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\n  \n 2023\n \n \n (84)\n \n \n
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\n \n\n \n \n \n \n \n \n Propionic acid induces alterations in mitochondrial morphology and dynamics in \\SH\\-\\SY5Y\\ cells.\n \n \n \n \n\n\n \n Buchanan, E.; Mahony, C.; Bam, S.; Jaffer, M.; Macleod, S.; Mangali, A.; Van Der Watt, M.; De Wet, S.; Theart, R.; Jacobs, C.; Loos, B.; and O'Ryan, C.\n\n\n \n\n\n\n Scientific Reports, 13(1): 13248. aug 2023.\n \n\n\n\n
\n\n\n\n \n \n \"PropionicPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{buchanan_propionic_2023,\nabstract = {Abstract\n\nPropionic acid (PPA) is used to study the role of mitochondrial dysfunction in neurodevelopmental conditions like autism spectrum disorders. PPA is known to disrupt mitochondrial biogenesis, metabolism, and turnover. However, the effect of PPA on mitochondrial dynamics, fission, and fusion remains challenging to study due to the complex temporal nature of these mechanisms. Here, we use complementary quantitative visualization techniques to examine how PPA influences mitochondrial ultrastructure, morphology, and dynamics in neuronal-like SH-SY5Y cells. PPA (5 mM) induced a significant decrease in mitochondrial area (\np\n{\\textless}0.01), Feret's diameter and perimeter (\np\n{\\textless}0.05), and in area\n2\n(\np\n{\\textless}0.01). Mitochondrial event localiser analysis demonstrated a significant increase in fission and fusion events (\np\n{\\textless}0.05) that preserved mitochondrial network integrity under stress. Moreover, mRNA expression of\ncMYC\n(\np\n{\\textless}0.0001),\nNRF1\n(\np\n{\\textless}0.01),\nTFAM\n(\np\n{\\textless}0.05),\nSTOML2\n(\np\n{\\textless}0.0001), and\nOPA1\n(\np\n{\\textless}0.01) was significantly decreased. This illustrates a remodeling of mitochondrial morphology, biogenesis, and dynamics to preserve function under stress. Our data provide new insights into the influence of PPA on mitochondrial dynamics and highlight the utility of visualization techniques to study the complex regulatory mechanisms involved in the mitochondrial stress response.},\nauthor = {Buchanan, Erin and Mahony, Caitlyn and Bam, Sophia and Jaffer, Mohamed and Macleod, Sarah and Mangali, Asandile and {Van Der Watt}, Mignon and {De Wet}, Sholto and Theart, Rensu and Jacobs, Caron and Loos, Ben and O'Ryan, Colleen},\ndoi = {10.1038/s41598-023-40130-8},\nfile = {:Users/jacquelinebracher/Zotero/storage/BBGUU6KB/Buchanan et al. - 2023 - Propionic acid induces alterations in mitochondria.pdf:pdf},\nissn = {2045-2322},\njournal = {Scientific Reports},\nmonth = {aug},\nnumber = {1},\npages = {13248},\ntitle = {{Propionic acid induces alterations in mitochondrial morphology and dynamics in {\\{}SH{\\}}-{\\{}SY5Y{\\}} cells}},\nurl = {https://www.nature.com/articles/s41598-023-40130-8},\nvolume = {13},\nyear = {2023}\n}\n
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\n Abstract Propionic acid (PPA) is used to study the role of mitochondrial dysfunction in neurodevelopmental conditions like autism spectrum disorders. PPA is known to disrupt mitochondrial biogenesis, metabolism, and turnover. However, the effect of PPA on mitochondrial dynamics, fission, and fusion remains challenging to study due to the complex temporal nature of these mechanisms. Here, we use complementary quantitative visualization techniques to examine how PPA influences mitochondrial ultrastructure, morphology, and dynamics in neuronal-like SH-SY5Y cells. PPA (5 mM) induced a significant decrease in mitochondrial area ( p \\textless0.01), Feret's diameter and perimeter ( p \\textless0.05), and in area 2 ( p \\textless0.01). Mitochondrial event localiser analysis demonstrated a significant increase in fission and fusion events ( p \\textless0.05) that preserved mitochondrial network integrity under stress. Moreover, mRNA expression of cMYC ( p \\textless0.0001), NRF1 ( p \\textless0.01), TFAM ( p \\textless0.05), STOML2 ( p \\textless0.0001), and OPA1 ( p \\textless0.01) was significantly decreased. This illustrates a remodeling of mitochondrial morphology, biogenesis, and dynamics to preserve function under stress. Our data provide new insights into the influence of PPA on mitochondrial dynamics and highlight the utility of visualization techniques to study the complex regulatory mechanisms involved in the mitochondrial stress response.\n
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\n \n\n \n \n \n \n \n \n Dehumanizing organizations: insidious effects of having one's human integrity denied at work.\n \n \n \n \n\n\n \n Baldissarri, C.; and Fourie, M. M\n\n\n \n\n\n\n Current Opinion in Behavioral Sciences, 49: 101244. feb 2023.\n \n\n\n\n
\n\n\n\n \n \n \"DehumanizingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{baldissarri_dehumanizing_2023,\nauthor = {Baldissarri, Cristina and Fourie, Melike M},\ndoi = {10.1016/j.cobeha.2022.101244},\nissn = {23521546},\njournal = {Current Opinion in Behavioral Sciences},\nmonth = {feb},\npages = {101244},\nshorttitle = {Dehumanizing organizations},\ntitle = {{Dehumanizing organizations: insidious effects of having one's human integrity denied at work}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S2352154622001504},\nvolume = {49},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Persistent accelerated epigenetic ageing in a longitudinal cohort of vertically infected \\HIV\\-positive adolescents.\n \n \n \n \n\n\n \n Heany, S. J; Levine, A. J; Lesosky, M.; Phillips, N.; Fouche, J.; Myer, L.; Zar, H. J; Stein, D. J; Horvath, S.; and Hoare, J.\n\n\n \n\n\n\n Journal of NeuroVirology, 29(3): 272–282. jun 2023.\n \n\n\n\n
\n\n\n\n \n \n \"PersistentPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{heany_persistent_2023,\nabstract = {Abstract\nWe have previously shown accelerated ageing in adolescents perinatally infected with HIV (PHIV +), based on discrepancies between epigenetic and chronological age. The current study examines follow-up longitudinal patterns of epigenetic ageing and the association of epigenetic ageing with cognition as well as whole brain structure changes in PHIV + and healthy controls enrolled in the Cape Town Adolescent Antiretroviral Cohort Study (CTAAC). The Illumina EPIC array was used to generate blood DNA methylation data from 60 PHIV + adolescents and 36 age-matched controls aged 9–12 years old at baseline and again at a 36-month follow-up. Epigenetic clock software estimated two measures of epigenetic age acceleration: extrinsic epigenetic accelerated ageing (EEAA) and age acceleration difference (AAD) at both time points. At follow-up, each participant completed neuropsychological testing, structural magnetic resonance imaging, and diffusion tensor imaging. At follow-up, PHIV infection remains associated with increased EEAA and AAD. Accelerated epigenetic ageing remained positively associated with viral load and negatively associated with CD4 ratio. EEAA was positively associated with whole brain grey matter volume and alterations in whole brain white matter integrity. AAD and EEAA were not associated with cognitive function within the PHIV + group. Measures of epigenetic ageing, as detected in DNA methylation patterns, remain increased in PHIV + adolescents across a 36-month period. Associations between epigenetic ageing measures, viral biomarkers, and alterations in brain micro- and macrostructure also persist at 36-month follow-up. Further study should determine if epigenetic age acceleration is associated with cognitive functional changes due to brain alterations in later life.},\nauthor = {Heany, Sarah J and Levine, Andrew J and Lesosky, Maia and Phillips, Nicole and Fouche, Jean-Paul and Myer, Landon and Zar, Heather J and Stein, Dan J and Horvath, Steve and Hoare, Jacqueline},\ndoi = {10.1007/s13365-023-01130-6},\nfile = {:Users/jacquelinebracher/Zotero/storage/Y38H36ZE/Heany et al. - 2023 - Persistent accelerated epigenetic ageing in a long.pdf:pdf},\nissn = {1355-0284, 1538-2443},\njournal = {Journal of NeuroVirology},\nmonth = {jun},\nnumber = {3},\npages = {272--282},\ntitle = {{Persistent accelerated epigenetic ageing in a longitudinal cohort of vertically infected {\\{}HIV{\\}}-positive adolescents}},\nurl = {https://link.springer.com/10.1007/s13365-023-01130-6},\nvolume = {29},\nyear = {2023}\n}\n
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\n Abstract We have previously shown accelerated ageing in adolescents perinatally infected with HIV (PHIV +), based on discrepancies between epigenetic and chronological age. The current study examines follow-up longitudinal patterns of epigenetic ageing and the association of epigenetic ageing with cognition as well as whole brain structure changes in PHIV + and healthy controls enrolled in the Cape Town Adolescent Antiretroviral Cohort Study (CTAAC). The Illumina EPIC array was used to generate blood DNA methylation data from 60 PHIV + adolescents and 36 age-matched controls aged 9–12 years old at baseline and again at a 36-month follow-up. Epigenetic clock software estimated two measures of epigenetic age acceleration: extrinsic epigenetic accelerated ageing (EEAA) and age acceleration difference (AAD) at both time points. At follow-up, each participant completed neuropsychological testing, structural magnetic resonance imaging, and diffusion tensor imaging. At follow-up, PHIV infection remains associated with increased EEAA and AAD. Accelerated epigenetic ageing remained positively associated with viral load and negatively associated with CD4 ratio. EEAA was positively associated with whole brain grey matter volume and alterations in whole brain white matter integrity. AAD and EEAA were not associated with cognitive function within the PHIV + group. Measures of epigenetic ageing, as detected in DNA methylation patterns, remain increased in PHIV + adolescents across a 36-month period. Associations between epigenetic ageing measures, viral biomarkers, and alterations in brain micro- and macrostructure also persist at 36-month follow-up. Further study should determine if epigenetic age acceleration is associated with cognitive functional changes due to brain alterations in later life.\n
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\n \n\n \n \n \n \n \n \n Epigenome-wide meta-analysis of prenatal maternal stressful life events and newborn \\DNA\\ methylation.\n \n \n \n \n\n\n \n Kotsakis Ruehlmann, A.; Sammallahti, S.; Cortés Hidalgo, A. P; Bakulski, K. M; Binder, E. B; Campbell, M. L.; Caramaschi, D.; Cecil, C. A M; Colicino, E.; Cruceanu, C.; Czamara, D.; Dieckmann, L.; Dou, J.; Felix, J. F; Frank, J.; Håberg, S. E; Herberth, G.; Hoang, T. T; Houtepen, L. C; Hüls, A.; Koen, N.; London, S. J; Magnus, M. C; Mancano, G.; Mulder, R. H; Page, C. M; Räikkönen, K.; Röder, S.; Schmidt, R. J; Send, T. S; Sharp, G.; Stein, D. J; Streit, F.; Tuhkanen, J.; Witt, S. H; Zar, H. J; Zenclussen, A. C; Zhang, Y.; Zillich, L.; Wright, R.; Lahti, J.; and Brunst, K. J\n\n\n \n\n\n\n Molecular Psychiatry. mar 2023.\n \n\n\n\n
\n\n\n\n \n \n \"Epigenome-widePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{kotsakis_ruehlmann_epigenome-wide_2023,\nauthor = {{Kotsakis Ruehlmann}, Anna and Sammallahti, Sara and {Cort{\\'{e}}s Hidalgo}, Andrea P and Bakulski, Kelly M and Binder, Elisabeth B and Campbell, Megan Loraine and Caramaschi, Doretta and Cecil, Charlotte A M and Colicino, Elena and Cruceanu, Cristiana and Czamara, Darina and Dieckmann, Linda and Dou, John and Felix, Janine F and Frank, Josef and H{\\aa}berg, Siri E and Herberth, Gunda and Hoang, Thanh T and Houtepen, Lotte C and H{\\"{u}}ls, Anke and Koen, Nastassja and London, Stephanie J and Magnus, Maria C and Mancano, Giulia and Mulder, Rosa H and Page, Christian M and R{\\"{a}}ikk{\\"{o}}nen, Katri and R{\\"{o}}der, Stefan and Schmidt, Rebecca J and Send, Tabea S and Sharp, Gemma and Stein, Dan J and Streit, Fabian and Tuhkanen, Johanna and Witt, Stephanie H and Zar, Heather J and Zenclussen, Ana C and Zhang, Yining and Zillich, Lea and Wright, Rosalind and Lahti, Jari and Brunst, Kelly J},\ndoi = {10.1038/s41380-023-02010-5},\nfile = {:Users/jacquelinebracher/Zotero/storage/HRTZ4GJV/Kotsakis Ruehlmann et al. - 2023 - Epigenome-wide meta-analysis of prenatal maternal .pdf:pdf},\nissn = {1359-4184, 1476-5578},\njournal = {Molecular Psychiatry},\nmonth = {mar},\ntitle = {{Epigenome-wide meta-analysis of prenatal maternal stressful life events and newborn {\\{}DNA{\\}} methylation}},\nurl = {https://www.nature.com/articles/s41380-023-02010-5},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Global multi‐center and multi‐modal magnetic resonance imaging study of obsessive‐compulsive disorder: \\Harmonization\\ and monitoring of protocols in healthy volunteers and phantoms.\n \n \n \n \n\n\n \n Pouwels, P. J W; Vriend, C.; Liu, F.; De Joode, N. T; Otaduy, M. C G; Pastorello, B.; Robertson, F. C; Venkatasubramanian, G.; Ipser, J.; Lee, S.; Batistuzzo, M. C; Hoexter, M. Q; Lochner, C.; Miguel, E. C; Narayanaswamy, J. C; Rao, R.; Janardhan Reddy, Y C; Shavitt, R. G; Sheshachala, K.; Stein, D. J; Van Balkom, A. J L M; Wall, M.; Simpson, H. B.; and Van Den Heuvel, O. A\n\n\n \n\n\n\n International Journal of Methods in Psychiatric Research, 32(1): e1931. mar 2023.\n \n\n\n\n
\n\n\n\n \n \n \"GlobalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{pouwels_global_2023,\nabstract = {Abstract\n\nObjectives\nWe describe the harmonized MRI acquisition and quality assessment of an ongoing global OCD study, with the aim to translate representative, well‐powered neuroimaging findings in neuropsychiatric research to worldwide populations.\n\n\nMethods\nWe report on T1‐weighted structural MRI, resting‐state functional MRI, and multi‐shell diffusion‐weighted imaging of 140 healthy participants (28 per site), two traveling controls, and regular phantom scans.\n\n\nResults\nHuman image quality measures (IQMs) and outcome measures showed smaller within‐site variation than between‐site variation. Outcome measures were less variable than IQMs, especially for the traveling controls. Phantom IQMs were stable regarding geometry, SNR, and mean diffusivity, while fMRI fluctuation was more variable between sites.\n\n\nConclusions\nVariation in IQMs persists, even for an a priori harmonized data acquisition protocol, but after pre‐processing they have less of an impact on the outcome measures. Continuous monitoring IQMs per site is valuable to detect potential artifacts and outliers. The inclusion of both cases and healthy participants at each site remains mandatory.},\nauthor = {Pouwels, Petra J W and Vriend, Chris and Liu, Feng and {De Joode}, Niels T and Otaduy, Maria C G and Pastorello, Bruno and Robertson, Frances C and Venkatasubramanian, Ganesan and Ipser, Jonathan and Lee, Seonjoo and Batistuzzo, Marcelo C and Hoexter, Marcelo Q and Lochner, Christine and Miguel, Euripedes C and Narayanaswamy, Janardhanan C and Rao, Rashmi and {Janardhan Reddy}, Y C and Shavitt, Roseli G and Sheshachala, Karthik and Stein, Dan J and {Van Balkom}, Anton J L M and Wall, Melanie and Simpson, Helen Blair and {Van Den Heuvel}, Odile A},\ndoi = {10.1002/mpr.1931},\nfile = {:Users/jacquelinebracher/Zotero/storage/JX86T8ET/Pouwels et al. - 2023 - Global multi‐center and multi‐modal magnetic reson.pdf:pdf},\nissn = {1049-8931, 1557-0657},\njournal = {International Journal of Methods in Psychiatric Research},\nmonth = {mar},\nnumber = {1},\npages = {e1931},\nshorttitle = {Global multi‐center and multi‐modal magnetic reson},\ntitle = {{Global multi‐center and multi‐modal magnetic resonance imaging study of obsessive‐compulsive disorder: {\\{}Harmonization{\\}} and monitoring of protocols in healthy volunteers and phantoms}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1002/mpr.1931},\nvolume = {32},\nyear = {2023}\n}\n
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\n Abstract Objectives We describe the harmonized MRI acquisition and quality assessment of an ongoing global OCD study, with the aim to translate representative, well‐powered neuroimaging findings in neuropsychiatric research to worldwide populations. Methods We report on T1‐weighted structural MRI, resting‐state functional MRI, and multi‐shell diffusion‐weighted imaging of 140 healthy participants (28 per site), two traveling controls, and regular phantom scans. Results Human image quality measures (IQMs) and outcome measures showed smaller within‐site variation than between‐site variation. Outcome measures were less variable than IQMs, especially for the traveling controls. Phantom IQMs were stable regarding geometry, SNR, and mean diffusivity, while fMRI fluctuation was more variable between sites. Conclusions Variation in IQMs persists, even for an a priori harmonized data acquisition protocol, but after pre‐processing they have less of an impact on the outcome measures. Continuous monitoring IQMs per site is valuable to detect potential artifacts and outliers. The inclusion of both cases and healthy participants at each site remains mandatory.\n
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\n \n\n \n \n \n \n \n \n What type of inclusion does epistemic injustice require?.\n \n \n \n \n\n\n \n Nyamnjoh, A.; and Ewuoso, C.\n\n\n \n\n\n\n Journal of Medical Ethics, 49(5): 341–342. may 2023.\n \n\n\n\n
\n\n\n\n \n \n \"WhatPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{nyamnjoh_what_2023,\nauthor = {Nyamnjoh, Anye-Nkwenti and Ewuoso, Cornelius},\ndoi = {10.1136/jme-2023-109091},\nissn = {0306-6800, 1473-4257},\njournal = {Journal of Medical Ethics},\nmonth = {may},\nnumber = {5},\npages = {341--342},\ntitle = {{What type of inclusion does epistemic injustice require?}},\nurl = {https://jme.bmj.com/lookup/doi/10.1136/jme-2023-109091},\nvolume = {49},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Freud's error.\n \n \n \n \n\n\n \n Solms, M.\n\n\n \n\n\n\n In The \\Ego\\ and the \\Id\\, pages 1–13. Routledge, London, 1 edition, may 2023.\n \n\n\n\n
\n\n\n\n \n \n \"Freud'sPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@incollection{busch_freuds_2023,\naddress = {London},\nauthor = {Solms, Mark},\nbooktitle = {The {\\{}Ego{\\}} and the {\\{}Id{\\}}},\ndoi = {10.4324/9781003336754-1},\nedition = {1},\nisbn = {978-1-00-333675-4},\nmonth = {may},\npages = {1--13},\npublisher = {Routledge},\ntitle = {{Freud's error}},\nurl = {https://www.taylorfrancis.com/books/9781003336754/chapters/10.4324/9781003336754-1},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Structural brain network connectivity in trichotillomania (hair-pulling disorder).\n \n \n \n \n\n\n \n Roos, A.; Fouche, J.; Stein, D. J; and Lochner, C.\n\n\n \n\n\n\n Brain Imaging and Behavior, 17(4): 395–402. aug 2023.\n \n\n\n\n
\n\n\n\n \n \n \"StructuralPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{roos_structural_2023,\nabstract = {Abstract\nNeuroimaging studies suggest involvement of frontal, striatal, limbic and cerebellar regions in trichotillomania, an obsessive-compulsive related disorder. However, findings regarding the underlying neural circuitry remains limited and inconsistent. Graph theoretical analysis offers a way to identify structural brain networks in trichotillomania. T1-weighted MRI scans were acquired in adult females with trichotillomania (n = 23) and healthy controls (n = 16). Graph theoretical analysis was used to investigate structural networks as derived from cortical thickness and volumetric FreeSurfer output. Hubs, brain regions with highest connectivity in the global network, were identified, and group differences were determined. Regions with highest connectivity on a regional level were also determined. There were no differences in small-worldness or other network measures between groups. Hubs in the global network of trichotillomania patients included temporal, parietal, and occipital regions (at 2SD above mean network connectivity), as well as frontal and striatal regions (at 1SD above mean network connectivity). In contrast, in healthy controls hubs at 2SD represented different frontal, parietal and temporal regions, while at 1SD hubs were widespread. The inferior temporal gyrus, involved in object recognition as part of the ventral visual pathway, had significantly higher connectivity on a global and regional level in trichotillomania. The study included women only and sample size was limited. This study adds to the trichotillomania literature on structural brain network connectivity. Our study findings are consistent with previous studies that have implicated somatosensory, sensorimotor and frontal-striatal circuitry in trichotillomania, and partially overlap with structural connectivity findings in obsessive-compulsive disorder.},\nauthor = {Roos, Annerine and Fouche, Jean-Paul and Stein, Dan J and Lochner, Christine},\ndoi = {10.1007/s11682-023-00767-5},\nfile = {:Users/jacquelinebracher/Zotero/storage/S8AQDCE8/Roos et al. - 2023 - Structural brain network connectivity in trichotil.pdf:pdf},\nissn = {1931-7557, 1931-7565},\njournal = {Brain Imaging and Behavior},\nmonth = {aug},\nnumber = {4},\npages = {395--402},\ntitle = {{Structural brain network connectivity in trichotillomania (hair-pulling disorder)}},\nurl = {https://link.springer.com/10.1007/s11682-023-00767-5},\nvolume = {17},\nyear = {2023}\n}\n
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\n Abstract Neuroimaging studies suggest involvement of frontal, striatal, limbic and cerebellar regions in trichotillomania, an obsessive-compulsive related disorder. However, findings regarding the underlying neural circuitry remains limited and inconsistent. Graph theoretical analysis offers a way to identify structural brain networks in trichotillomania. T1-weighted MRI scans were acquired in adult females with trichotillomania (n = 23) and healthy controls (n = 16). Graph theoretical analysis was used to investigate structural networks as derived from cortical thickness and volumetric FreeSurfer output. Hubs, brain regions with highest connectivity in the global network, were identified, and group differences were determined. Regions with highest connectivity on a regional level were also determined. There were no differences in small-worldness or other network measures between groups. Hubs in the global network of trichotillomania patients included temporal, parietal, and occipital regions (at 2SD above mean network connectivity), as well as frontal and striatal regions (at 1SD above mean network connectivity). In contrast, in healthy controls hubs at 2SD represented different frontal, parietal and temporal regions, while at 1SD hubs were widespread. The inferior temporal gyrus, involved in object recognition as part of the ventral visual pathway, had significantly higher connectivity on a global and regional level in trichotillomania. The study included women only and sample size was limited. This study adds to the trichotillomania literature on structural brain network connectivity. Our study findings are consistent with previous studies that have implicated somatosensory, sensorimotor and frontal-striatal circuitry in trichotillomania, and partially overlap with structural connectivity findings in obsessive-compulsive disorder.\n
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\n \n\n \n \n \n \n \n \n Population \\Pharmacokinetic\\ \\Analysis\\ of \\Rifampicin\\ in \\Plasma\\, \\Cerebrospinal\\ \\Fluid\\, and \\Brain\\ \\Extracellular\\ \\Fluid\\ in \\South\\ \\African\\ \\Children\\ with \\Tuberculous\\ \\Meningitis\\.\n \n \n \n \n\n\n \n Abdelgawad, N.; Tshavhungwe, M. (.; Rohlwink, U.; McIlleron, H.; Abdelwahab, M. T; Wiesner, L.; Castel, S.; Steele, C.; Enslin, J. (.; Thango, N. S.; Denti, P.; and Figaji, A.\n\n\n \n\n\n\n Antimicrobial Agents and Chemotherapy,e01474—-22. feb 2023.\n \n\n\n\n
\n\n\n\n \n \n \"PopulationPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{abdelgawad_population_2023,\nabstract = {Limited knowledge is available on the pharmacokinetics of rifampicin in children with tuberculous meningitis (TBM) and its penetration into brain tissue, which is the site of infection. In this analysis, we characterize the distribution of rifampicin in cerebrospinal fluid (CSF), lumbar (LCSF) and ventricular (VCSF), and brain extracellular fluid (ECF).\n, \nABSTRACT\nLimited knowledge is available on the pharmacokinetics of rifampicin in children with tuberculous meningitis (TBM) and its penetration into brain tissue, which is the site of infection. In this analysis, we characterize the distribution of rifampicin in cerebrospinal fluid (CSF), lumbar (LCSF) and ventricular (VCSF), and brain extracellular fluid (ECF). Children with TBM were included in this pharmacokinetic analysis. Sparse plasma, LCSF, and VCSF samples were collected opportunistically, as clinically indicated. Brain ECF was sampled using microdialysis (MD). Rifampicin was quantified with liquid chromatography with tandem mass spectrometry in all samples, and 25-desacetyl rifampicin in the plasma samples. The data were interpreted with nonlinear mixed-effects modeling, with the CSF and brain ECF modeled as “effect compartments.” Data were available from 61 children, with median (min-max) age of 2 (0.3 to 10) years and weight of 11.0 (4.8 to 49.0) kg. A one-compartment model for parent and metabolite with first-order absorption and elimination via saturable hepatic clearance described the data well. Allometric scaling, maturation, and auto-induction of clearance were included. The pseudopartition coefficient between plasma and LCSF/VCSF was {\\{}$\\backslash$textasciitilde{\\}}5{\\%}, while the value for ECF was only {\\{}$\\backslash$textasciitilde{\\}}0.5{\\%}, possibly reflecting low recovery of rifampicin using MD. The equilibration half-life between plasma and LCSF/VCSF was {\\{}$\\backslash$textasciitilde{\\}}4 h and between plasma and ECF {\\{}$\\backslash$textasciitilde{\\}}2 h. Our study confirms previous reports showing that rifampicin concentrations in the LCSF are lower than in plasma and provides novel knowledge about rifampicin in the VCSF and the brain tissue. Despite MD being semiquantitative because the relative recovery cannot be quantified, our study presents a proof-of-concept that rifampicin reaches the brain tissue and that MD is an attractive technique to study site-of-disease pharmacokinetics in TBM.},\nauthor = {Abdelgawad, Noha and Tshavhungwe, Mvuwo (Phophi) and Rohlwink, Ursula and McIlleron, Helen and Abdelwahab, Mahmoud T and Wiesner, Lubbe and Castel, Sandra and Steele, Chanel and Enslin, Johannes (Nico) and Thango, Nqobile Sindiswa and Denti, Paolo and Figaji, Anthony},\ndoi = {10.1128/aac.01474-22},\nfile = {:Users/jacquelinebracher/Zotero/storage/99IFNAEA/Abdelgawad et al. - 2023 - Population Pharmacokinetic Analysis of Rifampicin .pdf:pdf},\nissn = {0066-4804, 1098-6596},\njournal = {Antimicrobial Agents and Chemotherapy},\nmonth = {feb},\npages = {e01474----22},\ntitle = {{Population {\\{}Pharmacokinetic{\\}} {\\{}Analysis{\\}} of {\\{}Rifampicin{\\}} in {\\{}Plasma{\\}}, {\\{}Cerebrospinal{\\}} {\\{}Fluid{\\}}, and {\\{}Brain{\\}} {\\{}Extracellular{\\}} {\\{}Fluid{\\}} in {\\{}South{\\}} {\\{}African{\\}} {\\{}Children{\\}} with {\\{}Tuberculous{\\}} {\\{}Meningitis{\\}}}},\nurl = {https://journals.asm.org/doi/10.1128/aac.01474-22},\nyear = {2023}\n}\n
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\n Limited knowledge is available on the pharmacokinetics of rifampicin in children with tuberculous meningitis (TBM) and its penetration into brain tissue, which is the site of infection. In this analysis, we characterize the distribution of rifampicin in cerebrospinal fluid (CSF), lumbar (LCSF) and ventricular (VCSF), and brain extracellular fluid (ECF). , ABSTRACT Limited knowledge is available on the pharmacokinetics of rifampicin in children with tuberculous meningitis (TBM) and its penetration into brain tissue, which is the site of infection. In this analysis, we characterize the distribution of rifampicin in cerebrospinal fluid (CSF), lumbar (LCSF) and ventricular (VCSF), and brain extracellular fluid (ECF). Children with TBM were included in this pharmacokinetic analysis. Sparse plasma, LCSF, and VCSF samples were collected opportunistically, as clinically indicated. Brain ECF was sampled using microdialysis (MD). Rifampicin was quantified with liquid chromatography with tandem mass spectrometry in all samples, and 25-desacetyl rifampicin in the plasma samples. The data were interpreted with nonlinear mixed-effects modeling, with the CSF and brain ECF modeled as “effect compartments.” Data were available from 61 children, with median (min-max) age of 2 (0.3 to 10) years and weight of 11.0 (4.8 to 49.0) kg. A one-compartment model for parent and metabolite with first-order absorption and elimination via saturable hepatic clearance described the data well. Allometric scaling, maturation, and auto-induction of clearance were included. The pseudopartition coefficient between plasma and LCSF/VCSF was \\$\\$textasciitilde\\5%, while the value for ECF was only \\$\\$textasciitilde\\0.5%, possibly reflecting low recovery of rifampicin using MD. The equilibration half-life between plasma and LCSF/VCSF was \\$\\$textasciitilde\\4 h and between plasma and ECF \\$\\$textasciitilde\\2 h. Our study confirms previous reports showing that rifampicin concentrations in the LCSF are lower than in plasma and provides novel knowledge about rifampicin in the VCSF and the brain tissue. Despite MD being semiquantitative because the relative recovery cannot be quantified, our study presents a proof-of-concept that rifampicin reaches the brain tissue and that MD is an attractive technique to study site-of-disease pharmacokinetics in TBM.\n
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\n \n\n \n \n \n \n \n \n \\DNA\\ methylation as a potential mediator of the association between indoor air pollution and neurodevelopmental delay in a \\South\\ \\African\\ birth cohort.\n \n \n \n \n\n\n \n Feil, D.; Abrishamcar, S.; Christensen, G. M; Vanker, A.; Koen, N.; Kilanowski, A.; Hoffman, N.; Wedderburn, C. J; Donald, K. A; Kobor, M. S; Zar, H. J; Stein, D. J; and Hüls, A.\n\n\n \n\n\n\n Clinical Epigenetics, 15(1): 31. feb 2023.\n \n\n\n\n
\n\n\n\n \n \n \"\\DNA\\Paper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{feil_dna_2023,\nabstract = {Abstract\n\nBackground\n\nExposure to indoor air pollution during pregnancy has been linked to neurodevelopmental delay in toddlers. Epigenetic modification, particularly DNA methylation (DNAm), may explain this link. In this study, we employed three high-dimensional mediation analysis methods (HIMA, DACT, and gHMA) followed by causal mediation analysis to identify differentially methylated CpG sites and genes that mediate the association between indoor air pollution and neurodevelopmental delay. Analyses were performed using data from 142 mother to child pairs from a South African birth cohort, the Drakenstein Child Health Study. DNAm from cord blood was measured using the Infinium MethylationEPIC and HumanMethylation450 arrays. Neurodevelopment was assessed at age 2 years using the Bayley Scores of Infant and Toddler Development, 3rd edition across four domains (cognitive development, general adaptive behavior, language, and motor function). Particulate matter with an aerodynamic diameter of 10 $\\mu$m or less (PM\n10\n) was measured inside participants' homes during the second trimester of pregnancy.\n\n\n\nResults\n\nA total of 29 CpG sites and 4 genes (\nGOPC\n,\nRP11-74K11.1\n,\nDYRK1A\n,\nRNMT\n) were identified as significant mediators of the association between PM\n10\nand cognitive neurodevelopment. The estimated proportion mediated (95{\\%}-confidence interval) ranged from 0.29 [0.01, 0.86] for cg00694520 to 0.54 [0.11, 1.56] for cg05023582.\n\n\n\nConclusions\n\nOur findings suggest that DNAm may mediate the association between prenatal PM\n10\nexposure and cognitive neurodevelopment.\nDYRK1A\nand several genes that our CpG sites mapped to, including\nCNKSR1, IPO13, IFNGR1, LONP2,\nand\nCDH1,\nare associated with biological pathways implicated in cognitive neurodevelopment and three of our identified CpG sites (cg23560546 [\nDAPL1\n], cg22572779 [\nC6orf218\n], cg15000966 [\nNT5C\n]) have been previously associated with fetal brain development. These findings are novel and add to the limited literature investigating the relationship between indoor air pollution, DNAm, and neurodevelopment, particularly in low- and middle-income country settings and non-white populations.},\nauthor = {Feil, Dakotah and Abrishamcar, Sarina and Christensen, Grace M and Vanker, Aneesa and Koen, Nastassja and Kilanowski, Anna and Hoffman, Nadia and Wedderburn, Catherine J and Donald, Kirsten A and Kobor, Michael S and Zar, Heather J and Stein, Dan J and H{\\"{u}}ls, Anke},\ndoi = {10.1186/s13148-023-01444-6},\nfile = {:Users/jacquelinebracher/Zotero/storage/MZ8RS9MI/Feil et al. - 2023 - DNA methylation as a potential mediator of the ass.pdf:pdf},\nissn = {1868-7083},\njournal = {Clinical Epigenetics},\nmonth = {feb},\nnumber = {1},\npages = {31},\ntitle = {{{\\{}DNA{\\}} methylation as a potential mediator of the association between indoor air pollution and neurodevelopmental delay in a {\\{}South{\\}} {\\{}African{\\}} birth cohort}},\nurl = {https://clinicalepigeneticsjournal.biomedcentral.com/articles/10.1186/s13148-023-01444-6},\nvolume = {15},\nyear = {2023}\n}\n
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\n Abstract Background Exposure to indoor air pollution during pregnancy has been linked to neurodevelopmental delay in toddlers. Epigenetic modification, particularly DNA methylation (DNAm), may explain this link. In this study, we employed three high-dimensional mediation analysis methods (HIMA, DACT, and gHMA) followed by causal mediation analysis to identify differentially methylated CpG sites and genes that mediate the association between indoor air pollution and neurodevelopmental delay. Analyses were performed using data from 142 mother to child pairs from a South African birth cohort, the Drakenstein Child Health Study. DNAm from cord blood was measured using the Infinium MethylationEPIC and HumanMethylation450 arrays. Neurodevelopment was assessed at age 2 years using the Bayley Scores of Infant and Toddler Development, 3rd edition across four domains (cognitive development, general adaptive behavior, language, and motor function). Particulate matter with an aerodynamic diameter of 10 $μ$m or less (PM 10 ) was measured inside participants' homes during the second trimester of pregnancy. Results A total of 29 CpG sites and 4 genes ( GOPC , RP11-74K11.1 , DYRK1A , RNMT ) were identified as significant mediators of the association between PM 10 and cognitive neurodevelopment. The estimated proportion mediated (95%-confidence interval) ranged from 0.29 [0.01, 0.86] for cg00694520 to 0.54 [0.11, 1.56] for cg05023582. Conclusions Our findings suggest that DNAm may mediate the association between prenatal PM 10 exposure and cognitive neurodevelopment. DYRK1A and several genes that our CpG sites mapped to, including CNKSR1, IPO13, IFNGR1, LONP2, and CDH1, are associated with biological pathways implicated in cognitive neurodevelopment and three of our identified CpG sites (cg23560546 [ DAPL1 ], cg22572779 [ C6orf218 ], cg15000966 [ NT5C ]) have been previously associated with fetal brain development. These findings are novel and add to the limited literature investigating the relationship between indoor air pollution, DNAm, and neurodevelopment, particularly in low- and middle-income country settings and non-white populations.\n
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\n \n\n \n \n \n \n \n \n Romantic relationship dissolutions are significantly associated with posttraumatic stress symptoms as compared to a \\DSM\\-5 \\Criterion\\ \\A\\ event: a case-case–control comparison.\n \n \n \n \n\n\n \n Van Der Watt, A. S. J.; Kidd, M.; Roos, A.; Lesch, E.; and Seedat, S.\n\n\n \n\n\n\n European Journal of Psychotraumatology, 14(2): 2238585. nov 2023.\n \n\n\n\n
\n\n\n\n \n \n \"RomanticPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{van_der_watt_romantic_2023,\nauthor = {{Van Der Watt}, Alberta Susanna Johanna and Kidd, Martin and Roos, Annerine and Lesch, Elmien and Seedat, Soraya},\ndoi = {10.1080/20008066.2023.2238585},\nfile = {:Users/jacquelinebracher/Zotero/storage/JYS2PD7H/Van Der Watt et al. - 2023 - Romantic relationship dissolutions are significant.pdf:pdf},\nissn = {2000-8066},\njournal = {European Journal of Psychotraumatology},\nmonth = {nov},\nnumber = {2},\npages = {2238585},\nshorttitle = {Romantic relationship dissolutions are significant},\ntitle = {{Romantic relationship dissolutions are significantly associated with posttraumatic stress symptoms as compared to a {\\{}DSM{\\}}-5 {\\{}Criterion{\\}} {\\{}A{\\}} event: a case-case–control comparison}},\nurl = {https://www.tandfonline.com/doi/full/10.1080/20008066.2023.2238585},\nvolume = {14},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Predictors of within-individual variability in cognitive performance in schizophrenia in a \\South\\ \\African\\ case–control study.\n \n \n \n \n\n\n \n Wootton, O.; Dalvie, S.; MacGinty, R.; Ngqengelele, L.; Susser, E. S; Gur, R. C; and Stein, D. J\n\n\n \n\n\n\n Acta Neuropsychiatrica,1–7. jun 2023.\n \n\n\n\n
\n\n\n\n \n \n \"PredictorsPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{wootton_predictors_2023,\nabstract = {Abstract\n\nIntroduction:\nCognitive dysfunction in schizophrenia may be assessed by measuring within-individual variability (WIV) in performance across a range of cognitive tests. Previous studies have found increased WIV in people with schizophrenia, but no studies have been conducted in low- to middle-income countries where the different sociocultural context may affect WIV. We sought to address this gap by exploring the relationship between WIV and a range of clinical and demographic variables in a large study of people with schizophrenia and matched controls in South Africa.\n\n\nMethods:\n544 people with schizophrenia and 861 matched controls completed an adapted version of The University of Pennsylvania Computerized Neurocognitive Battery (PennCNB). Demographic and clinical information was collected using the Structured Clinical Interview for DSM-IV Diagnoses. Across-task WIV for performance speed and accuracy on the PennCNB was calculated. Multivariate linear regression was used to assess the relationship between WIV and a diagnosis of schizophrenia in the whole sample, and WIV and selected demographic and clinical variables in people with schizophrenia.\n\n\nResults:\nIncreased WIV of performance speed across cognitive tests was significantly associated with a diagnosis of schizophrenia. In people with schizophrenia, increased speed WIV was associated with older age, a lower level of education and a lower score on the Global Assessment of Functioning scale. Increased accuracy WIV was significantly associated with a younger age in people with schizophrenia.\n\n\nConclusions:\nMeasurements of WIV of performance speed can add to the knowledge gained from studies of cognitive dysfunction in schizophrenia in resource-limited settings.},\nauthor = {Wootton, Olivia and Dalvie, Shareefa and MacGinty, Rae and Ngqengelele, Linda and Susser, Ezra S and Gur, Ruben C and Stein, Dan J},\ndoi = {10.1017/neu.2023.28},\nfile = {:Users/jacquelinebracher/Zotero/storage/NMTEYEZ3/Wootton et al. - 2023 - Predictors of within-individual variability in cog.pdf:pdf},\nissn = {0924-2708, 1601-5215},\njournal = {Acta Neuropsychiatrica},\nmonth = {jun},\npages = {1--7},\ntitle = {{Predictors of within-individual variability in cognitive performance in schizophrenia in a {\\{}South{\\}} {\\{}African{\\}} case–control study}},\nurl = {https://www.cambridge.org/core/product/identifier/S0924270823000285/type/journal{\\_}article},\nyear = {2023}\n}\n
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\n Abstract Introduction: Cognitive dysfunction in schizophrenia may be assessed by measuring within-individual variability (WIV) in performance across a range of cognitive tests. Previous studies have found increased WIV in people with schizophrenia, but no studies have been conducted in low- to middle-income countries where the different sociocultural context may affect WIV. We sought to address this gap by exploring the relationship between WIV and a range of clinical and demographic variables in a large study of people with schizophrenia and matched controls in South Africa. Methods: 544 people with schizophrenia and 861 matched controls completed an adapted version of The University of Pennsylvania Computerized Neurocognitive Battery (PennCNB). Demographic and clinical information was collected using the Structured Clinical Interview for DSM-IV Diagnoses. Across-task WIV for performance speed and accuracy on the PennCNB was calculated. Multivariate linear regression was used to assess the relationship between WIV and a diagnosis of schizophrenia in the whole sample, and WIV and selected demographic and clinical variables in people with schizophrenia. Results: Increased WIV of performance speed across cognitive tests was significantly associated with a diagnosis of schizophrenia. In people with schizophrenia, increased speed WIV was associated with older age, a lower level of education and a lower score on the Global Assessment of Functioning scale. Increased accuracy WIV was significantly associated with a younger age in people with schizophrenia. Conclusions: Measurements of WIV of performance speed can add to the knowledge gained from studies of cognitive dysfunction in schizophrenia in resource-limited settings.\n
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\n \n\n \n \n \n \n \n \n Cognitive \\Impairment\\ in \\Tuberculous\\ \\Meningitis\\.\n \n \n \n \n\n\n \n Davis, A. G; Dreyer, A. J; Albertyn, C.; Maxebengula, M.; Stek, C.; Wasserman, S.; Marais, S.; Bateman, K.; Solms, M.; Joska, J.; Wilkinson, R. J; and Nightingale, S.\n\n\n \n\n\n\n Clinical Infectious Diseases, 76(5): 842–849. mar 2023.\n \n\n\n\n
\n\n\n\n \n \n \"CognitivePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{davis_cognitive_2023,\nabstract = {Abstract\n\nBackground\nCognitive impairment is reported as a common complication in adult tuberculous meningitis (TBM), yet few studies have systematically assessed the frequency and nature of impairment. Moreover, the impact of impairment on functioning and medication adherence has not been described.\n\n\nMethods\nA cognitive test battery (10 measures assessing 7 cognitive domains) was administered to 34 participants with human immunodeficiency virus (HIV)–associated TBM 6 months after diagnosis. Cognitive performance was compared with that a comparator group of 66 people with HIV without a history of tuberculosis. A secondary comparison was made between participants with TBM and 26 participants with HIV 6 months after diagnosis of tuberculosis outside the central nervous system (CNS). Impact on functioning was evaluated, including through assessment of medication adherence.\n\n\nResults\nOf 34 participants with TBM, 16 (47{\\%}) had low performance on cognitive testing. Cognition was impaired across all domains. Global cognitive performance was significantly lower in participants with TBM than in people with HIV (mean T score, 41 vs 48, respectively; P {\\textless} .001). These participants also had lower global cognition scores than those with non-CNS tuberculosis (mean global T score, 41 vs 46; P = .02). Functional outcomes were not significantly correlated with cognitive performance in the subgroup of participants in whom this was assessed (n = 19).\n\n\nConclusions\nLow cognitive performance following HIV-associated TBM is common. This effect is independent of, and additional to, effects of HIV and non-CNS tuberculosis disease. Further studies are needed to understand longer-term outcomes, clarify the association with treatment adherence, a key predictor of outcome in TBM, and develop context-specific tools to identify individuals with cognitive difficulties in order to improve outcomes in TBM.},\nauthor = {Davis, Angharad G and Dreyer, Anna J and Albertyn, Christine and Maxebengula, Mpumi and Stek, Cari and Wasserman, Sean and Marais, Suzaan and Bateman, Kathleen and Solms, Mark and Joska, John and Wilkinson, Robert J and Nightingale, Sam},\ndoi = {10.1093/cid/ciac831},\nfile = {:Users/jacquelinebracher/Zotero/storage/3MLP7SL4/Davis et al. - 2023 - Cognitive Impairment in Tuberculous Meningitis.pdf:pdf},\nissn = {1058-4838, 1537-6591},\njournal = {Clinical Infectious Diseases},\nmonth = {mar},\nnumber = {5},\npages = {842--849},\ntitle = {{Cognitive {\\{}Impairment{\\}} in {\\{}Tuberculous{\\}} {\\{}Meningitis{\\}}}},\nurl = {https://academic.oup.com/cid/article/76/5/842/6763738},\nvolume = {76},\nyear = {2023}\n}\n
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\n Abstract Background Cognitive impairment is reported as a common complication in adult tuberculous meningitis (TBM), yet few studies have systematically assessed the frequency and nature of impairment. Moreover, the impact of impairment on functioning and medication adherence has not been described. Methods A cognitive test battery (10 measures assessing 7 cognitive domains) was administered to 34 participants with human immunodeficiency virus (HIV)–associated TBM 6 months after diagnosis. Cognitive performance was compared with that a comparator group of 66 people with HIV without a history of tuberculosis. A secondary comparison was made between participants with TBM and 26 participants with HIV 6 months after diagnosis of tuberculosis outside the central nervous system (CNS). Impact on functioning was evaluated, including through assessment of medication adherence. Results Of 34 participants with TBM, 16 (47%) had low performance on cognitive testing. Cognition was impaired across all domains. Global cognitive performance was significantly lower in participants with TBM than in people with HIV (mean T score, 41 vs 48, respectively; P \\textless .001). These participants also had lower global cognition scores than those with non-CNS tuberculosis (mean global T score, 41 vs 46; P = .02). Functional outcomes were not significantly correlated with cognitive performance in the subgroup of participants in whom this was assessed (n = 19). Conclusions Low cognitive performance following HIV-associated TBM is common. This effect is independent of, and additional to, effects of HIV and non-CNS tuberculosis disease. Further studies are needed to understand longer-term outcomes, clarify the association with treatment adherence, a key predictor of outcome in TBM, and develop context-specific tools to identify individuals with cognitive difficulties in order to improve outcomes in TBM.\n
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\n \n\n \n \n \n \n \n \n Cerebral organoids as an in vitro model to study autism spectrum disorders.\n \n \n \n \n\n\n \n Rabeling, A.; and Goolam, M.\n\n\n \n\n\n\n Gene Therapy, 30(9): 659–669. sep 2023.\n \n\n\n\n
\n\n\n\n \n \n \"CerebralPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{rabeling_cerebral_2023,\nauthor = {Rabeling, Alexa and Goolam, Mubeen},\ndoi = {10.1038/s41434-022-00356-z},\nissn = {0969-7128, 1476-5462},\njournal = {Gene Therapy},\nmonth = {sep},\nnumber = {9},\npages = {659--669},\ntitle = {{Cerebral organoids as an in vitro model to study autism spectrum disorders}},\nurl = {https://www.nature.com/articles/s41434-022-00356-z},\nvolume = {30},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Volume of subcortical brain regions in social anxiety disorder: mega-analytic results from 37 samples in the \\ENIGMA\\-\\Anxiety\\ \\Working\\ \\Group\\.\n \n \n \n \n\n\n \n Groenewold, N. A; Bas-Hoogendam, J. M.; Amod, A. R; Laansma, M. A; Van Velzen, L. S; Aghajani, M.; Hilbert, K.; Oh, H.; Salas, R.; Jackowski, A. P; Pan, P. M; Salum, G. A; Blair, J. R; Blair, K. S; Hirsch, J.; Pantazatos, S. P; Schneier, F. R; Talati, A.; Roelofs, K.; Volman, I.; Blanco-Hinojo, L.; Cardoner, N.; Pujol, J.; Beesdo-Baum, K.; Ching, C. R K; Thomopoulos, S. I; Jansen, A.; Kircher, T.; Krug, A.; Nenadić, I.; Stein, F.; Dannlowski, U.; Grotegerd, D.; Lemke, H.; Meinert, S.; Winter, A.; Erb, M.; Kreifelts, B.; Gong, Q.; Lui, S.; Zhu, F.; Mwangi, B.; Soares, J. C; Wu, M.; Bayram, A.; Canli, M.; Tükel, R.; Westenberg, P M.; Heeren, A.; Cremers, H. R; Hofmann, D.; Straube, T.; Doruyter, A. G G; Lochner, C.; Peterburs, J.; Van Tol, M.; Gur, R. E; Kaczkurkin, A. N; Larsen, B.; Satterthwaite, T. D; Filippi, C. A; Gold, A. L; Harrewijn, A.; Zugman, A.; Bülow, R.; Grabe, H. J; Völzke, H.; Wittfeld, K.; Böhnlein, J.; Dohm, K.; Kugel, H.; Schrammen, E.; Zwanzger, P.; Leehr, E. J; Sindermann, L.; Ball, T. M; Fonzo, G. A; Paulus, M. P; Simmons, A.; Stein, M. B; Klumpp, H.; Phan, K L.; Furmark, T.; Månsson, K. N T; Manzouri, A.; Avery, S. N; Blackford, J. U.; Clauss, J. A; Feola, B.; Harper, J. C; Sylvester, C. M; Lueken, U.; Veltman, D. J; Winkler, A. M; Jahanshad, N.; Pine, D. S; Thompson, P. M; Stein, D. J; and Van Der Wee, N. J A\n\n\n \n\n\n\n Molecular Psychiatry, 28(3): 1079–1089. mar 2023.\n \n\n\n\n
\n\n\n\n \n \n \"VolumePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{groenewold_volume_2023,\nauthor = {Groenewold, Nynke A and Bas-Hoogendam, Janna Marie and Amod, Alyssa R and Laansma, Max A and {Van Velzen}, Laura S and Aghajani, Moji and Hilbert, Kevin and Oh, Hyuntaek and Salas, Ramiro and Jackowski, Andrea P and Pan, Pedro M and Salum, Giovanni A and Blair, James R and Blair, Karina S and Hirsch, Joy and Pantazatos, Spiro P and Schneier, Franklin R and Talati, Ardesheer and Roelofs, Karin and Volman, Inge and Blanco-Hinojo, Laura and Cardoner, Narc{\\'{i}}s and Pujol, Jesus and Beesdo-Baum, Katja and Ching, Christopher R K and Thomopoulos, Sophia I and Jansen, Andreas and Kircher, Tilo and Krug, Axel and Nenadi{\\'{c}}, Igor and Stein, Frederike and Dannlowski, Udo and Grotegerd, Dominik and Lemke, Hannah and Meinert, Susanne and Winter, Alexandra and Erb, Michael and Kreifelts, Benjamin and Gong, Qiyong and Lui, Su and Zhu, Fei and Mwangi, Benson and Soares, Jair C and Wu, Mon-Ju and Bayram, Ali and Canli, Mesut and T{\\"{u}}kel, Raşit and Westenberg, P Michiel and Heeren, Alexandre and Cremers, Henk R and Hofmann, David and Straube, Thomas and Doruyter, Alexander G G and Lochner, Christine and Peterburs, Jutta and {Van Tol}, Marie-Jos{\\'{e}} and Gur, Raquel E and Kaczkurkin, Antonia N and Larsen, Bart and Satterthwaite, Theodore D and Filippi, Courtney A and Gold, Andrea L and Harrewijn, Anita and Zugman, Andr{\\'{e}} and B{\\"{u}}low, Robin and Grabe, Hans J and V{\\"{o}}lzke, Henry and Wittfeld, Katharina and B{\\"{o}}hnlein, Joscha and Dohm, Katharina and Kugel, Harald and Schrammen, Elisabeth and Zwanzger, Peter and Leehr, Elisabeth J and Sindermann, Lisa and Ball, Tali M and Fonzo, Gregory A and Paulus, Martin P and Simmons, Alan and Stein, Murray B and Klumpp, Heide and Phan, K Luan and Furmark, Tomas and M{\\aa}nsson, Kristoffer N T and Manzouri, Amirhossein and Avery, Suzanne N and Blackford, Jennifer Urbano and Clauss, Jacqueline A and Feola, Brandee and Harper, Jennifer C and Sylvester, Chad M and Lueken, Ulrike and Veltman, Dick J and Winkler, Anderson M and Jahanshad, Neda and Pine, Daniel S and Thompson, Paul M and Stein, Dan J and {Van Der Wee}, Nic J A},\ndoi = {10.1038/s41380-022-01933-9},\nissn = {1359-4184, 1476-5578},\njournal = {Molecular Psychiatry},\nmonth = {mar},\nnumber = {3},\npages = {1079--1089},\nshorttitle = {Volume of subcortical brain regions in social anxi},\ntitle = {{Volume of subcortical brain regions in social anxiety disorder: mega-analytic results from 37 samples in the {\\{}ENIGMA{\\}}-{\\{}Anxiety{\\}} {\\{}Working{\\}} {\\{}Group{\\}}}},\nurl = {https://www.nature.com/articles/s41380-022-01933-9},\nvolume = {28},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Has maternal sensitivity been comprehensively investigated in sub-\\Saharan\\ \\Africa\\? \\A\\ narrative scoping review.\n \n \n \n \n\n\n \n Prag, A; Donald, K A; Weldon, E; Halligan, S L; Stein, D J; and Malcolm-Smith, S\n\n\n \n\n\n\n Acta Neuropsychiatrica,1–18. mar 2023.\n \n\n\n\n
\n\n\n\n \n \n \"HasPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{prag_has_2023,\nabstract = {Abstract\nChild development is strongly influenced by maternal characteristics. Maternal sensitivity, as well as risks to and outcomes of sensitive maternal style, are well studied in industrialised western contexts, but it is unclear if this is the case for other contexts. Sub-Saharan Africa has been subjected to and continues to negotiate socio-economic and psychological sequelae of colonial and race-based politics: exploring the nature and outcomes of early caregiver input in such challenging conditions is imperative. This scoping review thus aims to 1) evaluate the nature and extent of quantified observational assessments of dyadic interactions, with a focus on maternal sensitivity, in Sub-Saharan Africa and 2) ascertain which risk and outcome factors have been examined in relation to maternal sensitivity. Study quality and cross-cultural appropriateness will also be considered. The search using expanded search terms yielded 20 papers –four characterizing maternal sensitivity or style, eight examining maternal sensitivity in relation to risks and outcomes, and eight intervention studies examining efforts to improve maternal sensitivity. Most research was conducted in South Africa – only seven studies were conducted in four other countries. Researchers used a wide array of coding schemes, mostly developed in the west. Ten studies made some adaptations to measures. Language issues and cultural considerations were often not explicitly addressed. Taken together, very limited research on this important topic exists. For the work that does exist, questions around westernized assumptions, language, and appropriateness of measures remain. Substantially more research, informed by both culturally flexible conceptualizations and methodological rigour, is required.},\nauthor = {Prag, A and Donald, K A and Weldon, E and Halligan, S L and Stein, D J and Malcolm-Smith, S},\ndoi = {10.1017/neu.2023.20},\nissn = {0924-2708, 1601-5215},\njournal = {Acta Neuropsychiatrica},\nmonth = {mar},\npages = {1--18},\nshorttitle = {Has maternal sensitivity been comprehensively inve},\ntitle = {{Has maternal sensitivity been comprehensively investigated in sub-{\\{}Saharan{\\}} {\\{}Africa{\\}}? {\\{}A{\\}} narrative scoping review}},\nurl = {https://www.cambridge.org/core/product/identifier/S0924270823000200/type/journal{\\_}article},\nyear = {2023}\n}\n
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\n Abstract Child development is strongly influenced by maternal characteristics. Maternal sensitivity, as well as risks to and outcomes of sensitive maternal style, are well studied in industrialised western contexts, but it is unclear if this is the case for other contexts. Sub-Saharan Africa has been subjected to and continues to negotiate socio-economic and psychological sequelae of colonial and race-based politics: exploring the nature and outcomes of early caregiver input in such challenging conditions is imperative. This scoping review thus aims to 1) evaluate the nature and extent of quantified observational assessments of dyadic interactions, with a focus on maternal sensitivity, in Sub-Saharan Africa and 2) ascertain which risk and outcome factors have been examined in relation to maternal sensitivity. Study quality and cross-cultural appropriateness will also be considered. The search using expanded search terms yielded 20 papers –four characterizing maternal sensitivity or style, eight examining maternal sensitivity in relation to risks and outcomes, and eight intervention studies examining efforts to improve maternal sensitivity. Most research was conducted in South Africa – only seven studies were conducted in four other countries. Researchers used a wide array of coding schemes, mostly developed in the west. Ten studies made some adaptations to measures. Language issues and cultural considerations were often not explicitly addressed. Taken together, very limited research on this important topic exists. For the work that does exist, questions around westernized assumptions, language, and appropriateness of measures remain. Substantially more research, informed by both culturally flexible conceptualizations and methodological rigour, is required.\n
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\n \n\n \n \n \n \n \n \n Mouse \\Organotypic\\ \\Brain\\ \\Slice\\ \\Cultures\\: \\A\\ \\Novel\\ \\Model\\ for \\Studying\\ \\Neuroimmune\\ \\Responses\\ to \\Cryptococcal\\ \\Brain\\ \\Infections\\.\n \n \n \n \n\n\n \n Awala, A. N; Kauchali, M.; De Lange, A.; Higgitt, E. R.; Mbangiwa, T.; Raimondo, J. V; and Dangarembizi, R.\n\n\n \n\n\n\n In Drummond, R. A, editor(s), Antifungal \\Immunity\\, volume 2667, pages 31–45. Springer US, New York, NY, 2023.\n \n\n\n\n
\n\n\n\n \n \n \"MousePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@incollection{drummond_mouse_2023,\naddress = {New York, NY},\nannote = {Series Title: Methods in Molecular Biology},\nauthor = {Awala, Amalia N and Kauchali, Maahir and {De Lange}, Anja and Higgitt, Emily Ruth and Mbangiwa, Tshepiso and Raimondo, Joseph V and Dangarembizi, Rachael},\nbooktitle = {Antifungal {\\{}Immunity{\\}}},\ndoi = {10.1007/978-1-0716-3199-7_3},\neditor = {Drummond, Rebecca A},\nisbn = {978-1-07-163198-0 978-1-07-163199-7},\npages = {31--45},\npublisher = {Springer US},\nshorttitle = {Mouse {\\{}Organotypic{\\}} {\\{}Brain{\\}} {\\{}Slice{\\}} {\\{}Cultures{\\}}},\ntitle = {{Mouse {\\{}Organotypic{\\}} {\\{}Brain{\\}} {\\{}Slice{\\}} {\\{}Cultures{\\}}: {\\{}A{\\}} {\\{}Novel{\\}} {\\{}Model{\\}} for {\\{}Studying{\\}} {\\{}Neuroimmune{\\}} {\\{}Responses{\\}} to {\\{}Cryptococcal{\\}} {\\{}Brain{\\}} {\\{}Infections{\\}}}},\nurl = {https://link.springer.com/10.1007/978-1-0716-3199-7{\\_}3},\nvolume = {2667},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n The \\Global\\ \\Task\\ \\Force\\ for \\Chronic\\ \\Pain\\ in \\People\\ with \\HIV\\ (\\PWH\\): \\Developing\\ a research agenda in an emerging field.\n \n \n \n \n\n\n \n Merlin, J. S; Hamm, M; De Abril Cameron, F; Baker, V; Brown, D A; Cherry, C L; Edelman, E J; Evangeli, M; Harding, R; Josh, J; Kemp, H I; Lichius, C; Madden, V J; Nkhoma, K; O'Brien, K K; Parker, R; Rice, A; Robinson-Papp, J; Sabin, C A; Slawek, D; Scott, W; Tsui, J I; Uebelacker, L A; Wadley, A L; and Goodin, B R\n\n\n \n\n\n\n AIDS Care, 35(8): 1215–1223. aug 2023.\n \n\n\n\n
\n\n\n\n \n \n \"ThePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{merlin_global_2023,\nauthor = {Merlin, Jessica S and Hamm, M and {De Abril Cameron}, F and Baker, V and Brown, D A and Cherry, C L and Edelman, E J and Evangeli, M and Harding, R and Josh, J and Kemp, H I and Lichius, C and Madden, V J and Nkhoma, K and O'Brien, K K and Parker, R and Rice, A and Robinson-Papp, J and Sabin, C A and Slawek, D and Scott, W and Tsui, J I and Uebelacker, L A and Wadley, A L and Goodin, B R},\ndoi = {10.1080/09540121.2021.1902936},\nissn = {0954-0121, 1360-0451},\njournal = {AIDS Care},\nmonth = {aug},\nnumber = {8},\npages = {1215--1223},\nshorttitle = {The {\\{}Global{\\}} {\\{}Task{\\}} {\\{}Force{\\}} for {\\{}Chronic{\\}} {\\{}Pain{\\}} i},\ntitle = {{The {\\{}Global{\\}} {\\{}Task{\\}} {\\{}Force{\\}} for {\\{}Chronic{\\}} {\\{}Pain{\\}} in {\\{}People{\\}} with {\\{}HIV{\\}} ({\\{}PWH{\\}}): {\\{}Developing{\\}} a research agenda in an emerging field}},\nurl = {https://www.tandfonline.com/doi/full/10.1080/09540121.2021.1902936},\nvolume = {35},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n (\\Not\\) part of the team: \\Racial\\ empathy bias in a \\South\\ \\African\\ minimal group study.\n \n \n \n \n\n\n \n Deist, M.; and Fourie, M. M\n\n\n \n\n\n\n PLOS ONE, 18(4): e0283902. apr 2023.\n \n\n\n\n
\n\n\n\n \n \n \"(\\Not\\)Paper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{deist_not_2023,\nabstract = {Minimal Group Paradigm (MGP) research suggests that recategorization with an arbitrarily defined group may be sufficient to override empathy biases among salient social categories like race. However, most studies utilizing MGPs do not consider sufficiently the socio-historical contexts of social groups. Here we investigated whether the recategorization of White participants into arbitrarily defined mixed-race teams using a non-competitive MGP would ameliorate racial empathy biases towards ingroup team members in the South African context. Sixty participants rated their empathic and counter-empathic (\nSchadenfreude\n,\nGl{\\"{u}}ckschmerz\n) responses to ingroup and outgroup team members in physically painful, emotionally distressing, and positive situations. As anticipated, results indicated significant ingroup team biases in empathic and counter-empathic responses. However, mixed-race minimal teams were unable to override ingroup racial empathy biases, which persisted across events. Interestingly, a manipulation highlighting purported political ideological differences between White and Black African team members did not exacerbate racial empathy bias, suggesting that such perceptions were already salient. Across conditions, an internal motivation to respond without prejudice was most strongly associated with empathy for Black African target individuals, regardless of their team status. Together, these results suggest that racial identity continues to provide a salient motivational guide in addition to more arbitrary group memberships, even at an explicit level, for empathic responding in contexts characterized by historical power asymmetry. These data further problematize the continued official use of race-based categories in such contexts.},\nauthor = {Deist, Melanie and Fourie, Melike M},\ndoi = {10.1371/journal.pone.0283902},\neditor = {Weinberg, Ashley},\nfile = {:Users/jacquelinebracher/Zotero/storage/ZV72V7WQ/Deist and Fourie - 2023 - (Not) part of the team Racial empathy bias in a S.pdf:pdf},\nissn = {1932-6203},\njournal = {PLOS ONE},\nmonth = {apr},\nnumber = {4},\npages = {e0283902},\nshorttitle = {({\\{}Not{\\}}) part of the team},\ntitle = {{({\\{}Not{\\}}) part of the team: {\\{}Racial{\\}} empathy bias in a {\\{}South{\\}} {\\{}African{\\}} minimal group study}},\nurl = {https://dx.plos.org/10.1371/journal.pone.0283902},\nvolume = {18},\nyear = {2023}\n}\n
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\n Minimal Group Paradigm (MGP) research suggests that recategorization with an arbitrarily defined group may be sufficient to override empathy biases among salient social categories like race. However, most studies utilizing MGPs do not consider sufficiently the socio-historical contexts of social groups. Here we investigated whether the recategorization of White participants into arbitrarily defined mixed-race teams using a non-competitive MGP would ameliorate racial empathy biases towards ingroup team members in the South African context. Sixty participants rated their empathic and counter-empathic ( Schadenfreude , Glückschmerz ) responses to ingroup and outgroup team members in physically painful, emotionally distressing, and positive situations. As anticipated, results indicated significant ingroup team biases in empathic and counter-empathic responses. However, mixed-race minimal teams were unable to override ingroup racial empathy biases, which persisted across events. Interestingly, a manipulation highlighting purported political ideological differences between White and Black African team members did not exacerbate racial empathy bias, suggesting that such perceptions were already salient. Across conditions, an internal motivation to respond without prejudice was most strongly associated with empathy for Black African target individuals, regardless of their team status. Together, these results suggest that racial identity continues to provide a salient motivational guide in addition to more arbitrary group memberships, even at an explicit level, for empathic responding in contexts characterized by historical power asymmetry. These data further problematize the continued official use of race-based categories in such contexts.\n
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\n \n\n \n \n \n \n \n \n Systematic review of genome-wide association studies of anxiety disorders and neuroticism.\n \n \n \n \n\n\n \n Van Der Walt, K.; Campbell, M.; Stein, D. J; and Dalvie, S.\n\n\n \n\n\n\n The World Journal of Biological Psychiatry, 24(4): 280–291. apr 2023.\n \n\n\n\n
\n\n\n\n \n \n \"SystematicPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{van_der_walt_systematic_2023,\nauthor = {{Van Der Walt}, Kristien and Campbell, Megan and Stein, Dan J and Dalvie, Shareefa},\ndoi = {10.1080/15622975.2022.2099970},\nissn = {1562-2975, 1814-1412},\njournal = {The World Journal of Biological Psychiatry},\nmonth = {apr},\nnumber = {4},\npages = {280--291},\ntitle = {{Systematic review of genome-wide association studies of anxiety disorders and neuroticism}},\nurl = {https://www.tandfonline.com/doi/full/10.1080/15622975.2022.2099970},\nvolume = {24},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Advanced brain ageing in adult psychopathology: \\A\\ systematic review and meta-analysis of structural \\MRI\\ studies.\n \n \n \n \n\n\n \n Blake, K. V; Ntwatwa, Z.; Kaufmann, T.; Stein, D. J; Ipser, J. C; and Groenewold, N. A\n\n\n \n\n\n\n Journal of Psychiatric Research, 157: 180–191. jan 2023.\n \n\n\n\n
\n\n\n\n \n \n \"AdvancedPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{blake_advanced_2023,\nauthor = {Blake, Kimberly V and Ntwatwa, Ziphozihle and Kaufmann, Tobias and Stein, Dan J and Ipser, Jonathan C and Groenewold, Nynke A},\ndoi = {10.1016/j.jpsychires.2022.11.011},\nfile = {:Users/jacquelinebracher/Zotero/storage/7FX2TI7E/Blake et al. - 2023 - Advanced brain ageing in adult psychopathology A .pdf:pdf},\nissn = {00223956},\njournal = {Journal of Psychiatric Research},\nmonth = {jan},\npages = {180--191},\nshorttitle = {Advanced brain ageing in adult psychopathology},\ntitle = {{Advanced brain ageing in adult psychopathology: {\\{}A{\\}} systematic review and meta-analysis of structural {\\{}MRI{\\}} studies}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S0022395622006355},\nvolume = {157},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Prognostication and \\Goals\\ of \\Care\\ \\Decisions\\ in \\Severe\\ \\Traumatic\\ \\Brain\\ \\Injury\\: \\A\\ \\Survey\\ of \\The\\ \\Seattle\\ \\International\\ \\Severe\\ \\Traumatic\\ \\Brain\\ \\Injury\\ \\Consensus\\ \\Conference\\ \\Working\\ \\Group\\.\n \n \n \n \n\n\n \n Sarigul, B.; Bell, R. S; Chesnut, R.; Aguilera, S.; Buki, A.; Citerio, G.; Cooper, D J.; Diaz-Arrastia, R.; Diringer, M.; Figaji, A.; Gao, G.; Geocadin, R. G; Ghajar, J.; Harris, O.; Hoffer, A.; Hutchinson, P.; Joseph, M.; Kitagawa, R.; Manley, G.; Mayer, S. A; Menon, D. K; Meyfroidt, G.; Michael, D. B; Oddo, M.; Okonkwo, D. O; Patel, M. B; Robertson, C.; Rosenfeld, J. V; Rubiano, A. M; Sahuquillo, J.; Servadei, F.; Shutter, L.; Stein, D. D; Stocchetti, N.; Taccone, F. S.; Timmons, S. D; Tsai, E.; Ullman, J. S; Vespa, P.; Videtta, W.; Wright, D. W; Zammit, C.; and Hawryluk, G. W J\n\n\n \n\n\n\n Journal of Neurotrauma, 40(15-16): 1707–1717. aug 2023.\n \n\n\n\n
\n\n\n\n \n \n \"PrognosticationPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{sarigul_prognostication_2023,\nauthor = {Sarigul, Buse and Bell, Randy S and Chesnut, Randall and Aguilera, Sergio and Buki, Andras and Citerio, Giuseppe and Cooper, D Jamie and Diaz-Arrastia, Ramon and Diringer, Michael and Figaji, Anthony and Gao, Guoyi and Geocadin, Romergryko G and Ghajar, Jamshid and Harris, Odette and Hoffer, Alan and Hutchinson, Peter and Joseph, Mathew and Kitagawa, Ryan and Manley, Geoffrey and Mayer, Stephan A and Menon, David K and Meyfroidt, Geert and Michael, Daniel B and Oddo, Mauro and Okonkwo, David O and Patel, Mayur B and Robertson, Claudia and Rosenfeld, Jeffrey V and Rubiano, Andres M and Sahuquillo, Juan and Servadei, Franco and Shutter, Lori and Stein, Deborah D and Stocchetti, Nino and Taccone, Fabio Silvio and Timmons, Shelly D and Tsai, Eve and Ullman, Jamie S and Vespa, Paul and Videtta, Walter and Wright, David W and Zammit, Christopher and Hawryluk, Gregory W J},\ndoi = {10.1089/neu.2022.0414},\nfile = {:Users/jacquelinebracher/Zotero/storage/NFKDCQR8/Sarigul et al. - 2023 - Prognostication and Goals of Care Decisions in Sev.pdf:pdf},\nissn = {0897-7151, 1557-9042},\njournal = {Journal of Neurotrauma},\nmonth = {aug},\nnumber = {15-16},\npages = {1707--1717},\nshorttitle = {Prognostication and {\\{}Goals{\\}} of {\\{}Care{\\}} {\\{}Decisions{\\}} },\ntitle = {{Prognostication and {\\{}Goals{\\}} of {\\{}Care{\\}} {\\{}Decisions{\\}} in {\\{}Severe{\\}} {\\{}Traumatic{\\}} {\\{}Brain{\\}} {\\{}Injury{\\}}: {\\{}A{\\}} {\\{}Survey{\\}} of {\\{}The{\\}} {\\{}Seattle{\\}} {\\{}International{\\}} {\\{}Severe{\\}} {\\{}Traumatic{\\}} {\\{}Brain{\\}} {\\{}Injury{\\}} {\\{}Consensus{\\}} {\\{}Conference{\\}} {\\{}Working{\\}} {\\{}Group{\\}}}},\nurl = {https://www.liebertpub.com/doi/10.1089/neu.2022.0414},\nvolume = {40},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Similar cortical morphometry trajectories from 5 to 9 years in children with perinatal \\HIV\\ who started treatment before age 2 years and uninfected controls.\n \n \n \n \n\n\n \n Nwosu, E. C; Holmes, M. J; Cotton, M. F; Dobbels, E.; Little, F.; Laughton, B.; Van Der Kouwe, A.; Robertson, F.; and Meintjes, E. M\n\n\n \n\n\n\n BMC Neuroscience, 24(1): 15. feb 2023.\n \n\n\n\n
\n\n\n\n \n \n \"SimilarPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{nwosu_similar_2023,\nabstract = {Abstract\n\nBackground\nLife-long early ART (started before age 2 years), often with periods of treatment interruption, is now the standard of care in pediatric HIV infection. Although cross-sectional studies have investigated HIV-related differences in cortical morphology in the setting of early ART and ART interruption, the long-term impact on cortical developmental trajectories is unclear. This study compares the longitudinal trajectories of cortical thickness and folding (gyrification) from age 5 to 9 years in a subset of children perinatally infected with HIV (CPHIV) from the Children with HIV Early antiRetroviral therapy (CHER) trial to age-matched children without HIV infection.\n\n\nMethods\n\n75 CHER participants in follow-up care at FAMCRU (Family Centre for Research with Ubuntu), as well as 66 age-matched controls, received magnetic resonance imaging (MRI) on a 3 T Siemens Allegra at ages 5, 7 and/or 9 years. MR images were processed, and cortical surfaces reconstructed using the\nFreeSurfer\nlongitudinal processing stream. Vertex-wise linear mixed effects (LME) analyses were performed across the whole brain to compare the means and linear rates of change of cortical thickness and gyrification from 5 to 9 years between CPHIV and controls, as well as to examine effects of ART interruption.\n\n\n\nResults\n\nChildren without HIV demonstrated generalized cortical thinning from 5 to 9 years, with the rate of thinning varying by region, as well as regional age-related gyrification increases. Overall, the means and developmental trajectories of cortical thickness and gyrification were similar in CPHIV. However, at an uncorrected\np\n{\\textless}0.005, 6 regions were identified where the cortex of CPHIV was thicker than in uninfected children, namely bilateral insula, left supramarginal, lateral orbitofrontal and superior temporal, and right medial superior frontal regions. Planned ART interruption did not affect development of cortical morphometry.\n\n\n\nConclusions\nAlthough our results suggest that normal development of cortical morphometry between the ages of 5 and 9 years is preserved in CPHIV who started ART early, these findings require further confirmation with longitudinal follow-up through the vulnerable adolescent period.},\nauthor = {Nwosu, Emmanuel C and Holmes, Martha J and Cotton, Mark F and Dobbels, Els and Little, Francesca and Laughton, Barbara and {Van Der Kouwe}, Andre and Robertson, Frances and Meintjes, Ernesta M},\ndoi = {10.1186/s12868-023-00783-7},\nfile = {:Users/jacquelinebracher/Zotero/storage/HV2BXXX6/Nwosu et al. - 2023 - Similar cortical morphometry trajectories from 5 t.pdf:pdf},\nissn = {1471-2202},\njournal = {BMC Neuroscience},\nmonth = {feb},\nnumber = {1},\npages = {15},\ntitle = {{Similar cortical morphometry trajectories from 5 to 9 years in children with perinatal {\\{}HIV{\\}} who started treatment before age 2 years and uninfected controls}},\nurl = {https://bmcneurosci.biomedcentral.com/articles/10.1186/s12868-023-00783-7},\nvolume = {24},\nyear = {2023}\n}\n
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\n Abstract Background Life-long early ART (started before age 2 years), often with periods of treatment interruption, is now the standard of care in pediatric HIV infection. Although cross-sectional studies have investigated HIV-related differences in cortical morphology in the setting of early ART and ART interruption, the long-term impact on cortical developmental trajectories is unclear. This study compares the longitudinal trajectories of cortical thickness and folding (gyrification) from age 5 to 9 years in a subset of children perinatally infected with HIV (CPHIV) from the Children with HIV Early antiRetroviral therapy (CHER) trial to age-matched children without HIV infection. Methods 75 CHER participants in follow-up care at FAMCRU (Family Centre for Research with Ubuntu), as well as 66 age-matched controls, received magnetic resonance imaging (MRI) on a 3 T Siemens Allegra at ages 5, 7 and/or 9 years. MR images were processed, and cortical surfaces reconstructed using the FreeSurfer longitudinal processing stream. Vertex-wise linear mixed effects (LME) analyses were performed across the whole brain to compare the means and linear rates of change of cortical thickness and gyrification from 5 to 9 years between CPHIV and controls, as well as to examine effects of ART interruption. Results Children without HIV demonstrated generalized cortical thinning from 5 to 9 years, with the rate of thinning varying by region, as well as regional age-related gyrification increases. Overall, the means and developmental trajectories of cortical thickness and gyrification were similar in CPHIV. However, at an uncorrected p \\textless0.005, 6 regions were identified where the cortex of CPHIV was thicker than in uninfected children, namely bilateral insula, left supramarginal, lateral orbitofrontal and superior temporal, and right medial superior frontal regions. Planned ART interruption did not affect development of cortical morphometry. Conclusions Although our results suggest that normal development of cortical morphometry between the ages of 5 and 9 years is preserved in CPHIV who started ART early, these findings require further confirmation with longitudinal follow-up through the vulnerable adolescent period.\n
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\n \n\n \n \n \n \n \n \n Potential advantages of combining randomized controlled trials with qualitative research in mood and anxiety disorders - \\A\\ systematic review.\n \n \n \n \n\n\n \n Sørensen, C. W.; Sonne, C.; Sacha, M.; Kristiansen, M.; Hannemose, S. Z.; Stein, D. J; and Carlsson, J.\n\n\n \n\n\n\n Journal of Affective Disorders, 325: 701–712. mar 2023.\n \n\n\n\n
\n\n\n\n \n \n \"PotentialPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{sorensen_potential_2023,\nauthor = {S{\\o}rensen, Carina Winkler and Sonne, Charlotte and Sacha, Maria and Kristiansen, Maria and Hannemose, Sigrid Zeuthen and Stein, Dan J and Carlsson, Jessica},\ndoi = {10.1016/j.jad.2023.01.038},\nissn = {01650327},\njournal = {Journal of Affective Disorders},\nmonth = {mar},\npages = {701--712},\ntitle = {{Potential advantages of combining randomized controlled trials with qualitative research in mood and anxiety disorders - {\\{}A{\\}} systematic review}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S0165032723000496},\nvolume = {325},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Cognitive training and remediation interventions for substance use disorders: a \\Delphi\\ consensus study.\n \n \n \n \n\n\n \n Verdejo‐Garcia, A.; Rezapour, T.; Giddens, E.; Khojasteh Zonoozi, A.; Rafei, P.; Berry, J.; Caracuel, A.; Copersino, M. L; Field, M.; Garland, E. L; Lorenzetti, V.; Malloy‐Diniz, L.; Manning, V.; Marceau, E. M; Pennington, D. L; Strickland, J. C; Wiers, R.; Fairhead, R.; Anderson, A.; Bell, M.; Boendermaker, W. J; Brooks, S.; Bruno, R.; Campanella, S.; Cousijn, J.; Cox, W M.; Dean, A. C; Ersche, K. D; Franken, I.; Froeliger, B.; Gamito, P.; Gladwin, T. E; Goncalves, P. D; Houben, K.; Jacobus, J.; Jones, A.; Kaag, A. M; Lindenmeyer, J.; McGrath, E.; Nardo, T.; Oliveira, J.; Pennington, C. R; Perrykkad, K.; Piercy, H.; Rupp, C. I; Schulte, M. H J; Squeglia, L. M; Staiger, P.; Stein, D. J; Stein, J.; Stein, M.; Stoops, W. W; Sweeney, M.; Witkiewitz, K.; Woods, S. P; Yi, R.; Zhao, M.; and Ekhtiari, H.\n\n\n \n\n\n\n Addiction, 118(5): 935–951. may 2023.\n \n\n\n\n
\n\n\n\n \n \n \"CognitivePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{verdejogarcia_cognitive_2023,\nabstract = {Abstract\n\nAims\nSubstance use disorders (SUD) are associated with cognitive deficits that are not always addressed in current treatments, and this hampers recovery. Cognitive training and remediation interventions are well suited to fill the gap for managing cognitive deficits in SUD. We aimed to reach consensus on recommendations for developing and applying these interventions.\n\n\nDesign, Setting and Participants\n\nWe used a Delphi approach with two sequential phases: survey development and iterative surveying of experts. This was an on‐line study. During survey development, we engaged a group of 15 experts from a working group of the International Society of Addiction Medicine (Steering Committee). During the surveying process, we engaged a larger pool of experts (\nn\n= 54) identified via recommendations from the Steering Committee and a systematic review.\n\n\n\nMeasurements\nSurvey with 67 items covering four key areas of intervention development: targets, intervention approaches, active ingredients and modes of delivery.\n\n\nFindings\nAcross two iterative rounds (98{\\%} retention rate), the experts reached a consensus on 50 items including: (i) implicit biases, positive affect, arousal, executive functions and social processing as key targets of interventions; (ii) cognitive bias modification, contingency management, emotion regulation training and cognitive remediation as preferred approaches; (iii) practice, feedback, difficulty‐titration, bias modification, goal‐setting, strategy learning and meta‐awareness as active ingredients; and (iv) both addiction treatment work‐force and specialized neuropsychologists facilitating delivery, together with novel digital‐based delivery modalities.\n\n\nConclusions\nExpert recommendations on cognitive training and remediation for substance use disorders highlight the relevance of targeting implicit biases, reward, emotion regulation and higher‐order cognitive skills via well‐validated intervention approaches qualified with mechanistic techniques and flexible delivery options.},\nauthor = {Verdejo‐Garcia, Antonio and Rezapour, Tara and Giddens, Emily and {Khojasteh Zonoozi}, Arash and Rafei, Parnian and Berry, Jamie and Caracuel, Alfonso and Copersino, Marc L and Field, Matt and Garland, Eric L and Lorenzetti, Valentina and Malloy‐Diniz, Leandro and Manning, Victoria and Marceau, Ely M and Pennington, David L and Strickland, Justin C and Wiers, Reinout and Fairhead, Rahia and Anderson, Alexandra and Bell, Morris and Boendermaker, Wouter J and Brooks, Samantha and Bruno, Raimondo and Campanella, Salvatore and Cousijn, Janna and Cox, W Miles and Dean, Andrew C and Ersche, Karen D and Franken, Ingmar and Froeliger, Brett and Gamito, Pedro and Gladwin, Thomas E and Goncalves, Priscila D and Houben, Katrijn and Jacobus, Joanna and Jones, Andrew and Kaag, Anne M and Lindenmeyer, Johannes and McGrath, Elly and Nardo, Talia and Oliveira, Jorge and Pennington, Charlotte R and Perrykkad, Kelsey and Piercy, Hugh and Rupp, Claudia I and Schulte, Mieke H J and Squeglia, Lindsay M and Staiger, Petra and Stein, Dan J and Stein, Jeff and Stein, Maria and Stoops, William W and Sweeney, Mary and Witkiewitz, Katie and Woods, Steven P and Yi, Richard and Zhao, Min and Ekhtiari, Hamed},\ndoi = {10.1111/add.16109},\nfile = {:Users/jacquelinebracher/Zotero/storage/7K3LRRH9/Verdejo‐Garcia et al. - 2023 - Cognitive training and remediation interventions f.pdf:pdf},\nissn = {0965-2140, 1360-0443},\njournal = {Addiction},\nmonth = {may},\nnumber = {5},\npages = {935--951},\nshorttitle = {Cognitive training and remediation interventions f},\ntitle = {{Cognitive training and remediation interventions for substance use disorders: a {\\{}Delphi{\\}} consensus study}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1111/add.16109},\nvolume = {118},\nyear = {2023}\n}\n
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\n Abstract Aims Substance use disorders (SUD) are associated with cognitive deficits that are not always addressed in current treatments, and this hampers recovery. Cognitive training and remediation interventions are well suited to fill the gap for managing cognitive deficits in SUD. We aimed to reach consensus on recommendations for developing and applying these interventions. Design, Setting and Participants We used a Delphi approach with two sequential phases: survey development and iterative surveying of experts. This was an on‐line study. During survey development, we engaged a group of 15 experts from a working group of the International Society of Addiction Medicine (Steering Committee). During the surveying process, we engaged a larger pool of experts ( n = 54) identified via recommendations from the Steering Committee and a systematic review. Measurements Survey with 67 items covering four key areas of intervention development: targets, intervention approaches, active ingredients and modes of delivery. Findings Across two iterative rounds (98% retention rate), the experts reached a consensus on 50 items including: (i) implicit biases, positive affect, arousal, executive functions and social processing as key targets of interventions; (ii) cognitive bias modification, contingency management, emotion regulation training and cognitive remediation as preferred approaches; (iii) practice, feedback, difficulty‐titration, bias modification, goal‐setting, strategy learning and meta‐awareness as active ingredients; and (iv) both addiction treatment work‐force and specialized neuropsychologists facilitating delivery, together with novel digital‐based delivery modalities. Conclusions Expert recommendations on cognitive training and remediation for substance use disorders highlight the relevance of targeting implicit biases, reward, emotion regulation and higher‐order cognitive skills via well‐validated intervention approaches qualified with mechanistic techniques and flexible delivery options.\n
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\n \n\n \n \n \n \n \n \n What \\Causes\\ \\Seizures\\ in \\Neurocysticercosis\\?.\n \n \n \n \n\n\n \n Steyn, T. J. S.; Awala, A. N.; De Lange, A.; and Raimondo, J. V.\n\n\n \n\n\n\n Epilepsy Currents, 23(2): 105–112. mar 2023.\n \n\n\n\n
\n\n\n\n \n \n \"WhatPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{steyn_what_2023,\nabstract = {Neurocysticercosis (NCC) is the most prevalent parasitic infection of the central nervous system. It is caused by the presence of larvae of the cestode Taenia solium in the brain. The most common symptom of NCC is seizures, and it is widely considered the world's leading cause of preventable epilepsy. Despite the prevalence and impact of NCC, a thorough, mechanistic understanding of seizure generation is still lacking. In this review, we address the question “What causes seizures in NCC?” by summarizing and discussing the major theories that seek to explain the seizurogenic and epileptogenic processes in this disorder. In addition, we highlight the potential for recent advances in disease modeling to help accelerate progress in this area.},\nauthor = {Steyn, Teresa Julieta Sim{\\~{o}}es and Awala, Amalia Naita and {De Lange}, Anja and Raimondo, Joseph Valentino},\ndoi = {10.1177/15357597221137418},\nfile = {:Users/jacquelinebracher/Zotero/storage/CVGNR6HG/Steyn et al. - 2023 - What Causes Seizures in Neurocysticercosis.pdf:pdf},\nissn = {1535-7597, 1535-7511},\njournal = {Epilepsy Currents},\nmonth = {mar},\nnumber = {2},\npages = {105--112},\ntitle = {{What {\\{}Causes{\\}} {\\{}Seizures{\\}} in {\\{}Neurocysticercosis{\\}}?}},\nurl = {http://journals.sagepub.com/doi/10.1177/15357597221137418},\nvolume = {23},\nyear = {2023}\n}\n
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\n Neurocysticercosis (NCC) is the most prevalent parasitic infection of the central nervous system. It is caused by the presence of larvae of the cestode Taenia solium in the brain. The most common symptom of NCC is seizures, and it is widely considered the world's leading cause of preventable epilepsy. Despite the prevalence and impact of NCC, a thorough, mechanistic understanding of seizure generation is still lacking. In this review, we address the question “What causes seizures in NCC?” by summarizing and discussing the major theories that seek to explain the seizurogenic and epileptogenic processes in this disorder. In addition, we highlight the potential for recent advances in disease modeling to help accelerate progress in this area.\n
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\n \n\n \n \n \n \n \n \n Pruning and thresholding approach for methylation risk scores in multi-ancestry populations.\n \n \n \n \n\n\n \n Chen, J.; Gatev, E.; Everson, T.; Conneely, K. N; Koen, N.; Epstein, M. P; Kobor, M. S; Zar, H. J; Stein, D. J; and Hüls, A.\n\n\n \n\n\n\n Epigenetics, 18(1): 2187172. dec 2023.\n \n\n\n\n
\n\n\n\n \n \n \"PruningPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{chen_pruning_2023,\nauthor = {Chen, Junyu and Gatev, Evan and Everson, Todd and Conneely, Karen N and Koen, Nastassja and Epstein, Michael P and Kobor, Michael S and Zar, Heather J and Stein, Dan J and H{\\"{u}}ls, Anke},\ndoi = {10.1080/15592294.2023.2187172},\nfile = {:Users/jacquelinebracher/Zotero/storage/ISDT38MG/Chen et al. - 2023 - Pruning and thresholding approach for methylation .pdf:pdf},\nissn = {1559-2294, 1559-2308},\njournal = {Epigenetics},\nmonth = {dec},\nnumber = {1},\npages = {2187172},\ntitle = {{Pruning and thresholding approach for methylation risk scores in multi-ancestry populations}},\nurl = {https://www.tandfonline.com/doi/full/10.1080/15592294.2023.2187172},\nvolume = {18},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Decision-making tendencies and voucher spending independently support abstinence within contingency management for methamphetamine use disorder.\n \n \n \n \n\n\n \n Lake, M. T; Krishnamurti, T.; Murtaugh, K. L.; Van Nunen, L. J; Stein, D. J; and Shoptaw, S.\n\n\n \n\n\n\n Experimental and Clinical Psychopharmacology, 31(2): 324–329. apr 2023.\n \n\n\n\n
\n\n\n\n \n \n \"Decision-makingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{lake_decision-making_2023,\nauthor = {Lake, Marilyn T and Krishnamurti, Tamar and Murtaugh, Kimberly Ling and {Van Nunen}, Lara J and Stein, Dan J and Shoptaw, Steven},\ndoi = {10.1037/pha0000574},\nfile = {:Users/jacquelinebracher/Zotero/storage/K8CFMHP2/Lake et al. - 2023 - Decision-making tendencies and voucher spending in.pdf:pdf},\nissn = {1936-2293, 1064-1297},\njournal = {Experimental and Clinical Psychopharmacology},\nmonth = {apr},\nnumber = {2},\npages = {324--329},\ntitle = {{Decision-making tendencies and voucher spending independently support abstinence within contingency management for methamphetamine use disorder.}},\nurl = {http://doi.apa.org/getdoi.cfm?doi=10.1037/pha0000574},\nvolume = {31},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Exploring the unmet needs of adults with cerebral palsy living in urban \\South\\ \\Africa\\.\n \n \n \n \n\n\n \n Salie, R.; Kleintjes, S.; Eken, M. M; Donald, K. A; Fieggen, A G.; and Langerak, N. G\n\n\n \n\n\n\n Disability and Rehabilitation,1–9. feb 2023.\n \n\n\n\n
\n\n\n\n \n \n \"ExploringPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{salie_exploring_2023,\nauthor = {Salie, Roshaan and Kleintjes, Sharon and Eken, Maaike M and Donald, Kirsten A and Fieggen, A Graham and Langerak, Nelleke G},\ndoi = {10.1080/09638288.2023.2177358},\nissn = {0963-8288, 1464-5165},\njournal = {Disability and Rehabilitation},\nmonth = {feb},\npages = {1--9},\ntitle = {{Exploring the unmet needs of adults with cerebral palsy living in urban {\\{}South{\\}} {\\{}Africa{\\}}}},\nurl = {https://www.tandfonline.com/doi/full/10.1080/09638288.2023.2177358},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Emerging and re‐emerging fungal threats in \\Africa\\.\n \n \n \n \n\n\n \n Dangarembizi, R.; Wasserman, S.; and Hoving, J. C.\n\n\n \n\n\n\n Parasite Immunology, 45(2): e12953. feb 2023.\n \n\n\n\n
\n\n\n\n \n \n \"EmergingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{dangarembizi_emerging_2023,\nabstract = {Abstract\n\nThe emergence of deadly fungal infections in Africa is primarily driven by a disproportionately high burden of human immunodeficiency virus (HIV) infections, lack of access to quality health care, and the unavailability of effective antifungal drugs. Immunocompromised people in Africa are therefore at high risk of infection from opportunistic fungal pathogens such as\nCryptococcus neoformans\nand\nPneumocystis jirovecii\n, which are associated with high morbidity, mortality, and related socioeconomic impacts. Other emerging fungal threats include\nEmergomyces\nspp.,\nHistoplasma\nspp.,\nBlastomyces\nspp., and healthcare‐associated multi‐drug resistant\nCandida auris\n. Socioeconomic development and the Covid‐19 pandemic may influence shifts in epidemiology of invasive fungal diseases on the continent. This review discusses the epidemiology, clinical manifestations, and current management strategies available for these emerging fungal diseases in Africa. We also discuss gaps in knowledge, policy, and research to inform future efforts at managing these fungal threats.},\nauthor = {Dangarembizi, Rachael and Wasserman, Sean and Hoving, Jennifer Claire},\ndoi = {10.1111/pim.12953},\nfile = {:Users/jacquelinebracher/Zotero/storage/SCPHU43B/Dangarembizi et al. - 2023 - Emerging and re‐emerging fungal threats in Africa.pdf:pdf},\nissn = {0141-9838, 1365-3024},\njournal = {Parasite Immunology},\nmonth = {feb},\nnumber = {2},\npages = {e12953},\ntitle = {{Emerging and re‐emerging fungal threats in {\\{}Africa{\\}}}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1111/pim.12953},\nvolume = {45},\nyear = {2023}\n}\n
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\n Abstract The emergence of deadly fungal infections in Africa is primarily driven by a disproportionately high burden of human immunodeficiency virus (HIV) infections, lack of access to quality health care, and the unavailability of effective antifungal drugs. Immunocompromised people in Africa are therefore at high risk of infection from opportunistic fungal pathogens such as Cryptococcus neoformans and Pneumocystis jirovecii , which are associated with high morbidity, mortality, and related socioeconomic impacts. Other emerging fungal threats include Emergomyces spp., Histoplasma spp., Blastomyces spp., and healthcare‐associated multi‐drug resistant Candida auris . Socioeconomic development and the Covid‐19 pandemic may influence shifts in epidemiology of invasive fungal diseases on the continent. This review discusses the epidemiology, clinical manifestations, and current management strategies available for these emerging fungal diseases in Africa. We also discuss gaps in knowledge, policy, and research to inform future efforts at managing these fungal threats.\n
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\n \n\n \n \n \n \n \n \n Fellow \\Strangers\\: \\Physical\\ \\Distance\\ and \\Evaluations\\ of \\Blameworthiness\\.\n \n \n \n \n\n\n \n Hartford, A.\n\n\n \n\n\n\n The Journal of Value Inquiry, 57(2): 343–363. jun 2023.\n \n\n\n\n
\n\n\n\n \n \n \"FellowPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{hartford_fellow_2023,\nauthor = {Hartford, Anna},\ndoi = {10.1007/s10790-021-09830-0},\nfile = {:Users/jacquelinebracher/Zotero/storage/YLT3R3V8/Hartford - 2023 - Fellow Strangers Physical Distance and Evaluation.pdf:pdf},\nissn = {0022-5363, 1573-0492},\njournal = {The Journal of Value Inquiry},\nmonth = {jun},\nnumber = {2},\npages = {343--363},\nshorttitle = {Fellow {\\{}Strangers{\\}}},\ntitle = {{Fellow {\\{}Strangers{\\}}: {\\{}Physical{\\}} {\\{}Distance{\\}} and {\\{}Evaluations{\\}} of {\\{}Blameworthiness{\\}}}},\nurl = {https://link.springer.com/10.1007/s10790-021-09830-0},\nvolume = {57},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Post-\\TB\\ health and wellbeing.\n \n \n \n \n\n\n \n Nightingale, R; Carlin, F; Meghji, J; McMullen, K; Evans, D; Van Der Zalm, M M; Anthony, M G; Bittencourt, M; Byrne, A; Du Preez, K; Coetzee, M; Feris, C; Goussard, P; Hirasen, K; Bouwer, J; Hoddinott, G; Huaman, M A; Inglis-Jassiem, G; Ivanova, O; Karmadwala, F; Schaaf, H S; Schoeman, I; Seddon, J A; Sineke, T; Solomons, R; Thiart, M; Van Toorn, R; Fujiwara, P I; Romanowski, K; Marais, S; Hesseling, A C; Johnston, J; Allwood, B; Muhwa, J C; and Mortimer, K\n\n\n \n\n\n\n The International Journal of Tuberculosis and Lung Disease, 27(4): 248–283. apr 2023.\n \n\n\n\n
\n\n\n\n \n \n \"Post-\\TB\\Paper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{nightingale_post-tb_2023,\nabstract = {TB affects around 10.6 million people each year and there are now around 155 million TB survivors. TB and its treatments can lead to permanently impaired health and wellbeing. In 2019, representatives of TB affected communities attending the ‘1\nst\nInternational Post-Tuberculosis\nSymposium´ called for the development of clinical guidance on these issues. This clinical statement on post-TB health and wellbeing responds to this call and builds on the work of the symposium, which brought together TB survivors, healthcare professionals and researchers. Our document\noffers expert opinion and, where possible, evidence-based guidance to aid clinicians in the diagnosis and management of post-TB conditions and research in this field. It covers all aspects of post-TB, including economic, social and psychological wellbeing, post TB lung disease (PTLD), cardiovascular\nand pericardial disease, neurological disability, effects in adolescents and children, and future research needs.},\nauthor = {Nightingale, R and Carlin, F and Meghji, J and McMullen, K and Evans, D and {Van Der Zalm}, M M and Anthony, M G and Bittencourt, M and Byrne, A and {Du Preez}, K and Coetzee, M and Feris, C and Goussard, P and Hirasen, K and Bouwer, J and Hoddinott, G and Huaman, M A and Inglis-Jassiem, G and Ivanova, O and Karmadwala, F and Schaaf, H S and Schoeman, I and Seddon, J A and Sineke, T and Solomons, R and Thiart, M and {Van Toorn}, R and Fujiwara, P I and Romanowski, K and Marais, S and Hesseling, A C and Johnston, J and Allwood, B and Muhwa, J C and Mortimer, K},\ndoi = {10.5588/ijtld.22.0514},\nfile = {:Users/jacquelinebracher/Zotero/storage/LM23CP34/Nightingale et al. - 2023 - Post-TB health and wellbeing.pdf:pdf},\nissn = {1027-3719},\njournal = {The International Journal of Tuberculosis and Lung Disease},\nmonth = {apr},\nnumber = {4},\npages = {248--283},\ntitle = {{Post-{\\{}TB{\\}} health and wellbeing}},\nurl = {https://www.ingentaconnect.com/content/10.5588/ijtld.22.0514},\nvolume = {27},\nyear = {2023}\n}\n
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\n TB affects around 10.6 million people each year and there are now around 155 million TB survivors. TB and its treatments can lead to permanently impaired health and wellbeing. In 2019, representatives of TB affected communities attending the ‘1 st International Post-Tuberculosis Symposium´ called for the development of clinical guidance on these issues. This clinical statement on post-TB health and wellbeing responds to this call and builds on the work of the symposium, which brought together TB survivors, healthcare professionals and researchers. Our document offers expert opinion and, where possible, evidence-based guidance to aid clinicians in the diagnosis and management of post-TB conditions and research in this field. It covers all aspects of post-TB, including economic, social and psychological wellbeing, post TB lung disease (PTLD), cardiovascular and pericardial disease, neurological disability, effects in adolescents and children, and future research needs.\n
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\n \n\n \n \n \n \n \n \n Viral protein \\R\\ (\\Vpr\\)-induced neuroinflammation and its potential contribution to neuronal dysfunction: a scoping review.\n \n \n \n \n\n\n \n Williams, M. E.; Williams, A. A; and Naudé, P. J W\n\n\n \n\n\n\n BMC Infectious Diseases, 23(1): 512. aug 2023.\n \n\n\n\n
\n\n\n\n \n \n \"ViralPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{williams_viral_2023,\nabstract = {Abstract\nHIV-associated neurocognitive disorders (HAND) are the result of the activity of HIV-1 within the central nervous system (CNS). While the introduction of antiretroviral therapy (ART) has significantly reduced the occurrence of severe cases of HAND, milder cases still persist. The persistence of HAND in the modern ART era has been linked to a chronic dysregulated inflammatory profile. There is increasing evidence suggesting a potential role of Viral protein R (Vpr) in dysregulating the neuroinflammatory processes in people living with HIV (PLHIV), which may contribute to the development of HAND. Since the role of Vpr in neuroinflammatory mechanisms has not been clearly defined, we conducted a scoping review of fundamental research studies on this topic. The review aimed to assess the size and scope of available research literature on this topic and provide commentary on whether Vpr contributes to neuroinflammation, as highlighted in fundamental studies. Based on the specified selection criteria, 10 studies (6 of which were cell culture-based and 4 that included both animal and cell culture experiments) were eligible for inclusion. The main findings were that (1) Vpr can increase neuroinflammatory markers, with studies consistently reporting higher levels of TNF-$\\alpha$ and IL-8, (2) Vpr induces (neuro)inflammation via specific pathways, including the PI3K/AKT, p38-MAPk, JNK-SAPK and Sur1-Trpm4 channels in astrocytes and the p38 and JNK-SAPK in myeloid cells, and (3) Vpr-specific protein amino acid signatures (73R, 77R and 80A) may play an important role in exacerbating neuroinflammation and the neuropathophysiology of HAND. Therefore, Vpr should be investigated for its potential contribution to neuroinflammation in the development of HAND.},\nauthor = {Williams, Monray Edward and Williams, Aurelia A and Naud{\\'{e}}, Petrus J W},\ndoi = {10.1186/s12879-023-08495-3},\nfile = {:Users/jacquelinebracher/Zotero/storage/MC4FQXVV/Williams et al. - 2023 - Viral protein R (Vpr)-induced neuroinflammation an.pdf:pdf},\nissn = {1471-2334},\njournal = {BMC Infectious Diseases},\nmonth = {aug},\nnumber = {1},\npages = {512},\nshorttitle = {Viral protein {\\{}R{\\}} ({\\{}Vpr{\\}})-induced neuroinflammatio},\ntitle = {{Viral protein {\\{}R{\\}} ({\\{}Vpr{\\}})-induced neuroinflammation and its potential contribution to neuronal dysfunction: a scoping review}},\nurl = {https://bmcinfectdis.biomedcentral.com/articles/10.1186/s12879-023-08495-3},\nvolume = {23},\nyear = {2023}\n}\n
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\n Abstract HIV-associated neurocognitive disorders (HAND) are the result of the activity of HIV-1 within the central nervous system (CNS). While the introduction of antiretroviral therapy (ART) has significantly reduced the occurrence of severe cases of HAND, milder cases still persist. The persistence of HAND in the modern ART era has been linked to a chronic dysregulated inflammatory profile. There is increasing evidence suggesting a potential role of Viral protein R (Vpr) in dysregulating the neuroinflammatory processes in people living with HIV (PLHIV), which may contribute to the development of HAND. Since the role of Vpr in neuroinflammatory mechanisms has not been clearly defined, we conducted a scoping review of fundamental research studies on this topic. The review aimed to assess the size and scope of available research literature on this topic and provide commentary on whether Vpr contributes to neuroinflammation, as highlighted in fundamental studies. Based on the specified selection criteria, 10 studies (6 of which were cell culture-based and 4 that included both animal and cell culture experiments) were eligible for inclusion. The main findings were that (1) Vpr can increase neuroinflammatory markers, with studies consistently reporting higher levels of TNF-$α$ and IL-8, (2) Vpr induces (neuro)inflammation via specific pathways, including the PI3K/AKT, p38-MAPk, JNK-SAPK and Sur1-Trpm4 channels in astrocytes and the p38 and JNK-SAPK in myeloid cells, and (3) Vpr-specific protein amino acid signatures (73R, 77R and 80A) may play an important role in exacerbating neuroinflammation and the neuropathophysiology of HAND. Therefore, Vpr should be investigated for its potential contribution to neuroinflammation in the development of HAND.\n
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\n \n\n \n \n \n \n \n \n Cognitive \\Performance\\, as well as \\Depression\\, \\Alcohol\\ \\Use\\, and \\Gender\\, predict \\Anti\\-\\Retroviral\\ \\Therapy\\ \\Adherence\\ in a \\South\\ \\African\\ \\Cohort\\ of \\People\\ with \\HIV\\ and \\Comorbid\\ \\Major\\ \\Depressive\\ \\Disorder\\.\n \n \n \n \n\n\n \n Dreyer, A. J; Nightingale, S.; Andersen, L. S; Lee, J. S; Gouse, H.; Safren, S. A; O'Cleirigh, C.; Thomas, K. G F; and Joska, J.\n\n\n \n\n\n\n AIDS and Behavior, 27(8): 2681–2694. aug 2023.\n \n\n\n\n
\n\n\n\n \n \n \"CognitivePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{dreyer_cognitive_2023,\nabstract = {Abstract\n\nDepression and cognitive impairment, which commonly coexist in people with HIV (PWH), have been identified as potential barriers to optimal antiretroviral therapy (ART) adherence. We investigated associations between cognitive performance, depression (as well as other sociodemographic, psychosocial and psychiatric variables) and ART adherence in a South African cohort of PWH with comorbid major depressive disorder (MDD). Cognitive performance and ART adherence were assessed at two time points 8 months apart (\nN\nbaseline\n= 105,\nN\nfollow-up\n= 81). Adherence was indicated by self-report, objective measures (Wisepill usage and plasma tenofovir-diphosphate levels), and HIV viral suppression. Mixed-effects regression models examined associations across both time points. Univariate models detected no significant associations between cognitive performance (globally and within-domain) and ART adherence. Multivariate modelling showed increased depression severity (\n$\\beta$\n= − 0.54,\np\n{\\textless}0.001) and problematic alcohol use (\n$\\beta$\n= 0.73,\np\n= 0.015) were associated with worse adherence as measured subjectively. Being female (\nOR\n0.27,\np\n= 0.048) and having better global cognitive performance (\nOR\n1.83,\np\n= 0.043) were associated with better adherence as indicated by viral suppression. This study identifies poor global cognitive performance, as well as depression and problematic alcohol use, as potential barriers to optimal ART adherence in PWH and comorbid MDD. Hence, clinicians could consider assessing for cognitive deficits, depression, and problematic alcohol use, and should endeavour to provide the appropriate support so as to improve adherence.},\nauthor = {Dreyer, Anna J and Nightingale, Sam and Andersen, Lena S and Lee, Jasper S and Gouse, Hetta and Safren, Steven A and O'Cleirigh, Conall and Thomas, Kevin G F and Joska, John},\ndoi = {10.1007/s10461-023-03992-7},\nfile = {:Users/jacquelinebracher/Zotero/storage/6IUAKQ2L/Dreyer et al. - 2023 - Cognitive Performance, as well as Depression, Alco.pdf:pdf},\nissn = {1090-7165, 1573-3254},\njournal = {AIDS and Behavior},\nmonth = {aug},\nnumber = {8},\npages = {2681--2694},\ntitle = {{Cognitive {\\{}Performance{\\}}, as well as {\\{}Depression{\\}}, {\\{}Alcohol{\\}} {\\{}Use{\\}}, and {\\{}Gender{\\}}, predict {\\{}Anti{\\}}-{\\{}Retroviral{\\}} {\\{}Therapy{\\}} {\\{}Adherence{\\}} in a {\\{}South{\\}} {\\{}African{\\}} {\\{}Cohort{\\}} of {\\{}People{\\}} with {\\{}HIV{\\}} and {\\{}Comorbid{\\}} {\\{}Major{\\}} {\\{}Depressive{\\}} {\\{}Disorder{\\}}}},\nurl = {https://link.springer.com/10.1007/s10461-023-03992-7},\nvolume = {27},\nyear = {2023}\n}\n
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\n Abstract Depression and cognitive impairment, which commonly coexist in people with HIV (PWH), have been identified as potential barriers to optimal antiretroviral therapy (ART) adherence. We investigated associations between cognitive performance, depression (as well as other sociodemographic, psychosocial and psychiatric variables) and ART adherence in a South African cohort of PWH with comorbid major depressive disorder (MDD). Cognitive performance and ART adherence were assessed at two time points 8 months apart ( N baseline = 105, N follow-up = 81). Adherence was indicated by self-report, objective measures (Wisepill usage and plasma tenofovir-diphosphate levels), and HIV viral suppression. Mixed-effects regression models examined associations across both time points. Univariate models detected no significant associations between cognitive performance (globally and within-domain) and ART adherence. Multivariate modelling showed increased depression severity ( $β$ = − 0.54, p \\textless0.001) and problematic alcohol use ( $β$ = 0.73, p = 0.015) were associated with worse adherence as measured subjectively. Being female ( OR 0.27, p = 0.048) and having better global cognitive performance ( OR 1.83, p = 0.043) were associated with better adherence as indicated by viral suppression. This study identifies poor global cognitive performance, as well as depression and problematic alcohol use, as potential barriers to optimal ART adherence in PWH and comorbid MDD. Hence, clinicians could consider assessing for cognitive deficits, depression, and problematic alcohol use, and should endeavour to provide the appropriate support so as to improve adherence.\n
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\n \n\n \n \n \n \n \n \n Blood and cerebrospinal fluid biomarker changes in patients with \\HIV\\-associated neurocognitive impairment treated with lithium: analysis from a randomised placebo-controlled trial.\n \n \n \n \n\n\n \n Thela, L.; Decloedt, E.; Zetterberg, H.; Gisslén, M.; Lesosky, M.; Gleich, M.; Koutsilieri, E.; Scheller, C.; Hye, A.; and Joska, J.\n\n\n \n\n\n\n Journal of NeuroVirology, 29(2): 156–166. apr 2023.\n \n\n\n\n
\n\n\n\n \n \n \"BloodPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{thela_blood_2023,\nabstract = {Abstract\n\nHIV-associated neurocognitive disorders (HAND) persist in the era of antiretroviral therapy (ART). Thus, ART does not completely halt or reverse the pathological processes behind HAND. Adjuvant mitigating treatments are, therefore, prudent. Lithium treatment is known to promote neuronal brain–derived neurotrophic factors (BDNF). Lithium is also an inhibitor of glycogen synthase kinase-3 beta (GSK-3-$\\beta$). We analyzed biomarkers obtained from participants in a randomized placebo-controlled trial of lithium in ART-treated individuals with moderate or severe HAND. We assayed markers at baseline and 24 weeks across several pathways hypothesized to be affected by HIV, inflammation, or degeneration. Investigated biomarkers included dopamine, BDNF, neurofilament light chain, and CD8 + lymphocyte activation (CD38 + HLADR +). Alzheimer's Disease (AD) biomarkers included soluble amyloid precursor protein alpha and beta (sAPP$\\alpha$/$\\beta$), A$\\beta$38, 40, 42, and ten other biomarkers validated as predictors of mild cognitive impairment and progression in previous studies. These include apolipoprotein C3, pre-albumin, $\\alpha$1-acid glycoprotein, $\\alpha$1-antitrypsin, PEDF, CC4, ICAM-1, RANTES, clusterin, and cystatin c. We recruited 61 participants (placebo = 31; lithium = 30). The age baseline mean was 40 (± 8.35) years and the median CD4 + T-cell count was 498 (IQR: 389–651) cells/$\\mu$L. Biomarker concentrations between groups did not differ at baseline. However, both groups' blood dopamine levels decreased significantly after 24 weeks (adj.\np\n{\\textless}002). No other marker was significantly different between groups, and we concluded that lithium did not confer neuroprotection following 24 weeks of treatment. However, the study was limited in duration and sample size.},\nauthor = {Thela, Lindokuhle and Decloedt, Eric and Zetterberg, Henrik and Gissl{\\'{e}}n, Magnus and Lesosky, Maia and Gleich, Melanie and Koutsilieri, Eleni and Scheller, Carsten and Hye, Abdul and Joska, John},\ndoi = {10.1007/s13365-023-01116-4},\nfile = {:Users/jacquelinebracher/Zotero/storage/VEWRUZXG/Thela et al. - 2023 - Blood and cerebrospinal fluid biomarker changes in.pdf:pdf},\nissn = {1355-0284, 1538-2443},\njournal = {Journal of NeuroVirology},\nmonth = {apr},\nnumber = {2},\npages = {156--166},\nshorttitle = {Blood and cerebrospinal fluid biomarker changes in},\ntitle = {{Blood and cerebrospinal fluid biomarker changes in patients with {\\{}HIV{\\}}-associated neurocognitive impairment treated with lithium: analysis from a randomised placebo-controlled trial}},\nurl = {https://link.springer.com/10.1007/s13365-023-01116-4},\nvolume = {29},\nyear = {2023}\n}\n
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\n Abstract HIV-associated neurocognitive disorders (HAND) persist in the era of antiretroviral therapy (ART). Thus, ART does not completely halt or reverse the pathological processes behind HAND. Adjuvant mitigating treatments are, therefore, prudent. Lithium treatment is known to promote neuronal brain–derived neurotrophic factors (BDNF). Lithium is also an inhibitor of glycogen synthase kinase-3 beta (GSK-3-$β$). We analyzed biomarkers obtained from participants in a randomized placebo-controlled trial of lithium in ART-treated individuals with moderate or severe HAND. We assayed markers at baseline and 24 weeks across several pathways hypothesized to be affected by HIV, inflammation, or degeneration. Investigated biomarkers included dopamine, BDNF, neurofilament light chain, and CD8 + lymphocyte activation (CD38 + HLADR +). Alzheimer's Disease (AD) biomarkers included soluble amyloid precursor protein alpha and beta (sAPP$α$/$β$), A$β$38, 40, 42, and ten other biomarkers validated as predictors of mild cognitive impairment and progression in previous studies. These include apolipoprotein C3, pre-albumin, $α$1-acid glycoprotein, $α$1-antitrypsin, PEDF, CC4, ICAM-1, RANTES, clusterin, and cystatin c. We recruited 61 participants (placebo = 31; lithium = 30). The age baseline mean was 40 (± 8.35) years and the median CD4 + T-cell count was 498 (IQR: 389–651) cells/$μ$L. Biomarker concentrations between groups did not differ at baseline. However, both groups' blood dopamine levels decreased significantly after 24 weeks (adj. p \\textless002). No other marker was significantly different between groups, and we concluded that lithium did not confer neuroprotection following 24 weeks of treatment. However, the study was limited in duration and sample size.\n
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\n \n\n \n \n \n \n \n \n Precision medicine for developmental and epileptic encephalopathies in \\Africa\\—strategies for a resource-limited setting.\n \n \n \n \n\n\n \n Esterhuizen, A. I; Tiffin, N.; Riordan, G.; Wessels, M.; Burman, R. J; Aziz, M. C; Calhoun, J. D; Gunti, J.; Amiri, E. E; Ramamurthy, A.; Bamshad, M. J; Mefford, H. C; Ramesar, R.; Wilmshurst, J. M; Carvill, G. L; Bamshad, M. J; Leal, S. M; Nickerson, D. A; Anderson, P.; Bacus, T. J; Blue, E. E; Brower, K.; Buckingham, K. J; Chong, J. X; Cornejo Sánchez, D.; Davis, C. P; Davis, C. J; Frazar, C. D; Gomeztagle-Burgess, K.; Gordon, W. W; Horike-Pyne, M.; Hurless, J. R; Jarvik, G. P; Johanson, E.; Thomas Kolar, J; Marvin, C. T; McGee, S.; McGoldrick, D. J; Mekonnen, B.; Nielsen, P. M; Patterson, K.; Radhakrishnan, A.; Richardson, M. A; Roote, G. T; Ryke, E. L; Schrauwen, I.; Shively, K. M; Smith, J. D; Tackett, M.; Wang, G.; Weiss, J. M; Wheeler, M. M; Yi, Q.; and Zhang, X.\n\n\n \n\n\n\n Genetics in Medicine, 25(2): 100333. feb 2023.\n \n\n\n\n
\n\n\n\n \n \n \"PrecisionPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{esterhuizen_precision_2023,\nauthor = {Esterhuizen, Alina I and Tiffin, Nicki and Riordan, Gillian and Wessels, Marie and Burman, Richard J and Aziz, Miriam C and Calhoun, Jeffrey D and Gunti, Jonathan and Amiri, Ezra E and Ramamurthy, Aishwarya and Bamshad, Michael J and Mefford, Heather C and Ramesar, Raj and Wilmshurst, Jo M and Carvill, Gemma L and Bamshad, Michael J and Leal, Suzanne M and Nickerson, Deborah A and Anderson, Peter and Bacus, Tamara J and Blue, Elizabeth E and Brower, Katherine and Buckingham, Kati J and Chong, Jessica X and {Cornejo S{\\'{a}}nchez}, Diana and Davis, Colleen P and Davis, Chayna J and Frazar, Christian D and Gomeztagle-Burgess, Katherine and Gordon, William W and Horike-Pyne, Martha and Hurless, Jameson R and Jarvik, Gail P and Johanson, Eric and {Thomas Kolar}, J and Marvin, Colby T and McGee, Sean and McGoldrick, Daniel J and Mekonnen, Betselote and Nielsen, Patrick M and Patterson, Karynne and Radhakrishnan, Aparna and Richardson, Matthew A and Roote, Gwendolin T and Ryke, Erica L and Schrauwen, Isabelle and Shively, Kathryn M and Smith, Joshua D and Tackett, Monica and Wang, Gao and Weiss, Jeffrey M and Wheeler, Marsha M and Yi, Qian and Zhang, Xiaohong},\ndoi = {10.1016/j.gim.2022.11.002},\nfile = {:Users/jacquelinebracher/Zotero/storage/JWG2E5DM/Esterhuizen et al. - 2023 - Precision medicine for developmental and epileptic.pdf:pdf},\nissn = {10983600},\njournal = {Genetics in Medicine},\nmonth = {feb},\nnumber = {2},\npages = {100333},\ntitle = {{Precision medicine for developmental and epileptic encephalopathies in {\\{}Africa{\\}}—strategies for a resource-limited setting}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S1098360022010012},\nvolume = {25},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Bacterial meningitis in \\Africa\\.\n \n \n \n \n\n\n \n Barichello, T.; Rocha Catalão, C. H.; Rohlwink, U. K; Kuip, M. V. D.; Zaharie, D.; Solomons, R. S; Van Toorn, R.; Tutu Van Furth, M.; Hasbun, R.; Iovino, F.; and Namale, V. S.\n\n\n \n\n\n\n Frontiers in Neurology, 14: 822575. feb 2023.\n \n\n\n\n
\n\n\n\n \n \n \"BacterialPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{barichello_bacterial_2023,\nabstract = {Bacterial meningitis differs globally, and the incidence and case fatality rates vary by region, country, pathogen, and age group; being a life-threatening disease with a high case fatality rate and long-term complications in low-income countries. Africa has the most significant prevalence of bacterial meningitis illness, and the outbreaks typically vary with the season and the geographic location, with a high incidence in the meningitis belt of the sub-Saharan area from Senegal to Ethiopia.\nStreptococcus pneumoniae\n(pneumococcus) and\nNeisseria meningitidis\n(meningococcus) are the main etiological agents of bacterial meningitis in adults and children above the age of one.\nStreptococcus agalactiae\n(group B Streptococcus)\n, Escherichia coli\n, and\nStaphylococcus aureus\nare neonatal meningitis's most common causal agents. Despite efforts to vaccinate against the most common causes of bacterial neuro-infections, bacterial meningitis remains a significant cause of mortality and morbidity in Africa, with children below 5 years bearing the heaviest disease burden. The factors attributed to this continued high disease burden include poor infrastructure, continued war, instability, and difficulty in diagnosis of bacterial neuro-infections leading to delay in treatment and hence high morbidity. Despite having the highest disease burden, there is a paucity of African data on bacterial meningitis. In this article, we discuss the common etiologies of bacterial neuroinfectious diseases, diagnosis and the interplay between microorganisms and the immune system, and the value of neuroimmune changes in diagnostics and therapeutics.},\nauthor = {Barichello, Tatiana and {Rocha Catal{\\~{a}}o}, Carlos Henrique and Rohlwink, Ursula K and Kuip, Martijn Van Der and Zaharie, Dan and Solomons, Regan S and {Van Toorn}, Ronald and {Tutu Van Furth}, Marceline and Hasbun, Rodrigo and Iovino, Federico and Namale, Vivian Ssonko},\ndoi = {10.3389/fneur.2023.822575},\nfile = {:Users/jacquelinebracher/Zotero/storage/J6W6WA9N/Barichello et al. - 2023 - Bacterial meningitis in Africa.pdf:pdf},\nissn = {1664-2295},\njournal = {Frontiers in Neurology},\nmonth = {feb},\npages = {822575},\ntitle = {{Bacterial meningitis in {\\{}Africa{\\}}}},\nurl = {https://www.frontiersin.org/articles/10.3389/fneur.2023.822575/full},\nvolume = {14},\nyear = {2023}\n}\n
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\n Bacterial meningitis differs globally, and the incidence and case fatality rates vary by region, country, pathogen, and age group; being a life-threatening disease with a high case fatality rate and long-term complications in low-income countries. Africa has the most significant prevalence of bacterial meningitis illness, and the outbreaks typically vary with the season and the geographic location, with a high incidence in the meningitis belt of the sub-Saharan area from Senegal to Ethiopia. Streptococcus pneumoniae (pneumococcus) and Neisseria meningitidis (meningococcus) are the main etiological agents of bacterial meningitis in adults and children above the age of one. Streptococcus agalactiae (group B Streptococcus) , Escherichia coli , and Staphylococcus aureus are neonatal meningitis's most common causal agents. Despite efforts to vaccinate against the most common causes of bacterial neuro-infections, bacterial meningitis remains a significant cause of mortality and morbidity in Africa, with children below 5 years bearing the heaviest disease burden. The factors attributed to this continued high disease burden include poor infrastructure, continued war, instability, and difficulty in diagnosis of bacterial neuro-infections leading to delay in treatment and hence high morbidity. Despite having the highest disease burden, there is a paucity of African data on bacterial meningitis. In this article, we discuss the common etiologies of bacterial neuroinfectious diseases, diagnosis and the interplay between microorganisms and the immune system, and the value of neuroimmune changes in diagnostics and therapeutics.\n
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\n \n\n \n \n \n \n \n \n \\DNA\\ methylation and general psychopathology in childhood: an epigenome-wide meta-analysis from the \\PACE\\ consortium.\n \n \n \n \n\n\n \n Rijlaarsdam, J.; Cosin-Tomas, M.; Schellhas, L.; Abrishamcar, S.; Malmberg, A.; Neumann, A.; Felix, J. F; Sunyer, J.; Gutzkow, K. B; Grazuleviciene, R.; Wright, J.; Kampouri, M.; Zar, H. J; Stein, D. J; Heinonen, K.; Räikkönen, K.; Lahti, J.; Hüls, A.; Caramaschi, D.; Alemany, S.; and Cecil, C. A M\n\n\n \n\n\n\n Molecular Psychiatry, 28(3): 1128–1136. mar 2023.\n \n\n\n\n
\n\n\n\n \n \n \"\\DNA\\Paper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{rijlaarsdam_dna_2023,\nauthor = {Rijlaarsdam, Jolien and Cosin-Tomas, Marta and Schellhas, Laura and Abrishamcar, Sarina and Malmberg, Anni and Neumann, Alexander and Felix, Janine F and Sunyer, Jordi and Gutzkow, Kristine B and Grazuleviciene, Regina and Wright, John and Kampouri, Mariza and Zar, Heather J and Stein, Dan J and Heinonen, Kati and R{\\"{a}}ikk{\\"{o}}nen, Katri and Lahti, Jari and H{\\"{u}}ls, Anke and Caramaschi, Doretta and Alemany, Silvia and Cecil, Charlotte A M},\ndoi = {10.1038/s41380-022-01871-6},\nfile = {:Users/jacquelinebracher/Zotero/storage/JA8D6DYJ/Rijlaarsdam et al. - 2023 - DNA methylation and general psychopathology in chi.pdf:pdf},\nissn = {1359-4184, 1476-5578},\njournal = {Molecular Psychiatry},\nmonth = {mar},\nnumber = {3},\npages = {1128--1136},\nshorttitle = {{\\{}DNA{\\}} methylation and general psychopathology in c},\ntitle = {{{\\{}DNA{\\}} methylation and general psychopathology in childhood: an epigenome-wide meta-analysis from the {\\{}PACE{\\}} consortium}},\nurl = {https://www.nature.com/articles/s41380-022-01871-6},\nvolume = {28},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Associations between community-level patterns of prenatal alcohol and tobacco exposure on brain structure in a non-clinical sample of 6-year-old children: a \\South\\ \\African\\ pilot study.\n \n \n \n \n\n\n \n Uban, K. A; Jonker, D.; Donald, K. A; Bodison, S. C; Brooks, S. J; Kan, E.; Steigelmann, B.; Roos, A.; Marshall, A.; Adise, S.; Butler-Kruger, L.; Melly, B.; Narr, K. L; Joshi, S. H; Odendaal, H. J; Sowell, E. R; and Stein, D. J\n\n\n \n\n\n\n Acta Neuropsychiatrica,1–10. jan 2023.\n \n\n\n\n
\n\n\n\n \n \n \"AssociationsPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{uban_associations_2023,\nabstract = {Abstract\n\nThe current small study utilised prospective data collection of patterns of prenatal alcohol and tobacco exposure (PAE and PTE) to examine associations with structural brain outcomes in 6-year-olds and served as a pilot to determine the value of prospective data describing community-level patterns of PAE and PTE in a non-clinical sample of children. Participants from the Safe Passage Study in pregnancy were approached when their child was ∼6 years old and completed structural brain magnetic resonance imaging to examine with archived PAE and PTE data (\nn\n= 51 children–mother dyads). Linear regression was used to conduct whole-brain structural analyses, with false-discovery rate (FDR) correction, to examine: (a) main effects of PAE, PTE and their interaction; and (b) predictive potential of data that reflect\npatterns\nof PAE and PTE (e.g. quantity, frequency and timing (QFT)). Associations between PAE, PTE and their interaction with brain structural measures demonstrated unique profiles of cortical and subcortical alterations that were distinct between PAE only, PTE only and their interactive effects. Analyses examining associations between patterns of PAE and PTE (e.g. QFT) were able to significantly detect brain alterations (that survived FDR correction) in this small non-clinical sample of children. These findings support the hypothesis that considering QFT and co-exposures is important for identifying brain alterations following PAE and/or PTE in a small group of young children. Current results demonstrate that teratogenic outcomes on brain structure differ as a function PAE, PTE or their co-exposures, as well as the pattern (QFT) or exposure.},\nauthor = {Uban, Kristina A and Jonker, Deborah and Donald, Kirsten A and Bodison, Stefanie C and Brooks, Samantha J and Kan, Eric and Steigelmann, Babette and Roos, Annerine and Marshall, Andrew and Adise, Shana and Butler-Kruger, Letitia and Melly, Brigitte and Narr, Katherine L and Joshi, Shantanu H and Odendaal, Hein J and Sowell, Elizabeth R and Stein, Dan J},\ndoi = {10.1017/neu.2022.34},\nfile = {:Users/jacquelinebracher/Zotero/storage/QPECQXYV/Uban et al. - 2023 - Associations between community-level patterns of p.pdf:pdf},\nissn = {0924-2708, 1601-5215},\njournal = {Acta Neuropsychiatrica},\nmonth = {jan},\npages = {1--10},\nshorttitle = {Associations between community-level patterns of p},\ntitle = {{Associations between community-level patterns of prenatal alcohol and tobacco exposure on brain structure in a non-clinical sample of 6-year-old children: a {\\{}South{\\}} {\\{}African{\\}} pilot study}},\nurl = {https://www.cambridge.org/core/product/identifier/S0924270822000345/type/journal{\\_}article},\nyear = {2023}\n}\n
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\n Abstract The current small study utilised prospective data collection of patterns of prenatal alcohol and tobacco exposure (PAE and PTE) to examine associations with structural brain outcomes in 6-year-olds and served as a pilot to determine the value of prospective data describing community-level patterns of PAE and PTE in a non-clinical sample of children. Participants from the Safe Passage Study in pregnancy were approached when their child was ∼6 years old and completed structural brain magnetic resonance imaging to examine with archived PAE and PTE data ( n = 51 children–mother dyads). Linear regression was used to conduct whole-brain structural analyses, with false-discovery rate (FDR) correction, to examine: (a) main effects of PAE, PTE and their interaction; and (b) predictive potential of data that reflect patterns of PAE and PTE (e.g. quantity, frequency and timing (QFT)). Associations between PAE, PTE and their interaction with brain structural measures demonstrated unique profiles of cortical and subcortical alterations that were distinct between PAE only, PTE only and their interactive effects. Analyses examining associations between patterns of PAE and PTE (e.g. QFT) were able to significantly detect brain alterations (that survived FDR correction) in this small non-clinical sample of children. These findings support the hypothesis that considering QFT and co-exposures is important for identifying brain alterations following PAE and/or PTE in a small group of young children. Current results demonstrate that teratogenic outcomes on brain structure differ as a function PAE, PTE or their co-exposures, as well as the pattern (QFT) or exposure.\n
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\n \n\n \n \n \n \n \n \n Integrated psychological care services within seizure settings: \\Key\\ components and implementation factors among example services in four \\textlessspan style=\"font-variant:small-caps;\"\\textgreater\\ILAE\\\\textless/span\\textgreaterregions: \\A\\ report by the \\textlessspan style=\"font-variant:small-caps;.\n \n \n \n \n\n\n \n Gandy, M.; Michaelis, R.; Acraman, J.; Donald, K. A; Fitzpatrick, M.; LaFrance, W C.; Margolis, S. A; Modi, A. C; Reuber, M.; Tang, V.; Thayer, Z.; Verity, K.; Wagner, J. L; Wilmshurst, J.; Whittaker, S.; and Munger Clary, H. M\n\n\n \n\n\n\n Epilepsia, 64(7): 1766–1784. jul 2023.\n \n\n\n\n
\n\n\n\n \n \n \"IntegratedPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{gandy_integrated_2023,\nabstract = {Abstract\nMental health comorbidities are prevalent and problematic in patients with seizures but often suboptimally managed. To address common gaps in care, the Integrated Mental Health Care Pathways Task Force of the International League Against Epilepsy (ILAE) Psychiatry Commission was tasked with providing education and guidance on the integration of mental health management (e.g., screening, referral, treatment) into routine seizure care. This report aims to describe a variety of established services in this area, with a specific focus on psychological care models. Services were identified by members of the ILAE Psychiatry Commission and authors of psychological intervention trials in epilepsy. A total of eight services met inclusion criteria and agreed to be showcased. They include three pediatric and five adult services located across four distinct ILAE regions (Europe, North America, Africa, Asia Oceania). The report describes the core operations, known outcomes, and implementation factors (i.e., barriers and facilitators) of these services. The report concludes with a set of practical tips for building successful psychological care services within seizure settings, including the importance of having local champions, clearly defining the scope of the service, and establishing sustainable funding models. The breadth of exemplars demonstrates how models tailored to the local environment and resources can be implemented. This report is an initial step to disseminate information regarding integrated mental health care within seizure care settings. Future work is needed to systematically examine both psychological and pharmacological care models and to further establish the evidence base in this area, especially around clinical impact, and cost‐effectiveness.},\nauthor = {Gandy, Milena and Michaelis, Rosa and Acraman, Jayne and Donald, Kirsten A and Fitzpatrick, Michael and LaFrance, W Curt and Margolis, Seth A and Modi, Avani C and Reuber, Markus and Tang, Venus and Thayer, Zoe and Verity, Kirsten and Wagner, Janelle L and Wilmshurst, Jo and Whittaker, Sarah and {Munger Clary}, Heidi M},\ndoi = {10.1111/epi.17647},\nfile = {:Users/jacquelinebracher/Zotero/storage/LU2EVUIZ/Gandy et al. - 2023 - Integrated psychological care services within seiz.pdf:pdf},\nissn = {0013-9580, 1528-1167},\njournal = {Epilepsia},\nmonth = {jul},\nnumber = {7},\npages = {1766--1784},\nshorttitle = {Integrated psychological care services within seiz},\ntitle = {{Integrated psychological care services within seizure settings: {\\{}Key{\\}} components and implementation factors among example services in four {\\textless}span style="font-variant:small-caps;"{\\textgreater}{\\{}ILAE{\\}}{\\textless}/span{\\textgreater}regions: {\\{}A{\\}} report by the {\\textless}span style="font-variant:small-caps;}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1111/epi.17647},\nvolume = {64},\nyear = {2023}\n}\n
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\n Abstract Mental health comorbidities are prevalent and problematic in patients with seizures but often suboptimally managed. To address common gaps in care, the Integrated Mental Health Care Pathways Task Force of the International League Against Epilepsy (ILAE) Psychiatry Commission was tasked with providing education and guidance on the integration of mental health management (e.g., screening, referral, treatment) into routine seizure care. This report aims to describe a variety of established services in this area, with a specific focus on psychological care models. Services were identified by members of the ILAE Psychiatry Commission and authors of psychological intervention trials in epilepsy. A total of eight services met inclusion criteria and agreed to be showcased. They include three pediatric and five adult services located across four distinct ILAE regions (Europe, North America, Africa, Asia Oceania). The report describes the core operations, known outcomes, and implementation factors (i.e., barriers and facilitators) of these services. The report concludes with a set of practical tips for building successful psychological care services within seizure settings, including the importance of having local champions, clearly defining the scope of the service, and establishing sustainable funding models. The breadth of exemplars demonstrates how models tailored to the local environment and resources can be implemented. This report is an initial step to disseminate information regarding integrated mental health care within seizure care settings. Future work is needed to systematically examine both psychological and pharmacological care models and to further establish the evidence base in this area, especially around clinical impact, and cost‐effectiveness.\n
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\n \n\n \n \n \n \n \n \n In vitro and in vivo anti-seizure activity of hydromethanolic extract and fractions of \\Pterolobium\\ stellatum.\n \n \n \n \n\n\n \n Salile, S. S.; Lee, H. J.; Alberts, P. S. F.; Abula, T.; Raimondo, J. V.; and Stafford, G. I.\n\n\n \n\n\n\n Journal of Ethnopharmacology, 304: 116073. mar 2023.\n \n\n\n\n
\n\n\n\n \n \n \"InPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{salile_vitro_2023,\nauthor = {Salile, Samson Sahile and Lee, Hamin John and Alberts, Paul Sewes Frederick and Abula, Teferra and Raimondo, Joseph Valentino and Stafford, Gary Ivan},\ndoi = {10.1016/j.jep.2022.116073},\nissn = {03788741},\njournal = {Journal of Ethnopharmacology},\nmonth = {mar},\npages = {116073},\ntitle = {{In vitro and in vivo anti-seizure activity of hydromethanolic extract and fractions of {\\{}Pterolobium{\\}} stellatum}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S0378874122011126},\nvolume = {304},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Trauma exposure and psychometric properties of the life events checklist among adults in \\South\\ \\Africa\\.\n \n \n \n \n\n\n \n Stevenson, A.; Beltran, M.; Misra, S.; Ametaj, A. A; Bronkhorst, A.; Gelaye, B.; Koenen, K. C; Pretorius, A.; Stein, D. J; and Zingela, Z.\n\n\n \n\n\n\n European Journal of Psychotraumatology, 14(1): 2172257. dec 2023.\n \n\n\n\n
\n\n\n\n \n \n \"TraumaPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{stevenson_trauma_2023,\nauthor = {Stevenson, Anne and Beltran, Marine and Misra, Supriya and Ametaj, Amantia A and Bronkhorst, Aletta and Gelaye, Bizu and Koenen, Karestan C and Pretorius, Adele and Stein, Dan J and Zingela, Zukiswa},\ndoi = {10.1080/20008066.2023.2172257},\nfile = {:Users/jacquelinebracher/Zotero/storage/VP4JN5JH/Stevenson et al. - 2023 - Trauma exposure and psychometric properties of the.pdf:pdf},\nissn = {2000-8066},\njournal = {European Journal of Psychotraumatology},\nmonth = {dec},\nnumber = {1},\npages = {2172257},\ntitle = {{Trauma exposure and psychometric properties of the life events checklist among adults in {\\{}South{\\}} {\\{}Africa{\\}}}},\nurl = {https://www.tandfonline.com/doi/full/10.1080/20008066.2023.2172257},\nvolume = {14},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n World \\Federation\\ of \\Societies\\ of \\Biological\\ \\Psychiatry\\ (\\WFSBP\\) guidelines for treatment of anxiety, obsessive-compulsive and posttraumatic stress disorders – \\Version\\ 3. \\Part\\ \\I\\: \\Anxiety\\ disorders.\n \n \n \n \n\n\n \n Bandelow, B.; Allgulander, C.; Baldwin, D. S; Costa, D. L. D. C.; Denys, D.; Dilbaz, N.; Domschke, K.; Eriksson, E.; Fineberg, N. A; Hättenschwiler, J.; Hollander, E.; Kaiya, H.; Karavaeva, T.; Kasper, S.; Katzman, M.; Kim, Y.; Inoue, T.; Lim, L.; Masdrakis, V.; Menchón, J. M; Miguel, E. C; Möller, H.; Nardi, A. E; Pallanti, S.; Perna, G.; Rujescu, D.; Starcevic, V.; Stein, D. J; Tsai, S.; Van Ameringen, M.; Vasileva, A.; Wang, Z.; and Zohar, J.\n\n\n \n\n\n\n The World Journal of Biological Psychiatry, 24(2): 79–117. feb 2023.\n \n\n\n\n
\n\n\n\n \n \n \"WorldPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{bandelow_world_2023,\nauthor = {Bandelow, Borwin and Allgulander, Christer and Baldwin, David S and Costa, Daniel Lucas Da Concei{\\c{c}}{\\~{a}}o and Denys, Damiaan and Dilbaz, Nesrin and Domschke, Katharina and Eriksson, Elias and Fineberg, Naomi A and H{\\"{a}}ttenschwiler, Josef and Hollander, Eric and Kaiya, Hisanobu and Karavaeva, Tatiana and Kasper, Siegfried and Katzman, Martin and Kim, Yong-Ku and Inoue, Takeshi and Lim, Leslie and Masdrakis, Vasilios and Mench{\\'{o}}n, Jos{\\'{e}} M and Miguel, Euripedes C and M{\\"{o}}ller, Hans-J{\\"{u}}rgen and Nardi, Antonio E and Pallanti, Stefano and Perna, Giampaolo and Rujescu, Dan and Starcevic, Vladan and Stein, Dan J and Tsai, Shih-Jen and {Van Ameringen}, Michael and Vasileva, Anna and Wang, Zhen and Zohar, Joseph},\ndoi = {10.1080/15622975.2022.2086295},\nissn = {1562-2975, 1814-1412},\njournal = {The World Journal of Biological Psychiatry},\nmonth = {feb},\nnumber = {2},\npages = {79--117},\nshorttitle = {World {\\{}Federation{\\}} of {\\{}Societies{\\}} of {\\{}Biological{\\}} },\ntitle = {{World {\\{}Federation{\\}} of {\\{}Societies{\\}} of {\\{}Biological{\\}} {\\{}Psychiatry{\\}} ({\\{}WFSBP{\\}}) guidelines for treatment of anxiety, obsessive-compulsive and posttraumatic stress disorders – {\\{}Version{\\}} 3. {\\{}Part{\\}} {\\{}I{\\}}: {\\{}Anxiety{\\}} disorders}},\nurl = {https://www.tandfonline.com/doi/full/10.1080/15622975.2022.2086295},\nvolume = {24},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Antenatal maternal intimate partner violence exposure is associated with sex-specific alterations in brain structure among young infants: \\Evidence\\ from a \\South\\ \\African\\ birth cohort.\n \n \n \n \n\n\n \n Hiscox, L. V; Fairchild, G.; Donald, K. A; Groenewold, N. A; Koen, N.; Roos, A.; Narr, K. L; Lawrence, M.; Hoffman, N.; Wedderburn, C. J; Barnett, W.; Zar, H. J; Stein, D. J; and Halligan, S. L\n\n\n \n\n\n\n Developmental Cognitive Neuroscience, 60: 101210. apr 2023.\n \n\n\n\n
\n\n\n\n \n \n \"AntenatalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{hiscox_antenatal_2023,\nauthor = {Hiscox, Lucy V and Fairchild, Graeme and Donald, Kirsten A and Groenewold, Nynke A and Koen, Nastassja and Roos, Annerine and Narr, Katherine L and Lawrence, Marina and Hoffman, Nadia and Wedderburn, Catherine J and Barnett, Whitney and Zar, Heather J and Stein, Dan J and Halligan, Sarah L},\ndoi = {10.1016/j.dcn.2023.101210},\nfile = {:Users/jacquelinebracher/Zotero/storage/8BSN7VXQ/Hiscox et al. - 2023 - Antenatal maternal intimate partner violence expos.pdf:pdf},\nissn = {18789293},\njournal = {Developmental Cognitive Neuroscience},\nmonth = {apr},\npages = {101210},\nshorttitle = {Antenatal maternal intimate partner violence expos},\ntitle = {{Antenatal maternal intimate partner violence exposure is associated with sex-specific alterations in brain structure among young infants: {\\{}Evidence{\\}} from a {\\{}South{\\}} {\\{}African{\\}} birth cohort}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S1878929323000154},\nvolume = {60},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Global synergistic actions to improve brain health for human development.\n \n \n \n \n\n\n \n Owolabi, M. O; Leonardi, M.; Bassetti, C.; Jaarsma, J.; Hawrot, T.; Makanjuola, A. I; Dhamija, R. K; Feng, W.; Straub, V.; Camaradou, J.; Dodick, D. W; Sunna, R.; Menon, B.; Wright, C.; Lynch, C.; Chadha, A. S.; Ferretti, M. T.; Dé, A.; Catsman-Berrevoets, C. E; Gichu, M.; Tassorelli, C.; Oliver, D.; Paulus, W.; Mohammed, R. K; Charway-Felli, A.; Rostasy, K.; Feigin, V.; Craven, A.; Cunningham, E.; Galvin, O.; Perry, A. H.; Fink, E. L; Baneke, P.; Helme, A.; Laurson-Doube, J.; Medina, M. T; Roa, J. D.; Hogl, B.; O'Bryan, A.; Trenkwalder, C.; Wilmshurst, J.; Akinyemi, R. O; Yaria, J. O; Good, D. C; Hoemberg, V.; Boon, P.; Wiebe, S.; Cross, J H.; Haas, M.; Jabalpurwala, I.; Mojasevic, M.; DiLuca, M.; Barbarino, P.; Clarke, S.; Zuberi, S. M; Olowoyo, P.; Owolabi, A.; Oyesiku, N.; Maly-Sundgren, P. C; Norrving, B.; Soekadar, S. R; Van Doorn, P. A; Lewis, R.; Solomon, T.; and Servadei, F.\n\n\n \n\n\n\n Nature Reviews Neurology, 19(6): 371–383. jun 2023.\n \n\n\n\n
\n\n\n\n \n \n \"GlobalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{owolabi_global_2023,\nauthor = {Owolabi, Mayowa O and Leonardi, Matilde and Bassetti, Claudio and Jaarsma, Joke and Hawrot, Tadeusz and Makanjuola, Akintomiwa I and Dhamija, Rajinder K and Feng, Wuwei and Straub, Volker and Camaradou, Jennifer and Dodick, David W and Sunna, Rosita and Menon, Bindu and Wright, Claire and Lynch, Chris and Chadha, Antonella Santuccione and Ferretti, Maria Teresa and D{\\'{e}}, Anna and Catsman-Berrevoets, Coriene E and Gichu, Muthoni and Tassorelli, Cristina and Oliver, David and Paulus, Walter and Mohammed, Ramla K and Charway-Felli, Augustina and Rostasy, Kevin and Feigin, Valery and Craven, Audrey and Cunningham, Elizabeth and Galvin, Orla and Perry, Alexandra Heumber and Fink, Ericka L and Baneke, Peer and Helme, Anne and Laurson-Doube, Joanna and Medina, Marco T and Roa, Juan David and Hogl, Birgit and O'Bryan, Allan and Trenkwalder, Claudia and Wilmshurst, Jo and Akinyemi, Rufus O and Yaria, Joseph O and Good, David C and Hoemberg, Volker and Boon, Paul and Wiebe, Samuel and Cross, J Helen and Haas, Magali and Jabalpurwala, Inez and Mojasevic, Marijeta and DiLuca, Monica and Barbarino, Paola and Clarke, Stephanie and Zuberi, Sameer M and Olowoyo, Paul and Owolabi, Ayomide and Oyesiku, Nelson and Maly-Sundgren, Pia C and Norrving, Bo and Soekadar, Surjo R and {Van Doorn}, Pieter A and Lewis, Richard and Solomon, Tom and Servadei, Franco},\ndoi = {10.1038/s41582-023-00808-z},\nfile = {:Users/jacquelinebracher/Zotero/storage/4FA55VVH/Owolabi et al. - 2023 - Global synergistic actions to improve brain health.pdf:pdf},\nissn = {1759-4758, 1759-4766},\njournal = {Nature Reviews Neurology},\nmonth = {jun},\nnumber = {6},\npages = {371--383},\ntitle = {{Global synergistic actions to improve brain health for human development}},\nurl = {https://www.nature.com/articles/s41582-023-00808-z},\nvolume = {19},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Life years lost associated with mental illness: \\A\\ cohort study of beneficiaries of a \\South\\ \\African\\ medical insurance scheme.\n \n \n \n \n\n\n \n Ruffieux, Y.; Wettstein, A.; Maartens, G.; Folb, N.; Mesa-Vieira, C.; Didden, C.; Tlali, M.; Williams, C.; Cornell, M.; Schomaker, M.; Johnson, L. F; Joska, J. A; Egger, M.; and Haas, A. D\n\n\n \n\n\n\n Journal of Affective Disorders, 340: 204–212. nov 2023.\n \n\n\n\n
\n\n\n\n \n \n \"LifePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{ruffieux_life_2023,\nauthor = {Ruffieux, Yann and Wettstein, Anja and Maartens, Gary and Folb, Naomi and Mesa-Vieira, Cristina and Didden, Christiane and Tlali, Mpho and Williams, Chanwyn and Cornell, Morna and Schomaker, Michael and Johnson, Leigh F and Joska, John A and Egger, Matthias and Haas, Andreas D},\ndoi = {10.1016/j.jad.2023.08.013},\nfile = {:Users/jacquelinebracher/Zotero/storage/5AYRLUVT/Ruffieux et al. - 2023 - Life years lost associated with mental illness A .pdf:pdf},\nissn = {01650327},\njournal = {Journal of Affective Disorders},\nmonth = {nov},\npages = {204--212},\nshorttitle = {Life years lost associated with mental illness},\ntitle = {{Life years lost associated with mental illness: {\\{}A{\\}} cohort study of beneficiaries of a {\\{}South{\\}} {\\{}African{\\}} medical insurance scheme}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S0165032723009898},\nvolume = {340},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n World \\Federation\\ of \\Societies\\ of \\Biological\\ \\Psychiatry\\ (\\WFSBP\\) guidelines for treatment of anxiety, obsessive-compulsive and posttraumatic stress disorders – \\Version\\ 3. \\Part\\ \\II\\: \\OCD\\ and \\PTSD\\.\n \n \n \n \n\n\n \n Bandelow, B.; Allgulander, C.; Baldwin, D. S; Costa, D. L. D. C.; Denys, D.; Dilbaz, N.; Domschke, K.; Hollander, E.; Kasper, S.; Möller, H.; Eriksson, E.; Fineberg, N. A; Hättenschwiler, J.; Kaiya, H.; Karavaeva, T.; Katzman, M. A; Kim, Y.; Inoue, T.; Lim, L.; Masdrakis, V.; Menchón, J. M; Miguel, E. C; Nardi, A. E; Pallanti, S.; Perna, G.; Rujescu, D.; Starcevic, V.; Stein, D. J; Tsai, S.; Van Ameringen, M.; Vasileva, A.; Wang, Z.; and Zohar, J.\n\n\n \n\n\n\n The World Journal of Biological Psychiatry, 24(2): 118–134. feb 2023.\n \n\n\n\n
\n\n\n\n \n \n \"WorldPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{bandelow_world_2023-1,\nauthor = {Bandelow, Borwin and Allgulander, Christer and Baldwin, David S and Costa, Daniel Lucas Da Concei{\\c{c}}{\\~{a}}o and Denys, Damiaan and Dilbaz, Nesrin and Domschke, Katharina and Hollander, Eric and Kasper, Siegfried and M{\\"{o}}ller, Hans-J{\\"{u}}rgen and Eriksson, Elias and Fineberg, Naomi A and H{\\"{a}}ttenschwiler, Josef and Kaiya, Hisanobu and Karavaeva, Tatiana and Katzman, Martin A and Kim, Yong-Ku and Inoue, Takeshi and Lim, Leslie and Masdrakis, Vasilios and Mench{\\'{o}}n, Jos{\\'{e}} M and Miguel, Euripedes C and Nardi, Ant{\\^{o}}nio E and Pallanti, Stefano and Perna, Giampaolo and Rujescu, Dan and Starcevic, Vladan and Stein, Dan J and Tsai, Shih-Jen and {Van Ameringen}, Michael and Vasileva, Anna and Wang, Zhen and Zohar, Joseph},\ndoi = {10.1080/15622975.2022.2086296},\nissn = {1562-2975, 1814-1412},\njournal = {The World Journal of Biological Psychiatry},\nmonth = {feb},\nnumber = {2},\npages = {118--134},\nshorttitle = {World {\\{}Federation{\\}} of {\\{}Societies{\\}} of {\\{}Biological{\\}} },\ntitle = {{World {\\{}Federation{\\}} of {\\{}Societies{\\}} of {\\{}Biological{\\}} {\\{}Psychiatry{\\}} ({\\{}WFSBP{\\}}) guidelines for treatment of anxiety, obsessive-compulsive and posttraumatic stress disorders – {\\{}Version{\\}} 3. {\\{}Part{\\}} {\\{}II{\\}}: {\\{}OCD{\\}} and {\\{}PTSD{\\}}}},\nurl = {https://www.tandfonline.com/doi/full/10.1080/15622975.2022.2086296},\nvolume = {24},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Measurement fidelity of clinical assessment methods in a global study on identifying reproducible brain signatures of obsessive–compulsive disorder.\n \n \n \n \n\n\n \n Shavitt, R. G; Sheshachala, K.; Hezel, D. M; Wall, M. M; Balachander, S.; Lochner, C.; Narayanaswamy, J. C; Costa, D. L C; De Mathis, M. A.; Van Balkom, A. J L M; De Joode, N. T; Narayan, M.; Van Den Heuvel, O. A; Stein, D. J; Miguel, E. C; Simpson, H. B.; and Reddy, Y C J.\n\n\n \n\n\n\n Neuropsychology, 37(3): 330–343. mar 2023.\n \n\n\n\n
\n\n\n\n \n \n \"MeasurementPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{shavitt_measurement_2023,\nauthor = {Shavitt, Roseli G and Sheshachala, Karthik and Hezel, Dianne M and Wall, Melanie M and Balachander, Srinivas and Lochner, Christine and Narayanaswamy, Janardhanan C and Costa, Daniel L C and {De Mathis}, Maria Alice and {Van Balkom}, Anton J L M and {De Joode}, Niels T and Narayan, Madhuri and {Van Den Heuvel}, Odile A and Stein, Dan J and Miguel, Euripedes C and Simpson, Helen Blair and Reddy, Y C Janardhan},\ndoi = {10.1037/neu0000849},\nissn = {1931-1559, 0894-4105},\njournal = {Neuropsychology},\nmonth = {mar},\nnumber = {3},\npages = {330--343},\ntitle = {{Measurement fidelity of clinical assessment methods in a global study on identifying reproducible brain signatures of obsessive–compulsive disorder.}},\nurl = {http://doi.apa.org/getdoi.cfm?doi=10.1037/neu0000849},\nvolume = {37},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Medical treatment in infants and young children with epilepsy: \\Off\\‐label use of antiseizure medications. \\Survey\\ \\Report\\ of \\ILAE\\ \\Task\\ \\Force\\ \\Medical\\ \\Therapies\\ in \\Children\\.\n \n \n \n \n\n\n \n Sourbron, J.; Auvin, S.; Arzimanoglou, A.; Cross, J H.; Hartmann, H.; Pressler, R.; Riney, K.; Sugai, K.; Wilmshurst, J. M; Yozawitz, E.; and Lagae, L.\n\n\n \n\n\n\n Epilepsia Open, 8(1): 77–89. mar 2023.\n \n\n\n\n
\n\n\n\n \n \n \"MedicalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{sourbron_medical_2023,\nabstract = {Abstract\n\nObjective\n\nAntiseizure medications (ASMs) remain the mainstay of epilepsy treatment. These ASMs have mainly been tested in trials in adults with epilepsy, which subsequently led to market authorization (MA). For treatment of –\nespecially young\n– children with epilepsy, several ASMs do not have a MA and guidelines are lacking, subsequently leading to “off‐label” use of ASMs. Even though “off‐label” ASM prescriptions for children could lead to more adverse events, it can be clinically appropriate and rational if the benefits outweigh the risks. This could be the case if “on‐label” ASM, in mono‐ or polytherapy, fails to achieve adequate seizure control.\n\n\n\nMethods\nThe Medical Therapies Task Force of the International League Against Epilepsy (ILAE) Commission for Pediatrics performed a survey to study the current treatment practices in six classic, early life epilepsy scenarios. Our aim was not only to study first‐ and second‐line treatment preferences but also to illustrate the use of “off‐label” drugs in childhood epilepsies.\n\n\nResults\nOur results reveal that several ASMs (e.g. topiramate, oxcarbazepine, benzodiazepines) are prescribed “off‐label” in distinct scenarios of young children with epilepsy. In addition, recent scientific guidelines were not always adopted by several survey respondents, suggesting a potential knowledge gap.\n\n\nSignificance\nWe report the relatively common use of “off‐label” prescriptions that underlines the need for targeted and appropriately designed clinical trials, including younger patients, which will also result in the ability to generate evidence‐based guidelines.},\nauthor = {Sourbron, Jo and Auvin, St{\\'{e}}phane and Arzimanoglou, Alexis and Cross, J Helen and Hartmann, Hans and Pressler, Ronit and Riney, Kate and Sugai, Kenji and Wilmshurst, Jo M and Yozawitz, Elissa and Lagae, Lieven},\ndoi = {10.1002/epi4.12666},\nfile = {:Users/jacquelinebracher/Zotero/storage/5LHTRW2Y/Sourbron et al. - 2023 - Medical treatment in infants and young children wi.pdf:pdf},\nissn = {2470-9239, 2470-9239},\njournal = {Epilepsia Open},\nmonth = {mar},\nnumber = {1},\npages = {77--89},\nshorttitle = {Medical treatment in infants and young children wi},\ntitle = {{Medical treatment in infants and young children with epilepsy: {\\{}Off{\\}}‐label use of antiseizure medications. {\\{}Survey{\\}} {\\{}Report{\\}} of {\\{}ILAE{\\}} {\\{}Task{\\}} {\\{}Force{\\}} {\\{}Medical{\\}} {\\{}Therapies{\\}} in {\\{}Children{\\}}}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1002/epi4.12666},\nvolume = {8},\nyear = {2023}\n}\n
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\n Abstract Objective Antiseizure medications (ASMs) remain the mainstay of epilepsy treatment. These ASMs have mainly been tested in trials in adults with epilepsy, which subsequently led to market authorization (MA). For treatment of – especially young – children with epilepsy, several ASMs do not have a MA and guidelines are lacking, subsequently leading to “off‐label” use of ASMs. Even though “off‐label” ASM prescriptions for children could lead to more adverse events, it can be clinically appropriate and rational if the benefits outweigh the risks. This could be the case if “on‐label” ASM, in mono‐ or polytherapy, fails to achieve adequate seizure control. Methods The Medical Therapies Task Force of the International League Against Epilepsy (ILAE) Commission for Pediatrics performed a survey to study the current treatment practices in six classic, early life epilepsy scenarios. Our aim was not only to study first‐ and second‐line treatment preferences but also to illustrate the use of “off‐label” drugs in childhood epilepsies. Results Our results reveal that several ASMs (e.g. topiramate, oxcarbazepine, benzodiazepines) are prescribed “off‐label” in distinct scenarios of young children with epilepsy. In addition, recent scientific guidelines were not always adopted by several survey respondents, suggesting a potential knowledge gap. Significance We report the relatively common use of “off‐label” prescriptions that underlines the need for targeted and appropriately designed clinical trials, including younger patients, which will also result in the ability to generate evidence‐based guidelines.\n
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\n \n\n \n \n \n \n \n \n Factors associated with breakup distress following a romantic relationship dissolution among emerging adult students.\n \n \n \n \n\n\n \n Van Der Watt, A. S.; Roos, A.; Lesch, E.; and Seedat, S.\n\n\n \n\n\n\n Journal of Psychology in Africa, 33(2): 183–188. mar 2023.\n \n\n\n\n
\n\n\n\n \n \n \"FactorsPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{van_der_watt_factors_2023,\nauthor = {{Van Der Watt}, Alberta Sj and Roos, Annerine and Lesch, Elmien and Seedat, Soraya},\ndoi = {10.1080/14330237.2023.2190232},\nissn = {1433-0237, 1815-5626},\njournal = {Journal of Psychology in Africa},\nmonth = {mar},\nnumber = {2},\npages = {183--188},\ntitle = {{Factors associated with breakup distress following a romantic relationship dissolution among emerging adult students}},\nurl = {https://www.tandfonline.com/doi/full/10.1080/14330237.2023.2190232},\nvolume = {33},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Lessons learned from the translation of the \\Internalised\\ \\Stigma\\ of \\Mental\\ \\Illness\\ (\\ISMI\\) scale into \\isiXhosa\\ for use with \\South\\ \\African\\ \\Xhosa\\ people with schizophrenia.\n \n \n \n \n\n\n \n Matshabane, O. P; Appelbaum, P. S; Faure, M. C; Marshall, P. A; Stein, D. J; De Vries, J.; and Campbell, M. M\n\n\n \n\n\n\n Transcultural Psychiatry,13634615231168461. jun 2023.\n \n\n\n\n
\n\n\n\n \n \n \"LessonsPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{matshabane_lessons_2023,\nabstract = {Internalised stigma is highly prevalent among people with mental illness. This is concerning because internalised stigma is often associated with negative consequences affecting individuals' personal, familial, social, and overall wellbeing, employment opportunities and recovery. Currently, there is no psychometrically validated instrument to measure internalised stigma among Xhosa people in their home language. Our study aimed to translate the Internalised Stigma of Mental Illness (ISMI) scale into isiXhosa. Following WHO guidelines, the ISMI scale was translated using a five-stage translation design which included (i) forward-translation, (ii) back-translation, (iii) committee approach, (iv) quantitative piloting, and (v) qualitative piloting using cognitive interviews. The ISMI isiXhosa version (ISMI-X) underwent psychometric testing to establish utility, within-scale validity, convergent, divergent, and content validity (assessed using frequency of endorsements and cognitive interviewing) with n = 65 Xhosa people with schizophrenia. The resultant ISMI-X scale demonstrated good psychometric utility, internal consistency for the overall scale ($\\alpha$ = .90) and most subscales ($\\alpha$ {\\textgreater}.70, except the Stigma Resistance subscale where $\\alpha$ = .57), convergent validity between the ISMI Discrimination Experiences subscale and the Discrimination and Stigma (DISC) scale's Treated Unfairly subscale ( r = .34, p = .03) and divergent validity between the ISMI Stigma Resistance and DISC Treated Unfairly subscales ( r = .13, p = .49). But more importantly the study provides valuable insights into strengths and limitations of the present translation design. Specifically, validation methods such as assessing frequency of endorsements of scale items and using cognitive interviewing to establish conceptual clarity and relevance of items may be useful in small piloting sample sizes.},\nauthor = {Matshabane, Olivia P and Appelbaum, Paul S and Faure, Marlyn C and Marshall, Patricia A and Stein, Dan J and {De Vries}, Jantina and Campbell, Megan M},\ndoi = {10.1177/13634615231168461},\nfile = {:Users/jacquelinebracher/Zotero/storage/Q879JCKB/Matshabane et al. - 2023 - Lessons learned from the translation of the Intern.pdf:pdf},\nissn = {1363-4615, 1461-7471},\njournal = {Transcultural Psychiatry},\nmonth = {jun},\npages = {13634615231168461},\ntitle = {{Lessons learned from the translation of the {\\{}Internalised{\\}} {\\{}Stigma{\\}} of {\\{}Mental{\\}} {\\{}Illness{\\}} ({\\{}ISMI{\\}}) scale into {\\{}isiXhosa{\\}} for use with {\\{}South{\\}} {\\{}African{\\}} {\\{}Xhosa{\\}} people with schizophrenia}},\nurl = {http://journals.sagepub.com/doi/10.1177/13634615231168461},\nyear = {2023}\n}\n
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\n Internalised stigma is highly prevalent among people with mental illness. This is concerning because internalised stigma is often associated with negative consequences affecting individuals' personal, familial, social, and overall wellbeing, employment opportunities and recovery. Currently, there is no psychometrically validated instrument to measure internalised stigma among Xhosa people in their home language. Our study aimed to translate the Internalised Stigma of Mental Illness (ISMI) scale into isiXhosa. Following WHO guidelines, the ISMI scale was translated using a five-stage translation design which included (i) forward-translation, (ii) back-translation, (iii) committee approach, (iv) quantitative piloting, and (v) qualitative piloting using cognitive interviews. The ISMI isiXhosa version (ISMI-X) underwent psychometric testing to establish utility, within-scale validity, convergent, divergent, and content validity (assessed using frequency of endorsements and cognitive interviewing) with n = 65 Xhosa people with schizophrenia. The resultant ISMI-X scale demonstrated good psychometric utility, internal consistency for the overall scale ($α$ = .90) and most subscales ($α$ \\textgreater.70, except the Stigma Resistance subscale where $α$ = .57), convergent validity between the ISMI Discrimination Experiences subscale and the Discrimination and Stigma (DISC) scale's Treated Unfairly subscale ( r = .34, p = .03) and divergent validity between the ISMI Stigma Resistance and DISC Treated Unfairly subscales ( r = .13, p = .49). But more importantly the study provides valuable insights into strengths and limitations of the present translation design. Specifically, validation methods such as assessing frequency of endorsements of scale items and using cognitive interviewing to establish conceptual clarity and relevance of items may be useful in small piloting sample sizes.\n
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\n \n\n \n \n \n \n \n \n Right \\Prefrontal\\ \\Cortical\\ \\Thickness\\ \\Is\\ \\Associated\\ \\With\\ \\Response\\ to \\Cognitive\\-\\Behavioral\\ \\Therapy\\ in \\Children\\ \\With\\ \\Obsessive\\-\\Compulsive\\ \\Disorder\\.\n \n \n \n \n\n\n \n Bertolín, S.; Alonso, P.; Martínez-Zalacaín, I.; Menchón, J. M; Jimenez-Murcia, S.; Baker, J. T; Bargalló, N.; Batistuzzo, M. C.; Boedhoe, P. S W; Brennan, B. P; Feusner, J. D; Fitzgerald, K. D; Fontaine, M.; Hansen, B.; Hirano, Y.; Hoexter, M. Q; Huyser, C.; Jahanshad, N.; Jaspers-Fayer, F.; Kuno, M.; Kvale, G.; Lazaro, L.; Machado-Sousa, M.; Marsh, R.; Morgado, P.; Nakagawa, A.; Norman, L.; Nurmi, E. L; O'Neill, J.; Ortiz, A. E; Perriello, C.; Piacentini, J.; Picó-Pérez, M.; Shavitt, R. G; Shimizu, E.; Simpson, H. B.; Stewart, S E.; Thomopoulos, S. I; Thorsen, A. L.; Walitza, S.; Wolters, L. H; Thompson, P. M; Van Den Heuvel, O. A; Stein, D. J; Soriano-Mas, C.; Real, E.; Segalas, C.; Morer, A.; Brem, S.; Ferreira, S.; Moreira, P. S.; Hagen, K.; Hamatani, S.; Takahashi, J.; Yoshida, T.; De Mathis, M. A.; Miguel, E. C; Pariente, J. C; and Tang, J.\n\n\n \n\n\n\n Journal of the American Academy of Child & Adolescent Psychiatry, 62(4): 403–414. apr 2023.\n \n\n\n\n
\n\n\n\n \n \n \"RightPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{bertolin_right_2023,\nauthor = {Bertol{\\'{i}}n, Sara and Alonso, Pino and Mart{\\'{i}}nez-Zalaca{\\'{i}}n, Ignacio and Mench{\\'{o}}n, Jose M and Jimenez-Murcia, Susana and Baker, Justin T and Bargall{\\'{o}}, Nuria and Batistuzzo, Marcelo Camargo and Boedhoe, Premika S W and Brennan, Brian P and Feusner, Jamie D and Fitzgerald, Kate D and Fontaine, Martine and Hansen, Bjarne and Hirano, Yoshiyuki and Hoexter, Marcelo Q and Huyser, Chaim and Jahanshad, Neda and Jaspers-Fayer, Fern and Kuno, Masaru and Kvale, Gerd and Lazaro, Luisa and Machado-Sousa, Mafalda and Marsh, Rachel and Morgado, Pedro and Nakagawa, Akiko and Norman, Luke and Nurmi, Erika L and O'Neill, Joseph and Ortiz, Ana E and Perriello, Chris and Piacentini, John and Pic{\\'{o}}-P{\\'{e}}rez, Maria and Shavitt, Roseli G and Shimizu, Eiji and Simpson, Helen Blair and Stewart, S Evelyn and Thomopoulos, Sophia I and Thorsen, Anders Lillevik and Walitza, Susanne and Wolters, Lidewij H and Thompson, Paul M and {Van Den Heuvel}, Odile A and Stein, Dan J and Soriano-Mas, Carles and Real, Eva and Segalas, Cinto and Morer, Astrid and Brem, Silvia and Ferreira, Sonia and Moreira, Pedro Silva and Hagen, Kristen and Hamatani, Sayo and Takahashi, Jumpei and Yoshida, Tokiko and {De Mathis}, Maria Alice and Miguel, Euripedes C and Pariente, Jose C and Tang, Jinsong},\ndoi = {10.1016/j.jaac.2022.07.865},\nissn = {08908567},\njournal = {Journal of the American Academy of Child {\\&} Adolescent Psychiatry},\nmonth = {apr},\nnumber = {4},\npages = {403--414},\ntitle = {{Right {\\{}Prefrontal{\\}} {\\{}Cortical{\\}} {\\{}Thickness{\\}} {\\{}Is{\\}} {\\{}Associated{\\}} {\\{}With{\\}} {\\{}Response{\\}} to {\\{}Cognitive{\\}}-{\\{}Behavioral{\\}} {\\{}Therapy{\\}} in {\\{}Children{\\}} {\\{}With{\\}} {\\{}Obsessive{\\}}-{\\{}Compulsive{\\}} {\\{}Disorder{\\}}}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S0890856722019724},\nvolume = {62},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Maternal perinatal depression and child brain structure at 2-3 years in a \\South\\ \\African\\ birth cohort study.\n \n \n \n \n\n\n \n Pellowski, J. A; Wedderburn, C. J; Groenewold, N. A; Roos, A.; Subramoney, S.; Hoffman, N.; Fouche, J.; Joshi, S. H; Woods, R. P; Narr, K. L; Zar, H. J; Donald, K. A; and Stein, D. J\n\n\n \n\n\n\n Translational Psychiatry, 13(1): 96. mar 2023.\n \n\n\n\n
\n\n\n\n \n \n \"MaternalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{pellowski_maternal_2023,\nabstract = {Abstract\n\nMaternal perinatal depression is associated with risk of adverse child developmental outcomes and differences in offspring brain structure. Evidence from low- and middle-income countries is lacking as is an investigation of antenatal, postnatal, and persistent depression in the same sample. In a South African birth cohort, we investigated the effect of antenatal and postpartum maternal depressive symptoms on offspring brain structure at 2–3 years of age. Magnetic resonance imaging was performed, extracting cortical thickness and surface areas in frontal cortex regions of interest and subcortical volumes using FreeSurfer software. Maternal depressive symptoms were measured using the Edinburgh Postpartum Depression Scale and the Beck Depression Inventory II antenatally and at 6–10 weeks, 6 months, 12 months, and 18 months postpartum and analyzed dichotomously and continuously. Linear regressions were used controlling for child age, sex, intracranial volume, maternal education, age, smoking, alcohol use and HIV. 146 children were included with 38 (37{\\%}) exposed to depressive symptoms antenatally and 44 (35{\\%}) exposed postnatally. Of these, 16 (13{\\%}) were exposed to both. Postpartum, but not antenatal, depressive symptoms were associated with smaller amygdala volumes in children (B = −74.73,\np\n= 0.01). Persistent maternal depressive symptoms across pregnancy and postpartum were also independently associated with smaller amygdala volumes (B = −78.61,\np\n= 0.047). Differences in amygdala volumes among children exposed to postnatal as well as persistent maternal depressive symptomatology underscore the importance of identifying women at-risk for depression during the entire perinatal period.},\nauthor = {Pellowski, Jennifer A and Wedderburn, Catherine J and Groenewold, Nynke A and Roos, Annerine and Subramoney, Sivenesi and Hoffman, Nadia and Fouche, Jean-Paul and Joshi, Shantanu H and Woods, Roger P and Narr, Katherine L and Zar, Heather J and Donald, Kirsten A and Stein, Dan J},\ndoi = {10.1038/s41398-023-02395-5},\nfile = {:Users/jacquelinebracher/Zotero/storage/5J9RLF88/Pellowski et al. - 2023 - Maternal perinatal depression and child brain stru.pdf:pdf},\nissn = {2158-3188},\njournal = {Translational Psychiatry},\nmonth = {mar},\nnumber = {1},\npages = {96},\ntitle = {{Maternal perinatal depression and child brain structure at 2-3 years in a {\\{}South{\\}} {\\{}African{\\}} birth cohort study}},\nurl = {https://www.nature.com/articles/s41398-023-02395-5},\nvolume = {13},\nyear = {2023}\n}\n
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\n Abstract Maternal perinatal depression is associated with risk of adverse child developmental outcomes and differences in offspring brain structure. Evidence from low- and middle-income countries is lacking as is an investigation of antenatal, postnatal, and persistent depression in the same sample. In a South African birth cohort, we investigated the effect of antenatal and postpartum maternal depressive symptoms on offspring brain structure at 2–3 years of age. Magnetic resonance imaging was performed, extracting cortical thickness and surface areas in frontal cortex regions of interest and subcortical volumes using FreeSurfer software. Maternal depressive symptoms were measured using the Edinburgh Postpartum Depression Scale and the Beck Depression Inventory II antenatally and at 6–10 weeks, 6 months, 12 months, and 18 months postpartum and analyzed dichotomously and continuously. Linear regressions were used controlling for child age, sex, intracranial volume, maternal education, age, smoking, alcohol use and HIV. 146 children were included with 38 (37%) exposed to depressive symptoms antenatally and 44 (35%) exposed postnatally. Of these, 16 (13%) were exposed to both. Postpartum, but not antenatal, depressive symptoms were associated with smaller amygdala volumes in children (B = −74.73, p = 0.01). Persistent maternal depressive symptoms across pregnancy and postpartum were also independently associated with smaller amygdala volumes (B = −78.61, p = 0.047). Differences in amygdala volumes among children exposed to postnatal as well as persistent maternal depressive symptomatology underscore the importance of identifying women at-risk for depression during the entire perinatal period.\n
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\n \n\n \n \n \n \n \n \n Harmonizing \\PTSD\\ severity scales across instruments and sites.\n \n \n \n \n\n\n \n Kennedy, E.; Dennis, E. L; Lindsey, H. M; DeRoon-Cassini, T.; Du Plessis, S.; Fani, N.; Kaufman, M. L; Koen, N.; Larson, C. L; Laskowitz, S.; Lebois, L. A M; Morey, R. A; Newsome, M. R; Palermo, C.; Pastorek, N. J; Powers, A.; Scheibel, R.; Seedat, S.; Seligowski, A.; Stein, D. J; Stevens, J.; Sun, D.; Thompson, P.; Troyanskaya, M.; Van Rooij, S. J H; Watts, A. A; Tomas, C. W; Williams, W.; Hillary, F. G; Pugh, M. J.; Wilde, E. A; and Tate, D. F\n\n\n \n\n\n\n Neuropsychology, 37(4): 398–408. may 2023.\n \n\n\n\n
\n\n\n\n \n \n \"HarmonizingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{kennedy_harmonizing_2023,\nauthor = {Kennedy, Eamonn and Dennis, Emily L and Lindsey, Hannah M and DeRoon-Cassini, Terri and {Du Plessis}, Stefan and Fani, Negar and Kaufman, Milissa L and Koen, Nastassja and Larson, Christine L and Laskowitz, Sarah and Lebois, Lauren A M and Morey, Rajendra A and Newsome, Mary R and Palermo, Cori and Pastorek, Nicholas J and Powers, Abigail and Scheibel, Randall and Seedat, Soraya and Seligowski, Antonia and Stein, Dan J and Stevens, Jennifer and Sun, Delin and Thompson, Paul and Troyanskaya, Maya and {Van Rooij}, Sanne J H and Watts, Amanda A and Tomas, Carissa W and Williams, Wright and Hillary, Frank G and Pugh, Mary Jo and Wilde, Elisabeth A and Tate, David F},\ndoi = {10.1037/neu0000823},\nissn = {1931-1559, 0894-4105},\njournal = {Neuropsychology},\nmonth = {may},\nnumber = {4},\npages = {398--408},\ntitle = {{Harmonizing {\\{}PTSD{\\}} severity scales across instruments and sites.}},\nurl = {http://doi.apa.org/getdoi.cfm?doi=10.1037/neu0000823},\nvolume = {37},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Pain perception and physiological correlates in body-focused repetitive behavior disorders.\n \n \n \n \n\n\n \n Lochner, C.; Roos, J.; Kidd, M.; Hendricks, G.; Peris, T. S; Ricketts, E. J; Dougherty, D. D; Woods, D. W; Keuthen, N. J; Stein, D. J; Grant, J. E; and Piacentini, J.\n\n\n \n\n\n\n CNS Spectrums, 28(2): 197–204. apr 2023.\n \n\n\n\n
\n\n\n\n \n \n \"PainPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{lochner_pain_2023,\nabstract = {Abstract\n\nBackground\nBehaviors typical of body-focused repetitive behavior disorders such as trichotillomania (TTM) and skin-picking disorder (SPD) are often associated with pleasure or relief, and with little or no physical pain, suggesting aberrant pain perception. Conclusive evidence about pain perception and correlates in these conditions is, however, lacking.\n\n\nMethods\nA multisite international study examined pain perception and its physiological correlates in adults with TTM (n = 31), SPD (n = 24), and healthy controls (HCs; n = 26). The cold pressor test was administered, and measurements of pain perception and cardiovascular parameters were taken every 15 seconds. Pain perception, latency to pain tolerance, cardiovascular parameters and associations with illness severity, and comorbid depression, as well as interaction effects (group × time interval), were investigated across groups.\n\n\nResults\n\nThere were no group differences in pain ratings over time (\nP\n= .8) or latency to pain tolerance (\nP\n= .8). Illness severity was not associated with pain ratings (all\nP\n{\\textgreater}.05). In terms of diastolic blood pressure (DBP), the main effect of group was statistically significant (\nP\n= .01), with post hoc analyses indicating higher mean DBP in TTM (95{\\%} confidence intervals [CI], 84.0-93.5) compared to SPD (95{\\%} CI, 73.5-84.2;\nP\n= .01), and HCs (95{\\%} CI, 75.6-86.0;\nP\n= .03). Pain perception did not differ between those with and those without depression (TTM:\nP\n= .2, SPD:\nP\n= .4).\n\n\n\nConclusion\n\nThe study findings were mostly negative suggesting that\ngeneral\npain perception aberration is not involved in TTM and SPD. Other underlying drivers of hair-pulling and skin-picking behavior (eg, abnormal reward processing) should be investigated.},\nauthor = {Lochner, Christine and Roos, Janine and Kidd, Martin and Hendricks, Gaironeesa and Peris, Tara S and Ricketts, Emily J and Dougherty, Darin D and Woods, Douglas W and Keuthen, Nancy J and Stein, Dan J and Grant, Jon E and Piacentini, John},\ndoi = {10.1017/S1092852922000062},\nfile = {:Users/jacquelinebracher/Zotero/storage/JAFTYBBT/Lochner et al. - 2023 - Pain perception and physiological correlates in bo.pdf:pdf},\nissn = {1092-8529, 2165-6509},\njournal = {CNS Spectrums},\nmonth = {apr},\nnumber = {2},\npages = {197--204},\ntitle = {{Pain perception and physiological correlates in body-focused repetitive behavior disorders}},\nurl = {https://www.cambridge.org/core/product/identifier/S1092852922000062/type/journal{\\_}article},\nvolume = {28},\nyear = {2023}\n}\n
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\n Abstract Background Behaviors typical of body-focused repetitive behavior disorders such as trichotillomania (TTM) and skin-picking disorder (SPD) are often associated with pleasure or relief, and with little or no physical pain, suggesting aberrant pain perception. Conclusive evidence about pain perception and correlates in these conditions is, however, lacking. Methods A multisite international study examined pain perception and its physiological correlates in adults with TTM (n = 31), SPD (n = 24), and healthy controls (HCs; n = 26). The cold pressor test was administered, and measurements of pain perception and cardiovascular parameters were taken every 15 seconds. Pain perception, latency to pain tolerance, cardiovascular parameters and associations with illness severity, and comorbid depression, as well as interaction effects (group × time interval), were investigated across groups. Results There were no group differences in pain ratings over time ( P = .8) or latency to pain tolerance ( P = .8). Illness severity was not associated with pain ratings (all P \\textgreater.05). In terms of diastolic blood pressure (DBP), the main effect of group was statistically significant ( P = .01), with post hoc analyses indicating higher mean DBP in TTM (95% confidence intervals [CI], 84.0-93.5) compared to SPD (95% CI, 73.5-84.2; P = .01), and HCs (95% CI, 75.6-86.0; P = .03). Pain perception did not differ between those with and those without depression (TTM: P = .2, SPD: P = .4). Conclusion The study findings were mostly negative suggesting that general pain perception aberration is not involved in TTM and SPD. Other underlying drivers of hair-pulling and skin-picking behavior (eg, abnormal reward processing) should be investigated.\n
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\n \n\n \n \n \n \n \n \n Cross-national harmonization of neurocognitive assessment across five sites in a global study.\n \n \n \n \n\n\n \n Batistuzzo, M. C; Sheshachala, K.; Alschuler, D. M; Hezel, D. M; Lewis-Fernández, R.; De Joode, N. T; Vriend, C.; Lempert, K. M; Narayan, M.; Marincowitz, C.; Lochner, C.; Stein, D. J; Narayanaswamy, J. C; Van Den Heuvel, O. A; Simpson, H. B.; and Wall, M.\n\n\n \n\n\n\n Neuropsychology, 37(3): 284–300. mar 2023.\n \n\n\n\n
\n\n\n\n \n \n \"Cross-nationalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{batistuzzo_cross-national_2023,\nauthor = {Batistuzzo, Marcelo C and Sheshachala, Karthik and Alschuler, Daniel M and Hezel, Dianne M and Lewis-Fern{\\'{a}}ndez, Roberto and {De Joode}, Niels T and Vriend, Chris and Lempert, Karolina M and Narayan, Madhuri and Marincowitz, Clara and Lochner, Christine and Stein, Dan J and Narayanaswamy, Janardhanan C and {Van Den Heuvel}, Odile A and Simpson, Helen Blair and Wall, Melanie},\ndoi = {10.1037/neu0000838},\nissn = {1931-1559, 0894-4105},\njournal = {Neuropsychology},\nmonth = {mar},\nnumber = {3},\npages = {284--300},\ntitle = {{Cross-national harmonization of neurocognitive assessment across five sites in a global study.}},\nurl = {http://doi.apa.org/getdoi.cfm?doi=10.1037/neu0000838},\nvolume = {37},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Correction to: \\Similar\\ cortical morphometry trajectories from 5 to 9 years in children with perinatal \\HIV\\ who started treatment before age 2 years and uninfected controls.\n \n \n \n \n\n\n \n Nwosu, E. C; Holmes, M. J; Cotton, M. F; Dobbels, E.; Little, F.; Laughton, B.; Van Der Kouwe, A.; Robertson, F.; and Meintjes, E. M\n\n\n \n\n\n\n BMC Neuroscience, 24(1): 36. jul 2023.\n \n\n\n\n
\n\n\n\n \n \n \"CorrectionPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{nwosu_correction_2023,\nauthor = {Nwosu, Emmanuel C and Holmes, Martha J and Cotton, Mark F and Dobbels, Els and Little, Francesca and Laughton, Barbara and {Van Der Kouwe}, Andre and Robertson, Frances and Meintjes, Ernesta M},\ndoi = {10.1186/s12868-023-00802-7},\nfile = {:Users/jacquelinebracher/Zotero/storage/XCDM8TUE/Nwosu et al. - 2023 - Correction to Similar cortical morphometry trajec.pdf:pdf},\nissn = {1471-2202},\njournal = {BMC Neuroscience},\nmonth = {jul},\nnumber = {1},\npages = {36},\nshorttitle = {Correction to},\ntitle = {{Correction to: {\\{}Similar{\\}} cortical morphometry trajectories from 5 to 9 years in children with perinatal {\\{}HIV{\\}} who started treatment before age 2 years and uninfected controls}},\nurl = {https://bmcneurosci.biomedcentral.com/articles/10.1186/s12868-023-00802-7},\nvolume = {24},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Why monitor the neonatal brain—that is the important question.\n \n \n \n \n\n\n \n Vanhatalo, S.; Stevenson, N. J; Pressler, R. M; Abend, N. S; Auvin, S.; Brigo, F.; Cilio, M R.; Hahn, C. D; Hartmann, H.; Hellström-Westas, L.; Inder, T. E; Moshé, S. L; Nunes, M. L; Shellhaas, R. A; Vinayan, K. P; De Vries, L. S; Wilmshurst, J. M; Yozawitz, E.; and Boylan, G. B\n\n\n \n\n\n\n Pediatric Research, 93(1): 19–21. jan 2023.\n \n\n\n\n
\n\n\n\n \n \n \"WhyPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{vanhatalo_why_2023,\nauthor = {Vanhatalo, Sampsa and Stevenson, Nathan J and Pressler, Ronit M and Abend, Nicholas S and Auvin, St{\\'{e}}phane and Brigo, Francesco and Cilio, M Roberta and Hahn, Cecil D and Hartmann, Hans and Hellstr{\\"{o}}m-Westas, Lena and Inder, Terrie E and Mosh{\\'{e}}, Solomon L and Nunes, Magda L and Shellhaas, Ren{\\'{e}}e A and Vinayan, Kollencheri P and {De Vries}, Linda S and Wilmshurst, Jo M and Yozawitz, Elissa and Boylan, Geraldine B},\ndoi = {10.1038/s41390-022-02040-9},\nfile = {:Users/jacquelinebracher/Zotero/storage/R7CKAJLA/Vanhatalo et al. - 2023 - Why monitor the neonatal brain—that is the importa.pdf:pdf},\nissn = {0031-3998, 1530-0447},\njournal = {Pediatric Research},\nmonth = {jan},\nnumber = {1},\npages = {19--21},\ntitle = {{Why monitor the neonatal brain—that is the important question}},\nurl = {https://www.nature.com/articles/s41390-022-02040-9},\nvolume = {93},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Externalizing behavior in preschool children in a \\South\\ \\African\\ birth cohort: \\Predictive\\ pathways in a high-risk context.\n \n \n \n \n\n\n \n Malcolm-Smith, S.; Lake, M. T; Krwece, A.; Du Plooy, C. P; Hoffman, N.; Donald, K. A; Zar, H. J; and Stein, D. J\n\n\n \n\n\n\n Development and Psychopathology, 35(2): 982–999. may 2023.\n \n\n\n\n
\n\n\n\n \n \n \"ExternalizingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{malcolm-smith_externalizing_2023,\nabstract = {Abstract\nMental health problems often begin in early childhood. However, the associations of various individual and contextual risk factors with mental health in the preschool period are incompletely understood, particularly in low- to middle-income countries (LMICs) where multiple risk factors co-exist. To address this gap, we prospectively followed 981 children in a South African birth cohort, the Drakenstein Child Health Study, assessing pre-and postnatal exposures and risk factors. The predictive value of these factors for child mental health (assessed by the Child Behavior Checklist) was modeled using structural equation modeling. We identified two key pathways to greater externalizing behavior: (1) prenatal exposure to substances (alcohol and smoking) directly predicted increased externalizing behavior ($\\beta$ = 0.24, p {\\textless}0.001); this relationship was partially mediated by an aspect of infant temperament (negative emotionality; $\\beta$ = 0.05, p = 0.016); (2) lower socioeconomic status and associated maternal prenatal depression predicted more coercive parenting, which in turn predicted increased externalizing behavior ($\\beta$ = 0.18, p = 0.001). Findings in this high-risk LMIC cohort cohere with research from higher income contexts, and indicate the need to introduce integrated screening and intervention strategies for maternal prenatal substance use and depression, and promoting positive parenting across the preschool period.},\nauthor = {Malcolm-Smith, Susan and Lake, Marilyn T and Krwece, Akhona and {Du Plooy}, Christopher P and Hoffman, Nadia and Donald, Kirsten A and Zar, Heather J and Stein, Dan J},\ndoi = {10.1017/S095457942200027X},\nfile = {:Users/jacquelinebracher/Zotero/storage/LQFY2ULS/Malcolm-Smith et al. - 2023 - Externalizing behavior in preschool children in a .pdf:pdf},\nissn = {0954-5794, 1469-2198},\njournal = {Development and Psychopathology},\nmonth = {may},\nnumber = {2},\npages = {982--999},\nshorttitle = {Externalizing behavior in preschool children in a },\ntitle = {{Externalizing behavior in preschool children in a {\\{}South{\\}} {\\{}African{\\}} birth cohort: {\\{}Predictive{\\}} pathways in a high-risk context}},\nurl = {https://www.cambridge.org/core/product/identifier/S095457942200027X/type/journal{\\_}article},\nvolume = {35},\nyear = {2023}\n}\n
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\n Abstract Mental health problems often begin in early childhood. However, the associations of various individual and contextual risk factors with mental health in the preschool period are incompletely understood, particularly in low- to middle-income countries (LMICs) where multiple risk factors co-exist. To address this gap, we prospectively followed 981 children in a South African birth cohort, the Drakenstein Child Health Study, assessing pre-and postnatal exposures and risk factors. The predictive value of these factors for child mental health (assessed by the Child Behavior Checklist) was modeled using structural equation modeling. We identified two key pathways to greater externalizing behavior: (1) prenatal exposure to substances (alcohol and smoking) directly predicted increased externalizing behavior ($β$ = 0.24, p \\textless0.001); this relationship was partially mediated by an aspect of infant temperament (negative emotionality; $β$ = 0.05, p = 0.016); (2) lower socioeconomic status and associated maternal prenatal depression predicted more coercive parenting, which in turn predicted increased externalizing behavior ($β$ = 0.18, p = 0.001). Findings in this high-risk LMIC cohort cohere with research from higher income contexts, and indicate the need to introduce integrated screening and intervention strategies for maternal prenatal substance use and depression, and promoting positive parenting across the preschool period.\n
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\n \n\n \n \n \n \n \n \n Editorial: \\Broadening\\ our understanding of the impact of infections on the developing central nervous system - from basic to clinical sciences.\n \n \n \n \n\n\n \n Travassos, M. A; Rohlwink, U. K; and Tucker, E. W\n\n\n \n\n\n\n Frontiers in Neurology, 14: 1198518. may 2023.\n \n\n\n\n
\n\n\n\n \n \n \"Editorial:Paper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{travassos_editorial_2023,\nauthor = {Travassos, Mark A and Rohlwink, Ursula K and Tucker, Elizabeth W},\ndoi = {10.3389/fneur.2023.1198518},\nfile = {:Users/jacquelinebracher/Zotero/storage/TUAA7SMP/Travassos et al. - 2023 - Editorial Broadening our understanding of the imp.pdf:pdf},\nissn = {1664-2295},\njournal = {Frontiers in Neurology},\nmonth = {may},\npages = {1198518},\nshorttitle = {Editorial},\ntitle = {{Editorial: {\\{}Broadening{\\}} our understanding of the impact of infections on the developing central nervous system - from basic to clinical sciences}},\nurl = {https://www.frontiersin.org/articles/10.3389/fneur.2023.1198518/full},\nvolume = {14},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Low and differential polygenic score generalizability among \\African\\ populations due largely to genetic diversity.\n \n \n \n \n\n\n \n Majara, L.; Kalungi, A.; Koen, N.; Tsuo, K.; Wang, Y.; Gupta, R.; Nkambule, L. L; Zar, H.; Stein, D. J; Kinyanda, E.; Atkinson, E. G; and Martin, A. R\n\n\n \n\n\n\n Human Genetics and Genomics Advances, 4(2): 100184. apr 2023.\n \n\n\n\n
\n\n\n\n \n \n \"LowPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{majara_low_2023,\nauthor = {Majara, Lerato and Kalungi, Allan and Koen, Nastassja and Tsuo, Kristin and Wang, Ying and Gupta, Rahul and Nkambule, Lethukuthula L and Zar, Heather and Stein, Dan J and Kinyanda, Eugene and Atkinson, Elizabeth G and Martin, Alicia R},\ndoi = {10.1016/j.xhgg.2023.100184},\nfile = {:Users/jacquelinebracher/Zotero/storage/BHRCY434/Majara et al. - 2023 - Low and differential polygenic score generalizabil.pdf:pdf},\nissn = {26662477},\njournal = {Human Genetics and Genomics Advances},\nmonth = {apr},\nnumber = {2},\npages = {100184},\ntitle = {{Low and differential polygenic score generalizability among {\\{}African{\\}} populations due largely to genetic diversity}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S2666247723000167},\nvolume = {4},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Genetic \\Influences\\ on the \\Developing\\ \\Young\\ \\Brain\\ and \\Risk\\ for \\Neuropsychiatric\\ \\Disorders\\.\n \n \n \n \n\n\n \n Alex, A. M; Buss, C.; Davis, E. P.; Campos, G. D. L.; Donald, K. A; Fair, D. A; Gaab, N.; Gao, W.; Gilmore, J. H; Girault, J. B; Grewen, K.; Groenewold, N. A; Hankin, B. L; Ipser, J.; Kapoor, S.; Kim, P.; Lin, W.; Luo, S.; Norton, E. S; O'Connor, T. G; Piven, J.; Qiu, A.; Rasmussen, J. M; Skeide, M. A; Stein, D. J; Styner, M. A; Thompson, P. M; Wakschlag, L.; and Knickmeyer, R.\n\n\n \n\n\n\n Biological Psychiatry, 93(10): 905–920. may 2023.\n \n\n\n\n
\n\n\n\n \n \n \"GeneticPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{alex_genetic_2023,\nauthor = {Alex, Ann M and Buss, Claudia and Davis, Elysia Poggi and Campos, Gustavo De Los and Donald, Kirsten A and Fair, Damien A and Gaab, Nadine and Gao, Wei and Gilmore, John H and Girault, Jessica B and Grewen, Karen and Groenewold, Nynke A and Hankin, Benjamin L and Ipser, Jonathan and Kapoor, Shreya and Kim, Pilyoung and Lin, Weili and Luo, Shan and Norton, Elizabeth S and O'Connor, Thomas G and Piven, Joseph and Qiu, Anqi and Rasmussen, Jerod M and Skeide, Michael A and Stein, Dan J and Styner, Martin A and Thompson, Paul M and Wakschlag, Laurie and Knickmeyer, Rebecca},\ndoi = {10.1016/j.biopsych.2023.01.013},\nfile = {:Users/jacquelinebracher/Zotero/storage/XTKS9IDE/Alex et al. - 2023 - Genetic Influences on the Developing Young Brain a.pdf:pdf},\nissn = {00063223},\njournal = {Biological Psychiatry},\nmonth = {may},\nnumber = {10},\npages = {905--920},\ntitle = {{Genetic {\\{}Influences{\\}} on the {\\{}Developing{\\}} {\\{}Young{\\}} {\\{}Brain{\\}} and {\\{}Risk{\\}} for {\\{}Neuropsychiatric{\\}} {\\{}Disorders{\\}}}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S0006322323000409},\nvolume = {93},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n The functional connectome in obsessive-compulsive disorder: resting-state mega-analysis and machine learning classification for the \\ENIGMA\\-\\OCD\\ consortium.\n \n \n \n \n\n\n \n Bruin, W. B; Abe, Y.; Alonso, P.; Anticevic, A.; Backhausen, L. L; Balachander, S.; Bargallo, N.; Batistuzzo, M. C; Benedetti, F.; Bertolin Triquell, S.; Brem, S.; Calesella, F.; Couto, B.; Denys, D. A J P; Echevarria, M. A N; Eng, G. K.; Ferreira, S.; Feusner, J. D; Grazioplene, R. G; Gruner, P.; Guo, J. Y; Hagen, K.; Hansen, B.; Hirano, Y.; Hoexter, M. Q; Jahanshad, N.; Jaspers-Fayer, F.; Kasprzak, S.; Kim, M.; Koch, K.; Bin Kwak, Y.; Kwon, J. S.; Lazaro, L.; Li, C. R; Lochner, C.; Marsh, R.; Martínez-Zalacaín, I.; Menchon, J. M; Moreira, P. S; Morgado, P.; Nakagawa, A.; Nakao, T.; Narayanaswamy, J. C; Nurmi, E. L; Zorrilla, J. C P.; Piacentini, J.; Picó-Pérez, M.; Piras, F.; Piras, F.; Pittenger, C.; Reddy, J. Y C; Rodriguez-Manrique, D.; Sakai, Y.; Shimizu, E.; Shivakumar, V.; Simpson, B. H; Soriano-Mas, C.; Sousa, N.; Spalletta, G.; Stern, E. R; Evelyn Stewart, S; Szeszko, P. R; Tang, J.; Thomopoulos, S. I; Thorsen, A. L; Yoshida, T.; Tomiyama, H.; Vai, B.; Veer, I. M; Venkatasubramanian, G.; Vetter, N. C; Vriend, C.; Walitza, S.; Waller, L.; Wang, Z.; Watanabe, A.; Wolff, N.; Yun, J.; Zhao, Q.; Van Leeuwen, W. A; Van Marle, H. J F; Van De Mortel, L. A; Van Der Straten, A.; Van Der Werf, Y. D; ENIGMA-OCD Working Group; Arai, H.; Bollettini, I.; Escalona, R. C.; Coelho, A.; Colombo, F.; Darwich, L.; Fontaine, M.; Ikuta, T.; Ipser, J. C; Juaneda-Seguí, A.; Kitagawa, H.; Kvale, G.; Machado-Sousa, M.; Morer, A.; Nakamae, T.; Narumoto, J.; O'Neill, J.; Okawa, S.; Real, E.; Roessner, V.; Sato, J. R; Segalàs, C.; Shavitt, R. G; Veltman, D. J; Yamada, K.; Van Leeuwen, W. A; Van Marle, H. J F; Van De Mortel, L. A; Van Der Straten, A.; Van Der Werf, Y. D; Van Den Heuvel, O. A; Van Wingen, G. A; Thompson, P. M; Stein, D. J; Van Den Heuvel, O. A; and Van Wingen, G. A\n\n\n \n\n\n\n Molecular Psychiatry. may 2023.\n \n\n\n\n
\n\n\n\n \n \n \"ThePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{bruin_functional_2023,\nabstract = {Abstract\n\nCurrent knowledge about functional connectivity in obsessive-compulsive disorder (OCD) is based on small-scale studies, limiting the generalizability of results. Moreover, the majority of studies have focused only on predefined regions or functional networks rather than connectivity throughout the entire brain. Here, we investigated differences in resting-state functional connectivity between OCD patients and healthy controls (HC) using mega-analysis of data from 1024 OCD patients and 1028 HC from 28 independent samples of the ENIGMA-OCD consortium. We assessed group differences in whole-brain functional connectivity at both the regional and network level, and investigated whether functional connectivity could serve as biomarker to identify patient status at the individual level using machine learning analysis. The mega-analyses revealed widespread abnormalities in functional connectivity in OCD, with global hypo-connectivity (Cohen's\nd\n: -0.27 to -0.13) and few hyper-connections, mainly with the thalamus (Cohen's\nd\n: 0.19 to 0.22). Most hypo-connections were located within the sensorimotor network and no fronto-striatal abnormalities were found. Overall, classification performances were poor, with area-under-the-receiver-operating-characteristic curve (AUC) scores ranging between 0.567 and 0.673, with better classification for medicated (AUC = 0.702) than unmedicated (AUC = 0.608) patients versus healthy controls. These findings provide partial support for existing pathophysiological models of OCD and highlight the important role of the sensorimotor network in OCD. However, resting-state connectivity does not so far provide an accurate biomarker for identifying patients at the individual level.},\nauthor = {Bruin, Willem B and Abe, Yoshinari and Alonso, Pino and Anticevic, Alan and Backhausen, Lea L and Balachander, Srinivas and Bargallo, Nuria and Batistuzzo, Marcelo C and Benedetti, Francesco and {Bertolin Triquell}, Sara and Brem, Silvia and Calesella, Federico and Couto, Beatriz and Denys, Damiaan A J P and Echevarria, Marco A N and Eng, Goi Khia and Ferreira, S{\\'{o}}nia and Feusner, Jamie D and Grazioplene, Rachael G and Gruner, Patricia and Guo, Joyce Y and Hagen, Kristen and Hansen, Bjarne and Hirano, Yoshiyuki and Hoexter, Marcelo Q and Jahanshad, Neda and Jaspers-Fayer, Fern and Kasprzak, Selina and Kim, Minah and Koch, Kathrin and {Bin Kwak}, Yoo and Kwon, Jun Soo and Lazaro, Luisa and Li, Chiang-Shan R and Lochner, Christine and Marsh, Rachel and Mart{\\'{i}}nez-Zalaca{\\'{i}}n, Ignacio and Menchon, Jose M and Moreira, Pedro S and Morgado, Pedro and Nakagawa, Akiko and Nakao, Tomohiro and Narayanaswamy, Janardhanan C and Nurmi, Erika L and Zorrilla, Jose C Pariente and Piacentini, John and Pic{\\'{o}}-P{\\'{e}}rez, Maria and Piras, Fabrizio and Piras, Federica and Pittenger, Christopher and Reddy, Janardhan Y C and Rodriguez-Manrique, Daniela and Sakai, Yuki and Shimizu, Eiji and Shivakumar, Venkataram and Simpson, Blair H and Soriano-Mas, Carles and Sousa, Nuno and Spalletta, Gianfranco and Stern, Emily R and {Evelyn Stewart}, S and Szeszko, Philip R and Tang, Jinsong and Thomopoulos, Sophia I and Thorsen, Anders L and Yoshida, Tokiko and Tomiyama, Hirofumi and Vai, Benedetta and Veer, Ilya M and Venkatasubramanian, Ganesan and Vetter, Nora C and Vriend, Chris and Walitza, Susanne and Waller, Lea and Wang, Zhen and Watanabe, Anri and Wolff, Nicole and Yun, Je-Yeon and Zhao, Qing and {Van Leeuwen}, Wieke A and {Van Marle}, Hein J F and {Van De Mortel}, Laurens A and {Van Der Straten}, Anouk and {Van Der Werf}, Ysbrand D and {ENIGMA-OCD Working Group} and Arai, Honami and Bollettini, Irene and Escalona, Rosa Calvo and Coelho, Ana and Colombo, Federica and Darwich, Leila and Fontaine, Martine and Ikuta, Toshikazu and Ipser, Jonathan C and Juaneda-Segu{\\'{i}}, Asier and Kitagawa, Hitomi and Kvale, Gerd and Machado-Sousa, Mafalda and Morer, Astrid and Nakamae, Takashi and Narumoto, Jin and O'Neill, Joseph and Okawa, Sho and Real, Eva and Roessner, Veit and Sato, Joao R and Segal{\\`{a}}s, Cinto and Shavitt, Roseli G and Veltman, Dick J and Yamada, Kei and {Van Leeuwen}, Wieke A and {Van Marle}, Hein J F and {Van De Mortel}, Laurens A and {Van Der Straten}, Anouk and {Van Der Werf}, Ysbrand D and {Van Den Heuvel}, Odile A and {Van Wingen}, Guido A and Thompson, Paul M and Stein, Dan J and {Van Den Heuvel}, Odile A and {Van Wingen}, Guido A},\ndoi = {10.1038/s41380-023-02077-0},\nfile = {:Users/jacquelinebracher/Zotero/storage/EWDYMJPC/Bruin et al. - 2023 - The functional connectome in obsessive-compulsive .pdf:pdf},\nissn = {1359-4184, 1476-5578},\njournal = {Molecular Psychiatry},\nmonth = {may},\nshorttitle = {The functional connectome in obsessive-compulsive },\ntitle = {{The functional connectome in obsessive-compulsive disorder: resting-state mega-analysis and machine learning classification for the {\\{}ENIGMA{\\}}-{\\{}OCD{\\}} consortium}},\nurl = {https://www.nature.com/articles/s41380-023-02077-0},\nyear = {2023}\n}\n
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\n Abstract Current knowledge about functional connectivity in obsessive-compulsive disorder (OCD) is based on small-scale studies, limiting the generalizability of results. Moreover, the majority of studies have focused only on predefined regions or functional networks rather than connectivity throughout the entire brain. Here, we investigated differences in resting-state functional connectivity between OCD patients and healthy controls (HC) using mega-analysis of data from 1024 OCD patients and 1028 HC from 28 independent samples of the ENIGMA-OCD consortium. We assessed group differences in whole-brain functional connectivity at both the regional and network level, and investigated whether functional connectivity could serve as biomarker to identify patient status at the individual level using machine learning analysis. The mega-analyses revealed widespread abnormalities in functional connectivity in OCD, with global hypo-connectivity (Cohen's d : -0.27 to -0.13) and few hyper-connections, mainly with the thalamus (Cohen's d : 0.19 to 0.22). Most hypo-connections were located within the sensorimotor network and no fronto-striatal abnormalities were found. Overall, classification performances were poor, with area-under-the-receiver-operating-characteristic curve (AUC) scores ranging between 0.567 and 0.673, with better classification for medicated (AUC = 0.702) than unmedicated (AUC = 0.608) patients versus healthy controls. These findings provide partial support for existing pathophysiological models of OCD and highlight the important role of the sensorimotor network in OCD. However, resting-state connectivity does not so far provide an accurate biomarker for identifying patients at the individual level.\n
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\n \n\n \n \n \n \n \n \n Cognitive impairment in people living with \\HIV\\: consensus recommendations for a new approach.\n \n \n \n \n\n\n \n Nightingale, S.; Ances, B.; Cinque, P.; Dravid, A.; Dreyer, A. J; Gisslén, M.; Joska, J. A; Kwasa, J.; Meyer, A.; Mpongo, N.; Nakasujja, N.; Pebody, R.; Pozniak, A.; Price, R. W; Sandford, C.; Saylor, D.; Thomas, K. G F; Underwood, J.; Vera, J. H; and Winston, A.\n\n\n \n\n\n\n Nature Reviews Neurology, 19(7): 424–433. jul 2023.\n \n\n\n\n
\n\n\n\n \n \n \"CognitivePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{nightingale_cognitive_2023,\nauthor = {Nightingale, Sam and Ances, Beau and Cinque, Paola and Dravid, Ameet and Dreyer, Anna J and Gissl{\\'{e}}n, Magnus and Joska, John A and Kwasa, Judith and Meyer, Ana-Claire and Mpongo, Nombeko and Nakasujja, Noeline and Pebody, Roger and Pozniak, Anton and Price, Richard W and Sandford, Christopher and Saylor, Deanna and Thomas, Kevin G F and Underwood, Jonathan and Vera, Jaime H and Winston, Alan},\ndoi = {10.1038/s41582-023-00813-2},\nfile = {:Users/jacquelinebracher/Zotero/storage/2FVQ59V9/Nightingale et al. - 2023 - Cognitive impairment in people living with HIV co.pdf:pdf},\nissn = {1759-4758, 1759-4766},\njournal = {Nature Reviews Neurology},\nmonth = {jul},\nnumber = {7},\npages = {424--433},\nshorttitle = {Cognitive impairment in people living with {\\{}HIV{\\}}},\ntitle = {{Cognitive impairment in people living with {\\{}HIV{\\}}: consensus recommendations for a new approach}},\nurl = {https://www.nature.com/articles/s41582-023-00813-2},\nvolume = {19},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Editorial: \\Frontiers\\ in psychodynamic neuroscience.\n \n \n \n \n\n\n \n Cieri, F.; Carhart-Harris, R. L.; Mathys, C.; Turnbull, O.; and Solms, M.\n\n\n \n\n\n\n Frontiers in Human Neuroscience, 17: 1170480. mar 2023.\n \n\n\n\n
\n\n\n\n \n \n \"Editorial:Paper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{cieri_editorial_2023,\nauthor = {Cieri, Filippo and Carhart-Harris, Robin Lester and Mathys, Christoph and Turnbull, Oliver and Solms, Mark},\ndoi = {10.3389/fnhum.2023.1170480},\nfile = {:Users/jacquelinebracher/Zotero/storage/G3424ETP/Cieri et al. - 2023 - Editorial Frontiers in psychodynamic neuroscience.pdf:pdf},\nissn = {1662-5161},\njournal = {Frontiers in Human Neuroscience},\nmonth = {mar},\npages = {1170480},\nshorttitle = {Editorial},\ntitle = {{Editorial: {\\{}Frontiers{\\}} in psychodynamic neuroscience}},\nurl = {https://www.frontiersin.org/articles/10.3389/fnhum.2023.1170480/full},\nvolume = {17},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n \\PTSD\\ and comorbid \\MDD\\ is associated with activation of the right frontoparietal network.\n \n \n \n \n\n\n \n Koopowitz, S.; Zar, H. J; Stein, D. J; and Ipser, J. C\n\n\n \n\n\n\n Psychiatry Research: Neuroimaging, 331: 111630. jun 2023.\n \n\n\n\n
\n\n\n\n \n \n \"\\PTSD\\Paper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{koopowitz_ptsd_2023,\nauthor = {Koopowitz, Sheri-Michelle and Zar, Heather J and Stein, Dan J and Ipser, Jonathan C},\ndoi = {10.1016/j.pscychresns.2023.111630},\nfile = {:Users/jacquelinebracher/Zotero/storage/EPU4E59B/Koopowitz et al. - 2023 - PTSD and comorbid MDD is associated with activatio.pdf:pdf},\nissn = {09254927},\njournal = {Psychiatry Research: Neuroimaging},\nmonth = {jun},\npages = {111630},\ntitle = {{{\\{}PTSD{\\}} and comorbid {\\{}MDD{\\}} is associated with activation of the right frontoparietal network}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S0925492723000409},\nvolume = {331},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Epistemic justice in bioethics: interculturality and the possibility of reparations.\n \n \n \n \n\n\n \n De Vries, J.; and Pratt, B.\n\n\n \n\n\n\n Journal of Medical Ethics, 49(5): 347. may 2023.\n \n\n\n\n
\n\n\n\n \n \n \"EpistemicPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{de_vries_epistemic_2023,\nauthor = {{De Vries}, Jantina and Pratt, Bridget},\ndoi = {10.1136/jme-2023-109149},\nissn = {0306-6800, 1473-4257},\njournal = {Journal of Medical Ethics},\nmonth = {may},\nnumber = {5},\npages = {347},\nshorttitle = {Epistemic justice in bioethics},\ntitle = {{Epistemic justice in bioethics: interculturality and the possibility of reparations}},\nurl = {https://jme.bmj.com/lookup/doi/10.1136/jme-2023-109149},\nvolume = {49},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Economic evaluation of psychological treatments for common mental disorders in low- and middle-income countries: a systematic review.\n \n \n \n \n\n\n \n Mutyambizi-Mafunda, V.; Myers, B.; Sorsdahl, K.; Chanakira, E.; Lund, C.; and Cleary, S.\n\n\n \n\n\n\n Health Policy and Planning, 38(2): 239–260. feb 2023.\n \n\n\n\n
\n\n\n\n \n \n \"EconomicPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{mutyambizi-mafunda_economic_2023,\nabstract = {Abstract\nCommon mental disorders (CMDs) constitute a major public health and economic burden on low- and middle-income countries (LMICs). Systematic reviews of economic evaluations of psychological treatments for CMDs are limited. This systematic review examines methods, reports findings and appraises the quality of economic evaluations of psychological treatments for CMDs in LMICs. We searched a range of bibliographic databases (including PubMed, EconLit, APA-PsycINFO and Cochrane library) and the African Journals Online (AJoL) and Google Scholar platforms. We used a pre-populated template to extract data and the Drummond {\\&} Jefferson checklist for quality appraisal. We present results as a narrative synthesis. The review included 26 studies, mostly from Asia (12) and Africa (9). The majority were cost-effectiveness analyses (12), some were cost-utility analyses (5), with one cost–benefit analysis or combinations of economic evaluations (8). Most interventions were considered either cost-effective or potentially cost-effective (22), with 3 interventions being not cost-effective. Limitations were noted regarding appropriateness of conclusions drawn on cost-effectiveness, the use of cost-effectiveness thresholds and application of ‘societal' incremental cost-effectiveness ratios to reflect value for money (VfM) of treatments. Non-specialist health workers (NSHWs) delivered most of the treatments (16) for low-cost delivery at scale, and costs should reflect the true opportunity cost of NSHWs' time to support the development of a sustainable cadre of health care providers. There is a 4-fold increase in economic evaluations of CMD psychological treatments in the last decade over the previous one. Yet, findings from this review highlight the need for better application of economic evaluation methodology to support resource allocation towards the World Health Organization recommended first-line treatments of CMDs. We suggest impact inventories to capture societal economic gains and propose a VfM assessment framework to guide researchers in evaluating cost-effectiveness.},\nauthor = {Mutyambizi-Mafunda, Vimbayi and Myers, Bronwyn and Sorsdahl, Katherine and Chanakira, Esther and Lund, Crick and Cleary, Susan},\ndoi = {10.1093/heapol/czac069},\nfile = {:Users/jacquelinebracher/Zotero/storage/BTQG59YM/Mutyambizi-Mafunda et al. - 2023 - Economic evaluation of psychological treatments fo.pdf:pdf},\nissn = {1460-2237},\njournal = {Health Policy and Planning},\nmonth = {feb},\nnumber = {2},\npages = {239--260},\nshorttitle = {Economic evaluation of psychological treatments fo},\ntitle = {{Economic evaluation of psychological treatments for common mental disorders in low- and middle-income countries: a systematic review}},\nurl = {https://academic.oup.com/heapol/article/38/2/239/6675509},\nvolume = {38},\nyear = {2023}\n}\n
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\n Abstract Common mental disorders (CMDs) constitute a major public health and economic burden on low- and middle-income countries (LMICs). Systematic reviews of economic evaluations of psychological treatments for CMDs are limited. This systematic review examines methods, reports findings and appraises the quality of economic evaluations of psychological treatments for CMDs in LMICs. We searched a range of bibliographic databases (including PubMed, EconLit, APA-PsycINFO and Cochrane library) and the African Journals Online (AJoL) and Google Scholar platforms. We used a pre-populated template to extract data and the Drummond & Jefferson checklist for quality appraisal. We present results as a narrative synthesis. The review included 26 studies, mostly from Asia (12) and Africa (9). The majority were cost-effectiveness analyses (12), some were cost-utility analyses (5), with one cost–benefit analysis or combinations of economic evaluations (8). Most interventions were considered either cost-effective or potentially cost-effective (22), with 3 interventions being not cost-effective. Limitations were noted regarding appropriateness of conclusions drawn on cost-effectiveness, the use of cost-effectiveness thresholds and application of ‘societal' incremental cost-effectiveness ratios to reflect value for money (VfM) of treatments. Non-specialist health workers (NSHWs) delivered most of the treatments (16) for low-cost delivery at scale, and costs should reflect the true opportunity cost of NSHWs' time to support the development of a sustainable cadre of health care providers. There is a 4-fold increase in economic evaluations of CMD psychological treatments in the last decade over the previous one. Yet, findings from this review highlight the need for better application of economic evaluation methodology to support resource allocation towards the World Health Organization recommended first-line treatments of CMDs. We suggest impact inventories to capture societal economic gains and propose a VfM assessment framework to guide researchers in evaluating cost-effectiveness.\n
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\n \n\n \n \n \n \n \n \n Intersecting \\Relationships\\ of \\Psychosocial\\ and \\Structural\\ \\Syndemic\\ \\Problems\\ \\Among\\ \\People\\ with \\HIV\\ in \\South\\ \\Africa\\: \\Using\\ \\Network\\ \\Analysis\\ to \\Identify\\ \\Influential\\ \\Problems\\.\n \n \n \n \n\n\n \n Lee, J. S; Bainter, S. A; Tsai, A. C; Andersen, L. S; Stanton, A. M; Magidson, J. F; Kagee, A.; Joska, J. A; O'Cleirigh, C.; and Safren, S. A\n\n\n \n\n\n\n AIDS and Behavior, 27(6): 1741–1756. jun 2023.\n \n\n\n\n
\n\n\n\n \n \n \"IntersectingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{lee_intersecting_2023,\nauthor = {Lee, Jasper S and Bainter, Sierra A and Tsai, Alexander C and Andersen, Lena S and Stanton, Amelia M and Magidson, Jessica F and Kagee, Ashraf and Joska, John A and O'Cleirigh, Conall and Safren, Steven A},\ndoi = {10.1007/s10461-022-03906-z},\nissn = {1090-7165, 1573-3254},\njournal = {AIDS and Behavior},\nmonth = {jun},\nnumber = {6},\npages = {1741--1756},\nshorttitle = {Intersecting {\\{}Relationships{\\}} of {\\{}Psychosocial{\\}} and},\ntitle = {{Intersecting {\\{}Relationships{\\}} of {\\{}Psychosocial{\\}} and {\\{}Structural{\\}} {\\{}Syndemic{\\}} {\\{}Problems{\\}} {\\{}Among{\\}} {\\{}People{\\}} with {\\{}HIV{\\}} in {\\{}South{\\}} {\\{}Africa{\\}}: {\\{}Using{\\}} {\\{}Network{\\}} {\\{}Analysis{\\}} to {\\{}Identify{\\}} {\\{}Influential{\\}} {\\{}Problems{\\}}}},\nurl = {https://link.springer.com/10.1007/s10461-022-03906-z},\nvolume = {27},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Country-level gender inequality is associated with structural differences in the brains of women and men.\n \n \n \n \n\n\n \n Zugman, A.; Alliende, L. M.; Medel, V.; Bethlehem, R. A I; Seidlitz, J.; Ringlein, G.; Arango, C.; Arnatkevičiūtė, A.; Asmal, L.; Bellgrove, M.; Benegal, V.; Bernardo, M.; Billeke, P.; Bosch-Bayard, J.; Bressan, R.; Busatto, G. F; Castro, M. N; Chaim-Avancini, T.; Compte, A.; Costanzi, M.; Czepielewski, L.; Dazzan, P.; de la Fuente-Sandoval, C.; Di Forti, M.; Díaz-Caneja, C. M; María Díaz-Zuluaga, A.; Du Plessis, S.; Duran, F. L S; Fittipaldi, S.; Fornito, A.; Freimer, N. B; Gadelha, A.; Gama, C. S; Garani, R.; Garcia-Rizo, C.; Gonzalez Campo, C.; Gonzalez-Valderrama, A.; Guinjoan, S.; Holla, B.; Ibañez, A.; Ivanovic, D.; Jackowski, A.; Leon-Ortiz, P.; Lochner, C.; López-Jaramillo, C.; Luckhoff, H.; Massuda, R.; McGuire, P.; Miyata, J.; Mizrahi, R.; Murray, R.; Ozerdem, A.; Pan, P. M; Parellada, M.; Phahladira, L.; Ramirez-Mahaluf, J. P; Reckziegel, R.; Reis Marques, T.; Reyes-Madrigal, F.; Roos, A.; Rosa, P.; Salum, G.; Scheffler, F.; Schumann, G.; Serpa, M.; Stein, D. J; Tepper, A.; Tiego, J.; Ueno, T.; Undurraga, J.; Undurraga, E. A; Valdes-Sosa, P.; Valli, I.; Villarreal, M.; Winton-Brown, T. T; Yalin, N.; Zamorano, F.; Zanetti, M. V; CVEDA; Winkler, A. M; Pine, D. S; Evans-Lacko, S.; Crossley, N. A; Murthy, P.; Chakrabarti, A.; Basu, D.; Subodh, B N; Singh, L.; Singh, R.; Kalyanram, K.; Kartik, K.; Kumaran, K.; Krishnaveni, G.; Kuriyan, R.; Kurpad, S. S.; Barker, G. J; Bharath, R. D; Desrivieres, S.; Purushottam, M.; Orfanos, D. P; Sharma, E.; Hickman, M.; Heron, J.; Toledano, M. B; and Vaidya, N.\n\n\n \n\n\n\n Proceedings of the National Academy of Sciences, 120(20): e2218782120. may 2023.\n \n\n\n\n
\n\n\n\n \n \n \"Country-levelPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{zugman_country-level_2023,\nabstract = {Gender inequality across the world has been associated with a higher risk to mental health problems and lower academic achievement in women compared to men. We also know that the brain is shaped by nurturing and adverse socio-environmental experiences. Therefore, unequal exposure to harsher conditions for women compared to men in gender-unequal countries might be reflected in differences in their brain structure, and this could be the neural mechanism partly explaining women's worse outcomes in gender-unequal countries. We examined this through a random-effects meta-analysis on cortical thickness and surface area differences between adult healthy men and women, including a meta-regression in which country-level gender inequality acted as an explanatory variable for the observed differences. A total of 139 samples from 29 different countries, totaling 7,876 MRI scans, were included. Thickness of the right hemisphere, and particularly the right caudal anterior cingulate, right medial orbitofrontal, and left lateral occipital cortex, presented no differences or even thicker regional cortices in women compared to men in gender-equal countries, reversing to thinner cortices in countries with greater gender inequality. These results point to the potentially hazardous effect of gender inequality on women's brains and provide initial evidence for neuroscience-informed policies for gender equality.},\nauthor = {Zugman, Andr{\\'{e}} and Alliende, Luz Mar{\\'{i}}a and Medel, Vicente and Bethlehem, Richard A I and Seidlitz, Jakob and Ringlein, Grace and Arango, Celso and Arnatkevi{\\v{c}}iūtė, Aurina and Asmal, Laila and Bellgrove, Mark and Benegal, Vivek and Bernardo, Miquel and Billeke, Pablo and Bosch-Bayard, Jorge and Bressan, Rodrigo and Busatto, Geraldo F and Castro, Mariana N and Chaim-Avancini, Tiffany and Compte, Albert and Costanzi, Monise and Czepielewski, Leticia and Dazzan, Paola and de la Fuente-Sandoval, Camilo and {Di Forti}, Marta and D{\\'{i}}az-Caneja, Covadonga M and {Mar{\\'{i}}a D{\\'{i}}az-Zuluaga}, Ana and {Du Plessis}, Stefan and Duran, Fabio L S and Fittipaldi, Sol and Fornito, Alex and Freimer, Nelson B and Gadelha, Ary and Gama, Clarissa S and Garani, Ranjini and Garcia-Rizo, Clemente and {Gonzalez Campo}, Cecilia and Gonzalez-Valderrama, Alfonso and Guinjoan, Salvador and Holla, Bharath and Iba{\\~{n}}ez, Agust{\\'{i}}n and Ivanovic, Daniza and Jackowski, Andrea and Leon-Ortiz, Pablo and Lochner, Christine and L{\\'{o}}pez-Jaramillo, Carlos and Luckhoff, Hilmar and Massuda, Raffael and McGuire, Philip and Miyata, Jun and Mizrahi, Romina and Murray, Robin and Ozerdem, Aysegul and Pan, Pedro M and Parellada, Mara and Phahladira, Lebogan and Ramirez-Mahaluf, Juan P and Reckziegel, Ramiro and {Reis Marques}, Tiago and Reyes-Madrigal, Francisco and Roos, Annerine and Rosa, Pedro and Salum, Giovanni and Scheffler, Freda and Schumann, Gunter and Serpa, Mauricio and Stein, Dan J and Tepper, Angeles and Tiego, Jeggan and Ueno, Tsukasa and Undurraga, Juan and Undurraga, Eduardo A and Valdes-Sosa, Pedro and Valli, Isabel and Villarreal, Mirta and Winton-Brown, Toby T and Yalin, Nefize and Zamorano, Francisco and Zanetti, Marcus V and CVEDA and Winkler, Anderson M and Pine, Daniel S and Evans-Lacko, Sara and Crossley, Nicolas A and Murthy, Pratima and Chakrabarti, Amit and Basu, Debasish and Subodh, B N and Singh, Lenin and Singh, Roshan and Kalyanram, Kartik and Kartik, Kamakshi and Kumaran, Kalyanaraman and Krishnaveni, Ghattu and Kuriyan, Rebecca and Kurpad, Sunita Simon and Barker, Gareth J and Bharath, Rose D and Desrivieres, Sylvane and Purushottam, Meera and Orfanos, Dimitri P and Sharma, Eesha and Hickman, Matthew and Heron, Jon and Toledano, Mireille B and Vaidya, Nilakshi},\ndoi = {10.1073/pnas.2218782120},\nfile = {:Users/jacquelinebracher/Zotero/storage/PXRQUX47/Zugman et al. - 2023 - Country-level gender inequality is associated with.pdf:pdf},\nissn = {0027-8424, 1091-6490},\njournal = {Proceedings of the National Academy of Sciences},\nmonth = {may},\nnumber = {20},\npages = {e2218782120},\ntitle = {{Country-level gender inequality is associated with structural differences in the brains of women and men}},\nurl = {https://pnas.org/doi/10.1073/pnas.2218782120},\nvolume = {120},\nyear = {2023}\n}\n
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\n Gender inequality across the world has been associated with a higher risk to mental health problems and lower academic achievement in women compared to men. We also know that the brain is shaped by nurturing and adverse socio-environmental experiences. Therefore, unequal exposure to harsher conditions for women compared to men in gender-unequal countries might be reflected in differences in their brain structure, and this could be the neural mechanism partly explaining women's worse outcomes in gender-unequal countries. We examined this through a random-effects meta-analysis on cortical thickness and surface area differences between adult healthy men and women, including a meta-regression in which country-level gender inequality acted as an explanatory variable for the observed differences. A total of 139 samples from 29 different countries, totaling 7,876 MRI scans, were included. Thickness of the right hemisphere, and particularly the right caudal anterior cingulate, right medial orbitofrontal, and left lateral occipital cortex, presented no differences or even thicker regional cortices in women compared to men in gender-equal countries, reversing to thinner cortices in countries with greater gender inequality. These results point to the potentially hazardous effect of gender inequality on women's brains and provide initial evidence for neuroscience-informed policies for gender equality.\n
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\n \n\n \n \n \n \n \n \n The impact of coal mine dust characteristics on pathways to respiratory harm: investigating the pneumoconiotic potency of coals.\n \n \n \n \n\n\n \n Kamanzi, C.; Becker, M.; Jacobs, M.; Konečný, P.; Von Holdt, J.; and Broadhurst, J.\n\n\n \n\n\n\n Environmental Geochemistry and Health, 45(10): 7363–7388. oct 2023.\n \n\n\n\n
\n\n\n\n \n \n \"ThePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{kamanzi_impact_2023,\nabstract = {Abstract\nExposure to dust from the mining environment has historically resulted in epidemic levels of mortality and morbidity from pneumoconiotic diseases such as silicosis, coal workers' pneumoconiosis (CWP), and asbestosis. Studies have shown that CWP remains a critical issue at collieries across the globe, with some countries facing resurgent patterns of the disease and additional pathologies from long-term exposure. Compliance measures to reduce dust exposure rely primarily on the assumption that all “fine” particles are equally toxic irrespective of source or chemical composition. For several ore types, but more specifically coal, such an assumption is not practical due to the complex and highly variable nature of the material. Additionally, several studies have identified possible mechanisms of pathogenesis from the minerals and deleterious metals in coal. The purpose of this review was to provide a reassessment of the perspectives and strategies used to evaluate the pneumoconiotic potency of coal mine dust. Emphasis is on the physicochemical characteristics of coal mine dust such as mineralogy/mineral chemistry, particle shape, size, specific surface area, and free surface area—all of which have been highlighted as contributing factors to the expression of pro-inflammatory responses in the lung. The review also highlights the potential opportunity for more holistic risk characterisation strategies for coal mine dust, which consider the mineralogical and physicochemical aspects of the dust as variables relevant to the current proposed mechanisms for CWP pathogenesis.},\nauthor = {Kamanzi, Conchita and Becker, Megan and Jacobs, Muazzam and Kone{\\v{c}}n{\\'{y}}, Petr and {Von Holdt}, Johanna and Broadhurst, Jennifer},\ndoi = {10.1007/s10653-023-01583-y},\nfile = {:Users/jacquelinebracher/Zotero/storage/YUKJKNT2/Kamanzi et al. - 2023 - The impact of coal mine dust characteristics on pa.pdf:pdf},\nissn = {0269-4042, 1573-2983},\njournal = {Environmental Geochemistry and Health},\nmonth = {oct},\nnumber = {10},\npages = {7363--7388},\nshorttitle = {The impact of coal mine dust characteristics on pa},\ntitle = {{The impact of coal mine dust characteristics on pathways to respiratory harm: investigating the pneumoconiotic potency of coals}},\nurl = {https://link.springer.com/10.1007/s10653-023-01583-y},\nvolume = {45},\nyear = {2023}\n}\n
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\n Abstract Exposure to dust from the mining environment has historically resulted in epidemic levels of mortality and morbidity from pneumoconiotic diseases such as silicosis, coal workers' pneumoconiosis (CWP), and asbestosis. Studies have shown that CWP remains a critical issue at collieries across the globe, with some countries facing resurgent patterns of the disease and additional pathologies from long-term exposure. Compliance measures to reduce dust exposure rely primarily on the assumption that all “fine” particles are equally toxic irrespective of source or chemical composition. For several ore types, but more specifically coal, such an assumption is not practical due to the complex and highly variable nature of the material. Additionally, several studies have identified possible mechanisms of pathogenesis from the minerals and deleterious metals in coal. The purpose of this review was to provide a reassessment of the perspectives and strategies used to evaluate the pneumoconiotic potency of coal mine dust. Emphasis is on the physicochemical characteristics of coal mine dust such as mineralogy/mineral chemistry, particle shape, size, specific surface area, and free surface area—all of which have been highlighted as contributing factors to the expression of pro-inflammatory responses in the lung. The review also highlights the potential opportunity for more holistic risk characterisation strategies for coal mine dust, which consider the mineralogical and physicochemical aspects of the dust as variables relevant to the current proposed mechanisms for CWP pathogenesis.\n
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\n \n\n \n \n \n \n \n \n A cross-national validation of the \\Internet\\ \\Severity\\ and \\Activities\\ \\Addiction\\ \\Questionnaire\\ (\\ISAAQ\\).\n \n \n \n \n\n\n \n Omrawo, C.; Ioannidis, K.; Grant, J. E; Lutz, N.; Chamberlain, S. R; Stein, D. J; Tiego, J.; Kidd, M.; and Lochner, C.\n\n\n \n\n\n\n Comprehensive Psychiatry, 122: 152378. apr 2023.\n \n\n\n\n
\n\n\n\n \n \n \"APaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{omrawo_cross-national_2023,\nauthor = {Omrawo, Charlene and Ioannidis, Konstantinos and Grant, Jon E and Lutz, Nina and Chamberlain, Samuel R and Stein, Dan J and Tiego, Jeggan and Kidd, Martin and Lochner, Christine},\ndoi = {10.1016/j.comppsych.2023.152378},\nissn = {0010440X},\njournal = {Comprehensive Psychiatry},\nmonth = {apr},\npages = {152378},\ntitle = {{A cross-national validation of the {\\{}Internet{\\}} {\\{}Severity{\\}} and {\\{}Activities{\\}} {\\{}Addiction{\\}} {\\{}Questionnaire{\\}} ({\\{}ISAAQ{\\}})}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S0010440X23000159},\nvolume = {122},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Where is knowledge from the global \\South\\? \\An\\ account of epistemic justice for a global bioethics.\n \n \n \n \n\n\n \n Pratt, B.; and De Vries, J.\n\n\n \n\n\n\n Journal of Medical Ethics, 49(5): 325–334. may 2023.\n \n\n\n\n
\n\n\n\n \n \n \"WherePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{pratt_where_2023,\nabstract = {The silencing of the epistemologies, theories, principles, values, concepts and experiences of the global South constitutes a particularly egregious epistemic injustice in bioethics. Our shared responsibility to rectify that injustice should be at the top of the ethics agenda. That it is not, or only is in part, is deeply problematic and endangers the credibility of the entire field. As a first step towards reorienting the field, this paper offers a comprehensive account of epistemic justice for global health ethics. We first introduce several different conceptions of justice and decolonisation in relation to knowledge, purposefully drawing on work emanating from the global South as well as the global North. We then apply those conceptions to the global health ethics context to generate a tripartite account of the layers of epistemic justice in the field: who is producing ethics knowledge; what theories and concepts are being applied to produce ethics knowledge; and whose voices are sought, recorded and used to generate ethics knowledge. These layers reflect that the field spans conceptual and empirical research. We conclude by proposing that, going forward, three avenues are key to achieve greater epistemic justice at each layer and to help decolonise global health ethics: namely, understanding the problem, dialogue and structural change.},\nauthor = {Pratt, Bridget and {De Vries}, Jantina},\ndoi = {10.1136/jme-2022-108291},\nfile = {:Users/jacquelinebracher/Zotero/storage/TM47SAA6/Pratt and De Vries - 2023 - Where is knowledge from the global South An accou.pdf:pdf},\nissn = {0306-6800, 1473-4257},\njournal = {Journal of Medical Ethics},\nmonth = {may},\nnumber = {5},\npages = {325--334},\nshorttitle = {Where is knowledge from the global {\\{}South{\\}}?},\ntitle = {{Where is knowledge from the global {\\{}South{\\}}? {\\{}An{\\}} account of epistemic justice for a global bioethics}},\nurl = {https://jme.bmj.com/lookup/doi/10.1136/jme-2022-108291},\nvolume = {49},\nyear = {2023}\n}\n
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\n The silencing of the epistemologies, theories, principles, values, concepts and experiences of the global South constitutes a particularly egregious epistemic injustice in bioethics. Our shared responsibility to rectify that injustice should be at the top of the ethics agenda. That it is not, or only is in part, is deeply problematic and endangers the credibility of the entire field. As a first step towards reorienting the field, this paper offers a comprehensive account of epistemic justice for global health ethics. We first introduce several different conceptions of justice and decolonisation in relation to knowledge, purposefully drawing on work emanating from the global South as well as the global North. We then apply those conceptions to the global health ethics context to generate a tripartite account of the layers of epistemic justice in the field: who is producing ethics knowledge; what theories and concepts are being applied to produce ethics knowledge; and whose voices are sought, recorded and used to generate ethics knowledge. These layers reflect that the field spans conceptual and empirical research. We conclude by proposing that, going forward, three avenues are key to achieve greater epistemic justice at each layer and to help decolonise global health ethics: namely, understanding the problem, dialogue and structural change.\n
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\n \n\n \n \n \n \n \n \n Evaluating construct and criterion validity of \\NeuroScreen\\ in assessing neurocognition among hospitalized \\Ugandan\\ first-episode psychosis patients.\n \n \n \n \n\n\n \n Asiedu, N.; Mwesiga, E. K.; Akena, D.; Morrison, C.; Gumikiriza-Onoria, J. L.; Nanteza, A.; Nakku, J.; Koen, N.; Nakasujja, N.; Ssembajjwe, W.; Ferraris, C. M; Santoro, A. F; Stein, D. J; and Robbins, R. N\n\n\n \n\n\n\n Schizophrenia Research: Cognition, 32: 100276. jun 2023.\n \n\n\n\n
\n\n\n\n \n \n \"EvaluatingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{asiedu_evaluating_2023,\nauthor = {Asiedu, Nana and Mwesiga, Emmanuel Kiiza and Akena, Dickens and Morrison, Corey and Gumikiriza-Onoria, Joy Louise and Nanteza, Angel and Nakku, Juliet and Koen, Nastassja and Nakasujja, Noeline and Ssembajjwe, Wilber and Ferraris, Christopher M and Santoro, Anthony F and Stein, Dan J and Robbins, Reuben N},\ndoi = {10.1016/j.scog.2022.100276},\nfile = {:Users/jacquelinebracher/Zotero/storage/R5KBRMRG/Asiedu et al. - 2023 - Evaluating construct and criterion validity of Neu.pdf:pdf},\nissn = {22150013},\njournal = {Schizophrenia Research: Cognition},\nmonth = {jun},\npages = {100276},\ntitle = {{Evaluating construct and criterion validity of {\\{}NeuroScreen{\\}} in assessing neurocognition among hospitalized {\\{}Ugandan{\\}} first-episode psychosis patients}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S2215001322000415},\nvolume = {32},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n A genetically targeted ion sensor reveals distinct seizure-related chloride and \\pH\\ dynamics in \\GABAergic\\ interneuron populations.\n \n \n \n \n\n\n \n Călin, A.; Waseem, T.; Raimondo, J. V; Newey, S. E; and Akerman, C. J\n\n\n \n\n\n\n iScience, 26(4): 106363. apr 2023.\n \n\n\n\n
\n\n\n\n \n \n \"APaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{calin_genetically_2023,\nauthor = {Călin, Alexandru and Waseem, Tatiana and Raimondo, Joseph V and Newey, Sarah E and Akerman, Colin J},\ndoi = {10.1016/j.isci.2023.106363},\nfile = {:Users/jacquelinebracher/Zotero/storage/62MLKB2L/Călin et al. - 2023 - A genetically targeted ion sensor reveals distinct.pdf:pdf},\nissn = {25890042},\njournal = {iScience},\nmonth = {apr},\nnumber = {4},\npages = {106363},\ntitle = {{A genetically targeted ion sensor reveals distinct seizure-related chloride and {\\{}pH{\\}} dynamics in {\\{}GABAergic{\\}} interneuron populations}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S2589004223004406},\nvolume = {26},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Experiences of identifying pre-school children with disabilities in resource limited settings – an account from \\Malawi\\, \\Pakistan\\ and \\Uganda\\.\n \n \n \n \n\n\n \n Lynch, P.; Nabwera, H. M; Babikako, H. M; Rasheed, M.; Donald, K. A; Mbale, E. W; Stockdale, E.; Chand, P.; Van Den Heuvel, M.; Kakooza Mwesige, A.; and Gladstone, M.\n\n\n \n\n\n\n Disability & Society,1–21. feb 2023.\n \n\n\n\n
\n\n\n\n \n \n \"ExperiencesPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{lynch_experiences_2023,\nauthor = {Lynch, Paul and Nabwera, Helen M and Babikako, Harriet M and Rasheed, Muneera and Donald, Kirsten A and Mbale, Emmie W and Stockdale, Elizabeth and Chand, Prem and {Van Den Heuvel}, Meta and {Kakooza Mwesige}, Angelina and Gladstone, Melissa},\ndoi = {10.1080/09687599.2023.2181769},\nfile = {:Users/jacquelinebracher/Zotero/storage/LZEEGL8K/Lynch et al. - 2023 - Experiences of identifying pre-school children wit.pdf:pdf},\nissn = {0968-7599, 1360-0508},\njournal = {Disability {\\&} Society},\nmonth = {feb},\npages = {1--21},\ntitle = {{Experiences of identifying pre-school children with disabilities in resource limited settings – an account from {\\{}Malawi{\\}}, {\\{}Pakistan{\\}} and {\\{}Uganda{\\}}}},\nurl = {https://www.tandfonline.com/doi/full/10.1080/09687599.2023.2181769},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Gastruloids: \\A\\ \\Novel\\ \\System\\ for \\Disease\\ \\Modelling\\ and \\Drug\\ \\Testing\\.\n \n \n \n \n\n\n \n Amel, A.; Rossouw, S.; and Goolam, M.\n\n\n \n\n\n\n Stem Cell Reviews and Reports, 19(1): 104–113. jan 2023.\n \n\n\n\n
\n\n\n\n \n \n \"Gastruloids:Paper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{amel_gastruloids_2023,\nauthor = {Amel, Atoosa and Rossouw, Simon{\\'{e}} and Goolam, Mubeen},\ndoi = {10.1007/s12015-022-10462-5},\nissn = {2629-3269, 2629-3277},\njournal = {Stem Cell Reviews and Reports},\nmonth = {jan},\nnumber = {1},\npages = {104--113},\nshorttitle = {Gastruloids},\ntitle = {{Gastruloids: {\\{}A{\\}} {\\{}Novel{\\}} {\\{}System{\\}} for {\\{}Disease{\\}} {\\{}Modelling{\\}} and {\\{}Drug{\\}} {\\{}Testing{\\}}}},\nurl = {https://link.springer.com/10.1007/s12015-022-10462-5},\nvolume = {19},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Contextualizing the impact of prenatal alcohol and tobacco exposure on neurodevelopment in a \\South\\ \\African\\ birth cohort: an analysis from the socioecological perspective.\n \n \n \n \n\n\n \n Xia, Y.; Rebello, V.; Bodison, S. C; Jonker, D.; Steigelmann, B.; Donald, K. A; Charles, W.; Stein, D. J; Ipser, J.; Ahmadi, H.; Kan, E.; Sowell, E. R; Narr, K. L; Joshi, S. H; Odendaal, H. J; and Uban, K. A\n\n\n \n\n\n\n Frontiers in Integrative Neuroscience, 17: 1104788. jul 2023.\n \n\n\n\n
\n\n\n\n \n \n \"ContextualizingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{xia_contextualizing_2023,\nabstract = {Background\nAlcohol and tobacco are known teratogens. Historically, more severe prenatal alcohol exposure (PAE) and prenatal tobacco exposure (PTE) have been examined as the principal predictor of neurodevelopmental alterations, with little incorporation of lower doses or ecological contextual factors that can also impact neurodevelopment, such as socioeconomic resources (SER) or adverse childhood experiences (ACEs). Here, a novel analytical approach informed by a socio-ecological perspective was used to examine the associations between SER, PAE and/or PTE, and ACEs, and their effects on neurodevelopment.\n\n\nMethods\n\nN\n= 313 mother-child dyads were recruited from a prospective birth cohort with maternal report of PAE and PTE, and cross-sectional structural brain neuroimaging of child acquired via 3T scanner at ages 8–11 years.\nIn utero\nSER was measured by maternal education, household income, and home utility availability. The child's ACEs were measured by self-report assisted by the researcher. PAE was grouped into early exposure ({\\textless}12 weeks), continued exposure ({\\textgreater}=12 weeks), and no exposure controls. PTE was grouped into exposed and non-exposed controls.\n\n\n\nResults\n\nGreater access to SER during pregnancy was associated with fewer ACEs (maternal education: $\\beta$ = −0.293,\np\n= 0.01; phone access: $\\beta$ = −0.968,\np\n= 0.05). PTE partially mediated the association between SER and ACEs, where greater SER reduced the likelihood of PTE, which was positively associated with ACEs ($\\beta$ = 1.110,\np\n= 0.01). SER was associated with alterations in superior frontal ($\\beta$ = −1336.036,\nq\n= 0.046), lateral orbitofrontal ($\\beta$ = −513.865,\nq\n= 0.046), caudal anterior cingulate volumes ($\\beta$ = −222.982,\nq\n= 0.046), with access to phone negatively associated with all three brain volumes. Access to water was positively associated with superior frontal volume ($\\beta$=1569.527,\nq\n= 0.013). PTE was associated with smaller volumes of lateral orbitofrontal ($\\beta$ = −331.000,\nq\n= 0.033) and nucleus accumbens regions ($\\beta$ = −34.800,\nq\n= 0.033).\n\n\n\nConclusion\nResearch on neurodevelopment following community-levels of PAE and PTE should more regularly consider the ecological context to accelerate understanding of teratogenic outcomes. Further research is needed to replicate this novel conceptual approach with varying PAE and PTE patterns, to disentangle the interplay between dose, community-level and individual-level risk factors on neurodevelopment.},\nauthor = {Xia, Yingjing and Rebello, Vida and Bodison, Stefanie C and Jonker, Deborah and Steigelmann, Babette and Donald, Kirsten A and Charles, Weslin and Stein, Dan J and Ipser, Jonathan and Ahmadi, Hedyeh and Kan, Eric and Sowell, Elizabeth R and Narr, Katherine L and Joshi, Shantanu H and Odendaal, Hein J and Uban, Kristina A},\ndoi = {10.3389/fnint.2023.1104788},\nfile = {:Users/jacquelinebracher/Zotero/storage/Y65VCU8A/Xia et al. - 2023 - Contextualizing the impact of prenatal alcohol and.pdf:pdf},\nissn = {1662-5145},\njournal = {Frontiers in Integrative Neuroscience},\nmonth = {jul},\npages = {1104788},\nshorttitle = {Contextualizing the impact of prenatal alcohol and},\ntitle = {{Contextualizing the impact of prenatal alcohol and tobacco exposure on neurodevelopment in a {\\{}South{\\}} {\\{}African{\\}} birth cohort: an analysis from the socioecological perspective}},\nurl = {https://www.frontiersin.org/articles/10.3389/fnint.2023.1104788/full},\nvolume = {17},\nyear = {2023}\n}\n
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\n Background Alcohol and tobacco are known teratogens. Historically, more severe prenatal alcohol exposure (PAE) and prenatal tobacco exposure (PTE) have been examined as the principal predictor of neurodevelopmental alterations, with little incorporation of lower doses or ecological contextual factors that can also impact neurodevelopment, such as socioeconomic resources (SER) or adverse childhood experiences (ACEs). Here, a novel analytical approach informed by a socio-ecological perspective was used to examine the associations between SER, PAE and/or PTE, and ACEs, and their effects on neurodevelopment. Methods N = 313 mother-child dyads were recruited from a prospective birth cohort with maternal report of PAE and PTE, and cross-sectional structural brain neuroimaging of child acquired via 3T scanner at ages 8–11 years. In utero SER was measured by maternal education, household income, and home utility availability. The child's ACEs were measured by self-report assisted by the researcher. PAE was grouped into early exposure (\\textless12 weeks), continued exposure (\\textgreater=12 weeks), and no exposure controls. PTE was grouped into exposed and non-exposed controls. Results Greater access to SER during pregnancy was associated with fewer ACEs (maternal education: $β$ = −0.293, p = 0.01; phone access: $β$ = −0.968, p = 0.05). PTE partially mediated the association between SER and ACEs, where greater SER reduced the likelihood of PTE, which was positively associated with ACEs ($β$ = 1.110, p = 0.01). SER was associated with alterations in superior frontal ($β$ = −1336.036, q = 0.046), lateral orbitofrontal ($β$ = −513.865, q = 0.046), caudal anterior cingulate volumes ($β$ = −222.982, q = 0.046), with access to phone negatively associated with all three brain volumes. Access to water was positively associated with superior frontal volume ($β$=1569.527, q = 0.013). PTE was associated with smaller volumes of lateral orbitofrontal ($β$ = −331.000, q = 0.033) and nucleus accumbens regions ($β$ = −34.800, q = 0.033). Conclusion Research on neurodevelopment following community-levels of PAE and PTE should more regularly consider the ecological context to accelerate understanding of teratogenic outcomes. Further research is needed to replicate this novel conceptual approach with varying PAE and PTE patterns, to disentangle the interplay between dose, community-level and individual-level risk factors on neurodevelopment.\n
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\n \n\n \n \n \n \n \n \n Epileptic spasms: \\A\\ \\South\\ \\African\\ overview of aetiologies, interventions, and outcomes.\n \n \n \n \n\n\n \n Raga, S. V; Essajee, F.; Solomons, R.; Van Toorn, R.; and Wilmshurst, J. M\n\n\n \n\n\n\n Developmental Medicine & Child Neurology, 65(4): 526–533. apr 2023.\n \n\n\n\n
\n\n\n\n \n \n \"EpilepticPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{raga_epileptic_2023,\nabstract = {Abstract\n\nAim\nTo better understand the aetiologies of epileptic spasms in infants, as well as the safety and efficacy of high dose corticosteroids in tuberculosis and human immunodeficiency virus (HIV) endemic resource‐limited settings.\n\n\nMethod\nThis was a retrospective analysis of infants with epileptic spasms managed at the tertiary referral centres in the Western Cape, South Africa.\n\n\nResults\n\nOf 175 children with epileptic spasms, the median age at onset was 6 months (interquartile range 4–8 months). Structural aetiologies were most common (115 out of 175 [66{\\%}]), with two‐thirds related to perinatal insults. A lead time to treatment (LTTT) of less than 1 month was more likely in the epileptic encephalopathy/developmental and epileptic encephalopathy (DEE) group: 58 out of 92 (63{\\%}), compared to 28 out of 76 (37{\\%}) of those with developmental encephalopathy (\np\n= 0.001). Failure to recognize preceding developmental delay was common. Ninety‐nine children (57{\\%}) received first line hormonal therapy such as adrenocorticotropic hormone. A total of 111 out of 172 children (65{\\%}) from the developmental encephalopathy and epileptic encephalopathy/DEE groups had clinical and/or electroencephalogram resolution of spasms within 14 days. In our population, children in whom an aetiology could not be identified were statistically more likely to have moderate to profound developmental delay at 1 year of age: 33 out of 44 (\np\n= 0.001). Based on reported incidence of epileptic spasms, 23 to 58 cases per annum would be expected but a far smaller proportion presented to our centres.\n\n\n\nInterpretation\nWhilst this is the largest cohort of infants with epileptic spasms from sub‐Saharan Africa, the study size is less than expected; this may reflect misdiagnosis and failure of referral pathways. Despite a reported shorter LTTT, infants with DEE had worse developmental outcomes compared to international studies. Hormonal therapy was safe and effective in our setting, despite exposure to high levels of tuberculosis and HIV.\n\n\nWhat this paper adds\n\n\n\nThe number of unreferred cases of epileptic spasms in South Africa remains high.\n\n\nCaregivers and health care workers in primary care facilities often fail to recognize developmental delay.\n\n\nThe burden of disease from hypoxic‐ischaemic encephalopathy remains high in our resource‐limited setting.\n\n\nHormonal treatment (e.g. adrenocorticotropic hormone) was safe and effective despite the high prevalence of human immunodeficiency virus and tuberculosis.},\nauthor = {Raga, Sharika V and Essajee, Farida and Solomons, Regan and {Van Toorn}, Ronald and Wilmshurst, Jo M},\ndoi = {10.1111/dmcn.15433},\nissn = {0012-1622, 1469-8749},\njournal = {Developmental Medicine {\\&} Child Neurology},\nmonth = {apr},\nnumber = {4},\npages = {526--533},\nshorttitle = {Epileptic spasms},\ntitle = {{Epileptic spasms: {\\{}A{\\}} {\\{}South{\\}} {\\{}African{\\}} overview of aetiologies, interventions, and outcomes}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1111/dmcn.15433},\nvolume = {65},\nyear = {2023}\n}\n
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\n Abstract Aim To better understand the aetiologies of epileptic spasms in infants, as well as the safety and efficacy of high dose corticosteroids in tuberculosis and human immunodeficiency virus (HIV) endemic resource‐limited settings. Method This was a retrospective analysis of infants with epileptic spasms managed at the tertiary referral centres in the Western Cape, South Africa. Results Of 175 children with epileptic spasms, the median age at onset was 6 months (interquartile range 4–8 months). Structural aetiologies were most common (115 out of 175 [66%]), with two‐thirds related to perinatal insults. A lead time to treatment (LTTT) of less than 1 month was more likely in the epileptic encephalopathy/developmental and epileptic encephalopathy (DEE) group: 58 out of 92 (63%), compared to 28 out of 76 (37%) of those with developmental encephalopathy ( p = 0.001). Failure to recognize preceding developmental delay was common. Ninety‐nine children (57%) received first line hormonal therapy such as adrenocorticotropic hormone. A total of 111 out of 172 children (65%) from the developmental encephalopathy and epileptic encephalopathy/DEE groups had clinical and/or electroencephalogram resolution of spasms within 14 days. In our population, children in whom an aetiology could not be identified were statistically more likely to have moderate to profound developmental delay at 1 year of age: 33 out of 44 ( p = 0.001). Based on reported incidence of epileptic spasms, 23 to 58 cases per annum would be expected but a far smaller proportion presented to our centres. Interpretation Whilst this is the largest cohort of infants with epileptic spasms from sub‐Saharan Africa, the study size is less than expected; this may reflect misdiagnosis and failure of referral pathways. Despite a reported shorter LTTT, infants with DEE had worse developmental outcomes compared to international studies. Hormonal therapy was safe and effective in our setting, despite exposure to high levels of tuberculosis and HIV. What this paper adds The number of unreferred cases of epileptic spasms in South Africa remains high. Caregivers and health care workers in primary care facilities often fail to recognize developmental delay. The burden of disease from hypoxic‐ischaemic encephalopathy remains high in our resource‐limited setting. Hormonal treatment (e.g. adrenocorticotropic hormone) was safe and effective despite the high prevalence of human immunodeficiency virus and tuberculosis.\n
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\n \n\n \n \n \n \n \n \n Maternal \\ART\\ throughout gestation prevents caudate volume reductions in neonates who are \\HIV\\ exposed but uninfected.\n \n \n \n \n\n\n \n Ibrahim, A.; Warton, F. L; Fry, S.; Cotton, M. F; Jacobson, S. W; Jacobson, J. L; Molteno, C. D; Little, F.; Van Der Kouwe, A. J W; Laughton, B.; Meintjes, E. M; and Holmes, M. J\n\n\n \n\n\n\n Frontiers in Neuroscience, 17: 1085589. mar 2023.\n \n\n\n\n
\n\n\n\n \n \n \"MaternalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{ibrahim_maternal_2023,\nabstract = {Introduction\nSuccessful programmes for prevention of vertical HIV transmission have reduced the risk of infant HIV infection in South Africa from 8{\\%} in 2008 to below 1{\\%} in 2018/2019, resulting in an increasing population of children exposed to HIV perinatally but who are uninfected (HEU). However, the long-term effects of HIV and antiretroviral treatment (ART) exposure on the developing brain are not well understood. Whereas children who are HEU perform better than their HIV-infected counterparts, they demonstrate greater neurodevelopmental delay than children who are HIV unexposed and uninfected (HUU), especially in resource-poor settings. Here we investigate subcortical volumetric differences related to HIV and ART exposure in neonates.\n\n\nMethods\nWe included 120 infants (59 girls; 79 HEU) born to healthy women with and without HIV infection in Cape Town, South Africa, where HIV sero-prevalence approaches 30{\\%}. Of the 79 HEU infants, 40 were exposed to ART throughout gestation (i.e., mothers initiated ART pre conception; HEU-pre), and 39 were exposed to ART for part of gestation (i.e., mothers initiated ART post conception; HEU-post). Post-conception mothers had a mean (± SD) gestational age (GA) of 15.4 (± 5.7) weeks at ART initiation. Mothers with HIV received standard care fixed drug combination ART (Tenofovir/Efavirenz/Emtricitabine). Infants were imaged unsedated on a 3T Skyra (Siemens, Erlangen, Germany) at mean GA equivalent of 41.5 (± 1.0) weeks. Selected regions (caudate, putamen, pallidum, thalamus, cerebellar hemispheres and vermis, and corpus callosum) were manually traced on T1-weighted images using Freeview.\n\n\nResults\n\nHEU neonates had smaller left putamen volumes than HUU [$\\beta$ (SE) = −90.3 (45.3),\np\n= 0.05] and caudate volume reductions that depended on ART exposure duration\nin utero\n. While the HEU-pre group demonstrated no caudate volume reductions compared to HUU, the HEU-post group had smaller caudate volumes bilaterally [$\\beta$ (SE) = −145.5 (45.1),\np\n= 0.002, and −135.7 (49.7),\np\n= 0.008 for left and right caudate, respectively].\n\n\n\nDiscussion\nThese findings from the first postnatal month suggest that maternal ART throughout gestation is protective to the caudate nuclei. In contrast, left putamens were smaller across all HEU newborns, despite maternal ART.},\nauthor = {Ibrahim, Abdulmumin and Warton, Fleur L and Fry, Samantha and Cotton, Mark F and Jacobson, Sandra W and Jacobson, Joseph L and Molteno, Christopher D and Little, Francesca and {Van Der Kouwe}, Andre J W and Laughton, Barbara and Meintjes, Ernesta M and Holmes, Martha J},\ndoi = {10.3389/fnins.2023.1085589},\nfile = {:Users/jacquelinebracher/Zotero/storage/HGJJUUQG/Ibrahim et al. - 2023 - Maternal ART throughout gestation prevents caudate.pdf:pdf},\nissn = {1662-453X},\njournal = {Frontiers in Neuroscience},\nmonth = {mar},\npages = {1085589},\ntitle = {{Maternal {\\{}ART{\\}} throughout gestation prevents caudate volume reductions in neonates who are {\\{}HIV{\\}} exposed but uninfected}},\nurl = {https://www.frontiersin.org/articles/10.3389/fnins.2023.1085589/full},\nvolume = {17},\nyear = {2023}\n}\n
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\n Introduction Successful programmes for prevention of vertical HIV transmission have reduced the risk of infant HIV infection in South Africa from 8% in 2008 to below 1% in 2018/2019, resulting in an increasing population of children exposed to HIV perinatally but who are uninfected (HEU). However, the long-term effects of HIV and antiretroviral treatment (ART) exposure on the developing brain are not well understood. Whereas children who are HEU perform better than their HIV-infected counterparts, they demonstrate greater neurodevelopmental delay than children who are HIV unexposed and uninfected (HUU), especially in resource-poor settings. Here we investigate subcortical volumetric differences related to HIV and ART exposure in neonates. Methods We included 120 infants (59 girls; 79 HEU) born to healthy women with and without HIV infection in Cape Town, South Africa, where HIV sero-prevalence approaches 30%. Of the 79 HEU infants, 40 were exposed to ART throughout gestation (i.e., mothers initiated ART pre conception; HEU-pre), and 39 were exposed to ART for part of gestation (i.e., mothers initiated ART post conception; HEU-post). Post-conception mothers had a mean (± SD) gestational age (GA) of 15.4 (± 5.7) weeks at ART initiation. Mothers with HIV received standard care fixed drug combination ART (Tenofovir/Efavirenz/Emtricitabine). Infants were imaged unsedated on a 3T Skyra (Siemens, Erlangen, Germany) at mean GA equivalent of 41.5 (± 1.0) weeks. Selected regions (caudate, putamen, pallidum, thalamus, cerebellar hemispheres and vermis, and corpus callosum) were manually traced on T1-weighted images using Freeview. Results HEU neonates had smaller left putamen volumes than HUU [$β$ (SE) = −90.3 (45.3), p = 0.05] and caudate volume reductions that depended on ART exposure duration in utero . While the HEU-pre group demonstrated no caudate volume reductions compared to HUU, the HEU-post group had smaller caudate volumes bilaterally [$β$ (SE) = −145.5 (45.1), p = 0.002, and −135.7 (49.7), p = 0.008 for left and right caudate, respectively]. Discussion These findings from the first postnatal month suggest that maternal ART throughout gestation is protective to the caudate nuclei. In contrast, left putamens were smaller across all HEU newborns, despite maternal ART.\n
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\n \n\n \n \n \n \n \n \n Equity in access to antiseizure medications: \\Who\\ has the right to decide and what are the consequences of crisis decisions?.\n \n \n \n \n\n\n \n Wilmshurst, J. M; and Sperling, M. R\n\n\n \n\n\n\n Epilepsia, 64(8): 2011–2013. aug 2023.\n \n\n\n\n
\n\n\n\n \n \n \"EquityPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{wilmshurst_equity_2023,\nauthor = {Wilmshurst, Jo M and Sperling, Michael R},\ndoi = {10.1111/epi.17685},\nissn = {0013-9580, 1528-1167},\njournal = {Epilepsia},\nmonth = {aug},\nnumber = {8},\npages = {2011--2013},\nshorttitle = {Equity in access to antiseizure medications},\ntitle = {{Equity in access to antiseizure medications: {\\{}Who{\\}} has the right to decide and what are the consequences of crisis decisions?}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1111/epi.17685},\nvolume = {64},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Normal \\Outcome\\ \\With\\ \\Prenatal\\ \\Intervention\\ for \\Riboflavin\\ \\Transporter\\ \\Defect\\.\n \n \n \n \n\n\n \n Elks, N.; Wilmshurst, J. M; and Raga, S. V\n\n\n \n\n\n\n Pediatric Neurology, 144: 16–18. jul 2023.\n \n\n\n\n
\n\n\n\n \n \n \"NormalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{elks_normal_2023,\nauthor = {Elks, Natasha and Wilmshurst, Jo M and Raga, Sharika V},\ndoi = {10.1016/j.pediatrneurol.2023.04.004},\nissn = {08878994},\njournal = {Pediatric Neurology},\nmonth = {jul},\npages = {16--18},\ntitle = {{Normal {\\{}Outcome{\\}} {\\{}With{\\}} {\\{}Prenatal{\\}} {\\{}Intervention{\\}} for {\\{}Riboflavin{\\}} {\\{}Transporter{\\}} {\\{}Defect{\\}}}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S088789942300111X},\nvolume = {144},\nyear = {2023}\n}\n
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\n \n\n \n \n \n \n \n \n Gathering the \\Stakeholder\\'s \\Perspective\\: \\Experiences\\ and \\Opportunities\\ in \\Rare\\ \\Genetic\\ \\Disease\\ \\Research\\.\n \n \n \n \n\n\n \n White, L. K; Crowley, T B.; Finucane, B.; McClellan, E. J; Donoghue, S.; Garcia-Minaur, S.; Repetto, G. M; Fischer, M.; Jacquemont, S.; Gur, R. E; Maillard, A. M; Donald, K. A; Bassett, A. S; Swillen, A.; and McDonald-McGinn, D. M\n\n\n \n\n\n\n Genes, 14(1): 169. jan 2023.\n \n\n\n\n
\n\n\n\n \n \n \"GatheringPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{white_gathering_2023,\nabstract = {Background: Research participant feedback is rarely collected; therefore, investigators have limited understanding regarding stakeholders' (affected individuals/caregivers) motivation to participate. Members of the Genes to Mental Health Network (G2MH) surveyed stakeholders affected by copy number variants (CNVs) regarding perceived incentives for study participation, opinions concerning research priorities, and the necessity for future funding. Respondents were also asked about feelings of preparedness, research burden, and satisfaction with research study participation. Methods: Modified validated surveys were used to assess stakeholders´ views across three domains: (1) Research Study Enrollment, Retainment, Withdrawal, and Future Participation; (2) Overall Research Experience, Burden, and Preparedness; (3) Research Priorities and Obstacles. Top box score analyses were performed. Results: A total of 704 stakeholders´ responded from 29 countries representing 55 CNVs. The top reasons for initial participation in the research included reasons related to education and altruism. The top reasons for leaving a research study included treatment risks and side effects. The importance of sharing research findings and laboratory results with stakeholders was underscored by participants. Most stakeholders reported positive research experiences. Conclusions: This study provides important insight into how individuals and families affected with a rare CNV feel toward research participation and their overall experience in rare disease research. There are clear targets for areas of improvement for study teams, although many stakeholders reported positive research experiences. Key findings from this international survey may help advance collaborative research and improve the experience of participants, investigators, and other stakeholders moving forward.},\nauthor = {White, Lauren K and Crowley, T Blaine and Finucane, Brenda and McClellan, Emily J and Donoghue, Sarah and Garcia-Minaur, Sixto and Repetto, Gabriela M and Fischer, Matthias and Jacquemont, Sebastien and Gur, Raquel E and Maillard, Anne M and Donald, Kirsten A and Bassett, Anne S and Swillen, Ann and McDonald-McGinn, Donna M},\ndoi = {10.3390/genes14010169},\nfile = {:Users/jacquelinebracher/Zotero/storage/IYEKWK7J/White et al. - 2023 - Gathering the Stakeholder's Perspective Experienc.pdf:pdf},\nissn = {2073-4425},\njournal = {Genes},\nmonth = {jan},\nnumber = {1},\npages = {169},\nshorttitle = {Gathering the {\\{}Stakeholder{\\}}'s {\\{}Perspective{\\}}},\ntitle = {{Gathering the {\\{}Stakeholder{\\}}'s {\\{}Perspective{\\}}: {\\{}Experiences{\\}} and {\\{}Opportunities{\\}} in {\\{}Rare{\\}} {\\{}Genetic{\\}} {\\{}Disease{\\}} {\\{}Research{\\}}}},\nurl = {https://www.mdpi.com/2073-4425/14/1/169},\nvolume = {14},\nyear = {2023}\n}\n
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\n Background: Research participant feedback is rarely collected; therefore, investigators have limited understanding regarding stakeholders' (affected individuals/caregivers) motivation to participate. Members of the Genes to Mental Health Network (G2MH) surveyed stakeholders affected by copy number variants (CNVs) regarding perceived incentives for study participation, opinions concerning research priorities, and the necessity for future funding. Respondents were also asked about feelings of preparedness, research burden, and satisfaction with research study participation. Methods: Modified validated surveys were used to assess stakeholders´ views across three domains: (1) Research Study Enrollment, Retainment, Withdrawal, and Future Participation; (2) Overall Research Experience, Burden, and Preparedness; (3) Research Priorities and Obstacles. Top box score analyses were performed. Results: A total of 704 stakeholders´ responded from 29 countries representing 55 CNVs. The top reasons for initial participation in the research included reasons related to education and altruism. The top reasons for leaving a research study included treatment risks and side effects. The importance of sharing research findings and laboratory results with stakeholders was underscored by participants. Most stakeholders reported positive research experiences. Conclusions: This study provides important insight into how individuals and families affected with a rare CNV feel toward research participation and their overall experience in rare disease research. There are clear targets for areas of improvement for study teams, although many stakeholders reported positive research experiences. Key findings from this international survey may help advance collaborative research and improve the experience of participants, investigators, and other stakeholders moving forward.\n
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\n \n\n \n \n \n \n \n \n Cerebrovascular \\Pressure\\ \\Reactivity\\ \\Has\\ a \\Strong\\ and \\Independent\\ \\Association\\ \\With\\ \\Outcome\\ in \\Children\\ \\With\\ \\Severe\\ \\Traumatic\\ \\Brain\\ \\Injury\\*.\n \n \n \n \n\n\n \n Smith, C. A; Rohlwink, U. K; Mauff, K.; Thango, N. S; Hina, T. S; Salie, S.; Enslin, J. M N; and Figaji, A. A\n\n\n \n\n\n\n Critical Care Medicine, 51(5): 573–583. may 2023.\n \n\n\n\n
\n\n\n\n \n \n \"CerebrovascularPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{smith_cerebrovascular_2023,\nabstract = {OBJECTIVES:\nTo examine cerebrovascular pressure reactivity index (PRx) in a large cohort of children with severe traumatic brain injury (sTBI) in association with physiologic variables and outcome.\n\n\nDESIGN:\nRetrospective observational cohort study.\n\n\nSETTING:\nRed Cross War Memorial Children's Hospital in Cape Town, South Africa.\n\n\nPATIENTS:\nPediatric (≤ 14 yr old) sTBI patients with intracranial pressure (ICP) monitoring (postresuscitation Glasgow Coma Score [Glasgow Coma Scale (GCS)] of ≤ 8).\n\n\nMEASUREMENTS AND MAIN RESULTS:\n\nData were analyzed from ICM+ files sampled at 100Hz. PRx (a mathematical indicator of pressure reactivity) was calculated as a moving correlation coefficient between ICP and mean arterial pressure (MAP) as previously described. Associations between PRx, age, GCS, ICP, MAP, and cerebral perfusion pressure (CPP) were examined with summary measures and correlation analysis using high-frequency data. Associations between PRx and mortality/outcome were examined with multivariable logistic regression analysis and the prognostic ability of PRx with receiver operating characteristic (ROCs) curves. The dataset included over 1.7 million minutes (28,634 hr) of MAP and ICP data in 196 children. The series mortality was 10.7{\\%} (21/196), and unfavorable outcome 29.6{\\%} (58/196). PRx had a moderate positive correlation with ICP (\nr\n= 0.44;\np\n{\\textless}0.001), a moderate negative correlation with CPP (\nr\n= -0.43;\np\n{\\textless}0.001), and a weak negative correlation with MAP (\nr\n= –0.21;\np\n= 0.004). PRx was consistently higher in patients with poor outcome and had a strong, independent association with mortality (ROC area under the curve = 0.91). A PRx threshold of 0.25 showed the best predictive ability for mortality.\n\n\n\nCONCLUSIONS:\nThis is the largest cohort of children with PRx analysis of cerebrovascular reactivity to date. PRx had a strong association with outcome that was independent of ICP, CPP, GCS, and age. The data suggest that impaired autoregulation is an independent factor associated with poor outcome and may be useful in directing clinical care.},\nauthor = {Smith, Claudia A and Rohlwink, Ursula K and Mauff, Katya and Thango, Nqobile S and Hina, Thembani S and Salie, Shamiel and Enslin, Johannes M N and Figaji, Anthony A},\ndoi = {10.1097/CCM.0000000000005815},\nfile = {:Users/jacquelinebracher/Zotero/storage/NZNI6K5C/Smith et al. - 2023 - Cerebrovascular Pressure Reactivity Has a Strong a.pdf:pdf},\nissn = {0090-3493},\njournal = {Critical Care Medicine},\nmonth = {may},\nnumber = {5},\npages = {573--583},\ntitle = {{Cerebrovascular {\\{}Pressure{\\}} {\\{}Reactivity{\\}} {\\{}Has{\\}} a {\\{}Strong{\\}} and {\\{}Independent{\\}} {\\{}Association{\\}} {\\{}With{\\}} {\\{}Outcome{\\}} in {\\{}Children{\\}} {\\{}With{\\}} {\\{}Severe{\\}} {\\{}Traumatic{\\}} {\\{}Brain{\\}} {\\{}Injury{\\}}*}},\nurl = {https://journals.lww.com/10.1097/CCM.0000000000005815},\nvolume = {51},\nyear = {2023}\n}\n
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\n OBJECTIVES: To examine cerebrovascular pressure reactivity index (PRx) in a large cohort of children with severe traumatic brain injury (sTBI) in association with physiologic variables and outcome. DESIGN: Retrospective observational cohort study. SETTING: Red Cross War Memorial Children's Hospital in Cape Town, South Africa. PATIENTS: Pediatric (≤ 14 yr old) sTBI patients with intracranial pressure (ICP) monitoring (postresuscitation Glasgow Coma Score [Glasgow Coma Scale (GCS)] of ≤ 8). MEASUREMENTS AND MAIN RESULTS: Data were analyzed from ICM+ files sampled at 100Hz. PRx (a mathematical indicator of pressure reactivity) was calculated as a moving correlation coefficient between ICP and mean arterial pressure (MAP) as previously described. Associations between PRx, age, GCS, ICP, MAP, and cerebral perfusion pressure (CPP) were examined with summary measures and correlation analysis using high-frequency data. Associations between PRx and mortality/outcome were examined with multivariable logistic regression analysis and the prognostic ability of PRx with receiver operating characteristic (ROCs) curves. The dataset included over 1.7 million minutes (28,634 hr) of MAP and ICP data in 196 children. The series mortality was 10.7% (21/196), and unfavorable outcome 29.6% (58/196). PRx had a moderate positive correlation with ICP ( r = 0.44; p \\textless0.001), a moderate negative correlation with CPP ( r = -0.43; p \\textless0.001), and a weak negative correlation with MAP ( r = –0.21; p = 0.004). PRx was consistently higher in patients with poor outcome and had a strong, independent association with mortality (ROC area under the curve = 0.91). A PRx threshold of 0.25 showed the best predictive ability for mortality. CONCLUSIONS: This is the largest cohort of children with PRx analysis of cerebrovascular reactivity to date. PRx had a strong association with outcome that was independent of ICP, CPP, GCS, and age. The data suggest that impaired autoregulation is an independent factor associated with poor outcome and may be useful in directing clinical care.\n
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\n \n\n \n \n \n \n \n \n Shape analysis of subcortical structures in obsessive‐compulsive disorder and the relationship with comorbid anxiety, depression, and medication use: \\A\\ meta‐analysis by the \\OCD\\ \\Brain\\ \\Imaging\\ \\Consortium\\.\n \n \n \n \n\n\n \n Fouche, J.; Groenewold, N. A; Sevenoaks, T.; Heany, S.; Lochner, C.; Alonso, P.; Batistuzzo, M. C; Cardoner, N.; Ching, C. R K; De Wit, S. J; Gutman, B.; Hoexter, M. Q; Jahanshad, N.; Kim, M.; Kwon, J. S.; Mataix‐Cols, D.; Menchon, J. M; Miguel, E. C; Nakamae, T.; Phillips, M. L; Pujol, J.; Sakai, Y.; Yun, J.; Soriano‐Mas, C.; Thompson, P. M; Yamada, K.; Veltman, D. J; Van Den Heuvel, O. A; and Stein, D. J\n\n\n \n\n\n\n Brain and Behavior, 12(10): e2755. oct 2022.\n \n\n\n\n
\n\n\n\n \n \n \"ShapePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{fouche_shape_2022,\nabstract = {Abstract\n\nObjective\nNeuroimaging studies of obsessive‐compulsive disorder (OCD) patients have highlighted the important role of deep gray matter structures. Less work has however focused on subcortical shape in OCD patients.\n\n\nMethods\nHere we pooled brain MRI scans from 412 OCD patients and 368 controls to perform a meta‐analysis utilizing the ENIGMA‐Shape protocol. In addition, we investigated modulating effects of medication status, comorbid anxiety or depression, and disease duration on subcortical shape.\n\n\nResults\nThere was no significant difference in shape thickness or surface area between OCD patients and healthy controls. For the subgroup analyses, OCD patients with comorbid depression or anxiety had lower thickness of the hippocampus and caudate nucleus and higher thickness of the putamen and pallidum compared to controls. OCD patients with comorbid depression had lower shape surface area in the thalamus, caudate nucleus, putamen, hippocampus, and nucleus accumbens and higher shape surface area in the pallidum. OCD patients with comorbid anxiety had lower shape surface area in the putamen and the left caudate nucleus and higher shape surface area in the pallidum and the right caudate nucleus. Further, OCD patients on medication had lower shape thickness of the putamen, thalamus, and hippocampus and higher thickness of the pallidum and caudate nucleus, as well as lower shape surface area in the hippocampus and amygdala and higher surface area in the putamen, pallidum, and caudate nucleus compared to controls. There were no significant differences between OCD patients without co‐morbid anxiety and/or depression and healthy controls on shape measures. In addition, there were also no significant differences between OCD patients not using medication and healthy controls.\n\n\nConclusions\nThe findings here are partly consistent with prior work on brain volumes in OCD, insofar as they emphasize that alterations in subcortical brain morphology are associated with comorbidity and medication status. Further work is needed to understand the biological processes contributing to subcortical shape.},\nauthor = {Fouche, Jean‐Paul and Groenewold, Nynke A and Sevenoaks, Tatum and Heany, Sarah and Lochner, Christine and Alonso, Pino and Batistuzzo, Marcelo C and Cardoner, Narcis and Ching, Christopher R K and {De Wit}, Stella J and Gutman, Boris and Hoexter, Marcelo Q and Jahanshad, Neda and Kim, Minah and Kwon, Jun Soo and Mataix‐Cols, David and Menchon, Jose M and Miguel, Euripedes C and Nakamae, Takashi and Phillips, Mary L and Pujol, Jesus and Sakai, Yuki and Yun, Je‐Yeon and Soriano‐Mas, Carles and Thompson, Paul M and Yamada, Kei and Veltman, Dick J and {Van Den Heuvel}, Odile A and Stein, Dan J},\ndoi = {10.1002/brb3.2755},\nfile = {:Users/jacquelinebracher/Zotero/storage/KGPIVMCQ/Fouche et al. - 2022 - Shape analysis of subcortical structures in obsess.pdf:pdf},\nissn = {2162-3279, 2162-3279},\njournal = {Brain and Behavior},\nmonth = {oct},\nnumber = {10},\npages = {e2755},\nshorttitle = {Shape analysis of subcortical structures in obsess},\ntitle = {{Shape analysis of subcortical structures in obsessive‐compulsive disorder and the relationship with comorbid anxiety, depression, and medication use: {\\{}A{\\}} meta‐analysis by the {\\{}OCD{\\}} {\\{}Brain{\\}} {\\{}Imaging{\\}} {\\{}Consortium{\\}}}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1002/brb3.2755},\nvolume = {12},\nyear = {2022}\n}\n
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\n Abstract Objective Neuroimaging studies of obsessive‐compulsive disorder (OCD) patients have highlighted the important role of deep gray matter structures. Less work has however focused on subcortical shape in OCD patients. Methods Here we pooled brain MRI scans from 412 OCD patients and 368 controls to perform a meta‐analysis utilizing the ENIGMA‐Shape protocol. In addition, we investigated modulating effects of medication status, comorbid anxiety or depression, and disease duration on subcortical shape. Results There was no significant difference in shape thickness or surface area between OCD patients and healthy controls. For the subgroup analyses, OCD patients with comorbid depression or anxiety had lower thickness of the hippocampus and caudate nucleus and higher thickness of the putamen and pallidum compared to controls. OCD patients with comorbid depression had lower shape surface area in the thalamus, caudate nucleus, putamen, hippocampus, and nucleus accumbens and higher shape surface area in the pallidum. OCD patients with comorbid anxiety had lower shape surface area in the putamen and the left caudate nucleus and higher shape surface area in the pallidum and the right caudate nucleus. Further, OCD patients on medication had lower shape thickness of the putamen, thalamus, and hippocampus and higher thickness of the pallidum and caudate nucleus, as well as lower shape surface area in the hippocampus and amygdala and higher surface area in the putamen, pallidum, and caudate nucleus compared to controls. There were no significant differences between OCD patients without co‐morbid anxiety and/or depression and healthy controls on shape measures. In addition, there were also no significant differences between OCD patients not using medication and healthy controls. Conclusions The findings here are partly consistent with prior work on brain volumes in OCD, insofar as they emphasize that alterations in subcortical brain morphology are associated with comorbidity and medication status. Further work is needed to understand the biological processes contributing to subcortical shape.\n
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\n \n\n \n \n \n \n \n Prenatal depression exposure alters white matter integrity and neurodevelopment in early childhood.\n \n \n \n\n\n \n Roos, A.; Wedderburn, C.; Fouche, J.; Joshi, S.; Narr, K.; Woods, R.; Zar, H.; Stein, D.; and Donald, K.\n\n\n \n\n\n\n Brain Imaging and Behavior, 16(3): 1324–1336. 2022.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{Roos2022,\nabstract = {Prenatal exposure to maternal depression increases the risk for onset of emotional and behavioral disorders in children. We investigated the effects of exposure to prenatal depression on white matter microstructural integrity at birth and at 2-3 years, and associated neurodevelopment. Diffusion-weighted images were acquired for children of the Drakenstein Child Health Study at 2-4 weeks postpartum (n=70, 47{\\%} boys) and at 2-3 years of age (n=60, 58{\\%} boys). Tract-Based Spatial Statistics was used to compare, using an ROI based approach, diffusion tensor metrics across groups defined by presence ({\\textgreater}19 on Beck's Depression Inventory and/or {\\textgreater}12 on the Edinburgh Postnatal Depression Scale) or absence (below depression thresholds) of depression, and associations with neurodevelopmental measures at age 2-3 years were determined. We did not detect group differences in white matter integrity at neonatal age, but at 2-3 years, children in the exposed group demonstrated higher fractional anisotropy, and lower mean and radial diffusivity in association tracts compared to controls. This was notable in the sagittal stratum (radial diffusivity: p{\\textless}0.01). Altered white matter integrity metrics were also observed in projection tracts, including the corona radiata, which associated with cognitive and motor outcomes in exposed 2-3-year-olds (p{\\textless}0.05). Our findings of widespread white matter alterations in 2-3-year-old children with prenatal exposure to depression are consistent with previous findings, as well as with neuroimaging findings in adults with major depression. Further, we identified novel associations of altered white matter integrity with cognitive development in depression-exposed children, suggesting that these neuroimaging findings may have early functional impact.},\nauthor = {Roos, A. and Wedderburn, C.J. and Fouche, J.-P. and Joshi, S.H. and Narr, K.L. and Woods, R.P. and Zar, H.J. and Stein, D.J. and Donald, K.A.},\ndoi = {10.1007/s11682-021-00616-3},\nfile = {:Users/jacquelinebracher/Zotero/storage/EEXBHFRY/Roos et al. - 2022 - Prenatal depression exposure alters white matter i.pdf:pdf},\njournal = {Brain Imaging and Behavior},\nnumber = {3},\npages = {1324--1336},\ntitle = {{Prenatal depression exposure alters white matter integrity and neurodevelopment in early childhood}},\nvolume = {16},\nyear = {2022}\n}\n
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\n Prenatal exposure to maternal depression increases the risk for onset of emotional and behavioral disorders in children. We investigated the effects of exposure to prenatal depression on white matter microstructural integrity at birth and at 2-3 years, and associated neurodevelopment. Diffusion-weighted images were acquired for children of the Drakenstein Child Health Study at 2-4 weeks postpartum (n=70, 47% boys) and at 2-3 years of age (n=60, 58% boys). Tract-Based Spatial Statistics was used to compare, using an ROI based approach, diffusion tensor metrics across groups defined by presence (\\textgreater19 on Beck's Depression Inventory and/or \\textgreater12 on the Edinburgh Postnatal Depression Scale) or absence (below depression thresholds) of depression, and associations with neurodevelopmental measures at age 2-3 years were determined. We did not detect group differences in white matter integrity at neonatal age, but at 2-3 years, children in the exposed group demonstrated higher fractional anisotropy, and lower mean and radial diffusivity in association tracts compared to controls. This was notable in the sagittal stratum (radial diffusivity: p\\textless0.01). Altered white matter integrity metrics were also observed in projection tracts, including the corona radiata, which associated with cognitive and motor outcomes in exposed 2-3-year-olds (p\\textless0.05). Our findings of widespread white matter alterations in 2-3-year-old children with prenatal exposure to depression are consistent with previous findings, as well as with neuroimaging findings in adults with major depression. Further, we identified novel associations of altered white matter integrity with cognitive development in depression-exposed children, suggesting that these neuroimaging findings may have early functional impact.\n
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\n \n\n \n \n \n \n \n \n Post-\\Infectious\\ \\Autoimmunity\\ in the \\Central\\ (\\CNS\\) and \\Peripheral\\ (\\PNS\\) \\Nervous\\ \\Systems\\: \\An\\ \\African\\ \\Perspective\\.\n \n \n \n \n\n\n \n Ndondo, A. P.; Eley, B.; Wilmshurst, J. M.; Kakooza-Mwesige, A.; Giannoccaro, M. P.; Willison, H. J; Cruz, P. M R.; Heckmann, J. M; Bateman, K.; and Vincent, A.\n\n\n \n\n\n\n Frontiers in Immunology, 13: 833548. mar 2022.\n \n\n\n\n
\n\n\n\n \n \n \"Post-\\Infectious\\Paper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{ndondo_post-infectious_2022,\nabstract = {The direct impact and sequelae of infections in children and adults result in significant morbidity and mortality especially when they involve the central (CNS) or peripheral nervous system (PNS). The historical understanding of the pathophysiology has been mostly focused on the direct impact of the various pathogens through neural tissue invasion. However, with the better understanding of neuroimmunology, there is a rapidly growing realization of the contribution of the innate and adaptive host immune responses in the pathogenesis of many CNS and PNS diseases.\nThe balance between the protective and pathologic sequelae of immunity is fragile and can easily be tipped towards harm for the host. The matter of immune privilege and surveillance of the CNS/PNS compartments and the role of the blood-brain barrier (BBB) and blood nerve barrier (BNB) makes this even more complex. Our understanding of the pathogenesis of many post-infectious manifestations of various microbial agents remains elusive, especially in the diverse African setting. Our exploration and better understanding of the neuroimmunology of some of the infectious diseases that we encounter in the continent will go a long way into helping us to improve their management and therefore lessen the burden.\nAfrica is diverse and uniquely poised because of the mix of the classic, well described, autoimmune disease entities and the specifically “tropical” conditions. This review explores the current understanding of some of the para- and post-infectious autoimmune manifestations of CNS and PNS diseases in the African context. We highlight the clinical presentations, diagnosis and treatment of these neurological disorders and underscore the knowledge gaps and perspectives for future research using disease models of conditions that we see in the continent, some of which are not uniquely African and, where relevant, include discussion of the proposed mechanisms underlying pathogen-induced autoimmunity. This review covers the following conditions as models and highlight those in which a relationship with COVID-19 infection has been reported: a) Acute Necrotizing Encephalopathy; b) Measles-associated encephalopathies; c) Human Immunodeficiency Virus (HIV) neuroimmune disorders, and particularly the difficulties associated with classical post-infectious autoimmune disorders such as the Guillain-Barr{\\'{e}} syndrome in the context of HIV and other infections. Finally, we describe NMDA-R encephalitis, which can be post-HSV encephalitis, summarise other antibody-mediated CNS diseases and describe myasthenia gravis as the classic antibody-mediated disease but with special features in Africa.},\nauthor = {Ndondo, Alvin Pumelele and Eley, Brian and Wilmshurst, Jo Madeleine and Kakooza-Mwesige, Angelina and Giannoccaro, Maria Pia and Willison, Hugh J and Cruz, Pedro M Rodr{\\'{i}}guez and Heckmann, Jeannine M and Bateman, Kathleen and Vincent, Angela},\ndoi = {10.3389/fimmu.2022.833548},\nfile = {:Users/jacquelinebracher/Zotero/storage/TJUW5YPA/Ndondo et al. - 2022 - Post-Infectious Autoimmunity in the Central (CNS) .pdf:pdf},\nissn = {1664-3224},\njournal = {Frontiers in Immunology},\nmonth = {mar},\npages = {833548},\nshorttitle = {Post-{\\{}Infectious{\\}} {\\{}Autoimmunity{\\}} in the {\\{}Central{\\}} },\ntitle = {{Post-{\\{}Infectious{\\}} {\\{}Autoimmunity{\\}} in the {\\{}Central{\\}} ({\\{}CNS{\\}}) and {\\{}Peripheral{\\}} ({\\{}PNS{\\}}) {\\{}Nervous{\\}} {\\{}Systems{\\}}: {\\{}An{\\}} {\\{}African{\\}} {\\{}Perspective{\\}}}},\nurl = {https://www.frontiersin.org/articles/10.3389/fimmu.2022.833548/full},\nvolume = {13},\nyear = {2022}\n}\n
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\n The direct impact and sequelae of infections in children and adults result in significant morbidity and mortality especially when they involve the central (CNS) or peripheral nervous system (PNS). The historical understanding of the pathophysiology has been mostly focused on the direct impact of the various pathogens through neural tissue invasion. However, with the better understanding of neuroimmunology, there is a rapidly growing realization of the contribution of the innate and adaptive host immune responses in the pathogenesis of many CNS and PNS diseases. The balance between the protective and pathologic sequelae of immunity is fragile and can easily be tipped towards harm for the host. The matter of immune privilege and surveillance of the CNS/PNS compartments and the role of the blood-brain barrier (BBB) and blood nerve barrier (BNB) makes this even more complex. Our understanding of the pathogenesis of many post-infectious manifestations of various microbial agents remains elusive, especially in the diverse African setting. Our exploration and better understanding of the neuroimmunology of some of the infectious diseases that we encounter in the continent will go a long way into helping us to improve their management and therefore lessen the burden. Africa is diverse and uniquely poised because of the mix of the classic, well described, autoimmune disease entities and the specifically “tropical” conditions. This review explores the current understanding of some of the para- and post-infectious autoimmune manifestations of CNS and PNS diseases in the African context. We highlight the clinical presentations, diagnosis and treatment of these neurological disorders and underscore the knowledge gaps and perspectives for future research using disease models of conditions that we see in the continent, some of which are not uniquely African and, where relevant, include discussion of the proposed mechanisms underlying pathogen-induced autoimmunity. This review covers the following conditions as models and highlight those in which a relationship with COVID-19 infection has been reported: a) Acute Necrotizing Encephalopathy; b) Measles-associated encephalopathies; c) Human Immunodeficiency Virus (HIV) neuroimmune disorders, and particularly the difficulties associated with classical post-infectious autoimmune disorders such as the Guillain-Barré syndrome in the context of HIV and other infections. Finally, we describe NMDA-R encephalitis, which can be post-HSV encephalitis, summarise other antibody-mediated CNS diseases and describe myasthenia gravis as the classic antibody-mediated disease but with special features in Africa.\n
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\n \n\n \n \n \n \n \n \n A longitudinal and qualitative analysis of caregiver depression and quality of life in the Cape Town adolescent antiretroviral cohort.\n \n \n \n \n\n\n \n Sevenoaks, T; Fouche, J.; Mtukushe, B; Phillips, N; Heany, S; Myer, L; Zar, H J; Stein, D J; and Hoare, J\n\n\n \n\n\n\n 2022.\n \n\n\n\n
\n\n\n\n \n \n \"APaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@misc{Sevenoaks2022,\nannote = {Export Date: 29 December 2022},\nauthor = {Sevenoaks, T and Fouche, J.-P. and Mtukushe, B and Phillips, N and Heany, S and Myer, L and Zar, H J and Stein, D J and Hoare, J},\ndoi = {10.1016/j.jadr.2022.100396},\ntitle = {{A longitudinal and qualitative analysis of caregiver depression and quality of life in the Cape Town adolescent antiretroviral cohort}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85136458005{\\&}doi=10.1016{\\%}2Fj.jadr.2022.100396{\\&}partnerID=40{\\&}md5=f3e409b58b7e7dcc53a4ae0cdf7cafcf},\nvolume = {10},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n The Shared Pleasure Paradigm: A study in an observational birth cohort in South Africa.\n \n \n \n\n\n \n Lachman, A.; Jordaan, E.; Stern, M.; Donald, K.; Hoffman, N.; Lake, M.; Zar, H.; Niehaus, D.; Puura, K.; and Stein, D.\n\n\n \n\n\n\n Archives of Women's Mental Health, 25(1): 227–235. 2022.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{Lachman2022,\nabstract = {Mother–infant dyads in low- and middle-income countries (LMICs) may be exposed to a range of factors associated with suboptimal development. Optimal infant development is likely supported by synchronicity in the early mother–infant relationship, but limited corroborative research is available in LMICs. The Drakenstein Child Health Study (DCHS) provided an opportunity to study this synchronicity and its associations in South Africa. A South African birth cohort study investigating early-life determinants of child health in a LMIC context provided participants. The Shared Pleasure (SP) paradigm helped assess early mother–infant synchronicity in videos of a sub-set of 291 mother–infant dyads at their 14-week well baby visit. General linear regression models investigated the relationship between selected maternal and infant characteristics and the presence of Shared Pleasure moments. Out of a possible 291 dyads, 82{\\%} (n = 239) yielded Shared Pleasure moments. The mean age of mothers was 27 years, while infant sex distribution comprised 54{\\%} females and 46{\\%} males. The shortest single Shared Pleasure moment lasted at least 0.5 s and the longest 28 s. Shared Pleasure moments were associated with higher gestation age at delivery (p = 0.008) and higher infant birth weight (p = 0.006), but were not related to mother's mental health and infant health outcomes at 14 weeks. The high frequency of positive Shared Pleasure moments in reciprocal dyadic interactions in this sample suggests that significant disruption in shared pleasure may be present only in extreme cases (e.g. mothers with severe mental disorders). Further work is needed to investigate the mechanisms underlying the associations between early mother–infant synchronicity and better outcomes noted here, and to assess whether SP may serve as a culturally appropriate screen for assessing connectedness.},\nauthor = {Lachman, A. and Jordaan, E.R. and Stern, M. and Donald, K.A. and Hoffman, N. and Lake, M.T. and Zar, H.J. and Niehaus, D.J.H. and Puura, K. and Stein, D.J.},\ndoi = {10.1007/s00737-021-01199-0},\nfile = {:Users/jacquelinebracher/Zotero/storage/EUFFQ3W5/Lachman et al. - 2022 - The Shared Pleasure Paradigm A study in an observ.pdf:pdf},\njournal = {Archives of Women's Mental Health},\nnumber = {1},\npages = {227--235},\ntitle = {{The Shared Pleasure Paradigm: A study in an observational birth cohort in South Africa}},\nvolume = {25},\nyear = {2022}\n}\n
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\n Mother–infant dyads in low- and middle-income countries (LMICs) may be exposed to a range of factors associated with suboptimal development. Optimal infant development is likely supported by synchronicity in the early mother–infant relationship, but limited corroborative research is available in LMICs. The Drakenstein Child Health Study (DCHS) provided an opportunity to study this synchronicity and its associations in South Africa. A South African birth cohort study investigating early-life determinants of child health in a LMIC context provided participants. The Shared Pleasure (SP) paradigm helped assess early mother–infant synchronicity in videos of a sub-set of 291 mother–infant dyads at their 14-week well baby visit. General linear regression models investigated the relationship between selected maternal and infant characteristics and the presence of Shared Pleasure moments. Out of a possible 291 dyads, 82% (n = 239) yielded Shared Pleasure moments. The mean age of mothers was 27 years, while infant sex distribution comprised 54% females and 46% males. The shortest single Shared Pleasure moment lasted at least 0.5 s and the longest 28 s. Shared Pleasure moments were associated with higher gestation age at delivery (p = 0.008) and higher infant birth weight (p = 0.006), but were not related to mother's mental health and infant health outcomes at 14 weeks. The high frequency of positive Shared Pleasure moments in reciprocal dyadic interactions in this sample suggests that significant disruption in shared pleasure may be present only in extreme cases (e.g. mothers with severe mental disorders). Further work is needed to investigate the mechanisms underlying the associations between early mother–infant synchronicity and better outcomes noted here, and to assess whether SP may serve as a culturally appropriate screen for assessing connectedness.\n
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\n \n\n \n \n \n \n \n \n Fulfilling the specialist neurosurgical workforce needs in \\Africa\\: a systematic review and projection toward 2030.\n \n \n \n \n\n\n \n Ukachukwu, A. K; Still, M. E H; Seas, A.; Von Isenburg, M.; Fieggen, G.; Malomo, A. O; Shokunbi, M. T; Egger, J. R; Haglund, M. M; and Fuller, A. T\n\n\n \n\n\n\n Journal of Neurosurgery,1–12. aug 2022.\n \n\n\n\n
\n\n\n\n \n \n \"FulfillingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{ukachukwu_fulfilling_2022,\nabstract = {OBJECTIVE\nAfrica contributes significantly to the global neurosurgical disease burden but has only 1{\\%} of the neurosurgery workforce. This study appraises the neurosurgical workforce and training capacity in Africa and projects the workforce capacity by 2030.\n\n\nMETHODS\nThe authors conducted a systematic review of the online literature on neurosurgical workforce and training in Africa obtained from three journal databases (PubMed, Embase, and African Index Medicus), as well as from a gray literature search, between September and December 2020. Included literature passed a two-level screening conducted using a systematic review software by a team of two independent reviewers. Data were extracted from selected articles and documented and analyzed on spreadsheets.\n\n\nRESULTS\nOne hundred and fifty-nine eligible articles were analyzed: 1974 neurosurgeons serve 1.3 billion people in Africa (density 0.15 per 100,000 persons, ratio 1:678,740), with uneven distribution between the regions. North Africa has 64.39{\\%} of the neurosurgical workforce (n = 1271), followed by Southern Africa (12.66{\\%}, n = 250), West Africa (11.60{\\%}, n = 229), East Africa (8.26{\\%}, n = 163), and Central Africa (3.09{\\%}, n = 61). At an exponential growth rate of 7.03{\\%} (95{\\%} CI 5.83{\\%}–8.23{\\%}) per annum, Africa will have 3418 (95{\\%} CI 1811–6080) neurosurgeons by 2030, with a deficit of 5191 neurosurgeons, based on population workforce targets. In terms of training, there are 106 neurosurgery training institutions in 26 African countries. North Africa has 52 training centers (49.05{\\%}), West Africa 23 (21.70{\\%}), East Africa 15 (14.15{\\%}), Southern Africa 14 (13.21{\\%}), and Central Africa 2 (1.89{\\%}). The major regional training programs are those of the West African College of Surgeons (24 sites in 7 countries) and the College of Surgeons of East, Central, and Southern Africa (17 sites in 8 countries).\n\n\nCONCLUSIONS\nThe study is limited as it is based on the online literature, some of which includes modeled estimates with questionable reliability. However, the results indicate that while countries in North Africa are expected to surpass their population workforce requirements, sub-Saharan African countries are likely to have significant workforce deficits accentuated by the paucity of neurosurgery training programs. To meet the 2030 population workforce requirements, the continent's exponential growth rate should be scaled up to 15.87{\\%} per annum. Scaling up neurosurgical training would help to meet this target and requires collaborative efforts from continental, regional, and national agencies and international organizations.},\nauthor = {Ukachukwu, Alvan-Emeka K and Still, Megan E H and Seas, Andreas and {Von Isenburg}, Megan and Fieggen, Graham and Malomo, Adefolarin O and Shokunbi, Matthew T and Egger, Joseph R and Haglund, Michael M and Fuller, Anthony T},\ndoi = {10.3171/2022.2.JNS211984},\nissn = {0022-3085, 1933-0693},\njournal = {Journal of Neurosurgery},\nmonth = {aug},\npages = {1--12},\nshorttitle = {Fulfilling the specialist neurosurgical workforce },\ntitle = {{Fulfilling the specialist neurosurgical workforce needs in {\\{}Africa{\\}}: a systematic review and projection toward 2030}},\nurl = {https://thejns.org/view/journals/j-neurosurg/aop/article-10.3171-2022.2.JNS211984/article-10.3171-2022.2.JNS211984.xml},\nyear = {2022}\n}\n
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\n OBJECTIVE Africa contributes significantly to the global neurosurgical disease burden but has only 1% of the neurosurgery workforce. This study appraises the neurosurgical workforce and training capacity in Africa and projects the workforce capacity by 2030. METHODS The authors conducted a systematic review of the online literature on neurosurgical workforce and training in Africa obtained from three journal databases (PubMed, Embase, and African Index Medicus), as well as from a gray literature search, between September and December 2020. Included literature passed a two-level screening conducted using a systematic review software by a team of two independent reviewers. Data were extracted from selected articles and documented and analyzed on spreadsheets. RESULTS One hundred and fifty-nine eligible articles were analyzed: 1974 neurosurgeons serve 1.3 billion people in Africa (density 0.15 per 100,000 persons, ratio 1:678,740), with uneven distribution between the regions. North Africa has 64.39% of the neurosurgical workforce (n = 1271), followed by Southern Africa (12.66%, n = 250), West Africa (11.60%, n = 229), East Africa (8.26%, n = 163), and Central Africa (3.09%, n = 61). At an exponential growth rate of 7.03% (95% CI 5.83%–8.23%) per annum, Africa will have 3418 (95% CI 1811–6080) neurosurgeons by 2030, with a deficit of 5191 neurosurgeons, based on population workforce targets. In terms of training, there are 106 neurosurgery training institutions in 26 African countries. North Africa has 52 training centers (49.05%), West Africa 23 (21.70%), East Africa 15 (14.15%), Southern Africa 14 (13.21%), and Central Africa 2 (1.89%). The major regional training programs are those of the West African College of Surgeons (24 sites in 7 countries) and the College of Surgeons of East, Central, and Southern Africa (17 sites in 8 countries). CONCLUSIONS The study is limited as it is based on the online literature, some of which includes modeled estimates with questionable reliability. However, the results indicate that while countries in North Africa are expected to surpass their population workforce requirements, sub-Saharan African countries are likely to have significant workforce deficits accentuated by the paucity of neurosurgery training programs. To meet the 2030 population workforce requirements, the continent's exponential growth rate should be scaled up to 15.87% per annum. Scaling up neurosurgical training would help to meet this target and requires collaborative efforts from continental, regional, and national agencies and international organizations.\n
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\n \n\n \n \n \n \n \n \n Editorial: \\Insights\\ in pediatric neurology: 2021.\n \n \n \n \n\n\n \n Ni, H.; Striano, P.; and Wilmshurst, J. M\n\n\n \n\n\n\n Frontiers in Neurology, 13: 1041204. nov 2022.\n \n\n\n\n
\n\n\n\n \n \n \"Editorial:Paper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{ni_editorial_2022,\nauthor = {Ni, Hong and Striano, Pasquale and Wilmshurst, Jo M},\ndoi = {10.3389/fneur.2022.1041204},\nfile = {:Users/jacquelinebracher/Zotero/storage/YZEZXKB7/Ni et al. - 2022 - Editorial Insights in pediatric neurology 2021.pdf:pdf},\nissn = {1664-2295},\njournal = {Frontiers in Neurology},\nmonth = {nov},\npages = {1041204},\nshorttitle = {Editorial},\ntitle = {{Editorial: {\\{}Insights{\\}} in pediatric neurology: 2021}},\nurl = {https://www.frontiersin.org/articles/10.3389/fneur.2022.1041204/full},\nvolume = {13},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Cognitive performance in a South African cohort of people with HIV and comorbid major depressive disorder.\n \n \n \n \n\n\n \n Dreyer, A J; Nightingale, S; Andersen, L S; Lee, J S; Gouse, H; Safren, S A; O'Cleirigh, C; Thomas, K G F; and Joska, J\n\n\n \n\n\n\n 2022.\n \n\n\n\n
\n\n\n\n \n \n \"CognitivePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Dreyer2022a,\nannote = {Export Date: 29 December 2022},\nauthor = {Dreyer, A J and Nightingale, S and Andersen, L S and Lee, J S and Gouse, H and Safren, S A and O'Cleirigh, C and Thomas, K G F and Joska, J},\ndoi = {10.1007/s13365-022-01093-0},\ntitle = {{Cognitive performance in a South African cohort of people with HIV and comorbid major depressive disorder}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85137205265{\\&}doi=10.1007{\\%}2Fs13365-022-01093-0{\\&}partnerID=40{\\&}md5=178c160b8d741a738986fa918d33bc08},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n A case for genomic medicine in \\South\\ \\African\\ paediatric patients with neuromuscular disease.\n \n \n \n \n\n\n \n Raga, S. V; Wilmshurst, J. M.; Smuts, I.; Meldau, S.; Bardien, S.; Schoonen, M.; and Van Der Westhuizen, F. H.\n\n\n \n\n\n\n Frontiers in Pediatrics, 10: 1033299. nov 2022.\n \n\n\n\n
\n\n\n\n \n \n \"APaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{raga_case_2022,\nabstract = {Paediatric neuromuscular diseases are under-recognised and under-diagnosed in Africa, especially those of genetic origin. This may be attributable to various factors, inclusive of socioeconomic barriers, high burden of communicable and non-communicable diseases, resource constraints, lack of expertise in specialised fields and paucity of genetic testing facilities and biobanks in the African population, making access to and interpretation of results more challenging. As new treatments become available that are effective for specific sub-phenotypes, it is even more important to confirm a genetic diagnosis for affected children to be eligible for drug trials and potential treatments. This perspective article aims to create awareness of the major neuromuscular diseases clinically diagnosed in the South African paediatric populations, as well as the current challenges and possible solutions. With this in mind, we introduce a multi-centred research platform (ICGNMD), which aims to address the limited knowledge on NMD aetiology and to improve genetic diagnostic capacities in South African and other African populations.},\nauthor = {Raga, Sharika V and Wilmshurst, Jo Madeleine and Smuts, Izelle and Meldau, Surita and Bardien, Soraya and Schoonen, Maryke and {Van Der Westhuizen}, Francois Hendrikus},\ndoi = {10.3389/fped.2022.1033299},\nfile = {:Users/jacquelinebracher/Zotero/storage/8KGUBFWN/Raga et al. - 2022 - A case for genomic medicine in South African paedi.pdf:pdf},\nissn = {2296-2360},\njournal = {Frontiers in Pediatrics},\nmonth = {nov},\npages = {1033299},\ntitle = {{A case for genomic medicine in {\\{}South{\\}} {\\{}African{\\}} paediatric patients with neuromuscular disease}},\nurl = {https://www.frontiersin.org/articles/10.3389/fped.2022.1033299/full},\nvolume = {10},\nyear = {2022}\n}\n
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\n Paediatric neuromuscular diseases are under-recognised and under-diagnosed in Africa, especially those of genetic origin. This may be attributable to various factors, inclusive of socioeconomic barriers, high burden of communicable and non-communicable diseases, resource constraints, lack of expertise in specialised fields and paucity of genetic testing facilities and biobanks in the African population, making access to and interpretation of results more challenging. As new treatments become available that are effective for specific sub-phenotypes, it is even more important to confirm a genetic diagnosis for affected children to be eligible for drug trials and potential treatments. This perspective article aims to create awareness of the major neuromuscular diseases clinically diagnosed in the South African paediatric populations, as well as the current challenges and possible solutions. With this in mind, we introduce a multi-centred research platform (ICGNMD), which aims to address the limited knowledge on NMD aetiology and to improve genetic diagnostic capacities in South African and other African populations.\n
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\n \n\n \n \n \n \n \n \n The neurobiology of obsessive–compulsive personality disorder: a systematic review.\n \n \n \n \n\n\n \n Marincowitz, C.; Lochner, C.; and Stein, D. J\n\n\n \n\n\n\n CNS Spectrums, 27(6): 664–675. dec 2022.\n \n\n\n\n
\n\n\n\n \n \n \"ThePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{marincowitz_neurobiology_2022,\nabstract = {Abstract\n\nBackground\nA number of recent investigations have focused on the neurobiology of obsessive–compulsive personality disorder (OCPD). However, there have been few reviews of this literature with no detailed model proposed. We therefore undertook a systematic review of these investigations, aiming to map the available evidence and investigate whether it is possible to formulate a detailed model of the neurobiology of OCPD.\n\n\nMethods\nOCPD can be considered from both categorical and dimensional perspectives. An electronic search was therefore conducted using terms that would address not only OCPD as a category, but also related constructs, such as perfectionism, that would capture research on neuropsychology, neuroimaging, neurochemistry, and neurogenetics.\n\n\nResults\nA total of 1059 articles were retrieved, with 87 ultimately selected for abstract screening, resulting in a final selection of 49 articles focusing on neurobiological investigations relevant to OCPD. Impaired executive function and cognitive inflexibility are common neuropsychological traits in this condition, and suggest that obsessive–compulsive disorder (OCD) and OCPD may lie on a continuum. However, neuroimaging studies in OCPD indicate the involvement of specific neurocircuitry, including the precuneus and amygdala, and so suggest that OCD and OCPD may have important differences. Although OCPD has a heritable component, we found no well-powered genetic studies of OCPD.\n\n\nConclusion\nAlthough knowledge in this area has advanced, there are insufficient data on which to base a comprehensive model of the neurobiology of OCPD. Given the clinical importance of OCPD, further work to understand the mechanisms that underpin this condition is warranted.},\nauthor = {Marincowitz, Clara and Lochner, Christine and Stein, Dan J},\ndoi = {10.1017/S1092852921000754},\nissn = {1092-8529, 2165-6509},\njournal = {CNS Spectrums},\nmonth = {dec},\nnumber = {6},\npages = {664--675},\nshorttitle = {The neurobiology of obsessive–compulsive personali},\ntitle = {{The neurobiology of obsessive–compulsive personality disorder: a systematic review}},\nurl = {https://www.cambridge.org/core/product/identifier/S1092852921000754/type/journal{\\_}article},\nvolume = {27},\nyear = {2022}\n}\n
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\n Abstract Background A number of recent investigations have focused on the neurobiology of obsessive–compulsive personality disorder (OCPD). However, there have been few reviews of this literature with no detailed model proposed. We therefore undertook a systematic review of these investigations, aiming to map the available evidence and investigate whether it is possible to formulate a detailed model of the neurobiology of OCPD. Methods OCPD can be considered from both categorical and dimensional perspectives. An electronic search was therefore conducted using terms that would address not only OCPD as a category, but also related constructs, such as perfectionism, that would capture research on neuropsychology, neuroimaging, neurochemistry, and neurogenetics. Results A total of 1059 articles were retrieved, with 87 ultimately selected for abstract screening, resulting in a final selection of 49 articles focusing on neurobiological investigations relevant to OCPD. Impaired executive function and cognitive inflexibility are common neuropsychological traits in this condition, and suggest that obsessive–compulsive disorder (OCD) and OCPD may lie on a continuum. However, neuroimaging studies in OCPD indicate the involvement of specific neurocircuitry, including the precuneus and amygdala, and so suggest that OCD and OCPD may have important differences. Although OCPD has a heritable component, we found no well-powered genetic studies of OCPD. Conclusion Although knowledge in this area has advanced, there are insufficient data on which to base a comprehensive model of the neurobiology of OCPD. Given the clinical importance of OCPD, further work to understand the mechanisms that underpin this condition is warranted.\n
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\n \n\n \n \n \n \n \n \n White matter microstructure differences in individuals with dependence on cocaine, methamphetamine, and nicotine: \\Findings\\ from the \\ENIGMA\\-\\Addiction\\ working group.\n \n \n \n \n\n\n \n Ottino-González, J.; Uhlmann, A.; Hahn, S.; Cao, Z.; Cupertino, R. B; Schwab, N.; Allgaier, N.; Alia-Klein, N.; Ekhtiari, H.; Fouche, J.; Goldstein, R. Z; Li, C. R; Lochner, C.; London, E. D; Luijten, M.; Masjoodi, S.; Momenan, R.; Oghabian, M. A.; Roos, A.; Stein, D. J; Stein, E. A; Veltman, D. J; Verdejo-García, A.; Zhang, S.; Zhao, M.; Zhong, N.; Jahanshad, N.; Thompson, P. M; Conrod, P.; Mackey, S.; and Garavan, H.\n\n\n \n\n\n\n Drug and Alcohol Dependence, 230: 109185. jan 2022.\n \n\n\n\n
\n\n\n\n \n \n \"WhitePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{ottino-gonzalez_white_2022,\nauthor = {Ottino-Gonz{\\'{a}}lez, Jonatan and Uhlmann, Anne and Hahn, Sage and Cao, Zhipeng and Cupertino, Renata B and Schwab, Nathan and Allgaier, Nicholas and Alia-Klein, Nelly and Ekhtiari, Hamed and Fouche, Jean-Paul and Goldstein, Rita Z and Li, Chiang-Shan R and Lochner, Christine and London, Edythe D and Luijten, Maartje and Masjoodi, Sadegh and Momenan, Reza and Oghabian, Mohammad Ali and Roos, Annerine and Stein, Dan J and Stein, Elliot A and Veltman, Dick J and Verdejo-Garc{\\'{i}}a, Antonio and Zhang, Sheng and Zhao, Min and Zhong, Na and Jahanshad, Neda and Thompson, Paul M and Conrod, Patricia and Mackey, Scott and Garavan, Hugh},\ndoi = {10.1016/j.drugalcdep.2021.109185},\nfile = {:Users/jacquelinebracher/Zotero/storage/GD6D3T6J/Ottino-Gonz{\\'{a}}lez et al. - 2022 - White matter microstructure differences in individ.pdf:pdf},\nissn = {03768716},\njournal = {Drug and Alcohol Dependence},\nmonth = {jan},\npages = {109185},\nshorttitle = {White matter microstructure differences in individ},\ntitle = {{White matter microstructure differences in individuals with dependence on cocaine, methamphetamine, and nicotine: {\\{}Findings{\\}} from the {\\{}ENIGMA{\\}}-{\\{}Addiction{\\}} working group}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S0376871621006803},\nvolume = {230},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Psychiatric diagnosis and treatment in the 21st century: paradigm shifts versus incremental integration.\n \n \n \n \n\n\n \n Stein, D. J; Shoptaw, S. J; Vigo, D. V; Lund, C.; Cuijpers, P.; Bantjes, J.; Sartorius, N.; and Maj, M.\n\n\n \n\n\n\n World Psychiatry, 21(3): 393–414. oct 2022.\n \n\n\n\n
\n\n\n\n \n \n \"PsychiatricPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{stein_psychiatric_2022,\nabstract = {Psychiatry has always been characterized by a range of different models of and approaches to mental disorder, which have sometimes brought progress in clinical practice, but have often also been accompanied by critique from within and without the field. Psychiatric nosology has been a particular focus of debate in recent decades; successive editions of the DSM and ICD have strongly influenced both psychiatric practice and research, but have also led to assertions that psychiatry is in crisis, and to advocacy for entirely new paradigms for diagnosis and assessment. When thinking about etiology, many researchers currently refer to a biopsychosocial model, but this approach has received significant critique, being considered by some observers overly eclectic and vague. Despite the development of a range of evidence‐based pharmacotherapies and psychotherapies, current evidence points to both a treatment gap and a research‐practice gap in mental health. In this paper, after considering current clinical practice, we discuss some proposed novel perspectives that have recently achieved particular prominence and may significantly impact psychiatric practice and research in the future: clinical neuroscience and personalized pharmacotherapy; novel statistical approaches to psychiatric nosology, assessment and research; deinstitutionalization and community mental health care; the scale‐up of evidence‐based psychotherapy; digital phenotyping and digital therapies; and global mental health and task‐sharing approaches. We consider the extent to which proposed transitions from current practices to novel approaches reflect hype or hope. Our review indicates that each of the novel perspectives contributes important insights that allow hope for the future, but also that each provides only a partial view, and that any promise of a paradigm shift for the field is not well grounded. We conclude that there have been crucial advances in psychiatric diagnosis and treatment in recent decades; that, despite this important progress, there is considerable need for further improvements in assessment and intervention; and that such improvements will likely not be achieved by any specific paradigm shifts in psychiatric practice and research, but rather by incremental progress and iterative integration.},\nauthor = {Stein, Dan J and Shoptaw, Steven J and Vigo, Daniel V and Lund, Crick and Cuijpers, Pim and Bantjes, Jason and Sartorius, Norman and Maj, Mario},\ndoi = {10.1002/wps.20998},\nfile = {:Users/jacquelinebracher/Zotero/storage/YAW4MDNS/Stein et al. - 2022 - Psychiatric diagnosis and treatment in the 21st ce.pdf:pdf},\nissn = {1723-8617, 2051-5545},\njournal = {World Psychiatry},\nmonth = {oct},\nnumber = {3},\npages = {393--414},\nshorttitle = {Psychiatric diagnosis and treatment in the 21st ce},\ntitle = {{Psychiatric diagnosis and treatment in the 21st century: paradigm shifts versus incremental integration}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1002/wps.20998},\nvolume = {21},\nyear = {2022}\n}\n
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\n Psychiatry has always been characterized by a range of different models of and approaches to mental disorder, which have sometimes brought progress in clinical practice, but have often also been accompanied by critique from within and without the field. Psychiatric nosology has been a particular focus of debate in recent decades; successive editions of the DSM and ICD have strongly influenced both psychiatric practice and research, but have also led to assertions that psychiatry is in crisis, and to advocacy for entirely new paradigms for diagnosis and assessment. When thinking about etiology, many researchers currently refer to a biopsychosocial model, but this approach has received significant critique, being considered by some observers overly eclectic and vague. Despite the development of a range of evidence‐based pharmacotherapies and psychotherapies, current evidence points to both a treatment gap and a research‐practice gap in mental health. In this paper, after considering current clinical practice, we discuss some proposed novel perspectives that have recently achieved particular prominence and may significantly impact psychiatric practice and research in the future: clinical neuroscience and personalized pharmacotherapy; novel statistical approaches to psychiatric nosology, assessment and research; deinstitutionalization and community mental health care; the scale‐up of evidence‐based psychotherapy; digital phenotyping and digital therapies; and global mental health and task‐sharing approaches. We consider the extent to which proposed transitions from current practices to novel approaches reflect hype or hope. Our review indicates that each of the novel perspectives contributes important insights that allow hope for the future, but also that each provides only a partial view, and that any promise of a paradigm shift for the field is not well grounded. We conclude that there have been crucial advances in psychiatric diagnosis and treatment in recent decades; that, despite this important progress, there is considerable need for further improvements in assessment and intervention; and that such improvements will likely not be achieved by any specific paradigm shifts in psychiatric practice and research, but rather by incremental progress and iterative integration.\n
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\n \n\n \n \n \n \n \n DNA methylation as a potential mediator of the association between prenatal tobacco and alcohol exposure and child neurodevelopment in a South African birth cohort.\n \n \n \n\n\n \n Abrishamcar, S.; Chen, J.; Feil, D.; Kilanowski, A.; Koen, N.; Vanker, A.; Wedderburn, C.; Donald, K.; Zar, H.; Stein, D.; Stein, D.; and Hüls, A.\n\n\n \n\n\n\n Translational Psychiatry, 12(1). 2022.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{Abrishamcar2022,\nabstract = {Prenatal tobacco exposure (PTE) and prenatal alcohol exposure (PAE) have been associated with an increased risk of delayed neurodevelopment in children as well as differential newborn DNA methylation (DNAm). However, the biological mechanisms connecting PTE and PAE, DNAm, and neurodevelopment are largely unknown. Here we aim to determine whether differential DNAm mediates the association between PTE and PAE and neurodevelopment at 6 (N = 112) and 24 months (N = 184) in children from the South African Drakenstein Child Health Study. PTE and PAE were assessed antenatally using urine cotinine measurements and the ASSIST questionnaire, respectively. Cord blood DNAm was measured using the EPIC and 450 K BeadChips. Neurodevelopment (cognitive, language, motor, adaptive behavior, socioemotional) was measured using the Bayley Scales of Infant and Toddler Development, Third Edition. We constructed methylation risk scores (MRS) for PTE and PAE and conducted causal mediation analysis (CMA) with these MRS as mediators. Next, we conducted a high-dimensional mediation analysis to identify individual CpG sites as potential mediators, followed by a CMA to estimate the average causal mediation effects (ACME) and total effect (TE). PTE and PAE were associated with neurodevelopment at 6 but not at 24 months. PTE MRS reached a prediction accuracy (R2) of 0.23 but did not significantly mediate the association between PTE and neurodevelopment. PAE MRS was not predictive of PAE (R2 = 0.006). For PTE, 31 CpG sites and eight CpG sites were identified as significant mediators (ACME and TE P {\\textless} 0.05) for the cognitive and motor domains at 6 months, respectively. For PAE, 16 CpG sites and 1 CpG site were significant mediators for the motor and adaptive behavior domains at 6 months, respectively. Several of the associated genes, including MAD1L1, CAMTA1, and ALDH1A2 have been implicated in neurodevelopmental delay, suggesting that differential DNAm may partly explain the biological mechanisms underlying the relationship between PTE and PAE and child neurodevelopment.},\nauthor = {Abrishamcar, S. and Chen, J. and Feil, D. and Kilanowski, A. and Koen, N. and Vanker, A. and Wedderburn, C.J. and Donald, K.A. and Zar, H.J. and Stein, D.J. and Stein, D.J. and H{\\"{u}}ls, A.},\ndoi = {10.1038/s41398-022-02195-3},\nfile = {:Users/jacquelinebracher/Zotero/storage/XHX7N76K/Abrishamcar et al. - 2022 - DNA methylation as a potential mediator of the ass.pdf:pdf},\njournal = {Translational Psychiatry},\nnumber = {1},\ntitle = {{DNA methylation as a potential mediator of the association between prenatal tobacco and alcohol exposure and child neurodevelopment in a South African birth cohort}},\nvolume = {12},\nyear = {2022}\n}\n
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\n Prenatal tobacco exposure (PTE) and prenatal alcohol exposure (PAE) have been associated with an increased risk of delayed neurodevelopment in children as well as differential newborn DNA methylation (DNAm). However, the biological mechanisms connecting PTE and PAE, DNAm, and neurodevelopment are largely unknown. Here we aim to determine whether differential DNAm mediates the association between PTE and PAE and neurodevelopment at 6 (N = 112) and 24 months (N = 184) in children from the South African Drakenstein Child Health Study. PTE and PAE were assessed antenatally using urine cotinine measurements and the ASSIST questionnaire, respectively. Cord blood DNAm was measured using the EPIC and 450 K BeadChips. Neurodevelopment (cognitive, language, motor, adaptive behavior, socioemotional) was measured using the Bayley Scales of Infant and Toddler Development, Third Edition. We constructed methylation risk scores (MRS) for PTE and PAE and conducted causal mediation analysis (CMA) with these MRS as mediators. Next, we conducted a high-dimensional mediation analysis to identify individual CpG sites as potential mediators, followed by a CMA to estimate the average causal mediation effects (ACME) and total effect (TE). PTE and PAE were associated with neurodevelopment at 6 but not at 24 months. PTE MRS reached a prediction accuracy (R2) of 0.23 but did not significantly mediate the association between PTE and neurodevelopment. PAE MRS was not predictive of PAE (R2 = 0.006). For PTE, 31 CpG sites and eight CpG sites were identified as significant mediators (ACME and TE P \\textless 0.05) for the cognitive and motor domains at 6 months, respectively. For PAE, 16 CpG sites and 1 CpG site were significant mediators for the motor and adaptive behavior domains at 6 months, respectively. Several of the associated genes, including MAD1L1, CAMTA1, and ALDH1A2 have been implicated in neurodevelopmental delay, suggesting that differential DNAm may partly explain the biological mechanisms underlying the relationship between PTE and PAE and child neurodevelopment.\n
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\n \n\n \n \n \n \n \n \n Early pharmacological interventions for universal prevention of post-traumatic stress disorder (\\PTSD\\).\n \n \n \n \n\n\n \n Bertolini, F.; Robertson, L.; Bisson, J. I; Meader, N.; Churchill, R.; Ostuzzi, G.; Stein, D. J; Williams, T.; and Barbui, C.\n\n\n \n\n\n\n Cochrane Database of Systematic Reviews, 2022(2). feb 2022.\n \n\n\n\n
\n\n\n\n \n \n \"EarlyPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{cochrane_common_mental_disorders_group_early_2022,\nauthor = {Bertolini, Federico and Robertson, Lindsay and Bisson, Jonathan I and Meader, Nicholas and Churchill, Rachel and Ostuzzi, Giovanni and Stein, Dan J and Williams, Taryn and Barbui, Corrado},\ndoi = {10.1002/14651858.CD013443.pub2},\neditor = {{Cochrane Common Mental Disorders Group}},\nfile = {:Users/jacquelinebracher/Zotero/storage/S2C8XDL9/Bertolini et al. - 2022 - Early pharmacological interventions for universal .pdf:pdf},\nissn = {14651858},\njournal = {Cochrane Database of Systematic Reviews},\nmonth = {feb},\nnumber = {2},\ntitle = {{Early pharmacological interventions for universal prevention of post-traumatic stress disorder ({\\{}PTSD{\\}})}},\nurl = {http://doi.wiley.com/10.1002/14651858.CD013443.pub2},\nvolume = {2022},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Neuroimmunology of \\Common\\ \\Parasitic\\ \\Infections\\ in \\Africa\\.\n \n \n \n \n\n\n \n Idro, R.; Ogwang, R.; Barragan, A.; Raimondo, J. V.; and Masocha, W.\n\n\n \n\n\n\n Frontiers in Immunology, 13: 791488. feb 2022.\n \n\n\n\n
\n\n\n\n \n \n \"NeuroimmunologyPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{idro_neuroimmunology_2022,\nabstract = {Parasitic infections of the central nervous system are an important cause of morbidity and mortality in Africa. The neurological, cognitive, and psychiatric sequelae of these infections result from a complex interplay between the parasites and the host inflammatory response. Here we review some of the diseases caused by selected parasitic organisms known to infect the nervous system including\nPlasmodium falciparum\n,\nToxoplasma gondii\n,\nTrypanosoma brucei\nspp., and\nTaenia solium\nspecies. For each parasite, we describe the geographical distribution, prevalence, life cycle, and typical clinical symptoms of infection and pathogenesis. We pay particular attention to how the parasites infect the brain and the interaction between each organism and the host immune system. We describe how an understanding of these processes may guide optimal diagnostic and therapeutic strategies to treat these disorders. Finally, we highlight current gaps in our understanding of disease pathophysiology and call for increased interrogation of these often-neglected disorders of the nervous system.},\nauthor = {Idro, Richard and Ogwang, Rodney and Barragan, Antonio and Raimondo, Joseph Valentino and Masocha, Willias},\ndoi = {10.3389/fimmu.2022.791488},\nfile = {:Users/jacquelinebracher/Zotero/storage/QM24E3U4/Idro et al. - 2022 - Neuroimmunology of Common Parasitic Infections in .pdf:pdf},\nissn = {1664-3224},\njournal = {Frontiers in Immunology},\nmonth = {feb},\npages = {791488},\ntitle = {{Neuroimmunology of {\\{}Common{\\}} {\\{}Parasitic{\\}} {\\{}Infections{\\}} in {\\{}Africa{\\}}}},\nurl = {https://www.frontiersin.org/articles/10.3389/fimmu.2022.791488/full},\nvolume = {13},\nyear = {2022}\n}\n
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\n Parasitic infections of the central nervous system are an important cause of morbidity and mortality in Africa. The neurological, cognitive, and psychiatric sequelae of these infections result from a complex interplay between the parasites and the host inflammatory response. Here we review some of the diseases caused by selected parasitic organisms known to infect the nervous system including Plasmodium falciparum , Toxoplasma gondii , Trypanosoma brucei spp., and Taenia solium species. For each parasite, we describe the geographical distribution, prevalence, life cycle, and typical clinical symptoms of infection and pathogenesis. We pay particular attention to how the parasites infect the brain and the interaction between each organism and the host immune system. We describe how an understanding of these processes may guide optimal diagnostic and therapeutic strategies to treat these disorders. Finally, we highlight current gaps in our understanding of disease pathophysiology and call for increased interrogation of these often-neglected disorders of the nervous system.\n
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\n \n\n \n \n \n \n \n \n Computational models reveal how chloride dynamics determine the optimal distribution of inhibitory synapses to minimise dendritic excitability.\n \n \n \n \n\n\n \n Currin, C. B.; and Raimondo, J. V.\n\n\n \n\n\n\n PLOS Computational Biology, 18(9): e1010534. sep 2022.\n \n\n\n\n
\n\n\n\n \n \n \"ComputationalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n  \n \n 2 downloads\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{currin_computational_2022,\nabstract = {Many neurons in the mammalian central nervous system have complex dendritic arborisations and active dendritic conductances that enable these cells to perform sophisticated computations. How dendritically targeted inhibition affects local dendritic excitability is not fully understood. Here we use computational models of branched dendrites to investigate where GABAergic synapses should be placed to minimise dendritic excitability over time. To do so, we formulate a metric we term the “Inhibitory Level” (IL), which quantifies the effectiveness of synaptic inhibition for reducing the depolarising effect of nearby excitatory input. GABAergic synaptic inhibition is dependent on the reversal potential for GABA\nA\nreceptors (EGABA), which is primarily set by the transmembrane chloride ion (Cl\n-\n) concentration gradient. We, therefore, investigated how variable EGABA and dynamic chloride affects dendritic inhibition. We found that the inhibitory effectiveness of dendritic GABAergic synapses combines at an encircled branch junction. The extent of this inhibitory accumulation is dependent on the number of branches and location of synapses but is independent of EGABA. This inhibitory accumulation occurs even for very distally placed inhibitory synapses when they are hyperpolarising–but not when they are shunting. When accounting for Cl\n-\nfluxes and dynamics in Cl\n-\nconcentration, we observed that Cl\n-\nloading is detrimental to inhibitory effectiveness. This enabled us to determine the most inhibitory distribution of GABAergic synapses which is close to–but not at–a shared branch junction. This distribution balances a trade-off between a stronger combined\ninhibitory influence\nwhen synapses closely encircle a branch junction with the deleterious effects of increased Cl\n-\nby loading that occurs when inhibitory synapses are co-located.},\nauthor = {Currin, Christopher Brian and Raimondo, Joseph Valentino},\ndoi = {10.1371/journal.pcbi.1010534},\neditor = {Rubin, Jonathan},\nfile = {:Users/jacquelinebracher/Zotero/storage/6N8Q2PJ3/Currin and Raimondo - 2022 - Computational models reveal how chloride dynamics .pdf:pdf},\nissn = {1553-7358},\njournal = {PLOS Computational Biology},\nmonth = {sep},\nnumber = {9},\npages = {e1010534},\ntitle = {{Computational models reveal how chloride dynamics determine the optimal distribution of inhibitory synapses to minimise dendritic excitability}},\nurl = {https://dx.plos.org/10.1371/journal.pcbi.1010534},\nvolume = {18},\nyear = {2022}\n}\n
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\n Many neurons in the mammalian central nervous system have complex dendritic arborisations and active dendritic conductances that enable these cells to perform sophisticated computations. How dendritically targeted inhibition affects local dendritic excitability is not fully understood. Here we use computational models of branched dendrites to investigate where GABAergic synapses should be placed to minimise dendritic excitability over time. To do so, we formulate a metric we term the “Inhibitory Level” (IL), which quantifies the effectiveness of synaptic inhibition for reducing the depolarising effect of nearby excitatory input. GABAergic synaptic inhibition is dependent on the reversal potential for GABA A receptors (EGABA), which is primarily set by the transmembrane chloride ion (Cl - ) concentration gradient. We, therefore, investigated how variable EGABA and dynamic chloride affects dendritic inhibition. We found that the inhibitory effectiveness of dendritic GABAergic synapses combines at an encircled branch junction. The extent of this inhibitory accumulation is dependent on the number of branches and location of synapses but is independent of EGABA. This inhibitory accumulation occurs even for very distally placed inhibitory synapses when they are hyperpolarising–but not when they are shunting. When accounting for Cl - fluxes and dynamics in Cl - concentration, we observed that Cl - loading is detrimental to inhibitory effectiveness. This enabled us to determine the most inhibitory distribution of GABAergic synapses which is close to–but not at–a shared branch junction. This distribution balances a trade-off between a stronger combined inhibitory influence when synapses closely encircle a branch junction with the deleterious effects of increased Cl - by loading that occurs when inhibitory synapses are co-located.\n
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\n \n\n \n \n \n \n \n \n Engaging \\Patients\\ with \\Depression\\ in \\Treatment\\ \\Continuity\\.\n \n \n \n \n\n\n \n Stein, D. J\n\n\n \n\n\n\n Advances in Therapy, 39(S1): 13–19. apr 2022.\n \n\n\n\n
\n\n\n\n \n \n \"EngagingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{stein_engaging_2022,\nauthor = {Stein, Dan J},\ndoi = {10.1007/s12325-021-02029-6},\nfile = {:Users/jacquelinebracher/Zotero/storage/TFNPGTZY/Stein - 2022 - Engaging Patients with Depression in Treatment Con.pdf:pdf},\nissn = {0741-238X, 1865-8652},\njournal = {Advances in Therapy},\nmonth = {apr},\nnumber = {S1},\npages = {13--19},\ntitle = {{Engaging {\\{}Patients{\\}} with {\\{}Depression{\\}} in {\\{}Treatment{\\}} {\\{}Continuity{\\}}}},\nurl = {https://link.springer.com/10.1007/s12325-021-02029-6},\nvolume = {39},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n More than 25 years after selective dorsal rhizotomy: physical status, quality of life, and levels of anxiety and depression in adults with cerebral palsy.\n \n \n \n \n\n\n \n Veerbeek, B. E; Lamberts, R. P; Kosel, E.; Fieggen, A G.; and Langerak, N. G\n\n\n \n\n\n\n Journal of Neurosurgery, 136(3): 689–698. mar 2022.\n \n\n\n\n
\n\n\n\n \n \n \"MorePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{veerbeek_more_2022,\nabstract = {OBJECTIVE\nThe primary purpose of selective dorsal rhizotomy (SDR) is to ameliorate spasticity in the lower extremities of children with cerebral palsy (CP). In correctly selected patients, this neurosurgical procedure has been shown to have a beneficial effect on many aspects of the child's life. However, given the challenges faced by adults with CP, it would be valuable to document the status of this population compared to their peers later in adulthood. Therefore, the aim of this study was to determine the physical status, mental health, and health-related quality of life (HRQoL) of adults with CP who underwent SDR at least 25 years ago, compared to matched typically developing (TD) individuals. The second aim was to investigate relationships between physical status and the other outcome measures.\n\n\nMETHODS\nAdults with CP were recruited from a database of children who had undergone SDR performed using the technique introduced by Professor Warwick Peacock at Red Cross War Memorial Children's Hospital in Cape Town, South Africa, between 1981 and 1991. These individuals were matched for age, sex, body mass index, and socioeconomic status to a TD adult cohort from a similar background. The parameters assessed were lower-extremity muscle tone, passive range of motion, muscle strength, selectivity, functional mobility and dynamic balance (Timed Up and Go [TUG] test), HRQoL (SF-36), and anxiety and depression levels.\n\n\nRESULTS\nTwenty-six adults with CP who had a median age of 35.8 years (interquartile range 34.2–41.4 years) (female/male: n = 10/16; Gross Motor Function Classification System level I/II/III: n = 13/10/3), were compared to 26 TD adults. Muscle tone was similar, whereas passive range of motion, muscle strength, selectivity, TUG, and SF-36 physical functioning (concept and summary) scores differed between the cohorts. Other SF-36 parameters, anxiety levels, and depression levels were not different. Strong correlations were found between the muscle strength and TUG scores.\n\n\nCONCLUSIONS\nNormalized lower-extremity muscle tone was sustained 25–35 years after SDR. Whereas the lower scores for physical assessments are in line with findings in other CP populations, remarkably, relatively good mental health and HRQoL scores were reported in this CP group despite their physical limitations. The strong correlation between muscle strength and TUG suggests that strength training after SDR may have value in improving functional mobility and balance.},\nauthor = {Veerbeek, Berendina E and Lamberts, Robert P and Kosel, Elisa and Fieggen, A Graham and Langerak, Nelleke G},\ndoi = {10.3171/2021.3.JNS204096},\nissn = {0022-3085, 1933-0693},\njournal = {Journal of Neurosurgery},\nmonth = {mar},\nnumber = {3},\npages = {689--698},\nshorttitle = {More than 25 years after selective dorsal rhizotom},\ntitle = {{More than 25 years after selective dorsal rhizotomy: physical status, quality of life, and levels of anxiety and depression in adults with cerebral palsy}},\nurl = {https://thejns.org/view/journals/j-neurosurg/136/3/article-p689.xml},\nvolume = {136},\nyear = {2022}\n}\n
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\n OBJECTIVE The primary purpose of selective dorsal rhizotomy (SDR) is to ameliorate spasticity in the lower extremities of children with cerebral palsy (CP). In correctly selected patients, this neurosurgical procedure has been shown to have a beneficial effect on many aspects of the child's life. However, given the challenges faced by adults with CP, it would be valuable to document the status of this population compared to their peers later in adulthood. Therefore, the aim of this study was to determine the physical status, mental health, and health-related quality of life (HRQoL) of adults with CP who underwent SDR at least 25 years ago, compared to matched typically developing (TD) individuals. The second aim was to investigate relationships between physical status and the other outcome measures. METHODS Adults with CP were recruited from a database of children who had undergone SDR performed using the technique introduced by Professor Warwick Peacock at Red Cross War Memorial Children's Hospital in Cape Town, South Africa, between 1981 and 1991. These individuals were matched for age, sex, body mass index, and socioeconomic status to a TD adult cohort from a similar background. The parameters assessed were lower-extremity muscle tone, passive range of motion, muscle strength, selectivity, functional mobility and dynamic balance (Timed Up and Go [TUG] test), HRQoL (SF-36), and anxiety and depression levels. RESULTS Twenty-six adults with CP who had a median age of 35.8 years (interquartile range 34.2–41.4 years) (female/male: n = 10/16; Gross Motor Function Classification System level I/II/III: n = 13/10/3), were compared to 26 TD adults. Muscle tone was similar, whereas passive range of motion, muscle strength, selectivity, TUG, and SF-36 physical functioning (concept and summary) scores differed between the cohorts. Other SF-36 parameters, anxiety levels, and depression levels were not different. Strong correlations were found between the muscle strength and TUG scores. CONCLUSIONS Normalized lower-extremity muscle tone was sustained 25–35 years after SDR. Whereas the lower scores for physical assessments are in line with findings in other CP populations, remarkably, relatively good mental health and HRQoL scores were reported in this CP group despite their physical limitations. The strong correlation between muscle strength and TUG suggests that strength training after SDR may have value in improving functional mobility and balance.\n
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\n \n\n \n \n \n \n \n \n An overview of the first 5 years of the \\ENIGMA\\ obsessive–compulsive disorder working group: \\The\\ power of worldwide collaboration.\n \n \n \n \n\n\n \n Van Den Heuvel, O. A; Boedhoe, P. S W; Bertolin, S.; Bruin, W. B; Francks, C.; Ivanov, I.; Jahanshad, N.; Kong, X.; Kwon, J. S.; O'Neill, J.; Paus, T.; Patel, Y.; Piras, F.; Schmaal, L.; Soriano‐Mas, C.; Spalletta, G.; Van Wingen, G. A; Yun, J.; Vriend, C.; Simpson, H B.; Van Rooij, D.; Hoexter, M. Q; Hoogman, M.; Buitelaar, J. K; Arnold, P.; Beucke, J. C; Benedetti, F.; Bollettini, I.; Bose, A.; Brennan, B. P; De Nadai, A. S; Fitzgerald, K.; Gruner, P.; Grünblatt, E.; Hirano, Y.; Huyser, C.; James, A.; Koch, K.; Kvale, G.; Lazaro, L.; Lochner, C.; Marsh, R.; Mataix‐Cols, D.; Morgado, P.; Nakamae, T.; Nakao, T.; Narayanaswamy, J. C; Nurmi, E.; Pittenger, C.; Reddy, Y C J.; Sato, J. R; Soreni, N.; Stewart, S E.; Taylor, S. F; Tolin, D.; Thomopoulos, S. I; Veltman, D. J; Venkatasubramanian, G.; Walitza, S.; Wang, Z.; Thompson, P. M; Stein, D. J; and working group , E.\n\n\n \n\n\n\n Human Brain Mapping, 43(1): 23–36. jan 2022.\n \n\n\n\n
\n\n\n\n \n \n \"AnPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{van_den_heuvel_overview_2022,\nabstract = {Abstract\nNeuroimaging has played an important part in advancing our understanding of the neurobiology of obsessive–compulsive disorder (OCD). At the same time, neuroimaging studies of OCD have had notable limitations, including reliance on relatively small samples. International collaborative efforts to increase statistical power by combining samples from across sites have been bolstered by the ENIGMA consortium; this provides specific technical expertise for conducting multi‐site analyses, as well as access to a collaborative community of neuroimaging scientists. In this article, we outline the background to, development of, and initial findings from ENIGMA's OCD working group, which currently consists of 47 samples from 34 institutes in 15 countries on 5 continents, with a total sample of 2,323 OCD patients and 2,325 healthy controls. Initial work has focused on studies of cortical thickness and subcortical volumes, structural connectivity, and brain lateralization in children, adolescents and adults with OCD, also including the study on the commonalities and distinctions across different neurodevelopment disorders. Additional work is ongoing, employing machine learning techniques. Findings to date have contributed to the development of neurobiological models of OCD, have provided an important model of global scientific collaboration, and have had a number of clinical implications. Importantly, our work has shed new light on questions about whether structural and functional alterations found in OCD reflect neurodevelopmental changes, effects of the disease process, or medication impacts. We conclude with a summary of ongoing work by ENIGMA‐OCD, and a consideration of future directions for neuroimaging research on OCD within and beyond ENIGMA.},\nauthor = {{Van Den Heuvel}, Odile A and Boedhoe, Premika S W and Bertolin, Sara and Bruin, Willem B and Francks, Clyde and Ivanov, Iliyan and Jahanshad, Neda and Kong, Xiang‐Zhen and Kwon, Jun Soo and O'Neill, Joseph and Paus, Tomas and Patel, Yash and Piras, Fabrizio and Schmaal, Lianne and Soriano‐Mas, Carles and Spalletta, Gianfranco and {Van Wingen}, Guido A and Yun, Je‐Yeon and Vriend, Chris and Simpson, H Blair and {Van Rooij}, Daan and Hoexter, Marcelo Q and Hoogman, Martine and Buitelaar, Jan K and Arnold, Paul and Beucke, Jan C and Benedetti, Francesco and Bollettini, Irene and Bose, Anushree and Brennan, Brian P and {De Nadai}, Alessandro S and Fitzgerald, Kate and Gruner, Patricia and Gr{\\"{u}}nblatt, Edna and Hirano, Yoshiyuki and Huyser, Chaim and James, Anthony and Koch, Kathrin and Kvale, Gerd and Lazaro, Luisa and Lochner, Christine and Marsh, Rachel and Mataix‐Cols, David and Morgado, Pedro and Nakamae, Takashi and Nakao, Tomohiro and Narayanaswamy, Janardhanan C and Nurmi, Erika and Pittenger, Christopher and Reddy, Y C Janardhan and Sato, Jo{\\~{a}}o R and Soreni, Noam and Stewart, S Evelyn and Taylor, Stephan F and Tolin, David and Thomopoulos, Sophia I and Veltman, Dick J and Venkatasubramanian, Ganesan and Walitza, Susanne and Wang, Zhen and Thompson, Paul M and Stein, Dan J and ENIGMA‐OCD working group},\ndoi = {10.1002/hbm.24972},\nfile = {:Users/jacquelinebracher/Zotero/storage/9FMHCHJF/Van Den Heuvel et al. - 2022 - An overview of the first 5 years of the ENIGMA obs.pdf:pdf},\nissn = {1065-9471, 1097-0193},\njournal = {Human Brain Mapping},\nmonth = {jan},\nnumber = {1},\npages = {23--36},\nshorttitle = {An overview of the first 5 years of the {\\{}ENIGMA{\\}} o},\ntitle = {{An overview of the first 5 years of the {\\{}ENIGMA{\\}} obsessive–compulsive disorder working group: {\\{}The{\\}} power of worldwide collaboration}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1002/hbm.24972},\nvolume = {43},\nyear = {2022}\n}\n
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\n Abstract Neuroimaging has played an important part in advancing our understanding of the neurobiology of obsessive–compulsive disorder (OCD). At the same time, neuroimaging studies of OCD have had notable limitations, including reliance on relatively small samples. International collaborative efforts to increase statistical power by combining samples from across sites have been bolstered by the ENIGMA consortium; this provides specific technical expertise for conducting multi‐site analyses, as well as access to a collaborative community of neuroimaging scientists. In this article, we outline the background to, development of, and initial findings from ENIGMA's OCD working group, which currently consists of 47 samples from 34 institutes in 15 countries on 5 continents, with a total sample of 2,323 OCD patients and 2,325 healthy controls. Initial work has focused on studies of cortical thickness and subcortical volumes, structural connectivity, and brain lateralization in children, adolescents and adults with OCD, also including the study on the commonalities and distinctions across different neurodevelopment disorders. Additional work is ongoing, employing machine learning techniques. Findings to date have contributed to the development of neurobiological models of OCD, have provided an important model of global scientific collaboration, and have had a number of clinical implications. Importantly, our work has shed new light on questions about whether structural and functional alterations found in OCD reflect neurodevelopmental changes, effects of the disease process, or medication impacts. We conclude with a summary of ongoing work by ENIGMA‐OCD, and a consideration of future directions for neuroimaging research on OCD within and beyond ENIGMA.\n
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\n \n\n \n \n \n \n \n Brain charts for the human lifespan.\n \n \n \n\n\n \n Bethlehem, R.; Seidlitz, J.; White, S.; Vogel, J.; Anderson, K.; Adamson, C.; Adler, S.; Alexopoulos, G.; Anagnostou, E.; Areces-Gonzalez, A.; Bullmore, E.; and Alexander-Bloch, A.\n\n\n \n\n\n\n Nature, 604(7906): 525–533. 2022.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Bethlehem2022,\nabstract = {Over the past few decades, neuroimaging has become a ubiquitous tool in basic research and clinical studies of the human brain. However, no reference standards currently exist to quantify individual differences in neuroimaging metrics over time, in contrast to growth charts for anthropometric traits such as height and weight1. Here we assemble an interactive open resource to benchmark brain morphology derived from any current or future sample of MRI data (http://www.brainchart.io/). With the goal of basing these reference charts on the largest and most inclusive dataset available, acknowledging limitations due to known biases of MRI studies relative to the diversity of the global population, we aggregated 123,984 MRI scans, across more than 100 primary studies, from 101,457 human participants between 115 days post-conception to 100 years of age. MRI metrics were quantified by centile scores, relative to non-linear trajectories2 of brain structural changes, and rates of change, over the lifespan. Brain charts identified previously unreported neurodevelopmental milestones3, showed high stability of individuals across longitudinal assessments, and demonstrated robustness to technical and methodological differences between primary studies. Centile scores showed increased heritability compared with non-centiled MRI phenotypes, and provided a standardized measure of atypical brain structure that revealed patterns of neuroanatomical variation across neurological and psychiatric disorders. In summary, brain charts are an essential step towards robust quantification of individual variation benchmarked to normative trajectories in multiple, commonly used neuroimaging phenotypes.},\nauthor = {Bethlehem, R.A.I. and Seidlitz, J. and White, S.R. and Vogel, J.W. and Anderson, K.M. and Adamson, C. and Adler, S. and Alexopoulos, G.S. and Anagnostou, E. and Areces-Gonzalez, A. and Bullmore, E.T. and Alexander-Bloch, A.F.},\ndoi = {10.1038/s41586-022-04554-y},\nfile = {:Users/jacquelinebracher/Zotero/storage/426ZIGKI/Bethlehem et al. - 2022 - Brain charts for the human lifespan.pdf:pdf},\njournal = {Nature},\nnumber = {7906},\npages = {525--533},\ntitle = {{Brain charts for the human lifespan}},\nvolume = {604},\nyear = {2022}\n}\n
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\n Over the past few decades, neuroimaging has become a ubiquitous tool in basic research and clinical studies of the human brain. However, no reference standards currently exist to quantify individual differences in neuroimaging metrics over time, in contrast to growth charts for anthropometric traits such as height and weight1. Here we assemble an interactive open resource to benchmark brain morphology derived from any current or future sample of MRI data (http://www.brainchart.io/). With the goal of basing these reference charts on the largest and most inclusive dataset available, acknowledging limitations due to known biases of MRI studies relative to the diversity of the global population, we aggregated 123,984 MRI scans, across more than 100 primary studies, from 101,457 human participants between 115 days post-conception to 100 years of age. MRI metrics were quantified by centile scores, relative to non-linear trajectories2 of brain structural changes, and rates of change, over the lifespan. Brain charts identified previously unreported neurodevelopmental milestones3, showed high stability of individuals across longitudinal assessments, and demonstrated robustness to technical and methodological differences between primary studies. Centile scores showed increased heritability compared with non-centiled MRI phenotypes, and provided a standardized measure of atypical brain structure that revealed patterns of neuroanatomical variation across neurological and psychiatric disorders. In summary, brain charts are an essential step towards robust quantification of individual variation benchmarked to normative trajectories in multiple, commonly used neuroimaging phenotypes.\n
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\n \n\n \n \n \n \n \n \n \\ILAE\\ classification and definition of epilepsy syndromes with onset in neonates and infants: \\Position\\ statement by the \\ILAE\\ \\Task\\ \\Force\\ on \\Nosology\\ and \\Definitions\\.\n \n \n \n \n\n\n \n Zuberi, S. M; Wirrell, E.; Yozawitz, E.; Wilmshurst, J. M; Specchio, N.; Riney, K.; Pressler, R.; Auvin, S.; Samia, P.; Hirsch, E.; Galicchio, S.; Triki, C.; Snead, O C.; Wiebe, S.; Cross, J H.; Tinuper, P.; Scheffer, I. E; Perucca, E.; Moshé, S. L; and Nabbout, R.\n\n\n \n\n\n\n Epilepsia, 63(6): 1349–1397. jun 2022.\n \n\n\n\n
\n\n\n\n \n \n \"\\ILAE\\Paper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{zuberi_ilae_2022,\nabstract = {Abstract\n\nThe International League Against Epilepsy (ILAE) Task Force on Nosology and Definitions proposes a classification and definition of epilepsy syndromes in the neonate and infant with seizure onset up to 2 years of age. The incidence of epilepsy is high in this age group and epilepsy is frequently associated with significant comorbidities and mortality. The licensing of syndrome specific antiseizure medications following randomized controlled trials and the development of precision, gene‐related therapies are two of the drivers defining the electroclinical phenotypes of syndromes with onset in infancy. The principal aim of this proposal, consistent with the 2017 ILAE Classification of the Epilepsies, is to support epilepsy diagnosis and emphasize the importance of classifying epilepsy in an individual both by syndrome and etiology. For each syndrome, we report epidemiology, clinical course, seizure types, electroencephalography (EEG), neuroimaging, genetics, and differential diagnosis. Syndromes are separated into self‐limited syndromes, where there is likely to be spontaneous remission and\ndevelopmental and epileptic encephalopathies\n, diseases where there is developmental impairment related to both the underlying etiology independent of epileptiform activity and the epileptic encephalopathy. The emerging class of etiology‐specific epilepsy syndromes, where there is a specific etiology for the epilepsy that is associated with a clearly defined, relatively uniform, and distinct clinical phenotype in most affected individuals as well as consistent EEG, neuroimaging, and/or genetic correlates, is presented. The number of etiology‐defined syndromes will continue to increase, and these newly described syndromes will in time be incorporated into this classification. The tables summarize mandatory features, cautionary alerts, and exclusionary features for the common syndromes. Guidance is given on the criteria for syndrome diagnosis in resource‐limited regions where laboratory confirmation, including EEG, MRI, and genetic testing, might not be available.},\nauthor = {Zuberi, Sameer M and Wirrell, Elaine and Yozawitz, Elissa and Wilmshurst, Jo M and Specchio, Nicola and Riney, Kate and Pressler, Ronit and Auvin, Stephane and Samia, Pauline and Hirsch, Edouard and Galicchio, Santiago and Triki, Chahnez and Snead, O Carter and Wiebe, Samuel and Cross, J Helen and Tinuper, Paolo and Scheffer, Ingrid E and Perucca, Emilio and Mosh{\\'{e}}, Solomon L and Nabbout, Rima},\ndoi = {10.1111/epi.17239},\nfile = {:Users/jacquelinebracher/Zotero/storage/FZGZAUW9/Zuberi et al. - 2022 - ILAE classification and definition of epilepsy syn.pdf:pdf},\nissn = {0013-9580, 1528-1167},\njournal = {Epilepsia},\nmonth = {jun},\nnumber = {6},\npages = {1349--1397},\nshorttitle = {{\\{}ILAE{\\}} classification and definition of epilepsy s},\ntitle = {{{\\{}ILAE{\\}} classification and definition of epilepsy syndromes with onset in neonates and infants: {\\{}Position{\\}} statement by the {\\{}ILAE{\\}} {\\{}Task{\\}} {\\{}Force{\\}} on {\\{}Nosology{\\}} and {\\{}Definitions{\\}}}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1111/epi.17239},\nvolume = {63},\nyear = {2022}\n}\n
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\n Abstract The International League Against Epilepsy (ILAE) Task Force on Nosology and Definitions proposes a classification and definition of epilepsy syndromes in the neonate and infant with seizure onset up to 2 years of age. The incidence of epilepsy is high in this age group and epilepsy is frequently associated with significant comorbidities and mortality. The licensing of syndrome specific antiseizure medications following randomized controlled trials and the development of precision, gene‐related therapies are two of the drivers defining the electroclinical phenotypes of syndromes with onset in infancy. The principal aim of this proposal, consistent with the 2017 ILAE Classification of the Epilepsies, is to support epilepsy diagnosis and emphasize the importance of classifying epilepsy in an individual both by syndrome and etiology. For each syndrome, we report epidemiology, clinical course, seizure types, electroencephalography (EEG), neuroimaging, genetics, and differential diagnosis. Syndromes are separated into self‐limited syndromes, where there is likely to be spontaneous remission and developmental and epileptic encephalopathies , diseases where there is developmental impairment related to both the underlying etiology independent of epileptiform activity and the epileptic encephalopathy. The emerging class of etiology‐specific epilepsy syndromes, where there is a specific etiology for the epilepsy that is associated with a clearly defined, relatively uniform, and distinct clinical phenotype in most affected individuals as well as consistent EEG, neuroimaging, and/or genetic correlates, is presented. The number of etiology‐defined syndromes will continue to increase, and these newly described syndromes will in time be incorporated into this classification. The tables summarize mandatory features, cautionary alerts, and exclusionary features for the common syndromes. Guidance is given on the criteria for syndrome diagnosis in resource‐limited regions where laboratory confirmation, including EEG, MRI, and genetic testing, might not be available.\n
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\n \n\n \n \n \n \n \n \n International \\League\\ \\Against\\ \\Epilepsy\\ classification and definition of epilepsy syndromes with onset in childhood: \\Position\\ paper by the \\ILAE\\ \\Task\\ \\Force\\ on \\Nosology\\ and \\Definitions\\.\n \n \n \n \n\n\n \n Specchio, N.; Wirrell, E. C; Scheffer, I. E; Nabbout, R.; Riney, K.; Samia, P.; Guerreiro, M.; Gwer, S.; Zuberi, S. M; Wilmshurst, J. M; Yozawitz, E.; Pressler, R.; Hirsch, E.; Wiebe, S.; Cross, H. J; Perucca, E.; Moshé, S. L; Tinuper, P.; and Auvin, S.\n\n\n \n\n\n\n Epilepsia, 63(6): 1398–1442. jun 2022.\n \n\n\n\n
\n\n\n\n \n \n \"InternationalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{specchio_international_2022,\nabstract = {Abstract\nThe 2017 International League Against Epilepsy classification has defined a three‐tier system with epilepsy syndrome identification at the third level. Although a syndrome cannot be determined in all children with epilepsy, identification of a specific syndrome provides guidance on management and prognosis. In this paper, we describe the childhood onset epilepsy syndromes, most of which have both mandatory seizure type(s) and interictal electroencephalographic (EEG) features. Based on the 2017 Classification of Seizures and Epilepsies, some syndrome names have been updated using terms directly describing the seizure semiology. Epilepsy syndromes beginning in childhood have been divided into three categories: (1) self‐limited focal epilepsies, comprising four syndromes: self‐limited epilepsy with centrotemporal spikes, self‐limited epilepsy with autonomic seizures, childhood occipital visual epilepsy, and photosensitive occipital lobe epilepsy; (2) generalized epilepsies, comprising three syndromes: childhood absence epilepsy, epilepsy with myoclonic absence, and epilepsy with eyelid myoclonia; and (3) developmental and/or epileptic encephalopathies, comprising five syndromes: epilepsy with myoclonic–atonic seizures, Lennox–Gastaut syndrome, developmental and/or epileptic encephalopathy with spike‐and‐wave activation in sleep, hemiconvulsion–hemiplegia–epilepsy syndrome, and febrile infection‐related epilepsy syndrome. We define each, highlighting the mandatory seizure(s), EEG features, phenotypic variations, and findings from key investigations.},\nauthor = {Specchio, Nicola and Wirrell, Elaine C and Scheffer, Ingrid E and Nabbout, Rima and Riney, Kate and Samia, Pauline and Guerreiro, Marilisa and Gwer, Sam and Zuberi, Sameer M and Wilmshurst, Jo M and Yozawitz, Elissa and Pressler, Ronit and Hirsch, Edouard and Wiebe, Samuel and Cross, Helen J and Perucca, Emilio and Mosh{\\'{e}}, Solomon L and Tinuper, Paolo and Auvin, St{\\'{e}}phane},\ndoi = {10.1111/epi.17241},\nfile = {:Users/jacquelinebracher/Zotero/storage/ZZR9MFL4/Specchio et al. - 2022 - International League Against Epilepsy classificati.pdf:pdf},\nissn = {0013-9580, 1528-1167},\njournal = {Epilepsia},\nmonth = {jun},\nnumber = {6},\npages = {1398--1442},\nshorttitle = {International {\\{}League{\\}} {\\{}Against{\\}} {\\{}Epilepsy{\\}} classi},\ntitle = {{International {\\{}League{\\}} {\\{}Against{\\}} {\\{}Epilepsy{\\}} classification and definition of epilepsy syndromes with onset in childhood: {\\{}Position{\\}} paper by the {\\{}ILAE{\\}} {\\{}Task{\\}} {\\{}Force{\\}} on {\\{}Nosology{\\}} and {\\{}Definitions{\\}}}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1111/epi.17241},\nvolume = {63},\nyear = {2022}\n}\n
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\n Abstract The 2017 International League Against Epilepsy classification has defined a three‐tier system with epilepsy syndrome identification at the third level. Although a syndrome cannot be determined in all children with epilepsy, identification of a specific syndrome provides guidance on management and prognosis. In this paper, we describe the childhood onset epilepsy syndromes, most of which have both mandatory seizure type(s) and interictal electroencephalographic (EEG) features. Based on the 2017 Classification of Seizures and Epilepsies, some syndrome names have been updated using terms directly describing the seizure semiology. Epilepsy syndromes beginning in childhood have been divided into three categories: (1) self‐limited focal epilepsies, comprising four syndromes: self‐limited epilepsy with centrotemporal spikes, self‐limited epilepsy with autonomic seizures, childhood occipital visual epilepsy, and photosensitive occipital lobe epilepsy; (2) generalized epilepsies, comprising three syndromes: childhood absence epilepsy, epilepsy with myoclonic absence, and epilepsy with eyelid myoclonia; and (3) developmental and/or epileptic encephalopathies, comprising five syndromes: epilepsy with myoclonic–atonic seizures, Lennox–Gastaut syndrome, developmental and/or epileptic encephalopathy with spike‐and‐wave activation in sleep, hemiconvulsion–hemiplegia–epilepsy syndrome, and febrile infection‐related epilepsy syndrome. We define each, highlighting the mandatory seizure(s), EEG features, phenotypic variations, and findings from key investigations.\n
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\n \n\n \n \n \n \n \n \n How do substance use disorders compare to other psychiatric conditions on structural brain abnormalities? \\A\\ cross‐disorder meta‐analytic comparison using the \\textlessspan style=\"font-variant:small-caps;\"\\textgreater\\ENIGMA\\\\textless/span\\textgreaterconsortium findings.\n \n \n \n \n\n\n \n Navarri, X.; Afzali, M. H; Lavoie, J.; Sinha, R.; Stein, D. J; Momenan, R.; Veltman, D. J; Korucuoglu, O.; Sjoerds, Z.; Van Holst, R. J; Hester, R.; Orr, C.; Cousijn, J.; Yucel, M.; Lorenzetti, V.; Wiers, R.; Jahanshad, N.; Glahn, D. C; Thompson, P. M; Mackey, S.; and Conrod, P. J\n\n\n \n\n\n\n Human Brain Mapping, 43(1): 399–413. jan 2022.\n \n\n\n\n
\n\n\n\n \n \n \"HowPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{navarri_how_2022,\nabstract = {Abstract\n\nAlcohol use disorder (AUD) and cannabis use disorder (CUD) are associated with brain alterations particularly involving fronto‐cerebellar and meso‐cortico‐limbic circuitry. However, such abnormalities have additionally been reported in other psychiatric conditions, and until recently there has been few large‐scale investigations to compare such findings. The current study uses the Enhancing Neuroimaging Genetics through Meta‐Analysis (ENIGMA) consortium method of standardising structural brain measures to quantify case–control differences and to compare brain‐correlates of substance use disorders with those published in relation to other psychiatric disorders. Using the ENIGMA protocols, we report effect sizes derived from a meta‐analysis of alcohol (seven studies,\nN\n= 798, 54{\\%} are cases) and cannabis (seven studies,\nN\n= 447, 45{\\%} are cases) dependent cases and age‐ and sex‐matched controls. We conduct linear analyses using harmonised methods to process and parcellate brain data identical to those reported in the literature for ENIGMA case–control studies of major depression disorder (MDD), schizophrenia (SCZ) and bipolar disorder so that effect sizes are optimally comparable across disorders. R elationships between substance use disorder diagnosis and subcortical grey matter volumes and cortical thickness were assessed with intracranial volume, age and sex as co‐variates . After correcting for multiple comparisons, AUD case–control meta‐analysis of subcortical regions indicated significant differences in the thalamus, hippocampus, amygdala and accumbens, with effect sizes (0.23) generally equivalent to, or larger than {\\{}$\\backslash$textbar{\\}}0.23{\\{}$\\backslash$textbar{\\}} those previously reported for other psychiatric disorders (except for the pallidum and putamen). On measures of cortical thickness, AUD was associated with significant differences bilaterally in the fusiform gyrus, inferior temporal gyrus, temporal pole, superior frontal gyrus, and rostral and caudal anterior cingulate gyri. Meta‐analysis of CUD case–control studies indicated reliable reductions in amygdala, accumbens and hippocampus volumes, with the former effect size comparable to, and the latter effect size around half of that reported for alcohol and SCZ. CUD was associated with lower cortical thickness in the frontal regions, particularly the medial orbitofrontal region, but this effect was not significant after correcting for multiple testing. This study allowed for an unbiased cross‐disorder comparison of brain correlates of substance use disorders and showed alcohol‐related brain anomalies equivalent in effect size to that found in SCZ in several subcortical and cortical regions and significantly greater alterations than those found in MDD in several subcortical and cortical regions. Although modest, CUD results overlapped with findings reported for AUD and other psychiatric conditions, but appear to be most robustly related to reduce thickness of the medial orbitofrontal cortex.},\nauthor = {Navarri, Xavier and Afzali, Mohammad H and Lavoie, Jacob and Sinha, Rajita and Stein, Dan J and Momenan, Reza and Veltman, Dick J and Korucuoglu, Ozlem and Sjoerds, Zsuzsika and {Van Holst}, Ruth J and Hester, Rob and Orr, Catherine and Cousijn, Janna and Yucel, Murat and Lorenzetti, Valentina and Wiers, Reinout and Jahanshad, Neda and Glahn, David C and Thompson, Paul M and Mackey, Scott and Conrod, Patricia J},\ndoi = {10.1002/hbm.25114},\nfile = {:Users/jacquelinebracher/Zotero/storage/HU888PCE/Navarri et al. - 2022 - How do substance use disorders compare to other ps.pdf:pdf},\nissn = {1065-9471, 1097-0193},\njournal = {Human Brain Mapping},\nmonth = {jan},\nnumber = {1},\npages = {399--413},\nshorttitle = {How do substance use disorders compare to other ps},\ntitle = {{How do substance use disorders compare to other psychiatric conditions on structural brain abnormalities? {\\{}A{\\}} cross‐disorder meta‐analytic comparison using the {\\textless}span style="font-variant:small-caps;"{\\textgreater}{\\{}ENIGMA{\\}}{\\textless}/span{\\textgreater}consortium findings}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1002/hbm.25114},\nvolume = {43},\nyear = {2022}\n}\n
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\n Abstract Alcohol use disorder (AUD) and cannabis use disorder (CUD) are associated with brain alterations particularly involving fronto‐cerebellar and meso‐cortico‐limbic circuitry. However, such abnormalities have additionally been reported in other psychiatric conditions, and until recently there has been few large‐scale investigations to compare such findings. The current study uses the Enhancing Neuroimaging Genetics through Meta‐Analysis (ENIGMA) consortium method of standardising structural brain measures to quantify case–control differences and to compare brain‐correlates of substance use disorders with those published in relation to other psychiatric disorders. Using the ENIGMA protocols, we report effect sizes derived from a meta‐analysis of alcohol (seven studies, N = 798, 54% are cases) and cannabis (seven studies, N = 447, 45% are cases) dependent cases and age‐ and sex‐matched controls. We conduct linear analyses using harmonised methods to process and parcellate brain data identical to those reported in the literature for ENIGMA case–control studies of major depression disorder (MDD), schizophrenia (SCZ) and bipolar disorder so that effect sizes are optimally comparable across disorders. R elationships between substance use disorder diagnosis and subcortical grey matter volumes and cortical thickness were assessed with intracranial volume, age and sex as co‐variates . After correcting for multiple comparisons, AUD case–control meta‐analysis of subcortical regions indicated significant differences in the thalamus, hippocampus, amygdala and accumbens, with effect sizes (0.23) generally equivalent to, or larger than \\$\\$textbar\\0.23\\$\\$textbar\\ those previously reported for other psychiatric disorders (except for the pallidum and putamen). On measures of cortical thickness, AUD was associated with significant differences bilaterally in the fusiform gyrus, inferior temporal gyrus, temporal pole, superior frontal gyrus, and rostral and caudal anterior cingulate gyri. Meta‐analysis of CUD case–control studies indicated reliable reductions in amygdala, accumbens and hippocampus volumes, with the former effect size comparable to, and the latter effect size around half of that reported for alcohol and SCZ. CUD was associated with lower cortical thickness in the frontal regions, particularly the medial orbitofrontal region, but this effect was not significant after correcting for multiple testing. This study allowed for an unbiased cross‐disorder comparison of brain correlates of substance use disorders and showed alcohol‐related brain anomalies equivalent in effect size to that found in SCZ in several subcortical and cortical regions and significantly greater alterations than those found in MDD in several subcortical and cortical regions. Although modest, CUD results overlapped with findings reported for AUD and other psychiatric conditions, but appear to be most robustly related to reduce thickness of the medial orbitofrontal cortex.\n
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\n \n\n \n \n \n \n \n Infection in the Developing Brain: The Role of Unique Systemic Immune Vulnerabilities.\n \n \n \n\n\n \n Singh, G.; Tucker, E.; and Rohlwink, U.\n\n\n \n\n\n\n Frontiers in Neurology, 12. 2022.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Singh2022,\nabstract = {Central nervous system (CNS) infections remain a major burden of pediatric disease associated with significant long-term morbidity due to injury to the developing brain. Children are susceptible to various etiologies of CNS infection partly because of vulnerabilities in their peripheral immune system. Young children are known to have reduced numbers and functionality of innate and adaptive immune cells, poorer production of immune mediators, impaired responses to inflammatory stimuli and depressed antibody activity in comparison to adults. This has implications not only for their response to pathogen invasion, but also for the development of appropriate vaccines and vaccination strategies. Further, pediatric immune characteristics evolve across the span of childhood into adolescence as their broader physiological and hormonal landscape develop. In addition to intrinsic vulnerabilities, children are subject to external factors that impact their susceptibility to infections, including maternal immunity and exposure, and nutrition. In this review we summarize the current evidence for immune characteristics across childhood that render children at risk for CNS infection and introduce the link with the CNS through the modulatory role that the brain has on the immune response. This manuscript lays the foundation from which we explore the specifics of infection and inflammation within the CNS and the consequences to the maturing brain in part two of this review series.},\nauthor = {Singh, G. and Tucker, E.W. and Rohlwink, U.K.},\ndoi = {10.3389/fneur.2021.805643},\nfile = {:Users/jacquelinebracher/Zotero/storage/NKSWA8YN/Singh et al. - 2022 - Infection in the Developing Brain The Role of Uni.pdf:pdf},\njournal = {Frontiers in Neurology},\ntitle = {{Infection in the Developing Brain: The Role of Unique Systemic Immune Vulnerabilities}},\nvolume = {12},\nyear = {2022}\n}\n
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\n Central nervous system (CNS) infections remain a major burden of pediatric disease associated with significant long-term morbidity due to injury to the developing brain. Children are susceptible to various etiologies of CNS infection partly because of vulnerabilities in their peripheral immune system. Young children are known to have reduced numbers and functionality of innate and adaptive immune cells, poorer production of immune mediators, impaired responses to inflammatory stimuli and depressed antibody activity in comparison to adults. This has implications not only for their response to pathogen invasion, but also for the development of appropriate vaccines and vaccination strategies. Further, pediatric immune characteristics evolve across the span of childhood into adolescence as their broader physiological and hormonal landscape develop. In addition to intrinsic vulnerabilities, children are subject to external factors that impact their susceptibility to infections, including maternal immunity and exposure, and nutrition. In this review we summarize the current evidence for immune characteristics across childhood that render children at risk for CNS infection and introduce the link with the CNS through the modulatory role that the brain has on the immune response. This manuscript lays the foundation from which we explore the specifics of infection and inflammation within the CNS and the consequences to the maturing brain in part two of this review series.\n
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\n \n\n \n \n \n \n \n Infections in the Developing Brain: The Role of the Neuro-Immune Axis.\n \n \n \n\n\n \n Kim, J.; Erice, C.; Rohlwink, U.; and Tucker, E.\n\n\n \n\n\n\n Frontiers in Neurology, 13. 2022.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Kim2022,\nabstract = {Central nervous system (CNS) infections occur more commonly in young children than in adults and pose unique challenges in the developing brain. This review builds on the distinct vulnerabilities in children's peripheral immune system (outlined in part 1 of this review series) and focuses on how the developing brain responds once a CNS infection occurs. Although the protective blood-brain barrier (BBB) matures early, pathogens enter the CNS and initiate a localized innate immune response with release of cytokines and chemokines to recruit peripheral immune cells that contribute to the inflammatory cascade. This immune response is initiated by the resident brain cells, microglia and astrocytes, which are not only integral to fighting the infection but also have important roles during normal brain development. Additionally, cytokines and other immune mediators such as matrix metalloproteinases from neurons, glia, and endothelial cells not only play a role in BBB permeability and peripheral cell recruitment, but also in brain maturation. Consequently, these immune modulators and the activation of microglia and astrocytes during infection adversely impact normal neurodevelopment. Perturbations to normal brain development manifest as neurodevelopmental and neurocognitive impairments common among children who survive CNS infections and are often permanent. In part 2 of the review series, we broadly summarize the unique challenges CNS infections create in a developing brain and explore the interaction of regulators of neurodevelopment and CNS immune response as part of the neuro-immune axis.},\nauthor = {Kim, J. and Erice, C. and Rohlwink, U.K. and Tucker, E.W.},\ndoi = {10.3389/fneur.2022.805786},\nfile = {:Users/jacquelinebracher/Zotero/storage/HP6CYU5Z/Kim et al. - 2022 - Infections in the Developing Brain The Role of th.pdf:pdf},\njournal = {Frontiers in Neurology},\ntitle = {{Infections in the Developing Brain: The Role of the Neuro-Immune Axis}},\nvolume = {13},\nyear = {2022}\n}\n
\n
\n\n\n
\n Central nervous system (CNS) infections occur more commonly in young children than in adults and pose unique challenges in the developing brain. This review builds on the distinct vulnerabilities in children's peripheral immune system (outlined in part 1 of this review series) and focuses on how the developing brain responds once a CNS infection occurs. Although the protective blood-brain barrier (BBB) matures early, pathogens enter the CNS and initiate a localized innate immune response with release of cytokines and chemokines to recruit peripheral immune cells that contribute to the inflammatory cascade. This immune response is initiated by the resident brain cells, microglia and astrocytes, which are not only integral to fighting the infection but also have important roles during normal brain development. Additionally, cytokines and other immune mediators such as matrix metalloproteinases from neurons, glia, and endothelial cells not only play a role in BBB permeability and peripheral cell recruitment, but also in brain maturation. Consequently, these immune modulators and the activation of microglia and astrocytes during infection adversely impact normal neurodevelopment. Perturbations to normal brain development manifest as neurodevelopmental and neurocognitive impairments common among children who survive CNS infections and are often permanent. In part 2 of the review series, we broadly summarize the unique challenges CNS infections create in a developing brain and explore the interaction of regulators of neurodevelopment and CNS immune response as part of the neuro-immune axis.\n
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\n \n\n \n \n \n \n \n \n Brain microdialysis and applications to drug therapy in severe traumatic brain injury.\n \n \n \n \n\n\n \n Ketharanathan, N; Rohlwink, U K; Figaji, A A; Wildschut, E D; Tibboel, D; and de Lange, E C M\n\n\n \n\n\n\n 2022.\n \n\n\n\n
\n\n\n\n \n \n \"BrainPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Ketharanathan2022,\nannote = {Export Date: 29 December 2022},\nauthor = {Ketharanathan, N and Rohlwink, U K and Figaji, A A and Wildschut, E D and Tibboel, D and de Lange, E C M},\ndoi = {10.1016/B978-0-12-823036-7.00041-4},\npages = {231--242},\ntitle = {{Brain microdialysis and applications to drug therapy in severe traumatic brain injury}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85138905959{\\&}doi=10.1016{\\%}2FB978-0-12-823036-7.00041-4{\\&}partnerID=40{\\&}md5=1c0a3740ad65f0bd458c8cd3b6569049},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n What we learn about bipolar disorder from large‐scale neuroimaging: \\Findings\\ and future directions from the \\textlessspan style=\"font-variant:small-caps;\"\\textgreater\\ENIGMA\\\\textless/span\\textgreater\\Bipolar\\ \\Disorder\\ \\Working\\ \\Group\\.\n \n \n \n \n\n\n \n Ching, C. R K; Hibar, D. P; Gurholt, T. P; Nunes, A.; Thomopoulos, S. I; Abé, C.; Agartz, I.; Brouwer, R. M; Cannon, D. M; De Zwarte, S. M C; Eyler, L. T; Favre, P.; Hajek, T.; Haukvik, U. K; Houenou, J.; Landén, M.; Lett, T. A; McDonald, C.; Nabulsi, L.; Patel, Y.; Pauling, M. E; Paus, T.; Radua, J.; Soeiro‐de‐Souza, M. G; Tronchin, G.; Van Haren, N. E M; Vieta, E.; Walter, H.; Zeng, L.; Alda, M.; Almeida, J.; Alnæs, D.; Alonso‐Lana, S.; Altimus, C.; Bauer, M.; Baune, B. T; Bearden, C. E; Bellani, M.; Benedetti, F.; Berk, M.; Bilderbeck, A. C; Blumberg, H. P; Bøen, E.; Bollettini, I.; Del Mar Bonnin, C.; Brambilla, P.; Canales‐Rodríguez, E. J; Caseras, X.; Dandash, O.; Dannlowski, U.; Delvecchio, G.; Díaz‐Zuluaga, A. M; Dima, D.; Duchesnay, É.; Elvsåshagen, T.; Fears, S. C; Frangou, S.; Fullerton, J. M; Glahn, D. C; Goikolea, J. M; Green, M. J; Grotegerd, D.; Gruber, O.; Haarman, B. C M; Henry, C.; Howells, F. M; Ives‐Deliperi, V.; Jansen, A.; Kircher, T. T J; Knöchel, C.; Kramer, B.; Lafer, B.; López‐Jaramillo, C.; Machado‐Vieira, R.; MacIntosh, B. J; Melloni, E. M T; Mitchell, P. B; Nenadic, I.; Nery, F.; Nugent, A. C; Oertel, V.; Ophoff, R. A; Ota, M.; Overs, B. J; Pham, D. L; Phillips, M. L; Pineda‐Zapata, J. A; Poletti, S.; Polosan, M.; Pomarol‐Clotet, E.; Pouchon, A.; Quidé, Y.; Rive, M. M; Roberts, G.; Ruhe, H. G; Salvador, R.; Sarró, S.; Satterthwaite, T. D; Schene, A. H; Sim, K.; Soares, J. C; Stäblein, M.; Stein, D. J; Tamnes, C. K; Thomaidis, G. V; Upegui, C. V.; Veltman, D. J; Wessa, M.; Westlye, L. T; Whalley, H. C; Wolf, D. H; Wu, M.; Yatham, L. N; Zarate, C. A; Thompson, P. M; Andreassen, O. A; and ENIGMA Bipolar Disorder Working Group\n\n\n \n\n\n\n Human Brain Mapping, 43(1): 56–82. jan 2022.\n \n\n\n\n
\n\n\n\n \n \n \"WhatPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{ching_what_2022,\nabstract = {Abstract\nMRI‐derived brain measures offer a link between genes, the environment and behavior and have been widely studied in bipolar disorder (BD). However, many neuroimaging studies of BD have been underpowered, leading to varied results and uncertainty regarding effects. The Enhancing Neuro Imaging Genetics through Meta‐Analysis (ENIGMA) Bipolar Disorder Working Group was formed in 2012 to empower discoveries, generate consensus findings and inform future hypothesis‐driven studies of BD. Through this effort, over 150 researchers from 20 countries and 55 institutions pool data and resources to produce the largest neuroimaging studies of BD ever conducted. The ENIGMA Bipolar Disorder Working Group applies standardized processing and analysis techniques to empower large‐scale meta‐ and mega‐analyses of multimodal brain MRI and improve the replicability of studies relating brain variation to clinical and genetic data. Initial BD Working Group studies reveal widespread patterns of lower cortical thickness, subcortical volume and disrupted white matter integrity associated with BD. Findings also include mapping brain alterations of common medications like lithium, symptom patterns and clinical risk profiles and have provided further insights into the pathophysiological mechanisms of BD. Here we discuss key findings from the BD working group, its ongoing projects and future directions for large‐scale, collaborative studies of mental illness.},\nauthor = {Ching, Christopher R K and Hibar, Derrek P and Gurholt, Tiril P and Nunes, Abraham and Thomopoulos, Sophia I and Ab{\\'{e}}, Christoph and Agartz, Ingrid and Brouwer, Rachel M and Cannon, Dara M and {De Zwarte}, Sonja M C and Eyler, Lisa T and Favre, Pauline and Hajek, Tomas and Haukvik, Unn K and Houenou, Josselin and Land{\\'{e}}n, Mikael and Lett, Tristram A and McDonald, Colm and Nabulsi, Leila and Patel, Yash and Pauling, Melissa E and Paus, Tomas and Radua, Joaquim and Soeiro‐de‐Souza, Marcio G and Tronchin, Giulia and {Van Haren}, Neeltje E M and Vieta, Eduard and Walter, Henrik and Zeng, Ling‐Li and Alda, Martin and Almeida, Jorge and Aln{\\ae}s, Dag and Alonso‐Lana, Silvia and Altimus, Cara and Bauer, Michael and Baune, Bernhard T and Bearden, Carrie E and Bellani, Marcella and Benedetti, Francesco and Berk, Michael and Bilderbeck, Amy C and Blumberg, Hilary P and B{\\o}en, Erlend and Bollettini, Irene and {Del Mar Bonnin}, Caterina and Brambilla, Paolo and Canales‐Rodr{\\'{i}}guez, Erick J and Caseras, Xavier and Dandash, Orwa and Dannlowski, Udo and Delvecchio, Giuseppe and D{\\'{i}}az‐Zuluaga, Ana M and Dima, Danai and Duchesnay, {\\'{E}}douard and Elvs{\\aa}shagen, Torbj{\\o}rn and Fears, Scott C and Frangou, Sophia and Fullerton, Janice M and Glahn, David C and Goikolea, Jose M and Green, Melissa J and Grotegerd, Dominik and Gruber, Oliver and Haarman, Bartholomeus C M and Henry, Chantal and Howells, Fleur M and Ives‐Deliperi, Victoria and Jansen, Andreas and Kircher, Tilo T J and Kn{\\"{o}}chel, Christian and Kramer, Bernd and Lafer, Beny and L{\\'{o}}pez‐Jaramillo, Carlos and Machado‐Vieira, Rodrigo and MacIntosh, Bradley J and Melloni, Elisa M T and Mitchell, Philip B and Nenadic, Igor and Nery, Fabiano and Nugent, Allison C and Oertel, Viola and Ophoff, Roel A and Ota, Miho and Overs, Bronwyn J and Pham, Daniel L and Phillips, Mary L and Pineda‐Zapata, Julian A and Poletti, Sara and Polosan, Mircea and Pomarol‐Clotet, Edith and Pouchon, Arnaud and Quid{\\'{e}}, Yann and Rive, Maria M and Roberts, Gloria and Ruhe, Henricus G and Salvador, Raymond and Sarr{\\'{o}}, Salvador and Satterthwaite, Theodore D and Schene, Aart H and Sim, Kang and Soares, Jair C and St{\\"{a}}blein, Michael and Stein, Dan J and Tamnes, Christian K and Thomaidis, Georgios V and Upegui, Cristian Vargas and Veltman, Dick J and Wessa, Mich{\\`{e}}le and Westlye, Lars T and Whalley, Heather C and Wolf, Daniel H and Wu, Mon‐Ju and Yatham, Lakshmi N and Zarate, Carlos A and Thompson, Paul M and Andreassen, Ole A and {ENIGMA Bipolar Disorder Working Group}},\ndoi = {10.1002/hbm.25098},\nfile = {:Users/jacquelinebracher/Zotero/storage/RCLC28W7/Ching et al. - 2022 - What we learn about bipolar disorder from large‐sc.pdf:pdf},\nissn = {1065-9471, 1097-0193},\njournal = {Human Brain Mapping},\nmonth = {jan},\nnumber = {1},\npages = {56--82},\nshorttitle = {What we learn about bipolar disorder from large‐sc},\ntitle = {{What we learn about bipolar disorder from large‐scale neuroimaging: {\\{}Findings{\\}} and future directions from the {\\textless}span style="font-variant:small-caps;"{\\textgreater}{\\{}ENIGMA{\\}}{\\textless}/span{\\textgreater}{\\{}Bipolar{\\}} {\\{}Disorder{\\}} {\\{}Working{\\}} {\\{}Group{\\}}}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1002/hbm.25098},\nvolume = {43},\nyear = {2022}\n}\n
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\n Abstract MRI‐derived brain measures offer a link between genes, the environment and behavior and have been widely studied in bipolar disorder (BD). However, many neuroimaging studies of BD have been underpowered, leading to varied results and uncertainty regarding effects. The Enhancing Neuro Imaging Genetics through Meta‐Analysis (ENIGMA) Bipolar Disorder Working Group was formed in 2012 to empower discoveries, generate consensus findings and inform future hypothesis‐driven studies of BD. Through this effort, over 150 researchers from 20 countries and 55 institutions pool data and resources to produce the largest neuroimaging studies of BD ever conducted. The ENIGMA Bipolar Disorder Working Group applies standardized processing and analysis techniques to empower large‐scale meta‐ and mega‐analyses of multimodal brain MRI and improve the replicability of studies relating brain variation to clinical and genetic data. Initial BD Working Group studies reveal widespread patterns of lower cortical thickness, subcortical volume and disrupted white matter integrity associated with BD. Findings also include mapping brain alterations of common medications like lithium, symptom patterns and clinical risk profiles and have provided further insights into the pathophysiological mechanisms of BD. Here we discuss key findings from the BD working group, its ongoing projects and future directions for large‐scale, collaborative studies of mental illness.\n
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\n \n\n \n \n \n \n \n A Neurometabolic Pattern of Elevated Myo-Inositol in Children Who Are HIV-Exposed and Uninfected: A South African Birth Cohort Study.\n \n \n \n\n\n \n Bertran-Cobo, C.; Wedderburn, C.; Robertson, F.; Subramoney, S.; Narr, K.; Joshi, S.; Roos, A.; Rehman, A.; Hoffman, N.; Zar, H.; Stein, D.; and Donald, K.\n\n\n \n\n\n\n Frontiers in Immunology, 13. 2022.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Bertran-Cobo2022,\nabstract = {Introduction: Exposure to maternal HIV in pregnancy may be a risk factor for impaired child neurodevelopment during the first years of life. Altered neurometabolites have been associated with HIV exposure in older children and may help explain the mechanisms underlying this risk. For the first time, we explored neurometabolic profiles of children who are HIV-exposed and uninfected (CHEU) compared to children who are HIV-unexposed (CHU) at 2-3 years of age. Methods: The South African Drakenstein Child Health Study enrolled women during pregnancy and is following mother-child pairs through childhood. MRI scans were acquired on a sub-group of children at 2-3 years. We used single voxel magnetic resonance spectroscopy to measure brain metabolite ratios to total creatine in the parietal grey matter, and left and right parietal white matter of 83 children (36 CHEU; 47 CHU). Using factor analysis, we explored brain metabolite patterns in predefined parietal voxels in these groups using logistic regression models. Differences in relative concentrations of individual metabolites (n-acetyl-aspartate, myo-inositol, total choline, and glutamate) to total creatine between CHEU and CHU groups were also examined. Results: Factor analysis revealed four different metabolite patterns, each one characterized by covarying ratios of a single metabolite in parietal grey and white matter. The cross-regional pattern dominated by myo-inositol, a marker for glial reactivity and inflammation, was associated with HIV exposure status (OR 1.63; 95{\\%} CI 1.11–2.50) which held after adjusting for child age, sex, and maternal alcohol use during pregnancy (OR 1.59; 95{\\%} CI 1.07 –2.47). Additionally, higher relative concentrations of myo-inositol to total creatine were found in left and right parietal white matter of CHEU compared to CHU (p=0.025 and p=0.001 respectively). Discussion: Increased ratios of myo-inositol to total creatine in parietal brain regions at age 2-3 years in CHEU are suggestive of early and ongoing neuroinflammatory processes. Altered relative concentrations of neurometabolites were found predominantly in the white matter, which is sensitive to neuroinflammation, and may contribute to developmental risk in this population. Future work on the trajectory of myo-inositol over time in CHEU, alongside markers of neurocognitive development, and the potential for specific neurodevelopmental interventions will be useful.},\nauthor = {Bertran-Cobo, C. and Wedderburn, C.J. and Robertson, F.C. and Subramoney, S. and Narr, K.L. and Joshi, S.H. and Roos, A. and Rehman, A.M. and Hoffman, N. and Zar, H.J. and Stein, D.J. and Donald, K.A.},\ndoi = {10.3389/fimmu.2022.800273},\nfile = {:Users/jacquelinebracher/Zotero/storage/66T3Y68Q/Bertran-Cobo et al. - 2022 - A Neurometabolic Pattern of Elevated Myo-Inositol .pdf:pdf},\njournal = {Frontiers in Immunology},\ntitle = {{A Neurometabolic Pattern of Elevated Myo-Inositol in Children Who Are HIV-Exposed and Uninfected: A South African Birth Cohort Study}},\nvolume = {13},\nyear = {2022}\n}\n
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\n Introduction: Exposure to maternal HIV in pregnancy may be a risk factor for impaired child neurodevelopment during the first years of life. Altered neurometabolites have been associated with HIV exposure in older children and may help explain the mechanisms underlying this risk. For the first time, we explored neurometabolic profiles of children who are HIV-exposed and uninfected (CHEU) compared to children who are HIV-unexposed (CHU) at 2-3 years of age. Methods: The South African Drakenstein Child Health Study enrolled women during pregnancy and is following mother-child pairs through childhood. MRI scans were acquired on a sub-group of children at 2-3 years. We used single voxel magnetic resonance spectroscopy to measure brain metabolite ratios to total creatine in the parietal grey matter, and left and right parietal white matter of 83 children (36 CHEU; 47 CHU). Using factor analysis, we explored brain metabolite patterns in predefined parietal voxels in these groups using logistic regression models. Differences in relative concentrations of individual metabolites (n-acetyl-aspartate, myo-inositol, total choline, and glutamate) to total creatine between CHEU and CHU groups were also examined. Results: Factor analysis revealed four different metabolite patterns, each one characterized by covarying ratios of a single metabolite in parietal grey and white matter. The cross-regional pattern dominated by myo-inositol, a marker for glial reactivity and inflammation, was associated with HIV exposure status (OR 1.63; 95% CI 1.11–2.50) which held after adjusting for child age, sex, and maternal alcohol use during pregnancy (OR 1.59; 95% CI 1.07 –2.47). Additionally, higher relative concentrations of myo-inositol to total creatine were found in left and right parietal white matter of CHEU compared to CHU (p=0.025 and p=0.001 respectively). Discussion: Increased ratios of myo-inositol to total creatine in parietal brain regions at age 2-3 years in CHEU are suggestive of early and ongoing neuroinflammatory processes. Altered relative concentrations of neurometabolites were found predominantly in the white matter, which is sensitive to neuroinflammation, and may contribute to developmental risk in this population. Future work on the trajectory of myo-inositol over time in CHEU, alongside markers of neurocognitive development, and the potential for specific neurodevelopmental interventions will be useful.\n
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\n \n\n \n \n \n \n \n \n The experiences of early childhood development care centre staff in providing care and learning support in a low socioeconomic community in \\South\\ \\Africa\\.\n \n \n \n \n\n\n \n Coetzee, B.; Du Toit, S.; Crouse, R.; and Roos, A.\n\n\n \n\n\n\n Early Child Development and Care, 192(14): 2338–2352. oct 2022.\n \n\n\n\n
\n\n\n\n \n \n \"ThePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{coetzee_experiences_2022,\nauthor = {Coetzee, Bronwyn{\\`{e}} and {Du Toit}, Stefani and Crouse, Rhonda and Roos, Annerine},\ndoi = {10.1080/03004430.2021.2012172},\nissn = {0300-4430, 1476-8275},\njournal = {Early Child Development and Care},\nmonth = {oct},\nnumber = {14},\npages = {2338--2352},\ntitle = {{The experiences of early childhood development care centre staff in providing care and learning support in a low socioeconomic community in {\\{}South{\\}} {\\{}Africa{\\}}}},\nurl = {https://www.tandfonline.com/doi/full/10.1080/03004430.2021.2012172},\nvolume = {192},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n What is next in African neuroscience?.\n \n \n \n\n\n \n Donald, K.; Maina, M.; Patel, N.; Nguemeni, C.; Mohammed, W.; Abubakar, A.; Brown, M.; Stoyanova, R.; Welchman, A.; Walker, N.; Daniels, W.; and Newton, C.\n\n\n \n\n\n\n eLife, 11. 2022.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Donald2022,\nabstract = {Working in Africa provides neuroscientists with opportunities that are not available in other continents. Populations in this region exhibit the greatest genetic diversity; they live in ecosystems with diverse flora and fauna; and they face unique stresses to brain health, including child brain health and development, due to high levels of traumatic brain injury and diseases endemic to the region. However, the neuroscience community in Africa has yet to reach its full potential. In this article we report the outcomes from a series of meetings at which the African neuroscience community came together to identify barriers and opportunities, and to discuss ways forward. This exercise resulted in the identification of six domains of distinction in African neuroscience: the diverse DNA of African populations; diverse flora, fauna and ecosystems for comparative research; child brain health and development; the impact of climate change on mental and neurological health; access to clinical populations with important conditions less prevalent in the global North; and resourcefulness in the reuse and adaption of existing technologies and resources to answer new questions. The article also outlines plans to advance the field of neuroscience in Africa in order to unlock the potential of African neuroscientists to address regional and global mental health and neurological problems.},\nauthor = {Donald, K.A. and Maina, M. and Patel, N. and Nguemeni, C. and Mohammed, W. and Abubakar, A. and Brown, M. and Stoyanova, R. and Welchman, A. and Walker, N. and Daniels, W. and Newton, C.R.},\ndoi = {10.7554/eLife.80488},\nfile = {:Users/jacquelinebracher/Zotero/storage/NPX3GC8R/Donald et al. - 2022 - What is next in African neuroscience.pdf:pdf},\njournal = {eLife},\ntitle = {{What is next in African neuroscience?}},\nvolume = {11},\nyear = {2022}\n}\n
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\n Working in Africa provides neuroscientists with opportunities that are not available in other continents. Populations in this region exhibit the greatest genetic diversity; they live in ecosystems with diverse flora and fauna; and they face unique stresses to brain health, including child brain health and development, due to high levels of traumatic brain injury and diseases endemic to the region. However, the neuroscience community in Africa has yet to reach its full potential. In this article we report the outcomes from a series of meetings at which the African neuroscience community came together to identify barriers and opportunities, and to discuss ways forward. This exercise resulted in the identification of six domains of distinction in African neuroscience: the diverse DNA of African populations; diverse flora, fauna and ecosystems for comparative research; child brain health and development; the impact of climate change on mental and neurological health; access to clinical populations with important conditions less prevalent in the global North; and resourcefulness in the reuse and adaption of existing technologies and resources to answer new questions. The article also outlines plans to advance the field of neuroscience in Africa in order to unlock the potential of African neuroscientists to address regional and global mental health and neurological problems.\n
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\n \n\n \n \n \n \n \n \n Cellular \\Substrates\\ of \\Functional\\ \\Network\\ \\Integration\\ and \\Memory\\ in \\Temporal\\ \\Lobe\\ \\Epilepsy\\.\n \n \n \n \n\n\n \n Douw, L.; Nissen, I. A; Fitzsimmons, S. M D D; Santos, F. A N; Hillebrand, A.; Van Straaten, E. C W; Stam, C. J; De Witt Hamer, P. C; Baayen, J. C; Klein, M.; Reijneveld, J. C; Heyer, D. B; Verhoog, M. B; Wilbers, R.; Hunt, S.; Mansvelder, H. D; Geurts, J. J G; De Kock, C. P J; and Goriounova, N. A\n\n\n \n\n\n\n Cerebral Cortex, 32(11): 2424–2436. may 2022.\n \n\n\n\n
\n\n\n\n \n \n \"CellularPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{douw_cellular_2022,\nabstract = {Abstract\nTemporal lobe epilepsy (TLE) patients are at risk of memory deficits, which have been linked to functional network disturbances, particularly of integration of the default mode network (DMN). However, the cellular substrates of functional network integration are unknown. We leverage a unique cross-scale dataset of drug-resistant TLE patients (n = 31), who underwent pseudo resting-state functional magnetic resonance imaging (fMRI), resting-state magnetoencephalography (MEG) and/or neuropsychological testing before neurosurgery. fMRI and MEG underwent atlas-based connectivity analyses. Functional network centrality of the lateral middle temporal gyrus, part of the DMN, was used as a measure of local network integration. Subsequently, non-pathological cortical tissue from this region was used for single cell morphological and electrophysiological patch-clamp analysis, assessing integration in terms of total dendritic length and action potential rise speed. As could be hypothesized, greater network centrality related to better memory performance. Moreover, greater network centrality correlated with more integrative properties at the cellular level across patients. We conclude that individual differences in cognitively relevant functional network integration of a DMN region are mirrored by differences in cellular integrative properties of this region in TLE patients. These findings connect previously separate scales of investigation, increasing translational insight into focal pathology and large-scale network disturbances in TLE.},\nauthor = {Douw, Linda and Nissen, Ida A and Fitzsimmons, Sophie M D D and Santos, Fernando A N and Hillebrand, Arjan and {Van Straaten}, Elisabeth C W and Stam, Cornelis J and {De Witt Hamer}, Philip C and Baayen, Johannes C and Klein, Martin and Reijneveld, Jaap C and Heyer, Djai B and Verhoog, Matthijs B and Wilbers, Ren{\\'{e}} and Hunt, Sarah and Mansvelder, Huibert D and Geurts, Jeroen J G and {De Kock}, Christiaan P J and Goriounova, Natalia A},\ndoi = {10.1093/cercor/bhab349},\nfile = {:Users/jacquelinebracher/Zotero/storage/XDNYZ9CF/Douw et al. - 2022 - Cellular Substrates of Functional Network Integrat.pdf:pdf},\nissn = {1047-3211, 1460-2199},\njournal = {Cerebral Cortex},\nmonth = {may},\nnumber = {11},\npages = {2424--2436},\ntitle = {{Cellular {\\{}Substrates{\\}} of {\\{}Functional{\\}} {\\{}Network{\\}} {\\{}Integration{\\}} and {\\{}Memory{\\}} in {\\{}Temporal{\\}} {\\{}Lobe{\\}} {\\{}Epilepsy{\\}}}},\nurl = {https://academic.oup.com/cercor/article/32/11/2424/6375261},\nvolume = {32},\nyear = {2022}\n}\n
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\n Abstract Temporal lobe epilepsy (TLE) patients are at risk of memory deficits, which have been linked to functional network disturbances, particularly of integration of the default mode network (DMN). However, the cellular substrates of functional network integration are unknown. We leverage a unique cross-scale dataset of drug-resistant TLE patients (n = 31), who underwent pseudo resting-state functional magnetic resonance imaging (fMRI), resting-state magnetoencephalography (MEG) and/or neuropsychological testing before neurosurgery. fMRI and MEG underwent atlas-based connectivity analyses. Functional network centrality of the lateral middle temporal gyrus, part of the DMN, was used as a measure of local network integration. Subsequently, non-pathological cortical tissue from this region was used for single cell morphological and electrophysiological patch-clamp analysis, assessing integration in terms of total dendritic length and action potential rise speed. As could be hypothesized, greater network centrality related to better memory performance. Moreover, greater network centrality correlated with more integrative properties at the cellular level across patients. We conclude that individual differences in cognitively relevant functional network integration of a DMN region are mirrored by differences in cellular integrative properties of this region in TLE patients. These findings connect previously separate scales of investigation, increasing translational insight into focal pathology and large-scale network disturbances in TLE.\n
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\n \n\n \n \n \n \n \n \n Epistemic justice, African values and feedback of findings in African genomics research.\n \n \n \n \n\n\n \n Ewuoso, C; Wonkam, A; and de Vries, J\n\n\n \n\n\n\n 2022.\n \n\n\n\n
\n\n\n\n \n \n \"EpistemicPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Ewuoso2022a,\nannote = {Export Date: 29 December 2022},\nauthor = {Ewuoso, C and Wonkam, A and de Vries, J},\ndoi = {10.1080/11287462.2022.2124019},\nfile = {:Users/jacquelinebracher/Zotero/storage/PBI2HKVK/Ewuoso et al. - 2022 - Epistemic justice, African values and feedback of .pdf:pdf},\nnumber = {1},\npages = {122--132},\ntitle = {{Epistemic justice, African values and feedback of findings in African genomics research}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85138553035{\\&}doi=10.1080{\\%}2F11287462.2022.2124019{\\&}partnerID=40{\\&}md5=ef26c56b551ebba4b3a42ee0cd030392},\nvolume = {33},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n Traumatic brain injury: progress and challenges in prevention, clinical care, and research.\n \n \n \n\n\n \n Maas, A.; Menon, D.; Manley, G.; Abrams, M.; Åkerlund, C.; Andelic, N.; Aries, M.; Bashford, T.; Bell, M.; Bodien, Y.; Zeldovich, M.; and Zemek, R.\n\n\n \n\n\n\n The Lancet Neurology, 21(11): 1004–1060. 2022.\n \n\n\n\n
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@article{Maas2022,\nauthor = {Maas, A.I.R. and Menon, D.K. and Manley, G.T. and Abrams, M. and {\\AA}kerlund, C. and Andelic, N. and Aries, M. and Bashford, T. and Bell, M.J. and Bodien, Y.G. and Zeldovich, M. and Zemek, R.},\ndoi = {10.1016/S1474-4422(22)00309-X},\nfile = {:Users/jacquelinebracher/Zotero/storage/7RJ5WJCV/Maas et al. - 2022 - Traumatic brain injury progress and challenges in.pdf:pdf},\njournal = {The Lancet Neurology},\nnumber = {11},\npages = {1004--1060},\ntitle = {{Traumatic brain injury: progress and challenges in prevention, clinical care, and research}},\nvolume = {21},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Coordinated cortical thickness alterations across six neurodevelopmental and psychiatric disorders.\n \n \n \n \n\n\n \n Hettwer, M D; Larivière, S; Park, B Y; Van Den Heuvel, O A; Schmaal, L; Andreassen, O A; Ching, C R K; Hoogman, M; Buitelaar, J; Van Rooij, D; Veltman, D J; Stein, D J; Franke, B; Van Erp, T G M; ENIGMA ADHD Working Group; ENIGMA Autism Working Group; Van Rooij, D; ENIGMA Bipolar Disorder Working Group; ENIGMA Major Depression Working Group; ENIGMA OCD Working Group; Van Den Heuvel, O A; ENIGMA Schizophrenia Working Group; Van Erp, T G M; Jahanshad, N; Thompson, P M; Thomopoulos, S I; Bethlehem, R A I; Bernhardt, B C; Eickhoff, S B; and Valk, S L\n\n\n \n\n\n\n Nature Communications, 13(1): 6851. nov 2022.\n \n\n\n\n
\n\n\n\n \n \n \"CoordinatedPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{hettwer_coordinated_2022,\nabstract = {Abstract\nNeuropsychiatric disorders are increasingly conceptualized as overlapping spectra sharing multi-level neurobiological alterations. However, whether transdiagnostic cortical alterations covary in a biologically meaningful way is currently unknown. Here, we studied co-alteration networks across six neurodevelopmental and psychiatric disorders, reflecting pathological structural covariance. In 12,024 patients and 18,969 controls from the ENIGMA consortium, we observed that co-alteration patterns followed normative connectome organization and were anchored to prefrontal and temporal disease epicenters. Manifold learning revealed frontal-to-temporal and sensory/limbic-to-occipitoparietal transdiagnostic gradients, differentiating shared illness effects on cortical thickness along these axes. The principal gradient aligned with a normative cortical thickness covariance gradient and established a transcriptomic link to cortico-cerebello-thalamic circuits. Moreover, transdiagnostic gradients segregated functional networks involved in basic sensory, attentional/perceptual, and domain-general cognitive processes, and distinguished between regional cytoarchitectonic profiles. Together, our findings indicate that shared illness effects occur in a synchronized fashion and along multiple levels of hierarchical cortical organization.},\nauthor = {Hettwer, M D and Larivi{\\`{e}}re, S and Park, B Y and {Van Den Heuvel}, O A and Schmaal, L and Andreassen, O A and Ching, C R K and Hoogman, M and Buitelaar, J and {Van Rooij}, D and Veltman, D J and Stein, D J and Franke, B and {Van Erp}, T G M and {ENIGMA ADHD Working Group} and {ENIGMA Autism Working Group} and {Van Rooij}, D and {ENIGMA Bipolar Disorder Working Group} and {ENIGMA Major Depression Working Group} and {ENIGMA OCD Working Group} and {Van Den Heuvel}, O A and {ENIGMA Schizophrenia Working Group} and {Van Erp}, T G M and Jahanshad, N and Thompson, P M and Thomopoulos, S I and Bethlehem, R A I and Bernhardt, B C and Eickhoff, S B and Valk, S L},\ndoi = {10.1038/s41467-022-34367-6},\nfile = {:Users/jacquelinebracher/Zotero/storage/ASYHZ69F/Hettwer et al. - 2022 - Coordinated cortical thickness alterations across .pdf:pdf},\nissn = {2041-1723},\njournal = {Nature Communications},\nmonth = {nov},\nnumber = {1},\npages = {6851},\ntitle = {{Coordinated cortical thickness alterations across six neurodevelopmental and psychiatric disorders}},\nurl = {https://www.nature.com/articles/s41467-022-34367-6},\nvolume = {13},\nyear = {2022}\n}\n
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\n Abstract Neuropsychiatric disorders are increasingly conceptualized as overlapping spectra sharing multi-level neurobiological alterations. However, whether transdiagnostic cortical alterations covary in a biologically meaningful way is currently unknown. Here, we studied co-alteration networks across six neurodevelopmental and psychiatric disorders, reflecting pathological structural covariance. In 12,024 patients and 18,969 controls from the ENIGMA consortium, we observed that co-alteration patterns followed normative connectome organization and were anchored to prefrontal and temporal disease epicenters. Manifold learning revealed frontal-to-temporal and sensory/limbic-to-occipitoparietal transdiagnostic gradients, differentiating shared illness effects on cortical thickness along these axes. The principal gradient aligned with a normative cortical thickness covariance gradient and established a transcriptomic link to cortico-cerebello-thalamic circuits. Moreover, transdiagnostic gradients segregated functional networks involved in basic sensory, attentional/perceptual, and domain-general cognitive processes, and distinguished between regional cytoarchitectonic profiles. Together, our findings indicate that shared illness effects occur in a synchronized fashion and along multiple levels of hierarchical cortical organization.\n
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\n \n\n \n \n \n \n \n \n In vivo hippocampal subfield volumes in bipolar disorder—\\A\\ mega‐analysis from \\The\\ \\Enhancing\\ \\Neuro\\ \\Imaging\\ \\Genetics\\ through \\textlessspan style=\"font-variant:small-caps;\"\\textgreater\\Meta\\‐\\Analysis\\\\textless/span\\textgreater\\Bipolar\\ \\Disorder\\ \\Working\\ \\Group\\.\n \n \n \n \n\n\n \n Haukvik, U. K; Gurholt, T. P; Nerland, S.; Elvsåshagen, T.; Akudjedu, T. N; Alda, M.; Alnæs, D.; Alonso‐Lana, S.; Bauer, J.; Baune, B. T; Benedetti, F.; Berk, M.; Bettella, F.; Bøen, E.; Bonnín, C. M; Brambilla, P.; Canales‐Rodríguez, E. J; Cannon, D. M; Caseras, X.; Dandash, O.; Dannlowski, U.; Delvecchio, G.; Díaz‐Zuluaga, A. M; Van Erp, T. G M; Fatjó‐Vilas, M.; Foley, S. F; Förster, K.; Fullerton, J. M; Goikolea, J. M; Grotegerd, D.; Gruber, O.; Haarman, B. C M; Haatveit, B.; Hajek, T.; Hallahan, B.; Harris, M.; Hawkins, E. L; Howells, F. M; Hülsmann, C.; Jahanshad, N.; Jørgensen, K. N; Kircher, T.; Krämer, B.; Krug, A.; Kuplicki, R.; Lagerberg, T. V; Lancaster, T. M; Lenroot, R. K; Lonning, V.; López‐Jaramillo, C.; Malt, U. F; McDonald, C.; McIntosh, A. M; McPhilemy, G.; Van Der Meer, D.; Melle, I.; Melloni, E. M T; Mitchell, P. B; Nabulsi, L.; Nenadić, I.; Oertel, V.; Oldani, L.; Opel, N.; Otaduy, M. C G; Overs, B. J; Pineda‐Zapata, J. A; Pomarol‐Clotet, E.; Radua, J.; Rauer, L.; Redlich, R.; Repple, J.; Rive, M. M; Roberts, G.; Ruhe, H. G; Salminen, L. E; Salvador, R.; Sarró, S.; Savitz, J.; Schene, A. H; Sim, K.; Soeiro‐de‐Souza, M. G; Stäblein, M.; Stein, D. J; Stein, F.; Tamnes, C. K; Temmingh, H. S; Thomopoulos, S. I; Veltman, D. J; Vieta, E.; Waltemate, L.; Westlye, L. T; Whalley, H. C; Sämann, P. G; Thompson, P. M; Ching, C. R K; Andreassen, O. A; Agartz, I.; and ENIGMA Bipolar Disorder Working Group\n\n\n \n\n\n\n Human Brain Mapping, 43(1): 385–398. jan 2022.\n \n\n\n\n
\n\n\n\n \n \n \"InPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{haukvik_vivo_2022,\nabstract = {Abstract\n\nThe hippocampus consists of anatomically and functionally distinct subfields that may be differentially involved in the pathophysiology of bipolar disorder (BD). Here we, the Enhancing NeuroImaging Genetics through Meta‐Analysis Bipolar Disorder workinggroup, study hippocampal subfield volumetry in BD. T1‐weighted magnetic resonance imaging scans from 4,698 individuals (BD = 1,472, healthy controls [HC] = 3,226) from 23 sites worldwide were processed with FreeSurfer. We used linear mixed‐effects models and mega‐analysis to investigate differences in hippocampal subfield volumes between BD and HC, followed by analyses of clinical characteristics and medication use. BD showed significantly smaller volumes of the whole hippocampus (Cohen's\nd =\n−0.20), cornu ammonis (CA)1 (\nd =\n−0.18), CA2/3 (\nd =\n−0.11), CA4 (\nd =\n−0.19), molecular layer (\nd =\n−0.21), granule cell layer of dentate gyrus (\nd =\n−0.21), hippocampal tail (\nd =\n−0.10), subiculum (\nd =\n−0.15), presubiculum (\nd =\n−0.18), and hippocampal amygdala transition area (\nd =\n−0.17) compared to HC. Lithium users did not show volume differences compared to HC, while non‐users did. Antipsychotics or antiepileptic use was associated with smaller volumes. In this largest study of hippocampal subfields in BD to date, we show widespread reductions in nine of 12 subfields studied. The associations were modulated by medication use and specifically the lack of differences between lithium users and HC supports a possible protective role of lithium in BD.},\nauthor = {Haukvik, Unn K and Gurholt, Tiril P and Nerland, Stener and Elvs{\\aa}shagen, Torbj{\\o}rn and Akudjedu, Theophilus N and Alda, Martin and Aln{\\ae}s, Dag and Alonso‐Lana, Silvia and Bauer, Jochen and Baune, Bernhard T and Benedetti, Francesco and Berk, Michael and Bettella, Francesco and B{\\o}en, Erlend and Bonn{\\'{i}}n, Caterina M and Brambilla, Paolo and Canales‐Rodr{\\'{i}}guez, Erick J and Cannon, Dara M and Caseras, Xavier and Dandash, Orwa and Dannlowski, Udo and Delvecchio, Giuseppe and D{\\'{i}}az‐Zuluaga, Ana M and {Van Erp}, Theo G M and Fatj{\\'{o}}‐Vilas, Mar and Foley, Sonya F and F{\\"{o}}rster, Katharina and Fullerton, Janice M and Goikolea, Jos{\\'{e}} M and Grotegerd, Dominik and Gruber, Oliver and Haarman, Bartholomeus C M and Haatveit, Beathe and Hajek, Tomas and Hallahan, Brian and Harris, Mathew and Hawkins, Emma L and Howells, Fleur M and H{\\"{u}}lsmann, Carina and Jahanshad, Neda and J{\\o}rgensen, Kjetil N and Kircher, Tilo and Kr{\\"{a}}mer, Bernd and Krug, Axel and Kuplicki, Rayus and Lagerberg, Trine V and Lancaster, Thomas M and Lenroot, Rhoshel K and Lonning, Vera and L{\\'{o}}pez‐Jaramillo, Carlos and Malt, Ulrik F and McDonald, Colm and McIntosh, Andrew M and McPhilemy, Genevieve and {Van Der Meer}, Dennis and Melle, Ingrid and Melloni, Elisa M T and Mitchell, Philip B and Nabulsi, Leila and Nenadi{\\'{c}}, Igor and Oertel, Viola and Oldani, Lucio and Opel, Nils and Otaduy, Maria C G and Overs, Bronwyn J and Pineda‐Zapata, Julian A and Pomarol‐Clotet, Edith and Radua, Joaquim and Rauer, Lisa and Redlich, Ronny and Repple, Jonathan and Rive, Maria M and Roberts, Gloria and Ruhe, Henricus G and Salminen, Lauren E and Salvador, Raymond and Sarr{\\'{o}}, Salvador and Savitz, Jonathan and Schene, Aart H and Sim, Kang and Soeiro‐de‐Souza, Marcio G and St{\\"{a}}blein, Michael and Stein, Dan J and Stein, Frederike and Tamnes, Christian K and Temmingh, Henk S and Thomopoulos, Sophia I and Veltman, Dick J and Vieta, Eduard and Waltemate, Lena and Westlye, Lars T and Whalley, Heather C and S{\\"{a}}mann, Philipp G and Thompson, Paul M and Ching, Christopher R K and Andreassen, Ole A and Agartz, Ingrid and {ENIGMA Bipolar Disorder Working Group}},\ndoi = {10.1002/hbm.25249},\nfile = {:Users/jacquelinebracher/Zotero/storage/99GGP8GS/Haukvik et al. - 2022 - In vivo hippocampal subfield volumes in bipolar di.pdf:pdf},\nissn = {1065-9471, 1097-0193},\njournal = {Human Brain Mapping},\nmonth = {jan},\nnumber = {1},\npages = {385--398},\nshorttitle = {In vivo hippocampal subfield volumes in bipolar di},\ntitle = {{In vivo hippocampal subfield volumes in bipolar disorder—{\\{}A{\\}} mega‐analysis from {\\{}The{\\}} {\\{}Enhancing{\\}} {\\{}Neuro{\\}} {\\{}Imaging{\\}} {\\{}Genetics{\\}} through {\\textless}span style="font-variant:small-caps;"{\\textgreater}{\\{}Meta{\\}}‐{\\{}Analysis{\\}}{\\textless}/span{\\textgreater}{\\{}Bipolar{\\}} {\\{}Disorder{\\}} {\\{}Working{\\}} {\\{}Group{\\}}}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1002/hbm.25249},\nvolume = {43},\nyear = {2022}\n}\n
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\n Abstract The hippocampus consists of anatomically and functionally distinct subfields that may be differentially involved in the pathophysiology of bipolar disorder (BD). Here we, the Enhancing NeuroImaging Genetics through Meta‐Analysis Bipolar Disorder workinggroup, study hippocampal subfield volumetry in BD. T1‐weighted magnetic resonance imaging scans from 4,698 individuals (BD = 1,472, healthy controls [HC] = 3,226) from 23 sites worldwide were processed with FreeSurfer. We used linear mixed‐effects models and mega‐analysis to investigate differences in hippocampal subfield volumes between BD and HC, followed by analyses of clinical characteristics and medication use. BD showed significantly smaller volumes of the whole hippocampus (Cohen's d = −0.20), cornu ammonis (CA)1 ( d = −0.18), CA2/3 ( d = −0.11), CA4 ( d = −0.19), molecular layer ( d = −0.21), granule cell layer of dentate gyrus ( d = −0.21), hippocampal tail ( d = −0.10), subiculum ( d = −0.15), presubiculum ( d = −0.18), and hippocampal amygdala transition area ( d = −0.17) compared to HC. Lithium users did not show volume differences compared to HC, while non‐users did. Antipsychotics or antiepileptic use was associated with smaller volumes. In this largest study of hippocampal subfields in BD to date, we show widespread reductions in nine of 12 subfields studied. The associations were modulated by medication use and specifically the lack of differences between lithium users and HC supports a possible protective role of lithium in BD.\n
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\n \n\n \n \n \n \n \n \n Neural basis of associative learning in \\Trichotillomania\\ and skin-picking disorder.\n \n \n \n \n\n\n \n Dougherty, D. D; Peters, A. T; Grant, J. E; Peris, T. S; Ricketts, E. J; Migó, M.; Chou, T.; O'Neill, J.; Stein, D. J; Lochner, C.; Keuthen, N.; Piacentini, J.; and Deckersbach, T.\n\n\n \n\n\n\n Behavioural Brain Research, 425: 113801. may 2022.\n \n\n\n\n
\n\n\n\n \n \n \"NeuralPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{dougherty_neural_2022,\nauthor = {Dougherty, Darin D and Peters, Amy T and Grant, Jon E and Peris, Tara S and Ricketts, Emily J and Mig{\\'{o}}, Marta and Chou, Tina and O'Neill, Joseph and Stein, Dan J and Lochner, Christine and Keuthen, Nancy and Piacentini, John and Deckersbach, Thilo},\ndoi = {10.1016/j.bbr.2022.113801},\nfile = {:Users/jacquelinebracher/Zotero/storage/S53WCPET/Dougherty et al. - 2022 - Neural basis of associative learning in Trichotill.pdf:pdf},\nissn = {01664328},\njournal = {Behavioural Brain Research},\nmonth = {may},\npages = {113801},\ntitle = {{Neural basis of associative learning in {\\{}Trichotillomania{\\}} and skin-picking disorder}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S0166432822000699},\nvolume = {425},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Dreams and the \\Hard\\ \\Problem\\ of \\Consciousness\\.\n \n \n \n \n\n\n \n Solms, M.\n\n\n \n\n\n\n In Encyclopedia of \\Behavioral\\ \\Neuroscience\\, 2nd edition, pages 678–686. Elsevier, 2022.\n \n\n\n\n
\n\n\n\n \n \n \"DreamsPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@incollection{solms_dreams_2022,\nauthor = {Solms, Mark},\nbooktitle = {Encyclopedia of {\\{}Behavioral{\\}} {\\{}Neuroscience{\\}}, 2nd edition},\ndoi = {10.1016/B978-0-12-809324-5.24093-5},\nisbn = {978-0-12-821636-1},\npages = {678--686},\npublisher = {Elsevier},\ntitle = {{Dreams and the {\\{}Hard{\\}} {\\{}Problem{\\}} of {\\{}Consciousness{\\}}}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/B9780128093245240935},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n A review of the genetic spectrum of hereditary spastic paraplegias, inherited neuropathies and spinal muscular atrophies in \\Africans\\.\n \n \n \n \n\n\n \n Mahungu, A. C; Monnakgotla, N.; Nel, M.; and Heckmann, J. M\n\n\n \n\n\n\n Orphanet Journal of Rare Diseases, 17(1): 133. dec 2022.\n \n\n\n\n
\n\n\n\n \n \n \"APaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{mahungu_review_2022,\nabstract = {Abstract\n\nBackground\nGenetic investigations of inherited neuromuscular disorders in Africans, have been neglected. We aimed to summarise the published data and comment on the genetic evidence related to inherited neuropathies (Charcot-Marie-Tooth disease (CMT)), hereditary spastic paraplegias (HSP) and spinal muscular atrophy (SMA) in Africans.\n\n\nMethods\nPubMed was searched for relevant articles and manual checking of references and review publications were performed for African-ancestry participants with relevant phenotypes and identified genetic variants. For each case report we extracted phenotype information, inheritance pattern, variant segregation and variant frequency in population controls (including up to date frequencies from the gnomAD database).\n\n\nResults\n\nFor HSP, 23 reports were found spanning the years 2000–2019 of which 19 related to North Africans, with high consanguinity, and six included sub-Saharan Africans. For CMT, 19 reports spanning years 2002–2021, of which 16 related to North Africans and 3 to sub-Saharan Africans. Most genetic variants had not been previously reported. There were 12 reports spanning years 1999–2020 related to\nSMN1\n-SMA caused by homozygous exon 7 ± 8 deletion. Interestingly, the population frequency of heterozygous\nSMN1\n-exon 7 deletion mutations appeared 2 × lower in Africans compared to Europeans, in addition to differences in the architecture of the\nSMN2\nlocus which may impact\nSMN1\n-SMA prognosis.\n\n\n\nConclusions\nOverall, genetic data on inherited neuromuscular diseases in sub-Saharan Africa, are sparse. If African patients with rare neuromuscular diseases are to benefit from the expansion in genomics capabilities and therapeutic advancements, then it is critical to document the mutational spectrum of inherited neuromuscular disease in Africa.\n\n\nHighlights\n\n\n\nReview of genetic variants reported in hereditary spastic paraplegia in Africans\n\n\nReview of genetic variants reported in genetic neuropathies in Africans\n\n\nReview of genetic underpinnings of spinal muscular atrophies in Africans\n\n\nAssessment of pathogenic evidence for candidate variants},\nauthor = {Mahungu, Amokelani C and Monnakgotla, Nomakhosazana and Nel, Melissa and Heckmann, Jeannine M},\ndoi = {10.1186/s13023-022-02280-2},\nfile = {:Users/jacquelinebracher/Zotero/storage/RAXGJAGW/Mahungu et al. - 2022 - A review of the genetic spectrum of hereditary spa.pdf:pdf},\nissn = {1750-1172},\njournal = {Orphanet Journal of Rare Diseases},\nmonth = {dec},\nnumber = {1},\npages = {133},\ntitle = {{A review of the genetic spectrum of hereditary spastic paraplegias, inherited neuropathies and spinal muscular atrophies in {\\{}Africans{\\}}}},\nurl = {https://ojrd.biomedcentral.com/articles/10.1186/s13023-022-02280-2},\nvolume = {17},\nyear = {2022}\n}\n
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\n Abstract Background Genetic investigations of inherited neuromuscular disorders in Africans, have been neglected. We aimed to summarise the published data and comment on the genetic evidence related to inherited neuropathies (Charcot-Marie-Tooth disease (CMT)), hereditary spastic paraplegias (HSP) and spinal muscular atrophy (SMA) in Africans. Methods PubMed was searched for relevant articles and manual checking of references and review publications were performed for African-ancestry participants with relevant phenotypes and identified genetic variants. For each case report we extracted phenotype information, inheritance pattern, variant segregation and variant frequency in population controls (including up to date frequencies from the gnomAD database). Results For HSP, 23 reports were found spanning the years 2000–2019 of which 19 related to North Africans, with high consanguinity, and six included sub-Saharan Africans. For CMT, 19 reports spanning years 2002–2021, of which 16 related to North Africans and 3 to sub-Saharan Africans. Most genetic variants had not been previously reported. There were 12 reports spanning years 1999–2020 related to SMN1 -SMA caused by homozygous exon 7 ± 8 deletion. Interestingly, the population frequency of heterozygous SMN1 -exon 7 deletion mutations appeared 2 × lower in Africans compared to Europeans, in addition to differences in the architecture of the SMN2 locus which may impact SMN1 -SMA prognosis. Conclusions Overall, genetic data on inherited neuromuscular diseases in sub-Saharan Africa, are sparse. If African patients with rare neuromuscular diseases are to benefit from the expansion in genomics capabilities and therapeutic advancements, then it is critical to document the mutational spectrum of inherited neuromuscular disease in Africa. Highlights Review of genetic variants reported in hereditary spastic paraplegia in Africans Review of genetic variants reported in genetic neuropathies in Africans Review of genetic underpinnings of spinal muscular atrophies in Africans Assessment of pathogenic evidence for candidate variants\n
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\n \n\n \n \n \n \n \n \n Gender Moderates Results of a Randomized Clinical Trial for the Khanya Intervention for Substance Use and ART Adherence in HIV Care in South Africa.\n \n \n \n \n\n\n \n Belus, J M; Joska, J A; Bronsteyn, Y; Rose, A L; Andersen, L S; Regenauer, K S; Myers, B; Hahn, J A; Orrell, C; Safren, S A; and Magidson, J F\n\n\n \n\n\n\n 2022.\n \n\n\n\n
\n\n\n\n \n \n \"GenderPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Belus2022,\nannote = {Export Date: 29 December 2022},\nauthor = {Belus, J M and Joska, J A and Bronsteyn, Y and Rose, A L and Andersen, L S and Regenauer, K S and Myers, B and Hahn, J A and Orrell, C and Safren, S A and Magidson, J F},\ndoi = {10.1007/s10461-022-03765-8},\nfile = {:Users/jacquelinebracher/Zotero/storage/A7ZAXH9Q/Belus et al. - 2022 - Gender Moderates Results of a Randomized Clinical .pdf:pdf},\nnumber = {11},\npages = {3630--3641},\ntitle = {{Gender Moderates Results of a Randomized Clinical Trial for the Khanya Intervention for Substance Use and ART Adherence in HIV Care in South Africa}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85135263740{\\&}doi=10.1007{\\%}2Fs10461-022-03765-8{\\&}partnerID=40{\\&}md5=9dcec0e2c063688c71bb7ef845b8a5ef},\nvolume = {26},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n What is a clinical practice guideline? \\A\\ roadmap to their development. \\Special\\ report from the \\Guidelines\\ \\Task\\ \\Force\\ of the \\International\\ \\League\\ \\Against\\ \\Epilepsy\\.\n \n \n \n \n\n\n \n Jetté, N.; Kirkpatrick, M.; Lin, K.; Fernando, S. M S; French, J. A; Jehi, L.; Kumlien, E.; Triki, C. C; Wiebe, S.; Wilmshurst, J.; and Brigo, F.\n\n\n \n\n\n\n Epilepsia, 63(8): 1920–1929. aug 2022.\n \n\n\n\n
\n\n\n\n \n \n \"WhatPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{jette_what_2022,\nabstract = {Abstract\nClinical practice guidelines (CPGs) are statements that provide evidence‐based recommendations aimed at optimizing patient care. However, many other documents are often published as “guidelines” when they are not; these documents, although also important in clinical practice, are usually not systematically produced following rigorous processes linking the evidence to the recommendations. Specifically, the International League Against Epilepsy (ILAE) guideline development toolkit aims to ensure that high‐quality CPGs are developed to fill knowledge gaps and optimize the management of epilepsy. In addition to adhering to key methodological processes, guideline developers need to consider that effective CPGs should lead to improvements in clinical processes of care and health care outcomes. This requires monitoring the effectiveness of epilepsy‐related CPGs and interventions to remove the barriers to epilepsy CPG implementation. This article provides an overview of what distinguishes quality CPGs from other documents and discusses their benefits and limitations. We summarize the recently revised ILAE CPG development process and elaborate on the barriers and facilitators to guideline dissemination, implementation, and adaptation.},\nauthor = {Jett{\\'{e}}, Nathalie and Kirkpatrick, Martin and Lin, Katia and Fernando, Sanjaya M S and French, Jacqueline A and Jehi, Lara and Kumlien, Eva and Triki, Chahnez C and Wiebe, Samuel and Wilmshurst, Jo and Brigo, Francesco},\ndoi = {10.1111/epi.17312},\nissn = {0013-9580, 1528-1167},\njournal = {Epilepsia},\nmonth = {aug},\nnumber = {8},\npages = {1920--1929},\nshorttitle = {What is a clinical practice guideline?},\ntitle = {{What is a clinical practice guideline? {\\{}A{\\}} roadmap to their development. {\\{}Special{\\}} report from the {\\{}Guidelines{\\}} {\\{}Task{\\}} {\\{}Force{\\}} of the {\\{}International{\\}} {\\{}League{\\}} {\\{}Against{\\}} {\\{}Epilepsy{\\}}}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1111/epi.17312},\nvolume = {63},\nyear = {2022}\n}\n
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\n Abstract Clinical practice guidelines (CPGs) are statements that provide evidence‐based recommendations aimed at optimizing patient care. However, many other documents are often published as “guidelines” when they are not; these documents, although also important in clinical practice, are usually not systematically produced following rigorous processes linking the evidence to the recommendations. Specifically, the International League Against Epilepsy (ILAE) guideline development toolkit aims to ensure that high‐quality CPGs are developed to fill knowledge gaps and optimize the management of epilepsy. In addition to adhering to key methodological processes, guideline developers need to consider that effective CPGs should lead to improvements in clinical processes of care and health care outcomes. This requires monitoring the effectiveness of epilepsy‐related CPGs and interventions to remove the barriers to epilepsy CPG implementation. This article provides an overview of what distinguishes quality CPGs from other documents and discusses their benefits and limitations. We summarize the recently revised ILAE CPG development process and elaborate on the barriers and facilitators to guideline dissemination, implementation, and adaptation.\n
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\n \n\n \n \n \n \n \n The impact of prenatal alcohol and/or tobacco exposure on brain structure in a large sample of children from a South African birth cohort.\n \n \n \n\n\n \n Marshall, A.; Bodison, S.; Uban, K.; Adise, S.; Jonker, D.; Charles, W.; Donald, K.; Kan, E.; Ipser, J.; Butler-Kruger, L.; Stein, D.; and Sowell, E.\n\n\n \n\n\n\n Alcoholism: Clinical and Experimental Research, 46(11): 1980–1992. 2022.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Marshall2022,\nabstract = {Background: Neuroimaging studies have emphasized the impact of prenatal alcohol exposure (PAE) on brain development, traditionally in heavily exposed participants. However, less is known about how naturally occurring community patterns of PAE (including light to moderate exposure) affect brain development, particularly in consideration of commonly occurring concurrent impacts of prenatal tobacco exposure (PTE). Methods: Three hundred thirty-two children (ages 8 to 12) living in South Africa's Cape Flats townships underwent structural magnetic resonance imaging. During pregnancy, their mothers reported alcohol and tobacco use, which was used to evaluate PAE and PTE effects on their children's brain structure. Analyses involved the main effects of PAE and PTE (and their interaction) and the effects of PAE and PTE quantity on cortical thickness, surface area, and volume. Results: After false-discovery rate (FDR) correction, PAE was associated with thinner left parahippocampal cortices, while PTE was associated with smaller cortical surface area in the bilateral pericalcarine, left lateral orbitofrontal, right posterior cingulate, right rostral anterior cingulate, left caudal middle frontal, and right caudal anterior cingulate gyri. There were no PAE × PTE interactions nor any associations of PAE and PTE exposure on volumetrics that survived FDR correction. Conclusion: PAE was associated with reduction in the structure of the medial temporal lobe, a brain region critical for learning and memory. PTE had stronger and broader associations, including with regions associated with executive function, reward processing, and emotional regulation, potentially reflecting continued postnatal exposure to tobacco (i.e., second-hand smoke exposure). These differential effects are discussed with respect to reduced PAE quantity in our exposed group versus prior studies within this geographical location, the deep poverty in which participants live, and the consequences of apartheid and racially and economically driven payment practices that contributed to heavy drinking in the region. Longer-term follow-up is needed to determine potential environmental and other moderators of the brain findings here and assess the extent to which they endure over time.},\nauthor = {Marshall, A.T. and Bodison, S.C. and Uban, K.A. and Adise, S. and Jonker, D. and Charles, W. and Donald, K.A. and Kan, E. and Ipser, J.C. and Butler-Kruger, L. and Stein, D.J. and Sowell, E.R.},\ndoi = {10.1111/acer.14945},\njournal = {Alcoholism: Clinical and Experimental Research},\nnumber = {11},\npages = {1980--1992},\ntitle = {{The impact of prenatal alcohol and/or tobacco exposure on brain structure in a large sample of children from a South African birth cohort}},\nvolume = {46},\nyear = {2022}\n}\n
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\n Background: Neuroimaging studies have emphasized the impact of prenatal alcohol exposure (PAE) on brain development, traditionally in heavily exposed participants. However, less is known about how naturally occurring community patterns of PAE (including light to moderate exposure) affect brain development, particularly in consideration of commonly occurring concurrent impacts of prenatal tobacco exposure (PTE). Methods: Three hundred thirty-two children (ages 8 to 12) living in South Africa's Cape Flats townships underwent structural magnetic resonance imaging. During pregnancy, their mothers reported alcohol and tobacco use, which was used to evaluate PAE and PTE effects on their children's brain structure. Analyses involved the main effects of PAE and PTE (and their interaction) and the effects of PAE and PTE quantity on cortical thickness, surface area, and volume. Results: After false-discovery rate (FDR) correction, PAE was associated with thinner left parahippocampal cortices, while PTE was associated with smaller cortical surface area in the bilateral pericalcarine, left lateral orbitofrontal, right posterior cingulate, right rostral anterior cingulate, left caudal middle frontal, and right caudal anterior cingulate gyri. There were no PAE × PTE interactions nor any associations of PAE and PTE exposure on volumetrics that survived FDR correction. Conclusion: PAE was associated with reduction in the structure of the medial temporal lobe, a brain region critical for learning and memory. PTE had stronger and broader associations, including with regions associated with executive function, reward processing, and emotional regulation, potentially reflecting continued postnatal exposure to tobacco (i.e., second-hand smoke exposure). These differential effects are discussed with respect to reduced PAE quantity in our exposed group versus prior studies within this geographical location, the deep poverty in which participants live, and the consequences of apartheid and racially and economically driven payment practices that contributed to heavy drinking in the region. Longer-term follow-up is needed to determine potential environmental and other moderators of the brain findings here and assess the extent to which they endure over time.\n
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\n \n\n \n \n \n \n \n \n A large-scale \\ENIGMA\\ multisite replication study of brain age in depression.\n \n \n \n \n\n\n \n Han, L. K M; Dinga, R.; Leenings, R.; Hahn, T.; Cole, J. H; Aftanas, L. I; Amod, A. R; Besteher, B.; Colle, R.; Corruble, E.; Couvy-Duchesne, B.; Danilenko, K. V; Fuentes-Claramonte, P.; Gonul, A. S.; Gotlib, I. H; Goya-Maldonado, R.; Groenewold, N. A; Hamilton, P.; Ichikawa, N.; Ipser, J. C; Itai, E.; Koopowitz, S.; Li, M.; Okada, G.; Okamoto, Y.; Churikova, O. S; Osipov, E. A; Penninx, B. W J H; Pomarol-Clotet, E.; Rodríguez-Cano, E.; Sacchet, M. D; Shinzato, H.; Sim, K.; Stein, D. J; Uyar-Demir, A.; Veltman, D. J; and Schmaal, L.\n\n\n \n\n\n\n Neuroimage: Reports, 2(4): 100149. dec 2022.\n \n\n\n\n
\n\n\n\n \n \n \"APaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{han_large-scale_2022,\nauthor = {Han, Laura K M and Dinga, Richard and Leenings, Ramona and Hahn, Tim and Cole, James H and Aftanas, Lyubomir I and Amod, Alyssa R and Besteher, Bianca and Colle, Romain and Corruble, Emmanuelle and Couvy-Duchesne, Baptiste and Danilenko, Konstantin V and Fuentes-Claramonte, Paola and Gonul, Ali Saffet and Gotlib, Ian H and Goya-Maldonado, Roberto and Groenewold, Nynke A and Hamilton, Paul and Ichikawa, Naho and Ipser, Jonathan C and Itai, Eri and Koopowitz, Sheri-Michelle and Li, Meng and Okada, Go and Okamoto, Yasumasa and Churikova, Olga S and Osipov, Evgeny A and Penninx, Brenda W J H and Pomarol-Clotet, Edith and Rodr{\\'{i}}guez-Cano, Elena and Sacchet, Matthew D and Shinzato, Hotaka and Sim, Kang and Stein, Dan J and Uyar-Demir, Aslihan and Veltman, Dick J and Schmaal, Lianne},\ndoi = {10.1016/j.ynirp.2022.100149},\nfile = {:Users/jacquelinebracher/Zotero/storage/CFKMWRK4/Han et al. - 2022 - A large-scale ENIGMA multisite replication study o.pdf:pdf},\nissn = {26669560},\njournal = {Neuroimage: Reports},\nmonth = {dec},\nnumber = {4},\npages = {100149},\ntitle = {{A large-scale {\\{}ENIGMA{\\}} multisite replication study of brain age in depression}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S2666956022000733},\nvolume = {2},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n The \\COVID\\-19 pandemic and problematic usage of the internet: \\Findings\\ from a diverse adult sample in \\South\\ \\Africa\\.\n \n \n \n \n\n\n \n Lochner, C.; Albertella, L.; Kidd, M.; Kilic, Z.; Ioannidis, K.; Grant, J. E; Yücel, M.; Stein, D. J; and Chamberlain, S. R\n\n\n \n\n\n\n Journal of Psychiatric Research, 153: 229–235. sep 2022.\n \n\n\n\n
\n\n\n\n \n \n \"ThePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{lochner_covid-19_2022,\nauthor = {Lochner, Christine and Albertella, Lucy and Kidd, Martin and Kilic, Zelal and Ioannidis, Konstantinos and Grant, Jon E and Y{\\"{u}}cel, Murat and Stein, Dan J and Chamberlain, Samuel R},\ndoi = {10.1016/j.jpsychires.2022.06.035},\nfile = {:Users/jacquelinebracher/Zotero/storage/9FR9VBLV/Lochner et al. - 2022 - The COVID-19 pandemic and problematic usage of the.pdf:pdf},\nissn = {00223956},\njournal = {Journal of Psychiatric Research},\nmonth = {sep},\npages = {229--235},\nshorttitle = {The {\\{}COVID{\\}}-19 pandemic and problematic usage of t},\ntitle = {{The {\\{}COVID{\\}}-19 pandemic and problematic usage of the internet: {\\{}Findings{\\}} from a diverse adult sample in {\\{}South{\\}} {\\{}Africa{\\}}}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S0022395622003405},\nvolume = {153},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Prevalence, profile and associations of cognitive impairment in \\Ugandan\\ first-episode psychosis patients.\n \n \n \n \n\n\n \n Mwesiga, E. K; Robbins, R.; Akena, D.; Koen, N.; Nakku, J.; Nakasujja, N.; and Stein, D. J\n\n\n \n\n\n\n Schizophrenia Research: Cognition, 28: 100234. jun 2022.\n \n\n\n\n
\n\n\n\n \n \n \"Prevalence,Paper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{mwesiga_prevalence_2022,\nauthor = {Mwesiga, Emmanuel K and Robbins, Reuben and Akena, Dickens and Koen, Nastassja and Nakku, Juliet and Nakasujja, Noeline and Stein, Dan J},\ndoi = {10.1016/j.scog.2021.100234},\nfile = {:Users/jacquelinebracher/Zotero/storage/LG62WZS5/Mwesiga et al. - 2022 - Prevalence, profile and associations of cognitive .pdf:pdf},\nissn = {22150013},\njournal = {Schizophrenia Research: Cognition},\nmonth = {jun},\npages = {100234},\ntitle = {{Prevalence, profile and associations of cognitive impairment in {\\{}Ugandan{\\}} first-episode psychosis patients}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S221500132100041X},\nvolume = {28},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n HIV-Related Stigma and Psychological Adjustment Among Perinatally HIV-Infected Youth in Cape Town, South Africa.\n \n \n \n \n\n\n \n Perez, A; Brittain, K; Phillips, N; Stein, D J; Zar, H J; Myer, L; and Hoare, J\n\n\n \n\n\n\n 2022.\n \n\n\n\n
\n\n\n\n \n \n \"HIV-RelatedPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Perez2022,\nannote = {Export Date: 29 December 2022},\nauthor = {Perez, A and Brittain, K and Phillips, N and Stein, D J and Zar, H J and Myer, L and Hoare, J},\ndoi = {10.1007/s10461-021-03398-3},\nnumber = {2},\npages = {434--442},\ntitle = {{HIV-Related Stigma and Psychological Adjustment Among Perinatally HIV-Infected Youth in Cape Town, South Africa}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85111589397{\\&}doi=10.1007{\\%}2Fs10461-021-03398-3{\\&}partnerID=40{\\&}md5=b64a38e02097832a10b6fa5e7c721df9},\nvolume = {26},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Self‐navigated prospective motion correction for \\textlessspan style=\"font-variant:small-caps;\"\\textgreater\\3D\\‐\\EPI\\\\textless/span\\textgreateracquisition.\n \n \n \n \n\n\n \n Bayih, S. G.; Jankiewicz, M.; Alhamud, A; Van Der Kouwe, A. J W; and Meintjes, E. M\n\n\n \n\n\n\n Magnetic Resonance in Medicine, 88(1): 211–223. jul 2022.\n \n\n\n\n
\n\n\n\n \n \n \"Self‐navigatedPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{bayih_selfnavigated_2022,\nabstract = {Purpose\nAlthough 3D EPI is more susceptible to motion artifacts than 2D EPI, it presents some benefits for functional MRI, including the absence of spin‐history artifacts, greater potential for parallel imaging acceleration, and better functional sensitivity in high‐resolution imaging. Here we present a self‐navigated 3D‐EPI sequence suitable for prospective motion‐corrected functional MRI without additional hardware or pulses.\n\n\nMethods\n\nFor each volume acquisition, the first 24 of the 52 partitions being acquired are accumulated to a new feedback block that was added to the image reconstruction pipeline. After zero‐filling the remaining partitions, the feedback block constructs a volumetric self‐navigator (\nvSNav\n), co‐registers it to the reference\nvSNav\nacquired during the first volume acquisition, and sends motion estimates to the sequence. The sequence then updates its FOV and acquires subsequent partitions with the adjusted FOV, until the next update is received. The sequence was validated without and with intentional motion in phantom and in vivo on a 3T Skyra.\n\n\n\nResults\n\nFor phantom scans, the FOV was updated 0.704 s after acquisition of the\nvSNav\npartitions, and for in vivo scans after 0.768 s. Both phantom and in vivo data demonstrated stable motion estimates in the absence of motion. For in vivo acquisitions, prospective head‐pose estimates using the\nvSNav'\ns and retrospective estimates with FLIRT (FMRIB's Linear Image Registration Tool) agreed to within 0.23 mm ({\\textless}10{\\%} of the slice thickness) and 0.14° in all directions.\n\n\n\nConclusion\nDepending when motion occurs during a volume acquisition, the proposed method fully corrects the FOV and recovers image quality within one volume acquisition.},\nauthor = {Bayih, Samuel Getaneh and Jankiewicz, Marcin and Alhamud, A and {Van Der Kouwe}, Andr{\\'{e}} J W and Meintjes, Ernesta M},\ndoi = {10.1002/mrm.29202},\nissn = {0740-3194, 1522-2594},\njournal = {Magnetic Resonance in Medicine},\nmonth = {jul},\nnumber = {1},\npages = {211--223},\nshorttitle = {Self‐navigated prospective motion correction for {\\textless}},\ntitle = {{Self‐navigated prospective motion correction for {\\textless}span style="font-variant:small-caps;"{\\textgreater}{\\{}3D{\\}}‐{\\{}EPI{\\}}{\\textless}/span{\\textgreater}acquisition}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1002/mrm.29202},\nvolume = {88},\nyear = {2022}\n}\n
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\n Purpose Although 3D EPI is more susceptible to motion artifacts than 2D EPI, it presents some benefits for functional MRI, including the absence of spin‐history artifacts, greater potential for parallel imaging acceleration, and better functional sensitivity in high‐resolution imaging. Here we present a self‐navigated 3D‐EPI sequence suitable for prospective motion‐corrected functional MRI without additional hardware or pulses. Methods For each volume acquisition, the first 24 of the 52 partitions being acquired are accumulated to a new feedback block that was added to the image reconstruction pipeline. After zero‐filling the remaining partitions, the feedback block constructs a volumetric self‐navigator ( vSNav ), co‐registers it to the reference vSNav acquired during the first volume acquisition, and sends motion estimates to the sequence. The sequence then updates its FOV and acquires subsequent partitions with the adjusted FOV, until the next update is received. The sequence was validated without and with intentional motion in phantom and in vivo on a 3T Skyra. Results For phantom scans, the FOV was updated 0.704 s after acquisition of the vSNav partitions, and for in vivo scans after 0.768 s. Both phantom and in vivo data demonstrated stable motion estimates in the absence of motion. For in vivo acquisitions, prospective head‐pose estimates using the vSNav' s and retrospective estimates with FLIRT (FMRIB's Linear Image Registration Tool) agreed to within 0.23 mm (\\textless10% of the slice thickness) and 0.14° in all directions. Conclusion Depending when motion occurs during a volume acquisition, the proposed method fully corrects the FOV and recovers image quality within one volume acquisition.\n
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\n \n\n \n \n \n \n \n \n Compromised interhemispheric transfer of information partially mediates cognitive function deficits in adolescents with fetal alcohol syndrome.\n \n \n \n \n\n\n \n Biffen, S. C; Dodge, N. C; Warton, C. M R; Molteno, C. D; Jacobson, J. L; Meintjes, E. M; and Jacobson, S. W\n\n\n \n\n\n\n Alcoholism: Clinical and Experimental Research, 46(4): 517–529. apr 2022.\n \n\n\n\n
\n\n\n\n \n \n \"CompromisedPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{biffen_compromised_2022,\nabstract = {Abstract\n\nBackground\nPrenatal alcohol exposure (PAE) has been associated with compromised interhemispheric transfer of tactile stimuli in childhood and structural changes to the corpus callosum (CC). In this study, we used a finger localization task (FLT) to investigate whether interhemispheric transfer deficits persist in adolescence; whether effects of PAE on perceptual reasoning, working memory, and executive function are mediated by deficits in interhemispheric transfer of information; and whether CC size in childhood predicts FLT performance in adolescence.\n\n\nMethods\nParticipants, aged 16 to 17 years, were from the Cape Town Longitudinal Cohort, whose mothers were recruited during pregnancy and interviewed regarding their alcohol use using the timeline follow‐back method. Diagnoses of fetal alcohol syndrome (FAS) and partial FAS (PFAS) were determined by two expert dysmorphologists; nonsyndromal exposed children were designated as heavily exposed (HE); those born to abstainers or light drinkers, as controls. The FLT was administered to 74 participants (12 FAS, 16 PFAS, 14 HE and 32 controls). CC size at age 9 to 12 years was available for 35 participants (7 FAS, 13 PFAS, 5 HE and 10 control).\n\n\nResults\nAlthough the degree of PAE was similar in the FAS, PFAS, and HE groups, only the adolescents with FAS showed more transfer‐related errors than controls in conditions in which one finger was stimulated. FLT performance mediated the effects of FAS on perceptual reasoning and executive function. In the subsample for which neuroimaging data from childhood were available, there was an association among adolescents with PAE of smaller CC volumes with more transfer‐related errors on the one‐finger/hand hidden condition, suggesting that CC damage previously seen in childhood continues to impact function through adolescence.\n\n\nConclusions\nThis study provides evidence of compromised interhemispheric transfer of information in adolescents with FAS, while those with PFAS or heavy exposed nonsyndromal individuals are apparently spared. It is the first to show that PAE effects on important aspects of cognitive function are partially mediated by deficits in the interhemispheric transfer of information.},\nauthor = {Biffen, Stevie C and Dodge, Neil C and Warton, Christopher M R and Molteno, Christopher D and Jacobson, Joseph L and Meintjes, Ernesta M and Jacobson, Sandra W},\ndoi = {10.1111/acer.14795},\nfile = {:Users/jacquelinebracher/Zotero/storage/T9S9P8KD/Biffen et al. - 2022 - Compromised interhemispheric transfer of informati.pdf:pdf},\nissn = {0145-6008, 1530-0277},\njournal = {Alcoholism: Clinical and Experimental Research},\nmonth = {apr},\nnumber = {4},\npages = {517--529},\ntitle = {{Compromised interhemispheric transfer of information partially mediates cognitive function deficits in adolescents with fetal alcohol syndrome}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1111/acer.14795},\nvolume = {46},\nyear = {2022}\n}\n
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\n Abstract Background Prenatal alcohol exposure (PAE) has been associated with compromised interhemispheric transfer of tactile stimuli in childhood and structural changes to the corpus callosum (CC). In this study, we used a finger localization task (FLT) to investigate whether interhemispheric transfer deficits persist in adolescence; whether effects of PAE on perceptual reasoning, working memory, and executive function are mediated by deficits in interhemispheric transfer of information; and whether CC size in childhood predicts FLT performance in adolescence. Methods Participants, aged 16 to 17 years, were from the Cape Town Longitudinal Cohort, whose mothers were recruited during pregnancy and interviewed regarding their alcohol use using the timeline follow‐back method. Diagnoses of fetal alcohol syndrome (FAS) and partial FAS (PFAS) were determined by two expert dysmorphologists; nonsyndromal exposed children were designated as heavily exposed (HE); those born to abstainers or light drinkers, as controls. The FLT was administered to 74 participants (12 FAS, 16 PFAS, 14 HE and 32 controls). CC size at age 9 to 12 years was available for 35 participants (7 FAS, 13 PFAS, 5 HE and 10 control). Results Although the degree of PAE was similar in the FAS, PFAS, and HE groups, only the adolescents with FAS showed more transfer‐related errors than controls in conditions in which one finger was stimulated. FLT performance mediated the effects of FAS on perceptual reasoning and executive function. In the subsample for which neuroimaging data from childhood were available, there was an association among adolescents with PAE of smaller CC volumes with more transfer‐related errors on the one‐finger/hand hidden condition, suggesting that CC damage previously seen in childhood continues to impact function through adolescence. Conclusions This study provides evidence of compromised interhemispheric transfer of information in adolescents with FAS, while those with PFAS or heavy exposed nonsyndromal individuals are apparently spared. It is the first to show that PAE effects on important aspects of cognitive function are partially mediated by deficits in the interhemispheric transfer of information.\n
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\n \n\n \n \n \n \n \n \n Tailored community engagement to address the genetics diversity gap.\n \n \n \n \n\n\n \n Hanchard, N A; Chahrour, M; and de Vries, J\n\n\n \n\n\n\n 2022.\n \n\n\n\n
\n\n\n\n \n \n \"TailoredPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Hanchard2022,\nannote = {Export Date: 29 December 2022},\nauthor = {Hanchard, N A and Chahrour, M and de Vries, J},\ndoi = {10.1016/j.medj.2022.05.010},\nfile = {:Users/jacquelinebracher/Zotero/storage/7YR6EJ8D/Hanchard et al. - 2022 - Tailored community engagement to address the genet.pdf:pdf},\nnumber = {6},\npages = {369--370},\ntitle = {{Tailored community engagement to address the genetics diversity gap}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85131663283{\\&}doi=10.1016{\\%}2Fj.medj.2022.05.010{\\&}partnerID=40{\\&}md5=fc9e327426d73bb32e0f0a60a65b9618},\nvolume = {3},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Capacity for cortical excitation is reduced in psychotic disorders: \\An\\ investigation of the \\TMS\\-\\EMG\\ cortical silent period.\n \n \n \n \n\n\n \n Howells, F. M; Hsieh, J. H; Temmingh, H. S; Baldwin, D. S; and Stein, D. J\n\n\n \n\n\n\n Schizophrenia Research, 240: 73–77. feb 2022.\n \n\n\n\n
\n\n\n\n \n \n \"CapacityPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{howells_capacity_2022,\nauthor = {Howells, Fleur M and Hsieh, Jennifer H and Temmingh, Henk S and Baldwin, David S and Stein, Dan J},\ndoi = {10.1016/j.schres.2021.12.012},\nfile = {:Users/jacquelinebracher/Zotero/storage/BVUN543H/Howells et al. - 2022 - Capacity for cortical excitation is reduced in psy.pdf:pdf},\nissn = {09209964},\njournal = {Schizophrenia Research},\nmonth = {feb},\npages = {73--77},\nshorttitle = {Capacity for cortical excitation is reduced in psy},\ntitle = {{Capacity for cortical excitation is reduced in psychotic disorders: {\\{}An{\\}} investigation of the {\\{}TMS{\\}}-{\\{}EMG{\\}} cortical silent period}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S0920996421004965},\nvolume = {240},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n A structured, blended learning program towards proficiency in epileptology: the launch of the \\ILAE\\ \\Academy\\ \\Level\\ 2 \\Program\\.\n \n \n \n \n\n\n \n Blümcke, I.; Biesel, E.; Bedenlier, S.; Händel, M.; Wilmshurst, J.; Mehndiratta, M. M.; Yacubian, E. M.; Cendes, F.; Arzimanoglou, A.; Beniczky, S.; Wolf, P.; Giavasi, C.; Baxendale, S.; Shisler, P.; and Wiebe, S.\n\n\n \n\n\n\n Epileptic Disorders, 24(5): 737–750. oct 2022.\n \n\n\n\n
\n\n\n\n \n \n \"APaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{blumcke_structured_2022,\nabstract = {Abstract\n\nThe ILAE Academy is the online learning platform of the International League Against Epilepsy (ILAE) and offers a structured educational program addressing the competency‐based ILAE curriculum in epileptology. The platform was launched in July 2020 with a self‐paced course portfolio of interactive e‐learning modules addressing ILAE Level 1 learning objectives, defined as the entry level in epileptology. Using feedback questionnaires from completed Level 1 courses as well as sociodemographic and learning‐related data obtained from 47 participants, we show that over 50{\\%} of learners have an entry level in epileptology and do not have access to on‐site training and over 40{\\%} do not have access to on‐site training. Most respondents found the case‐based e‐learning modules relevant to their practice needs, and the time for completion was regarded as viable for most, reiterating the value of an online self‐paced training in the field. Participants who have successfully completed all compulsory e‐learning material of the Level 1 program and received their final certificate will now be eligible to subscribe to the Level 2 program. The Level 2 program addressing the proficiency level of the ILAE curriculum of epileptology was launched on the ILAE Academy platform in May 2022. The Level 2 program will offer an evolving series of self‐paced, interactive, case‐based e‐learning modules on diagnosis, treatment, and counseling of common as well as rare epilepsies at a higher level of care. An interactive online EEG and MRI reader was developed and is embedded into the course content to satisfy the demands of the learners. The hallmark of this level will be the blended learning with tutored online courses,\ne.g.\n, the established VIREPA courses on EEG and the newly introduced VIREPA MRI program. Our distinguished faculty will hold live tutored online courses in small groups in various languages and continental time zones. Finally, the ILAE face‐to‐face curricular teaching courses at summer schools and congresses will represent another pillar of this advanced teaching level. The ILAE Academy will also provide Continuing Medical Education (CME) credits to support career planning in epileptology.},\nauthor = {Bl{\\"{u}}mcke, Ingmar and Biesel, Eva and Bedenlier, Svenja and H{\\"{a}}ndel, Marion and Wilmshurst, Jo and Mehndiratta, Man Mohan and Yacubian, Elza M{\\'{a}}rcia and Cendes, Fernando and Arzimanoglou, Alexis and Beniczky, Sandor and Wolf, Peter and Giavasi, Christina and Baxendale, Sallie and Shisler, Priscilla and Wiebe, Samuel},\ndoi = {10.1684/epd.2022.1462},\nfile = {:Users/jacquelinebracher/Zotero/storage/NKMTWQ7F/Bl{\\"{u}}mcke et al. - 2022 - A structured, blended learning program towards pro.pdf:pdf},\nissn = {1294-9361, 1950-6945},\njournal = {Epileptic Disorders},\nmonth = {oct},\nnumber = {5},\npages = {737--750},\nshorttitle = {A structured, blended learning program towards pro},\ntitle = {{A structured, blended learning program towards proficiency in epileptology: the launch of the {\\{}ILAE{\\}} {\\{}Academy{\\}} {\\{}Level{\\}} 2 {\\{}Program{\\}}}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1684/epd.2022.1462},\nvolume = {24},\nyear = {2022}\n}\n
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\n Abstract The ILAE Academy is the online learning platform of the International League Against Epilepsy (ILAE) and offers a structured educational program addressing the competency‐based ILAE curriculum in epileptology. The platform was launched in July 2020 with a self‐paced course portfolio of interactive e‐learning modules addressing ILAE Level 1 learning objectives, defined as the entry level in epileptology. Using feedback questionnaires from completed Level 1 courses as well as sociodemographic and learning‐related data obtained from 47 participants, we show that over 50% of learners have an entry level in epileptology and do not have access to on‐site training and over 40% do not have access to on‐site training. Most respondents found the case‐based e‐learning modules relevant to their practice needs, and the time for completion was regarded as viable for most, reiterating the value of an online self‐paced training in the field. Participants who have successfully completed all compulsory e‐learning material of the Level 1 program and received their final certificate will now be eligible to subscribe to the Level 2 program. The Level 2 program addressing the proficiency level of the ILAE curriculum of epileptology was launched on the ILAE Academy platform in May 2022. The Level 2 program will offer an evolving series of self‐paced, interactive, case‐based e‐learning modules on diagnosis, treatment, and counseling of common as well as rare epilepsies at a higher level of care. An interactive online EEG and MRI reader was developed and is embedded into the course content to satisfy the demands of the learners. The hallmark of this level will be the blended learning with tutored online courses, e.g. , the established VIREPA courses on EEG and the newly introduced VIREPA MRI program. Our distinguished faculty will hold live tutored online courses in small groups in various languages and continental time zones. Finally, the ILAE face‐to‐face curricular teaching courses at summer schools and congresses will represent another pillar of this advanced teaching level. The ILAE Academy will also provide Continuing Medical Education (CME) credits to support career planning in epileptology.\n
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\n \n\n \n \n \n \n \n \n Pain, health-related quality of life, and mental health of adolescents and adults with cerebral palsy in urban South Africa.\n \n \n \n \n\n\n \n Salie, R; Eken, M M; Donald, K A; Fieggen, A G; and Langerak, N G\n\n\n \n\n\n\n 2022.\n \n\n\n\n
\n\n\n\n \n \n \"Pain,Paper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Salie2022,\nannote = {Export Date: 29 December 2022},\nauthor = {Salie, R and Eken, M M and Donald, K A and Fieggen, A G and Langerak, N G},\ndoi = {10.1080/09638288.2021.1916101},\nnumber = {17},\npages = {4672--4680},\ntitle = {{Pain, health-related quality of life, and mental health of adolescents and adults with cerebral palsy in urban South Africa}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85105145219{\\&}doi=10.1080{\\%}2F09638288.2021.1916101{\\&}partnerID=40{\\&}md5=818432f7e3aca8c3e48bdee5d54915eb},\nvolume = {44},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n A comparison of methods to harmonize cortical thickness measurements across scanners and sites.\n \n \n \n \n\n\n \n Sun, D; Rakesh, G; Haswell, C C; Logue, M; Baird, C L; O'Leary, E N; Cotton, A S; Xie, H; Tamburrino, M; Chen, T; Dennis, E L; Jahanshad, N; Salminen, L E; Thomopoulos, S I; Rashid, F; Ching, C R K; Koch, S B J; Frijling, J L; Nawijn, L; van Zuiden, M; Zhu, X; Suarez-Jimenez, B; Sierk, A; Walter, H; Manthey, A; Stevens, J S; Fani, N; van Rooij, S J H; Stein, M; Bomyea, J; Koerte, I K; Choi, K; van der Werff, S J A; Vermeiren, R.; Herzog, J; Lebois, L A M; Baker, J T; Olson, E A; Straube, T; Korgaonkar, M S; Andrew, E; Zhu, Y; Li, G; Ipser, J; Hudson, A R; Peverill, M; Sambrook, K; Gordon, E; Baugh, L; Forster, G; Simons, R M; Simons, J S; Magnotta, V; Maron-Katz, A; du Plessis, S; Disner, S G; Davenport, N; Grupe, D W; Nitschke, J B; DeRoon-Cassini, T A; Fitzgerald, J M; Krystal, J H; Levy, I; Olff, M; Veltman, D J; Wang, L; Neria, Y; De Bellis, M D; Jovanovic, T; Daniels, J K; Shenton, M; van de Wee, N J A; Schmahl, C; Kaufman, M L; Rosso, I M; Sponheim, S R; Hofmann, D B; Bryant, R A; Fercho, K A; Stein, D J; Mueller, S C; Hosseini, B; Phan, K L; McLaughlin, K A; Davidson, R J; Larson, C L; May, G; Nelson, S M; Abdallah, C G; Gomaa, H; Etkin, A; Seedat, S; Harpaz-Rotem, I; Liberzon, I; van Erp, T G M; Quidé, Y; Wang, X; Thompson, P M; and Morey, R A\n\n\n \n\n\n\n 2022.\n \n\n\n\n
\n\n\n\n \n \n \"APaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Sun2022a,\nannote = {Export Date: 29 December 2022},\nauthor = {Sun, D and Rakesh, G and Haswell, C C and Logue, M and Baird, C L and O'Leary, E N and Cotton, A S and Xie, H and Tamburrino, M and Chen, T and Dennis, E L and Jahanshad, N and Salminen, L E and Thomopoulos, S I and Rashid, F and Ching, C R K and Koch, S B J and Frijling, J L and Nawijn, L and van Zuiden, M and Zhu, X and Suarez-Jimenez, B and Sierk, A and Walter, H and Manthey, A and Stevens, J S and Fani, N and van Rooij, S J H and Stein, M and Bomyea, J and Koerte, I K and Choi, K and van der Werff, S J A and Vermeiren, R.R.J.M. and Herzog, J and Lebois, L A M and Baker, J T and Olson, E A and Straube, T and Korgaonkar, M S and Andrew, E and Zhu, Y and Li, G and Ipser, J and Hudson, A R and Peverill, M and Sambrook, K and Gordon, E and Baugh, L and Forster, G and Simons, R M and Simons, J S and Magnotta, V and Maron-Katz, A and du Plessis, S and Disner, S G and Davenport, N and Grupe, D W and Nitschke, J B and DeRoon-Cassini, T A and Fitzgerald, J M and Krystal, J H and Levy, I and Olff, M and Veltman, D J and Wang, L and Neria, Y and {De Bellis}, M D and Jovanovic, T and Daniels, J K and Shenton, M and van de Wee, N J A and Schmahl, C and Kaufman, M L and Rosso, I M and Sponheim, S R and Hofmann, D B and Bryant, R A and Fercho, K A and Stein, D J and Mueller, S C and Hosseini, B and Phan, K L and McLaughlin, K A and Davidson, R J and Larson, C L and May, G and Nelson, S M and Abdallah, C G and Gomaa, H and Etkin, A and Seedat, S and Harpaz-Rotem, I and Liberzon, I and van Erp, T G M and Quid{\\'{e}}, Y and Wang, X and Thompson, P M and Morey, R A},\ndoi = {10.1016/j.neuroimage.2022.119509},\nfile = {:Users/jacquelinebracher/Zotero/storage/JN3KCHVC/Sun et al. - 2022 - A comparison of methods to harmonize cortical thic.pdf:pdf},\ntitle = {{A comparison of methods to harmonize cortical thickness measurements across scanners and sites}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85135967385{\\&}doi=10.1016{\\%}2Fj.neuroimage.2022.119509{\\&}partnerID=40{\\&}md5=2197d841f324439283f0972c94b34baf},\nvolume = {261},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Greater male than female variability in regional brain structure across the lifespan.\n \n \n \n \n\n\n \n Wierenga, L M; Doucet, G E; Dima, D; Agartz, I; Aghajani, M; Akudjedu, T N; Albajes-Eizagirre, A; Alnæs, D; Alpert, K I; Andreassen, O A; Anticevic, A; Asherson, P; Banaschewski, T; Bargallo, N; Baumeister, S; Baur-Streubel, R; Bertolino, A; Bonvino, A; Boomsma, D I; Borgwardt, S; Bourque, J; den Braber, A; Brandeis, D; Breier, A; Brodaty, H; Brouwer, R M; Buitelaar, J K; Busatto, G F; Calhoun, V D; Canales-Rodríguez, E J; Cannon, D M; Caseras, X; Castellanos, F X; Chaim-Avancini, T M; Ching, C R K; Clark, V P; Conrod, P J; Conzelmann, A; Crivello, F; Davey, C G; Dickie, E W; Ehrlich, S; van't Ent, D; Fisher, S E; Fouche, J.; Franke, B; Fuentes-Claramonte, P; de Geus, E J C; Di Giorgio, A; Glahn, D C; Gotlib, I H; Grabe, H J; Gruber, O; Gruner, P; Gur, R E; Gur, R C; Gurholt, T P; de Haan, L; Haatveit, B; Harrison, B J; Hartman, C A; Hatton, S N; Heslenfeld, D J; van den Heuvel, O A; Hickie, I B; Hoekstra, P J; Hohmann, S; Holmes, A J; Hoogman, M; Hosten, N; Howells, F M; Hulshoff Pol, H E; Huyser, C; Jahanshad, N; James, A C; Jiang, J; Jönsson, E G; Joska, J A; Kalnin, A J; Klein, M; Koenders, L; Kolskår, K K; Krämer, B; Kuntsi, J; Lagopoulos, J; Lazaro, L; Lebedeva, I S; Lee, P H; Lochner, C; Machielsen, M W J; Maingault, S; Martin, N G; Martínez-Zalacaín, I; Mataix-Cols, D; Mazoyer, B; McDonald, B C; McDonald, C; McIntosh, A M; McMahon, K L; McPhilemy, G; van der Meer, D; Menchón, J M; Naaijen, J; Nyberg, L; Oosterlaan, J; Paloyelis, Y; Pauli, P; Pergola, G; Pomarol-Clotet, E; Portella, M J; Radua, J; Reif, A; Richard, G; Roffman, J L; Rosa, P G P; Sacchet, M D; Sachdev, P S; Salvador, R; Sarró, S; Satterthwaite, T D; Saykin, A J; Serpa, M H; Sim, K; Simmons, A; Smoller, J W; Sommer, I E; Soriano-Mas, C; Stein, D J; Strike, L T; Szeszko, P R; Temmingh, H S; Thomopoulos, S I; Tomyshev, A S; Trollor, J N; Uhlmann, A; Veer, I M; Veltman, D J; Voineskos, A; Völzke, H; Walter, H; Wang, L; Wang, Y; Weber, B; Wen, W; West, J D; Westlye, L T; Whalley, H C; Williams, S C R; Wittfeld, K; Wolf, D H; Wright, M J; Yoncheva, Y N; Zanetti, M V; Ziegler, G C; de Zubicaray, G I; Thompson, P M; Crone, E A; Frangou, S; Tamnes, C K; and Consortium, K. S. P. (.\n\n\n \n\n\n\n 2022.\n \n\n\n\n
\n\n\n\n \n \n \"GreaterPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Wierenga2022,\nannote = {Export Date: 29 December 2022},\nauthor = {Wierenga, L M and Doucet, G E and Dima, D and Agartz, I and Aghajani, M and Akudjedu, T N and Albajes-Eizagirre, A and Aln{\\ae}s, D and Alpert, K I and Andreassen, O A and Anticevic, A and Asherson, P and Banaschewski, T and Bargallo, N and Baumeister, S and Baur-Streubel, R and Bertolino, A and Bonvino, A and Boomsma, D I and Borgwardt, S and Bourque, J and den Braber, A and Brandeis, D and Breier, A and Brodaty, H and Brouwer, R M and Buitelaar, J K and Busatto, G F and Calhoun, V D and Canales-Rodr{\\'{i}}guez, E J and Cannon, D M and Caseras, X and Castellanos, F X and Chaim-Avancini, T M and Ching, C R K and Clark, V P and Conrod, P J and Conzelmann, A and Crivello, F and Davey, C G and Dickie, E W and Ehrlich, S and van't Ent, D and Fisher, S E and Fouche, J.-P. and Franke, B and Fuentes-Claramonte, P and de Geus, E J C and {Di Giorgio}, A and Glahn, D C and Gotlib, I H and Grabe, H J and Gruber, O and Gruner, P and Gur, R E and Gur, R C and Gurholt, T P and de Haan, L and Haatveit, B and Harrison, B J and Hartman, C A and Hatton, S N and Heslenfeld, D J and van den Heuvel, O A and Hickie, I B and Hoekstra, P J and Hohmann, S and Holmes, A J and Hoogman, M and Hosten, N and Howells, F M and {Hulshoff Pol}, H E and Huyser, C and Jahanshad, N and James, A C and Jiang, J and J{\\"{o}}nsson, E G and Joska, J A and Kalnin, A J and Klein, M and Koenders, L and Kolsk{\\aa}r, K K and Kr{\\"{a}}mer, B and Kuntsi, J and Lagopoulos, J and Lazaro, L and Lebedeva, I S and Lee, P H and Lochner, C and Machielsen, M W J and Maingault, S and Martin, N G and Mart{\\'{i}}nez-Zalaca{\\'{i}}n, I and Mataix-Cols, D and Mazoyer, B and McDonald, B C and McDonald, C and McIntosh, A M and McMahon, K L and McPhilemy, G and van der Meer, D and Mench{\\'{o}}n, J M and Naaijen, J and Nyberg, L and Oosterlaan, J and Paloyelis, Y and Pauli, P and Pergola, G and Pomarol-Clotet, E and Portella, M J and Radua, J and Reif, A and Richard, G and Roffman, J L and Rosa, P G P and Sacchet, M D and Sachdev, P S and Salvador, R and Sarr{\\'{o}}, S and Satterthwaite, T D and Saykin, A J and Serpa, M H and Sim, K and Simmons, A and Smoller, J W and Sommer, I E and Soriano-Mas, C and Stein, D J and Strike, L T and Szeszko, P R and Temmingh, H S and Thomopoulos, S I and Tomyshev, A S and Trollor, J N and Uhlmann, A and Veer, I M and Veltman, D J and Voineskos, A and V{\\"{o}}lzke, H and Walter, H and Wang, L and Wang, Y and Weber, B and Wen, W and West, J D and Westlye, L T and Whalley, H C and Williams, S C R and Wittfeld, K and Wolf, D H and Wright, M J and Yoncheva, Y N and Zanetti, M V and Ziegler, G C and de Zubicaray, G I and Thompson, P M and Crone, E A and Frangou, S and Tamnes, C K and Consortium, Karolinska Schizophrenia Project (KaSP)},\ndoi = {10.1002/hbm.25204},\nfile = {:Users/jacquelinebracher/Zotero/storage/9C6ULM4Z/Wierenga et al. - 2022 - Greater male than female variability in regional b.pdf:pdf},\nnumber = {1},\npages = {470--499},\ntitle = {{Greater male than female variability in regional brain structure across the lifespan}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85092397145{\\&}doi=10.1002{\\%}2Fhbm.25204{\\&}partnerID=40{\\&}md5=6f2ab6e92af575fd7f41e80449a3e25d},\nvolume = {43},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Advances in problematic usage of the internet research – \\A\\ narrative review by experts from the \\European\\ network for problematic usage of the internet.\n \n \n \n \n\n\n \n Fineberg, N. A; Menchón, J. M; Hall, N.; Dell'Osso, B.; Brand, M.; Potenza, M. N; Chamberlain, S. R; Cirnigliaro, G.; Lochner, C.; Billieux, J.; Demetrovics, Z.; Rumpf, H. J.; Müller, A.; Castro-Calvo, J.; Hollander, E.; Burkauskas, J.; Grünblatt, E.; Walitza, S.; Corazza, O.; King, D. L; Stein, D. J; Grant, J. E; Pallanti, S.; Bowden-Jones, H.; Ameringen, M. V.; Ioannidis, K.; Carmi, L.; Goudriaan, A. E; Martinotti, G.; Sales, C. M D; Jones, J.; Gjoneska, B.; Király, O.; Benatti, B.; Vismara, M.; Pellegrini, L.; Conti, D.; Cataldo, I.; Riva, G. M; Yücel, M.; Flayelle, M.; Hall, T.; Griffiths, M.; and Zohar, J.\n\n\n \n\n\n\n Comprehensive Psychiatry, 118: 152346. oct 2022.\n \n\n\n\n
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@article{fineberg_advances_2022,\nauthor = {Fineberg, Naomi A and Mench{\\'{o}}n, Jos{\\'{e}} M and Hall, Natalie and Dell'Osso, Bernardo and Brand, Matthias and Potenza, Marc N and Chamberlain, Samuel R and Cirnigliaro, Giovanna and Lochner, Christine and Billieux, Jo{\\"{e}}l and Demetrovics, Zsolt and Rumpf, Hans J{\\"{u}}rgen and M{\\"{u}}ller, Astrid and Castro-Calvo, Jes{\\'{u}}s and Hollander, Eric and Burkauskas, Julius and Gr{\\"{u}}nblatt, Edna and Walitza, Susanne and Corazza, Ornella and King, Daniel L and Stein, Dan J and Grant, Jon E and Pallanti, Stefano and Bowden-Jones, Henrietta and Ameringen, Michael Van and Ioannidis, Konstantinos and Carmi, Lior and Goudriaan, Anna E and Martinotti, Giovanni and Sales, C{\\'{e}}lia M D and Jones, Julia and Gjoneska, Biljiana and Kir{\\'{a}}ly, Orsolya and Benatti, Beatrice and Vismara, Matteo and Pellegrini, Luca and Conti, Dario and Cataldo, Ilaria and Riva, Gianluigi M and Y{\\"{u}}cel, Murat and Flayelle, Ma{\\`{e}}va and Hall, Thomas and Griffiths, Morgan and Zohar, Joseph},\ndoi = {10.1016/j.comppsych.2022.152346},\nfile = {:Users/jacquelinebracher/Zotero/storage/HNGB7SBC/Fineberg et al. - 2022 - Advances in problematic usage of the internet rese.pdf:pdf},\nissn = {0010440X},\njournal = {Comprehensive Psychiatry},\nmonth = {oct},\npages = {152346},\ntitle = {{Advances in problematic usage of the internet research – {\\{}A{\\}} narrative review by experts from the {\\{}European{\\}} network for problematic usage of the internet}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S0010440X22000529},\nvolume = {118},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Associations of medication with subcortical morphology across the lifespan in \\OCD\\: \\Results\\ from the international \\ENIGMA\\ \\Consortium\\.\n \n \n \n \n\n\n \n Ivanov, I.; Boedhoe, P. S W; Abe, Y.; Alonso, P.; Ameis, S. H; Arnold, P. D; Balachander, S.; Baker, J. T; Banaj, N.; Bargalló, N.; Batistuzzo, M. C; Benedetti, F.; Beucke, J. C; Bollettini, I.; Brem, S.; Brennan, B. P; Buitelaar, J.; Calvo, R.; Cheng, Y.; Cho, K. I. K; Dallaspezia, S.; Denys, D.; Diniz, J. B; Ely, B. A; Feusner, J. D; Ferreira, S.; Fitzgerald, K. D; Fontaine, M.; Gruner, P.; Hanna, G. L; Hirano, Y.; Hoexter, M. Q; Huyser, C.; Ikari, K.; James, A.; Jaspers-Fayer, F.; Jiang, H.; Kathmann, N.; Kaufmann, C.; Kim, M.; Koch, K.; Kwon, J. S.; Lázaro, L.; Liu, Y.; Lochner, C.; Marsh, R.; Martínez-Zalacaín, I.; Mataix-Cols, D.; Menchón, J. M; Minuzzi, L.; Morer, A.; Morgado, P.; Nakagawa, A.; Nakamae, T.; Nakao, T.; Narayanaswamy, J. C; Nurmi, E. L; Oh, S.; Perriello, C.; Piacentini, J. C; Picó-Pérez, M.; Piras, F.; Piras, F.; Reddy, Y C J.; Manrique, D. R.; Sakai, Y.; Shimizu, E.; Simpson, H B.; Soreni, N.; Soriano-Mas, C.; Spalletta, G.; Stern, E. R; Stevens, M. C; Stewart, S E.; Szeszko, P. R; Tolin, D. F; Van Rooij, D.; Veltman, D. J; Van Der Werf, Y. D; Van Wingen, G. A; Venkatasubramanian, G.; Walitza, S.; Wang, Z.; Watanabe, A.; Wolters, L. H; Xu, X.; Yun, J.; Zarei, M.; Zhang, F.; Zhao, Q.; Jahanshad, N.; Thomopoulos, S. I; Thompson, P. M; Stein, D. J; Van Den Heuvel, O. A; O'Neill, J.; Poletti, S.; Fridgeirsson, E. A.; Ikuta, T.; De Wit, S. J; Vriend, C.; Kasprzak, S.; Kuno, M.; Takahashi, J.; Miguel, E. C; Shavitt, R. G; Hough, M.; Pariente, J. C; Ortiz, A. E; Bertolín, S.; Real, E.; Segalàs, C.; Moreira, P. S.; Sousa, N.; Narumoto, J.; Yamada, K.; Tang, J.; Fouche, J.; Kim, T.; Choi, S.; Ha, M.; and Park, S.\n\n\n \n\n\n\n Journal of Affective Disorders, 318: 204–216. dec 2022.\n \n\n\n\n
\n\n\n\n \n \n \"AssociationsPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{ivanov_associations_2022,\nauthor = {Ivanov, Iliyan and Boedhoe, Premika S W and Abe, Yoshinari and Alonso, Pino and Ameis, Stephanie H and Arnold, Paul D and Balachander, Srinivas and Baker, Justin T and Banaj, Nerisa and Bargall{\\'{o}}, Nuria and Batistuzzo, Marcelo C and Benedetti, Francesco and Beucke, Jan C and Bollettini, Irene and Brem, Silvia and Brennan, Brian P and Buitelaar, Jan and Calvo, Rosa and Cheng, Yuqi and Cho, Kang Ik K and Dallaspezia, Sara and Denys, Damiaan and Diniz, Juliana B and Ely, Benjamin A and Feusner, Jamie D and Ferreira, S{\\'{o}}nia and Fitzgerald, Kate D and Fontaine, Martine and Gruner, Patricia and Hanna, Gregory L and Hirano, Yoshiyuki and Hoexter, Marcelo Q and Huyser, Chaim and Ikari, Keisuke and James, Anthony and Jaspers-Fayer, Fern and Jiang, Hongyan and Kathmann, Norbert and Kaufmann, Christian and Kim, Minah and Koch, Kathrin and Kwon, Jun Soo and L{\\'{a}}zaro, Luisa and Liu, Yanni and Lochner, Christine and Marsh, Rachel and Mart{\\'{i}}nez-Zalaca{\\'{i}}n, Ignacio and Mataix-Cols, David and Mench{\\'{o}}n, Jos{\\'{e}} M and Minuzzi, Luciano and Morer, Astrid and Morgado, Pedro and Nakagawa, Akiko and Nakamae, Takashi and Nakao, Tomohiro and Narayanaswamy, Janardhanan C and Nurmi, Erika L and Oh, Sanghoon and Perriello, Chris and Piacentini, John C and Pic{\\'{o}}-P{\\'{e}}rez, Maria and Piras, Fabrizio and Piras, Federica and Reddy, Y C Janardhan and Manrique, Daniela Rodriguez and Sakai, Yuki and Shimizu, Eiji and Simpson, H Blair and Soreni, Noam and Soriano-Mas, Carles and Spalletta, Gianfranco and Stern, Emily R and Stevens, Michael C and Stewart, S Evelyn and Szeszko, Philip R and Tolin, David F and {Van Rooij}, Daan and Veltman, Dick J and {Van Der Werf}, Ysbrand D and {Van Wingen}, Guido A and Venkatasubramanian, Ganesan and Walitza, Susanne and Wang, Zhen and Watanabe, Anri and Wolters, Lidewij H and Xu, Xiufeng and Yun, Je-Yeon and Zarei, Mojtaba and Zhang, Fengrui and Zhao, Qing and Jahanshad, Neda and Thomopoulos, Sophia I and Thompson, Paul M and Stein, Dan J and {Van Den Heuvel}, Odile A and O'Neill, Joseph and Poletti, Sara and Fridgeirsson, Egill Axfjord and Ikuta, Toshikazu and {De Wit}, Stella J and Vriend, Chris and Kasprzak, Selina and Kuno, Masaru and Takahashi, Jumpei and Miguel, Euripedes C and Shavitt, Roseli G and Hough, Morgan and Pariente, Jose C and Ortiz, Ana E and Bertol{\\'{i}}n, Sara and Real, Eva and Segal{\\`{a}}s, Cinto and Moreira, Pedro Silva and Sousa, Nuno and Narumoto, Jin and Yamada, Kei and Tang, Jinsong and Fouche, Jean-Paul and Kim, Taekwan and Choi, Sunah and Ha, Minji and Park, Sunghyun},\ndoi = {10.1016/j.jad.2022.08.084},\nissn = {01650327},\njournal = {Journal of Affective Disorders},\nmonth = {dec},\npages = {204--216},\nshorttitle = {Associations of medication with subcortical morpho},\ntitle = {{Associations of medication with subcortical morphology across the lifespan in {\\{}OCD{\\}}: {\\{}Results{\\}} from the international {\\{}ENIGMA{\\}} {\\{}Consortium{\\}}}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S0165032722009405},\nvolume = {318},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Alcohol use and alcohol use disorder differ in their genetic relationships with \\PTSD\\: \\A\\ genomic structural equation modelling approach.\n \n \n \n \n\n\n \n Bountress, K. E; Brick, L. A; Sheerin, C.; Grotzinger, A.; Bustamante, D.; Hawn, S. E; Gillespie, N.; Kirkpatrick, R. M; Kranzler, H.; Morey, R.; Edenberg, H. J; Maihofer, A. X; Disner, S.; Ashley-Koch, A.; Peterson, R.; Lori, A.; Stein, D. J; Kimbrel, N.; Nievergelt, C.; Andreassen, O. A; Luykx, J.; Javanbakht, A.; Youssef, N. A; and Amstadter, A. B\n\n\n \n\n\n\n Drug and Alcohol Dependence, 234: 109430. may 2022.\n \n\n\n\n
\n\n\n\n \n \n \"AlcoholPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{bountress_alcohol_2022,\nauthor = {Bountress, Kaitlin E and Brick, Leslie A and Sheerin, Christina and Grotzinger, Andrew and Bustamante, Daniel and Hawn, Sage E and Gillespie, Nathan and Kirkpatrick, Robert M and Kranzler, Henry and Morey, Rajendra and Edenberg, Howard J and Maihofer, Adam X and Disner, Seth and Ashley-Koch, Allison and Peterson, Roseann and Lori, Adriana and Stein, Dan J and Kimbrel, Nathan and Nievergelt, Caroline and Andreassen, Ole A and Luykx, Jurjen and Javanbakht, Arash and Youssef, Nagy A and Amstadter, Ananda B},\ndoi = {10.1016/j.drugalcdep.2022.109430},\nfile = {:Users/jacquelinebracher/Zotero/storage/ZX2886DW/Bountress et al. - 2022 - Alcohol use and alcohol use disorder differ in the.pdf:pdf},\nissn = {03768716},\njournal = {Drug and Alcohol Dependence},\nmonth = {may},\npages = {109430},\nshorttitle = {Alcohol use and alcohol use disorder differ in the},\ntitle = {{Alcohol use and alcohol use disorder differ in their genetic relationships with {\\{}PTSD{\\}}: {\\{}A{\\}} genomic structural equation modelling approach}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S0376871622001673},\nvolume = {234},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Publisher \\Correction\\: \\Brain\\ charts for the human lifespan.\n \n \n \n \n\n\n \n Bethlehem, R A I; Seidlitz, J; White, S R; Vogel, J W; Anderson, K M; Adamson, C; Adler, S; Alexopoulos, G S; Anagnostou, E; Areces-Gonzalez, A; Astle, D E; Auyeung, B; Ayub, M; Bae, J; Ball, G; Baron-Cohen, S; Beare, R; Bedford, S A; Benegal, V; Beyer, F; Blangero, J; Blesa Cábez, M; Boardman, J P; Borzage, M; Bosch-Bayard, J F; Bourke, N; Calhoun, V D; Chakravarty, M M; Chen, C; Chertavian, C; Chetelat, G; Chong, Y S; Cole, J H; Corvin, A; Costantino, M; Courchesne, E; Crivello, F; Cropley, V L; Crosbie, J; Crossley, N; Delarue, M; Delorme, R; Desrivieres, S; Devenyi, G A; Di Biase, M A; Dolan, R; Donald, K A; Donohoe, G; Dunlop, K; Edwards, A D; Elison, J T; Ellis, C T; Elman, J A; Eyler, L; Fair, D A; Feczko, E; Fletcher, P C; Fonagy, P; Franz, C E; Galan-Garcia, L; Gholipour, A; Giedd, J; Gilmore, J H; Glahn, D C; Goodyer, I M; Grant, P E; Groenewold, N A; Gunning, F M; Gur, R E; Gur, R C; Hammill, C F; Hansson, O; Hedden, T; Heinz, A; Henson, R N; Heuer, K; Hoare, J; Holla, B; Holmes, A J; Holt, R; Huang, H; Im, K; Ipser, J; Jack, C R; Jackowski, A P; Jia, T; Johnson, K A; Jones, P B; Jones, D T; Kahn, R S; Karlsson, H; Karlsson, L; Kawashima, R; Kelley, E A; Kern, S; Kim, K W; Kitzbichler, M G; Kremen, W S; Lalonde, F; Landeau, B; Lee, S; Lerch, J; Lewis, J D; Li, J; Liao, W; Liston, C; Lombardo, M V; Lv, J; Lynch, C; Mallard, T T; Marcelis, M; Markello, R D; Mathias, S R; Mazoyer, B; McGuire, P; Meaney, M J; Mechelli, A; Medic, N; Misic, B; Morgan, S E; Mothersill, D; Nigg, J; Ong, M Q W; Ortinau, C; Ossenkoppele, R; Ouyang, M; Palaniyappan, L; Paly, L; Pan, P M; Pantelis, C; Park, M M; Paus, T; Pausova, Z; Paz-Linares, D; Pichet Binette, A; Pierce, K; Qian, X; Qiu, J; Qiu, A; Raznahan, A; Rittman, T; Rodrigue, A; Rollins, C K; Romero-Garcia, R; Ronan, L; Rosenberg, M D; Rowitch, D H; Salum, G A; Satterthwaite, T D; Schaare, H L; Schachar, R J; Schultz, A P; Schumann, G; Schöll, M; Sharp, D; Shinohara, R T; Skoog, I; Smyser, C D; Sperling, R A; Stein, D J; Stolicyn, A; Suckling, J; Sullivan, G; Taki, Y; Thyreau, B; Toro, R; Traut, N; Tsvetanov, K A; Turk-Browne, N B; Tuulari, J J; Tzourio, C; Vachon-Presseau, É; Valdes-Sosa, M J; Valdes-Sosa, P A; Valk, S L; Van Amelsvoort, T; Vandekar, S N; Vasung, L; Victoria, L W; Villeneuve, S; Villringer, A; Vértes, P E; Wagstyl, K; Wang, Y S; Warfield, S K; Warrier, V; Westman, E; Westwater, M L; Whalley, H C; Witte, A V; Yang, N; Yeo, B; Yun, H; Zalesky, A; Zar, H J; Zettergren, A; Zhou, J H; Ziauddeen, H; Zugman, A; Zuo, X N; 3R-BRAIN; AIBL; Rowe, C; Alzheimer's Disease Neuroimaging Initiative; Alzheimer's Disease Repository Without Borders Investigators; Frisoni, G B; CALM Team; Cam-CAN; CCNP; COBRE; CVEDA; ENIGMA Developmental Brain Age Working Group; Developing Human Connectome Project; FinnBrain; Harvard Aging Brain Study; IMAGEN; KNE96; The Mayo Clinic Study of Aging; NSPN; POND; The PREVENT-AD Research Group; Binette, A P.; VETSA; Bullmore, E T; and Alexander-Bloch, A F\n\n\n \n\n\n\n Nature, 610(7931): E6—-E6. oct 2022.\n \n\n\n\n
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@article{bethlehem_publisher_2022,\nauthor = {Bethlehem, R A I and Seidlitz, J and White, S R and Vogel, J W and Anderson, K M and Adamson, C and Adler, S and Alexopoulos, G S and Anagnostou, E and Areces-Gonzalez, A and Astle, D E and Auyeung, B and Ayub, M and Bae, J and Ball, G and Baron-Cohen, S and Beare, R and Bedford, S A and Benegal, V and Beyer, F and Blangero, J and {Blesa C{\\'{a}}bez}, M and Boardman, J P and Borzage, M and Bosch-Bayard, J F and Bourke, N and Calhoun, V D and Chakravarty, M M and Chen, C and Chertavian, C and Chetelat, G and Chong, Y S and Cole, J H and Corvin, A and Costantino, M and Courchesne, E and Crivello, F and Cropley, V L and Crosbie, J and Crossley, N and Delarue, M and Delorme, R and Desrivieres, S and Devenyi, G A and {Di Biase}, M A and Dolan, R and Donald, K A and Donohoe, G and Dunlop, K and Edwards, A D and Elison, J T and Ellis, C T and Elman, J A and Eyler, L and Fair, D A and Feczko, E and Fletcher, P C and Fonagy, P and Franz, C E and Galan-Garcia, L and Gholipour, A and Giedd, J and Gilmore, J H and Glahn, D C and Goodyer, I M and Grant, P E and Groenewold, N A and Gunning, F M and Gur, R E and Gur, R C and Hammill, C F and Hansson, O and Hedden, T and Heinz, A and Henson, R N and Heuer, K and Hoare, J and Holla, B and Holmes, A J and Holt, R and Huang, H and Im, K and Ipser, J and Jack, C R and Jackowski, A P and Jia, T and Johnson, K A and Jones, P B and Jones, D T and Kahn, R S and Karlsson, H and Karlsson, L and Kawashima, R and Kelley, E A and Kern, S and Kim, K W and Kitzbichler, M G and Kremen, W S and Lalonde, F and Landeau, B and Lee, S and Lerch, J and Lewis, J D and Li, J and Liao, W and Liston, C and Lombardo, M V and Lv, J and Lynch, C and Mallard, T T and Marcelis, M and Markello, R D and Mathias, S R and Mazoyer, B and McGuire, P and Meaney, M J and Mechelli, A and Medic, N and Misic, B and Morgan, S E and Mothersill, D and Nigg, J and Ong, M Q W and Ortinau, C and Ossenkoppele, R and Ouyang, M and Palaniyappan, L and Paly, L and Pan, P M and Pantelis, C and Park, M M and Paus, T and Pausova, Z and Paz-Linares, D and {Pichet Binette}, A and Pierce, K and Qian, X and Qiu, J and Qiu, A and Raznahan, A and Rittman, T and Rodrigue, A and Rollins, C K and Romero-Garcia, R and Ronan, L and Rosenberg, M D and Rowitch, D H and Salum, G A and Satterthwaite, T D and Schaare, H L and Schachar, R J and Schultz, A P and Schumann, G and Sch{\\"{o}}ll, M and Sharp, D and Shinohara, R T and Skoog, I and Smyser, C D and Sperling, R A and Stein, D J and Stolicyn, A and Suckling, J and Sullivan, G and Taki, Y and Thyreau, B and Toro, R and Traut, N and Tsvetanov, K A and Turk-Browne, N B and Tuulari, J J and Tzourio, C and Vachon-Presseau, {\\'{E}} and Valdes-Sosa, M J and Valdes-Sosa, P A and Valk, S L and {Van Amelsvoort}, T and Vandekar, S N and Vasung, L and Victoria, L W and Villeneuve, S and Villringer, A and V{\\'{e}}rtes, P E and Wagstyl, K and Wang, Y S and Warfield, S K and Warrier, V and Westman, E and Westwater, M L and Whalley, H C and Witte, A V and Yang, N and Yeo, B and Yun, H and Zalesky, A and Zar, H J and Zettergren, A and Zhou, J H and Ziauddeen, H and Zugman, A and Zuo, X N and 3R-BRAIN and AIBL and Rowe, C and {Alzheimer's Disease Neuroimaging Initiative} and {Alzheimer's Disease Repository Without Borders Investigators} and Frisoni, G B and {CALM Team} and Cam-CAN and CCNP and COBRE and CVEDA and {ENIGMA Developmental Brain Age Working Group} and {Developing Human Connectome Project} and FinnBrain and {Harvard Aging Brain Study} and IMAGEN and KNE96 and {The Mayo Clinic Study of Aging} and NSPN and POND and {The PREVENT-AD Research Group} and Binette, A Pichet and VETSA and Bullmore, E T and Alexander-Bloch, A F},\ndoi = {10.1038/s41586-022-05300-0},\nfile = {:Users/jacquelinebracher/Zotero/storage/F82KR5PA/Bethlehem et al. - 2022 - Publisher Correction Brain charts for the human l.pdf:pdf},\nissn = {0028-0836, 1476-4687},\njournal = {Nature},\nmonth = {oct},\nnumber = {7931},\npages = {E6----E6},\nshorttitle = {Publisher {\\{}Correction{\\}}},\ntitle = {{Publisher {\\{}Correction{\\}}: {\\{}Brain{\\}} charts for the human lifespan}},\nurl = {https://www.nature.com/articles/s41586-022-05300-0},\nvolume = {610},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Development of a \\Mobile\\ \\Application\\ for \\Detection\\ of \\Adolescent\\ \\Mental\\ \\Health\\ \\Problems\\ and \\Feasibility\\ \\Assessment\\ with \\Primary\\ \\Health\\ \\Care\\ \\Workers\\.\n \n \n \n \n\n\n \n Groen, G.; Jörns-Presentati, A.; Dessauvagie, A.; Seedat, S.; Van Den Heuvel, L. L; Suliman, S.; Grobler, G.; Jansen, R.; Mwape, L.; Mukwato, P.; Chapima, F.; Korhonen, J.; Stein, D. J; Jonker, D.; Mudenda, J.; Turunen, T.; Valtiņš, K.; Beinaroviča, A.; Grada, L.; and Lahti, M.\n\n\n \n\n\n\n Issues in Mental Health Nursing, 43(11): 1046–1055. nov 2022.\n \n\n\n\n
\n\n\n\n \n \n \"DevelopmentPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{groen_development_2022,\nauthor = {Groen, Gunter and J{\\"{o}}rns-Presentati, Astrid and Dessauvagie, Anja and Seedat, Soraya and {Van Den Heuvel}, Leigh L and Suliman, Sharain and Grobler, Gerhard and Jansen, Ronelle and Mwape, Lonia and Mukwato, Patricia and Chapima, Fabian and Korhonen, Joonas and Stein, Dan J and Jonker, Deborah and Mudenda, John and Turunen, Timo and Valtiņ{\\v{s}}, Kārlis and Beinarovi{\\v{c}}a, Anete and Grada, Leva and Lahti, Mari},\ndoi = {10.1080/01612840.2022.2124003},\nissn = {0161-2840, 1096-4673},\njournal = {Issues in Mental Health Nursing},\nmonth = {nov},\nnumber = {11},\npages = {1046--1055},\ntitle = {{Development of a {\\{}Mobile{\\}} {\\{}Application{\\}} for {\\{}Detection{\\}} of {\\{}Adolescent{\\}} {\\{}Mental{\\}} {\\{}Health{\\}} {\\{}Problems{\\}} and {\\{}Feasibility{\\}} {\\{}Assessment{\\}} with {\\{}Primary{\\}} {\\{}Health{\\}} {\\{}Care{\\}} {\\{}Workers{\\}}}},\nurl = {https://www.tandfonline.com/doi/full/10.1080/01612840.2022.2124003},\nvolume = {43},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Philosophy and psychiatry: problems of clinicians and problems of life.\n \n \n \n \n\n\n \n Stein, D. J\n\n\n \n\n\n\n Brazilian Journal of Psychiatry, 44(3): 227–228. jun 2022.\n \n\n\n\n
\n\n\n\n \n \n \"PhilosophyPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{stein_philosophy_2022,\nauthor = {Stein, Dan J},\ndoi = {10.1590/1516-4446-2021-0033},\nfile = {:Users/jacquelinebracher/Zotero/storage/9IUD8QE5/Stein - 2022 - Philosophy and psychiatry problems of clinicians .pdf:pdf},\nissn = {1809-452X, 1516-4446},\njournal = {Brazilian Journal of Psychiatry},\nmonth = {jun},\nnumber = {3},\npages = {227--228},\nshorttitle = {Philosophy and psychiatry},\ntitle = {{Philosophy and psychiatry: problems of clinicians and problems of life}},\nurl = {http://www.scielo.br/scielo.php?script=sci{\\_}arttext{\\&}pid=S1516-44462022000300227{\\&}tlng=en},\nvolume = {44},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n The \\Emergence\\ of \\Embryonic\\ \\Myosin\\ \\Heavy\\ \\Chain\\ during \\Branchiomeric\\ \\Muscle\\ \\Development\\.\n \n \n \n \n\n\n \n Yahya, I.; Böing, M.; Hockman, D.; Brand-Saberi, B.; and Morosan-Puopolo, G.\n\n\n \n\n\n\n Life, 12(6): 785. may 2022.\n \n\n\n\n
\n\n\n\n \n \n \"ThePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{yahya_emergence_2022,\nabstract = {A prerequisite for discovering the properties and therapeutic potential of branchiomeric muscles is an understanding of their fate determination, pattering and differentiation. Although the expression of differentiation markers such as myosin heavy chain (MyHC) during trunk myogenesis has been more intensively studied, little is known about its expression in the developing branchiomeric muscle anlagen. To shed light on this, we traced the onset of MyHC expression in the facial and neck muscle anlagen by using the whole-mount in situ hybridization between embryonic days E9.5 and E15.5 in the mouse. Unlike trunk muscle, the facial and neck muscle anlagen express MyHC at late stages. Within the branchiomeric muscles, our results showed variation in the emergence of MyHC expression. MyHC was first detected in the first arch-derived muscle anlagen, while its expression in the second arch-derived muscle and non-somitic neck muscle began at a later time point. Additionally, we show that non-ectomesenchymal neural crest invasion of the second branchial arch is delayed compared with that of the first brachial arch in chicken embryos. Thus, our findings reflect the timing underlying branchiomeric muscle differentiation.},\nauthor = {Yahya, Imadeldin and B{\\"{o}}ing, Marion and Hockman, Dorit and Brand-Saberi, Beate and Morosan-Puopolo, Gabriela},\ndoi = {10.3390/life12060785},\nfile = {:Users/jacquelinebracher/Zotero/storage/NXN9IQCI/Yahya et al. - 2022 - The Emergence of Embryonic Myosin Heavy Chain duri.pdf:pdf},\nissn = {2075-1729},\njournal = {Life},\nmonth = {may},\nnumber = {6},\npages = {785},\ntitle = {{The {\\{}Emergence{\\}} of {\\{}Embryonic{\\}} {\\{}Myosin{\\}} {\\{}Heavy{\\}} {\\{}Chain{\\}} during {\\{}Branchiomeric{\\}} {\\{}Muscle{\\}} {\\{}Development{\\}}}},\nurl = {https://www.mdpi.com/2075-1729/12/6/785},\nvolume = {12},\nyear = {2022}\n}\n
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\n A prerequisite for discovering the properties and therapeutic potential of branchiomeric muscles is an understanding of their fate determination, pattering and differentiation. Although the expression of differentiation markers such as myosin heavy chain (MyHC) during trunk myogenesis has been more intensively studied, little is known about its expression in the developing branchiomeric muscle anlagen. To shed light on this, we traced the onset of MyHC expression in the facial and neck muscle anlagen by using the whole-mount in situ hybridization between embryonic days E9.5 and E15.5 in the mouse. Unlike trunk muscle, the facial and neck muscle anlagen express MyHC at late stages. Within the branchiomeric muscles, our results showed variation in the emergence of MyHC expression. MyHC was first detected in the first arch-derived muscle anlagen, while its expression in the second arch-derived muscle and non-somitic neck muscle began at a later time point. Additionally, we show that non-ectomesenchymal neural crest invasion of the second branchial arch is delayed compared with that of the first brachial arch in chicken embryos. Thus, our findings reflect the timing underlying branchiomeric muscle differentiation.\n
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\n \n\n \n \n \n \n \n \n An international survey examining the impact of the \\COVID\\-19 pandemic on telehealth use among mental health professionals.\n \n \n \n \n\n\n \n Montoya, M. I; Kogan, C. S; Rebello, T. J; Sadowska, K.; Garcia-Pacheco, J. A; Khoury, B.; Kulygina, M.; Matsumoto, C.; Robles, R.; Huang, J.; Andrews, H. F; Ayuso-Mateos, J. L.; Denny, K.; Gaebel, W.; Gureje, O.; Kanba, S.; Maré, K.; Medina-Mora, M. E.; Pike, K. M; Roberts, M. C; Sharan, P.; Stein, D. J; Scott Stroup, T; Zhao, M.; and Reed, G. M\n\n\n \n\n\n\n Journal of Psychiatric Research, 148: 188–196. apr 2022.\n \n\n\n\n
\n\n\n\n \n \n \"AnPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{montoya_international_2022,\nauthor = {Montoya, Madeline I and Kogan, Cary S and Rebello, Tahilia J and Sadowska, Karolina and Garcia-Pacheco, Jos{\\'{e}} A and Khoury, Brigitte and Kulygina, Maya and Matsumoto, Chihiro and Robles, Rebeca and Huang, Jingjing and Andrews, Howard F and Ayuso-Mateos, Jos{\\'{e}} Luis and Denny, Keith and Gaebel, Wolfgang and Gureje, Oye and Kanba, Shigenobu and Mar{\\'{e}}, Karen and Medina-Mora, Mar{\\'{i}}a Elena and Pike, Kathleen M and Roberts, Michael C and Sharan, Pratap and Stein, Dan J and {Scott Stroup}, T and Zhao, Min and Reed, Geoffrey M},\ndoi = {10.1016/j.jpsychires.2022.01.050},\nfile = {:Users/jacquelinebracher/Zotero/storage/QB84E8GA/Montoya et al. - 2022 - An international survey examining the impact of th.pdf:pdf},\nissn = {00223956},\njournal = {Journal of Psychiatric Research},\nmonth = {apr},\npages = {188--196},\ntitle = {{An international survey examining the impact of the {\\{}COVID{\\}}-19 pandemic on telehealth use among mental health professionals}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S0022395622000590},\nvolume = {148},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Pharmacotherapy for post traumatic stress disorder (PTSD).\n \n \n \n \n\n\n \n Williams, T; Phillips, N J; Stein, D J; and Ipser, J C\n\n\n \n\n\n\n 2022.\n \n\n\n\n
\n\n\n\n \n \n \"PharmacotherapyPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Williams2022,\nannote = {Export Date: 29 December 2022},\nauthor = {Williams, T and Phillips, N J and Stein, D J and Ipser, J C},\ndoi = {10.1002/14651858.CD002795.pub3},\nfile = {:Users/jacquelinebracher/Zotero/storage/472EJGUP/Williams et al. - 2022 - Pharmacotherapy for post traumatic stress disorder.pdf:pdf},\nnumber = {3},\ntitle = {{Pharmacotherapy for post traumatic stress disorder (PTSD)}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85125596115{\\&}doi=10.1002{\\%}2F14651858.CD002795.pub3{\\&}partnerID=40{\\&}md5=225fb4a3ecaf955dd7e0895755df1864},\nvolume = {2022},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Competency‐based \\EEG\\ education: a list of “must‐know” \\EEG\\ findings for adult and child neurology residents.\n \n \n \n \n\n\n \n Nascimento, F. A; Jing, J.; Strowd, R.; Sheikh, I. S; Weber, D.; Gavvala, J. R; Maheshwari, A.; Tanner, A.; Ng, M.; Vinayan, K P; Sinha, S. R; Yacubian, E. M; Rao, V. R; Perry, M S.; Fountain, N. B; Karakis, I.; Wirrell, E.; Yuan, F.; Friedman, D.; Tankisi, H.; Rampp, S.; Fasano, R.; Wilmshurst, J. M; O'Donovan, C.; Schomer, D.; Kaplan, P. W; Sperling, M. R; Benbadis, S.; Westover, M B.; and Beniczky, S.\n\n\n \n\n\n\n Epileptic Disorders, 24(5): 979–982. oct 2022.\n \n\n\n\n
\n\n\n\n \n \n \"Competency‐basedPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{nascimento_competencybased_2022,\nauthor = {Nascimento, F{\\'{a}}bio A and Jing, Jin and Strowd, Roy and Sheikh, Irfan S and Weber, Dan and Gavvala, Jay R and Maheshwari, Atul and Tanner, Adriana and Ng, Marcus and Vinayan, K P and Sinha, Saurabh R and Yacubian, Elza M and Rao, Vikram R and Perry, M Scott and Fountain, Nathan B and Karakis, Ioannis and Wirrell, Elaine and Yuan, Fang and Friedman, Daniel and Tankisi, Hatice and Rampp, Stefan and Fasano, Rebecca and Wilmshurst, Jo M and O'Donovan, Cormac and Schomer, Donald and Kaplan, Peter W and Sperling, Michael R and Benbadis, Selim and Westover, M Brandon and Beniczky, S{\\'{a}}ndor},\ndoi = {10.1684/epd.2022.1476},\nfile = {:Users/jacquelinebracher/Zotero/storage/CB72ME57/Nascimento et al. - 2022 - Competency‐based EEG education a list of “must‐kn.pdf:pdf},\nissn = {1294-9361, 1950-6945},\njournal = {Epileptic Disorders},\nmonth = {oct},\nnumber = {5},\npages = {979--982},\nshorttitle = {Competency‐based {\\{}EEG{\\}} education},\ntitle = {{Competency‐based {\\{}EEG{\\}} education: a list of “must‐know” {\\{}EEG{\\}} findings for adult and child neurology residents}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1684/epd.2022.1476},\nvolume = {24},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n \\ENIGMA\\‐\\DTI\\: \\Translating\\ reproducible white matter deficits into personalized vulnerability metrics in cross‐diagnostic psychiatric research.\n \n \n \n \n\n\n \n Kochunov, P.; Hong, L E.; Dennis, E. L; Morey, R. A; Tate, D. F; Wilde, E. A; Logue, M.; Kelly, S.; Donohoe, G.; Favre, P.; Houenou, J.; Ching, C. R K; Holleran, L.; Andreassen, O. A; Van Velzen, L. S; Schmaal, L.; Villalón‐Reina, J. E; Bearden, C. E; Piras, F.; Spalletta, G.; Van Den Heuvel, O. A; Veltman, D. J; Stein, D. J; Ryan, M. C; Tan, Y.; Van Erp, T. G M; Turner, J. A; Haddad, L.; Nir, T. M; Glahn, D. C; Thompson, P. M; and Jahanshad, N.\n\n\n \n\n\n\n Human Brain Mapping, 43(1): 194–206. jan 2022.\n \n\n\n\n
\n\n\n\n \n \n \"\\ENIGMA\\‐\\DTI\\:Paper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{kochunov_enigmadti_2022,\nabstract = {Abstract\nThe ENIGMA‐DTI (diffusion tensor imaging) workgroup supports analyses that examine the effects of psychiatric, neurological, and developmental disorders on the white matter pathways of the human brain, as well as the effects of normal variation and its genetic associations. The seven ENIGMA disorder‐oriented working groups used the ENIGMA‐DTI workflow to derive patterns of deficits using coherent and coordinated analyses that model the disease effects across cohorts worldwide. This yielded the largest studies detailing patterns of white matter deficits in schizophrenia spectrum disorder (SSD), bipolar disorder (BD), major depressive disorder (MDD), obsessive–compulsive disorder (OCD), posttraumatic stress disorder (PTSD), traumatic brain injury (TBI), and 22q11 deletion syndrome. These deficit patterns are informative of the underlying neurobiology and reproducible in independent cohorts. We reviewed these findings, demonstrated their reproducibility in independent cohorts, and compared the deficit patterns across illnesses. We discussed translating ENIGMA‐defined deficit patterns on the level of individual subjects using a metric called the regional vulnerability index (RVI), a correlation of an individual's brain metrics with the expected pattern for a disorder. We discussed the similarity in white matter deficit patterns among SSD, BD, MDD, and OCD and provided a rationale for using this index in cross‐diagnostic neuropsychiatric research. We also discussed the difference in deficit patterns between idiopathic schizophrenia and 22q11 deletion syndrome, which is used as a developmental and genetic model of schizophrenia. Together, these findings highlight the importance of collaborative large‐scale research to provide robust and reproducible effects that offer insights into individual vulnerability and cross‐diagnosis features.},\nauthor = {Kochunov, Peter and Hong, L Elliot and Dennis, Emily L and Morey, Rajendra A and Tate, David F and Wilde, Elisabeth A and Logue, Mark and Kelly, Sinead and Donohoe, Gary and Favre, Pauline and Houenou, Josselin and Ching, Christopher R K and Holleran, Laurena and Andreassen, Ole A and {Van Velzen}, Laura S and Schmaal, Lianne and Villal{\\'{o}}n‐Reina, Julio E and Bearden, Carrie E and Piras, Fabrizio and Spalletta, Gianfranco and {Van Den Heuvel}, Odile A and Veltman, Dick J and Stein, Dan J and Ryan, Meghann C and Tan, Yunlong and {Van Erp}, Theo G M and Turner, Jessica A and Haddad, Liz and Nir, Talia M and Glahn, David C and Thompson, Paul M and Jahanshad, Neda},\ndoi = {10.1002/hbm.24998},\nfile = {:Users/jacquelinebracher/Zotero/storage/UAQQ9MJG/Kochunov et al. - 2022 - ENIGMA‐DTI Translating reproducible white matter .pdf:pdf},\nissn = {1065-9471, 1097-0193},\njournal = {Human Brain Mapping},\nmonth = {jan},\nnumber = {1},\npages = {194--206},\nshorttitle = {{\\{}ENIGMA{\\}}‐{\\{}DTI{\\}}},\ntitle = {{{\\{}ENIGMA{\\}}‐{\\{}DTI{\\}}: {\\{}Translating{\\}} reproducible white matter deficits into personalized vulnerability metrics in cross‐diagnostic psychiatric research}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1002/hbm.24998},\nvolume = {43},\nyear = {2022}\n}\n
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\n Abstract The ENIGMA‐DTI (diffusion tensor imaging) workgroup supports analyses that examine the effects of psychiatric, neurological, and developmental disorders on the white matter pathways of the human brain, as well as the effects of normal variation and its genetic associations. The seven ENIGMA disorder‐oriented working groups used the ENIGMA‐DTI workflow to derive patterns of deficits using coherent and coordinated analyses that model the disease effects across cohorts worldwide. This yielded the largest studies detailing patterns of white matter deficits in schizophrenia spectrum disorder (SSD), bipolar disorder (BD), major depressive disorder (MDD), obsessive–compulsive disorder (OCD), posttraumatic stress disorder (PTSD), traumatic brain injury (TBI), and 22q11 deletion syndrome. These deficit patterns are informative of the underlying neurobiology and reproducible in independent cohorts. We reviewed these findings, demonstrated their reproducibility in independent cohorts, and compared the deficit patterns across illnesses. We discussed translating ENIGMA‐defined deficit patterns on the level of individual subjects using a metric called the regional vulnerability index (RVI), a correlation of an individual's brain metrics with the expected pattern for a disorder. We discussed the similarity in white matter deficit patterns among SSD, BD, MDD, and OCD and provided a rationale for using this index in cross‐diagnostic neuropsychiatric research. We also discussed the difference in deficit patterns between idiopathic schizophrenia and 22q11 deletion syndrome, which is used as a developmental and genetic model of schizophrenia. Together, these findings highlight the importance of collaborative large‐scale research to provide robust and reproducible effects that offer insights into individual vulnerability and cross‐diagnosis features.\n
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\n \n\n \n \n \n \n \n \n Why won't it stop? \\The\\ dynamics of benzodiazepine resistance in status epilepticus.\n \n \n \n \n\n\n \n Burman, R. J; Rosch, R. E; Wilmshurst, J. M; Sen, A.; Ramantani, G.; Akerman, C. J; and Raimondo, J. V\n\n\n \n\n\n\n Nature Reviews Neurology, 18(7): 428–441. jul 2022.\n \n\n\n\n
\n\n\n\n \n \n \"WhyPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{burman_why_2022,\nauthor = {Burman, Richard J and Rosch, Richard E and Wilmshurst, Jo M and Sen, Arjune and Ramantani, Georgia and Akerman, Colin J and Raimondo, Joseph V},\ndoi = {10.1038/s41582-022-00664-3},\nissn = {1759-4758, 1759-4766},\njournal = {Nature Reviews Neurology},\nmonth = {jul},\nnumber = {7},\npages = {428--441},\nshorttitle = {Why won't it stop?},\ntitle = {{Why won't it stop? {\\{}The{\\}} dynamics of benzodiazepine resistance in status epilepticus}},\nurl = {https://www.nature.com/articles/s41582-022-00664-3},\nvolume = {18},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n Newborn differential DNA methylation and subcortical brain volumes as early signs of severe neurodevelopmental delay in a South African Birth Cohort Study.\n \n \n \n\n\n \n Hüls, A.; Wedderburn, C.; Groenewold, N.; Gladish, N.; Jones, M.; Koen, N.; MacIsaac, J.; Lin, D.; Ramadori, K.; Epstein, M.; Zar, H.; and Stein, D.\n\n\n \n\n\n\n World Journal of Biological Psychiatry, 23(8): 601–612. 2022.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Huls2022,\nabstract = {Objectives: Early detection of neurodevelopmental delay is crucial for intervention and treatment strategies. We analysed associations between newborn DNA methylation (DNAm), neonatal magnetic resonance imaging (MRI) neuroimaging data, and neurodevelopment. Methods: Neurodevelopment was assessed in 161 children from the South African Drakenstein Child Health Study at 2 years of age using the Bayley Scales of Infant and Toddler Development III. We performed an epigenome-wide association study of neurodevelopmental delay using DNAm from cord blood. Subsequently, we analysed if associations between DNAm and neurodevelopmental delay were mediated by altered neonatal brain volumes (subset of 51 children). Results: Differential DNAm at SPTBN4 (cg26971411, $\\Delta$beta = −0.024, p-value = 3.28 × 10−08), and two intergenic regions (chromosome 11: cg00490349, $\\Delta$beta = −0.036, p-value = 3.02 × 10−08; chromosome 17: cg15660740, $\\Delta$beta = −0.078, p-value = 6.49 × 10−08) were significantly associated with severe neurodevelopmental delay. While these associations were not mediated by neonatal brain volume, neonatal caudate volumes were independently associated with neurodevelopmental delay, particularly in language ($\\Delta$caudate volume = 165.30 mm3, p = 0.0443) and motor ($\\Delta$caudate volume = 365.36 mm3, p-value = 0.0082) domains. Conclusions: Differential DNAm from cord blood and increased neonatal caudate volumes were independently associated with severe neurodevelopmental delay at 2 years of age. These findings suggest that neurobiological signals for severe developmental delay may be detectable in very early life.},\nauthor = {H{\\"{u}}ls, A. and Wedderburn, C.J. and Groenewold, N.A. and Gladish, N. and Jones, M.J. and Koen, N. and MacIsaac, J.L. and Lin, D.T.S. and Ramadori, K.E. and Epstein, M.P. and Zar, H.J. and Stein, D.J.},\ndoi = {10.1080/15622975.2021.2016955},\njournal = {World Journal of Biological Psychiatry},\nnumber = {8},\npages = {601--612},\ntitle = {{Newborn differential DNA methylation and subcortical brain volumes as early signs of severe neurodevelopmental delay in a South African Birth Cohort Study}},\nvolume = {23},\nyear = {2022}\n}\n
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\n Objectives: Early detection of neurodevelopmental delay is crucial for intervention and treatment strategies. We analysed associations between newborn DNA methylation (DNAm), neonatal magnetic resonance imaging (MRI) neuroimaging data, and neurodevelopment. Methods: Neurodevelopment was assessed in 161 children from the South African Drakenstein Child Health Study at 2 years of age using the Bayley Scales of Infant and Toddler Development III. We performed an epigenome-wide association study of neurodevelopmental delay using DNAm from cord blood. Subsequently, we analysed if associations between DNAm and neurodevelopmental delay were mediated by altered neonatal brain volumes (subset of 51 children). Results: Differential DNAm at SPTBN4 (cg26971411, $Δ$beta = −0.024, p-value = 3.28 × 10−08), and two intergenic regions (chromosome 11: cg00490349, $Δ$beta = −0.036, p-value = 3.02 × 10−08; chromosome 17: cg15660740, $Δ$beta = −0.078, p-value = 6.49 × 10−08) were significantly associated with severe neurodevelopmental delay. While these associations were not mediated by neonatal brain volume, neonatal caudate volumes were independently associated with neurodevelopmental delay, particularly in language ($Δ$caudate volume = 165.30 mm3, p = 0.0443) and motor ($Δ$caudate volume = 365.36 mm3, p-value = 0.0082) domains. Conclusions: Differential DNAm from cord blood and increased neonatal caudate volumes were independently associated with severe neurodevelopmental delay at 2 years of age. These findings suggest that neurobiological signals for severe developmental delay may be detectable in very early life.\n
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\n \n\n \n \n \n \n \n \n Event‐based modeling in temporal lobe epilepsy demonstrates progressive atrophy from cross‐sectional data.\n \n \n \n \n\n\n \n Lopez, S. M; Aksman, L. M; Oxtoby, N. P; Vos, S. B; Rao, J.; Kaestner, E.; Alhusaini, S.; Alvim, M.; Bender, B.; Bernasconi, A.; Bernasconi, N.; Bernhardt, B.; Bonilha, L.; Caciagli, L.; Caldairou, B.; Caligiuri, M. E.; Calvet, A.; Cendes, F.; Concha, L.; Conde‐Blanco, E.; Davoodi‐Bojd, E.; De Bézenac, C.; Delanty, N.; Desmond, P. M; Devinsky, O.; Domin, M.; Duncan, J. S; Focke, N. K; Foley, S.; Fortunato, F.; Galovic, M.; Gambardella, A.; Gleichgerrcht, E.; Guerrini, R.; Hamandi, K.; Ives‐Deliperi, V.; Jackson, G. D; Jahanshad, N.; Keller, S. S; Kochunov, P.; Kotikalapudi, R.; Kreilkamp, B. A K; Labate, A.; Larivière, S.; Lenge, M.; Lui, E.; Malpas, C.; Martin, P.; Mascalchi, M.; Medland, S. E; Meletti, S.; Morita‐Sherman, M. E; Owen, T. W; Richardson, M.; Riva, A.; Rüber, T.; Sinclair, B.; Soltanian‐Zadeh, H.; Stein, D. J; Striano, P.; Taylor, P. N; Thomopoulos, S. I; Thompson, P. M; Tondelli, M.; Vaudano, A. E.; Vivash, L.; Wang, Y.; Weber, B.; Whelan, C. D; Wiest, R.; Winston, G. P; Yasuda, C. L.; McDonald, C. R; Alexander, D. C; Sisodiya, S. M; Altmann, A.; and for the ENIGMA‐Epilepsy Working Group\n\n\n \n\n\n\n Epilepsia, 63(8): 2081–2095. aug 2022.\n \n\n\n\n
\n\n\n\n \n \n \"Event‐basedPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{lopez_eventbased_2022,\nabstract = {Abstract\n\nObjective\nRecent work has shown that people with common epilepsies have characteristic patterns of cortical thinning, and that these changes may be progressive over time. Leveraging a large multicenter cross‐sectional cohort, we investigated whether regional morphometric changes occur in a sequential manner, and whether these changes in people with mesial temporal lobe epilepsy and hippocampal sclerosis (MTLE‐HS) correlate with clinical features.\n\n\nMethods\n\nWe extracted regional measures of cortical thickness, surface area, and subcortical brain volumes from T1‐weighted (T1W) magnetic resonance imaging (MRI) scans collected by the ENIGMA‐Epilepsy consortium, comprising 804 people with MTLE‐HS and 1625 healthy controls from 25 centers. Features with a moderate case–control effect size (Cohen\nd\n≥ .5) were used to train an event‐based model (EBM), which estimates a sequence of disease‐specific biomarker changes from cross‐sectional data and assigns a biomarker‐based fine‐grained disease stage to individual patients. We tested for associations between EBM disease stage and duration of epilepsy, age at onset, and antiseizure medicine (ASM) resistance.\n\n\n\nResults\n\nIn MTLE‐HS, decrease in ipsilateral hippocampal volume along with increased asymmetry in hippocampal volume was followed by reduced thickness in neocortical regions, reduction in ipsilateral thalamus volume, and finally, increase in ipsilateral lateral ventricle volume. EBM stage was correlated with duration of illness (Spearman\n$\\rho$ =\n.293,\np\n= 7.03 × 10\n−16\n), age at onset (\n$\\rho$ =\n−.18,\np =\n9.82 × 10\n−7\n), and ASM resistance (area under the curve = .59,\np\n= .043, Mann–Whitney\nU\ntest). However, associations were driven by cases assigned to EBM Stage 0, which represents MTLE‐HS with mild or nondetectable abnormality on T1W MRI.\n\n\n\nSignificance\nFrom cross‐sectional MRI, we reconstructed a disease progression model that highlights a sequence of MRI changes that aligns with previous longitudinal studies. This model could be used to stage MTLE‐HS subjects in other cohorts and help establish connections between imaging‐based progression staging and clinical features.},\nauthor = {Lopez, Seymour M and Aksman, Leon M and Oxtoby, Neil P and Vos, Sjoerd B and Rao, Jun and Kaestner, Erik and Alhusaini, Saud and Alvim, Marina and Bender, Benjamin and Bernasconi, Andrea and Bernasconi, Neda and Bernhardt, Boris and Bonilha, Leonardo and Caciagli, Lorenzo and Caldairou, Benoit and Caligiuri, Maria Eugenia and Calvet, Angels and Cendes, Fernando and Concha, Luis and Conde‐Blanco, Estefania and Davoodi‐Bojd, Esmaeil and {De B{\\'{e}}zenac}, Christophe and Delanty, Norman and Desmond, Patricia M and Devinsky, Orrin and Domin, Martin and Duncan, John S and Focke, Niels K and Foley, Sonya and Fortunato, Francesco and Galovic, Marian and Gambardella, Antonio and Gleichgerrcht, Ezequiel and Guerrini, Renzo and Hamandi, Khalid and Ives‐Deliperi, Victoria and Jackson, Graeme D and Jahanshad, Neda and Keller, Simon S and Kochunov, Peter and Kotikalapudi, Raviteja and Kreilkamp, Barbara A K and Labate, Angelo and Larivi{\\`{e}}re, Sara and Lenge, Matteo and Lui, Elaine and Malpas, Charles and Martin, Pascal and Mascalchi, Mario and Medland, Sarah E and Meletti, Stefano and Morita‐Sherman, Marcia E and Owen, Thomas W and Richardson, Mark and Riva, Antonella and R{\\"{u}}ber, Theodor and Sinclair, Ben and Soltanian‐Zadeh, Hamid and Stein, Dan J and Striano, Pasquale and Taylor, Peter N and Thomopoulos, Sophia I and Thompson, Paul M and Tondelli, Manuela and Vaudano, Anna Elisabetta and Vivash, Lucy and Wang, Yujiang and Weber, Bernd and Whelan, Christopher D and Wiest, Roland and Winston, Gavin P and Yasuda, Clarissa Lin and McDonald, Carrie R and Alexander, Daniel C and Sisodiya, Sanjay M and Altmann, Andre and {for the ENIGMA‐Epilepsy Working Group}},\ndoi = {10.1111/epi.17316},\nfile = {:Users/jacquelinebracher/Zotero/storage/APCVVCJ7/Lopez et al. - 2022 - Event‐based modeling in temporal lobe epilepsy dem.pdf:pdf},\nissn = {0013-9580, 1528-1167},\njournal = {Epilepsia},\nmonth = {aug},\nnumber = {8},\npages = {2081--2095},\ntitle = {{Event‐based modeling in temporal lobe epilepsy demonstrates progressive atrophy from cross‐sectional data}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1111/epi.17316},\nvolume = {63},\nyear = {2022}\n}\n
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\n Abstract Objective Recent work has shown that people with common epilepsies have characteristic patterns of cortical thinning, and that these changes may be progressive over time. Leveraging a large multicenter cross‐sectional cohort, we investigated whether regional morphometric changes occur in a sequential manner, and whether these changes in people with mesial temporal lobe epilepsy and hippocampal sclerosis (MTLE‐HS) correlate with clinical features. Methods We extracted regional measures of cortical thickness, surface area, and subcortical brain volumes from T1‐weighted (T1W) magnetic resonance imaging (MRI) scans collected by the ENIGMA‐Epilepsy consortium, comprising 804 people with MTLE‐HS and 1625 healthy controls from 25 centers. Features with a moderate case–control effect size (Cohen d ≥ .5) were used to train an event‐based model (EBM), which estimates a sequence of disease‐specific biomarker changes from cross‐sectional data and assigns a biomarker‐based fine‐grained disease stage to individual patients. We tested for associations between EBM disease stage and duration of epilepsy, age at onset, and antiseizure medicine (ASM) resistance. Results In MTLE‐HS, decrease in ipsilateral hippocampal volume along with increased asymmetry in hippocampal volume was followed by reduced thickness in neocortical regions, reduction in ipsilateral thalamus volume, and finally, increase in ipsilateral lateral ventricle volume. EBM stage was correlated with duration of illness (Spearman $ρ$ = .293, p = 7.03 × 10 −16 ), age at onset ( $ρ$ = −.18, p = 9.82 × 10 −7 ), and ASM resistance (area under the curve = .59, p = .043, Mann–Whitney U test). However, associations were driven by cases assigned to EBM Stage 0, which represents MTLE‐HS with mild or nondetectable abnormality on T1W MRI. Significance From cross‐sectional MRI, we reconstructed a disease progression model that highlights a sequence of MRI changes that aligns with previous longitudinal studies. This model could be used to stage MTLE‐HS subjects in other cohorts and help establish connections between imaging‐based progression staging and clinical features.\n
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\n \n\n \n \n \n \n \n \n \\textlessspan style=\"font-variant:small-caps;\"\\textgreater\\Mega\\‐analysis\\textless/span\\textgreatermethods in \\textlessspan style=\"font-variant:small-caps;\"\\textgreater\\ENIGMA\\\\textless/span\\textgreater: \\The\\ experience of the generalized anxiety disorder working group.\n \n \n \n \n\n\n \n Zugman, A.; Harrewijn, A.; Cardinale, E. M; Zwiebel, H.; Freitag, G. F; Werwath, K. E; Bas‐Hoogendam, J. M; Groenewold, N. A; Aghajani, M.; Hilbert, K.; Cardoner, N.; Porta‐Casteràs, D.; Gosnell, S.; Salas, R.; Blair, K. S; Blair, J. R; Hammoud, M. Z; Milad, M.; Burkhouse, K.; Phan, K L.; Schroeder, H. K; Strawn, J. R; Beesdo‐Baum, K.; Thomopoulos, S. I; Grabe, H. J; Van Der Auwera, S.; Wittfeld, K.; Nielsen, J. A; Buckner, R.; Smoller, J. W; Mwangi, B.; Soares, J. C; Wu, M.; Zunta‐Soares, G. B; Jackowski, A. P; Pan, P. M; Salum, G. A; Assaf, M.; Diefenbach, G. J; Brambilla, P.; Maggioni, E.; Hofmann, D.; Straube, T.; Andreescu, C.; Berta, R.; Tamburo, E.; Price, R.; Manfro, G. G; Critchley, H. D; Makovac, E.; Mancini, M.; Meeten, F.; Ottaviani, C.; Agosta, F.; Canu, E.; Cividini, C.; Filippi, M.; Kostić, M.; Munjiza, A.; Filippi, C. A; Leibenluft, E.; Alberton, B. A V; Balderston, N. L; Ernst, M.; Grillon, C.; Mujica‐Parodi, L. R; Van Nieuwenhuizen, H.; Fonzo, G. A; Paulus, M. P; Stein, M. B; Gur, R. E; Gur, R. C; Kaczkurkin, A. N; Larsen, B.; Satterthwaite, T. D; Harper, J.; Myers, M.; Perino, M. T; Yu, Q.; Sylvester, C. M; Veltman, D. J; Lueken, U.; Van Der Wee, N. J A; Stein, D. J; Jahanshad, N.; Thompson, P. M; Pine, D. S; and Winkler, A. M\n\n\n \n\n\n\n Human Brain Mapping, 43(1): 255–277. jan 2022.\n \n\n\n\n
\n\n\n\n \n \n \"\\textlessspanPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{zugman_span_2022,\nabstract = {Abstract\nThe ENIGMA group on Generalized Anxiety Disorder (ENIGMA‐Anxiety/GAD) is part of a broader effort to investigate anxiety disorders using imaging and genetic data across multiple sites worldwide. The group is actively conducting a mega‐analysis of a large number of brain structural scans. In this process, the group was confronted with many methodological challenges related to study planning and implementation, between‐country transfer of subject‐level data, quality control of a considerable amount of imaging data, and choices related to statistical methods and efficient use of resources. This report summarizes the background information and rationale for the various methodological decisions, as well as the approach taken to implement them. The goal is to document the approach and help guide other research groups working with large brain imaging data sets as they develop their own analytic pipelines for mega‐analyses.},\nauthor = {Zugman, Andr{\\'{e}} and Harrewijn, Anita and Cardinale, Elise M and Zwiebel, Hannah and Freitag, Gabrielle F and Werwath, Katy E and Bas‐Hoogendam, Janna M and Groenewold, Nynke A and Aghajani, Moji and Hilbert, Kevin and Cardoner, Narcis and Porta‐Caster{\\`{a}}s, Daniel and Gosnell, Savannah and Salas, Ramiro and Blair, Karina S and Blair, James R and Hammoud, Mira Z and Milad, Mohammed and Burkhouse, Katie and Phan, K Luan and Schroeder, Heidi K and Strawn, Jeffrey R and Beesdo‐Baum, Katja and Thomopoulos, Sophia I and Grabe, Hans J and {Van Der Auwera}, Sandra and Wittfeld, Katharina and Nielsen, Jared A and Buckner, Randy and Smoller, Jordan W and Mwangi, Benson and Soares, Jair C and Wu, Mon‐Ju and Zunta‐Soares, Giovana B and Jackowski, Andrea P and Pan, Pedro M and Salum, Giovanni A and Assaf, Michal and Diefenbach, Gretchen J and Brambilla, Paolo and Maggioni, Eleonora and Hofmann, David and Straube, Thomas and Andreescu, Carmen and Berta, Rachel and Tamburo, Erica and Price, Rebecca and Manfro, Gisele G and Critchley, Hugo D and Makovac, Elena and Mancini, Matteo and Meeten, Frances and Ottaviani, Cristina and Agosta, Federica and Canu, Elisa and Cividini, Camilla and Filippi, Massimo and Kosti{\\'{c}}, Milutin and Munjiza, Ana and Filippi, Courtney A and Leibenluft, Ellen and Alberton, Bianca A V and Balderston, Nicholas L and Ernst, Monique and Grillon, Christian and Mujica‐Parodi, Lilianne R and {Van Nieuwenhuizen}, Helena and Fonzo, Gregory A and Paulus, Martin P and Stein, Murray B and Gur, Raquel E and Gur, Ruben C and Kaczkurkin, Antonia N and Larsen, Bart and Satterthwaite, Theodore D and Harper, Jennifer and Myers, Michael and Perino, Michael T and Yu, Qiongru and Sylvester, Chad M and Veltman, Dick J and Lueken, Ulrike and {Van Der Wee}, Nic J A and Stein, Dan J and Jahanshad, Neda and Thompson, Paul M and Pine, Daniel S and Winkler, Anderson M},\ndoi = {10.1002/hbm.25096},\nfile = {:Users/jacquelinebracher/Zotero/storage/ZJ4BCNS9/Zugman et al. - 2022 - Mega‐analys.pdf:pdf},\nissn = {1065-9471, 1097-0193},\njournal = {Human Brain Mapping},\nmonth = {jan},\nnumber = {1},\npages = {255--277},\nshorttitle = {{\\textless}span style="font-variant},\ntitle = {{{\\textless}span style="font-variant:small-caps;"{\\textgreater}{\\{}Mega{\\}}‐analysis{\\textless}/span{\\textgreater}methods in {\\textless}span style="font-variant:small-caps;"{\\textgreater}{\\{}ENIGMA{\\}}{\\textless}/span{\\textgreater}: {\\{}The{\\}} experience of the generalized anxiety disorder working group}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1002/hbm.25096},\nvolume = {43},\nyear = {2022}\n}\n
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\n Abstract The ENIGMA group on Generalized Anxiety Disorder (ENIGMA‐Anxiety/GAD) is part of a broader effort to investigate anxiety disorders using imaging and genetic data across multiple sites worldwide. The group is actively conducting a mega‐analysis of a large number of brain structural scans. In this process, the group was confronted with many methodological challenges related to study planning and implementation, between‐country transfer of subject‐level data, quality control of a considerable amount of imaging data, and choices related to statistical methods and efficient use of resources. This report summarizes the background information and rationale for the various methodological decisions, as well as the approach taken to implement them. The goal is to document the approach and help guide other research groups working with large brain imaging data sets as they develop their own analytic pipelines for mega‐analyses.\n
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\n \n\n \n \n \n \n \n \n Nosology of behavioral addictions: \\Intersections\\ with philosophy of psychiatry •: \\Commentary\\ to the debate: “\\Behavioral\\ addictions in the \\ICD\\-11”.\n \n \n \n \n\n\n \n Stein, D. J; and Lochner, C.\n\n\n \n\n\n\n Journal of Behavioral Addictions, 11(2): 186–190. jul 2022.\n \n\n\n\n
\n\n\n\n \n \n \"NosologyPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{stein_nosology_2022,\nabstract = {Abstract\nWriting in this journal, Brand and colleagues have proposed criteria for other specified disorders due to addictive behaviors. Their proposal intersects with key debates in philosophy of psychiatry, including how best to define mental disorders, to validate them, and to optimize their meta-structure. Review of these debates in the context of behavioral addictions suggests several conclusions. First, these debates involve “essentially contested” constructs that require ongoing consideration and judgment. Second, the complexity of psychopathology suggests multiple legitimate approaches to delineating traits and explicating mechanisms. Third, in optimizing meta-structure, non-psychobiological considerations are crucial - the overlapping public mental health approach to addictive disorders is paramount.},\nauthor = {Stein, Dan J and Lochner, Christine},\ndoi = {10.1556/2006.2022.00033},\nfile = {:Users/jacquelinebracher/Zotero/storage/XWD2I9P9/Stein and Lochner - 2022 - Nosology of behavioral addictions Intersections w.pdf:pdf},\nissn = {2062-5871, 2063-5303},\njournal = {Journal of Behavioral Addictions},\nmonth = {jul},\nnumber = {2},\npages = {186--190},\nshorttitle = {Nosology of behavioral addictions},\ntitle = {{Nosology of behavioral addictions: {\\{}Intersections{\\}} with philosophy of psychiatry •: {\\{}Commentary{\\}} to the debate: “{\\{}Behavioral{\\}} addictions in the {\\{}ICD{\\}}-11”}},\nurl = {https://akjournals.com/view/journals/2006/11/2/article-p186.xml},\nvolume = {11},\nyear = {2022}\n}\n
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\n Abstract Writing in this journal, Brand and colleagues have proposed criteria for other specified disorders due to addictive behaviors. Their proposal intersects with key debates in philosophy of psychiatry, including how best to define mental disorders, to validate them, and to optimize their meta-structure. Review of these debates in the context of behavioral addictions suggests several conclusions. First, these debates involve “essentially contested” constructs that require ongoing consideration and judgment. Second, the complexity of psychopathology suggests multiple legitimate approaches to delineating traits and explicating mechanisms. Third, in optimizing meta-structure, non-psychobiological considerations are crucial - the overlapping public mental health approach to addictive disorders is paramount.\n
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\n \n\n \n \n \n \n \n \n Expanding the heuristic neurocircuit-based taxonomy to guide treatment for \\OCD\\: reply to the commentary “\\Probing\\ the genetic and molecular correlates of connectome alterations in obsessive-compulsive disorder”.\n \n \n \n \n\n\n \n Shephard, E.; Stern, E. R; Van Den Heuvel, O. A; Costa, D. L C; Batistuzzo, M. C; Godoy, P. B G; Lopes, A. C; Brunoni, A. R; Hoexter, M. Q; Shavitt, R. G; Janardhan Reddy, Y C; Lochner, C.; Stein, D. J; Simpson, H B.; and Miguel, E. C\n\n\n \n\n\n\n Molecular Psychiatry, 27(9): 3560–3561. sep 2022.\n \n\n\n\n
\n\n\n\n \n \n \"ExpandingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{shephard_expanding_2022,\nauthor = {Shephard, Elizabeth and Stern, Emily R and {Van Den Heuvel}, Odile A and Costa, Daniel L C and Batistuzzo, Marcelo C and Godoy, Priscilla B G and Lopes, Antonio C and Brunoni, Andre R and Hoexter, Marcelo Q and Shavitt, Roseli G and {Janardhan Reddy}, Y C and Lochner, Christine and Stein, Dan J and Simpson, H Blair and Miguel, Euripedes C},\ndoi = {10.1038/s41380-022-01645-0},\nissn = {1359-4184, 1476-5578},\njournal = {Molecular Psychiatry},\nmonth = {sep},\nnumber = {9},\npages = {3560--3561},\nshorttitle = {Expanding the heuristic neurocircuit-based taxonom},\ntitle = {{Expanding the heuristic neurocircuit-based taxonomy to guide treatment for {\\{}OCD{\\}}: reply to the commentary “{\\{}Probing{\\}} the genetic and molecular correlates of connectome alterations in obsessive-compulsive disorder”}},\nurl = {https://www.nature.com/articles/s41380-022-01645-0},\nvolume = {27},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Association of Maternal and Child Anemia With Brain Structure in Early Life in South Africa.\n \n \n \n \n\n\n \n Wedderburn, C J; Ringshaw, J E; Donald, K A; Joshi, S H; Subramoney, S; Fouche, J.; Stadler, J A M; Barnett, W; Rehman, A M; Hoffman, N; Roos, A; Narr, K L; Zar, H J; and Stein, D J\n\n\n \n\n\n\n 2022.\n \n\n\n\n
\n\n\n\n \n \n \"AssociationPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Wedderburn2022b,\nannote = {Export Date: 29 December 2022},\nauthor = {Wedderburn, C J and Ringshaw, J E and Donald, K A and Joshi, S H and Subramoney, S and Fouche, J.-P. and Stadler, J A M and Barnett, W and Rehman, A M and Hoffman, N and Roos, A and Narr, K L and Zar, H J and Stein, D J},\ndoi = {10.1001/jamanetworkopen.2022.44772},\nfile = {:Users/jacquelinebracher/Zotero/storage/ACVZAQ8D/Wedderburn et al. - 2022 - Association of Maternal and Child Anemia With Brai.pdf:pdf},\nnumber = {12},\npages = {e2244772},\ntitle = {{Association of Maternal and Child Anemia With Brain Structure in Early Life in South Africa}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85143379679{\\&}doi=10.1001{\\%}2Fjamanetworkopen.2022.44772{\\&}partnerID=40{\\&}md5=da3cba342ffb4867bed3c8d8fb8b810b},\nvolume = {5},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Psychopharmacotherapy of \\Obsessive\\-\\Compulsive\\ and \\Related\\ \\Disorders\\.\n \n \n \n \n\n\n \n Hoffman, J.; and Stein, D. J\n\n\n \n\n\n\n In Riederer, P.; Laux, G.; Nagatsu, T.; Le, W.; and Riederer, C., editor(s), NeuroPsychopharmacotherapy, pages 3935–3954. Springer International Publishing, Cham, 2022.\n \n\n\n\n
\n\n\n\n \n \n \"PsychopharmacotherapyPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@incollection{riederer_psychopharmacotherapy_2022,\naddress = {Cham},\nauthor = {Hoffman, Jacob and Stein, Dan J},\nbooktitle = {NeuroPsychopharmacotherapy},\ndoi = {10.1007/978-3-030-62059-2_433},\neditor = {Riederer, Peter and Laux, Gerd and Nagatsu, Toshiharu and Le, Weidong and Riederer, Christian},\nisbn = {978-3-030-62058-5 978-3-030-62059-2},\npages = {3935--3954},\npublisher = {Springer International Publishing},\ntitle = {{Psychopharmacotherapy of {\\{}Obsessive{\\}}-{\\{}Compulsive{\\}} and {\\{}Related{\\}} {\\{}Disorders{\\}}}},\nurl = {https://link.springer.com/10.1007/978-3-030-62059-2{\\_}433},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n A neuropsychoanalytic note on omnipotence.\n \n \n \n \n\n\n \n Solms, M.\n\n\n \n\n\n\n In The \\Omnipotent\\ \\State\\ of \\Mind\\, pages 115–121. Routledge, London, 1 edition, apr 2022.\n \n\n\n\n
\n\n\n\n \n \n \"APaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@incollection{arundale_neuropsychoanalytic_2022,\naddress = {London},\nauthor = {Solms, Mark},\nbooktitle = {The {\\{}Omnipotent{\\}} {\\{}State{\\}} of {\\{}Mind{\\}}},\ndoi = {10.4324/9781003185192-12},\nedition = {1},\nisbn = {978-1-00-318519-2},\nmonth = {apr},\npages = {115--121},\npublisher = {Routledge},\ntitle = {{A neuropsychoanalytic note on omnipotence}},\nurl = {https://www.taylorfrancis.com/books/9781003185192/chapters/10.4324/9781003185192-12},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Targeted transcript analysis in muscles from patients with genetically diverse congenital myopathies.\n \n \n \n \n\n\n \n Bachmann, C.; Franchini, M.; Van Den Bersselaar, L. R; Kruijt, N.; Voermans, N. C; Bouman, K.; Kamsteeg, E.; Knop, K. C.; Ruggiero, L.; Santoro, L.; Nevo, Y.; Wilmshurst, J.; Vissing, J.; Sinnreich, M.; Zorzato, D.; Muntoni, F.; Jungbluth, H.; Zorzato, F.; and Treves, S.\n\n\n \n\n\n\n Brain Communications, 4(5): fcac224. sep 2022.\n \n\n\n\n
\n\n\n\n \n \n \"TargetedPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{bachmann_targeted_2022,\nabstract = {Abstract\nCongenital myopathies are a group of early onset muscle diseases of variable severity often with characteristic muscle biopsy findings and involvement of specific muscle types. The clinical diagnosis of patients typically relies on histopathological findings and is confirmed by genetic analysis. The most commonly mutated genes encode proteins involved in skeletal muscle excitation–contraction coupling, calcium regulation, sarcomeric proteins and thin–thick filament interaction. However, mutations in genes encoding proteins involved in other physiological functions (for example mutations in SELENON and MTM1, which encode for ubiquitously expressed proteins of low tissue specificity) have also been identified. This intriguing observation indicates that the presence of a genetic mutation impacts the expression of other genes whose product is important for skeletal muscle function. The aim of the present investigation was to verify if there are common changes in transcript and microRNA expression in muscles from patients with genetically heterogeneous congenital myopathies, focusing on genes encoding proteins involved in excitation–contraction coupling and calcium homeostasis, sarcomeric proteins, transcription factors and epigenetic enzymes. Our results identify RYR1, ATPB2B and miRNA-22 as common transcripts whose expression is decreased in muscles from congenital myopathy patients. The resulting protein deficiency may contribute to the muscle weakness observed in these patients. This study also provides information regarding potential biomarkers for monitoring disease progression and response to pharmacological treatments in patients with congenital myopathies.},\nauthor = {Bachmann, Christoph and Franchini, Martina and {Van Den Bersselaar}, Luuk R and Kruijt, Nick and Voermans, Nicol C and Bouman, Karlijn and Kamsteeg, Erik-Jan and Knop, Karl Christian and Ruggiero, Lucia and Santoro, Lucio and Nevo, Yoram and Wilmshurst, Jo and Vissing, John and Sinnreich, Michael and Zorzato, Daniele and Muntoni, Francesco and Jungbluth, Heinz and Zorzato, Francesco and Treves, Susan},\ndoi = {10.1093/braincomms/fcac224},\nfile = {:Users/jacquelinebracher/Zotero/storage/BLN895K8/Bachmann et al. - 2022 - Targeted transcript analysis in muscles from patie.pdf:pdf},\nissn = {2632-1297},\njournal = {Brain Communications},\nmonth = {sep},\nnumber = {5},\npages = {fcac224},\ntitle = {{Targeted transcript analysis in muscles from patients with genetically diverse congenital myopathies}},\nurl = {https://academic.oup.com/braincomms/article/doi/10.1093/braincomms/fcac224/6687656},\nvolume = {4},\nyear = {2022}\n}\n
\n
\n\n\n
\n Abstract Congenital myopathies are a group of early onset muscle diseases of variable severity often with characteristic muscle biopsy findings and involvement of specific muscle types. The clinical diagnosis of patients typically relies on histopathological findings and is confirmed by genetic analysis. The most commonly mutated genes encode proteins involved in skeletal muscle excitation–contraction coupling, calcium regulation, sarcomeric proteins and thin–thick filament interaction. However, mutations in genes encoding proteins involved in other physiological functions (for example mutations in SELENON and MTM1, which encode for ubiquitously expressed proteins of low tissue specificity) have also been identified. This intriguing observation indicates that the presence of a genetic mutation impacts the expression of other genes whose product is important for skeletal muscle function. The aim of the present investigation was to verify if there are common changes in transcript and microRNA expression in muscles from patients with genetically heterogeneous congenital myopathies, focusing on genes encoding proteins involved in excitation–contraction coupling and calcium homeostasis, sarcomeric proteins, transcription factors and epigenetic enzymes. Our results identify RYR1, ATPB2B and miRNA-22 as common transcripts whose expression is decreased in muscles from congenital myopathy patients. The resulting protein deficiency may contribute to the muscle weakness observed in these patients. This study also provides information regarding potential biomarkers for monitoring disease progression and response to pharmacological treatments in patients with congenital myopathies.\n
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\n \n\n \n \n \n \n \n \n The utility of mobile telephone-recorded videos as adjuncts to the diagnosis of seizures and paroxysmal events in children with suspected epileptic seizures.\n \n \n \n \n\n\n \n Oyieke, K; and Wilmshurst, J.\n\n\n \n\n\n\n South African Medical Journal, 113(1): 42–48. dec 2022.\n \n\n\n\n
\n\n\n\n \n \n \"ThePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{oyieke_utility_2022,\nabstract = {Background. Epilepsy is often diagnosed through clinical description, but inter-observer interpretations can be diverse and misleading.Objective. To assess the utility of smartphone videos in the diagnosis of paediatric epilepsy.Methods. The literature was reviewed for evidence to support the use of smartphone videos, inclusive of advantages, ethical practiceand potential disadvantages. An existing adult-based quality of video (QOV) scoring tool was adapted for use in children. A pilot studyused convenience sampling of videos from 25 patients, which were reviewed to assess the viability of the adapted QOV tool againstthe subsequent diagnosis for the patients with videos. The referral mechanism of the videos was reviewed for the source and consentprocesses followed.Results. A total of 14 studies were identified. Methodologies varied; only three focused on videos of children, and QOV was formally scored in three. Studies found that smartphone videos of good quality assisted the differentiation of epilepsy from non-epileptic events, especially with accompanying history and with more experienced clinicians. The ethics and risks of circulation of smartphone videos were briefly considered in a minority of the reports. The pilot study found that the adapted QOV tool correlated with videos of moderate and high quality and subsequent diagnostic closure.Conclusions. Data relating to the role of smartphone video of events in children is lacking, especially from low- and middle-incomesettings. Guidelines for caregivers to acquire good-quality videos are not part of routine practice. The ethical implications of transfer ofsensitive material have not been adequately addressed for this group. Prospective multicentre studies are needed to formally assess the viability of the adapted QOV tool for paediatric videos.},\nauthor = {Oyieke, K and Wilmshurst, Jm},\ndoi = {10.7196/SAMJ.2023.v113i1.16661},\nfile = {:Users/jacquelinebracher/Zotero/storage/YMI82ZNA/Oyieke and Wilmshurst - 2022 - The utility of mobile telephone-recorded videos as.pdf:pdf},\nissn = {2078-5135, 0256-9574},\njournal = {South African Medical Journal},\nmonth = {dec},\nnumber = {1},\npages = {42--48},\ntitle = {{The utility of mobile telephone-recorded videos as adjuncts to the diagnosis of seizures and paroxysmal events in children with suspected epileptic seizures}},\nurl = {https://samajournals.co.za/index.php/samj/article/view/627},\nvolume = {113},\nyear = {2022}\n}\n
\n
\n\n\n
\n Background. Epilepsy is often diagnosed through clinical description, but inter-observer interpretations can be diverse and misleading.Objective. To assess the utility of smartphone videos in the diagnosis of paediatric epilepsy.Methods. The literature was reviewed for evidence to support the use of smartphone videos, inclusive of advantages, ethical practiceand potential disadvantages. An existing adult-based quality of video (QOV) scoring tool was adapted for use in children. A pilot studyused convenience sampling of videos from 25 patients, which were reviewed to assess the viability of the adapted QOV tool againstthe subsequent diagnosis for the patients with videos. The referral mechanism of the videos was reviewed for the source and consentprocesses followed.Results. A total of 14 studies were identified. Methodologies varied; only three focused on videos of children, and QOV was formally scored in three. Studies found that smartphone videos of good quality assisted the differentiation of epilepsy from non-epileptic events, especially with accompanying history and with more experienced clinicians. The ethics and risks of circulation of smartphone videos were briefly considered in a minority of the reports. The pilot study found that the adapted QOV tool correlated with videos of moderate and high quality and subsequent diagnostic closure.Conclusions. Data relating to the role of smartphone video of events in children is lacking, especially from low- and middle-incomesettings. Guidelines for caregivers to acquire good-quality videos are not part of routine practice. The ethical implications of transfer ofsensitive material have not been adequately addressed for this group. Prospective multicentre studies are needed to formally assess the viability of the adapted QOV tool for paediatric videos.\n
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\n \n\n \n \n \n \n \n Should institutions fund the feedback of individual findings in genomic research?.\n \n \n \n\n\n \n Ewuoso, C.; Berkman, B.; Wonkam, A.; and De Vries, J.\n\n\n \n\n\n\n Journal of Medical Ethics. 2022.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{Ewuoso2022,\nabstract = {The article argues the thesis that institutions have a prima facie obligation to fund the feedback of individual findings in genomic research conducted on the African continent by drawing arguments from an underexplored Afro-communitarian view of distributive justice and rights of researchers to be aided. Whilst some studies have explored how institutions have a duty to support return as a form of ancillary care or additional foreseeable service in research by mostly appealing to dominant principles and theories in the Global North, this mostly normative study explores this question by appealing to underexplored African philosophy. This is a new way of thinking about institutional responsibility to fund feedback and responds to the call to decolonise health research in Africa. Further studies are required to study how this prima facie obligation will interact with social contexts and an institution's extant relationships to find an actual duty. The research community should also work out procedures, policies and governance structures to facilitate feedback. In our opinion, though the impacts of feeding back can inform how institutions think about their actual duty, these do not obliterate the binding duty to fund feedback.},\nauthor = {Ewuoso, C. and Berkman, B. and Wonkam, A. and {De Vries}, J.},\ndoi = {10.1136/medethics-2021-107992},\njournal = {Journal of Medical Ethics},\ntitle = {{Should institutions fund the feedback of individual findings in genomic research?}},\nyear = {2022}\n}\n
\n
\n\n\n
\n The article argues the thesis that institutions have a prima facie obligation to fund the feedback of individual findings in genomic research conducted on the African continent by drawing arguments from an underexplored Afro-communitarian view of distributive justice and rights of researchers to be aided. Whilst some studies have explored how institutions have a duty to support return as a form of ancillary care or additional foreseeable service in research by mostly appealing to dominant principles and theories in the Global North, this mostly normative study explores this question by appealing to underexplored African philosophy. This is a new way of thinking about institutional responsibility to fund feedback and responds to the call to decolonise health research in Africa. Further studies are required to study how this prima facie obligation will interact with social contexts and an institution's extant relationships to find an actual duty. The research community should also work out procedures, policies and governance structures to facilitate feedback. In our opinion, though the impacts of feeding back can inform how institutions think about their actual duty, these do not obliterate the binding duty to fund feedback.\n
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\n \n\n \n \n \n \n \n \n Author \\Correction\\: \\Why\\ won't it stop? \\The\\ dynamics of benzodiazepine resistance in status epilepticus.\n \n \n \n \n\n\n \n Burman, R. J; Rosch, R. E; Wilmshurst, J. M; Sen, A.; Ramantani, G.; Akerman, C. J; and Raimondo, J. V\n\n\n \n\n\n\n Nature Reviews Neurology, 18(7): 442. jul 2022.\n \n\n\n\n
\n\n\n\n \n \n \"AuthorPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{burman_author_2022,\nauthor = {Burman, Richard J and Rosch, Richard E and Wilmshurst, Jo M and Sen, Arjune and Ramantani, Georgia and Akerman, Colin J and Raimondo, Joseph V},\ndoi = {10.1038/s41582-022-00673-2},\nfile = {:Users/jacquelinebracher/Zotero/storage/WM2DYBID/Burman et al. - 2022 - Author Correction Why won't it stop The dynamics.pdf:pdf},\nissn = {1759-4758, 1759-4766},\njournal = {Nature Reviews Neurology},\nmonth = {jul},\nnumber = {7},\npages = {442},\nshorttitle = {Author {\\{}Correction{\\}}},\ntitle = {{Author {\\{}Correction{\\}}: {\\{}Why{\\}} won't it stop? {\\{}The{\\}} dynamics of benzodiazepine resistance in status epilepticus}},\nurl = {https://www.nature.com/articles/s41582-022-00673-2},\nvolume = {18},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n The ‘\\Hard\\ \\Problem\\' of \\Consciousness\\ 1.\n \n \n \n \n\n\n \n Solms, M.\n\n\n \n\n\n\n In Psychoanalysis and the \\Mind\\-\\Body\\ \\Problem\\, pages 153–185. Routledge, London, 1 edition, mar 2022.\n \n\n\n\n
\n\n\n\n \n \n \"ThePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@incollection{mills_hard_2022,\naddress = {London},\nauthor = {Solms, Mark},\nbooktitle = {Psychoanalysis and the {\\{}Mind{\\}}-{\\{}Body{\\}} {\\{}Problem{\\}}},\ndoi = {10.4324/9781003090755-8},\nedition = {1},\nisbn = {978-1-00-309075-5},\nmonth = {mar},\npages = {153--185},\npublisher = {Routledge},\ntitle = {{The ‘{\\{}Hard{\\}} {\\{}Problem{\\}}' of {\\{}Consciousness{\\}} 1}},\nurl = {https://www.taylorfrancis.com/books/9781003090755/chapters/10.4324/9781003090755-8},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n Cortical thickness across the lifespan: Data from 17,075 healthy individuals aged 3–90 years.\n \n \n \n\n\n \n Frangou, S.; Modabbernia, A.; Williams, S.; Papachristou, E.; Doucet, G.; Agartz, I.; Aghajani, M.; Akudjedu, T.; Albajes-Eizagirre, A.; Alnæs, D.; Thompson, P.; and Dima, D.\n\n\n \n\n\n\n Human Brain Mapping, 43(1): 431–451. 2022.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{Frangou2022,\nabstract = {Delineating the association of age and cortical thickness in healthy individuals is critical given the association of cortical thickness with cognition and behavior. Previous research has shown that robust estimates of the association between age and brain morphometry require large-scale studies. In response, we used cross-sectional data from 17,075 individuals aged 3–90 years from the Enhancing Neuroimaging Genetics through Meta-Analysis (ENIGMA) Consortium to infer age-related changes in cortical thickness. We used fractional polynomial (FP) regression to quantify the association between age and cortical thickness, and we computed normalized growth centiles using the parametric Lambda, Mu, and Sigma method. Interindividual variability was estimated using meta-analysis and one-way analysis of variance. For most regions, their highest cortical thickness value was observed in childhood. Age and cortical thickness showed a negative association; the slope was steeper up to the third decade of life and more gradual thereafter; notable exceptions to this general pattern were entorhinal, temporopolar, and anterior cingulate cortices. Interindividual variability was largest in temporal and frontal regions across the lifespan. Age and its FP combinations explained up to 59{\\%} variance in cortical thickness. These results may form the basis of further investigation on normative deviation in cortical thickness and its significance for behavioral and cognitive outcomes.},\nauthor = {Frangou, S. and Modabbernia, A. and Williams, S.C.R. and Papachristou, E. and Doucet, G.E. and Agartz, I. and Aghajani, M. and Akudjedu, T.N. and Albajes-Eizagirre, A. and Aln{\\ae}s, D. and Thompson, P.M. and Dima, D.},\ndoi = {10.1002/hbm.25364},\nfile = {:Users/jacquelinebracher/Zotero/storage/7YIAK2JB/Frangou et al. - 2022 - Cortical thickness across the lifespan Data from .pdf:pdf},\njournal = {Human Brain Mapping},\nnumber = {1},\npages = {431--451},\ntitle = {{Cortical thickness across the lifespan: Data from 17,075 healthy individuals aged 3–90 years}},\nvolume = {43},\nyear = {2022}\n}\n
\n
\n\n\n
\n Delineating the association of age and cortical thickness in healthy individuals is critical given the association of cortical thickness with cognition and behavior. Previous research has shown that robust estimates of the association between age and brain morphometry require large-scale studies. In response, we used cross-sectional data from 17,075 individuals aged 3–90 years from the Enhancing Neuroimaging Genetics through Meta-Analysis (ENIGMA) Consortium to infer age-related changes in cortical thickness. We used fractional polynomial (FP) regression to quantify the association between age and cortical thickness, and we computed normalized growth centiles using the parametric Lambda, Mu, and Sigma method. Interindividual variability was estimated using meta-analysis and one-way analysis of variance. For most regions, their highest cortical thickness value was observed in childhood. Age and cortical thickness showed a negative association; the slope was steeper up to the third decade of life and more gradual thereafter; notable exceptions to this general pattern were entorhinal, temporopolar, and anterior cingulate cortices. Interindividual variability was largest in temporal and frontal regions across the lifespan. Age and its FP combinations explained up to 59% variance in cortical thickness. These results may form the basis of further investigation on normative deviation in cortical thickness and its significance for behavioral and cognitive outcomes.\n
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\n \n\n \n \n \n \n \n \n Breakdown of utilitarian moral judgement after basolateral amygdala damage.\n \n \n \n \n\n\n \n Van Honk, J.; Terburg, D.; Montoya, E. R; Grafman, J.; Stein, D. J; and Morgan, B.\n\n\n \n\n\n\n Proceedings of the National Academy of Sciences, 119(31): e2119072119. aug 2022.\n \n\n\n\n
\n\n\n\n \n \n \"BreakdownPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{van_honk_breakdown_2022,\nabstract = {Most of us would regard killing another person as morally wrong, but when the death of one saves multiple others, it can be morally permitted. According to a prominent computational dual-systems framework, in these life-and-death dilemmas, deontological (nonsacrificial) moral judgments stem from a model-free algorithm that emphasizes the intrinsic value of the sacrificial action, while utilitarian (sacrificial) moral judgments are derived from a model-based algorithm that emphasizes the outcome of the sacrificial action. Rodent decision-making research suggests that the model-based algorithm depends on the basolateral amygdala (BLA), but these findings have not yet been translated to human moral decision-making. Here, in five humans with selective, bilateral BLA damage, we show a breakdown of utilitarian sacrificial moral judgments, pointing at deficient model-based moral decision-making. Across an established set of moral dilemmas, healthy controls frequently sacrifice one person to save numerous others, but BLA-damaged humans withhold such sacrificial judgments even at the cost of thousands of lives. Our translational research confirms a neurocomputational hypothesis drawn from rodent decision-making research by indicating that the model-based algorithm which underlies outcome-based, utilitarian moral judgements in humans critically depends on the BLA.},\nauthor = {{Van Honk}, Jack and Terburg, David and Montoya, Estrella R and Grafman, Jordan and Stein, Dan J and Morgan, Barak},\ndoi = {10.1073/pnas.2119072119},\nfile = {:Users/jacquelinebracher/Zotero/storage/AZVK9SEP/Van Honk et al. - 2022 - Breakdown of utilitarian moral judgement after bas.pdf:pdf},\nissn = {0027-8424, 1091-6490},\njournal = {Proceedings of the National Academy of Sciences},\nmonth = {aug},\nnumber = {31},\npages = {e2119072119},\ntitle = {{Breakdown of utilitarian moral judgement after basolateral amygdala damage}},\nurl = {https://pnas.org/doi/full/10.1073/pnas.2119072119},\nvolume = {119},\nyear = {2022}\n}\n
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\n Most of us would regard killing another person as morally wrong, but when the death of one saves multiple others, it can be morally permitted. According to a prominent computational dual-systems framework, in these life-and-death dilemmas, deontological (nonsacrificial) moral judgments stem from a model-free algorithm that emphasizes the intrinsic value of the sacrificial action, while utilitarian (sacrificial) moral judgments are derived from a model-based algorithm that emphasizes the outcome of the sacrificial action. Rodent decision-making research suggests that the model-based algorithm depends on the basolateral amygdala (BLA), but these findings have not yet been translated to human moral decision-making. Here, in five humans with selective, bilateral BLA damage, we show a breakdown of utilitarian sacrificial moral judgments, pointing at deficient model-based moral decision-making. Across an established set of moral dilemmas, healthy controls frequently sacrifice one person to save numerous others, but BLA-damaged humans withhold such sacrificial judgments even at the cost of thousands of lives. Our translational research confirms a neurocomputational hypothesis drawn from rodent decision-making research by indicating that the model-based algorithm which underlies outcome-based, utilitarian moral judgements in humans critically depends on the BLA.\n
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\n \n\n \n \n \n \n \n \n Subcortical brain volumes in young infants exposed to antenatal maternal depression: Findings from a South African birth cohort.\n \n \n \n \n\n\n \n Groenewold, N A; Wedderburn, C J; Pellowski, J A; Fouché, J.; Michalak, L; Roos, A; Woods, R P; Narr, K L; Zar, H J; Donald, K A; and Stein, D J\n\n\n \n\n\n\n 2022.\n \n\n\n\n
\n\n\n\n \n \n \"SubcorticalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Groenewold2022,\nannote = {Export Date: 29 December 2022},\nauthor = {Groenewold, N A and Wedderburn, C J and Pellowski, J A and Fouch{\\'{e}}, J.-P. and Michalak, L and Roos, A and Woods, R P and Narr, K L and Zar, H J and Donald, K A and Stein, D J},\ndoi = {10.1016/j.nicl.2022.103206},\nfile = {:Users/jacquelinebracher/Zotero/storage/I6FLR2QM/Groenewold et al. - 2022 - Subcortical brain volumes in young infants exposed.pdf:pdf},\ntitle = {{Subcortical brain volumes in young infants exposed to antenatal maternal depression: Findings from a South African birth cohort}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85138385346{\\&}doi=10.1016{\\%}2Fj.nicl.2022.103206{\\&}partnerID=40{\\&}md5=a3b3b8f32751f9141d77d29b53715b3f},\nvolume = {36},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Attentional \\Harms\\ and \\Digital\\ \\Inequalities\\.\n \n \n \n \n\n\n \n Hartford, A.; and Stein, D. J\n\n\n \n\n\n\n JMIR Mental Health, 9(2): e30838. feb 2022.\n \n\n\n\n
\n\n\n\n \n \n \"AttentionalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{hartford_attentional_2022,\nabstract = {Recent years have seen growing public concern about the effects of persuasive digital technologies on public mental health and well-being. As the draws on our attention reach such staggering scales and as our ability to focus our attention on our own considered ends erodes ever further, the need to understand and articulate what is at stake has become pressing. In this ethical viewpoint, we explore the concept of attentional harms and emphasize their potential seriousness. We further argue that the acknowledgment of these harms has relevance for evolving debates on digital inequalities. An underdiscussed aspect of web-based inequality concerns the persuasions, and even the manipulations, that help to generate sustained attentional loss. These inequalities are poised to grow, and as they do, so will concerns about justice with regard to the psychological and self-regulatory burdens of web-based participation for different internet users. In line with calls for multidimensional approaches to digital inequalities, it is important to recognize these potential harms as well as to empower internet users against them even while expanding high-quality access.},\nauthor = {Hartford, Anna and Stein, Dan J},\ndoi = {10.2196/30838},\nfile = {:Users/jacquelinebracher/Zotero/storage/SDIJ3MGQ/Hartford and Stein - 2022 - Attentional Harms and Digital Inequalities.pdf:pdf},\nissn = {2368-7959},\njournal = {JMIR Mental Health},\nmonth = {feb},\nnumber = {2},\npages = {e30838},\ntitle = {{Attentional {\\{}Harms{\\}} and {\\{}Digital{\\}} {\\{}Inequalities{\\}}}},\nurl = {https://mental.jmir.org/2022/2/e30838},\nvolume = {9},\nyear = {2022}\n}\n
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\n Recent years have seen growing public concern about the effects of persuasive digital technologies on public mental health and well-being. As the draws on our attention reach such staggering scales and as our ability to focus our attention on our own considered ends erodes ever further, the need to understand and articulate what is at stake has become pressing. In this ethical viewpoint, we explore the concept of attentional harms and emphasize their potential seriousness. We further argue that the acknowledgment of these harms has relevance for evolving debates on digital inequalities. An underdiscussed aspect of web-based inequality concerns the persuasions, and even the manipulations, that help to generate sustained attentional loss. These inequalities are poised to grow, and as they do, so will concerns about justice with regard to the psychological and self-regulatory burdens of web-based participation for different internet users. In line with calls for multidimensional approaches to digital inequalities, it is important to recognize these potential harms as well as to empower internet users against them even while expanding high-quality access.\n
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\n \n\n \n \n \n \n \n ImpACT+, a coping intervention to improve clinical outcomes for women living with HIV and sexual trauma in South Africa: study protocol for a randomized controlled trial.\n \n \n \n\n\n \n Sikkema, K.; Rabie, S.; King, A.; Watt, M.; Mulawa, M.; Andersen, L.; Wilson, P.; Marais, A.; Ndwandwa, E.; Majokweni, S.; Orrell, C.; and Joska, J.\n\n\n \n\n\n\n Trials, 23(1). 2022.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Sikkema2022,\nabstract = {Background: Addressing sexual trauma in the context of HIV care is essential to improve clinical outcomes and mental health among women in South Africa. Women living with HIV (WLH) report disproportionately high levels of sexual trauma and have higher rates of posttraumatic stress disorder. Adherence to antiretroviral therapy (ART) may be difficult for traumatized women, as sexual trauma compounds the stress associated with managing HIV and is often comorbid with other mental health disorders, further compromising care engagement and adherence. ART initiation represents a unique window of opportunity for intervention to enhance motivation, increase care engagement, and address the negative effects of trauma on avoidant coping behaviors. Mental health interventions delivered by non-specialists in low- and middle-income countries have potential to treat depression, trauma, and effects of intimate partner violence among WLH. This study will examine the effectiveness of Improving AIDS Care after Trauma (ImpACT +), a task-shared, trauma-focused coping intervention, to promote viral suppression among WLH initiating ART in a South African clinic setting. Methods: This study will be conducted in Khayelitsha, a peri-urban settlement situated near Cape Town, South Africa. Using a hybrid type 1 effectiveness-implementation design, we will randomize 350 WLH initiating ART to the ImpACT + experimental condition or the control condition (three weekly sessions of adapted problem-solving therapy) to examine the effectiveness of ImpACT + on viral suppression, ART adherence, and the degree to which mental health outcomes mediate intervention effects. ImpACT + participants will receive six once-a-week coping intervention sessions and six monthly maintenance sessions over the follow-up period. We will conduct mental health and bio-behavioral assessments at baseline, 4, 8, and 12 months, with care engagement data extracted from medical records. We will explore scalability using the Consolidated Framework for Implementation Research (CFIR). Discussion: This trial is expected to yield important new information on psychologically informed intervention models that benefit the mental health and clinical outcomes of WLH with histories of sexual trauma. The proposed ImpACT + intervention, with its focus on building coping skills to address traumatic stress and engagement in HIV care and treatment, could have widespread impact on the health and wellbeing of individuals and communities in sub-Saharan Africa. Trial registration: Clinicaltrials.gov NCT04793217. Retrospectively registered on 11 March 2021.},\nauthor = {Sikkema, K.J. and Rabie, S. and King, A. and Watt, M.H. and Mulawa, M.I. and Andersen, L.S. and Wilson, P.A. and Marais, A. and Ndwandwa, E. and Majokweni, S. and Orrell, C. and Joska, J.A.},\ndoi = {10.1186/s13063-022-06655-5},\nfile = {:Users/jacquelinebracher/Zotero/storage/6ZGGMENL/Sikkema et al. - 2022 - ImpACT+, a coping intervention to improve clinical.pdf:pdf},\njournal = {Trials},\nnumber = {1},\ntitle = {{ImpACT+, a coping intervention to improve clinical outcomes for women living with HIV and sexual trauma in South Africa: study protocol for a randomized controlled trial}},\nvolume = {23},\nyear = {2022}\n}\n
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\n Background: Addressing sexual trauma in the context of HIV care is essential to improve clinical outcomes and mental health among women in South Africa. Women living with HIV (WLH) report disproportionately high levels of sexual trauma and have higher rates of posttraumatic stress disorder. Adherence to antiretroviral therapy (ART) may be difficult for traumatized women, as sexual trauma compounds the stress associated with managing HIV and is often comorbid with other mental health disorders, further compromising care engagement and adherence. ART initiation represents a unique window of opportunity for intervention to enhance motivation, increase care engagement, and address the negative effects of trauma on avoidant coping behaviors. Mental health interventions delivered by non-specialists in low- and middle-income countries have potential to treat depression, trauma, and effects of intimate partner violence among WLH. This study will examine the effectiveness of Improving AIDS Care after Trauma (ImpACT +), a task-shared, trauma-focused coping intervention, to promote viral suppression among WLH initiating ART in a South African clinic setting. Methods: This study will be conducted in Khayelitsha, a peri-urban settlement situated near Cape Town, South Africa. Using a hybrid type 1 effectiveness-implementation design, we will randomize 350 WLH initiating ART to the ImpACT + experimental condition or the control condition (three weekly sessions of adapted problem-solving therapy) to examine the effectiveness of ImpACT + on viral suppression, ART adherence, and the degree to which mental health outcomes mediate intervention effects. ImpACT + participants will receive six once-a-week coping intervention sessions and six monthly maintenance sessions over the follow-up period. We will conduct mental health and bio-behavioral assessments at baseline, 4, 8, and 12 months, with care engagement data extracted from medical records. We will explore scalability using the Consolidated Framework for Implementation Research (CFIR). Discussion: This trial is expected to yield important new information on psychologically informed intervention models that benefit the mental health and clinical outcomes of WLH with histories of sexual trauma. The proposed ImpACT + intervention, with its focus on building coping skills to address traumatic stress and engagement in HIV care and treatment, could have widespread impact on the health and wellbeing of individuals and communities in sub-Saharan Africa. Trial registration: Clinicaltrials.gov NCT04793217. Retrospectively registered on 11 March 2021.\n
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\n \n\n \n \n \n \n \n \n Oxytocin receptor expression patterns in the human brain across development.\n \n \n \n \n\n\n \n Rokicki, J.; Kaufmann, T.; De Lange, A. G; Van Der Meer, D.; Bahrami, S.; Sartorius, A. M; Haukvik, U. K; Steen, N. E.; Schwarz, E.; Stein, D. J; Nærland, T.; Andreassen, O. A; Westlye, L. T; and Quintana, D. S\n\n\n \n\n\n\n Neuropsychopharmacology, 47(8): 1550–1560. jul 2022.\n \n\n\n\n
\n\n\n\n \n \n \"OxytocinPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{rokicki_oxytocin_2022,\nauthor = {Rokicki, Jaroslav and Kaufmann, Tobias and {De Lange}, Ann-Marie G and {Van Der Meer}, Dennis and Bahrami, Shahram and Sartorius, Alina M and Haukvik, Unn K and Steen, Nils Eiel and Schwarz, Emanuel and Stein, Dan J and N{\\ae}rland, Terje and Andreassen, Ole A and Westlye, Lars T and Quintana, Daniel S},\ndoi = {10.1038/s41386-022-01305-5},\nfile = {:Users/jacquelinebracher/Zotero/storage/YW4GMJVJ/Rokicki et al. - 2022 - Oxytocin receptor expression patterns in the human.pdf:pdf},\nissn = {0893-133X, 1740-634X},\njournal = {Neuropsychopharmacology},\nmonth = {jul},\nnumber = {8},\npages = {1550--1560},\ntitle = {{Oxytocin receptor expression patterns in the human brain across development}},\nurl = {https://www.nature.com/articles/s41386-022-01305-5},\nvolume = {47},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Predicting alcohol dependence from \\textlessspan style=\"font-variant:small-caps;\"\\textgreatermulti‐site\\textless/span\\textgreaterbrain structural measures.\n \n \n \n \n\n\n \n Hahn, S.; Mackey, S.; Cousijn, J.; Foxe, J. J; Heinz, A.; Hester, R.; Hutchinson, K.; Kiefer, F.; Korucuoglu, O.; Lett, T.; Li, C. R; London, E.; Lorenzetti, V.; Maartje, L.; Momenan, R.; Orr, C.; Paulus, M.; Schmaal, L.; Sinha, R.; Sjoerds, Z.; Stein, D. J; Stein, E.; Van Holst, R. J; Veltman, D.; Walter, H.; Wiers, R. W; Yucel, M.; Thompson, P. M; Conrod, P.; Allgaier, N.; and Garavan, H.\n\n\n \n\n\n\n Human Brain Mapping, 43(1): 555–565. jan 2022.\n \n\n\n\n
\n\n\n\n \n \n \"PredictingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{hahn_predicting_2022,\nabstract = {Abstract\nTo identify neuroimaging biomarkers of alcohol dependence (AD) from structural magnetic resonance imaging, it may be useful to develop classification models that are explicitly generalizable to unseen sites and populations. This problem was explored in a mega‐analysis of previously published datasets from 2,034 AD and comparison participants spanning 27 sites curated by the ENIGMA Addiction Working Group. Data were grouped into a training set used for internal validation including 1,652 participants (692 AD, 24 sites), and a test set used for external validation with 382 participants (146 AD, 3 sites). An exploratory data analysis was first conducted, followed by an evolutionary search based feature selection to site generalizable and high performing subsets of brain measurements. Exploratory data analysis revealed that inclusion of case‐ and control‐only sites led to the inadvertent learning of site‐effects. Cross validation methods that do not properly account for site can drastically overestimate results. Evolutionary‐based feature selection leveraging leave‐one‐site‐out cross‐validation, to combat unintentional learning, identified cortical thickness in the left superior frontal gyrus and right lateral orbitofrontal cortex, cortical surface area in the right transverse temporal gyrus, and left putamen volume as final features. Ridge regression restricted to these features yielded a test‐set area under the receiver operating characteristic curve of 0.768. These findings evaluate strategies for handling multi‐site data with varied underlying class distributions and identify potential biomarkers for individuals with current AD.},\nauthor = {Hahn, Sage and Mackey, Scott and Cousijn, Janna and Foxe, John J and Heinz, Andreas and Hester, Robert and Hutchinson, Kent and Kiefer, Falk and Korucuoglu, Ozlem and Lett, Tristram and Li, Chiang‐Shan R and London, Edythe and Lorenzetti, Valentina and Maartje, Luijten and Momenan, Reza and Orr, Catherine and Paulus, Martin and Schmaal, Lianne and Sinha, Rajita and Sjoerds, Zsuzsika and Stein, Dan J and Stein, Elliot and {Van Holst}, Ruth J and Veltman, Dick and Walter, Henrik and Wiers, Reinout W and Yucel, Murat and Thompson, Paul M and Conrod, Patricia and Allgaier, Nicholas and Garavan, Hugh},\ndoi = {10.1002/hbm.25248},\nfile = {:Users/jacquelinebracher/Zotero/storage/VMIHGVV7/Hahn et al. - 2022 - Predicting alcohol dependence from span style=fo.pdf:pdf},\nissn = {1065-9471, 1097-0193},\njournal = {Human Brain Mapping},\nmonth = {jan},\nnumber = {1},\npages = {555--565},\nshorttitle = {Predicting alcohol dependence from {\\textless}span style="fo},\ntitle = {{Predicting alcohol dependence from {\\textless}span style="font-variant:small-caps;"{\\textgreater}multi‐site{\\textless}/span{\\textgreater}brain structural measures}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1002/hbm.25248},\nvolume = {43},\nyear = {2022}\n}\n
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\n Abstract To identify neuroimaging biomarkers of alcohol dependence (AD) from structural magnetic resonance imaging, it may be useful to develop classification models that are explicitly generalizable to unseen sites and populations. This problem was explored in a mega‐analysis of previously published datasets from 2,034 AD and comparison participants spanning 27 sites curated by the ENIGMA Addiction Working Group. Data were grouped into a training set used for internal validation including 1,652 participants (692 AD, 24 sites), and a test set used for external validation with 382 participants (146 AD, 3 sites). An exploratory data analysis was first conducted, followed by an evolutionary search based feature selection to site generalizable and high performing subsets of brain measurements. Exploratory data analysis revealed that inclusion of case‐ and control‐only sites led to the inadvertent learning of site‐effects. Cross validation methods that do not properly account for site can drastically overestimate results. Evolutionary‐based feature selection leveraging leave‐one‐site‐out cross‐validation, to combat unintentional learning, identified cortical thickness in the left superior frontal gyrus and right lateral orbitofrontal cortex, cortical surface area in the right transverse temporal gyrus, and left putamen volume as final features. Ridge regression restricted to these features yielded a test‐set area under the receiver operating characteristic curve of 0.768. These findings evaluate strategies for handling multi‐site data with varied underlying class distributions and identify potential biomarkers for individuals with current AD.\n
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\n \n\n \n \n \n \n \n \n Coulrophobia: \\An\\ investigation of clinical features.\n \n \n \n \n\n\n \n Planting, T.; Koopowitz, S.; and Stein, D. J\n\n\n \n\n\n\n South African Journal of Psychiatry, 28. jan 2022.\n \n\n\n\n
\n\n\n\n \n \n \"Coulrophobia:Paper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{planting_coulrophobia_2022,\nauthor = {Planting, Talia and Koopowitz, Sheri-Michelle and Stein, Dan J},\ndoi = {10.4102/sajpsychiatry.v28i0.1653},\nfile = {:Users/jacquelinebracher/Zotero/storage/S5GJXAGY/Planting et al. - 2022 - Coulrophobia An investigation of clinical feature.pdf:pdf},\nissn = {2078-6786, 1608-9685},\njournal = {South African Journal of Psychiatry},\nmonth = {jan},\nshorttitle = {Coulrophobia},\ntitle = {{Coulrophobia: {\\{}An{\\}} investigation of clinical features}},\nurl = {http://www.sajpsychiatry.org/index.php/sajp/article/view/1653},\nvolume = {28},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Increasing diversity in genomics requires investment in equitable partnerships and capacity building.\n \n \n \n \n\n\n \n Martin, A. R; Stroud, R. E; Abebe, T.; Akena, D.; Alemayehu, M.; Atwoli, L.; Chapman, S. B; Flowers, K.; Gelaye, B.; Gichuru, S.; Kariuki, S. M; Kinyanjui, S.; Korte, K. J; Koen, N.; Koenen, K. C; Newton, C. R J C; Olivares, A. M.; Pollock, S.; Post, K.; Singh, I.; Stein, D. J; Teferra, S.; Zingela, Z.; and Chibnik, L. B\n\n\n \n\n\n\n Nature Genetics, 54(6): 740–745. jun 2022.\n \n\n\n\n
\n\n\n\n \n \n \"IncreasingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{martin_increasing_2022,\nauthor = {Martin, Alicia R and Stroud, Rocky E and Abebe, Tamrat and Akena, Dickens and Alemayehu, Melkam and Atwoli, Lukoye and Chapman, Sin{\\'{e}}ad B and Flowers, Katelyn and Gelaye, Bizu and Gichuru, Stella and Kariuki, Symon M and Kinyanjui, Sam and Korte, Kristina J and Koen, Nastassja and Koenen, Karestan C and Newton, Charles R J C and Olivares, Ana Maria and Pollock, Sam and Post, Kristianna and Singh, Ilina and Stein, Dan J and Teferra, Solomon and Zingela, Zukiswa and Chibnik, Lori B},\ndoi = {10.1038/s41588-022-01095-y},\nfile = {:Users/jacquelinebracher/Zotero/storage/DQPTFS2V/Martin et al. - 2022 - Increasing diversity in genomics requires investme.pdf:pdf},\nissn = {1061-4036, 1546-1718},\njournal = {Nature Genetics},\nmonth = {jun},\nnumber = {6},\npages = {740--745},\ntitle = {{Increasing diversity in genomics requires investment in equitable partnerships and capacity building}},\nurl = {https://www.nature.com/articles/s41588-022-01095-y},\nvolume = {54},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Current practice in diagnostic genetic testing of the epilepsies.\n \n \n \n \n\n\n \n Krey, I.; Platzer, K.; Esterhuizen, A.; Berkovic, S. F; Helbig, I.; Hildebrand, M. S; Lerche, H.; Lowenstein, D.; Møller, R. S; Poduri, A.; Sadleir, L.; Sisodiya, S. M; Weckhuysen, S.; Wilmshurst, J. M; Weber, Y.; and Lemke, J. R\n\n\n \n\n\n\n Epileptic Disorders, 24(5): 765–786. oct 2022.\n \n\n\n\n
\n\n\n\n \n \n \"CurrentPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{krey_current_2022,\nabstract = {Abstract\nEpilepsy genetics is a rapidly developing field, in which novel disease‐associated genes, novel mechanisms associated with epilepsy, and precision medicine approaches are continuously being identified. In the past decade, advances in genomic knowledge and analysis platforms have begun to make clinical genetic testing accessible for, in principle, people of all ages with epilepsy. For this reason, the Genetics Commission of the International League Against Epilepsy (ILAE) presents this update on clinical genetic testing practice, including current techniques, indications, yield of genetic testing, recommendations for pre‐ and post‐test counseling, and follow‐up after genetic testing is completed. We acknowledge that the resources vary across different settings but highlight that genetic diagnostic testing for epilepsy should be prioritized when the likelihood of an informative finding is high. Results of genetic testing, in particular the identification of causative genetic variants, are likely to improve individual care. We emphasize the importance of genetic testing for individuals with epilepsy as we enter the era of precision therapy.},\nauthor = {Krey, Ilona and Platzer, Konrad and Esterhuizen, Alina and Berkovic, Samuel F and Helbig, Ingo and Hildebrand, Michael S and Lerche, Holger and Lowenstein, Daniel and M{\\o}ller, Rikke S and Poduri, Annapurna and Sadleir, Lynette and Sisodiya, Sanjay M and Weckhuysen, Sarah and Wilmshurst, Jo M and Weber, Yvonne and Lemke, Johannes R},\ndoi = {10.1684/epd.2022.1448},\nfile = {:Users/jacquelinebracher/Zotero/storage/MCMU4237/Krey et al. - 2022 - Current practice in diagnostic genetic testing of .pdf:pdf},\nissn = {1294-9361, 1950-6945},\njournal = {Epileptic Disorders},\nmonth = {oct},\nnumber = {5},\npages = {765--786},\ntitle = {{Current practice in diagnostic genetic testing of the epilepsies}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1684/epd.2022.1448},\nvolume = {24},\nyear = {2022}\n}\n
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\n Abstract Epilepsy genetics is a rapidly developing field, in which novel disease‐associated genes, novel mechanisms associated with epilepsy, and precision medicine approaches are continuously being identified. In the past decade, advances in genomic knowledge and analysis platforms have begun to make clinical genetic testing accessible for, in principle, people of all ages with epilepsy. For this reason, the Genetics Commission of the International League Against Epilepsy (ILAE) presents this update on clinical genetic testing practice, including current techniques, indications, yield of genetic testing, recommendations for pre‐ and post‐test counseling, and follow‐up after genetic testing is completed. We acknowledge that the resources vary across different settings but highlight that genetic diagnostic testing for epilepsy should be prioritized when the likelihood of an informative finding is high. Results of genetic testing, in particular the identification of causative genetic variants, are likely to improve individual care. We emphasize the importance of genetic testing for individuals with epilepsy as we enter the era of precision therapy.\n
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\n \n\n \n \n \n \n \n \n International consensus on diagnosis and management of \\Dravet\\ syndrome.\n \n \n \n \n\n\n \n Wirrell, E. C; Hood, V.; Knupp, K. G; Meskis, M. A.; Nabbout, R.; Scheffer, I. E; Wilmshurst, J.; and Sullivan, J.\n\n\n \n\n\n\n Epilepsia, 63(7): 1761–1777. jul 2022.\n \n\n\n\n
\n\n\n\n \n \n \"InternationalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{wirrell_international_2022,\nabstract = {Abstract\n\nObjective\nThis study was undertaken to gain consensus from experienced physicians and caregivers regarding optimal diagnosis and management of Dravet syndrome (DS), in the context of recently approved, DS‐specific therapies and emerging disease‐modifying treatments.\n\n\nMethods\nA core working group was convened consisting of six physicians with recognized expertise in DS and two representatives of the Dravet Syndrome Foundation. This core group summarized the current literature (focused on clinical presentation, comorbidities, maintenance and rescue therapies, and evolving disease‐modifying therapies) and nominated the 31‐member expert panel (ensuring international representation), which participated in two rounds of a Delphi process to gain consensus on diagnosis and management of DS.\n\n\nResults\nThere was strong consensus that infants 2–15 months old, presenting with either a first prolonged hemiclonic seizure or first convulsive status epilepticus with fever or following vaccination, in the absence of another cause, should undergo genetic testing for DS. Panelists agreed on evolution of specific comorbidities with time, but less agreement was achieved on optimal management. There was also agreement on appropriate first‐ to third‐line maintenance therapies, which included the newly approved agents. Whereas there was agreement for recommendation of disease‐modifying therapies, if they are proven safe and efficacious for seizures and/or reduction of comorbidities, there was less consensus for when these should be started, with caregivers being more conservative than physicians.\n\n\nSignificance\nThis International DS Consensus, informed by both experienced global caregiver and physician voices, provides a strong overview of the impact of DS, therapeutic goals and optimal management strategies incorporating the recent therapeutic advances in DS, and evolving disease‐modifying therapies.},\nauthor = {Wirrell, Elaine C and Hood, Veronica and Knupp, Kelly G and Meskis, Mary Anne and Nabbout, Rima and Scheffer, Ingrid E and Wilmshurst, Jo and Sullivan, Joseph},\ndoi = {10.1111/epi.17274},\nfile = {:Users/jacquelinebracher/Zotero/storage/TXQWNMI2/Wirrell et al. - 2022 - International consensus on diagnosis and managemen.pdf:pdf},\nissn = {0013-9580, 1528-1167},\njournal = {Epilepsia},\nmonth = {jul},\nnumber = {7},\npages = {1761--1777},\ntitle = {{International consensus on diagnosis and management of {\\{}Dravet{\\}} syndrome}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1111/epi.17274},\nvolume = {63},\nyear = {2022}\n}\n
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\n Abstract Objective This study was undertaken to gain consensus from experienced physicians and caregivers regarding optimal diagnosis and management of Dravet syndrome (DS), in the context of recently approved, DS‐specific therapies and emerging disease‐modifying treatments. Methods A core working group was convened consisting of six physicians with recognized expertise in DS and two representatives of the Dravet Syndrome Foundation. This core group summarized the current literature (focused on clinical presentation, comorbidities, maintenance and rescue therapies, and evolving disease‐modifying therapies) and nominated the 31‐member expert panel (ensuring international representation), which participated in two rounds of a Delphi process to gain consensus on diagnosis and management of DS. Results There was strong consensus that infants 2–15 months old, presenting with either a first prolonged hemiclonic seizure or first convulsive status epilepticus with fever or following vaccination, in the absence of another cause, should undergo genetic testing for DS. Panelists agreed on evolution of specific comorbidities with time, but less agreement was achieved on optimal management. There was also agreement on appropriate first‐ to third‐line maintenance therapies, which included the newly approved agents. Whereas there was agreement for recommendation of disease‐modifying therapies, if they are proven safe and efficacious for seizures and/or reduction of comorbidities, there was less consensus for when these should be started, with caregivers being more conservative than physicians. Significance This International DS Consensus, informed by both experienced global caregiver and physician voices, provides a strong overview of the impact of DS, therapeutic goals and optimal management strategies incorporating the recent therapeutic advances in DS, and evolving disease‐modifying therapies.\n
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\n \n\n \n \n \n \n \n \n Efficacy and tolerability of pharmacotherapy for obsessive-compulsive personality disorder: a systematic review of randomized controlled trials.\n \n \n \n \n\n\n \n Gecaite-Stonciene, J.; Williams, T.; Lochner, C.; Hoffman, J.; and Stein, D. J\n\n\n \n\n\n\n Expert Opinion on Pharmacotherapy, 23(11): 1351–1358. jul 2022.\n \n\n\n\n
\n\n\n\n \n \n \"EfficacyPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{gecaite-stonciene_efficacy_2022,\nauthor = {Gecaite-Stonciene, Julija and Williams, Taryn and Lochner, Christine and Hoffman, Jacob and Stein, Dan J},\ndoi = {10.1080/14656566.2022.2100695},\nissn = {1465-6566, 1744-7666},\njournal = {Expert Opinion on Pharmacotherapy},\nmonth = {jul},\nnumber = {11},\npages = {1351--1358},\nshorttitle = {Efficacy and tolerability of pharmacotherapy for o},\ntitle = {{Efficacy and tolerability of pharmacotherapy for obsessive-compulsive personality disorder: a systematic review of randomized controlled trials}},\nurl = {https://www.tandfonline.com/doi/full/10.1080/14656566.2022.2100695},\nvolume = {23},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Early neurodevelopment of HIV-exposed uninfected children in the era of antiretroviral therapy: a systematic review and meta-analysis.\n \n \n \n \n\n\n \n Wedderburn, C J; Weldon, E; Bertran-Cobo, C; Rehman, A M; Stein, D J; Gibb, D M; Yeung, S; Prendergast, A J; and Donald, K A\n\n\n \n\n\n\n 2022.\n \n\n\n\n
\n\n\n\n \n \n \"EarlyPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Wedderburn2022a,\nannote = {Export Date: 29 December 2022},\nauthor = {Wedderburn, C J and Weldon, E and Bertran-Cobo, C and Rehman, A M and Stein, D J and Gibb, D M and Yeung, S and Prendergast, A J and Donald, K A},\ndoi = {10.1016/S2352-4642(22)00071-2},\nfile = {:Users/jacquelinebracher/Zotero/storage/EVYSUJ4S/Wedderburn et al. - 2022 - Early neurodevelopment of HIV-exposed uninfected c.pdf:pdf},\nnumber = {6},\npages = {393--408},\ntitle = {{Early neurodevelopment of HIV-exposed uninfected children in the era of antiretroviral therapy: a systematic review and meta-analysis}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85129955066{\\&}doi=10.1016{\\%}2FS2352-4642{\\%}2822{\\%}2900071-2{\\&}partnerID=40{\\&}md5=7a4f3f260f87133fa1ad82befa708fde},\nvolume = {6},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Adaptation and norming of the \\Edinburgh\\ \\Cognitive\\ and behavioural amyotrophic lateral sclerosis screen (\\ECAS\\) for three language groups in \\South\\ \\Africa\\.\n \n \n \n \n\n\n \n Albertyn, C. H; Hardy, A.; Bakker, L. A; Hlangani, M.; Van Der Walt, K.; Zeilinga, B.; Thomas, K. G F; and Heckmann, J. M\n\n\n \n\n\n\n Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 23(7-8): 532–541. oct 2022.\n \n\n\n\n
\n\n\n\n \n \n \"AdaptationPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{albertyn_adaptation_2022,\nauthor = {Albertyn, Christine H and Hardy, Anneli and Bakker, Leonhard A and Hlangani, Makhaya and {Van Der Walt}, Kristien and Zeilinga, Braam and Thomas, Kevin G F and Heckmann, Jeannine M},\ndoi = {10.1080/21678421.2022.2030361},\nissn = {2167-8421, 2167-9223},\njournal = {Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration},\nmonth = {oct},\nnumber = {7-8},\npages = {532--541},\ntitle = {{Adaptation and norming of the {\\{}Edinburgh{\\}} {\\{}Cognitive{\\}} and behavioural amyotrophic lateral sclerosis screen ({\\{}ECAS{\\}}) for three language groups in {\\{}South{\\}} {\\{}Africa{\\}}}},\nurl = {https://www.tandfonline.com/doi/full/10.1080/21678421.2022.2030361},\nvolume = {23},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Executive function in methamphetamine users with and without psychosis.\n \n \n \n \n\n\n \n Koopowitz, S.; Cotton, S. M; Uhlmann, A.; Thomas, K. G F; and Stein, D. J\n\n\n \n\n\n\n Psychiatry Research, 317: 114820. nov 2022.\n \n\n\n\n
\n\n\n\n \n \n \"ExecutivePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{koopowitz_executive_2022,\nauthor = {Koopowitz, Sheri-Michelle and Cotton, Sarah M and Uhlmann, Anne and Thomas, Kevin G F and Stein, Dan J},\ndoi = {10.1016/j.psychres.2022.114820},\nissn = {01651781},\njournal = {Psychiatry Research},\nmonth = {nov},\npages = {114820},\ntitle = {{Executive function in methamphetamine users with and without psychosis}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S0165178122004139},\nvolume = {317},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Mental disorders and \\COVID\\-19: \\Towards\\ a precision public mental health approach.\n \n \n \n \n\n\n \n Stein, D. J; and Wessely, S.\n\n\n \n\n\n\n European Neuropsychopharmacology, 58: 42–43. may 2022.\n \n\n\n\n
\n\n\n\n \n \n \"MentalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{stein_mental_2022,\nauthor = {Stein, Dan J and Wessely, Simon},\ndoi = {10.1016/j.euroneuro.2022.02.008},\nfile = {:Users/jacquelinebracher/Zotero/storage/F7FR5H8K/Stein and Wessely - 2022 - Mental disorders and COVID-19 Towards a precision.pdf:pdf},\nissn = {0924977X},\njournal = {European Neuropsychopharmacology},\nmonth = {may},\npages = {42--43},\nshorttitle = {Mental disorders and {\\{}COVID{\\}}-19},\ntitle = {{Mental disorders and {\\{}COVID{\\}}-19: {\\{}Towards{\\}} a precision public mental health approach}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S0924977X2200133X},\nvolume = {58},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Truly minimal criteria for animal sentience.\n \n \n \n \n\n\n \n Solms, M.\n\n\n \n\n\n\n Animal Sentience, 7(32). jan 2022.\n \n\n\n\n
\n\n\n\n \n \n \"TrulyPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{solms_truly_2022,\nauthor = {Solms, Mark},\ndoi = {10.51291/2377-7478.1711},\nfile = {:Users/jacquelinebracher/Zotero/storage/P4EQGADK/Solms - 2022 - Truly minimal criteria for animal sentience.pdf:pdf},\nissn = {2377-7478},\njournal = {Animal Sentience},\nmonth = {jan},\nnumber = {32},\ntitle = {{Truly minimal criteria for animal sentience}},\nurl = {https://www.wellbeingintlstudiesrepository.org/animsent/vol7/iss32/2},\nvolume = {7},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Assessing effective treatment coverage for depression.\n \n \n \n \n\n\n \n De Girolamo, G.; and Stein, D. J\n\n\n \n\n\n\n The Lancet Regional Health - Europe, 17: 100384. jun 2022.\n \n\n\n\n
\n\n\n\n \n \n \"AssessingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{de_girolamo_assessing_2022,\nauthor = {{De Girolamo}, Giovanni and Stein, Dan J},\ndoi = {10.1016/j.lanepe.2022.100384},\nfile = {:Users/jacquelinebracher/Zotero/storage/SBQR5M8A/De Girolamo and Stein - 2022 - Assessing effective treatment coverage for depress.pdf:pdf},\nissn = {26667762},\njournal = {The Lancet Regional Health - Europe},\nmonth = {jun},\npages = {100384},\ntitle = {{Assessing effective treatment coverage for depression}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S2666776222000771},\nvolume = {17},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n The effect of the COVID-19 lockdown on mental health care use in South Africa: an interrupted time-series analysis.\n \n \n \n \n\n\n \n Wettstein, A; Tlali, M; Joska, J A; Cornell, M; Skrivankova, V W; Seedat, S; Mouton, J P; Van Den Heuvel, L L; Maxwell, N; Davies, M.; Maartens, G; Egger, M; and Haas, A D\n\n\n \n\n\n\n 2022.\n \n\n\n\n
\n\n\n\n \n \n \"ThePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Wettstein2022,\nannote = {Export Date: 29 December 2022},\nauthor = {Wettstein, A and Tlali, M and Joska, J A and Cornell, M and Skrivankova, V W and Seedat, S and Mouton, J P and {Van Den Heuvel}, L L and Maxwell, N and Davies, M.-A. and Maartens, G and Egger, M and Haas, A D},\ndoi = {10.1017/S2045796022000270},\nfile = {:Users/jacquelinebracher/Zotero/storage/ITLAXZAK/Wettstein et al. - 2022 - The effect of the COVID-19 lockdown on mental heal.pdf:pdf},\ntitle = {{The effect of the COVID-19 lockdown on mental health care use in South Africa: an interrupted time-series analysis}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85132079192{\\&}doi=10.1017{\\%}2FS2045796022000270{\\&}partnerID=40{\\&}md5=a100bb795b1b25f5f58844bee8f15a47},\nvolume = {31},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Increasing \\African\\ genomic data generation and sharing to resolve rare and undiagnosed diseases in \\Africa\\: a call-to-action by the \\H3Africa\\ rare diseases working group.\n \n \n \n \n\n\n \n Lumaka, A.; Carstens, N.; Devriendt, K.; Krause, A.; Kulohoma, B.; Kumuthini, J.; Mubungu, G.; Mukisa, J.; Nel, M.; Olanrewaju, T. O; Lombard, Z.; Landouré, G.; and as members of the Rare Disease Working Group of the H3Africa Consortium\n\n\n \n\n\n\n Orphanet Journal of Rare Diseases, 17(1): 230. dec 2022.\n \n\n\n\n
\n\n\n\n \n \n \"IncreasingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{lumaka_increasing_2022,\nabstract = {Abstract\nThe rich and diverse genomics of African populations is significantly underrepresented in reference and in disease-associated databases. This renders interpreting the Next Generation Sequencing (NGS) data and reaching a diagnostic more difficult in Africa and for the African diaspora. It increases chances for false positives with variants being misclassified as pathogenic due to their novelty or rarity. We can increase African genomic data by (1) making consent for sharing aggregate frequency data an essential component of research toolkit; (2) encouraging investigators with African data to share available data through public resources such as gnomAD, AVGD, ClinVar, DECIPHER and to use MatchMaker Exchange; (3) educating African research participants on the meaning and value of sharing aggregate frequency data; and (4) increasing funding to scale-up the production of African genomic data that will be more representative of the geographical and ethno-linguistic variation on the continent. The RDWG of H3Africa is hereby calling to action because this underrepresentation accentuates the health disparities. Applying the NGS to shorten the diagnostic odyssey or to guide therapeutic options for rare diseases will fully work for Africans only when public repositories include sufficient data from African subjects.},\nauthor = {Lumaka, Aim{\\'{e}} and Carstens, Nadia and Devriendt, Koenraad and Krause, Amanda and Kulohoma, Benard and Kumuthini, Judit and Mubungu, Gerrye and Mukisa, John and Nel, Melissa and Olanrewaju, Timothy O and Lombard, Zan{\\'{e}} and Landour{\\'{e}}, Guida and {as members of the Rare Disease Working Group of the H3Africa Consortium}},\ndoi = {10.1186/s13023-022-02391-w},\nfile = {:Users/jacquelinebracher/Zotero/storage/746RW85B/Lumaka et al. - 2022 - Increasing African genomic data generation and sha.pdf:pdf},\nissn = {1750-1172},\njournal = {Orphanet Journal of Rare Diseases},\nmonth = {dec},\nnumber = {1},\npages = {230},\nshorttitle = {Increasing {\\{}African{\\}} genomic data generation and s},\ntitle = {{Increasing {\\{}African{\\}} genomic data generation and sharing to resolve rare and undiagnosed diseases in {\\{}Africa{\\}}: a call-to-action by the {\\{}H3Africa{\\}} rare diseases working group}},\nurl = {https://ojrd.biomedcentral.com/articles/10.1186/s13023-022-02391-w},\nvolume = {17},\nyear = {2022}\n}\n
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\n Abstract The rich and diverse genomics of African populations is significantly underrepresented in reference and in disease-associated databases. This renders interpreting the Next Generation Sequencing (NGS) data and reaching a diagnostic more difficult in Africa and for the African diaspora. It increases chances for false positives with variants being misclassified as pathogenic due to their novelty or rarity. We can increase African genomic data by (1) making consent for sharing aggregate frequency data an essential component of research toolkit; (2) encouraging investigators with African data to share available data through public resources such as gnomAD, AVGD, ClinVar, DECIPHER and to use MatchMaker Exchange; (3) educating African research participants on the meaning and value of sharing aggregate frequency data; and (4) increasing funding to scale-up the production of African genomic data that will be more representative of the geographical and ethno-linguistic variation on the continent. The RDWG of H3Africa is hereby calling to action because this underrepresentation accentuates the health disparities. Applying the NGS to shorten the diagnostic odyssey or to guide therapeutic options for rare diseases will fully work for Africans only when public repositories include sufficient data from African subjects.\n
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\n \n\n \n \n \n \n \n \n Multimodal magnetic resonance neuroimaging measures characteristic of early \\textlessspan style=\"font-variant:small-caps;\"\\textgreater\\cART\\\\textless/span\\textgreater‐treated pediatric \\textlessspan style=\"font-variant:small-caps;\"\\textgreater\\HIV\\\\textless/span\\textgreater: \\A\\ feature selection approach.\n \n \n \n \n\n\n \n Khobo, I. L; Jankiewicz, M.; Holmes, M. J; Little, F.; Cotton, M. F; Laughton, B.; Van Der Kouwe, A. J W; Moreau, A.; Nwosu, E.; Meintjes, E. M; and Robertson, F. C\n\n\n \n\n\n\n Human Brain Mapping, 43(13): 4128–4144. sep 2022.\n \n\n\n\n
\n\n\n\n \n \n \"MultimodalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{khobo_multimodal_2022,\nabstract = {Abstract\n\nChildren with perinatally acquired HIV (CPHIV) have poor cognitive outcomes despite early combination antiretroviral therapy (cART). While CPHIV‐related brain alterations can be investigated separately using proton magnetic resonance spectroscopy (\n1\nH‐MRS), structural magnetic resonance imaging (sMRI), diffusion tensor imaging (DTI), and functional MRI (fMRI), a set of multimodal MRI measures characteristic of children on cART has not been previously identified. We used the embedded feature selection of a logistic elastic‐net (EN) regularization to select neuroimaging measures that distinguish CPHIV from controls and measured their classification performance via the area under the receiver operating characteristic curve (AUC) using repeated cross validation. We also wished to establish whether combining MRI modalities improved the models. In single modality analysis, sMRI volumes performed best followed by DTI, whereas individual EN models on spectroscopic, gyrification, and cortical thickness measures showed no class discrimination capability. Adding DTI and\n1\nH‐MRS in basal measures to sMRI volumes produced the highest classification performance . The best multimodal MRI set consisted of 22 DTI and sMRI volume features, which included reduced volumes of the bilateral globus pallidus and amygdala, as well as increased mean diffusivity (MD) and radial diffusivity (RD) in the right corticospinal tract in cART‐treated CPHIV. Consistent with previous studies of CPHIV, select subcortical volumes obtained from sMRI provide reasonable discrimination between CPHIV and controls. This may give insight into neuroimaging measures that are relevant in understanding the effects of HIV on the brain, thereby providing a starting point for evaluating their link with cognitive performance in CPHIV.},\nauthor = {Khobo, Isaac L and Jankiewicz, Marcin and Holmes, Martha J and Little, Francesca and Cotton, Mark F and Laughton, Barbara and {Van Der Kouwe}, Andre J W and Moreau, Allison and Nwosu, Emmanuel and Meintjes, Ernesta M and Robertson, Frances C},\ndoi = {10.1002/hbm.25907},\nfile = {:Users/jacquelinebracher/Zotero/storage/CFD5PJB5/Khobo et al. - 2022 - Multimodal magnetic resonance neuroimaging measure.pdf:pdf},\nissn = {1065-9471, 1097-0193},\njournal = {Human Brain Mapping},\nmonth = {sep},\nnumber = {13},\npages = {4128--4144},\nshorttitle = {Multimodal magnetic resonance neuroimaging measure},\ntitle = {{Multimodal magnetic resonance neuroimaging measures characteristic of early {\\textless}span style="font-variant:small-caps;"{\\textgreater}{\\{}cART{\\}}{\\textless}/span{\\textgreater}‐treated pediatric {\\textless}span style="font-variant:small-caps;"{\\textgreater}{\\{}HIV{\\}}{\\textless}/span{\\textgreater}: {\\{}A{\\}} feature selection approach}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1002/hbm.25907},\nvolume = {43},\nyear = {2022}\n}\n
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\n Abstract Children with perinatally acquired HIV (CPHIV) have poor cognitive outcomes despite early combination antiretroviral therapy (cART). While CPHIV‐related brain alterations can be investigated separately using proton magnetic resonance spectroscopy ( 1 H‐MRS), structural magnetic resonance imaging (sMRI), diffusion tensor imaging (DTI), and functional MRI (fMRI), a set of multimodal MRI measures characteristic of children on cART has not been previously identified. We used the embedded feature selection of a logistic elastic‐net (EN) regularization to select neuroimaging measures that distinguish CPHIV from controls and measured their classification performance via the area under the receiver operating characteristic curve (AUC) using repeated cross validation. We also wished to establish whether combining MRI modalities improved the models. In single modality analysis, sMRI volumes performed best followed by DTI, whereas individual EN models on spectroscopic, gyrification, and cortical thickness measures showed no class discrimination capability. Adding DTI and 1 H‐MRS in basal measures to sMRI volumes produced the highest classification performance . The best multimodal MRI set consisted of 22 DTI and sMRI volume features, which included reduced volumes of the bilateral globus pallidus and amygdala, as well as increased mean diffusivity (MD) and radial diffusivity (RD) in the right corticospinal tract in cART‐treated CPHIV. Consistent with previous studies of CPHIV, select subcortical volumes obtained from sMRI provide reasonable discrimination between CPHIV and controls. This may give insight into neuroimaging measures that are relevant in understanding the effects of HIV on the brain, thereby providing a starting point for evaluating their link with cognitive performance in CPHIV.\n
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\n \n\n \n \n \n \n \n \n Enhancing neuroimaging genetics through meta-analysis for \\Tourette\\ syndrome (\\ENIGMA\\-\\TS\\): \\A\\ worldwide platform for collaboration.\n \n \n \n \n\n\n \n Paschou, P.; Jin, Y.; Müller-Vahl, K.; Möller, H. E; Rizzo, R.; Hoekstra, P. J; Roessner, V.; Mol Debes, N.; Worbe, Y.; Hartmann, A.; Mir, P.; Cath, D.; Neuner, I.; Eichele, H.; Zhang, C.; Lewandowska, K.; Munchau, A.; Verrel, J.; Musil, R.; Silk, T. J; Hanlon, C. A; Bihun, E. D; Brandt, V.; Dietrich, A.; Forde, N.; Ganos, C.; Greene, D. J; Chu, C.; Grothe, M. J; Hershey, T.; Janik, P.; Koller, J. M; Martin-Rodriguez, J. F.; Müller, K.; Palmucci, S.; Prato, A.; Ramkiran, S.; Saia, F.; Szejko, N.; Torrecuso, R.; Tumer, Z.; Uhlmann, A.; Veselinovic, T.; Wolańczyk, T.; Zouki, J.; Jain, P.; Topaloudi, A.; Kaka, M.; Yang, Z.; Drineas, P.; Thomopoulos, S. I; White, T.; Veltman, D. J; Schmaal, L.; Stein, D. J; Buitelaar, J.; Franke, B.; Van Den Heuvel, O.; Jahanshad, N.; Thompson, P. M; and Black, K. J\n\n\n \n\n\n\n Frontiers in Psychiatry, 13: 958688. aug 2022.\n \n\n\n\n
\n\n\n\n \n \n \"EnhancingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{paschou_enhancing_2022,\nabstract = {Tourette syndrome (TS) is characterized by multiple motor and vocal tics, and high-comorbidity rates with other neuropsychiatric disorders. Obsessive compulsive disorder (OCD), attention deficit hyperactivity disorder (ADHD), autism spectrum disorders (ASDs), major depressive disorder (MDD), and anxiety disorders (AXDs) are among the most prevalent TS comorbidities. To date, studies on TS brain structure and function have been limited in size with efforts mostly fragmented. This leads to low-statistical power, discordant results due to differences in approaches, and hinders the ability to stratify patients according to clinical parameters and investigate comorbidity patterns. Here, we present the scientific premise, perspectives, and key goals that have motivated the establishment of the Enhancing Neuroimaging Genetics through Meta-Analysis for TS (ENIGMA-TS) working group. The ENIGMA-TS working group is an international collaborative effort bringing together a large network of investigators who aim to understand brain structure and function in TS and dissect the underlying neurobiology that leads to observed comorbidity patterns and clinical heterogeneity. Previously collected TS neuroimaging data will be analyzed jointly and integrated with TS genomic data, as well as equivalently large and already existing studies of highly comorbid OCD, ADHD, ASD, MDD, and AXD. Our work highlights the power of collaborative efforts and transdiagnostic approaches, and points to the existence of different TS subtypes. ENIGMA-TS will offer large-scale, high-powered studies that will lead to important insights toward understanding brain structure and function and genetic effects in TS and related disorders, and the identification of biomarkers that could help inform improved clinical practice.},\nauthor = {Paschou, Peristera and Jin, Yin and M{\\"{u}}ller-Vahl, Kirsten and M{\\"{o}}ller, Harald E and Rizzo, Renata and Hoekstra, Pieter J and Roessner, Veit and {Mol Debes}, Nanette and Worbe, Yulia and Hartmann, Andreas and Mir, Pablo and Cath, Danielle and Neuner, Irene and Eichele, Heike and Zhang, Chencheng and Lewandowska, Katarzyna and Munchau, Alexander and Verrel, Julius and Musil, Richard and Silk, Tim J and Hanlon, Colleen A and Bihun, Emily D and Brandt, Valerie and Dietrich, Andrea and Forde, Natalie and Ganos, Christos and Greene, Deanna J and Chu, Chunguang and Grothe, Michel J and Hershey, Tamara and Janik, Piotr and Koller, Jonathan M and Martin-Rodriguez, Juan Francisco and M{\\"{u}}ller, Karsten and Palmucci, Stefano and Prato, Adriana and Ramkiran, Shukti and Saia, Federica and Szejko, Natalia and Torrecuso, Renzo and Tumer, Zeynep and Uhlmann, Anne and Veselinovic, Tanja and Wola{\\'{n}}czyk, Tomasz and Zouki, Jade-Jocelyne and Jain, Pritesh and Topaloudi, Apostolia and Kaka, Mary and Yang, Zhiyu and Drineas, Petros and Thomopoulos, Sophia I and White, Tonya and Veltman, Dick J and Schmaal, Lianne and Stein, Dan J and Buitelaar, Jan and Franke, Barbara and {Van Den Heuvel}, Odile and Jahanshad, Neda and Thompson, Paul M and Black, Kevin J},\ndoi = {10.3389/fpsyt.2022.958688},\nfile = {:Users/jacquelinebracher/Zotero/storage/AQL2T5IH/Paschou et al. - 2022 - Enhancing neuroimaging genetics through meta-analy.pdf:pdf},\nissn = {1664-0640},\njournal = {Frontiers in Psychiatry},\nmonth = {aug},\npages = {958688},\nshorttitle = {Enhancing neuroimaging genetics through meta-analy},\ntitle = {{Enhancing neuroimaging genetics through meta-analysis for {\\{}Tourette{\\}} syndrome ({\\{}ENIGMA{\\}}-{\\{}TS{\\}}): {\\{}A{\\}} worldwide platform for collaboration}},\nurl = {https://www.frontiersin.org/articles/10.3389/fpsyt.2022.958688/full},\nvolume = {13},\nyear = {2022}\n}\n
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\n Tourette syndrome (TS) is characterized by multiple motor and vocal tics, and high-comorbidity rates with other neuropsychiatric disorders. Obsessive compulsive disorder (OCD), attention deficit hyperactivity disorder (ADHD), autism spectrum disorders (ASDs), major depressive disorder (MDD), and anxiety disorders (AXDs) are among the most prevalent TS comorbidities. To date, studies on TS brain structure and function have been limited in size with efforts mostly fragmented. This leads to low-statistical power, discordant results due to differences in approaches, and hinders the ability to stratify patients according to clinical parameters and investigate comorbidity patterns. Here, we present the scientific premise, perspectives, and key goals that have motivated the establishment of the Enhancing Neuroimaging Genetics through Meta-Analysis for TS (ENIGMA-TS) working group. The ENIGMA-TS working group is an international collaborative effort bringing together a large network of investigators who aim to understand brain structure and function in TS and dissect the underlying neurobiology that leads to observed comorbidity patterns and clinical heterogeneity. Previously collected TS neuroimaging data will be analyzed jointly and integrated with TS genomic data, as well as equivalently large and already existing studies of highly comorbid OCD, ADHD, ASD, MDD, and AXD. Our work highlights the power of collaborative efforts and transdiagnostic approaches, and points to the existence of different TS subtypes. ENIGMA-TS will offer large-scale, high-powered studies that will lead to important insights toward understanding brain structure and function and genetic effects in TS and related disorders, and the identification of biomarkers that could help inform improved clinical practice.\n
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\n \n\n \n \n \n \n \n \n Utility of genetic testing in children with developmental and epileptic encephalopathy (\\DEE\\) at a tertiary hospital in \\South\\ \\Africa\\: \\A\\ prospective study.\n \n \n \n \n\n\n \n Essajee, F.; Urban, M.; Smit, L.; Wilmshurst, J. M; Solomons, R.; Van Toorn, R.; and Moosa, S.\n\n\n \n\n\n\n Seizure, 101: 197–204. oct 2022.\n \n\n\n\n
\n\n\n\n \n \n \"UtilityPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{essajee_utility_2022,\nauthor = {Essajee, Farida and Urban, Michael and Smit, Liani and Wilmshurst, Jo M and Solomons, Regan and {Van Toorn}, Ronald and Moosa, Shahida},\ndoi = {10.1016/j.seizure.2022.09.001},\nfile = {:Users/jacquelinebracher/Zotero/storage/GS7CV5FT/Essajee et al. - 2022 - Utility of genetic testing in children with develo.pdf:pdf},\nissn = {10591311},\njournal = {Seizure},\nmonth = {oct},\npages = {197--204},\nshorttitle = {Utility of genetic testing in children with develo},\ntitle = {{Utility of genetic testing in children with developmental and epileptic encephalopathy ({\\{}DEE{\\}}) at a tertiary hospital in {\\{}South{\\}} {\\{}Africa{\\}}: {\\{}A{\\}} prospective study}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S1059131122001935},\nvolume = {101},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Decreased reward circuit connectivity during reward anticipation in major depression.\n \n \n \n \n\n\n \n Geugies, H.; Groenewold, N. A; Meurs, M.; Doornbos, B.; De Klerk-Sluis, J. M; Van Eijndhoven, P.; Roest, A. M; and Ruhé, H. G\n\n\n \n\n\n\n NeuroImage: Clinical, 36: 103226. 2022.\n \n\n\n\n
\n\n\n\n \n \n \"DecreasedPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{geugies_decreased_2022,\nauthor = {Geugies, Hanneke and Groenewold, Nynke A and Meurs, Maaike and Doornbos, Bennard and {De Klerk-Sluis}, Jessica M and {Van Eijndhoven}, Philip and Roest, Annelieke M and Ruh{\\'{e}}, Henricus G},\ndoi = {10.1016/j.nicl.2022.103226},\nfile = {:Users/jacquelinebracher/Zotero/storage/WRU7K563/Geugies et al. - 2022 - Decreased reward circuit connectivity during rewar.pdf:pdf},\nissn = {22131582},\njournal = {NeuroImage: Clinical},\npages = {103226},\ntitle = {{Decreased reward circuit connectivity during reward anticipation in major depression}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S2213158222002911},\nvolume = {36},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Mental \\Health\\ in a \\Digital\\ \\World\\.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Elsevier, 2022.\n \n\n\n\n
\n\n\n\n \n \n \"MentalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@book{noauthor_mental_2022,\ndoi = {10.1016/C2019-0-00197-5},\nisbn = {978-0-12-822201-0},\npublisher = {Elsevier},\ntitle = {{Mental {\\{}Health{\\}} in a {\\{}Digital{\\}} {\\{}World{\\}}}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/C20190001975},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Cognitive Differences between Men and Women with HIV: A Systematic Review and Meta-Analysis.\n \n \n \n \n\n\n \n Dreyer, A J; Munsami, A; Williams, T; Andersen, L S; Nightingale, S; Gouse, H; Joska, J; and Thomas, K G F\n\n\n \n\n\n\n 2022.\n \n\n\n\n
\n\n\n\n \n \n \"CognitivePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Dreyer2022,\nannote = {Export Date: 29 December 2022},\nauthor = {Dreyer, A J and Munsami, A and Williams, T and Andersen, L S and Nightingale, S and Gouse, H and Joska, J and Thomas, K G F},\ndoi = {10.1093/arclin/acab068},\nfile = {:Users/jacquelinebracher/Zotero/storage/N5QMENET/Dreyer et al. - 2022 - Cognitive Differences between Men and Women with H.pdf:pdf},\nnumber = {2},\npages = {479--496},\ntitle = {{Cognitive Differences between Men and Women with HIV: A Systematic Review and Meta-Analysis}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85125212310{\\&}doi=10.1093{\\%}2Farclin{\\%}2Facab068{\\&}partnerID=40{\\&}md5=04bdafe97cd9ca3a52b4571c04e2533c},\nvolume = {37},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Early structural brain development in infants exposed to \\HIV\\ and antiretroviral therapy $\\$textit\\in utero\\ in a \\South\\ \\African\\ birth cohort.\n \n \n \n \n\n\n \n Wedderburn, C. J; Groenewold, N. A; Roos, A.; Yeung, S.; Fouche, J.; Rehman, A. M; Gibb, D. M; Narr, K. L; Zar, H. J; Stein, D. J; and Donald, K. A\n\n\n \n\n\n\n Journal of the International AIDS Society, 25(1): e25863. jan 2022.\n \n\n\n\n
\n\n\n\n \n \n \"EarlyPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{wedderburn_early_2022-1,\nabstract = {Abstract\n\nIntroduction\n\nThere is a growing population of children who are HIV‐exposed and uninfected (HEU) with the successful expansion of antiretroviral therapy (ART) use in pregnancy. Children who are HEU are at risk of delayed neurodevelopment; however, there is limited research on early brain growth and maturation. We aimed to investigate the effects of\nin utero\nexposure to HIV/ART on brain structure of infants who are HEU compared to HIV‐unexposed (HU).\n\n\n\nMethods\nMagnetic resonance imaging using a T2‐weighted sequence was undertaken in a subgroup of infants aged 2–6 weeks enrolled in the Drakenstein Child Health Study birth cohort, South Africa, between 2012 and 2015. Mother–child pairs received antenatal and postnatal HIV testing and ART per local guidelines. We compared subcortical and total grey matter volumes between HEU and HU groups using multivariable linear regression adjusting for infant age, sex, intracranial volume and socio‐economic variables. We further assessed associations between brain volumes with maternal CD4 cell count and ART exposure.\n\n\nResults\n\nOne hundred forty‐six infants (40 HEU; 106 HU) with high‐resolution images were included in this analysis (mean age 3 weeks; 50.7{\\%} male). All infants who were HEU were exposed to ART (88{\\%} maternal triple ART). Infants who were HEU had smaller caudate volumes bilaterally (5.4{\\%} reduction,\np\n{\\textless}0.05) compared to HU infants. There were no group differences in other subcortical volumes (all\np\n{\\textgreater}0.2). Total grey matter volume was also reduced in infants who were HEU (2.1{\\%} reduction,\np\n{\\textless}0.05). Exploratory analyses showed that low maternal CD4 cell count ({\\textless}350 cells/mm\n3\n) was associated with decreased infant grey matter volumes. There was no relationship between timing of ART exposure and grey matter volumes.\n\n\n\nConclusions\nLower caudate and total grey matter volumes were found in infants who were HEU compared to HU in the first weeks of life, and maternal immunosuppression was associated with reduced volumes. These findings suggest that antenatal HIV exposure may impact early structural brain development and improved antenatal HIV management may have the potential to optimize neurodevelopmental outcomes of children who are HEU.},\nauthor = {Wedderburn, Catherine J and Groenewold, Nynke A and Roos, Annerine and Yeung, Shunmay and Fouche, Jean‐Paul and Rehman, Andrea M and Gibb, Diana M and Narr, Katherine L and Zar, Heather J and Stein, Dan J and Donald, Kirsten A},\ndoi = {10.1002/jia2.25863},\nfile = {:Users/jacquelinebracher/Zotero/storage/WXDWH4FV/Wedderburn et al. - 2022 - Early structural brain development in infants expo.pdf:pdf},\nissn = {1758-2652, 1758-2652},\njournal = {Journal of the International AIDS Society},\nmonth = {jan},\nnumber = {1},\npages = {e25863},\ntitle = {{Early structural brain development in infants exposed to {\\{}HIV{\\}} and antiretroviral therapy $\\backslash$textit{\\{}in utero{\\}} in a {\\{}South{\\}} {\\{}African{\\}} birth cohort}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1002/jia2.25863},\nvolume = {25},\nyear = {2022}\n}\n
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\n Abstract Introduction There is a growing population of children who are HIV‐exposed and uninfected (HEU) with the successful expansion of antiretroviral therapy (ART) use in pregnancy. Children who are HEU are at risk of delayed neurodevelopment; however, there is limited research on early brain growth and maturation. We aimed to investigate the effects of in utero exposure to HIV/ART on brain structure of infants who are HEU compared to HIV‐unexposed (HU). Methods Magnetic resonance imaging using a T2‐weighted sequence was undertaken in a subgroup of infants aged 2–6 weeks enrolled in the Drakenstein Child Health Study birth cohort, South Africa, between 2012 and 2015. Mother–child pairs received antenatal and postnatal HIV testing and ART per local guidelines. We compared subcortical and total grey matter volumes between HEU and HU groups using multivariable linear regression adjusting for infant age, sex, intracranial volume and socio‐economic variables. We further assessed associations between brain volumes with maternal CD4 cell count and ART exposure. Results One hundred forty‐six infants (40 HEU; 106 HU) with high‐resolution images were included in this analysis (mean age 3 weeks; 50.7% male). All infants who were HEU were exposed to ART (88% maternal triple ART). Infants who were HEU had smaller caudate volumes bilaterally (5.4% reduction, p \\textless0.05) compared to HU infants. There were no group differences in other subcortical volumes (all p \\textgreater0.2). Total grey matter volume was also reduced in infants who were HEU (2.1% reduction, p \\textless0.05). Exploratory analyses showed that low maternal CD4 cell count (\\textless350 cells/mm 3 ) was associated with decreased infant grey matter volumes. There was no relationship between timing of ART exposure and grey matter volumes. Conclusions Lower caudate and total grey matter volumes were found in infants who were HEU compared to HU in the first weeks of life, and maternal immunosuppression was associated with reduced volumes. These findings suggest that antenatal HIV exposure may impact early structural brain development and improved antenatal HIV management may have the potential to optimize neurodevelopmental outcomes of children who are HEU.\n
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\n \n\n \n \n \n \n \n \n Classically conditioned modulation of pain depends on stimulus intensity.\n \n \n \n \n\n\n \n Harvie, D. S; Poolman, E. Y; Madden, V. J; Olthof, N. A; and Coppieters, M. W\n\n\n \n\n\n\n Experimental Brain Research, 240(4): 1151–1158. apr 2022.\n \n\n\n\n
\n\n\n\n \n \n \"ClassicallyPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{harvie_classically_2022,\nabstract = {Abstract\n\nInnocuous cues that become associated with pain can enhance pain. This is termed classically conditioned hyperalgesia. The size of this effect varies under different conditions. We aimed to test whether the sensitising effect of pain-associated cues depends on the intensity of the paired test stimulus. To do this, two virtual reality environments were paired with either painful or non-painful vibrotactile stimuli in a counterbalanced fashion. The differential effect of the two environments was evaluated using pain intensity ratings of paired electrocutaneous test stimuli at three different intensity levels. Forty healthy participants were included in the study; 30 participants experienced sufficient pain during the learning phase and were included in the main analysis. An effect of environment (\np\n= 0.014) and interaction between environment and test stimulus intensity was found (\np\n= 0.046). Only the most intense test stimulus was modulated by environment. While the effect was small, the results are consistent with the proposition that pain-associated cues may induce hyperalgesia to some degree, under certain conditions. In particular, results highlight the potential relevance of stimulus intensity during and after the initial painful experience. Further attention is needed to comprehensively understand the variables that impact classically conditioned hyperalgesia.},\nauthor = {Harvie, Daniel S and Poolman, Eva Y and Madden, Victoria J and Olthof, Nick A and Coppieters, Michel W},\ndoi = {10.1007/s00221-021-06285-4},\nfile = {:Users/jacquelinebracher/Zotero/storage/4885M8XT/Harvie et al. - 2022 - Classically conditioned modulation of pain depends.pdf:pdf},\nissn = {0014-4819, 1432-1106},\njournal = {Experimental Brain Research},\nmonth = {apr},\nnumber = {4},\npages = {1151--1158},\ntitle = {{Classically conditioned modulation of pain depends on stimulus intensity}},\nurl = {https://link.springer.com/10.1007/s00221-021-06285-4},\nvolume = {240},\nyear = {2022}\n}\n
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\n Abstract Innocuous cues that become associated with pain can enhance pain. This is termed classically conditioned hyperalgesia. The size of this effect varies under different conditions. We aimed to test whether the sensitising effect of pain-associated cues depends on the intensity of the paired test stimulus. To do this, two virtual reality environments were paired with either painful or non-painful vibrotactile stimuli in a counterbalanced fashion. The differential effect of the two environments was evaluated using pain intensity ratings of paired electrocutaneous test stimuli at three different intensity levels. Forty healthy participants were included in the study; 30 participants experienced sufficient pain during the learning phase and were included in the main analysis. An effect of environment ( p = 0.014) and interaction between environment and test stimulus intensity was found ( p = 0.046). Only the most intense test stimulus was modulated by environment. While the effect was small, the results are consistent with the proposition that pain-associated cues may induce hyperalgesia to some degree, under certain conditions. In particular, results highlight the potential relevance of stimulus intensity during and after the initial painful experience. Further attention is needed to comprehensively understand the variables that impact classically conditioned hyperalgesia.\n
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\n \n\n \n \n \n \n \n \n Preventing birth defects, saving lives, and promoting health equity: an urgent call to action for universal mandatory food fortification with folic acid.\n \n \n \n \n\n\n \n Kancherla, V.; Botto, L. D; Rowe, L. A; Shlobin, N. A; Caceres, A.; Arynchyna-Smith, A.; Zimmerman, K.; Blount, J.; Kibruyisfaw, Z.; Ghotme, K. A; Karmarkar, S.; Fieggen, G.; Roozen, S.; Oakley, G. P; Rosseau, G.; and Berry, R. J\n\n\n \n\n\n\n The Lancet Global Health, 10(7): e1053—-e1057. jul 2022.\n \n\n\n\n
\n\n\n\n \n \n \"PreventingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{kancherla_preventing_2022,\nauthor = {Kancherla, Vijaya and Botto, Lorenzo D and Rowe, Laura A and Shlobin, Nathan A and Caceres, Adrian and Arynchyna-Smith, Anastasia and Zimmerman, Kathrin and Blount, Jeffrey and Kibruyisfaw, Zewdie and Ghotme, Kemel A and Karmarkar, Santosh and Fieggen, Graham and Roozen, Sylvia and Oakley, Godfrey P and Rosseau, Gail and Berry, Robert J},\ndoi = {10.1016/S2214-109X(22)00213-3},\nfile = {:Users/jacquelinebracher/Zotero/storage/RQ8BX65P/Kancherla et al. - 2022 - Preventing birth defects, saving lives, and promot.pdf:pdf},\nissn = {2214109X},\njournal = {The Lancet Global Health},\nmonth = {jul},\nnumber = {7},\npages = {e1053----e1057},\nshorttitle = {Preventing birth defects, saving lives, and promot},\ntitle = {{Preventing birth defects, saving lives, and promoting health equity: an urgent call to action for universal mandatory food fortification with folic acid}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S2214109X22002133},\nvolume = {10},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Diagnosis of bipolar disorders and body mass index predict clustering based on similarities in cortical thickness—\\ENIGMA\\ study in 2436 individuals.\n \n \n \n \n\n\n \n McWhinney, S. R; Abé, C.; Alda, M.; Benedetti, F.; Bøen, E.; Del Mar Bonnin, C.; Borgers, T.; Brosch, K.; Canales‐Rodríguez, E. J; Cannon, D. M; Dannlowski, U.; Diaz‐Zuluaga, A. M; Dietze, L.; Elvsåshagen, T.; Eyler, L. T; Fullerton, J. M; Goikolea, J. M; Goltermann, J.; Grotegerd, D.; Haarman, B. C M; Hahn, T.; Howells, F. M; Ingvar, M.; Kircher, T. T J; Krug, A.; Kuplicki, R. T; Landén, M.; Lemke, H.; Liberg, B.; Lopez‐Jaramillo, C.; Malt, U. F; Martyn, F. M; Mazza, E.; McDonald, C.; McPhilemy, G.; Meier, S.; Meinert, S.; Meller, T.; Melloni, E. M T; Mitchell, P. B; Nabulsi, L.; Nenadic, I.; Opel, N.; Ophoff, R. A; Overs, B. J; Pfarr, J.; Pineda‐Zapata, J. A; Pomarol‐Clotet, E.; Raduà, J.; Repple, J.; Richter, M.; Ringwald, K. G; Roberts, G.; Ross, A.; Salvador, R.; Savitz, J.; Schmitt, S.; Schofield, P. R; Sim, K.; Stein, D. J; Stein, F.; Temmingh, H. S; Thiel, K.; Thomopoulos, S. I; Van Haren, N. E M; Van Gestel, H.; Vargas, C.; Vieta, E.; Vreeker, A.; Waltemate, L.; Yatham, L. N; Ching, C. R K; Andreassen, O. A; Thompson, P. M; Hajek, T.; and for the ENIGMA Bipolar Disorders Working Group\n\n\n \n\n\n\n Bipolar Disorders, 24(5): 509–520. aug 2022.\n \n\n\n\n
\n\n\n\n \n \n \"DiagnosisPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{mcwhinney_diagnosis_2022,\nabstract = {Abstract\n\nAims\nRates of obesity have reached epidemic proportions, especially among people with psychiatric disorders. While the effects of obesity on the brain are of major interest in medicine, they remain markedly under‐researched in psychiatry.\n\n\nMethods\nWe obtained body mass index (BMI) and magnetic resonance imaging‐derived regional cortical thickness, surface area from 836 bipolar disorders (BD) and 1600 control individuals from 14 sites within the ENIGMA‐BD Working Group. We identified regionally specific profiles of cortical thickness using K‐means clustering and studied clinical characteristics associated with individual cortical profiles.\n\n\nResults\nWe detected two clusters based on similarities among participants in cortical thickness. The lower thickness cluster (46.8{\\%} of the sample) showed thinner cortex, especially in the frontal and temporal lobes and was associated with diagnosis of BD, higher BMI, and older age. BD individuals in the low thickness cluster were more likely to have the diagnosis of bipolar disorder I and less likely to be treated with lithium. In contrast, clustering based on similarities in the cortical surface area was unrelated to BD or BMI and only tracked age and sex.\n\n\nConclusions\nWe provide evidence that both BD and obesity are associated with similar alterations in cortical thickness, but not surface area. The fact that obesity increased the chance of having low cortical thickness could explain differences in cortical measures among people with BD. The thinner cortex in individuals with higher BMI, which was additive and similar to the BD‐associated alterations, may suggest that treating obesity could lower the extent of cortical thinning in BD.},\nauthor = {McWhinney, Sean R and Ab{\\'{e}}, Christoph and Alda, Martin and Benedetti, Francesco and B{\\o}en, Erlend and {Del Mar Bonnin}, Caterina and Borgers, Tiana and Brosch, Katharina and Canales‐Rodr{\\'{i}}guez, Erick J and Cannon, Dara M and Dannlowski, Udo and Diaz‐Zuluaga, Ana M and Dietze, Lorielle and Elvs{\\aa}shagen, Torbj{\\o}rn and Eyler, Lisa T and Fullerton, Janice M and Goikolea, Jose M and Goltermann, Janik and Grotegerd, Dominik and Haarman, Bartholomeus C M and Hahn, Tim and Howells, Fleur M and Ingvar, Martin and Kircher, Tilo T J and Krug, Axel and Kuplicki, Rayus T and Land{\\'{e}}n, Mikael and Lemke, Hannah and Liberg, Benny and Lopez‐Jaramillo, Carlos and Malt, Ulrik F and Martyn, Fiona M and Mazza, Elena and McDonald, Colm and McPhilemy, Genevieve and Meier, Sandra and Meinert, Susanne and Meller, Tina and Melloni, Elisa M T and Mitchell, Philip B and Nabulsi, Leila and Nenadic, Igor and Opel, Nils and Ophoff, Roel A and Overs, Bronwyn J and Pfarr, Julia‐Katharina and Pineda‐Zapata, Julian A and Pomarol‐Clotet, Edith and Radu{\\`{a}}, Joaquim and Repple, Jonathan and Richter, Maike and Ringwald, Kai G and Roberts, Gloria and Ross, Alex and Salvador, Raymond and Savitz, Jonathan and Schmitt, Simon and Schofield, Peter R and Sim, Kang and Stein, Dan J and Stein, Frederike and Temmingh, Henk S and Thiel, Katharina and Thomopoulos, Sophia I and {Van Haren}, Neeltje E M and {Van Gestel}, Holly and Vargas, Cristian and Vieta, Eduard and Vreeker, Annabel and Waltemate, Lena and Yatham, Lakshmi N and Ching, Christopher R K and Andreassen, Ole A and Thompson, Paul M and Hajek, Tomas and {for the ENIGMA Bipolar Disorders Working Group}},\ndoi = {10.1111/bdi.13172},\nfile = {:Users/jacquelinebracher/Zotero/storage/I5GSRS9E/McWhinney et al. - 2022 - Diagnosis of bipolar disorders and body mass index.pdf:pdf},\nissn = {1398-5647, 1399-5618},\njournal = {Bipolar Disorders},\nmonth = {aug},\nnumber = {5},\npages = {509--520},\ntitle = {{Diagnosis of bipolar disorders and body mass index predict clustering based on similarities in cortical thickness—{\\{}ENIGMA{\\}} study in 2436 individuals}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1111/bdi.13172},\nvolume = {24},\nyear = {2022}\n}\n
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\n Abstract Aims Rates of obesity have reached epidemic proportions, especially among people with psychiatric disorders. While the effects of obesity on the brain are of major interest in medicine, they remain markedly under‐researched in psychiatry. Methods We obtained body mass index (BMI) and magnetic resonance imaging‐derived regional cortical thickness, surface area from 836 bipolar disorders (BD) and 1600 control individuals from 14 sites within the ENIGMA‐BD Working Group. We identified regionally specific profiles of cortical thickness using K‐means clustering and studied clinical characteristics associated with individual cortical profiles. Results We detected two clusters based on similarities among participants in cortical thickness. The lower thickness cluster (46.8% of the sample) showed thinner cortex, especially in the frontal and temporal lobes and was associated with diagnosis of BD, higher BMI, and older age. BD individuals in the low thickness cluster were more likely to have the diagnosis of bipolar disorder I and less likely to be treated with lithium. In contrast, clustering based on similarities in the cortical surface area was unrelated to BD or BMI and only tracked age and sex. Conclusions We provide evidence that both BD and obesity are associated with similar alterations in cortical thickness, but not surface area. The fact that obesity increased the chance of having low cortical thickness could explain differences in cortical measures among people with BD. The thinner cortex in individuals with higher BMI, which was additive and similar to the BD‐associated alterations, may suggest that treating obesity could lower the extent of cortical thinning in BD.\n
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\n \n\n \n \n \n \n \n \n \\COVID\\-19 and the global acceleration of digital psychiatry.\n \n \n \n \n\n\n \n Stein, D. J; Naslund, J. A; and Bantjes, J.\n\n\n \n\n\n\n The Lancet Psychiatry, 9(1): 8–9. jan 2022.\n \n\n\n\n
\n\n\n\n \n \n \"\\COVID\\-19Paper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{stein_covid-19_2022,\nauthor = {Stein, Dan J and Naslund, John A and Bantjes, Jason},\ndoi = {10.1016/S2215-0366(21)00474-0},\nfile = {:Users/jacquelinebracher/Zotero/storage/QJ658CI7/Stein et al. - 2022 - COVID-19 and the global acceleration of digital ps.pdf:pdf},\nissn = {22150366},\njournal = {The Lancet Psychiatry},\nmonth = {jan},\nnumber = {1},\npages = {8--9},\ntitle = {{{\\{}COVID{\\}}-19 and the global acceleration of digital psychiatry}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S2215036621004740},\nvolume = {9},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Addiction, autonomy, and the \\Internet\\: \\Some\\ ethical considerations.\n \n \n \n \n\n\n \n Hartford, A.; and Stein, D. J\n\n\n \n\n\n\n In Mental \\Health\\ in a \\Digital\\ \\World\\, pages 481–495. Elsevier, 2022.\n \n\n\n\n
\n\n\n\n \n \n \"Addiction,Paper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@incollection{hartford_addiction_2022,\nauthor = {Hartford, Anna and Stein, Dan J},\nbooktitle = {Mental {\\{}Health{\\}} in a {\\{}Digital{\\}} {\\{}World{\\}}},\ndoi = {10.1016/B978-0-12-822201-0.00003-4},\nisbn = {978-0-12-822201-0},\npages = {481--495},\npublisher = {Elsevier},\nshorttitle = {Addiction, autonomy, and the {\\{}Internet{\\}}},\ntitle = {{Addiction, autonomy, and the {\\{}Internet{\\}}: {\\{}Some{\\}} ethical considerations}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/B9780128222010000034},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Awareness is in the eye of the observer: \\Preserved\\ third-person awareness of deficit in anosognosia for hemiplegia.\n \n \n \n \n\n\n \n Besharati, S.; Jenkinson, P. M; Kopelman, M.; Solms, M.; Moro, V.; and Fotopoulou, A.\n\n\n \n\n\n\n Neuropsychologia, 170: 108227. jun 2022.\n \n\n\n\n
\n\n\n\n \n \n \"AwarenessPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{besharati_awareness_2022,\nauthor = {Besharati, Sahba and Jenkinson, Paul M and Kopelman, Michael and Solms, Mark and Moro, Valentina and Fotopoulou, Aikaterini},\ndoi = {10.1016/j.neuropsychologia.2022.108227},\nfile = {:Users/jacquelinebracher/Zotero/storage/Z5M56KZ7/Besharati et al. - 2022 - Awareness is in the eye of the observer Preserved.pdf:pdf},\nissn = {00283932},\njournal = {Neuropsychologia},\nmonth = {jun},\npages = {108227},\nshorttitle = {Awareness is in the eye of the observer},\ntitle = {{Awareness is in the eye of the observer: {\\{}Preserved{\\}} third-person awareness of deficit in anosognosia for hemiplegia}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S0028393222000860},\nvolume = {170},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Remodeling of the Cortical Structural Connectome in Posttraumatic Stress Disorder: Results From the ENIGMA-PGC Posttraumatic Stress Disorder Consortium.\n \n \n \n \n\n\n \n Sun, D; Rakesh, G; Clarke-Rubright, E K; Haswell, C C; Logue, M W; O'Leary, E N; Cotton, A S; Xie, H; Dennis, E L; Jahanshad, N; Salminen, L E; Thomopoulos, S I; Rashid, F M; Ching, C R K; Koch, S B J; Frijling, J L; Nawijn, L; van Zuiden, M; Zhu, X; Suarez-Jimenez, B; Sierk, A; Walter, H; Manthey, A; Stevens, J S; Fani, N; van Rooij, S J H; Stein, M B; Bomyea, J; Koerte, I; Choi, K; van der Werff, S J A; Vermeiren, R.; Herzog, J I; Lebois, L A M; Baker, J T; Ressler, K J; Olson, E A; Straube, T; Korgaonkar, M S; Andrew, E; Zhu, Y; Li, G; Ipser, J; Hudson, A R; Peverill, M; Sambrook, K; Gordon, E; Baugh, L A; Forster, G; Simons, R M; Simons, J S; Magnotta, V A; Maron-Katz, A; du Plessis, S; Disner, S G; Davenport, N D; Grupe, D; Nitschke, J B; DeRoon-Cassini, T A; Fitzgerald, J; Krystal, J H; Levy, I; Olff, M; Veltman, D J; Wang, L; Neria, Y; De Bellis, M D; Jovanovic, T; Daniels, J K; Shenton, M E; van de Wee, N J A; Schmahl, C; Kaufman, M L; Rosso, I M; Sponheim, S R; Hofmann, D B; Bryant, R A; Fercho, K A; Stein, D J; Mueller, S C; Phan, K L; McLaughlin, K A; Davidson, R J; Larson, C; May, G; Nelson, S M; Abdallah, C G; Gomaa, H; Etkin, A; Seedat, S; Harpaz-Rotem, I; Liberzon, I; Wang, X; Thompson, P M; and Morey, R A\n\n\n \n\n\n\n 2022.\n \n\n\n\n
\n\n\n\n \n \n \"RemodelingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Sun2022,\nannote = {Export Date: 29 December 2022},\nauthor = {Sun, D and Rakesh, G and Clarke-Rubright, E K and Haswell, C C and Logue, M W and O'Leary, E N and Cotton, A S and Xie, H and Dennis, E L and Jahanshad, N and Salminen, L E and Thomopoulos, S I and Rashid, F M and Ching, C R K and Koch, S B J and Frijling, J L and Nawijn, L and van Zuiden, M and Zhu, X and Suarez-Jimenez, B and Sierk, A and Walter, H and Manthey, A and Stevens, J S and Fani, N and van Rooij, S J H and Stein, M B and Bomyea, J and Koerte, I and Choi, K and van der Werff, S J A and Vermeiren, R.R.J.M. and Herzog, J I and Lebois, L A M and Baker, J T and Ressler, K J and Olson, E A and Straube, T and Korgaonkar, M S and Andrew, E and Zhu, Y and Li, G and Ipser, J and Hudson, A R and Peverill, M and Sambrook, K and Gordon, E and Baugh, L A and Forster, G and Simons, R M and Simons, J S and Magnotta, V A and Maron-Katz, A and du Plessis, S and Disner, S G and Davenport, N D and Grupe, D and Nitschke, J B and DeRoon-Cassini, T A and Fitzgerald, J and Krystal, J H and Levy, I and Olff, M and Veltman, D J and Wang, L and Neria, Y and {De Bellis}, M D and Jovanovic, T and Daniels, J K and Shenton, M E and van de Wee, N J A and Schmahl, C and Kaufman, M L and Rosso, I M and Sponheim, S R and Hofmann, D B and Bryant, R A and Fercho, K A and Stein, D J and Mueller, S C and Phan, K L and McLaughlin, K A and Davidson, R J and Larson, C and May, G and Nelson, S M and Abdallah, C G and Gomaa, H and Etkin, A and Seedat, S and Harpaz-Rotem, I and Liberzon, I and Wang, X and Thompson, P M and Morey, R A},\ndoi = {10.1016/j.bpsc.2022.02.008},\nfile = {:Users/jacquelinebracher/Zotero/storage/JCHQNRE7/Sun et al. - 2022 - Remodeling of the Cortical Structural Connectome i.pdf:pdf},\nnumber = {9},\npages = {935--948},\ntitle = {{Remodeling of the Cortical Structural Connectome in Posttraumatic Stress Disorder: Results From the ENIGMA-PGC Posttraumatic Stress Disorder Consortium}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85130467346{\\&}doi=10.1016{\\%}2Fj.bpsc.2022.02.008{\\&}partnerID=40{\\&}md5=a22e24992fe00d40f12dd6f8639bb2e3},\nvolume = {7},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n A \\textlessspan style=\"font-variant:small-caps;\"\\textgreatermeta‐analysis\\textless/span\\textgreaterof deep brain structural shape and asymmetry abnormalities in 2,833 individuals with schizophrenia compared with 3,929 healthy volunteers via the \\textlessspan style=\"font-variant:small-caps;\"\\textgreater\\ENIGMA\\ .\n \n \n \n \n\n\n \n Gutman, B. A; Van Erp, T. G M; Alpert, K.; Ching, C. R K; Isaev, D.; Ragothaman, A.; Jahanshad, N.; Saremi, A.; Zavaliangos‐Petropulu, A.; Glahn, D. C; Shen, L.; Cong, S.; Alnæs, D.; Andreassen, O. A.; Doan, N. T.; Westlye, L. T; Kochunov, P.; Satterthwaite, T. D; Wolf, D. H; Huang, A. J; Kessler, C.; Weideman, A.; Nguyen, D.; Mueller, B. A; Faziola, L.; Potkin, S. G; Preda, A.; Mathalon, D. H; Bustillo, J.; Calhoun, V.; Ford, J. M; Walton, E.; Ehrlich, S.; Ducci, G.; Banaj, N.; Piras, F.; Piras, F.; Spalletta, G.; Canales‐Rodríguez, E. J; Fuentes‐Claramonte, P.; Pomarol‐Clotet, E.; Radua, J.; Salvador, R.; Sarró, S.; Dickie, E. W; Voineskos, A.; Tordesillas‐Gutiérrez, D.; Crespo‐Facorro, B.; Setién‐Suero, E.; Van Son, J. M.; Borgwardt, S.; Schönborn‐Harrisberger, F.; Morris, D.; Donohoe, G.; Holleran, L.; Cannon, D.; McDonald, C.; Corvin, A.; Gill, M.; Filho, G. B.; Rosa, P. G P; Serpa, M. H; Zanetti, M. V; Lebedeva, I.; Kaleda, V.; Tomyshev, A.; Crow, T.; James, A.; Cervenka, S.; Sellgren, C. M; Fatouros‐Bergman, H.; Agartz, I.; Howells, F.; Stein, D. J; Temmingh, H.; Uhlmann, A.; De Zubicaray, G. I; McMahon, K. L; Wright, M.; Cobia, D.; Csernansky, J. G; Thompson, P. M; Turner, J. A; and Wang, L.\n\n\n \n\n\n\n Human Brain Mapping, 43(1): 352–372. jan 2022.\n \n\n\n\n
\n\n\n\n \n \n \"APaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{gutman_span_2022,\nabstract = {Abstract\nSchizophrenia is associated with widespread alterations in subcortical brain structure. While analytic methods have enabled more detailed morphometric characterization, findings are often equivocal. In this meta‐analysis, we employed the harmonized ENIGMA shape analysis protocols to collaboratively investigate subcortical brain structure shape differences between individuals with schizophrenia and healthy control participants. The study analyzed data from 2,833 individuals with schizophrenia and 3,929 healthy control participants contributed by 21 worldwide research groups participating in the ENIGMA Schizophrenia Working Group. Harmonized shape analysis protocols were applied to each site's data independently for bilateral hippocampus, amygdala, caudate, accumbens, putamen, pallidum, and thalamus obtained from T1‐weighted structural MRI scans. Mass univariate meta‐analyses revealed more‐concave‐than‐convex shape differences in the hippocampus, amygdala, accumbens, and thalamus in individuals with schizophrenia compared with control participants, more‐convex‐than‐concave shape differences in the putamen and pallidum, and both concave and convex shape differences in the caudate. Patterns of exaggerated asymmetry were observed across the hippocampus, amygdala, and thalamus in individuals with schizophrenia compared to control participants, while diminished asymmetry encompassed ventral striatum and ventral and dorsal thalamus. Our analyses also revealed that higher chlorpromazine dose equivalents and increased positive symptom levels were associated with patterns of contiguous convex shape differences across multiple subcortical structures. Findings from our shape meta‐analysis suggest that common neurobiological mechanisms may contribute to gray matter reduction across multiple subcortical regions, thus enhancing our understanding of the nature of network disorganization in schizophrenia.},\nauthor = {Gutman, Boris A and {Van Erp}, Theo G M and Alpert, Kathryn and Ching, Christopher R K and Isaev, Dmitry and Ragothaman, Anjani and Jahanshad, Neda and Saremi, Arvin and Zavaliangos‐Petropulu, Artemis and Glahn, David C and Shen, Li and Cong, Shan and Aln{\\ae}s, Dag and Andreassen, Ole Andreas and Doan, Nhat Trung and Westlye, Lars T and Kochunov, Peter and Satterthwaite, Theodore D and Wolf, Daniel H and Huang, Alexander J and Kessler, Charles and Weideman, Andrea and Nguyen, Dana and Mueller, Bryon A and Faziola, Lawrence and Potkin, Steven G and Preda, Adrian and Mathalon, Daniel H and Bustillo, Juan and Calhoun, Vince and Ford, Judith M and Walton, Esther and Ehrlich, Stefan and Ducci, Giuseppe and Banaj, Nerisa and Piras, Fabrizio and Piras, Federica and Spalletta, Gianfranco and Canales‐Rodr{\\'{i}}guez, Erick J and Fuentes‐Claramonte, Paola and Pomarol‐Clotet, Edith and Radua, Joaquim and Salvador, Raymond and Sarr{\\'{o}}, Salvador and Dickie, Erin W and Voineskos, Aristotle and Tordesillas‐Guti{\\'{e}}rrez, Diana and Crespo‐Facorro, Benedicto and Seti{\\'{e}}n‐Suero, Esther and {Van Son}, Jacqueline Mayoral and Borgwardt, Stefan and Sch{\\"{o}}nborn‐Harrisberger, Fabienne and Morris, Derek and Donohoe, Gary and Holleran, Laurena and Cannon, Dara and McDonald, Colm and Corvin, Aiden and Gill, Michael and Filho, Geraldo Busatto and Rosa, Pedro G P and Serpa, Mauricio H and Zanetti, Marcus V and Lebedeva, Irina and Kaleda, Vasily and Tomyshev, Alexander and Crow, Tim and James, Anthony and Cervenka, Simon and Sellgren, Carl M and Fatouros‐Bergman, Helena and Agartz, Ingrid and Howells, Fleur and Stein, Dan J and Temmingh, Henk and Uhlmann, Anne and {De Zubicaray}, Greig I and McMahon, Katie L and Wright, Margie and Cobia, Derin and Csernansky, John G and Thompson, Paul M and Turner, Jessica A and Wang, Lei},\ndoi = {10.1002/hbm.25625},\nfile = {:Users/jacquelinebracher/Zotero/storage/FWEG78QX/Gutman et al. - 2022 - A meta‐anal.pdf:pdf},\nissn = {1065-9471, 1097-0193},\njournal = {Human Brain Mapping},\nmonth = {jan},\nnumber = {1},\npages = {352--372},\nshorttitle = {A {\\textless}span style="font-variant},\ntitle = {{A {\\textless}span style="font-variant:small-caps;"{\\textgreater}meta‐analysis{\\textless}/span{\\textgreater}of deep brain structural shape and asymmetry abnormalities in 2,833 individuals with schizophrenia compared with 3,929 healthy volunteers via the {\\textless}span style="font-variant:small-caps;"{\\textgreater}{\\{}ENIGMA{\\}} }},\nurl = {https://onlinelibrary.wiley.com/doi/10.1002/hbm.25625},\nvolume = {43},\nyear = {2022}\n}\n
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\n Abstract Schizophrenia is associated with widespread alterations in subcortical brain structure. While analytic methods have enabled more detailed morphometric characterization, findings are often equivocal. In this meta‐analysis, we employed the harmonized ENIGMA shape analysis protocols to collaboratively investigate subcortical brain structure shape differences between individuals with schizophrenia and healthy control participants. The study analyzed data from 2,833 individuals with schizophrenia and 3,929 healthy control participants contributed by 21 worldwide research groups participating in the ENIGMA Schizophrenia Working Group. Harmonized shape analysis protocols were applied to each site's data independently for bilateral hippocampus, amygdala, caudate, accumbens, putamen, pallidum, and thalamus obtained from T1‐weighted structural MRI scans. Mass univariate meta‐analyses revealed more‐concave‐than‐convex shape differences in the hippocampus, amygdala, accumbens, and thalamus in individuals with schizophrenia compared with control participants, more‐convex‐than‐concave shape differences in the putamen and pallidum, and both concave and convex shape differences in the caudate. Patterns of exaggerated asymmetry were observed across the hippocampus, amygdala, and thalamus in individuals with schizophrenia compared to control participants, while diminished asymmetry encompassed ventral striatum and ventral and dorsal thalamus. Our analyses also revealed that higher chlorpromazine dose equivalents and increased positive symptom levels were associated with patterns of contiguous convex shape differences across multiple subcortical structures. Findings from our shape meta‐analysis suggest that common neurobiological mechanisms may contribute to gray matter reduction across multiple subcortical regions, thus enhancing our understanding of the nature of network disorganization in schizophrenia.\n
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\n \n\n \n \n \n \n \n In-utero exposure to indoor air pollution or tobacco smoke and cognitive development in a South African birth cohort study.\n \n \n \n\n\n \n Christensen, G.; Rowcliffe, C.; Chen, J.; Vanker, A.; Koen, N.; Jones, M.; Gladish, N.; Hoffman, N.; Donald, K.; Wedderburn, C.; Stein, D.; and Hüls, A.\n\n\n \n\n\n\n Science of the Total Environment, 834. 2022.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Christensen2022,\nabstract = {Background and Aims: There is increasing evidence indicating that air pollution exposure is associated with neuronal damage. Since pregnancy is a critical window of vulnerability, air pollution exposure during this period could have adverse effects on neurodevelopment. This study aims 1) to analyze associations of prenatal exposure to indoor air pollution (particulate matter with diameters ≤10 $\\mu$m, PM10) and tobacco smoke with neurodevelopment and 2) to determine whether these associations are mediated by deviations of epigenetic gestational age from chronological gestational age ($\\Delta$GA). Methods: Data of 734 children from the South African Drakenstein Child Health Study were analyzed. Prenatal PM10 exposure was measured using devices placed in the families' homes. Maternal smoking during pregnancy was determined by maternal urine cotinine measures. The Bayley Scales of Infant and Toddler Development III (BSID-III) was used to measure cognition, language and motor development and adaptive behavior at two years of age. Linear regression models adjusted for maternal age, gestational age, sex of child, ancestry, birth weight/length, and socioeconomic status were used to explore associations between air pollutants and BSID-III scores. A mediation analysis was conducted to analyze if these associations were mediated by $\\Delta$GA using DNA methylation measurements from cord blood. Results: An increase of one interquartile range in natural-log transformed PM10 (lnPM10; 1.58 $\\mu$g/m3) was significantly associated with lower composite scores in cognition, language, and adaptive behavior sub-scores (composite score $\\beta$-estimate [95{\\%}-confidence interval]: −0.950 [−1.821, −0.120]). Maternal smoking was significantly associated with lower adaptive behavior scores (−3.386 [−5.632, −1.139]). Associations were not significantly mediated by $\\Delta$GA (e.g., for PM10 and cognition, proportion mediated [p-value]: 4{\\%} [0.52]). Conclusion: We found an association of prenatal exposure to indoor air pollution (PM10) and tobacco smoke on neurodevelopment at two years of age, particularly cognition, language, and adaptive behavior. Further research is needed to understand underlying biological mediators.},\nauthor = {Christensen, G.M. and Rowcliffe, C. and Chen, J. and Vanker, A. and Koen, N. and Jones, M.J. and Gladish, N. and Hoffman, N. and Donald, K.A. and Wedderburn, C.J. and Stein, D.J. and H{\\"{u}}ls, A.},\ndoi = {10.1016/j.scitotenv.2022.155394},\njournal = {Science of the Total Environment},\ntitle = {{In-utero exposure to indoor air pollution or tobacco smoke and cognitive development in a South African birth cohort study}},\nvolume = {834},\nyear = {2022}\n}\n
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\n Background and Aims: There is increasing evidence indicating that air pollution exposure is associated with neuronal damage. Since pregnancy is a critical window of vulnerability, air pollution exposure during this period could have adverse effects on neurodevelopment. This study aims 1) to analyze associations of prenatal exposure to indoor air pollution (particulate matter with diameters ≤10 $μ$m, PM10) and tobacco smoke with neurodevelopment and 2) to determine whether these associations are mediated by deviations of epigenetic gestational age from chronological gestational age ($Δ$GA). Methods: Data of 734 children from the South African Drakenstein Child Health Study were analyzed. Prenatal PM10 exposure was measured using devices placed in the families' homes. Maternal smoking during pregnancy was determined by maternal urine cotinine measures. The Bayley Scales of Infant and Toddler Development III (BSID-III) was used to measure cognition, language and motor development and adaptive behavior at two years of age. Linear regression models adjusted for maternal age, gestational age, sex of child, ancestry, birth weight/length, and socioeconomic status were used to explore associations between air pollutants and BSID-III scores. A mediation analysis was conducted to analyze if these associations were mediated by $Δ$GA using DNA methylation measurements from cord blood. Results: An increase of one interquartile range in natural-log transformed PM10 (lnPM10; 1.58 $μ$g/m3) was significantly associated with lower composite scores in cognition, language, and adaptive behavior sub-scores (composite score $β$-estimate [95%-confidence interval]: −0.950 [−1.821, −0.120]). Maternal smoking was significantly associated with lower adaptive behavior scores (−3.386 [−5.632, −1.139]). Associations were not significantly mediated by $Δ$GA (e.g., for PM10 and cognition, proportion mediated [p-value]: 4% [0.52]). Conclusion: We found an association of prenatal exposure to indoor air pollution (PM10) and tobacco smoke on neurodevelopment at two years of age, particularly cognition, language, and adaptive behavior. Further research is needed to understand underlying biological mediators.\n
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\n \n\n \n \n \n \n \n \n Construct validity and factor structure of the \\Kessler\\-10 in \\South\\ \\Africa\\.\n \n \n \n \n\n\n \n Hoffman, J.; Cossie, Q.; Ametaj, A. A; Kim, H. H; James, R.; Stroud, R. E; Stevenson, A.; Zingela, Z.; Stein, D. J; and Gelaye, B.\n\n\n \n\n\n\n BMC Psychology, 10(1): 177. dec 2022.\n \n\n\n\n
\n\n\n\n \n \n \"ConstructPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{hoffman_construct_2022,\nabstract = {Abstract\n\nBackground\nThe Kessler Psychological Distress Scale (K-10) is a short screening tool developed to identify, with good sensitivity, non-specific psychological distress in the general population. Sensitivity and specificity of the K-10 have been examined in various clinical populations in South Africa; however, other psychometric properties, such as construct validity and factor structure, have not been evaluated. We present evidence of the prevalence and severity of psychological distress in an outpatient setting in South Africa and evaluate the internal reliability, construct validity, and factor structure of the K-10 in this population.\n\n\nMethods\nWe explored prevalence estimates of psychological distress using previously established cutoffs and assessed the reliability (consistency) of the K-10 by calculating Cronbach's alpha, item-total correlations and omega total and hierarchical coefficients. Construct validity and factor structure of the K-10 were examined through split-sample exploratory factor analysis (EFA) followed by confirmatory factor analysis (CFA), comparing several theoretical models and the EFA.\n\n\nResults\nOverall, there was low prevalence of psychological distress in our sample of 2591 adults, the majority of whom were between the ages of 18–44 (77.7{\\%}). The K-10 showed good construct validity and reliability, with a Cronbach's alpha of 0.84 and omega total of 0.88. EFA yielded a four-factor solution with likely measurement artifacts. CFA showed that the four-factor model from EFA displayed the best comparative fit indices, but was likely overfitted. The unidimensional model with correlated errors was deemed the best fitting model based on fit indices, prior theory, and previous studies.\n\n\nConclusion\nThe K-10 displays adequate psychometric properties, good internal reliability, and good fit with a unidimensional-factor structure with correlated errors. Further work is required to determine appropriate cutoff values in different populations and clinical subgroups within South Africa to aid in determining the K-10's clinical utility.},\nauthor = {Hoffman, Jacob and Cossie, Qhama and Ametaj, Amantia A and Kim, Hannah H and James, Roxanne and Stroud, Rocky E and Stevenson, Anne and Zingela, Zukiswa and Stein, Dan J and Gelaye, Bizu},\ndoi = {10.1186/s40359-022-00883-9},\nfile = {:Users/jacquelinebracher/Zotero/storage/Y8GV9FA2/Hoffman et al. - 2022 - Construct validity and factor structure of the Kes.pdf:pdf},\nissn = {2050-7283},\njournal = {BMC Psychology},\nmonth = {dec},\nnumber = {1},\npages = {177},\ntitle = {{Construct validity and factor structure of the {\\{}Kessler{\\}}-10 in {\\{}South{\\}} {\\{}Africa{\\}}}},\nurl = {https://bmcpsychology.biomedcentral.com/articles/10.1186/s40359-022-00883-9},\nvolume = {10},\nyear = {2022}\n}\n
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\n Abstract Background The Kessler Psychological Distress Scale (K-10) is a short screening tool developed to identify, with good sensitivity, non-specific psychological distress in the general population. Sensitivity and specificity of the K-10 have been examined in various clinical populations in South Africa; however, other psychometric properties, such as construct validity and factor structure, have not been evaluated. We present evidence of the prevalence and severity of psychological distress in an outpatient setting in South Africa and evaluate the internal reliability, construct validity, and factor structure of the K-10 in this population. Methods We explored prevalence estimates of psychological distress using previously established cutoffs and assessed the reliability (consistency) of the K-10 by calculating Cronbach's alpha, item-total correlations and omega total and hierarchical coefficients. Construct validity and factor structure of the K-10 were examined through split-sample exploratory factor analysis (EFA) followed by confirmatory factor analysis (CFA), comparing several theoretical models and the EFA. Results Overall, there was low prevalence of psychological distress in our sample of 2591 adults, the majority of whom were between the ages of 18–44 (77.7%). The K-10 showed good construct validity and reliability, with a Cronbach's alpha of 0.84 and omega total of 0.88. EFA yielded a four-factor solution with likely measurement artifacts. CFA showed that the four-factor model from EFA displayed the best comparative fit indices, but was likely overfitted. The unidimensional model with correlated errors was deemed the best fitting model based on fit indices, prior theory, and previous studies. Conclusion The K-10 displays adequate psychometric properties, good internal reliability, and good fit with a unidimensional-factor structure with correlated errors. Further work is required to determine appropriate cutoff values in different populations and clinical subgroups within South Africa to aid in determining the K-10's clinical utility.\n
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\n \n\n \n \n \n \n \n \n \\textlessspan style=\"font-variant:small-caps;\"\\textgreater\\ENIGMA\\‐anxiety\\textless/span\\textgreaterworking group: \\Rationale\\ for and organization of \\textlessspan style=\"font-variant:small-caps;\"\\textgreaterlarge‐scale\\textless/span\\textgreaterneuroimaging studies of anxiety disorders.\n \n \n \n \n\n\n \n Bas‐Hoogendam, J. M.; Groenewold, N. A; Aghajani, M.; Freitag, G. F; Harrewijn, A.; Hilbert, K.; Jahanshad, N.; Thomopoulos, S. I; Thompson, P. M; Veltman, D. J; Winkler, A. M; Lueken, U.; Pine, D. S; Van Der Wee, N. J A; Stein, D. J; and ENIGMA‐Anxiety Working Group\n\n\n \n\n\n\n Human Brain Mapping, 43(1): 83–112. jan 2022.\n \n\n\n\n
\n\n\n\n \n \n \"\\textlessspanPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{bashoogendam_span_2022,\nabstract = {Abstract\nAnxiety disorders are highly prevalent and disabling but seem particularly tractable to investigation with translational neuroscience methodologies. Neuroimaging has informed our understanding of the neurobiology of anxiety disorders, but research has been limited by small sample sizes and low statistical power, as well as heterogenous imaging methodology. The ENIGMA‐Anxiety Working Group has brought together researchers from around the world, in a harmonized and coordinated effort to address these challenges and generate more robust and reproducible findings. This paper elaborates on the concepts and methods informing the work of the working group to date, and describes the initial approach of the four subgroups studying generalized anxiety disorder, panic disorder, social anxiety disorder, and specific phobia. At present, the ENIGMA‐Anxiety database contains information about more than 100 unique samples, from 16 countries and 59 institutes. Future directions include examining additional imaging modalities, integrating imaging and genetic data, and collaborating with other ENIGMA working groups. The ENIGMA consortium creates synergy at the intersection of global mental health and clinical neuroscience, and the ENIGMA‐Anxiety Working Group extends the promise of this approach to neuroimaging research on anxiety disorders.},\nauthor = {Bas‐Hoogendam, Janna Marie and Groenewold, Nynke A and Aghajani, Moji and Freitag, Gabrielle F and Harrewijn, Anita and Hilbert, Kevin and Jahanshad, Neda and Thomopoulos, Sophia I and Thompson, Paul M and Veltman, Dick J and Winkler, Anderson M and Lueken, Ulrike and Pine, Daniel S and {Van Der Wee}, Nic J A and Stein, Dan J and {ENIGMA‐Anxiety Working Group}},\ndoi = {10.1002/hbm.25100},\nfile = {:Users/jacquelinebracher/Zotero/storage/GXIKSNK8/Bas‐Hoogendam et al. - 2022 - ENIGMA‐anxi.pdf:pdf},\nissn = {1065-9471, 1097-0193},\njournal = {Human Brain Mapping},\nmonth = {jan},\nnumber = {1},\npages = {83--112},\nshorttitle = {{\\textless}span style="font-variant},\ntitle = {{{\\textless}span style="font-variant:small-caps;"{\\textgreater}{\\{}ENIGMA{\\}}‐anxiety{\\textless}/span{\\textgreater}working group: {\\{}Rationale{\\}} for and organization of {\\textless}span style="font-variant:small-caps;"{\\textgreater}large‐scale{\\textless}/span{\\textgreater}neuroimaging studies of anxiety disorders}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1002/hbm.25100},\nvolume = {43},\nyear = {2022}\n}\n
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\n Abstract Anxiety disorders are highly prevalent and disabling but seem particularly tractable to investigation with translational neuroscience methodologies. Neuroimaging has informed our understanding of the neurobiology of anxiety disorders, but research has been limited by small sample sizes and low statistical power, as well as heterogenous imaging methodology. The ENIGMA‐Anxiety Working Group has brought together researchers from around the world, in a harmonized and coordinated effort to address these challenges and generate more robust and reproducible findings. This paper elaborates on the concepts and methods informing the work of the working group to date, and describes the initial approach of the four subgroups studying generalized anxiety disorder, panic disorder, social anxiety disorder, and specific phobia. At present, the ENIGMA‐Anxiety database contains information about more than 100 unique samples, from 16 countries and 59 institutes. Future directions include examining additional imaging modalities, integrating imaging and genetic data, and collaborating with other ENIGMA working groups. The ENIGMA consortium creates synergy at the intersection of global mental health and clinical neuroscience, and the ENIGMA‐Anxiety Working Group extends the promise of this approach to neuroimaging research on anxiety disorders.\n
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\n \n\n \n \n \n \n \n \n What are the pharmacotherapeutic options for adjustment disorder?.\n \n \n \n \n\n\n \n Hoffman, J.; and Stein, D. J\n\n\n \n\n\n\n Expert Opinion on Pharmacotherapy, 23(6): 643–646. apr 2022.\n \n\n\n\n
\n\n\n\n \n \n \"WhatPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{hoffman_what_2022,\nauthor = {Hoffman, Jacob and Stein, Dan J},\ndoi = {10.1080/14656566.2022.2033209},\nissn = {1465-6566, 1744-7666},\njournal = {Expert Opinion on Pharmacotherapy},\nmonth = {apr},\nnumber = {6},\npages = {643--646},\ntitle = {{What are the pharmacotherapeutic options for adjustment disorder?}},\nurl = {https://www.tandfonline.com/doi/full/10.1080/14656566.2022.2033209},\nvolume = {23},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Study protocol: an observational study of distress, immune function and persistent pain in HIV.\n \n \n \n \n\n\n \n Madden, V J; Msolo, N; Mqadi, L; Lesosky, M; Bedwell, G J; Hutchinson, M R; Peter, J G; Parker, R; Schrepf, A; Edwards, R R; and Joska, J A\n\n\n \n\n\n\n 2022.\n \n\n\n\n
\n\n\n\n \n \n \"StudyPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Madden2022,\nannote = {Export Date: 29 December 2022},\nauthor = {Madden, V J and Msolo, N and Mqadi, L and Lesosky, M and Bedwell, G J and Hutchinson, M R and Peter, J G and Parker, R and Schrepf, A and Edwards, R R and Joska, J A},\ndoi = {10.1136/bmjopen-2021-059723},\nfile = {:Users/jacquelinebracher/Zotero/storage/5PHLDRLL/Madden et al. - 2022 - Study protocol an observational study of distress.pdf:pdf},\nnumber = {6},\ntitle = {{Study protocol: an observational study of distress, immune function and persistent pain in HIV}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85132108828{\\&}doi=10.1136{\\%}2Fbmjopen-2021-059723{\\&}partnerID=40{\\&}md5=6ab6a30ce71a276a009f519e3d8e1c1b},\nvolume = {12},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n The \\textlessspan style=\"font-variant:small-caps;\"\\textgreater\\ENIGMA\\‐\\Epilepsy\\\\textless/span\\textgreaterworking group: \\Mapping\\ disease from large data sets.\n \n \n \n \n\n\n \n Sisodiya, S. M; Whelan, C. D; Hatton, S. N; Huynh, K.; Altmann, A.; Ryten, M.; Vezzani, A.; Caligiuri, M. E.; Labate, A.; Gambardella, A.; Ives‐Deliperi, V.; Meletti, S.; Munsell, B. C; Bonilha, L.; Tondelli, M.; Rebsamen, M.; Rummel, C.; Vaudano, A. E.; Wiest, R.; Balachandra, A. R; Bargalló, N.; Bartolini, E.; Bernasconi, A.; Bernasconi, N.; Bernhardt, B.; Caldairou, B.; Carr, S. J A; Cavalleri, G. L; Cendes, F.; Concha, L.; Desmond, P. M; Domin, M.; Duncan, J. S; Focke, N. K; Guerrini, R.; Hamandi, K.; Jackson, G. D; Jahanshad, N.; Kälviäinen, R.; Keller, S. S; Kochunov, P.; Kowalczyk, M. A; Kreilkamp, B. A K; Kwan, P.; Lariviere, S.; Lenge, M.; Lopez, S. M; Martin, P.; Mascalchi, M.; Moreira, J. C V; Morita‐Sherman, M. E; Pardoe, H. R; Pariente, J. C; Raviteja, K.; Rocha, C. S; Rodríguez‐Cruces, R.; Seeck, M.; Semmelroch, M. K H G; Sinclair, B.; Soltanian‐Zadeh, H.; Stein, D. J; Striano, P.; Taylor, P. N; Thomas, R. H; Thomopoulos, S. I; Velakoulis, D.; Vivash, L.; Weber, B.; Yasuda, C. L.; Zhang, J.; Thompson, P. M; McDonald, C. R; and ENIGMA Consortium Epilepsy Working Group\n\n\n \n\n\n\n Human Brain Mapping, 43(1): 113–128. jan 2022.\n \n\n\n\n
\n\n\n\n \n \n \"ThePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{sisodiya_span_2022,\nabstract = {Abstract\nEpilepsy is a common and serious neurological disorder, with many different constituent conditions characterized by their electro clinical, imaging, and genetic features. MRI has been fundamental in advancing our understanding of brain processes in the epilepsies. Smaller‐scale studies have identified many interesting imaging phenomena, with implications both for understanding pathophysiology and improving clinical care. Through the infrastructure and concepts now well‐established by the ENIGMA Consortium, ENIGMA‐Epilepsy was established to strengthen epilepsy neuroscience by greatly increasing sample sizes, leveraging ideas and methods established in other ENIGMA projects, and generating a body of collaborating scientists and clinicians to drive forward robust research. Here we review published, current, and future projects, that include structural MRI, diffusion tensor imaging (DTI), and resting state functional MRI (rsfMRI), and that employ advanced methods including structural covariance, and event‐based modeling analysis. We explore age of onset‐ and duration‐related features, as well as phenomena‐specific work focusing on particular epilepsy syndromes or phenotypes, multimodal analyses focused on understanding the biology of disease progression, and deep learning approaches. We encourage groups who may be interested in participating to make contact to further grow and develop ENIGMA‐Epilepsy.},\nauthor = {Sisodiya, Sanjay M and Whelan, Christopher D and Hatton, Sean N and Huynh, Khoa and Altmann, Andre and Ryten, Mina and Vezzani, Annamaria and Caligiuri, Maria Eugenia and Labate, Angelo and Gambardella, Antonio and Ives‐Deliperi, Victoria and Meletti, Stefano and Munsell, Brent C and Bonilha, Leonardo and Tondelli, Manuela and Rebsamen, Michael and Rummel, Christian and Vaudano, Anna Elisabetta and Wiest, Roland and Balachandra, Akshara R and Bargall{\\'{o}}, N{\\'{u}}ria and Bartolini, Emanuele and Bernasconi, Andrea and Bernasconi, Neda and Bernhardt, Boris and Caldairou, Benoit and Carr, Sarah J A and Cavalleri, Gianpiero L and Cendes, Fernando and Concha, Luis and Desmond, Patricia M and Domin, Martin and Duncan, John S and Focke, Niels K and Guerrini, Renzo and Hamandi, Khalid and Jackson, Graeme D and Jahanshad, Neda and K{\\"{a}}lvi{\\"{a}}inen, Reetta and Keller, Simon S and Kochunov, Peter and Kowalczyk, Magdalena A and Kreilkamp, Barbara A K and Kwan, Patrick and Lariviere, Sara and Lenge, Matteo and Lopez, Seymour M and Martin, Pascal and Mascalchi, Mario and Moreira, Jos{\\'{e}} C V and Morita‐Sherman, Marcia E and Pardoe, Heath R and Pariente, Jose C and Raviteja, Kotikalapudi and Rocha, Cristiane S and Rodr{\\'{i}}guez‐Cruces, Ra{\\'{u}}l and Seeck, Margitta and Semmelroch, Mira K H G and Sinclair, Benjamin and Soltanian‐Zadeh, Hamid and Stein, Dan J and Striano, Pasquale and Taylor, Peter N and Thomas, Rhys H and Thomopoulos, Sophia I and Velakoulis, Dennis and Vivash, Lucy and Weber, Bernd and Yasuda, Clarissa Lin and Zhang, Junsong and Thompson, Paul M and McDonald, Carrie R and {ENIGMA Consortium Epilepsy Working Group}},\ndoi = {10.1002/hbm.25037},\nfile = {:Users/jacquelinebracher/Zotero/storage/AF2GR6FZ/Sisodiya et al. - 2022 - The ENIGMA‐.pdf:pdf},\nissn = {1065-9471, 1097-0193},\njournal = {Human Brain Mapping},\nmonth = {jan},\nnumber = {1},\npages = {113--128},\nshorttitle = {The {\\textless}span style="font-variant},\ntitle = {{The {\\textless}span style="font-variant:small-caps;"{\\textgreater}{\\{}ENIGMA{\\}}‐{\\{}Epilepsy{\\}}{\\textless}/span{\\textgreater}working group: {\\{}Mapping{\\}} disease from large data sets}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1002/hbm.25037},\nvolume = {43},\nyear = {2022}\n}\n
\n
\n\n\n
\n Abstract Epilepsy is a common and serious neurological disorder, with many different constituent conditions characterized by their electro clinical, imaging, and genetic features. MRI has been fundamental in advancing our understanding of brain processes in the epilepsies. Smaller‐scale studies have identified many interesting imaging phenomena, with implications both for understanding pathophysiology and improving clinical care. Through the infrastructure and concepts now well‐established by the ENIGMA Consortium, ENIGMA‐Epilepsy was established to strengthen epilepsy neuroscience by greatly increasing sample sizes, leveraging ideas and methods established in other ENIGMA projects, and generating a body of collaborating scientists and clinicians to drive forward robust research. Here we review published, current, and future projects, that include structural MRI, diffusion tensor imaging (DTI), and resting state functional MRI (rsfMRI), and that employ advanced methods including structural covariance, and event‐based modeling analysis. We explore age of onset‐ and duration‐related features, as well as phenomena‐specific work focusing on particular epilepsy syndromes or phenotypes, multimodal analyses focused on understanding the biology of disease progression, and deep learning approaches. We encourage groups who may be interested in participating to make contact to further grow and develop ENIGMA‐Epilepsy.\n
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\n \n\n \n \n \n \n \n \n Investigating pupillometry to detect emotional regulation difficulties in post-traumatic stress disorder.\n \n \n \n \n\n\n \n Ginton, L. M; Vuong, E.; Lake, M. T; Nhapi, R. T; Zar, H. J; Yrttiaho, S.; and Stein, D. J\n\n\n \n\n\n\n The World Journal of Biological Psychiatry, 23(2): 127–135. feb 2022.\n \n\n\n\n
\n\n\n\n \n \n \"InvestigatingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{ginton_investigating_2022,\nauthor = {Ginton, Lee M and Vuong, Eileen and Lake, Marilyn T and Nhapi, Raymond T and Zar, Heather J and Yrttiaho, Santeri and Stein, Dan J},\ndoi = {10.1080/15622975.2021.1935316},\nissn = {1562-2975, 1814-1412},\njournal = {The World Journal of Biological Psychiatry},\nmonth = {feb},\nnumber = {2},\npages = {127--135},\ntitle = {{Investigating pupillometry to detect emotional regulation difficulties in post-traumatic stress disorder}},\nurl = {https://www.tandfonline.com/doi/full/10.1080/15622975.2021.1935316},\nvolume = {23},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Brain structural covariance network differences in adults with alcohol dependence and heavy‐drinking adolescents.\n \n \n \n \n\n\n \n Ottino‐González, J.; Garavan, H.; The ENIGMA‐Addiction; and consortiums , I.\n\n\n \n\n\n\n Addiction, 117(5): 1312–1325. may 2022.\n \n\n\n\n
\n\n\n\n \n \n \"BrainPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{ottinogonzalez_brain_2022,\nabstract = {Abstract\n\nBackground and aims\nGraph theoretic analysis of structural covariance networks (SCN) provides an assessment of brain organization that has not yet been applied to alcohol dependence (AD). We estimated whether SCN differences are present in adults with AD and heavy‐drinking adolescents at age 19 and age 14, prior to substantial exposure to alcohol.\n\n\nDesign\nCross‐sectional sample of adults and a cohort of adolescents. Correlation matrices for cortical thicknesses across 68 regions were summarized with graph theoretic metrics.\n\n\nSetting and participants\nA total of 745 adults with AD and 979 non‐dependent controls from 24 sites curated by the Enhancing NeuroImaging Genetics through Meta Analysis (ENIGMA)–Addiction consortium, and 297 hazardous drinking adolescents and 594 controls at ages 19 and 14 from the IMAGEN study, all from Europe.\n\n\nMeasurements\nMetrics of network segregation (modularity, clustering coefficient and local efficiency) and integration (average shortest path length and global efficiency).\n\n\nFindings\n\nThe younger AD adults had lower network segregation and higher integration relative to non‐dependent controls. Compared with controls, the hazardous drinkers at age 19 showed lower modularity [area‐under‐the‐curve (AUC) difference = −0.0142, 95{\\%} confidence interval (CI) = −0.1333, 0.0092;\nP\n‐value = 0.017], clustering coefficient (AUC difference = −0.0164, 95{\\%} CI = −0.1456, 0.0043;\nP\n‐value = 0.008) and local efficiency (AUC difference = −0.0141, 95{\\%} CI = −0.0097, 0.0034;\nP\n‐value = 0.010), as well as lower average shortest path length (AUC difference = −0.0405, 95{\\%} CI = −0.0392, 0.0096;\nP\n‐value = 0.021) and higher global efficiency (AUC difference = 0.0044, 95{\\%} CI = −0.0011, 0.0043;\nP\n‐value = 0.023). The same pattern was present at age 14 with lower clustering coefficient (AUC difference = −0.0131, 95{\\%} CI = −0.1304, 0.0033;\nP\n‐value = 0.024), lower average shortest path length (AUC difference = −0.0362, 95{\\%} CI = −0.0334, 0.0118;\nP\n‐value = 0.019) and higher global efficiency (AUC difference = 0.0035, 95{\\%} CI = −0.0011, 0.0038;\nP\n‐value = 0.048).\n\n\n\nConclusions\nCross‐sectional analyses indicate that a specific structural covariance network profile is an early marker of alcohol dependence in adults. Similar effects in a cohort of heavy‐drinking adolescents, observed at age 19 and prior to substantial alcohol exposure at age 14, suggest that this pattern may be a pre‐existing risk factor for problematic drinking.},\nauthor = {Ottino‐Gonz{\\'{a}}lez, Jonatan and Garavan, Hugh and {The ENIGMA‐Addiction and IMAGEN consortiums}},\ndoi = {10.1111/add.15772},\nfile = {:Users/jacquelinebracher/Zotero/storage/DRL6XHCS/Ottino‐Gonz{\\'{a}}lez et al. - 2022 - Brain structural covariance network differences in.pdf:pdf},\nissn = {0965-2140, 1360-0443},\njournal = {Addiction},\nmonth = {may},\nnumber = {5},\npages = {1312--1325},\ntitle = {{Brain structural covariance network differences in adults with alcohol dependence and heavy‐drinking adolescents}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1111/add.15772},\nvolume = {117},\nyear = {2022}\n}\n
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\n Abstract Background and aims Graph theoretic analysis of structural covariance networks (SCN) provides an assessment of brain organization that has not yet been applied to alcohol dependence (AD). We estimated whether SCN differences are present in adults with AD and heavy‐drinking adolescents at age 19 and age 14, prior to substantial exposure to alcohol. Design Cross‐sectional sample of adults and a cohort of adolescents. Correlation matrices for cortical thicknesses across 68 regions were summarized with graph theoretic metrics. Setting and participants A total of 745 adults with AD and 979 non‐dependent controls from 24 sites curated by the Enhancing NeuroImaging Genetics through Meta Analysis (ENIGMA)–Addiction consortium, and 297 hazardous drinking adolescents and 594 controls at ages 19 and 14 from the IMAGEN study, all from Europe. Measurements Metrics of network segregation (modularity, clustering coefficient and local efficiency) and integration (average shortest path length and global efficiency). Findings The younger AD adults had lower network segregation and higher integration relative to non‐dependent controls. Compared with controls, the hazardous drinkers at age 19 showed lower modularity [area‐under‐the‐curve (AUC) difference = −0.0142, 95% confidence interval (CI) = −0.1333, 0.0092; P ‐value = 0.017], clustering coefficient (AUC difference = −0.0164, 95% CI = −0.1456, 0.0043; P ‐value = 0.008) and local efficiency (AUC difference = −0.0141, 95% CI = −0.0097, 0.0034; P ‐value = 0.010), as well as lower average shortest path length (AUC difference = −0.0405, 95% CI = −0.0392, 0.0096; P ‐value = 0.021) and higher global efficiency (AUC difference = 0.0044, 95% CI = −0.0011, 0.0043; P ‐value = 0.023). The same pattern was present at age 14 with lower clustering coefficient (AUC difference = −0.0131, 95% CI = −0.1304, 0.0033; P ‐value = 0.024), lower average shortest path length (AUC difference = −0.0362, 95% CI = −0.0334, 0.0118; P ‐value = 0.019) and higher global efficiency (AUC difference = 0.0035, 95% CI = −0.0011, 0.0038; P ‐value = 0.048). Conclusions Cross‐sectional analyses indicate that a specific structural covariance network profile is an early marker of alcohol dependence in adults. Similar effects in a cohort of heavy‐drinking adolescents, observed at age 19 and prior to substantial alcohol exposure at age 14, suggest that this pattern may be a pre‐existing risk factor for problematic drinking.\n
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\n \n\n \n \n \n \n \n \n Whole Exome Sequencing in South Africa: Stakeholder Views on Return of Individual Research Results and Incidental Findings.\n \n \n \n \n\n\n \n Van Der Merwe, N; Ramesar, R; and De Vries, J\n\n\n \n\n\n\n 2022.\n \n\n\n\n
\n\n\n\n \n \n \"WholePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{VanDerMerwe2022,\nannote = {Export Date: 29 December 2022},\nauthor = {{Van Der Merwe}, N and Ramesar, R and {De Vries}, J},\ndoi = {10.3389/fgene.2022.864822},\nfile = {:Users/jacquelinebracher/Zotero/storage/DXQKQ6KQ/Van Der Merwe et al. - 2022 - Whole Exome Sequencing in South Africa Stakeholde.pdf:pdf},\ntitle = {{Whole Exome Sequencing in South Africa: Stakeholder Views on Return of Individual Research Results and Incidental Findings}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85133366160{\\&}doi=10.3389{\\%}2Ffgene.2022.864822{\\&}partnerID=40{\\&}md5=4088d86222f9277236d248524eb12e70},\nvolume = {13},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n A new approach to cognitive impairment in people with HIV.\n \n \n \n\n\n \n Nightingale, S.; Cinque, P.; Joska, J.; Price, R.; and Underwood, J.\n\n\n \n\n\n\n The lancet. HIV, 9(12): e815–e817. 2022.\n \n\n\n\n
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@article{Nightingale2022,\nauthor = {Nightingale, S. and Cinque, P. and Joska, J.A. and Price, R.W. and Underwood, J.},\ndoi = {10.1016/S2352-3018(22)00267-3},\nfile = {:Users/jacquelinebracher/Zotero/storage/NCVKBZ5F/Nightingale et al. - 2022 - A new approach to cognitive impairment in people w.pdf:pdf},\njournal = {The lancet. HIV},\nnumber = {12},\npages = {e815--e817},\ntitle = {{A new approach to cognitive impairment in people with HIV}},\nvolume = {9},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Health \\Service\\ \\Utilization\\ by \\Young\\ \\Children\\ with \\Autism\\ \\Spectrum\\ \\Disorder\\ \\Versus\\ \\Global\\ \\Developmental\\ \\Delay\\ at a \\Tertiary\\ \\Center\\ in a \\Resource\\-\\Limited\\ \\Setting\\.\n \n \n \n \n\n\n \n Okwara, F. N O; Le Roux, S. M; and Donald, K. A\n\n\n \n\n\n\n Journal of Developmental & Behavioral Pediatrics, 43(5): e320—-e329. jun 2022.\n \n\n\n\n
\n\n\n\n \n \n \"HealthPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{okwara_health_2022,\nabstract = {ABSTRACT:\n\nObjective:\nWe investigated patterns and predictors of health service utilization (HSU) among children with autism spectrum disorder (ASD) and global developmental delays (GDD, non-ASD) attending tertiary services in a resource-constrained setting.\n\n\nMethod:\nCaregivers and children (diagnosed with either ASD or GDD) attending the developmental service were enrolled into a retrospective cohort study. Sociodemographic factors, clinical factors, and service use over the preceding year were collected using structured questionnaires and medical record reviews.\n\n\nResults:\n\nWe enrolled 240 households (116 ASD, 124 GDD; ages 3–8 years; male:female ratio 2:1). The majority (84{\\%}) had moderate-to-severe symptoms, and 42{\\%} were nonverbal. Children with GDD had higher levels of underlying syndromic diagnoses than those with ASD (46, 37.1{\\%}; 14, 9.5{\\%}); (\np\n{\\textless}0.01) and more co-occurring comorbidities (51, 41.0{\\%}; 14, 12.1{\\%};\np =\n0.0001). Those with GDD had higher mean total HSU visits (13.3; 11.5;\np\n= 0.02), higher mean specialist visits (4.0:2.0;\np\n= 0.001), and more hospitalizations than those with ASD (38, 31{\\%}; 16, 14{\\%};\np\n= 0.02). Other services were similarly attended by both groups: therapy 6.0 (2.0–10.0), emergency visits 1.0 (1.0–2.0), auxiliary services 0 (0–1.0), and primary care visits 0 (0–1.0). Having an employed parent was the strongest predictor of increased HSU (\np\n= 0.05).\n\n\n\nConclusion:\nDespite high functional impairment in this cohort, many households underutilized therapy services. There was skewed attendance of emergency and specialist services over primary care services. Children with GDD had greater HSU compared with those with ASD, primarily because of more specialist visits. HSU could be improved by caregiver education, household economic empowerment, and strengthening of primary care services.},\nauthor = {Okwara, Florence N O and {Le Roux}, Stanzi M and Donald, Kirsten A},\ndoi = {10.1097/DBP.0000000000001034},\nissn = {0196-206X},\njournal = {Journal of Developmental {\\&} Behavioral Pediatrics},\nmonth = {jun},\nnumber = {5},\npages = {e320----e329},\ntitle = {{Health {\\{}Service{\\}} {\\{}Utilization{\\}} by {\\{}Young{\\}} {\\{}Children{\\}} with {\\{}Autism{\\}} {\\{}Spectrum{\\}} {\\{}Disorder{\\}} {\\{}Versus{\\}} {\\{}Global{\\}} {\\{}Developmental{\\}} {\\{}Delay{\\}} at a {\\{}Tertiary{\\}} {\\{}Center{\\}} in a {\\{}Resource{\\}}-{\\{}Limited{\\}} {\\{}Setting{\\}}}},\nurl = {https://journals.lww.com/10.1097/DBP.0000000000001034},\nvolume = {43},\nyear = {2022}\n}\n
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\n ABSTRACT: Objective: We investigated patterns and predictors of health service utilization (HSU) among children with autism spectrum disorder (ASD) and global developmental delays (GDD, non-ASD) attending tertiary services in a resource-constrained setting. Method: Caregivers and children (diagnosed with either ASD or GDD) attending the developmental service were enrolled into a retrospective cohort study. Sociodemographic factors, clinical factors, and service use over the preceding year were collected using structured questionnaires and medical record reviews. Results: We enrolled 240 households (116 ASD, 124 GDD; ages 3–8 years; male:female ratio 2:1). The majority (84%) had moderate-to-severe symptoms, and 42% were nonverbal. Children with GDD had higher levels of underlying syndromic diagnoses than those with ASD (46, 37.1%; 14, 9.5%); ( p \\textless0.01) and more co-occurring comorbidities (51, 41.0%; 14, 12.1%; p = 0.0001). Those with GDD had higher mean total HSU visits (13.3; 11.5; p = 0.02), higher mean specialist visits (4.0:2.0; p = 0.001), and more hospitalizations than those with ASD (38, 31%; 16, 14%; p = 0.02). Other services were similarly attended by both groups: therapy 6.0 (2.0–10.0), emergency visits 1.0 (1.0–2.0), auxiliary services 0 (0–1.0), and primary care visits 0 (0–1.0). Having an employed parent was the strongest predictor of increased HSU ( p = 0.05). Conclusion: Despite high functional impairment in this cohort, many households underutilized therapy services. There was skewed attendance of emergency and specialist services over primary care services. Children with GDD had greater HSU compared with those with ASD, primarily because of more specialist visits. HSU could be improved by caregiver education, household economic empowerment, and strengthening of primary care services.\n
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\n \n\n \n \n \n \n \n Biomarkers of Tuberculous Meningitis and Pediatric Human Immunodeficiency Virus on the African Continent.\n \n \n \n\n\n \n Teunissen, C.; Rohlwink, U.; Pajkrt, D.; and Naudé, P.\n\n\n \n\n\n\n Frontiers in Neurology, 13. 2022.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Teunissen2022,\nabstract = {Biomarkers in body fluids are helpful objective tools in diagnosis, prognosis and monitoring of (therapeutic) responses of many neurological diseases. Cerebrospinal fluid (CSF) biomarkers are part of the diagnostic toolbox for infectious neurological diseases. Tuberculous meningitis (TBM) and Human immunodeficiency virus (HIV), are important burdens of disease in Africa and can negatively affect brain health. Two thirds of the world's population of people living with HIV reside in sub-Saharan Africa and 25{\\%} of the global burden of tuberculosis (TB) is carried by the African continent. Neuroinflammation and damage of specific neuronal cell types are key constituents in the pathophysiology of these central nervous system (CNS) diseases, and important potential sources of circulating biomarkers. In this review, we summarize current research in the use of biomarkers in TBM and pediatric HIV as case demonstrations for high prevalence neurological diseases in Africa. Inflammatory molecules, primarily when detected in CSF, appear to have diagnostic value in these diseases, especially when measured as profiles. Brain injury molecules, such as S100, Neuron specific enolase and glial fibrillary acidic protein may have prognostic value in TBM, but more studies are needed. There is a need for more cost-economic and high sensitivity technologies to drive further biomarker discoveries and translate into healthcare improvements for these important healthcare problems in a globally fair way.},\nauthor = {Teunissen, C.E. and Rohlwink, U. and Pajkrt, D. and Naud{\\'{e}}, P.J.W.},\ndoi = {10.3389/fneur.2022.793080},\nfile = {:Users/jacquelinebracher/Zotero/storage/INFUENK3/Teunissen et al. - 2022 - Biomarkers of Tuberculous Meningitis and Pediatric.pdf:pdf},\njournal = {Frontiers in Neurology},\ntitle = {{Biomarkers of Tuberculous Meningitis and Pediatric Human Immunodeficiency Virus on the African Continent}},\nvolume = {13},\nyear = {2022}\n}\n
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\n Biomarkers in body fluids are helpful objective tools in diagnosis, prognosis and monitoring of (therapeutic) responses of many neurological diseases. Cerebrospinal fluid (CSF) biomarkers are part of the diagnostic toolbox for infectious neurological diseases. Tuberculous meningitis (TBM) and Human immunodeficiency virus (HIV), are important burdens of disease in Africa and can negatively affect brain health. Two thirds of the world's population of people living with HIV reside in sub-Saharan Africa and 25% of the global burden of tuberculosis (TB) is carried by the African continent. Neuroinflammation and damage of specific neuronal cell types are key constituents in the pathophysiology of these central nervous system (CNS) diseases, and important potential sources of circulating biomarkers. In this review, we summarize current research in the use of biomarkers in TBM and pediatric HIV as case demonstrations for high prevalence neurological diseases in Africa. Inflammatory molecules, primarily when detected in CSF, appear to have diagnostic value in these diseases, especially when measured as profiles. Brain injury molecules, such as S100, Neuron specific enolase and glial fibrillary acidic protein may have prognostic value in TBM, but more studies are needed. There is a need for more cost-economic and high sensitivity technologies to drive further biomarker discoveries and translate into healthcare improvements for these important healthcare problems in a globally fair way.\n
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\n \n\n \n \n \n \n \n \n Mandatory food fortification with folic acid – \\Authors\\' reply.\n \n \n \n \n\n\n \n Kancherla, V.; Botto, L. D; Rowe, L. A; Shlobin, N. A; Caceres, A.; Arynchyna-Smith, A.; Zimmerman, K.; Blount, J.; Kibruyisfaw, Z.; Ghotme, K. A; Karmarkar, S.; Fieggen, G.; Roozen, S.; Oakley, G. P; Rosseau, G.; and Berry, R. J\n\n\n \n\n\n\n The Lancet Global Health, 10(10): e1391—-e1392. oct 2022.\n \n\n\n\n
\n\n\n\n \n \n \"MandatoryPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{kancherla_mandatory_2022,\nauthor = {Kancherla, Vijaya and Botto, Lorenzo D and Rowe, Laura A and Shlobin, Nathan A and Caceres, Adrian and Arynchyna-Smith, Anastasia and Zimmerman, Kathrin and Blount, Jeffrey and Kibruyisfaw, Zewdie and Ghotme, Kemel A and Karmarkar, Santosh and Fieggen, Graham and Roozen, Sylvia and Oakley, Godfrey P and Rosseau, Gail and Berry, Robert J},\ndoi = {10.1016/S2214-109X(22)00375-8},\nfile = {:Users/jacquelinebracher/Zotero/storage/4HGUZCHM/Kancherla et al. - 2022 - Mandatory food fortification with folic acid – Aut.pdf:pdf},\nissn = {2214109X},\njournal = {The Lancet Global Health},\nmonth = {oct},\nnumber = {10},\npages = {e1391----e1392},\ntitle = {{Mandatory food fortification with folic acid – {\\{}Authors{\\}}' reply}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S2214109X22003758},\nvolume = {10},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Virtual Ontogeny of Cortical Growth Preceding Mental Illness.\n \n \n \n \n\n\n \n Patel, Y; Shin, J; Abé, C; Agartz, I; Alloza, C; Alnæs, D; Ambrogi, S; Antonucci, L A; Arango, C; Arolt, V; Auzias, G; Ayesa-Arriola, R; Banaj, N; Banaschewski, T; Bandeira, C; Başgöze, Z; Cupertino, R B; Bau, C H D; Bauer, J; Baumeister, S; Bernardoni, F; Bertolino, A; Bonnin, C D M; Brandeis, D; Brem, S; Bruggemann, J; Bülow, R; Bustillo, J R; Calderoni, S; Calvo, R; Canales-Rodríguez, E J; Cannon, D M; Carmona, S; Carr, V J; Catts, S V; Chenji, S; Chew, Q H; Coghill, D; Connolly, C G; Conzelmann, A; Craven, A R; Crespo-Facorro, B; Cullen, K; Dahl, A; Dannlowski, U; Davey, C G; Deruelle, C; Díaz-Caneja, C M; Dohm, K; Ehrlich, S; Epstein, J; Erwin-Grabner, T; Eyler, L T; Fedor, J; Fitzgerald, J; Foran, W; Ford, J M; Fortea, L; Fuentes-Claramonte, P; Fullerton, J; Furlong, L; Gallagher, L; Gao, B; Gao, S; Goikolea, J M; Gotlib, I; Goya-Maldonado, R; Grabe, H J; Green, M; Grevet, E H; Groenewold, N A; Grotegerd, D; Gruber, O; Haavik, J; Hahn, T; Harrison, B J; Heindel, W; Henskens, F; Heslenfeld, D J; Hilland, E; Hoekstra, P J; Hohmann, S; Holz, N; Howells, F M; Ipser, J C; Jahanshad, N; Jakobi, B; Jansen, A; Janssen, J; Jonassen, R; Kaiser, A; Kaleda, V; Karantonis, J; King, J A; Kircher, T; Kochunov, P; Koopowitz, S.; Landén, M; Landrø, N I; Lawrie, S; Lebedeva, I; Luna, B; Lundervold, A J; MacMaster, F P; Maglanoc, L A; Mathalon, D H; McDonald, C; McIntosh, A; Meinert, S; Michie, P T; Mitchell, P; Moreno-Alcázar, A; Mowry, B; Muratori, F; Nabulsi, L; Nenadić, I; O'Gorman Tuura, R; Oosterlaan, J; Overs, B; Pantelis, C; Parellada, M; Pariente, J C; Pauli, P; Pergola, G; Piarulli, F M; Picon, F; Piras, F; Pomarol-Clotet, E; Pretus, C; Quidé, Y; Radua, J; Ramos-Quiroga, J A; Rasser, P E; Reif, A; Retico, A; Roberts, G; Rossell, S; Rovaris, D L; Rubia, K; Sacchet, M; Salavert, J; Salvador, R; Sarró, S; Sawa, A; Schall, U; Scott, R; Selvaggi, P; Silk, T; Sim, K; Skoch, A; Spalletta, G; Spaniel, F; Stein, D J; Steinsträter, O; Stolicyn, A; Takayanagi, Y; Tamm, L; Tavares, M; Teumer, A; Thiel, K; Thomopoulos, S I; Tomecek, D; Tomyshev, A S; Tordesillas-Gutiérrez, D; Tosetti, M; Uhlmann, A; Van Rheenen, T; Vazquez-Bourgón, J; Vernooij, M W; Vieta, E; Vilarroya, O; Weickert, C; Weickert, T; Westlye, L T; Whalley, H; Willinger, D; Winter, A; Wittfeld, K; Yang, T T; Yoncheva, Y; Zijlmans, J L; Hoogman, M; Franke, B; van Rooij, D; Buitelaar, J; Ching, C R K; Andreassen, O A; Pozzi, E; Veltman, D; Schmaal, L; van Erp, T G M; Turner, J; Castellanos, F X; Pausova, Z; Thompson, P; and Paus, T\n\n\n \n\n\n\n 2022.\n \n\n\n\n
\n\n\n\n \n \n \"VirtualPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Patel2022,\nannote = {Export Date: 29 December 2022},\nauthor = {Patel, Y and Shin, J and Ab{\\'{e}}, C and Agartz, I and Alloza, C and Aln{\\ae}s, D and Ambrogi, S and Antonucci, L A and Arango, C and Arolt, V and Auzias, G and Ayesa-Arriola, R and Banaj, N and Banaschewski, T and Bandeira, C and Başg{\\"{o}}ze, Z and Cupertino, R B and Bau, C H D and Bauer, J and Baumeister, S and Bernardoni, F and Bertolino, A and Bonnin, C D M and Brandeis, D and Brem, S and Bruggemann, J and B{\\"{u}}low, R and Bustillo, J R and Calderoni, S and Calvo, R and Canales-Rodr{\\'{i}}guez, E J and Cannon, D M and Carmona, S and Carr, V J and Catts, S V and Chenji, S and Chew, Q H and Coghill, D and Connolly, C G and Conzelmann, A and Craven, A R and Crespo-Facorro, B and Cullen, K and Dahl, A and Dannlowski, U and Davey, C G and Deruelle, C and D{\\'{i}}az-Caneja, C M and Dohm, K and Ehrlich, S and Epstein, J and Erwin-Grabner, T and Eyler, L T and Fedor, J and Fitzgerald, J and Foran, W and Ford, J M and Fortea, L and Fuentes-Claramonte, P and Fullerton, J and Furlong, L and Gallagher, L and Gao, B and Gao, S and Goikolea, J M and Gotlib, I and Goya-Maldonado, R and Grabe, H J and Green, M and Grevet, E H and Groenewold, N A and Grotegerd, D and Gruber, O and Haavik, J and Hahn, T and Harrison, B J and Heindel, W and Henskens, F and Heslenfeld, D J and Hilland, E and Hoekstra, P J and Hohmann, S and Holz, N and Howells, F M and Ipser, J C and Jahanshad, N and Jakobi, B and Jansen, A and Janssen, J and Jonassen, R and Kaiser, A and Kaleda, V and Karantonis, J and King, J A and Kircher, T and Kochunov, P and Koopowitz, S.-M. and Land{\\'{e}}n, M and Landr{\\o}, N I and Lawrie, S and Lebedeva, I and Luna, B and Lundervold, A J and MacMaster, F P and Maglanoc, L A and Mathalon, D H and McDonald, C and McIntosh, A and Meinert, S and Michie, P T and Mitchell, P and Moreno-Alc{\\'{a}}zar, A and Mowry, B and Muratori, F and Nabulsi, L and Nenadi{\\'{c}}, I and {O'Gorman Tuura}, R and Oosterlaan, J and Overs, B and Pantelis, C and Parellada, M and Pariente, J C and Pauli, P and Pergola, G and Piarulli, F M and Picon, F and Piras, F and Pomarol-Clotet, E and Pretus, C and Quid{\\'{e}}, Y and Radua, J and Ramos-Quiroga, J A and Rasser, P E and Reif, A and Retico, A and Roberts, G and Rossell, S and Rovaris, D L and Rubia, K and Sacchet, M and Salavert, J and Salvador, R and Sarr{\\'{o}}, S and Sawa, A and Schall, U and Scott, R and Selvaggi, P and Silk, T and Sim, K and Skoch, A and Spalletta, G and Spaniel, F and Stein, D J and Steinstr{\\"{a}}ter, O and Stolicyn, A and Takayanagi, Y and Tamm, L and Tavares, M and Teumer, A and Thiel, K and Thomopoulos, S I and Tomecek, D and Tomyshev, A S and Tordesillas-Guti{\\'{e}}rrez, D and Tosetti, M and Uhlmann, A and {Van Rheenen}, T and Vazquez-Bourg{\\'{o}}n, J and Vernooij, M W and Vieta, E and Vilarroya, O and Weickert, C and Weickert, T and Westlye, L T and Whalley, H and Willinger, D and Winter, A and Wittfeld, K and Yang, T T and Yoncheva, Y and Zijlmans, J L and Hoogman, M and Franke, B and van Rooij, D and Buitelaar, J and Ching, C R K and Andreassen, O A and Pozzi, E and Veltman, D and Schmaal, L and van Erp, T G M and Turner, J and Castellanos, F X and Pausova, Z and Thompson, P and Paus, T},\ndoi = {10.1016/j.biopsych.2022.02.959},\nfile = {:Users/jacquelinebracher/Zotero/storage/CWGHE48Q/Patel et al. - 2022 - Virtual Ontogeny of Cortical Growth Preceding Ment.pdf:pdf},\nnumber = {4},\npages = {299--313},\ntitle = {{Virtual Ontogeny of Cortical Growth Preceding Mental Illness}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85129809360{\\&}doi=10.1016{\\%}2Fj.biopsych.2022.02.959{\\&}partnerID=40{\\&}md5=48fad31b58289871faebead4eee0744d},\nvolume = {92},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Local molecular and global connectomic contributions to cross-disorder cortical abnormalities.\n \n \n \n \n\n\n \n Hansen, J. Y; Shafiei, G.; Vogel, J. W; Smart, K.; Bearden, C. E; Hoogman, M.; Franke, B.; Van Rooij, D.; Buitelaar, J.; McDonald, C. R; Sisodiya, S. M; Schmaal, L.; Veltman, D. J; Van Den Heuvel, O. A; Stein, D. J; Van Erp, T. G M; Ching, C. R K; Andreassen, O. A; Hajek, T.; Opel, N.; Modinos, G.; Aleman, A.; Van Der Werf, Y.; Jahanshad, N.; Thomopoulos, S. I; Thompson, P. M; Carson, R. E; Dagher, A.; and Misic, B.\n\n\n \n\n\n\n Nature Communications, 13(1): 4682. aug 2022.\n \n\n\n\n
\n\n\n\n \n \n \"LocalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{hansen_local_2022,\nabstract = {Abstract\n\nNumerous brain disorders demonstrate structural brain abnormalities, which are thought to arise from molecular perturbations or connectome miswiring. The unique and shared contributions of these molecular and connectomic vulnerabilities to brain disorders remain unknown, and has yet to be studied in a single multi-disorder framework. Using MRI morphometry from the ENIGMA consortium, we construct maps of cortical abnormalities for thirteen neurodevelopmental, neurological, and psychiatric disorders from\nN\n= 21,000 participants and\nN\n= 26,000 controls, collected using a harmonised processing protocol. We systematically compare cortical maps to multiple micro-architectural measures, including gene expression, neurotransmitter density, metabolism, and myelination (molecular vulnerability), as well as global connectomic measures including number of connections, centrality, and connection diversity (connectomic vulnerability). We find a relationship between molecular vulnerability and white-matter architecture that drives cortical disorder profiles. Local attributes, particularly neurotransmitter receptor profiles, constitute the best predictors of both disorder-specific cortical morphology and cross-disorder similarity. Finally, we find that cross-disorder abnormalities are consistently subtended by a small subset of network epicentres in bilateral sensory-motor, inferior temporal lobe, precuneus, and superior parietal cortex. Collectively, our results highlight how local molecular attributes and global connectivity jointly shape cross-disorder cortical abnormalities.},\nauthor = {Hansen, Justine Y and Shafiei, Golia and Vogel, Jacob W and Smart, Kelly and Bearden, Carrie E and Hoogman, Martine and Franke, Barbara and {Van Rooij}, Daan and Buitelaar, Jan and McDonald, Carrie R and Sisodiya, Sanjay M and Schmaal, Lianne and Veltman, Dick J and {Van Den Heuvel}, Odile A and Stein, Dan J and {Van Erp}, Theo G M and Ching, Christopher R K and Andreassen, Ole A and Hajek, Tomas and Opel, Nils and Modinos, Gemma and Aleman, Andr{\\'{e}} and {Van Der Werf}, Ysbrand and Jahanshad, Neda and Thomopoulos, Sophia I and Thompson, Paul M and Carson, Richard E and Dagher, Alain and Misic, Bratislav},\ndoi = {10.1038/s41467-022-32420-y},\nfile = {:Users/jacquelinebracher/Zotero/storage/KRENN9MT/Hansen et al. - 2022 - Local molecular and global connectomic contributio.pdf:pdf},\nissn = {2041-1723},\njournal = {Nature Communications},\nmonth = {aug},\nnumber = {1},\npages = {4682},\ntitle = {{Local molecular and global connectomic contributions to cross-disorder cortical abnormalities}},\nurl = {https://www.nature.com/articles/s41467-022-32420-y},\nvolume = {13},\nyear = {2022}\n}\n
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\n Abstract Numerous brain disorders demonstrate structural brain abnormalities, which are thought to arise from molecular perturbations or connectome miswiring. The unique and shared contributions of these molecular and connectomic vulnerabilities to brain disorders remain unknown, and has yet to be studied in a single multi-disorder framework. Using MRI morphometry from the ENIGMA consortium, we construct maps of cortical abnormalities for thirteen neurodevelopmental, neurological, and psychiatric disorders from N = 21,000 participants and N = 26,000 controls, collected using a harmonised processing protocol. We systematically compare cortical maps to multiple micro-architectural measures, including gene expression, neurotransmitter density, metabolism, and myelination (molecular vulnerability), as well as global connectomic measures including number of connections, centrality, and connection diversity (connectomic vulnerability). We find a relationship between molecular vulnerability and white-matter architecture that drives cortical disorder profiles. Local attributes, particularly neurotransmitter receptor profiles, constitute the best predictors of both disorder-specific cortical morphology and cross-disorder similarity. Finally, we find that cross-disorder abnormalities are consistently subtended by a small subset of network epicentres in bilateral sensory-motor, inferior temporal lobe, precuneus, and superior parietal cortex. Collectively, our results highlight how local molecular attributes and global connectivity jointly shape cross-disorder cortical abnormalities.\n
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\n \n\n \n \n \n \n \n \n The influence of a manipulation of threat on experimentally-induced secondary hyperalgesia.\n \n \n \n \n\n\n \n Bedwell, G. J; Louw, C.; Parker, R.; Van Den Broeke, E.; Vlaeyen, J. W; Moseley, G L.; and Madden, V. J\n\n\n \n\n\n\n PeerJ, 10: e13512. jun 2022.\n \n\n\n\n
\n\n\n\n \n \n \"ThePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{bedwell_influence_2022,\nabstract = {Pain is thought to be influenced by the threat value of the particular context in which it occurs. However, the mechanisms by which a threat achieves this influence on pain are unclear. Here, we explore how threat influences experimentally-induced secondary hyperalgesia, which is thought to be a manifestation of central sensitization. We developed an experimental study to investigate the effect of a manipulation of threat on experimentally-induced secondary hyperalgesia in 26 healthy human adults (16 identifying as female; 10 as male). We induced secondary hyperalgesia at both forearms using high-frequency electrical stimulation. Prior to the induction, we used a previously successful method to manipulate threat of tissue damage at one forearm (threat site). The effect of the threat manipulation was determined by comparing participant-rated anxiety, perceived threat, and pain during the experimental induction of secondary hyperalgesia, between the threat and control sites. We hypothesized that the threat site would show greater secondary hyperalgesia (primary outcome) and greater surface area (secondary outcome) of induced secondary hyperalgesia than the control site. Despite a thorough piloting procedure to test the threat manipulation, our data showed no main effect of site on pain, anxiety, or threat ratings during high-frequency electrical stimulation. In the light of no difference in threat between sites, the primary and secondary hypotheses cannot be tested. We discuss reasons why we were unable to replicate the efficacy of this established threat manipulation in our sample, including: (1) competition between threats, (2) generalization of learned threat value, (3) safety cues, (4) trust, and requirements for participant safety, (5) sampling bias, (6) sample-specific habituation to threat, and (7) implausibility of (sham) skin examination and report. Better strategies to manipulate threat are required for further research on the mechanisms by which threat influences pain.},\nauthor = {Bedwell, Gillian J and Louw, Caron and Parker, Romy and {Van Den Broeke}, Emanuel and Vlaeyen, Johan W and Moseley, G Lorimer and Madden, Victoria J},\ndoi = {10.7717/peerj.13512},\nfile = {:Users/jacquelinebracher/Zotero/storage/3KSWD3NF/Bedwell et al. - 2022 - The influence of a manipulation of threat on exper.pdf:pdf},\nissn = {2167-8359},\njournal = {PeerJ},\nmonth = {jun},\npages = {e13512},\ntitle = {{The influence of a manipulation of threat on experimentally-induced secondary hyperalgesia}},\nurl = {https://peerj.com/articles/13512},\nvolume = {10},\nyear = {2022}\n}\n
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\n Pain is thought to be influenced by the threat value of the particular context in which it occurs. However, the mechanisms by which a threat achieves this influence on pain are unclear. Here, we explore how threat influences experimentally-induced secondary hyperalgesia, which is thought to be a manifestation of central sensitization. We developed an experimental study to investigate the effect of a manipulation of threat on experimentally-induced secondary hyperalgesia in 26 healthy human adults (16 identifying as female; 10 as male). We induced secondary hyperalgesia at both forearms using high-frequency electrical stimulation. Prior to the induction, we used a previously successful method to manipulate threat of tissue damage at one forearm (threat site). The effect of the threat manipulation was determined by comparing participant-rated anxiety, perceived threat, and pain during the experimental induction of secondary hyperalgesia, between the threat and control sites. We hypothesized that the threat site would show greater secondary hyperalgesia (primary outcome) and greater surface area (secondary outcome) of induced secondary hyperalgesia than the control site. Despite a thorough piloting procedure to test the threat manipulation, our data showed no main effect of site on pain, anxiety, or threat ratings during high-frequency electrical stimulation. In the light of no difference in threat between sites, the primary and secondary hypotheses cannot be tested. We discuss reasons why we were unable to replicate the efficacy of this established threat manipulation in our sample, including: (1) competition between threats, (2) generalization of learned threat value, (3) safety cues, (4) trust, and requirements for participant safety, (5) sampling bias, (6) sample-specific habituation to threat, and (7) implausibility of (sham) skin examination and report. Better strategies to manipulate threat are required for further research on the mechanisms by which threat influences pain.\n
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\n \n\n \n \n \n \n \n \n The impact of prenatal alcohol exposure on gray matter volume and cortical surface area of 2 to 3-year-old children in a South African birth cohort.\n \n \n \n \n\n\n \n Subramoney, S; Joshi, S H; Wedderburn, C J; Lee, D; Roos, A; Woods, R P; Zar, H J; Narr, K; Stein, D J; and Donald, K A\n\n\n \n\n\n\n 2022.\n \n\n\n\n
\n\n\n\n \n \n \"ThePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Subramoney2022,\nannote = {Export Date: 29 December 2022},\nauthor = {Subramoney, S and Joshi, S H and Wedderburn, C J and Lee, D and Roos, A and Woods, R P and Zar, H J and Narr, K and Stein, D J and Donald, K A},\ndoi = {10.1111/acer.14873},\nfile = {:Users/jacquelinebracher/Zotero/storage/3LBECXDX/Subramoney et al. - 2022 - The impact of prenatal alcohol exposure on gray ma.pdf:pdf},\nnumber = {7},\npages = {1233--1247},\ntitle = {{The impact of prenatal alcohol exposure on gray matter volume and cortical surface area of 2 to 3-year-old children in a South African birth cohort}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85130871409{\\&}doi=10.1111{\\%}2Facer.14873{\\&}partnerID=40{\\&}md5=9619f4f40703fe8a26fbae172474a05b},\nvolume = {46},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n An investigation of the HIV Tat C31S and R57S mutation on peripheral immune marker levels in South African participants: A pilot study.\n \n \n \n \n\n\n \n Williams, M E; Ruhanya, V; Paul, R H; Ipser, J C; Stein, D J; Joska, J A; and Naudé, P J W\n\n\n \n\n\n\n 2022.\n \n\n\n\n
\n\n\n\n \n \n \"AnPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Williams2022a,\nannote = {Export Date: 29 December 2022},\nauthor = {Williams, M E and Ruhanya, V and Paul, R H and Ipser, J C and Stein, D J and Joska, J A and Naud{\\'{e}}, P J W},\ndoi = {10.1002/jmv.27720},\nnumber = {7},\npages = {2936--2938},\ntitle = {{An investigation of the HIV Tat C31S and R57S mutation on peripheral immune marker levels in South African participants: A pilot study}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85127292669{\\&}doi=10.1002{\\%}2Fjmv.27720{\\&}partnerID=40{\\&}md5=00064d5cc9feb6d49d482f027a505b1f},\nvolume = {94},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Antenatal maternal depression, early life inflammation and neurodevelopment in a South African birth cohort.\n \n \n \n \n\n\n \n Naudé, P J W; Pariante, C; Hoffman, N; Koopowitz, S.; Donald, K A; Zar, H J; and Stein, D J\n\n\n \n\n\n\n 2022.\n \n\n\n\n
\n\n\n\n \n \n \"AntenatalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Naude2022,\nannote = {Export Date: 29 December 2022},\nauthor = {Naud{\\'{e}}, P J W and Pariante, C and Hoffman, N and Koopowitz, S.-M. and Donald, K A and Zar, H J and Stein, D J},\ndoi = {10.1016/j.bbi.2022.07.001},\nfile = {:Users/jacquelinebracher/Zotero/storage/4K78XPCB/Naud{\\'{e}} et al. - 2022 - Antenatal maternal depression, early life inflamma.pdf:pdf},\npages = {160--168},\ntitle = {{Antenatal maternal depression, early life inflammation and neurodevelopment in a South African birth cohort}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85134596330{\\&}doi=10.1016{\\%}2Fj.bbi.2022.07.001{\\&}partnerID=40{\\&}md5=f7e62e77f65a020ef329ba3d908cca0c},\nvolume = {105},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Epilepsy research in \\Africa\\: \\A\\ scoping review by the \\textlessspan style=\"font-variant:small-caps;\"\\textgreater\\ILAE\\\\textless/span\\textgreater\\Pediatric\\ \\Commission\\ \\Research\\ \\Advocacy\\ \\Task\\ \\Force\\.\n \n \n \n \n\n\n \n Samia, P.; Hassell, J.; Hudson, J.; Ahmed, A.; Shah, J.; Hammond, C.; Kija, E.; Auvin, S.; and Wilmshurst, J.\n\n\n \n\n\n\n Epilepsia, 63(9): 2225–2241. sep 2022.\n \n\n\n\n
\n\n\n\n \n \n \"EpilepsyPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{samia_epilepsy_2022,\nabstract = {Abstract\n\nObjective\nDespite the high prevalence of epilepsy in Africa, evaluation of epilepsy research trends on the continent is lacking. Without establishing effective research, improvement in care for people with epilepsy cannot be effectively strategized or targeted.\n\n\nMethods\nA scoping review of the peer‐reviewed literature on epilepsy from Africa (1989–2019) was conducted. The aim was to understand from this what areas are well researched versus underresearched based on published epilepsy topics.\n\n\nResults\nA total of 1227 publications were identified and assessed. A significant increase in publications occurred over the 30 years assessed. African author leadership was evident in most reports. Nine countries had {\\textgreater}50 publications identified; the remaining 45 countries had {\\textless}50 or no publications. Research studies were typically of lower quality (case series and observational studies). Research themes were more focused on clinical epilepsy (descriptive observational studies) and social aspects (qualitative surveys). However, there were a number of unique and strong themes, specifically for neurocysticercosis and nodding syndrome, where strong research collaborations were evident, basic science understandings were explored, and interventional models were established.\n\n\nSignificance\nDespite Africa being the continent with the most countries, it is lacking in the quantity, quality, and for some areas, relevance of research on epilepsy. Targeted approaches are needed to upskill the strength of research undertaken with more basic science, interventional, and randomized controlled studies. Themes of research need to promote those with unique African content but also to align with current international research areas that have impact on care delivery, such as epilepsy surgery and epilepsy genetics. For this to be possible, it is important to strengthen research hubs with collaborations that empower Africa to own its epilepsy research journey.},\nauthor = {Samia, Pauline and Hassell, Jane and Hudson, Jessica and Ahmed, Azim and Shah, Jasmit and Hammond, Charles and Kija, Edward and Auvin, St{\\'{e}}phane and Wilmshurst, Jo},\ndoi = {10.1111/epi.17321},\nfile = {:Users/jacquelinebracher/Zotero/storage/R6NKR5KG/Samia et al. - 2022 - Epilepsy research in Africa A scoping review by t.pdf:pdf},\nissn = {0013-9580, 1528-1167},\njournal = {Epilepsia},\nmonth = {sep},\nnumber = {9},\npages = {2225--2241},\nshorttitle = {Epilepsy research in {\\{}Africa{\\}}},\ntitle = {{Epilepsy research in {\\{}Africa{\\}}: {\\{}A{\\}} scoping review by the {\\textless}span style="font-variant:small-caps;"{\\textgreater}{\\{}ILAE{\\}}{\\textless}/span{\\textgreater}{\\{}Pediatric{\\}} {\\{}Commission{\\}} {\\{}Research{\\}} {\\{}Advocacy{\\}} {\\{}Task{\\}} {\\{}Force{\\}}}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1111/epi.17321},\nvolume = {63},\nyear = {2022}\n}\n
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\n Abstract Objective Despite the high prevalence of epilepsy in Africa, evaluation of epilepsy research trends on the continent is lacking. Without establishing effective research, improvement in care for people with epilepsy cannot be effectively strategized or targeted. Methods A scoping review of the peer‐reviewed literature on epilepsy from Africa (1989–2019) was conducted. The aim was to understand from this what areas are well researched versus underresearched based on published epilepsy topics. Results A total of 1227 publications were identified and assessed. A significant increase in publications occurred over the 30 years assessed. African author leadership was evident in most reports. Nine countries had \\textgreater50 publications identified; the remaining 45 countries had \\textless50 or no publications. Research studies were typically of lower quality (case series and observational studies). Research themes were more focused on clinical epilepsy (descriptive observational studies) and social aspects (qualitative surveys). However, there were a number of unique and strong themes, specifically for neurocysticercosis and nodding syndrome, where strong research collaborations were evident, basic science understandings were explored, and interventional models were established. Significance Despite Africa being the continent with the most countries, it is lacking in the quantity, quality, and for some areas, relevance of research on epilepsy. Targeted approaches are needed to upskill the strength of research undertaken with more basic science, interventional, and randomized controlled studies. Themes of research need to promote those with unique African content but also to align with current international research areas that have impact on care delivery, such as epilepsy surgery and epilepsy genetics. For this to be possible, it is important to strengthen research hubs with collaborations that empower Africa to own its epilepsy research journey.\n
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\n \n\n \n \n \n \n \n \n Limited evidence for a moderating effect of HIV status on brain age in heavy episodic drinkers.\n \n \n \n \n\n\n \n Ipser, J C; Joska, J; Sevenoaks, T; Gouse, H; Freeman, C; Kaufmann, T; Andreassen, O A; Shoptaw, S; and Stein, D J\n\n\n \n\n\n\n 2022.\n \n\n\n\n
\n\n\n\n \n \n \"LimitedPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@misc{Ipser2022,\nannote = {Export Date: 29 December 2022},\nauthor = {Ipser, J C and Joska, J and Sevenoaks, T and Gouse, H and Freeman, C and Kaufmann, T and Andreassen, O A and Shoptaw, S and Stein, D J},\ndoi = {10.1007/s13365-022-01072-5},\nnumber = {3},\npages = {383--391},\ntitle = {{Limited evidence for a moderating effect of HIV status on brain age in heavy episodic drinkers}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85127374767{\\&}doi=10.1007{\\%}2Fs13365-022-01072-5{\\&}partnerID=40{\\&}md5=db40f93cf7c74f37fd4e9e56a31c35e9},\nvolume = {28},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n Intimate partner violence and growth outcomes through infancy: A longitudinal investigation of multiple mediators in a South African birth cohort.\n \n \n \n\n\n \n Barnett, W.; Nhapi, R.; Zar, H.; Halligan, S.; Pellowski, J.; Donald, K.; and Stein, D.\n\n\n \n\n\n\n Maternal and Child Nutrition, 18(1). 2022.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Barnett2022,\nabstract = {Intimate partner violence (IPV) has been linked to poor fetal and infant growth. However, factors underlying this relationship are not well understood, particularly in the postnatal time period. In a South African cohort, we investigated (1) associations between IPV in pregnancy and growth at birth as well as postnatal IPV and child growth at 12 months and (2) whether maternal depression, tobacco or alcohol use or infant hospitalizations mediated IPV-growth relationships. Mothers were enrolled in pregnancy. Maternal IPV was measured during pregnancy and 10 weeks postpartum; depression, alcohol and tobacco use were measured during pregnancy and at 6 months postpartum. Child weight and length were measured at birth and 12 months and converted to z-scores for analysis. Linear regression and structural equation models investigated interrelationships between IPV and potential mediators of IPV-growth relationships. At birth, among 1,111 mother–infant pairs, maternal emotional and physical IPV were associated with reduced weight-for-age z-scores (WFAZ). Only physical IPV was associated with length-for-age z-scores (LFAZ) at birth. Antenatal maternal alcohol and tobacco use mediated IPV-growth relationships at birth. Postnatally, among 783 mother–infant pairs, emotional and physical IPV were associated with reduced WFAZ at 12 months. Only emotional IPV was associated with LFAZ at 12 months. Maternal tobacco use was a mediator postnatally. Findings highlight the role of physical and emotional IPV as risk factors for compromised fetal and infant growth. Findings underscore the importance of programmes to address interrelated risk factors for compromised infant growth, specifically IPV and substance use, which are prevalent in high-risk settings.},\nauthor = {Barnett, W. and Nhapi, R. and Zar, H.J. and Halligan, S.L. and Pellowski, J. and Donald, K.A. and Stein, D.J.},\ndoi = {10.1111/mcn.13281},\nfile = {:Users/jacquelinebracher/Zotero/storage/WEWTZ9QW/Barnett et al. - 2022 - Intimate partner violence and growth outcomes thro.pdf:pdf},\njournal = {Maternal and Child Nutrition},\nnumber = {1},\ntitle = {{Intimate partner violence and growth outcomes through infancy: A longitudinal investigation of multiple mediators in a South African birth cohort}},\nvolume = {18},\nyear = {2022}\n}\n
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\n Intimate partner violence (IPV) has been linked to poor fetal and infant growth. However, factors underlying this relationship are not well understood, particularly in the postnatal time period. In a South African cohort, we investigated (1) associations between IPV in pregnancy and growth at birth as well as postnatal IPV and child growth at 12 months and (2) whether maternal depression, tobacco or alcohol use or infant hospitalizations mediated IPV-growth relationships. Mothers were enrolled in pregnancy. Maternal IPV was measured during pregnancy and 10 weeks postpartum; depression, alcohol and tobacco use were measured during pregnancy and at 6 months postpartum. Child weight and length were measured at birth and 12 months and converted to z-scores for analysis. Linear regression and structural equation models investigated interrelationships between IPV and potential mediators of IPV-growth relationships. At birth, among 1,111 mother–infant pairs, maternal emotional and physical IPV were associated with reduced weight-for-age z-scores (WFAZ). Only physical IPV was associated with length-for-age z-scores (LFAZ) at birth. Antenatal maternal alcohol and tobacco use mediated IPV-growth relationships at birth. Postnatally, among 783 mother–infant pairs, emotional and physical IPV were associated with reduced WFAZ at 12 months. Only emotional IPV was associated with LFAZ at 12 months. Maternal tobacco use was a mediator postnatally. Findings highlight the role of physical and emotional IPV as risk factors for compromised fetal and infant growth. Findings underscore the importance of programmes to address interrelated risk factors for compromised infant growth, specifically IPV and substance use, which are prevalent in high-risk settings.\n
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\n \n\n \n \n \n \n \n \n Difficulty & quality of will: implications for moral ignorance.\n \n \n \n \n\n\n \n Hartford, A.\n\n\n \n\n\n\n Philosophical Explorations, 25(2): 141–158. may 2022.\n \n\n\n\n
\n\n\n\n \n \n \"DifficultyPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{hartford_difficulty_2022,\nauthor = {Hartford, Anna},\ndoi = {10.1080/13869795.2022.2042585},\nissn = {1386-9795, 1741-5918},\njournal = {Philosophical Explorations},\nmonth = {may},\nnumber = {2},\npages = {141--158},\nshorttitle = {Difficulty {\\&} quality of will},\ntitle = {{Difficulty {\\&} quality of will: implications for moral ignorance}},\nurl = {https://www.tandfonline.com/doi/full/10.1080/13869795.2022.2042585},\nvolume = {25},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Childhood Trauma and Mental Health in the Cape Town Adolescent Antiretroviral Cohort.\n \n \n \n \n\n\n \n Sevenoaks, T; Fouche, J.; Phillips, N; Heany, S; Myer, L; Zar, H J; Stein, D J; and Hoare, J\n\n\n \n\n\n\n 2022.\n \n\n\n\n
\n\n\n\n \n \n \"ChildhoodPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Sevenoaks2022a,\nannote = {Export Date: 29 December 2022},\nauthor = {Sevenoaks, T and Fouche, J.-P. and Phillips, N and Heany, S and Myer, L and Zar, H J and Stein, D J and Hoare, J},\ndoi = {10.1007/s40653-021-00362-0},\nfile = {:Users/jacquelinebracher/Zotero/storage/FVDRNSM6/Sevenoaks et al. - 2022 - Childhood Trauma and Mental Health in the Cape Tow.pdf:pdf},\nnumber = {2},\npages = {353--363},\ntitle = {{Childhood Trauma and Mental Health in the Cape Town Adolescent Antiretroviral Cohort}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85106493339{\\&}doi=10.1007{\\%}2Fs40653-021-00362-0{\\&}partnerID=40{\\&}md5=678dedc8527c4711b6dd909fa816f5bd},\nvolume = {15},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n A systematic review of brain imaging findings in neurological infection with \\Japanese\\ encephalitis virus compared with \\Dengue\\ virus.\n \n \n \n \n\n\n \n Pichl, T.; Wedderburn, C. J; Hoskote, C.; Turtle, L.; and Bharucha, T.\n\n\n \n\n\n\n International Journal of Infectious Diseases, 119: 102–110. jun 2022.\n \n\n\n\n
\n\n\n\n \n \n \"APaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{pichl_systematic_2022,\nauthor = {Pichl, Thomas and Wedderburn, Catherine J and Hoskote, Chandrashekar and Turtle, Lance and Bharucha, Tehmina},\ndoi = {10.1016/j.ijid.2022.03.010},\nfile = {:Users/jacquelinebracher/Zotero/storage/HWIGPKBL/Pichl et al. - 2022 - A systematic review of brain imaging findings in n.pdf:pdf},\nissn = {12019712},\njournal = {International Journal of Infectious Diseases},\nmonth = {jun},\npages = {102--110},\ntitle = {{A systematic review of brain imaging findings in neurological infection with {\\{}Japanese{\\}} encephalitis virus compared with {\\{}Dengue{\\}} virus}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S1201971222001485},\nvolume = {119},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Revealing the \\Mutational\\ \\Spectrum\\ in \\Southern\\ \\Africans\\ \\With\\ \\Amyotrophic\\ \\Lateral\\ \\Sclerosis\\.\n \n \n \n \n\n\n \n Nel, M.; Mahungu, A. C; Monnakgotla, N.; Botha, G. R; Mulder, N. J; Wu, G.; Rampersaud, E.; Van Blitterswijk, M.; Wuu, J.; Cooley, A.; Myers, J.; Rademakers, R.; Taylor, J P.; Benatar, M.; and Heckmann, J. M\n\n\n \n\n\n\n Neurology Genetics, 8(1): e654. feb 2022.\n \n\n\n\n
\n\n\n\n \n \n \"RevealingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{nel_revealing_2022,\nabstract = {Background and Objectives\nTo perform the first screen of 44 amyotrophic lateral sclerosis (ALS) genes in a cohort of African genetic ancestry individuals with ALS using whole-genome sequencing (WGS) data.\n\n\nMethods\nOne hundred three consecutive cases with probable/definite ALS (using the revised El Escorial criteria), and self-categorized as African genetic ancestry, underwent WGS using various Illumina platforms. As population controls, 238 samples from various African WGS data sets were included. Our analysis was restricted to 44 ALS genes, which were curated for rare sequence variants and classified according to the American College of Medical Genetics guidelines as likely benign, uncertain significance, likely pathogenic, or pathogenic variants.\n\n\nResults\n\nThirteen percent of 103 ALS cases harbored pathogenic variants; 5 different\nSOD1\nvariants (N87S, G94D, I114T, L145S, and L145F) in 5 individuals (5{\\%}, 1 familial case), pathogenic\nC9orf72\nrepeat expansions in 7 individuals (7{\\%}, 1 familial case) and a likely pathogenic\nANXA11\n(G38R) variant in 1 individual. Thirty individuals (29{\\%}) harbored ≥1 variant of uncertain significance; 10 of these variants had limited pathogenic evidence, although this was insufficient to permit confident classification as pathogenic.\n\n\n\nDiscussion\n\nOur findings show that known ALS genes can be expected to identify a genetic cause of disease in {\\textgreater}11{\\%} of sporadic ALS cases of African genetic ancestry. Similar to European cohorts, the 2 most frequent genes harboring pathogenic variants in this population group are\nC9orf72\nand\nSOD1\n.},\nauthor = {Nel, Melissa and Mahungu, Amokelani C and Monnakgotla, Nomakhosazana and Botha, Gerrit R and Mulder, Nicola J and Wu, Gang and Rampersaud, Evadnie and {Van Blitterswijk}, Marka and Wuu, Joanne and Cooley, Anne and Myers, Jason and Rademakers, Rosa and Taylor, J Paul and Benatar, Michael and Heckmann, Jeannine M},\ndoi = {10.1212/NXG.0000000000000654},\nfile = {:Users/jacquelinebracher/Zotero/storage/N5N5IGEE/Nel et al. - 2022 - Revealing the Mutational Spectrum in Southern Afri.pdf:pdf},\nissn = {2376-7839},\njournal = {Neurology Genetics},\nmonth = {feb},\nnumber = {1},\npages = {e654},\ntitle = {{Revealing the {\\{}Mutational{\\}} {\\{}Spectrum{\\}} in {\\{}Southern{\\}} {\\{}Africans{\\}} {\\{}With{\\}} {\\{}Amyotrophic{\\}} {\\{}Lateral{\\}} {\\{}Sclerosis{\\}}}},\nurl = {http://ng.neurology.org/lookup/doi/10.1212/NXG.0000000000000654},\nvolume = {8},\nyear = {2022}\n}\n
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\n Background and Objectives To perform the first screen of 44 amyotrophic lateral sclerosis (ALS) genes in a cohort of African genetic ancestry individuals with ALS using whole-genome sequencing (WGS) data. Methods One hundred three consecutive cases with probable/definite ALS (using the revised El Escorial criteria), and self-categorized as African genetic ancestry, underwent WGS using various Illumina platforms. As population controls, 238 samples from various African WGS data sets were included. Our analysis was restricted to 44 ALS genes, which were curated for rare sequence variants and classified according to the American College of Medical Genetics guidelines as likely benign, uncertain significance, likely pathogenic, or pathogenic variants. Results Thirteen percent of 103 ALS cases harbored pathogenic variants; 5 different SOD1 variants (N87S, G94D, I114T, L145S, and L145F) in 5 individuals (5%, 1 familial case), pathogenic C9orf72 repeat expansions in 7 individuals (7%, 1 familial case) and a likely pathogenic ANXA11 (G38R) variant in 1 individual. Thirty individuals (29%) harbored ≥1 variant of uncertain significance; 10 of these variants had limited pathogenic evidence, although this was insufficient to permit confident classification as pathogenic. Discussion Our findings show that known ALS genes can be expected to identify a genetic cause of disease in \\textgreater11% of sporadic ALS cases of African genetic ancestry. Similar to European cohorts, the 2 most frequent genes harboring pathogenic variants in this population group are C9orf72 and SOD1 .\n
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\n \n\n \n \n \n \n \n \n Clinical \\Characteristics\\ of \\Youth\\ with \\Trichotillomania\\ (\\Hair\\-\\Pulling\\ \\Disorder\\) and \\Excoriation\\ (\\Skin\\-\\Picking\\) \\Disorder\\.\n \n \n \n \n\n\n \n Ricketts, E. J; Peris, T. S; Grant, J. E; Valle, S.; Cavic, E.; Lerner, J. E; Lochner, C.; Stein, D. J; Dougherty, D. D; O'Neill, J.; Woods, D. W; Keuthen, N. J; and Piacentini, J.\n\n\n \n\n\n\n Child Psychiatry & Human Development. oct 2022.\n \n\n\n\n
\n\n\n\n \n \n \"ClinicalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{ricketts_clinical_2022,\nauthor = {Ricketts, Emily J and Peris, Tara S and Grant, Jon E and Valle, Stephanie and Cavic, Elizabeth and Lerner, Juliette E and Lochner, Christine and Stein, Dan J and Dougherty, Darin D and O'Neill, Joseph and Woods, Douglas W and Keuthen, Nancy J and Piacentini, John},\ndoi = {10.1007/s10578-022-01458-w},\nissn = {0009-398X, 1573-3327},\njournal = {Child Psychiatry {\\&} Human Development},\nmonth = {oct},\ntitle = {{Clinical {\\{}Characteristics{\\}} of {\\{}Youth{\\}} with {\\{}Trichotillomania{\\}} ({\\{}Hair{\\}}-{\\{}Pulling{\\}} {\\{}Disorder{\\}}) and {\\{}Excoriation{\\}} ({\\{}Skin{\\}}-{\\{}Picking{\\}}) {\\{}Disorder{\\}}}},\nurl = {https://link.springer.com/10.1007/s10578-022-01458-w},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n Cultural diversity is crucial for African neuroethics.\n \n \n \n\n\n \n Matshabane, O.; Mgweba-Bewana, L.; Atuire, C.; de Vries, J.; and Koehly, L.\n\n\n \n\n\n\n Nature Human Behaviour, 6(9): 1185–1187. 2022.\n \n\n\n\n
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@article{Matshabane2022,\nauthor = {Matshabane, O.P. and Mgweba-Bewana, L. and Atuire, C.A. and de Vries, J. and Koehly, L.M.},\ndoi = {10.1038/s41562-022-01436-1},\nfile = {:Users/jacquelinebracher/Zotero/storage/9BPXWLGN/Matshabane et al. - 2022 - Cultural diversity is crucial for African neuroeth.pdf:pdf},\njournal = {Nature Human Behaviour},\nnumber = {9},\npages = {1185--1187},\ntitle = {{Cultural diversity is crucial for African neuroethics}},\nvolume = {6},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Cross-country variations in the reporting of psychotic symptoms among sub-\\Saharan\\ \\African\\ adults: \\A\\ psychometric evaluation of the \\Psychosis\\ \\Screening\\ \\Questionnaire\\.\n \n \n \n \n\n\n \n Bitta, M.; Thungana, Y.; Kim, H. H; Denckla, C. A; Ametaj, A.; Yared, M.; Kwagala, C.; Ongeri, L.; Stroud, R. E; Kwobah, E.; Koenen, K. C; Kariuki, S.; Zingela, Z.; Akena, D.; Newton, C.; Atwoli, L.; Teferra, S.; Stein, D. J; and Gelaye, B.\n\n\n \n\n\n\n Journal of Affective Disorders, 304: 85–92. may 2022.\n \n\n\n\n
\n\n\n\n \n \n \"Cross-countryPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{bitta_cross-country_2022,\nauthor = {Bitta, Mary and Thungana, Yanga and Kim, Hannah H and Denckla, Christy A and Ametaj, Amantia and Yared, Mahlet and Kwagala, Claire and Ongeri, Linnet and Stroud, Rocky E and Kwobah, Edith and Koenen, Karestan C and Kariuki, Symon and Zingela, Zukiswa and Akena, Dickens and Newton, Charles and Atwoli, Lukoye and Teferra, Solomon and Stein, Dan J and Gelaye, Bizu},\ndoi = {10.1016/j.jad.2022.02.048},\nfile = {:Users/jacquelinebracher/Zotero/storage/4RW7BXGD/Bitta et al. - 2022 - Cross-country variations in the reporting of psych.pdf:pdf},\nissn = {01650327},\njournal = {Journal of Affective Disorders},\nmonth = {may},\npages = {85--92},\nshorttitle = {Cross-country variations in the reporting of psych},\ntitle = {{Cross-country variations in the reporting of psychotic symptoms among sub-{\\{}Saharan{\\}} {\\{}African{\\}} adults: {\\{}A{\\}} psychometric evaluation of the {\\{}Psychosis{\\}} {\\{}Screening{\\}} {\\{}Questionnaire{\\}}}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S0165032722001963},\nvolume = {304},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Escitalopram and lorazepam differentially affect nesting and open field behaviour in deer mice exposed to an anxiogenic environment.\n \n \n \n \n\n\n \n Wolmarans, D. W.; Prinsloo, M.; Seedat, S.; Stein, D. J; Harvey, B. H; and De Brouwer, G.\n\n\n \n\n\n\n Neuroscience Research, 177: 85–93. apr 2022.\n \n\n\n\n
\n\n\n\n \n \n \"EscitalopramPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{wolmarans_escitalopram_2022,\nauthor = {Wolmarans, De Wet and Prinsloo, Michelle and Seedat, Soraya and Stein, Dan J and Harvey, Brian H and {De Brouwer}, Geoffrey},\ndoi = {10.1016/j.neures.2021.10.011},\nissn = {01680102},\njournal = {Neuroscience Research},\nmonth = {apr},\npages = {85--93},\ntitle = {{Escitalopram and lorazepam differentially affect nesting and open field behaviour in deer mice exposed to an anxiogenic environment}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S0168010221002194},\nvolume = {177},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Gait status 26–35 years after selective dorsal rhizotomy: \\A\\ 9 year follow up study.\n \n \n \n \n\n\n \n Langerak, N. G; Veerbeek, B. E; Fieggen, A G.; and Lamberts, R. P\n\n\n \n\n\n\n Gait & Posture, 91: 284–289. jan 2022.\n \n\n\n\n
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@article{langerak_gait_2022,\nauthor = {Langerak, Nelleke G and Veerbeek, Berendina E and Fieggen, A Graham and Lamberts, Robert P},\ndoi = {10.1016/j.gaitpost.2021.10.031},\nissn = {09666362},\njournal = {Gait {\\&} Posture},\nmonth = {jan},\npages = {284--289},\nshorttitle = {Gait status 26–35 years after selective dorsal rhi},\ntitle = {{Gait status 26–35 years after selective dorsal rhizotomy: {\\{}A{\\}} 9 year follow up study}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S0966636221005658},\nvolume = {91},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Verbal and \\General\\ \\IQ\\ \\Associate\\ with \\Supragranular\\ \\Layer\\ \\Thickness\\ and \\Cell\\ \\Properties\\ of the \\Left\\ \\Temporal\\ \\Cortex\\.\n \n \n \n \n\n\n \n Heyer, D B; Wilbers, R; Galakhova, A A; Hartsema, E; Braak, S; Hunt, S; Verhoog, M B; Muijtjens, M L; Mertens, E J; Idema, S; Baayen, J C; De Witt Hamer, P; Klein, M; McGraw, M; Lein, E S; De Kock, C P J; Mansvelder, H D; and Goriounova, N A\n\n\n \n\n\n\n Cerebral Cortex, 32(11): 2343–2357. may 2022.\n \n\n\n\n
\n\n\n\n \n \n \"VerbalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{heyer_verbal_2022,\nabstract = {Abstract\nThe left temporal lobe is an integral part of the language system and its cortical structure and function associate with general intelligence. However, whether cortical laminar architecture and cellular properties of this brain area relate to verbal intelligence is unknown. Here, we addressed this using histological analysis and cellular recordings of neurosurgically resected temporal cortex in combination with presurgical IQ scores. We find that subjects with higher general and verbal IQ scores have thicker left (but not right) temporal cortex (Brodmann area 21, BA21). The increased thickness is due to the selective increase in layers 2 and 3 thickness, accompanied by lower neuron densities, and larger dendrites and cell body size of pyramidal neurons in these layers. Furthermore, these neurons sustain faster action potential kinetics, which improves information processing. Our results indicate that verbal mental ability associates with selective adaptations of supragranular layers and their cellular micro-architecture and function in left, but not right temporal cortex.},\nauthor = {Heyer, D B and Wilbers, R and Galakhova, A A and Hartsema, E and Braak, S and Hunt, S and Verhoog, M B and Muijtjens, M L and Mertens, E J and Idema, S and Baayen, J C and {De Witt Hamer}, P and Klein, M and McGraw, M and Lein, E S and {De Kock}, C P J and Mansvelder, H D and Goriounova, N A},\ndoi = {10.1093/cercor/bhab330},\nfile = {:Users/jacquelinebracher/Zotero/storage/HSJXYSFP/Heyer et al. - 2022 - Verbal and General IQ Associate with Supragranular.pdf:pdf},\nissn = {1047-3211, 1460-2199},\njournal = {Cerebral Cortex},\nmonth = {may},\nnumber = {11},\npages = {2343--2357},\ntitle = {{Verbal and {\\{}General{\\}} {\\{}IQ{\\}} {\\{}Associate{\\}} with {\\{}Supragranular{\\}} {\\{}Layer{\\}} {\\{}Thickness{\\}} and {\\{}Cell{\\}} {\\{}Properties{\\}} of the {\\{}Left{\\}} {\\{}Temporal{\\}} {\\{}Cortex{\\}}}},\nurl = {https://academic.oup.com/cercor/article/32/11/2343/6373557},\nvolume = {32},\nyear = {2022}\n}\n
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\n Abstract The left temporal lobe is an integral part of the language system and its cortical structure and function associate with general intelligence. However, whether cortical laminar architecture and cellular properties of this brain area relate to verbal intelligence is unknown. Here, we addressed this using histological analysis and cellular recordings of neurosurgically resected temporal cortex in combination with presurgical IQ scores. We find that subjects with higher general and verbal IQ scores have thicker left (but not right) temporal cortex (Brodmann area 21, BA21). The increased thickness is due to the selective increase in layers 2 and 3 thickness, accompanied by lower neuron densities, and larger dendrites and cell body size of pyramidal neurons in these layers. Furthermore, these neurons sustain faster action potential kinetics, which improves information processing. Our results indicate that verbal mental ability associates with selective adaptations of supragranular layers and their cellular micro-architecture and function in left, but not right temporal cortex.\n
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\n \n\n \n \n \n \n \n \n Mental health literacy among primary healthcare workers in \\South\\ \\Africa\\ and \\Zambia\\.\n \n \n \n \n\n\n \n Korhonen, J.; Axelin, A.; Stein, D. J; Seedat, S.; Mwape, L.; Jansen, R.; Groen, G.; Grobler, G.; Jörns‐Presentati, A.; Katajisto, J.; Lahti, M.; and MEGA Consortium/Research Team\n\n\n \n\n\n\n Brain and Behavior, 12(12): e2807. dec 2022.\n \n\n\n\n
\n\n\n\n \n \n \"MentalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{korhonen_mental_2022,\nabstract = {Abstract\n\nBackground\nIn developing countries, mental health literacy (MHL) still needs to be improved due to the high prevalence of mental disorders. It is widely recognized that MHL can improve health outcomes for both individuals and populations. Healthcare professionals' development in MHL is crucial to the prevention of mental disorders. The aim of this study was to assess MHL of primary healthcare (PHC) workers in South Africa (SA) and Zambia and determinants thereof. Limited evidence is available on the levels of MHL among PHC workers in the sub‐Saharan Africa region, which faces a large burden of mental disorders.\n\n\nMethods\n\nThe study population for this cross‐sectional survey comprised PHC workers (\nn\n= 250) in five provinces of SA and Zambia. MHL was measured with the Mental Health Literacy Scale (MHLS). We conducted a multivariate analysis to explore determinants of MHL.\n\n\n\nResults\nResults showed moderate MHL among PHC professionals, but with a wide range from low to high MHL. Knowledge‐related items had a greater dispersion than other attributes of MHL. PHC workers with more education showed a greater ability to recognize mental health‐related disorders. Those who had experience in the use of mental health‐related assessment scales or screening tools reported a higher total MHL. The results confirmed strong internal consistency for the MHLS.\n\n\nConclusion\nThe results highlighted varying mental health perceptions and knowledge in PHC. Implementation of specifically developed formal training programs and interventions to improve MHL in PHC workers to strengthen their competence may help bridge the treatment gap.},\nauthor = {Korhonen, Joonas and Axelin, Anna and Stein, Dan J and Seedat, Soraya and Mwape, Lonia and Jansen, Ronelle and Groen, Gunter and Grobler, Gerhard and J{\\"{o}}rns‐Presentati, Astrid and Katajisto, Jouko and Lahti, Mari and {MEGA Consortium/Research Team}},\ndoi = {10.1002/brb3.2807},\nfile = {:Users/jacquelinebracher/Zotero/storage/KEGWNKSA/Korhonen et al. - 2022 - Mental health literacy among primary healthcare wo.pdf:pdf},\nissn = {2162-3279, 2162-3279},\njournal = {Brain and Behavior},\nmonth = {dec},\nnumber = {12},\npages = {e2807},\ntitle = {{Mental health literacy among primary healthcare workers in {\\{}South{\\}} {\\{}Africa{\\}} and {\\{}Zambia{\\}}}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1002/brb3.2807},\nvolume = {12},\nyear = {2022}\n}\n
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\n Abstract Background In developing countries, mental health literacy (MHL) still needs to be improved due to the high prevalence of mental disorders. It is widely recognized that MHL can improve health outcomes for both individuals and populations. Healthcare professionals' development in MHL is crucial to the prevention of mental disorders. The aim of this study was to assess MHL of primary healthcare (PHC) workers in South Africa (SA) and Zambia and determinants thereof. Limited evidence is available on the levels of MHL among PHC workers in the sub‐Saharan Africa region, which faces a large burden of mental disorders. Methods The study population for this cross‐sectional survey comprised PHC workers ( n = 250) in five provinces of SA and Zambia. MHL was measured with the Mental Health Literacy Scale (MHLS). We conducted a multivariate analysis to explore determinants of MHL. Results Results showed moderate MHL among PHC professionals, but with a wide range from low to high MHL. Knowledge‐related items had a greater dispersion than other attributes of MHL. PHC workers with more education showed a greater ability to recognize mental health‐related disorders. Those who had experience in the use of mental health‐related assessment scales or screening tools reported a higher total MHL. The results confirmed strong internal consistency for the MHLS. Conclusion The results highlighted varying mental health perceptions and knowledge in PHC. Implementation of specifically developed formal training programs and interventions to improve MHL in PHC workers to strengthen their competence may help bridge the treatment gap.\n
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\n \n\n \n \n \n \n \n \n Genetic structure correlates with ethnolinguistic diversity in eastern and southern \\Africa\\.\n \n \n \n \n\n\n \n Atkinson, E. G; Dalvie, S.; Pichkar, Y.; Kalungi, A.; Majara, L.; Stevenson, A.; Abebe, T.; Akena, D.; Alemayehu, M.; Ashaba, F. K; Atwoli, L.; Baker, M.; Chibnik, L. B; Creanza, N.; Daly, M. J; Fekadu, A.; Gelaye, B.; Gichuru, S.; Injera, W. E; James, R.; Kariuki, S. M; Kigen, G.; Koen, N.; Koenen, K. C; Koenig, Z.; Kwobah, E.; Kyebuzibwa, J.; Musinguzi, H.; Mwema, R. M; Neale, B. M; Newman, C. P; Newton, C. R J C; Ongeri, L.; Ramachandran, S.; Ramesar, R.; Shiferaw, W.; Stein, D. J; Stroud, R. E; Teferra, S.; Yohannes, M. T; Zingela, Z.; and Martin, A. R\n\n\n \n\n\n\n The American Journal of Human Genetics, 109(9): 1667–1679. sep 2022.\n \n\n\n\n
\n\n\n\n \n \n \"GeneticPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{atkinson_genetic_2022,\nauthor = {Atkinson, Elizabeth G and Dalvie, Shareefa and Pichkar, Yakov and Kalungi, Allan and Majara, Lerato and Stevenson, Anne and Abebe, Tamrat and Akena, Dickens and Alemayehu, Melkam and Ashaba, Fred K and Atwoli, Lukoye and Baker, Mark and Chibnik, Lori B and Creanza, Nicole and Daly, Mark J and Fekadu, Abebaw and Gelaye, Bizu and Gichuru, Stella and Injera, Wilfred E and James, Roxanne and Kariuki, Symon M and Kigen, Gabriel and Koen, Nastassja and Koenen, Karestan C and Koenig, Zan and Kwobah, Edith and Kyebuzibwa, Joseph and Musinguzi, Henry and Mwema, Rehema M and Neale, Benjamin M and Newman, Carter P and Newton, Charles R J C and Ongeri, Linnet and Ramachandran, Sohini and Ramesar, Raj and Shiferaw, Welelta and Stein, Dan J and Stroud, Rocky E and Teferra, Solomon and Yohannes, Mary T and Zingela, Zukiswa and Martin, Alicia R},\ndoi = {10.1016/j.ajhg.2022.07.013},\nfile = {:Users/jacquelinebracher/Zotero/storage/BZQMC5PI/Atkinson et al. - 2022 - Genetic structure correlates with ethnolinguistic .pdf:pdf},\nissn = {00029297},\njournal = {The American Journal of Human Genetics},\nmonth = {sep},\nnumber = {9},\npages = {1667--1679},\ntitle = {{Genetic structure correlates with ethnolinguistic diversity in eastern and southern {\\{}Africa{\\}}}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S0002929722003172},\nvolume = {109},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Introduction.\n \n \n \n \n\n\n \n Stein, D. J; Lochner, C.; Chamberlain, S. R; and Fineberg, N. A\n\n\n \n\n\n\n In Mental \\Health\\ in a \\Digital\\ \\World\\, pages 1–7. Elsevier, 2022.\n \n\n\n\n
\n\n\n\n \n \n \"IntroductionPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@incollection{stein_introduction_2022,\nauthor = {Stein, Dan J and Lochner, Christine and Chamberlain, Samuel R and Fineberg, Naomi A},\nbooktitle = {Mental {\\{}Health{\\}} in a {\\{}Digital{\\}} {\\{}World{\\}}},\ndoi = {10.1016/B978-0-12-822201-0.00020-4},\nisbn = {978-0-12-822201-0},\npages = {1--7},\npublisher = {Elsevier},\ntitle = {{Introduction}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/B9780128222010000204},\nyear = {2022}\n}\n
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\n \n\n \n \n \n \n \n \n Cochrane systematic review and meta-analysis of the impact of psychological treatment on health-related quality of life in people with epilepsy: an update by the ILAE Psychology Task Force, highlighting methodological changes∗.\n \n \n \n \n\n\n \n Michaelis, R; Tang, V; Nevitt, S J; Wagner, J L; Modi, A C; LaFrance Jr., W C; Goldstein, L H; Gandy, M; Bresnahan, R; Valente, K; Donald, K A; and Reuber, M\n\n\n \n\n\n\n 2021.\n \n\n\n\n
\n\n\n\n \n \n \"CochranePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Michaelis2021,\nannote = {Export Date: 29 December 2022},\nauthor = {Michaelis, R and Tang, V and Nevitt, S J and Wagner, J L and Modi, A C and {LaFrance  Jr.}, W C and Goldstein, L H and Gandy, M and Bresnahan, R and Valente, K and Donald, K A and Reuber, M},\ndoi = {10.1684/epd.2021.1357},\nfile = {:Users/jacquelinebracher/Zotero/storage/XL9FWQ4Z/Michaelis et al. - 2021 - Cochrane systematic review and meta‐analysis of th.pdf:pdf},\nnumber = {6},\npages = {803--811},\ntitle = {{Cochrane systematic review and meta-analysis of the impact of psychological treatment on health-related quality of life in people with epilepsy: an update by the ILAE Psychology Task Force, highlighting methodological changes∗}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85122671327{\\&}doi=10.1684{\\%}2Fepd.2021.1357{\\&}partnerID=40{\\&}md5=7cd1bec396b2a75320f586cd6fb04648},\nvolume = {23},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Reimagining the future of \\African\\ brain health: \\Perspectives\\ for basic research on the pathogenesis of cryptococcal meningitis.\n \n \n \n \n\n\n \n Dangarembizi, R\n\n\n \n\n\n\n Brain, Behavior, & Immunity - Health, 18: 100388. dec 2021.\n \n\n\n\n
\n\n\n\n \n \n \"ReimaginingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{dangarembizi_reimagining_2021,\nauthor = {Dangarembizi, R},\ndoi = {10.1016/j.bbih.2021.100388},\nfile = {:Users/jacquelinebracher/Zotero/storage/2JHPKTEQ/Dangarembizi - 2021 - Reimagining the future of African brain health Pe.pdf:pdf},\nissn = {26663546},\njournal = {Brain, Behavior, {\\&} Immunity - Health},\nmonth = {dec},\npages = {100388},\nshorttitle = {Reimagining the future of {\\{}African{\\}} brain health},\ntitle = {{Reimagining the future of {\\{}African{\\}} brain health: {\\{}Perspectives{\\}} for basic research on the pathogenesis of cryptococcal meningitis}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S2666354621001915},\nvolume = {18},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Serum and cerebrospinal fluid \\Neutrophil\\ gelatinase-associated lipocalin (\\NGAL\\) levels as biomarkers for the conversion from mild cognitive impairment to \\Alzheimer\\'s disease dementia.\n \n \n \n \n\n\n \n Naudé, P. J W; Ramakers, I. H G B; Van Der Flier, W. M; Jiskoot, L. C; Reesink, F. E; Claassen, J. A H R; Koek, H. L; Eisel, U. L M; and De Deyn, P. P\n\n\n \n\n\n\n Neurobiology of Aging, 107: 1–10. nov 2021.\n \n\n\n\n
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@article{naude_serum_2021,\nauthor = {Naud{\\'{e}}, Petrus J W and Ramakers, Inez H G B and {Van Der Flier}, Wiesje M and Jiskoot, Lize C and Reesink, Fransje E and Claassen, Jurgen A H R and Koek, Huiberdina L and Eisel, Ulrich L M and {De Deyn}, Peter P},\ndoi = {10.1016/j.neurobiolaging.2021.07.001},\nfile = {:Users/jacquelinebracher/Zotero/storage/54F2HGEW/Naud{\\'{e}} et al. - 2021 - Serum and cerebrospinal fluid Neutrophil gelatinas.pdf:pdf},\nissn = {01974580},\njournal = {Neurobiology of Aging},\nmonth = {nov},\npages = {1--10},\ntitle = {{Serum and cerebrospinal fluid {\\{}Neutrophil{\\}} gelatinase-associated lipocalin ({\\{}NGAL{\\}}) levels as biomarkers for the conversion from mild cognitive impairment to {\\{}Alzheimer{\\}}'s disease dementia}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S0197458021002256},\nvolume = {107},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Cortical structural changes related to early antiretroviral therapy (\\ART\\) interruption in perinatally \\HIV\\-infected children at 5 years of age.\n \n \n \n \n\n\n \n Nwosu, E. C; Holmes, M. J; Cotton, M. F; Dobbels, E.; Little, F.; Laughton, B.; Van Der Kouwe, A.; Meintjes, E. M; and Robertson, F.\n\n\n \n\n\n\n IBRO Neuroscience Reports, 10: 161–170. jun 2021.\n \n\n\n\n
\n\n\n\n \n \n \"CorticalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{nwosu_cortical_2021,\nauthor = {Nwosu, Emmanuel C and Holmes, Martha J and Cotton, Mark F and Dobbels, Els and Little, Francesca and Laughton, Barbara and {Van Der Kouwe}, Andre and Meintjes, Ernesta M and Robertson, Frances},\ndoi = {10.1016/j.ibneur.2021.02.001},\nfile = {:Users/jacquelinebracher/Zotero/storage/69JFF264/Nwosu et al. - 2021 - Cortical structural changes related to early antir.pdf:pdf},\nissn = {26672421},\njournal = {IBRO Neuroscience Reports},\nmonth = {jun},\npages = {161--170},\ntitle = {{Cortical structural changes related to early antiretroviral therapy ({\\{}ART{\\}}) interruption in perinatally {\\{}HIV{\\}}-infected children at 5 years of age}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S2667242121000105},\nvolume = {10},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Cortical volume abnormalities in posttraumatic stress disorder: an ENIGMA-psychiatric genomics consortium PTSD workgroup mega-analysis.\n \n \n \n \n\n\n \n Wang, X; Xie, H; Chen, T; Cotton, A S; Salminen, L E; Logue, M W; Clarke-Rubright, E K; Wall, J; Dennis, E L; O'Leary, B M; Abdallah, C G; Andrew, E; Baugh, L A; Bomyea, J; Bruce, S E; Bryant, R; Choi, K; Daniels, J K; Davenport, N D; Davidson, R J; DeBellis, M; DeRoon-Cassini, T; Disner, S G; Fani, N; Fercho, K A; Fitzgerald, J; Forster, G L; Frijling, J L; Geuze, E; Gomaa, H; Gordon, E M; Grupe, D; Harpaz-Rotem, I; Haswell, C C; Herzog, J I; Hofmann, D; Hollifield, M; Hosseini, B; Hudson, A R; Ipser, J; Jahanshad, N; Jovanovic, T; Kaufman, M L; King, A P; Koch, S B J; Koerte, I K; Korgaonkar, M S; Krystal, J H; Larson, C; Lebois, L A M; Levy, I; Li, G; Magnotta, V A; Manthey, A; May, G; McLaughlin, K A; Mueller, S C; Nawijn, L; Nelson, S M; Neria, Y; Nitschke, J B; Olff, M; Olson, E A; Peverill, M; Luan Phan, K; Rashid, F M; Ressler, K; Rosso, I M; Sambrook, K; Schmahl, C; Shenton, M E; Sierk, A; Simons, J S; Simons, R M; Sponheim, S R; Stein, M B; Stein, D J; Stevens, J S; Straube, T; Suarez-Jimenez, B; Tamburrino, M; Thomopoulos, S I; van der Wee, N J A; van der Werff, S J A; van Erp, T G M; van Rooij, S J H; van Zuiden, M; Varkevisser, T; Veltman, D J; Vermeiren, R.; Walter, H; Wang, L; Zhu, Y; Zhu, X; Thompson, P M; Morey, R A; and Liberzon, I\n\n\n \n\n\n\n 2021.\n \n\n\n\n
\n\n\n\n \n \n \"CorticalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Wang2021,\nannote = {Export Date: 29 December 2022},\nauthor = {Wang, X and Xie, H and Chen, T and Cotton, A S and Salminen, L E and Logue, M W and Clarke-Rubright, E K and Wall, J and Dennis, E L and O'Leary, B M and Abdallah, C G and Andrew, E and Baugh, L A and Bomyea, J and Bruce, S E and Bryant, R and Choi, K and Daniels, J K and Davenport, N D and Davidson, R J and DeBellis, M and DeRoon-Cassini, T and Disner, S G and Fani, N and Fercho, K A and Fitzgerald, J and Forster, G L and Frijling, J L and Geuze, E and Gomaa, H and Gordon, E M and Grupe, D and Harpaz-Rotem, I and Haswell, C C and Herzog, J I and Hofmann, D and Hollifield, M and Hosseini, B and Hudson, A R and Ipser, J and Jahanshad, N and Jovanovic, T and Kaufman, M L and King, A P and Koch, S B J and Koerte, I K and Korgaonkar, M S and Krystal, J H and Larson, C and Lebois, L A M and Levy, I and Li, G and Magnotta, V A and Manthey, A and May, G and McLaughlin, K A and Mueller, S C and Nawijn, L and Nelson, S M and Neria, Y and Nitschke, J B and Olff, M and Olson, E A and Peverill, M and {Luan Phan}, K and Rashid, F M and Ressler, K and Rosso, I M and Sambrook, K and Schmahl, C and Shenton, M E and Sierk, A and Simons, J S and Simons, R M and Sponheim, S R and Stein, M B and Stein, D J and Stevens, J S and Straube, T and Suarez-Jimenez, B and Tamburrino, M and Thomopoulos, S I and van der Wee, N J A and van der Werff, S J A and van Erp, T G M and van Rooij, S J H and van Zuiden, M and Varkevisser, T and Veltman, D J and Vermeiren, R.R.J.M. and Walter, H and Wang, L and Zhu, Y and Zhu, X and Thompson, P M and Morey, R A and Liberzon, I},\ndoi = {10.1038/s41380-020-00967-1},\nfile = {:Users/jacquelinebracher/Zotero/storage/JGDNPXKD/Wang et al. - 2021 - Cortical volume abnormalities in posttraumatic str.pdf:pdf},\nnumber = {8},\npages = {4331--4343},\ntitle = {{Cortical volume abnormalities in posttraumatic stress disorder: an ENIGMA-psychiatric genomics consortium PTSD workgroup mega-analysis}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85097223053{\\&}doi=10.1038{\\%}2Fs41380-020-00967-1{\\&}partnerID=40{\\&}md5=598cbb4c91411d83bab55bd1f7ca2713},\nvolume = {26},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Proteomics and metabolomics of \\HIV\\‐associated neurocognitive disorders: \\A\\ systematic review.\n \n \n \n \n\n\n \n Williams, M. E; Naudé, P. J W; and Van Der Westhuizen, F. H\n\n\n \n\n\n\n Journal of Neurochemistry, 157(3): 429–449. may 2021.\n \n\n\n\n
\n\n\n\n \n \n \"ProteomicsPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{williams_proteomics_2021,\nabstract = {Abstract\n\n\nHIV‐associated neurocognitive disorders (HAND) are common features of the effect of human immunodeficiency virus (HIV)‐1 within the central nervous system (CNS). The underlying neuropathophysiology of HAND is incompletely known. Furthermore, there are no markers to effectively predict or stratify the risk of HAND. Recent advancements in the fields of proteomics and metabolomics have shown promise in addressing these concerns, however, it is not clear if these approaches may provide new insight into pathways and markers related to HAND. We therefore conducted a systematic review of studies using proteomic and/or metabolomic approaches in the aim of identifying pathways or markers associated with neurocognitive impairment in people living with HIV (PLWH). Thirteen studies were eligible, including 11 proteomic and 2 metabolomic investigations of HIV‐positive clinical samples (cerebrospinal fluid (CSF), brain tissue, and serum). Across varying profiling techniques and sample types, the majority of studies found an association of markers with neurocognitive function in PLWH. These included metabolic marker myo‐inositol and proteomic markers superoxide dismutase, gelsolin, afamin, sphingomyelin, and ceramide. Certain markers were found to be dysregulated across various sample types. Afamin and gelsolin overlapped in studies of blood and CSF and sphingomyelin and ceramide overlapped in studies of CSF and brain tissue. The association of these markers with neurocognitive functioning may indicate the activity of certain pathways, potentially those related to the underlying neuropathophysiology of HAND.\n\n\n\n\n\n\nimage},\nauthor = {Williams, Monray E and Naud{\\'{e}}, Petrus J W and {Van Der Westhuizen}, Francois H},\ndoi = {10.1111/jnc.15295},\nissn = {0022-3042, 1471-4159},\njournal = {Journal of Neurochemistry},\nmonth = {may},\nnumber = {3},\npages = {429--449},\nshorttitle = {Proteomics and metabolomics of {\\{}HIV{\\}}‐associated ne},\ntitle = {{Proteomics and metabolomics of {\\{}HIV{\\}}‐associated neurocognitive disorders: {\\{}A{\\}} systematic review}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1111/jnc.15295},\nvolume = {157},\nyear = {2021}\n}\n
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\n Abstract HIV‐associated neurocognitive disorders (HAND) are common features of the effect of human immunodeficiency virus (HIV)‐1 within the central nervous system (CNS). The underlying neuropathophysiology of HAND is incompletely known. Furthermore, there are no markers to effectively predict or stratify the risk of HAND. Recent advancements in the fields of proteomics and metabolomics have shown promise in addressing these concerns, however, it is not clear if these approaches may provide new insight into pathways and markers related to HAND. We therefore conducted a systematic review of studies using proteomic and/or metabolomic approaches in the aim of identifying pathways or markers associated with neurocognitive impairment in people living with HIV (PLWH). Thirteen studies were eligible, including 11 proteomic and 2 metabolomic investigations of HIV‐positive clinical samples (cerebrospinal fluid (CSF), brain tissue, and serum). Across varying profiling techniques and sample types, the majority of studies found an association of markers with neurocognitive function in PLWH. These included metabolic marker myo‐inositol and proteomic markers superoxide dismutase, gelsolin, afamin, sphingomyelin, and ceramide. Certain markers were found to be dysregulated across various sample types. Afamin and gelsolin overlapped in studies of blood and CSF and sphingomyelin and ceramide overlapped in studies of CSF and brain tissue. The association of these markers with neurocognitive functioning may indicate the activity of certain pathways, potentially those related to the underlying neuropathophysiology of HAND. image\n
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\n \n\n \n \n \n \n \n \n Maternal anxiety during pregnancy and newborn epigenome-wide \\DNA\\ methylation.\n \n \n \n \n\n\n \n Sammallahti, S.; Cortes Hidalgo, A. P; Tuominen, S.; Malmberg, A.; Mulder, R. H; Brunst, K. J; Alemany, S.; McBride, N. S; Yousefi, P.; Heiss, J. A; McRae, N.; Page, C. M; Jin, J.; Pesce, G.; Caramaschi, D.; Rifas-Shiman, S. L; Koen, N.; Adams, C. D; Magnus, M. C; Baïz, N.; Ratanatharathorn, A.; Czamara, D.; Håberg, S. E; Colicino, E.; Baccarelli, A. A; Cardenas, A.; DeMeo, D. L; Lawlor, D. A; Relton, C. L; Felix, J. F; Van IJzendoorn, M. H; Bakermans-Kranenburg, M. J; Kajantie, E.; Räikkönen, K.; Sunyer, J.; Sharp, G. C; Houtepen, L. C; Nohr, E. A; Sørensen, T. I A; Téllez-Rojo, M. M; Wright, R. O; Annesi-Maesano, I.; Wright, J.; Hivert, M.; Wright, R. J; Zar, H. J; Stein, D. J; London, S. J; Cecil, C. A M; Tiemeier, H.; and Lahti, J.\n\n\n \n\n\n\n Molecular Psychiatry, 26(6): 1832–1845. jun 2021.\n \n\n\n\n
\n\n\n\n \n \n \"MaternalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{sammallahti_maternal_2021,\nauthor = {Sammallahti, Sara and {Cortes Hidalgo}, Andrea P and Tuominen, Samuli and Malmberg, Anni and Mulder, Rosa H and Brunst, Kelly J and Alemany, Silvia and McBride, Nancy S and Yousefi, Paul and Heiss, Jonathan A and McRae, Nia and Page, Christian M and Jin, Jianping and Pesce, Giancarlo and Caramaschi, Doretta and Rifas-Shiman, Sheryl L and Koen, Nastassja and Adams, Charleen D and Magnus, Maria C and Ba{\\"{i}}z, Nour and Ratanatharathorn, Andrew and Czamara, Darina and H{\\aa}berg, Siri E and Colicino, Elena and Baccarelli, Andrea A and Cardenas, Andres and DeMeo, Dawn L and Lawlor, Deborah A and Relton, Caroline L and Felix, Janine F and {Van IJzendoorn}, Marinus H and Bakermans-Kranenburg, Marian J and Kajantie, Eero and R{\\"{a}}ikk{\\"{o}}nen, Katri and Sunyer, Jordi and Sharp, Gemma C and Houtepen, Lotte C and Nohr, Ellen A and S{\\o}rensen, Thorkild I A and T{\\'{e}}llez-Rojo, Martha M and Wright, Robert O and Annesi-Maesano, Isabella and Wright, John and Hivert, Marie-France and Wright, Rosalind J and Zar, Heather J and Stein, Dan J and London, Stephanie J and Cecil, Charlotte A M and Tiemeier, Henning and Lahti, Jari},\ndoi = {10.1038/s41380-020-00976-0},\nfile = {:Users/jacquelinebracher/Zotero/storage/D5IJGAI7/Sammallahti et al. - 2021 - Maternal anxiety during pregnancy and newborn epig.pdf:pdf},\nissn = {1359-4184, 1476-5578},\njournal = {Molecular Psychiatry},\nmonth = {jun},\nnumber = {6},\npages = {1832--1845},\ntitle = {{Maternal anxiety during pregnancy and newborn epigenome-wide {\\{}DNA{\\}} methylation}},\nurl = {https://www.nature.com/articles/s41380-020-00976-0},\nvolume = {26},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Implications of the \\COVID\\-19 pandemic for people with bipolar disorders: \\A\\ scoping review.\n \n \n \n \n\n\n \n Fornaro, M.; De Prisco, M.; Billeci, M.; Ermini, E.; Young, A. H; Lafer, B.; Soares, J. C; Vieta, E.; Quevedo, J.; De Bartolomeis, A.; Sim, K.; Yatham, L. N; Bauer, M.; Stein, D. J; Solmi, M.; Berk, M.; and Carvalho, A. F\n\n\n \n\n\n\n Journal of Affective Disorders, 295: 740–751. dec 2021.\n \n\n\n\n
\n\n\n\n \n \n \"ImplicationsPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{fornaro_implications_2021,\nauthor = {Fornaro, Michele and {De Prisco}, Michele and Billeci, Martina and Ermini, Eleonora and Young, Allan H and Lafer, Beny and Soares, Jair C and Vieta, Eduard and Quevedo, Joao and {De Bartolomeis}, Andrea and Sim, Kang and Yatham, Lakshmi N and Bauer, Michael and Stein, Dan J and Solmi, Marco and Berk, Michael and Carvalho, Andre F},\ndoi = {10.1016/j.jad.2021.08.091},\nfile = {:Users/jacquelinebracher/Zotero/storage/PY93QJYS/Fornaro et al. - 2021 - Implications of the COVID-19 pandemic for people w.pdf:pdf},\nissn = {01650327},\njournal = {Journal of Affective Disorders},\nmonth = {dec},\npages = {740--751},\nshorttitle = {Implications of the {\\{}COVID{\\}}-19 pandemic for people},\ntitle = {{Implications of the {\\{}COVID{\\}}-19 pandemic for people with bipolar disorders: {\\{}A{\\}} scoping review}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S016503272100896X},\nvolume = {295},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Brain structural abnormalities in obesity: relation to age, genetic risk, and common psychiatric disorders: \\Evidence\\ through univariate and multivariate mega-analysis including 6420 participants from the \\ENIGMA\\ \\MDD\\ working group.\n \n \n \n \n\n\n \n Opel, N.; Thalamuthu, A.; Milaneschi, Y.; Grotegerd, D.; Flint, C.; Leenings, R.; Goltermann, J.; Richter, M.; Hahn, T.; Woditsch, G.; Berger, K.; Hermesdorf, M.; McIntosh, A.; Whalley, H. C; Harris, M. A; MacMaster, F. P; Walter, H.; Veer, I. M; Frodl, T.; Carballedo, A.; Krug, A.; Nenadic, I.; Kircher, T.; Aleman, A.; Groenewold, N. A; Stein, D. J; Soares, J. C; Zunta-Soares, G. B; Mwangi, B.; Wu, M.; Walter, M.; Li, M.; Harrison, B. J; Davey, C. G; Cullen, K. R; Klimes-Dougan, B.; Mueller, B. A; Sämann, P. G; Penninx, B.; Nawijn, L.; Veltman, D. J; Aftanas, L.; Brak, I. V; Filimonova, E. A; Osipov, E. A; Reneman, L.; Schrantee, A.; Grabe, H. J; Van Der Auwera, S.; Wittfeld, K.; Hosten, N.; Völzke, H.; Sim, K.; Gotlib, I. H; Sacchet, M. D; Lagopoulos, J.; Hatton, S. N; Hickie, I.; Pozzi, E.; Thompson, P. M; Jahanshad, N.; Schmaal, L.; Baune, B. T; and Dannlowski, U.\n\n\n \n\n\n\n Molecular Psychiatry, 26(9): 4839–4852. sep 2021.\n \n\n\n\n
\n\n\n\n \n \n \"BrainPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{opel_brain_2021,\nabstract = {Abstract\n\nEmerging evidence suggests that obesity impacts brain physiology at multiple levels. Here we aimed to clarify the relationship between obesity and brain structure using structural MRI (\nn\n= 6420) and genetic data (\nn\n= 3907) from the ENIGMA Major Depressive Disorder (MDD) working group. Obesity (BMI {\\textgreater}30) was significantly associated with cortical and subcortical abnormalities in both mass-univariate and multivariate pattern recognition analyses independent of MDD diagnosis. The most pronounced effects were found for associations between obesity and lower temporo-frontal cortical thickness (maximum Cohen´s\nd\n(left fusiform gyrus) = −0.33). The observed regional distribution and effect size of cortical thickness reductions in obesity revealed considerable similarities with corresponding patterns of lower cortical thickness in previously published studies of neuropsychiatric disorders. A higher polygenic risk score for obesity significantly correlated with lower occipital surface area. In addition, a significant age-by-obesity interaction on cortical thickness emerged driven by lower thickness in older participants. Our findings suggest a neurobiological interaction between obesity and brain structure under physiological and pathological brain conditions.},\nauthor = {Opel, Nils and Thalamuthu, Anbupalam and Milaneschi, Yuri and Grotegerd, Dominik and Flint, Claas and Leenings, Ramona and Goltermann, Janik and Richter, Maike and Hahn, Tim and Woditsch, Georg and Berger, Klaus and Hermesdorf, Marco and McIntosh, Andrew and Whalley, Heather C and Harris, Mathew A and MacMaster, Frank P and Walter, Henrik and Veer, Ilya M and Frodl, Thomas and Carballedo, Angela and Krug, Axel and Nenadic, Igor and Kircher, Tilo and Aleman, Andre and Groenewold, Nynke A and Stein, Dan J and Soares, Jair C and Zunta-Soares, Giovana B and Mwangi, Benson and Wu, Mon-Ju and Walter, Martin and Li, Meng and Harrison, Ben J and Davey, Christopher G and Cullen, Kathryn R and Klimes-Dougan, Bonnie and Mueller, Bryon A and S{\\"{a}}mann, Philipp G and Penninx, Brenda and Nawijn, Laura and Veltman, Dick J and Aftanas, Lyubomir and Brak, Ivan V and Filimonova, Elena A and Osipov, Evgeniy A and Reneman, Liesbeth and Schrantee, Anouk and Grabe, Hans J and {Van Der Auwera}, Sandra and Wittfeld, Katharina and Hosten, Norbert and V{\\"{o}}lzke, Henry and Sim, Kang and Gotlib, Ian H and Sacchet, Matthew D and Lagopoulos, Jim and Hatton, Sean N and Hickie, Ian and Pozzi, Elena and Thompson, Paul M and Jahanshad, Neda and Schmaal, Lianne and Baune, Bernhard T and Dannlowski, Udo},\ndoi = {10.1038/s41380-020-0774-9},\nfile = {:Users/jacquelinebracher/Zotero/storage/JKQHTEYB/Opel et al. - 2021 - Brain structural abnormalities in obesity relatio.pdf:pdf},\nissn = {1359-4184, 1476-5578},\njournal = {Molecular Psychiatry},\nmonth = {sep},\nnumber = {9},\npages = {4839--4852},\nshorttitle = {Brain structural abnormalities in obesity},\ntitle = {{Brain structural abnormalities in obesity: relation to age, genetic risk, and common psychiatric disorders: {\\{}Evidence{\\}} through univariate and multivariate mega-analysis including 6420 participants from the {\\{}ENIGMA{\\}} {\\{}MDD{\\}} working group}},\nurl = {https://www.nature.com/articles/s41380-020-0774-9},\nvolume = {26},\nyear = {2021}\n}\n
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\n Abstract Emerging evidence suggests that obesity impacts brain physiology at multiple levels. Here we aimed to clarify the relationship between obesity and brain structure using structural MRI ( n = 6420) and genetic data ( n = 3907) from the ENIGMA Major Depressive Disorder (MDD) working group. Obesity (BMI \\textgreater30) was significantly associated with cortical and subcortical abnormalities in both mass-univariate and multivariate pattern recognition analyses independent of MDD diagnosis. The most pronounced effects were found for associations between obesity and lower temporo-frontal cortical thickness (maximum Cohen´s d (left fusiform gyrus) = −0.33). The observed regional distribution and effect size of cortical thickness reductions in obesity revealed considerable similarities with corresponding patterns of lower cortical thickness in previously published studies of neuropsychiatric disorders. A higher polygenic risk score for obesity significantly correlated with lower occipital surface area. In addition, a significant age-by-obesity interaction on cortical thickness emerged driven by lower thickness in older participants. Our findings suggest a neurobiological interaction between obesity and brain structure under physiological and pathological brain conditions.\n
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\n \n\n \n \n \n \n \n The treatment gap for mental disorders in adults enrolled in HIV treatment programmes in South Africa: A cohort study using linked electronic health records.\n \n \n \n\n\n \n Ruffieux, Y.; Efthimiou, O.; Van Den Heuvel, L.; Joska, J.; Cornell, M.; Seedat, S.; Mouton, J.; Prozesky, H.; Lund, C.; Maxwell, N.; Maartens, G.; and Haas, A.\n\n\n \n\n\n\n Epidemiology and Psychiatric Sciences. 2021.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n  \n \n 11 downloads\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Ruffieux2021,\nabstract = {Aims Mental disorders are common in people living with HIV (PLWH) but often remain untreated. This study aimed to explore the treatment gap for mental disorders in adults followed-up in antiretroviral therapy (ART) programmes in South Africa and disparities between ART programmes regarding the provision of mental health services. Methods We conducted a cohort study using ART programme data and linked pharmacy and hospitalisation data to examine the 12-month prevalence of treatment for mental disorders and factors associated with the rate of treatment for mental disorders among adults, aged 15-49 years, followed-up from 1 January 2012 to 31 December 2017 at one private care, one public tertiary care and two pubic primary care ART programmes in South Africa. We calculated the treatment gap for mental disorders as the discrepancy between the 12-month prevalence of mental disorders in PLWH (aged 15-49 years) in South Africa (estimated based on data from the Global Burden of Disease study) and the 12-month prevalence of treatment for mental disorders in ART programmes. We calculated adjusted rate ratios (aRRs) for factors associated with the treatment rate of mental disorders using Poisson regression. Results In total, 182 285 ART patients were followed-up over 405 153 person-years. In 2017, the estimated treatment gap for mental disorders was 40.5{\\%} (95{\\%} confidence interval [CI] 19.5-52.9) for patients followed-up in private care, 96.5{\\%} (95{\\%} CI 95.0-97.5) for patients followed-up in public primary care and 65.0{\\%} (95{\\%} CI 36.5-85.1) for patients followed-up in public tertiary care ART programmes. Rates of treatment with antidepressants, anxiolytics and antipsychotics were 17 (aRR 0.06, 95{\\%} CI 0.06-0.07), 50 (aRR 0.02, 95{\\%} CI 0.01-0.03) and 2.6 (aRR 0.39, 95{\\%} CI 0.35-0.43) times lower in public primary care programmes than in the private sector programmes. Conclusions There is a large treatment gap for mental disorders in PLWH in South Africa and substantial disparities in access to mental health services between patients receiving ART in the public vs the private sector. In the public sector and especially in public primary care, PLWH with common mental disorders remain mostly untreated.},\nauthor = {Ruffieux, Y. and Efthimiou, O. and {Van Den Heuvel}, L.L. and Joska, J.A. and Cornell, M. and Seedat, S. and Mouton, J.P. and Prozesky, H. and Lund, C. and Maxwell, N. and Maartens, G. and Haas, A.D.},\ndoi = {10.1017/S2045796021000196},\nfile = {:Users/jacquelinebracher/Zotero/storage/BQPUJTMH/Ruffieux et al. - 2021 - The treatment gap for mental disorders in adults e.pdf:pdf},\njournal = {Epidemiology and Psychiatric Sciences},\ntitle = {{The treatment gap for mental disorders in adults enrolled in HIV treatment programmes in South Africa: A cohort study using linked electronic health records}},\nyear = {2021}\n}\n
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\n Aims Mental disorders are common in people living with HIV (PLWH) but often remain untreated. This study aimed to explore the treatment gap for mental disorders in adults followed-up in antiretroviral therapy (ART) programmes in South Africa and disparities between ART programmes regarding the provision of mental health services. Methods We conducted a cohort study using ART programme data and linked pharmacy and hospitalisation data to examine the 12-month prevalence of treatment for mental disorders and factors associated with the rate of treatment for mental disorders among adults, aged 15-49 years, followed-up from 1 January 2012 to 31 December 2017 at one private care, one public tertiary care and two pubic primary care ART programmes in South Africa. We calculated the treatment gap for mental disorders as the discrepancy between the 12-month prevalence of mental disorders in PLWH (aged 15-49 years) in South Africa (estimated based on data from the Global Burden of Disease study) and the 12-month prevalence of treatment for mental disorders in ART programmes. We calculated adjusted rate ratios (aRRs) for factors associated with the treatment rate of mental disorders using Poisson regression. Results In total, 182 285 ART patients were followed-up over 405 153 person-years. In 2017, the estimated treatment gap for mental disorders was 40.5% (95% confidence interval [CI] 19.5-52.9) for patients followed-up in private care, 96.5% (95% CI 95.0-97.5) for patients followed-up in public primary care and 65.0% (95% CI 36.5-85.1) for patients followed-up in public tertiary care ART programmes. Rates of treatment with antidepressants, anxiolytics and antipsychotics were 17 (aRR 0.06, 95% CI 0.06-0.07), 50 (aRR 0.02, 95% CI 0.01-0.03) and 2.6 (aRR 0.39, 95% CI 0.35-0.43) times lower in public primary care programmes than in the private sector programmes. Conclusions There is a large treatment gap for mental disorders in PLWH in South Africa and substantial disparities in access to mental health services between patients receiving ART in the public vs the private sector. In the public sector and especially in public primary care, PLWH with common mental disorders remain mostly untreated.\n
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\n \n\n \n \n \n \n \n \n \\ENIGMA\\‐\\Sleep\\: \\Challenges\\, opportunities, and the road map.\n \n \n \n \n\n\n \n Tahmasian, M.; Aleman, A.; Andreassen, O. A; Arab, Z.; Baillet, M.; Benedetti, F.; Bresser, T.; Bright, J.; Chee, M. W L; Chylinski, D.; Cheng, W.; Deantoni, M.; Dresler, M.; Eickhoff, S. B; Eickhoff, C. R; Elvsåshagen, T.; Feng, J.; Foster‐Dingley, J. C; Ganjgahi, H.; Grabe, H. J; Groenewold, N. A; Ho, T. C; Bong Hong, S.; Houenou, J.; Irungu, B.; Jahanshad, N.; Khazaie, H.; Kim, H.; Koshmanova, E.; Kocevska, D.; Kochunov, P.; Lakbila‐Kamal, O.; Leerssen, J.; Li, M.; Luik, A. I; Muto, V.; Narbutas, J.; Nilsonne, G.; O'Callaghan, V. S; Olsen, A.; Osorio, R. S; Poletti, S.; Poudel, G.; Reesen, J. E; Reneman, L.; Reyt, M.; Riemann, D.; Rosenzweig, I.; Rostampour, M.; Saberi, A.; Schiel, J.; Schmidt, C.; Schrantee, A.; Sciberras, E.; Silk, T. J; Sim, K.; Smevik, H.; Soares, J. C; Spiegelhalder, K.; Stein, D. J; Talwar, P.; Tamm, S.; Teresi, G. L; Valk, S. L; Van Someren, E.; Vandewalle, G.; Van Egroo, M.; Völzke, H.; Walter, M.; Wassing, R.; Weber, F. D; Weihs, A.; Westlye, L. T.; Wright, M. J; Wu, M.; Zak, N.; and Zarei, M.\n\n\n \n\n\n\n Journal of Sleep Research, 30(6): e13347. dec 2021.\n \n\n\n\n
\n\n\n\n \n \n \"\\ENIGMA\\‐\\Sleep\\:Paper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{tahmasian_enigmasleep_2021,\nabstract = {Summary\nNeuroimaging and genetics studies have advanced our understanding of the neurobiology of sleep and its disorders. However, individual studies usually have limitations to identifying consistent and reproducible effects, including modest sample sizes, heterogeneous clinical characteristics and varied methodologies. These issues call for a large‐scale multi‐centre effort in sleep research, in order to increase the number of samples, and harmonize the methods of data collection, preprocessing and analysis using pre‐registered well‐established protocols. The Enhancing NeuroImaging Genetics through Meta‐Analysis (ENIGMA) consortium provides a powerful collaborative framework for combining datasets across individual sites. Recently, we have launched the ENIGMA‐Sleep working group with the collaboration of several institutes from 15 countries to perform large‐scale worldwide neuroimaging and genetics studies for better understanding the neurobiology of impaired sleep quality in population‐based healthy individuals, the neural consequences of sleep deprivation, pathophysiology of sleep disorders, as well as neural correlates of sleep disturbances across various neuropsychiatric disorders. In this introductory review, we describe the details of our currently available datasets and our ongoing projects in the ENIGMA‐Sleep group, and discuss both the potential challenges and opportunities of a collaborative initiative in sleep medicine.},\nauthor = {Tahmasian, Masoud and Aleman, Andr{\\'{e}} and Andreassen, Ole A and Arab, Zahra and Baillet, Marion and Benedetti, Francesco and Bresser, Tom and Bright, Joanna and Chee, Michael W L and Chylinski, Daphne and Cheng, Wei and Deantoni, Michele and Dresler, Martin and Eickhoff, Simon B and Eickhoff, Claudia R and Elvs{\\aa}shagen, Torbj{\\o}rn and Feng, Jianfeng and Foster‐Dingley, Jessica C and Ganjgahi, Habib and Grabe, Hans J and Groenewold, Nynke A and Ho, Tiffany C and {Bong Hong}, Seung and Houenou, Josselin and Irungu, Benson and Jahanshad, Neda and Khazaie, Habibolah and Kim, Hosung and Koshmanova, Ekaterina and Kocevska, Desi and Kochunov, Peter and Lakbila‐Kamal, Oti and Leerssen, Jeanne and Li, Meng and Luik, Annemarie I and Muto, Vincenzo and Narbutas, Justinas and Nilsonne, Gustav and O'Callaghan, Victoria S and Olsen, Alexander and Osorio, Ricardo S and Poletti, Sara and Poudel, Govinda and Reesen, Joyce E and Reneman, Liesbeth and Reyt, Mathilde and Riemann, Dieter and Rosenzweig, Ivana and Rostampour, Masoumeh and Saberi, Amin and Schiel, Julian and Schmidt, Christina and Schrantee, Anouk and Sciberras, Emma and Silk, Tim J and Sim, Kang and Smevik, Hanne and Soares, Jair C and Spiegelhalder, Kai and Stein, Dan J and Talwar, Puneet and Tamm, Sandra and Teresi, Giana L and Valk, Sofie L and {Van Someren}, Eus and Vandewalle, Gilles and {Van Egroo}, Maxime and V{\\"{o}}lzke, Henry and Walter, Martin and Wassing, Rick and Weber, Frederik D and Weihs, Antoine and Westlye, Lars Tjelta and Wright, Margaret J and Wu, Mon‐Ju and Zak, Nathalia and Zarei, Mojtaba},\ndoi = {10.1111/jsr.13347},\nfile = {:Users/jacquelinebracher/Zotero/storage/UBFUHT2B/Tahmasian et al. - 2021 - ENIGMA‐Sleep Challenges, opportunities, and the r.pdf:pdf},\nissn = {0962-1105, 1365-2869},\njournal = {Journal of Sleep Research},\nmonth = {dec},\nnumber = {6},\npages = {e13347},\nshorttitle = {{\\{}ENIGMA{\\}}‐{\\{}Sleep{\\}}},\ntitle = {{{\\{}ENIGMA{\\}}‐{\\{}Sleep{\\}}: {\\{}Challenges{\\}}, opportunities, and the road map}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1111/jsr.13347},\nvolume = {30},\nyear = {2021}\n}\n
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\n Summary Neuroimaging and genetics studies have advanced our understanding of the neurobiology of sleep and its disorders. However, individual studies usually have limitations to identifying consistent and reproducible effects, including modest sample sizes, heterogeneous clinical characteristics and varied methodologies. These issues call for a large‐scale multi‐centre effort in sleep research, in order to increase the number of samples, and harmonize the methods of data collection, preprocessing and analysis using pre‐registered well‐established protocols. The Enhancing NeuroImaging Genetics through Meta‐Analysis (ENIGMA) consortium provides a powerful collaborative framework for combining datasets across individual sites. Recently, we have launched the ENIGMA‐Sleep working group with the collaboration of several institutes from 15 countries to perform large‐scale worldwide neuroimaging and genetics studies for better understanding the neurobiology of impaired sleep quality in population‐based healthy individuals, the neural consequences of sleep deprivation, pathophysiology of sleep disorders, as well as neural correlates of sleep disturbances across various neuropsychiatric disorders. In this introductory review, we describe the details of our currently available datasets and our ongoing projects in the ENIGMA‐Sleep group, and discuss both the potential challenges and opportunities of a collaborative initiative in sleep medicine.\n
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\n \n\n \n \n \n \n \n \n Association between body mass index and subcortical brain volumes in bipolar disorders–\\ENIGMA\\ study in 2735 individuals.\n \n \n \n \n\n\n \n McWhinney, S. R; Abé, C.; Alda, M.; Benedetti, F.; Bøen, E.; Del Mar Bonnin, C.; Borgers, T.; Brosch, K.; Canales-Rodríguez, E. J; Cannon, D. M; Dannlowski, U.; Díaz-Zuluaga, A. M; Elvsåshagen, T.; Eyler, L. T; Fullerton, J. M; Goikolea, J. M; Goltermann, J.; Grotegerd, D.; Haarman, B. C M; Hahn, T.; Howells, F. M; Ingvar, M.; Kircher, T. T J; Krug, A.; Kuplicki, R. T; Landén, M.; Lemke, H.; Liberg, B.; Lopez-Jaramillo, C.; Malt, U. F; Martyn, F. M; Mazza, E.; McDonald, C.; McPhilemy, G.; Meier, S.; Meinert, S.; Meller, T.; Melloni, E. M T; Mitchell, P. B; Nabulsi, L.; Nenadic, I.; Opel, N.; Ophoff, R. A; Overs, B. J; Pfarr, J.; Pineda-Zapata, J. A; Pomarol-Clotet, E.; Raduà, J.; Repple, J.; Richter, M.; Ringwald, K. G; Roberts, G.; Salvador, R.; Savitz, J.; Schmitt, S.; Schofield, P. R; Sim, K.; Stein, D. J; Stein, F.; Temmingh, H. S; Thiel, K.; Van Haren, N. E M; Gestel, H. V.; Vargas, C.; Vieta, E.; Vreeker, A.; Waltemate, L.; Yatham, L. N; Ching, C. R K; Andreassen, O.; Thompson, P. M; Hajek, T.; and for the ENIGMA Bipolar Disorders Working Group\n\n\n \n\n\n\n Molecular Psychiatry, 26(11): 6806–6819. nov 2021.\n \n\n\n\n
\n\n\n\n \n \n \"AssociationPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{mcwhinney_association_2021,\nabstract = {Abstract\n\nIndividuals with bipolar disorders (BD) frequently suffer from obesity, which is often associated with neurostructural alterations. Yet, the effects of obesity on brain structure in BD are under-researched. We obtained MRI-derived brain subcortical volumes and body mass index (BMI) from 1134 BD and 1601 control individuals from 17 independent research sites within the ENIGMA-BD Working Group. We jointly modeled the effects of BD and BMI on subcortical volumes using mixed-effects modeling and tested for mediation of group differences by obesity using nonparametric bootstrapping. All models controlled for age, sex, hemisphere, total intracranial volume, and data collection site. Relative to controls, individuals with BD had significantly higher BMI, larger lateral ventricular volume, and smaller volumes of amygdala, hippocampus, pallidum, caudate, and thalamus. BMI was positively associated with ventricular and amygdala and negatively with pallidal volumes. When analyzed jointly, both BD and BMI remained associated with volumes of lateral ventricles and amygdala. Adjusting for BMI decreased the BD vs control differences in ventricular volume. Specifically, 18.41{\\%} of the association between BD and ventricular volume was mediated by BMI (\nZ\n= 2.73,\np\n= 0.006). BMI was associated with similar regional brain volumes as BD, including lateral ventricles, amygdala, and pallidum. Higher BMI may in part account for larger ventricles, one of the most replicated findings in BD. Comorbidity with obesity could explain why neurostructural alterations are more pronounced in some individuals with BD. Future prospective brain imaging studies should investigate whether obesity could be a modifiable risk factor for neuroprogression.},\nauthor = {McWhinney, Sean R and Ab{\\'{e}}, Christoph and Alda, Martin and Benedetti, Francesco and B{\\o}en, Erlend and {Del Mar Bonnin}, Caterina and Borgers, Tiana and Brosch, Katharina and Canales-Rodr{\\'{i}}guez, Erick J and Cannon, Dara M and Dannlowski, Udo and D{\\'{i}}az-Zuluaga, Ana M and Elvs{\\aa}shagen, Torbj{\\o}rn and Eyler, Lisa T and Fullerton, Janice M and Goikolea, Jose M and Goltermann, Janik and Grotegerd, Dominik and Haarman, Bartholomeus C M and Hahn, Tim and Howells, Fleur M and Ingvar, Martin and Kircher, Tilo T J and Krug, Axel and Kuplicki, Rayus T and Land{\\'{e}}n, Mikael and Lemke, Hannah and Liberg, Benny and Lopez-Jaramillo, Carlos and Malt, Ulrik F and Martyn, Fiona M and Mazza, Elena and McDonald, Colm and McPhilemy, Genevieve and Meier, Sandra and Meinert, Susanne and Meller, Tina and Melloni, Elisa M T and Mitchell, Philip B and Nabulsi, Leila and Nenadic, Igor and Opel, Nils and Ophoff, Roel A and Overs, Bronwyn J and Pfarr, Julia-Katharina and Pineda-Zapata, Julian A and Pomarol-Clotet, Edith and Radu{\\`{a}}, Joaquim and Repple, Jonathan and Richter, Maike and Ringwald, Kai G and Roberts, Gloria and Salvador, Raymond and Savitz, Jonathan and Schmitt, Simon and Schofield, Peter R and Sim, Kang and Stein, Dan J and Stein, Frederike and Temmingh, Henk S and Thiel, Katharina and {Van Haren}, Neeltje E M and Gestel, Holly Van and Vargas, Cristian and Vieta, Eduard and Vreeker, Annabel and Waltemate, Lena and Yatham, Lakshmi N and Ching, Christopher R K and Andreassen, Ole and Thompson, Paul M and Hajek, Tomas and {for the ENIGMA Bipolar Disorders Working Group}},\ndoi = {10.1038/s41380-021-01098-x},\nfile = {:Users/jacquelinebracher/Zotero/storage/RB6S8WYI/McWhinney et al. - 2021 - Association between body mass index and subcortica.pdf:pdf},\nissn = {1359-4184, 1476-5578},\njournal = {Molecular Psychiatry},\nmonth = {nov},\nnumber = {11},\npages = {6806--6819},\ntitle = {{Association between body mass index and subcortical brain volumes in bipolar disorders–{\\{}ENIGMA{\\}} study in 2735 individuals}},\nurl = {https://www.nature.com/articles/s41380-021-01098-x},\nvolume = {26},\nyear = {2021}\n}\n
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\n Abstract Individuals with bipolar disorders (BD) frequently suffer from obesity, which is often associated with neurostructural alterations. Yet, the effects of obesity on brain structure in BD are under-researched. We obtained MRI-derived brain subcortical volumes and body mass index (BMI) from 1134 BD and 1601 control individuals from 17 independent research sites within the ENIGMA-BD Working Group. We jointly modeled the effects of BD and BMI on subcortical volumes using mixed-effects modeling and tested for mediation of group differences by obesity using nonparametric bootstrapping. All models controlled for age, sex, hemisphere, total intracranial volume, and data collection site. Relative to controls, individuals with BD had significantly higher BMI, larger lateral ventricular volume, and smaller volumes of amygdala, hippocampus, pallidum, caudate, and thalamus. BMI was positively associated with ventricular and amygdala and negatively with pallidal volumes. When analyzed jointly, both BD and BMI remained associated with volumes of lateral ventricles and amygdala. Adjusting for BMI decreased the BD vs control differences in ventricular volume. Specifically, 18.41% of the association between BD and ventricular volume was mediated by BMI ( Z = 2.73, p = 0.006). BMI was associated with similar regional brain volumes as BD, including lateral ventricles, amygdala, and pallidum. Higher BMI may in part account for larger ventricles, one of the most replicated findings in BD. Comorbidity with obesity could explain why neurostructural alterations are more pronounced in some individuals with BD. Future prospective brain imaging studies should investigate whether obesity could be a modifiable risk factor for neuroprogression.\n
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\n \n\n \n \n \n \n \n \n Mapping cortical and subcortical asymmetries in substance dependence: \\Findings\\ from the \\ENIGMA\\ \\Addiction\\ \\Working\\ \\Group\\.\n \n \n \n \n\n\n \n Cao, Z.; Ottino‐Gonzalez, J.; Cupertino, R. B; Schwab, N.; Hoke, C.; Catherine, O.; Cousijn, J.; Dagher, A.; Foxe, J. J; Goudriaan, A. E; Hester, R.; Hutchison, K.; Li, C. R; London, E. D; Lorenzetti, V.; Luijten, M.; Martin‐Santos, R.; Momenan, R.; Paulus, M. P; Schmaal, L.; Sinha, R.; Sjoerds, Z.; Solowij, N.; Stein, D. J; Stein, E. A; Uhlmann, A.; Van Holst, R. J; Veltman, D. J; Wiers, R. W; Yücel, M.; Zhang, S.; Jahanshad, N.; Thompson, P. M; Conrod, P.; Mackey, S.; and Garavan, H.\n\n\n \n\n\n\n Addiction Biology, 26(5): e13010. sep 2021.\n \n\n\n\n
\n\n\n\n \n \n \"MappingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{cao_mapping_2021,\nabstract = {Abstract\n\nBrain asymmetry reflects left‐right hemispheric differentiation, which is a quantitative brain phenotype that develops with age and can vary with psychiatric diagnoses. Previous studies have shown that substance dependence is associated with altered brain structure and function. However, it is unknown whether structural brain asymmetries are different in individuals with substance dependence compared with nondependent participants. Here, a mega‐analysis was performed using a collection of 22 structural brain MRI datasets from the ENIGMA Addiction Working Group. Structural asymmetries of cortical and subcortical regions were compared between individuals who were dependent on alcohol, nicotine, cocaine, methamphetamine, or cannabis (\nn\n= 1,796) and nondependent participants (\nn\n= 996). Substance‐general and substance‐specific effects on structural asymmetry were examined using separate models. We found that substance dependence was significantly associated with differences in volume asymmetry of the nucleus accumbens (NAcc; less rightward; Cohen's\nd\n= 0.15). This effect was driven by differences from controls in individuals with alcohol dependence (less rightward; Cohen's\nd\n= 0.10) and nicotine dependence (less rightward; Cohen's\nd\n= 0.11). These findings suggest that disrupted structural asymmetry in the NAcc may be a characteristic of substance dependence.},\nauthor = {Cao, Zhipeng and Ottino‐Gonzalez, Jonatan and Cupertino, Renata B and Schwab, Nathan and Hoke, Colin and Catherine, Orr and Cousijn, Janna and Dagher, Alain and Foxe, John J and Goudriaan, Anna E and Hester, Robert and Hutchison, Kent and Li, Chiang‐Shan R and London, Edythe D and Lorenzetti, Valentina and Luijten, Maartje and Martin‐Santos, Rocio and Momenan, Reza and Paulus, Martin P and Schmaal, Lianne and Sinha, Rajita and Sjoerds, Zsuzsika and Solowij, Nadia and Stein, Dan J and Stein, Elliot A and Uhlmann, Anne and {Van Holst}, Ruth J and Veltman, Dick J and Wiers, Reinout W and Y{\\"{u}}cel, Murat and Zhang, Sheng and Jahanshad, Neda and Thompson, Paul M and Conrod, Patricia and Mackey, Scott and Garavan, Hugh},\ndoi = {10.1111/adb.13010},\nfile = {:Users/jacquelinebracher/Zotero/storage/QXAFJL8L/Cao et al. - 2021 - Mapping cortical and subcortical asymmetries in su.pdf:pdf},\nissn = {1355-6215, 1369-1600},\njournal = {Addiction Biology},\nmonth = {sep},\nnumber = {5},\npages = {e13010},\nshorttitle = {Mapping cortical and subcortical asymmetries in su},\ntitle = {{Mapping cortical and subcortical asymmetries in substance dependence: {\\{}Findings{\\}} from the {\\{}ENIGMA{\\}} {\\{}Addiction{\\}} {\\{}Working{\\}} {\\{}Group{\\}}}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1111/adb.13010},\nvolume = {26},\nyear = {2021}\n}\n
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\n Abstract Brain asymmetry reflects left‐right hemispheric differentiation, which is a quantitative brain phenotype that develops with age and can vary with psychiatric diagnoses. Previous studies have shown that substance dependence is associated with altered brain structure and function. However, it is unknown whether structural brain asymmetries are different in individuals with substance dependence compared with nondependent participants. Here, a mega‐analysis was performed using a collection of 22 structural brain MRI datasets from the ENIGMA Addiction Working Group. Structural asymmetries of cortical and subcortical regions were compared between individuals who were dependent on alcohol, nicotine, cocaine, methamphetamine, or cannabis ( n = 1,796) and nondependent participants ( n = 996). Substance‐general and substance‐specific effects on structural asymmetry were examined using separate models. We found that substance dependence was significantly associated with differences in volume asymmetry of the nucleus accumbens (NAcc; less rightward; Cohen's d = 0.15). This effect was driven by differences from controls in individuals with alcohol dependence (less rightward; Cohen's d = 0.10) and nicotine dependence (less rightward; Cohen's d = 0.11). These findings suggest that disrupted structural asymmetry in the NAcc may be a characteristic of substance dependence.\n
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\n \n\n \n \n \n \n \n \n Mental health interventions for persons living with \\HIV\\ in low‐ and middle‐income countries: a systematic review.\n \n \n \n \n\n\n \n Nakimuli‐Mpungu, E.; Musisi, S.; Smith, C. M; Von Isenburg, M.; Akimana, B.; Shakarishvili, A.; Nachega, J. B; Mills, E. J; Chibanda, D.; Ribeiro, M.; V Williams, A.; and Joska, J. A\n\n\n \n\n\n\n Journal of the International AIDS Society, 24(S2): e25722. jun 2021.\n \n\n\n\n
\n\n\n\n \n \n \"MentalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{nakimulimpungu_mental_2021,\nabstract = {Abstract\n\nIntroduction\nAddressing the intersection between mental health and HIV is critical for the wellbeing of persons living with HIV (PLWH). This systematic review synthesized the literature on mental health interventions for PLWH in low‐ and middle‐income countries (LMICs) to determine intervention components and explore their relationship with intervention effectiveness.\n\n\nMethods\nWe included only controlled clinical trials of interventions aiming to improve the mental health of PLWH. We conducted a search in the following databases: PubMed, CINAHL, PsycINFO and EMBASE for eligible studies describing the evaluation of interventions for mental health problems among PLWH in LMICs published through August 2020. Two reviewers independently screened references in two successive stages of title/abstract screening and then full‐text screening for references meeting title/abstract criteria.\n\n\nResults\n\nWe identified a total of 30 eligible articles representing 6477 PLWH who were assigned to either the intervention arm (n = 3182) or control arm (n = 3346). The mental health interventions evaluated were psychological (n = 17, 56.67{\\%}), pharmacological (n = 6, 20.00{\\%}), combined psychological and pharmacological (n = 1, 3.33{\\%}) and complementary/alternative treatments (n = 6, 20.00{\\%}). The mental health problems targeted were depression (n = 22, 73.33 {\\%}), multiple psychological symptoms (n = 1, 3.33{\\%}), alcohol and substance use problems (n = 4, 13.33{\\%}), post‐traumatic stress disorder (n = 1, 3.33{\\%}) and HIV‐related neuro‐cognitive impairment (n = 2, 6.67{\\%}). Studies of interventions with significant effects had significantly a higher number of active ingredients than those without significant effects [3.41 (2.24) vs. 1.84 (1.46) Mean (SD)] [Mean difference = −1.56, 95{\\%} CI = −3.03 to −0.09,\np\n= 0.037].\n\n\n\nConclusions\nThere continue to be advances in mental health interventions for PLWH with mental illness in LMICs. However, more research is needed to elucidate how intervention components lead to intervention effectiveness. We recommend scale up of culturally appropriate interventions that have been successfully evaluated in low‐ and middle‐income countries.},\nauthor = {Nakimuli‐Mpungu, Etheldreda and Musisi, Seggane and Smith, Colin M and {Von Isenburg}, Megan and Akimana, Benedict and Shakarishvili, Ani and Nachega, Jean B and Mills, Edward J and Chibanda, Dixon and Ribeiro, Marcelo and {V Williams}, Anna and Joska, John A},\ndoi = {10.1002/jia2.25722},\nfile = {:Users/jacquelinebracher/Zotero/storage/QIZ2RZSQ/Nakimuli‐Mpungu et al. - 2021 - Mental health interventions for persons living wit.pdf:pdf},\nissn = {1758-2652, 1758-2652},\njournal = {Journal of the International AIDS Society},\nmonth = {jun},\nnumber = {S2},\npages = {e25722},\nshorttitle = {Mental health interventions for persons living wit},\ntitle = {{Mental health interventions for persons living with {\\{}HIV{\\}} in low‐ and middle‐income countries: a systematic review}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1002/jia2.25722},\nvolume = {24},\nyear = {2021}\n}\n
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\n Abstract Introduction Addressing the intersection between mental health and HIV is critical for the wellbeing of persons living with HIV (PLWH). This systematic review synthesized the literature on mental health interventions for PLWH in low‐ and middle‐income countries (LMICs) to determine intervention components and explore their relationship with intervention effectiveness. Methods We included only controlled clinical trials of interventions aiming to improve the mental health of PLWH. We conducted a search in the following databases: PubMed, CINAHL, PsycINFO and EMBASE for eligible studies describing the evaluation of interventions for mental health problems among PLWH in LMICs published through August 2020. Two reviewers independently screened references in two successive stages of title/abstract screening and then full‐text screening for references meeting title/abstract criteria. Results We identified a total of 30 eligible articles representing 6477 PLWH who were assigned to either the intervention arm (n = 3182) or control arm (n = 3346). The mental health interventions evaluated were psychological (n = 17, 56.67%), pharmacological (n = 6, 20.00%), combined psychological and pharmacological (n = 1, 3.33%) and complementary/alternative treatments (n = 6, 20.00%). The mental health problems targeted were depression (n = 22, 73.33 %), multiple psychological symptoms (n = 1, 3.33%), alcohol and substance use problems (n = 4, 13.33%), post‐traumatic stress disorder (n = 1, 3.33%) and HIV‐related neuro‐cognitive impairment (n = 2, 6.67%). Studies of interventions with significant effects had significantly a higher number of active ingredients than those without significant effects [3.41 (2.24) vs. 1.84 (1.46) Mean (SD)] [Mean difference = −1.56, 95% CI = −3.03 to −0.09, p = 0.037]. Conclusions There continue to be advances in mental health interventions for PLWH with mental illness in LMICs. However, more research is needed to elucidate how intervention components lead to intervention effectiveness. We recommend scale up of culturally appropriate interventions that have been successfully evaluated in low‐ and middle‐income countries.\n
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\n \n\n \n \n \n \n \n Physical Activity Levels of Adolescents and Adults With Cerebral Palsy in Urban South Africa.\n \n \n \n\n\n \n Salie, R.; Eken, M.; Donald, K.; Fieggen, A.; and Langerak, N.\n\n\n \n\n\n\n Frontiers in Neurology, 12. 2021.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Salie2021,\nabstract = {Background: Research in high income countries shows that people with cerebral palsy (CP) are less physically active than typically developing (TD) peers, but less is known regarding physical activity (PA) in those with CP in low-to-middle income countries. The aim of this study was to determine daily step count and levels of PA in adolescents and adults with CP living in urban South Africa, compared to TD peers, and to determine associations with sex, Gross Motor Function Classification System (GMFCS) level, body mass index and socio-economic status. Materials and Methods: This case–control study included 26 adolescents and 22 adults with CP (GMFCS Level I-V) and matched TD peers (25 and 30, respectively). Participants wore an ActiGraph GT3X for 7 consecutive days to determine step count and time (minutes per hour) spent in PA levels, including sedentary (SED), low physical activity (LPA) and moderate to vigorous physical activity (MVPA). Results: The daily step count and PA levels for ambulant adolescents with CP (GMFCS level I-III) were similar to TD peers, while this was less for adolescents classified in GMFCS level IV-V. Daily step count, SED and MVPA were similar for adults classified in GMFCS level I-II compared to TD adults, while all parameters were lower for adults using assistive devices (GMFCS level III) and non-ambulant adults (GMFCS level IV-V) compared to TD peers. Daily step count and PA levels were inversely associated with GMFCS, while no other associations were found. Conclusion: People with CP who were more mobile dependent (higher GMFCS level) were less active. However, adolescents and adults with CP classified as GMFCS levels I-II living in urban South Africa recorded similar step count and PA levels as their TD peers. This was also the case for adolescents using assistive devices, though not for those in the adult group (GMFCS level III). Furthermore, it was apparent that even the ambulant individuals with CP and TD cohorts were relatively inactive. Intervention programs for CP and TD adolescents should be aimed at finding strategies to keep adolescents physically active well into adulthood, in order to promote physical health, social and emotional well-being and independence.},\nauthor = {Salie, R. and Eken, M.M. and Donald, K.A. and Fieggen, A.G. and Langerak, N.G.},\ndoi = {10.3389/fneur.2021.747361},\nfile = {:Users/jacquelinebracher/Zotero/storage/CN6KH3SA/Salie et al. - 2021 - Physical Activity Levels of Adolescents and Adults.pdf:pdf},\njournal = {Frontiers in Neurology},\ntitle = {{Physical Activity Levels of Adolescents and Adults With Cerebral Palsy in Urban South Africa}},\nvolume = {12},\nyear = {2021}\n}\n
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\n Background: Research in high income countries shows that people with cerebral palsy (CP) are less physically active than typically developing (TD) peers, but less is known regarding physical activity (PA) in those with CP in low-to-middle income countries. The aim of this study was to determine daily step count and levels of PA in adolescents and adults with CP living in urban South Africa, compared to TD peers, and to determine associations with sex, Gross Motor Function Classification System (GMFCS) level, body mass index and socio-economic status. Materials and Methods: This case–control study included 26 adolescents and 22 adults with CP (GMFCS Level I-V) and matched TD peers (25 and 30, respectively). Participants wore an ActiGraph GT3X for 7 consecutive days to determine step count and time (minutes per hour) spent in PA levels, including sedentary (SED), low physical activity (LPA) and moderate to vigorous physical activity (MVPA). Results: The daily step count and PA levels for ambulant adolescents with CP (GMFCS level I-III) were similar to TD peers, while this was less for adolescents classified in GMFCS level IV-V. Daily step count, SED and MVPA were similar for adults classified in GMFCS level I-II compared to TD adults, while all parameters were lower for adults using assistive devices (GMFCS level III) and non-ambulant adults (GMFCS level IV-V) compared to TD peers. Daily step count and PA levels were inversely associated with GMFCS, while no other associations were found. Conclusion: People with CP who were more mobile dependent (higher GMFCS level) were less active. However, adolescents and adults with CP classified as GMFCS levels I-II living in urban South Africa recorded similar step count and PA levels as their TD peers. This was also the case for adolescents using assistive devices, though not for those in the adult group (GMFCS level III). Furthermore, it was apparent that even the ambulant individuals with CP and TD cohorts were relatively inactive. Intervention programs for CP and TD adolescents should be aimed at finding strategies to keep adolescents physically active well into adulthood, in order to promote physical health, social and emotional well-being and independence.\n
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\n \n\n \n \n \n \n \n \n The relationship between childhood trauma, socioeconomic status, and maternal depression among pregnant women in a \\South\\ \\African\\ birth cohort study.\n \n \n \n \n\n\n \n Mal-Sarkar, T.; Keyes, K.; Koen, N.; Barnett, W.; Myer, L.; Rutherford, C.; Zar, H. J; Stein, D. J; and Lund, C.\n\n\n \n\n\n\n SSM - Population Health, 14: 100770. jun 2021.\n \n\n\n\n
\n\n\n\n \n \n \"ThePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{mal-sarkar_relationship_2021,\nauthor = {Mal-Sarkar, Tatini and Keyes, Katherine and Koen, Nastassja and Barnett, Whitney and Myer, Landon and Rutherford, Caroline and Zar, Heather J and Stein, Dan J and Lund, Crick},\ndoi = {10.1016/j.ssmph.2021.100770},\nfile = {:Users/jacquelinebracher/Zotero/storage/WKTUR43K/Mal-Sarkar et al. - 2021 - The relationship between childhood trauma, socioec.pdf:pdf},\nissn = {23528273},\njournal = {SSM - Population Health},\nmonth = {jun},\npages = {100770},\ntitle = {{The relationship between childhood trauma, socioeconomic status, and maternal depression among pregnant women in a {\\{}South{\\}} {\\{}African{\\}} birth cohort study}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S2352827321000458},\nvolume = {14},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Response to: Asymptomatic neurocognitive impairment is a risk for symptomatic decline over a 3-year study period.\n \n \n \n \n\n\n \n Nightingale, S; Dreyer, A J; Gisslén, M; Winston, A; and Joska, J A\n\n\n \n\n\n\n 2021.\n \n\n\n\n
\n\n\n\n \n \n \"ResponsePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Nightingale2021a,\nannote = {Export Date: 29 December 2022},\nauthor = {Nightingale, S and Dreyer, A J and Gissl{\\'{e}}n, M and Winston, A and Joska, J A},\ndoi = {10.1097/QAD.0000000000002848},\nnumber = {7},\npages = {1152--1153},\ntitle = {{Response to: Asymptomatic neurocognitive impairment is a risk for symptomatic decline over a 3-year study period}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85105541612{\\&}doi=10.1097{\\%}2FQAD.0000000000002848{\\&}partnerID=40{\\&}md5=b05621b392f4e1f3837d51c7ed4c1900},\nvolume = {35},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Cerebrospinal fluid immune markers and HIV-associated neurocognitive impairments: A systematic review.\n \n \n \n \n\n\n \n Williams, M E; Stein, D J; Joska, J A; and Naudé, P J W\n\n\n \n\n\n\n 2021.\n \n\n\n\n
\n\n\n\n \n \n \"CerebrospinalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Williams2021,\nannote = {Export Date: 29 December 2022},\nauthor = {Williams, M E and Stein, D J and Joska, J A and Naud{\\'{e}}, P J W},\ndoi = {10.1016/j.jneuroim.2021.577649},\ntitle = {{Cerebrospinal fluid immune markers and HIV-associated neurocognitive impairments: A systematic review}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85110514165{\\&}doi=10.1016{\\%}2Fj.jneuroim.2021.577649{\\&}partnerID=40{\\&}md5=a47383d2bf1369aef527d5cd86f49ba4},\nvolume = {358},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Challenges and opportunities for neuroimaging in young patients with traumatic brain injury: a coordinated effort towards advancing discovery from the ENIGMA pediatric moderate/severe TBI group.\n \n \n \n \n\n\n \n Dennis, E L; Caeyenberghs, K; Asarnow, R F; Babikian, T; Bartnik-Olson, B; Bigler, E D; Figaji, A; Giza, C C; Goodrich-Hunsaker, N J; Hodges, C B; Hoskinson, K R; Königs, M; Levin, H S; Lindsey, H M; Livny, A; Max, J E; Merkley, T L; Newsome, M R; Olsen, A; Ryan, N P; Spruiell, M S; Suskauer, S J; Thomopoulos, S I; Ware, A L; Watson, C G; Wheeler, A L; Yeates, K O; Zielinski, B A; Thompson, P M; Tate, D F; and Wilde, E A\n\n\n \n\n\n\n 2021.\n \n\n\n\n
\n\n\n\n \n \n \"ChallengesPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Dennis2021,\nannote = {Export Date: 29 December 2022},\nauthor = {Dennis, E L and Caeyenberghs, K and Asarnow, R F and Babikian, T and Bartnik-Olson, B and Bigler, E D and Figaji, A and Giza, C C and Goodrich-Hunsaker, N J and Hodges, C B and Hoskinson, K R and K{\\"{o}}nigs, M and Levin, H S and Lindsey, H M and Livny, A and Max, J E and Merkley, T L and Newsome, M R and Olsen, A and Ryan, N P and Spruiell, M S and Suskauer, S J and Thomopoulos, S I and Ware, A L and Watson, C G and Wheeler, A L and Yeates, K O and Zielinski, B A and Thompson, P M and Tate, D F and Wilde, E A},\ndoi = {10.1007/s11682-020-00363-x},\nfile = {:Users/jacquelinebracher/Zotero/storage/KV7ZCR6B/Dennis et al. - 2021 - Challenges and opportunities for neuroimaging in y.pdf:pdf},\nnumber = {2},\npages = {555--575},\ntitle = {{Challenges and opportunities for neuroimaging in young patients with traumatic brain injury: a coordinated effort towards advancing discovery from the ENIGMA pediatric moderate/severe TBI group}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85089009747{\\&}doi=10.1007{\\%}2Fs11682-020-00363-x{\\&}partnerID=40{\\&}md5=ef3a3eb69a1405c0c668983fe8e3b81c},\nvolume = {15},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Imprecise \\Visual\\ \\Feedback\\ \\About\\ \\Hand\\ \\Location\\ \\Increases\\ a \\Classically\\ \\Conditioned\\ \\Pain\\ \\Expectancy\\ \\Effect\\.\n \n \n \n \n\n\n \n Chaves, T. C.; Stanton, T. R; Grant, A.; Pulling, B. W; Madden, V. J; Newport, R.; and Moseley, G L.\n\n\n \n\n\n\n The Journal of Pain, 22(6): 748–761. jun 2021.\n \n\n\n\n
\n\n\n\n \n \n \"ImprecisePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{chaves_imprecise_2021,\nauthor = {Chaves, Thais Cristina and Stanton, Tasha R and Grant, Ashley and Pulling, Brian W and Madden, Victoria J and Newport, Roger and Moseley, G Lorimer},\ndoi = {10.1016/j.jpain.2021.01.004},\nfile = {:Users/jacquelinebracher/Zotero/storage/68RCD6EE/Chaves et al. - 2021 - Imprecise Visual Feedback About Hand Location Incr.pdf:pdf},\nissn = {15265900},\njournal = {The Journal of Pain},\nmonth = {jun},\nnumber = {6},\npages = {748--761},\ntitle = {{Imprecise {\\{}Visual{\\}} {\\{}Feedback{\\}} {\\{}About{\\}} {\\{}Hand{\\}} {\\{}Location{\\}} {\\{}Increases{\\}} a {\\{}Classically{\\}} {\\{}Conditioned{\\}} {\\{}Pain{\\}} {\\{}Expectancy{\\}} {\\{}Effect{\\}}}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S1526590021000134},\nvolume = {22},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n Central white matter integrity alterations in 2-3-year-old children following prenatal alcohol exposure.\n \n \n \n\n\n \n Roos, A.; Wedderburn, C.; Fouche, J.; Subramoney, S.; Joshi, S.; Woods, R.; Zar, H.; Narr, K.; Stein, D.; and Donald, K.\n\n\n \n\n\n\n Drug and Alcohol Dependence, 225. 2021.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Roos2021,\nabstract = {Background: Prenatal alcohol exposure (PAE) remains a potentially preventable, but pervasive risk factor to neurodevelopment. Yet, evidence is lacking on the impact of alcohol on brain development in toddlers. This study aimed to investigate the impact of PAE on brain white matter integrity in 2–3-year-old children. Methods: Children (n = 83, 30–37 months old) of the Drakenstein Child Health Study birth cohort, underwent diffusion MRI on a 3 T Siemens scanner during natural sleep. Parameters were extracted in children with PAE (n = 25, 56 {\\%} boys) and unexposed controls (n = 58, 62 {\\%} boys) using Tract-based Spatial Statistics, and compared by group. The contribution of maternal tobacco smoking to white matter differences was also explored. Results: Children with PAE had altered fractional anisotropy, radial diffusivity and axial diffusivity in brain stem, limbic and association tracts compared to unexposed controls. Notably lower fractional anisotropy was found in the uncinate fasciculus, and lower mean and radial diffusivity were found in the fornix stria terminalis and corticospinal tract (FDR corrected p {\\textless} 0.05). There was a significant interaction effect of PAE and prenatal tobacco exposure which lowered mean, radial and axial diffusivity in the corticospinal tract significantly in the PAE group but not controls. Conclusion: Widespread altered white matter microstructural integrity at 2–3 years of age is consistent with findings in neonates in the same and other cohorts, indicating persistence of effects of PAE through early life. Findings also highlight that prenatal tobacco exposure impacts the association of PAE on white matter alterations, amplifying effects in tracts underlying motor function.},\nauthor = {Roos, A. and Wedderburn, C.J. and Fouche, J.-P. and Subramoney, S. and Joshi, S.H. and Woods, R.P. and Zar, H.J. and Narr, K.L. and Stein, D.J. and Donald, K.A.},\ndoi = {10.1016/j.drugalcdep.2021.108826},\nfile = {:Users/jacquelinebracher/Zotero/storage/3HP5IK7V/Roos et al. - 2021 - Central white matter integrity alterations in 2-3-.pdf:pdf},\njournal = {Drug and Alcohol Dependence},\ntitle = {{Central white matter integrity alterations in 2-3-year-old children following prenatal alcohol exposure}},\nvolume = {225},\nyear = {2021}\n}\n
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\n Background: Prenatal alcohol exposure (PAE) remains a potentially preventable, but pervasive risk factor to neurodevelopment. Yet, evidence is lacking on the impact of alcohol on brain development in toddlers. This study aimed to investigate the impact of PAE on brain white matter integrity in 2–3-year-old children. Methods: Children (n = 83, 30–37 months old) of the Drakenstein Child Health Study birth cohort, underwent diffusion MRI on a 3 T Siemens scanner during natural sleep. Parameters were extracted in children with PAE (n = 25, 56 % boys) and unexposed controls (n = 58, 62 % boys) using Tract-based Spatial Statistics, and compared by group. The contribution of maternal tobacco smoking to white matter differences was also explored. Results: Children with PAE had altered fractional anisotropy, radial diffusivity and axial diffusivity in brain stem, limbic and association tracts compared to unexposed controls. Notably lower fractional anisotropy was found in the uncinate fasciculus, and lower mean and radial diffusivity were found in the fornix stria terminalis and corticospinal tract (FDR corrected p \\textless 0.05). There was a significant interaction effect of PAE and prenatal tobacco exposure which lowered mean, radial and axial diffusivity in the corticospinal tract significantly in the PAE group but not controls. Conclusion: Widespread altered white matter microstructural integrity at 2–3 years of age is consistent with findings in neonates in the same and other cohorts, indicating persistence of effects of PAE through early life. Findings also highlight that prenatal tobacco exposure impacts the association of PAE on white matter alterations, amplifying effects in tracts underlying motor function.\n
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\n \n\n \n \n \n \n \n \n Expert appraisal of criteria for assessing gaming disorder: an international \\Delphi\\ study.\n \n \n \n \n\n\n \n Castro‐Calvo, J.; King, D. L; Stein, D. J; Brand, M.; Carmi, L.; Chamberlain, S. R; Demetrovics, Z.; Fineberg, N. A; Rumpf, H.; Yücel, M.; Achab, S.; Ambekar, A.; Bahar, N.; Blaszczynski, A.; Bowden‐Jones, H.; Carbonell, X.; Chan, E. M. L.; Ko, C.; De Timary, P.; Dufour, M.; Grall‐Bronnec, M.; Lee, H. K.; Higuchi, S.; Jimenez‐Murcia, S.; Király, O.; Kuss, D. J; Long, J.; Müller, A.; Pallanti, S.; Potenza, M. N; Rahimi‐Movaghar, A.; Saunders, J. B; Schimmenti, A.; Lee, S.; Siste, K.; Spritzer, D. T; Starcevic, V.; Weinstein, A. M; Wölfling, K.; and Billieux, J.\n\n\n \n\n\n\n Addiction, 116(9): 2463–2475. sep 2021.\n \n\n\n\n
\n\n\n\n \n \n \"ExpertPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{castrocalvo_expert_2021,\nabstract = {Abstract\n\nBackground and aims\nFollowing the recognition of ‘internet gaming disorder' (IGD) as a condition requiring further study by the DSM‐5, ‘gaming disorder' (GD) was officially included as a diagnostic entity by the World Health Organization (WHO) in the 11th revision of the International Classification of Diseases (ICD‐11). However, the proposed diagnostic criteria for gaming disorder remain the subject of debate, and there has been no systematic attempt to integrate the views of different groups of experts. To achieve a more systematic agreement on this new disorder, this study employed the Delphi expert consensus method to obtain expert agreement on the diagnostic validity, clinical utility and prognostic value of the DSM‐5 criteria and ICD‐11 clinical guidelines for GD.\n\n\nMethods\nA total of 29 international experts with clinical and/or research experience in GD completed three iterative rounds of a Delphi survey. Experts rated proposed criteria in progressive rounds until a pre‐determined level of agreement was achieved.\n\n\nResults\nFor DSM‐5 IGD criteria, there was an agreement both that a subset had high diagnostic validity, clinical utility and prognostic value and that some (e.g. tolerance, deception) had low diagnostic validity, clinical utility and prognostic value. Crucially, some DSM‐5 criteria (e.g. escapism/mood regulation, tolerance) were regarded as incapable of distinguishing between problematic and non‐problematic gaming. In contrast, ICD‐11 diagnostic guidelines for GD (except for the criterion relating to diminished non‐gaming interests) were judged as presenting high diagnostic validity, clinical utility and prognostic value.\n\n\nConclusions\nThis Delphi survey provides a foundation for identifying the most diagnostically valid and clinically useful criteria for GD. There was expert agreement that some DSM‐5 criteria were not clinically relevant and may pathologize non‐problematic patterns of gaming, whereas ICD‐11 diagnostic guidelines are likely to diagnose GD adequately and avoid pathologizing.},\nauthor = {Castro‐Calvo, Jes{\\'{u}}s and King, Daniel L and Stein, Dan J and Brand, Matthias and Carmi, Lior and Chamberlain, Samuel R and Demetrovics, Zsolt and Fineberg, Naomi A and Rumpf, Hans‐J{\\"{u}}rgen and Y{\\"{u}}cel, Murat and Achab, Sophia and Ambekar, Atul and Bahar, Norharlina and Blaszczynski, Alexander and Bowden‐Jones, Henrietta and Carbonell, Xavier and Chan, Elda Mei Lo and Ko, Chih‐Hung and {De Timary}, Philippe and Dufour, Magali and Grall‐Bronnec, Marie and Lee, Hae Kook and Higuchi, Susumu and Jimenez‐Murcia, Susana and Kir{\\'{a}}ly, Orsolya and Kuss, Daria J and Long, Jiang and M{\\"{u}}ller, Astrid and Pallanti, Stefano and Potenza, Marc N and Rahimi‐Movaghar, Afarin and Saunders, John B and Schimmenti, Adriano and Lee, Seung‐Yup and Siste, Kristiana and Spritzer, Daniel T and Starcevic, Vladan and Weinstein, Aviv M and W{\\"{o}}lfling, Klaus and Billieux, Jo{\\"{e}}l},\ndoi = {10.1111/add.15411},\nfile = {:Users/jacquelinebracher/Zotero/storage/IJ5HSAK8/Castro‐Calvo et al. - 2021 - Expert appraisal of criteria for assessing gaming .pdf:pdf},\nissn = {0965-2140, 1360-0443},\njournal = {Addiction},\nmonth = {sep},\nnumber = {9},\npages = {2463--2475},\nshorttitle = {Expert appraisal of criteria for assessing gaming },\ntitle = {{Expert appraisal of criteria for assessing gaming disorder: an international {\\{}Delphi{\\}} study}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1111/add.15411},\nvolume = {116},\nyear = {2021}\n}\n
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\n Abstract Background and aims Following the recognition of ‘internet gaming disorder' (IGD) as a condition requiring further study by the DSM‐5, ‘gaming disorder' (GD) was officially included as a diagnostic entity by the World Health Organization (WHO) in the 11th revision of the International Classification of Diseases (ICD‐11). However, the proposed diagnostic criteria for gaming disorder remain the subject of debate, and there has been no systematic attempt to integrate the views of different groups of experts. To achieve a more systematic agreement on this new disorder, this study employed the Delphi expert consensus method to obtain expert agreement on the diagnostic validity, clinical utility and prognostic value of the DSM‐5 criteria and ICD‐11 clinical guidelines for GD. Methods A total of 29 international experts with clinical and/or research experience in GD completed three iterative rounds of a Delphi survey. Experts rated proposed criteria in progressive rounds until a pre‐determined level of agreement was achieved. Results For DSM‐5 IGD criteria, there was an agreement both that a subset had high diagnostic validity, clinical utility and prognostic value and that some (e.g. tolerance, deception) had low diagnostic validity, clinical utility and prognostic value. Crucially, some DSM‐5 criteria (e.g. escapism/mood regulation, tolerance) were regarded as incapable of distinguishing between problematic and non‐problematic gaming. In contrast, ICD‐11 diagnostic guidelines for GD (except for the criterion relating to diminished non‐gaming interests) were judged as presenting high diagnostic validity, clinical utility and prognostic value. Conclusions This Delphi survey provides a foundation for identifying the most diagnostically valid and clinically useful criteria for GD. There was expert agreement that some DSM‐5 criteria were not clinically relevant and may pathologize non‐problematic patterns of gaming, whereas ICD‐11 diagnostic guidelines are likely to diagnose GD adequately and avoid pathologizing.\n
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\n \n\n \n \n \n \n \n \n 1q21.1 distal copy number variants are associated with cerebral and cognitive alterations in humans.\n \n \n \n \n\n\n \n Sønderby, I. E; Van Der Meer, D.; Moreau, C.; Kaufmann, T.; Walters, G B.; Ellegaard, M.; Abdellaoui, A.; Ames, D.; Amunts, K.; Andersson, M.; Armstrong, N. J; Bernard, M.; Blackburn, N. B; Blangero, J.; Boomsma, D. I; Brodaty, H.; Brouwer, R. M; Bülow, R.; Bøen, R.; Cahn, W.; Calhoun, V. D; Caspers, S.; Ching, C. R K; Cichon, S.; Ciufolini, S.; Crespo-Facorro, B.; Curran, J. E; Dale, A. M; Dalvie, S.; Dazzan, P.; De Geus, E. J C; De Zubicaray, G. I; De Zwarte, S. M C; Desrivieres, S.; Doherty, J. L; Donohoe, G.; Draganski, B.; Ehrlich, S.; Eising, E.; Espeseth, T.; Fejgin, K.; Fisher, S. E; Fladby, T.; Frei, O.; Frouin, V.; Fukunaga, M.; Gareau, T.; Ge, T.; Glahn, D. C; Grabe, H. J; Groenewold, N. A; Gústafsson, Ó.; Haavik, J.; Haberg, A. K; Hall, J.; Hashimoto, R.; Hehir-Kwa, J. Y; Hibar, D. P; Hillegers, M. H J; Hoffmann, P.; Holleran, L.; Holmes, A. J; Homuth, G.; Hottenga, J.; Hulshoff Pol, H. E; Ikeda, M.; Jahanshad, N.; Jockwitz, C.; Johansson, S.; Jönsson, E. G; Jørgensen, N. R; Kikuchi, M.; Knowles, E. E M; Kumar, K.; Le Hellard, S.; Leu, C.; Linden, D. E J; Liu, J.; Lundervold, A.; Lundervold, A. J.; Maillard, A. M; Martin, N. G; Martin-Brevet, S.; Mather, K. A; Mathias, S. R; McMahon, K. L; McRae, A. F; Medland, S. E; Meyer-Lindenberg, A.; Moberget, T.; Modenato, C.; Sánchez, J. M.; Morris, D. W; Mühleisen, T. W; Murray, R. M; Nielsen, J.; Nordvik, J. E; Nyberg, L.; Loohuis, L. M O.; Ophoff, R. A; Owen, M. J; Paus, T.; Pausova, Z.; Peralta, J. M; Pike, G B.; Prieto, C.; Quinlan, E. B; Reinbold, C. S; Marques, T. R.; Rucker, J. J H; Sachdev, P. S; Sando, S. B; Schofield, P. R; Schork, A. J; Schumann, G.; Shin, J.; Shumskaya, E.; Silva, A. I; Sisodiya, S. M; Steen, V. M; Stein, D. J; Strike, L. T; Suzuki, I. K; Tamnes, C. K; Teumer, A.; Thalamuthu, A.; Tordesillas-Gutiérrez, D.; Uhlmann, A.; Ulfarsson, M. O; Van ‘T Ent, D.; Van Den Bree, M. B M; Vanderhaeghen, P.; Vassos, E.; Wen, W.; Wittfeld, K.; Wright, M. J; Agartz, I.; Djurovic, S.; Westlye, L. T; Stefansson, H.; Stefansson, K.; Jacquemont, S.; Thompson, P. M; Andreassen, O. A; for the ENIGMA-CNV working group ; Van Der Meer, D.; De Geus, E. J C; De Zubicaray, G. I; De Zwarte, S. M C; Le Hellard, S.; Van ‘T Ent, D.; and Van Den Bree, M. B M\n\n\n \n\n\n\n Translational Psychiatry, 11(1): 182. mar 2021.\n \n\n\n\n
\n\n\n\n \n \n \"1q21.1Paper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{sonderby_1q211_2021,\nabstract = {Abstract\nLow-frequency 1q21.1 distal deletion and duplication copy number variant (CNV) carriers are predisposed to multiple neurodevelopmental disorders, including schizophrenia, autism and intellectual disability. Human carriers display a high prevalence of micro- and macrocephaly in deletion and duplication carriers, respectively. The underlying brain structural diversity remains largely unknown. We systematically called CNVs in 38 cohorts from the large-scale ENIGMA-CNV collaboration and the UK Biobank and identified 28 1q21.1 distal deletion and 22 duplication carriers and 37,088 non-carriers (48{\\%} male) derived from 15 distinct magnetic resonance imaging scanner sites. With standardized methods, we compared subcortical and cortical brain measures (all) and cognitive performance (UK Biobank only) between carrier groups also testing for mediation of brain structure on cognition. We identified positive dosage effects of copy number on intracranial volume (ICV) and total cortical surface area, with the largest effects in frontal and cingulate cortices, and negative dosage effects on caudate and hippocampal volumes. The carriers displayed distinct cognitive deficit profiles in cognitive tasks from the UK Biobank with intermediate decreases in duplication carriers and somewhat larger in deletion carriers—the latter potentially mediated by ICV or cortical surface area. These results shed light on pathobiological mechanisms of neurodevelopmental disorders, by demonstrating gene dose effect on specific brain structures and effect on cognitive function.},\nauthor = {S{\\o}nderby, Ida E and {Van Der Meer}, Dennis and Moreau, Clara and Kaufmann, Tobias and Walters, G Bragi and Ellegaard, Maria and Abdellaoui, Abdel and Ames, David and Amunts, Katrin and Andersson, Micael and Armstrong, Nicola J and Bernard, Manon and Blackburn, Nicholas B and Blangero, John and Boomsma, Dorret I and Brodaty, Henry and Brouwer, Rachel M and B{\\"{u}}low, Robin and B{\\o}en, Rune and Cahn, Wiepke and Calhoun, Vince D and Caspers, Svenja and Ching, Christopher R K and Cichon, Sven and Ciufolini, Simone and Crespo-Facorro, Benedicto and Curran, Joanne E and Dale, Anders M and Dalvie, Shareefa and Dazzan, Paola and {De Geus}, Eco J C and {De Zubicaray}, Greig I and {De Zwarte}, Sonja M C and Desrivieres, Sylvane and Doherty, Joanne L and Donohoe, Gary and Draganski, Bogdan and Ehrlich, Stefan and Eising, Else and Espeseth, Thomas and Fejgin, Kim and Fisher, Simon E and Fladby, Tormod and Frei, Oleksandr and Frouin, Vincent and Fukunaga, Masaki and Gareau, Thomas and Ge, Tian and Glahn, David C and Grabe, Hans J and Groenewold, Nynke A and G{\\'{u}}stafsson, {\\'{O}}mar and Haavik, Jan and Haberg, Asta K and Hall, Jeremy and Hashimoto, Ryota and Hehir-Kwa, Jayne Y and Hibar, Derrek P and Hillegers, Manon H J and Hoffmann, Per and Holleran, Laurena and Holmes, Avram J and Homuth, Georg and Hottenga, Jouke-Jan and {Hulshoff Pol}, Hilleke E and Ikeda, Masashi and Jahanshad, Neda and Jockwitz, Christiane and Johansson, Stefan and J{\\"{o}}nsson, Erik G and J{\\o}rgensen, Niklas R and Kikuchi, Masataka and Knowles, Emma E M and Kumar, Kuldeep and {Le Hellard}, Stephanie and Leu, Costin and Linden, David E J and Liu, Jingyu and Lundervold, Arvid and Lundervold, Astri Johansen and Maillard, Anne M and Martin, Nicholas G and Martin-Brevet, Sandra and Mather, Karen A and Mathias, Samuel R and McMahon, Katie L and McRae, Allan F and Medland, Sarah E and Meyer-Lindenberg, Andreas and Moberget, Torgeir and Modenato, Claudia and S{\\'{a}}nchez, Jennifer Monereo and Morris, Derek W and M{\\"{u}}hleisen, Thomas W and Murray, Robin M and Nielsen, Jacob and Nordvik, Jan E and Nyberg, Lars and Loohuis, Loes M Olde and Ophoff, Roel A and Owen, Michael J and Paus, Tomas and Pausova, Zdenka and Peralta, Juan M and Pike, G Bruce and Prieto, Carlos and Quinlan, Erin B and Reinbold, C{\\'{e}}line S and Marques, Tiago Reis and Rucker, James J H and Sachdev, Perminder S and Sando, Sigrid B and Schofield, Peter R and Schork, Andrew J and Schumann, Gunter and Shin, Jean and Shumskaya, Elena and Silva, Ana I and Sisodiya, Sanjay M and Steen, Vidar M and Stein, Dan J and Strike, Lachlan T and Suzuki, Ikuo K and Tamnes, Christian K and Teumer, Alexander and Thalamuthu, Anbupalam and Tordesillas-Guti{\\'{e}}rrez, Diana and Uhlmann, Anne and Ulfarsson, Magnus O and {Van ‘T Ent}, Dennis and {Van Den Bree}, Marianne B M and Vanderhaeghen, Pierre and Vassos, Evangelos and Wen, Wei and Wittfeld, Katharina and Wright, Margaret J and Agartz, Ingrid and Djurovic, Srdjan and Westlye, Lars T and Stefansson, Hreinn and Stefansson, Kari and Jacquemont, S{\\'{e}}bastien and Thompson, Paul M and Andreassen, Ole A and for the ENIGMA-CNV working group and {Van Der Meer}, Dennis and {De Geus}, Eco J C and {De Zubicaray}, Greig I and {De Zwarte}, Sonja M C and {Le Hellard}, Stephanie and {Van ‘T Ent}, Dennis and {Van Den Bree}, Marianne B M},\ndoi = {10.1038/s41398-021-01213-0},\nfile = {:Users/jacquelinebracher/Zotero/storage/UFC8IZDQ/S{\\o}nderby et al. - 2021 - 1q21.1 distal copy number variants are associated .pdf:pdf},\nissn = {2158-3188},\njournal = {Translational Psychiatry},\nmonth = {mar},\nnumber = {1},\npages = {182},\ntitle = {1q21.1 distal copy number variants are associated with cerebral and cognitive alterations in humans},\nurl = {https://www.nature.com/articles/s41398-021-01213-0},\nvolume = {11},\nyear = {2021}\n}\n
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\n Abstract Low-frequency 1q21.1 distal deletion and duplication copy number variant (CNV) carriers are predisposed to multiple neurodevelopmental disorders, including schizophrenia, autism and intellectual disability. Human carriers display a high prevalence of micro- and macrocephaly in deletion and duplication carriers, respectively. The underlying brain structural diversity remains largely unknown. We systematically called CNVs in 38 cohorts from the large-scale ENIGMA-CNV collaboration and the UK Biobank and identified 28 1q21.1 distal deletion and 22 duplication carriers and 37,088 non-carriers (48% male) derived from 15 distinct magnetic resonance imaging scanner sites. With standardized methods, we compared subcortical and cortical brain measures (all) and cognitive performance (UK Biobank only) between carrier groups also testing for mediation of brain structure on cognition. We identified positive dosage effects of copy number on intracranial volume (ICV) and total cortical surface area, with the largest effects in frontal and cingulate cortices, and negative dosage effects on caudate and hippocampal volumes. The carriers displayed distinct cognitive deficit profiles in cognitive tasks from the UK Biobank with intermediate decreases in duplication carriers and somewhat larger in deletion carriers—the latter potentially mediated by ICV or cortical surface area. These results shed light on pathobiological mechanisms of neurodevelopmental disorders, by demonstrating gene dose effect on specific brain structures and effect on cognitive function.\n
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\n \n\n \n \n \n \n \n \n Study protocol for a phase 2A trial of the safety and tolerability of increased dose rifampicin and adjunctive linezolid, with or without aspirin, for HIV-associated tuberculous meningitis [LASER-TBM].\n \n \n \n \n\n\n \n Davis, A G; Wasserman, S; Maxebengula, M; Stek, C; Bremer, M; Daroowala, R; Aziz, S; Goliath, R; Stegmann, S; Koekemoer, S; Jackson, A; Lai Sai, L; Kadernani, Y; Sihoyiya, T; Liang, C J; Dodd, L; Denti, P; Crede, T; Naude, J; Szymanski, P; Vallie, Y; Banderker, I; Moosa, S; Raubenheimer, P; Lai, R P J; Joska, J; Nightingale, S; Dreyer, A; Wahl, G; Offiah, C; Vorster, I; Candy, S; Robertson, F; Meintjes, E; Maartens, G; Black, J; Meintjes, G; and Wilkinson, R J\n\n\n \n\n\n\n 2021.\n \n\n\n\n
\n\n\n\n \n \n \"StudyPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@misc{Davis2021,\nannote = {Export Date: 29 December 2022},\nauthor = {Davis, A G and Wasserman, S and Maxebengula, M and Stek, C and Bremer, M and Daroowala, R and Aziz, S and Goliath, R and Stegmann, S and Koekemoer, S and Jackson, A and {Lai Sai}, L and Kadernani, Y and Sihoyiya, T and Liang, C J and Dodd, L and Denti, P and Crede, T and Naude, J and Szymanski, P and Vallie, Y and Banderker, I and Moosa, S and Raubenheimer, P and Lai, R P J and Joska, J and Nightingale, S and Dreyer, A and Wahl, G and Offiah, C and Vorster, I and Candy, S and Robertson, F and Meintjes, E and Maartens, G and Black, J and Meintjes, G and Wilkinson, R J},\ndoi = {10.12688/wellcomeopenres.16783.1},\nfile = {:Users/jacquelinebracher/Zotero/storage/8UB2BC67/Davis et al. - 2021 - Study protocol for a phase 2A trial of the safety .pdf:pdf},\ntitle = {{Study protocol for a phase 2A trial of the safety and tolerability of increased dose rifampicin and adjunctive linezolid, with or without aspirin, for HIV-associated tuberculous meningitis [LASER-TBM]}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85110437837{\\&}doi=10.12688{\\%}2Fwellcomeopenres.16783.1{\\&}partnerID=40{\\&}md5=5c6bb2895cc5de6d50cd5eb61d9278a9},\nvolume = {6},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Understanding the landscape of electrophysiology services for children in sub‐\\Saharan\\ \\Africa\\.\n \n \n \n \n\n\n \n Kander, V.; Hardman, J.; and Wilmshurst, J. M\n\n\n \n\n\n\n Epileptic Disorders, 23(6): 812–822. dec 2021.\n \n\n\n\n
\n\n\n\n \n \n \"UnderstandingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{kander_understanding_2021,\nabstract = {Abstract\n\nObjective\n. Incidence of epilepsy is greatest in infancy and childhood; this is especially evident in sub‐Saharan Africa (SSA). The aim of this study was to understand access to electrophysiology services in SSA including which health practitioner performs and interprets paediatric electroencephalogram (EEG) studies as well as their training in paediatric EEG.\n\n\nMethods\n. A web‐based survey was sent to a cohort of health care practitioners who manage children with epilepsy in SSA. The questions addressed whether EEG was available to these health care practitioners, how the practitioners accessed EEG and who assisted interpretation of the study results. The survey was circulated (June‐December 2019) to 305 participants from 32 African countries.\n\n\nResults\n. A total of 73 (16 partial and 57 complete) surveys were returned from 18 countries. The respondents fell into two main categories: those with access to an EEG machine (44/73; 60{\\%}) and those without access to an EEG machine (29/73; 40{\\%}). For 32{\\%} (23/73), there was no dedicated technician and for 34{\\%} (25/73) no neurologist. Access to a neurologist resulted in the highest proportion of EEGs performed per annum. Of the respondents, 77{\\%} (56/73) agreed that there was a need for a paediatric apprenticeship in EEG skills. Qualitative data to justify need for paediatric EEG training was grouped into three themes: (1) “professional development”; (2) “better care”; and (3) “help paediatric patients and neurologists”.\n\n\nSignificance\n. There is a lack of paediatric EEG training amongst doctors and technicians working with epilepsy in SSA. Expanding training beyond current capacity in SSA, for technicians and practitioners involved in EEG, is necessary.},\nauthor = {Kander, Veena and Hardman, Joanne and Wilmshurst, Jo M},\ndoi = {10.1684/epd.2021.1351},\nissn = {1294-9361, 1950-6945},\njournal = {Epileptic Disorders},\nmonth = {dec},\nnumber = {6},\npages = {812--822},\ntitle = {{Understanding the landscape of electrophysiology services for children in sub‐{\\{}Saharan{\\}} {\\{}Africa{\\}}}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1684/epd.2021.1351},\nvolume = {23},\nyear = {2021}\n}\n
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\n Abstract Objective . Incidence of epilepsy is greatest in infancy and childhood; this is especially evident in sub‐Saharan Africa (SSA). The aim of this study was to understand access to electrophysiology services in SSA including which health practitioner performs and interprets paediatric electroencephalogram (EEG) studies as well as their training in paediatric EEG. Methods . A web‐based survey was sent to a cohort of health care practitioners who manage children with epilepsy in SSA. The questions addressed whether EEG was available to these health care practitioners, how the practitioners accessed EEG and who assisted interpretation of the study results. The survey was circulated (June‐December 2019) to 305 participants from 32 African countries. Results . A total of 73 (16 partial and 57 complete) surveys were returned from 18 countries. The respondents fell into two main categories: those with access to an EEG machine (44/73; 60%) and those without access to an EEG machine (29/73; 40%). For 32% (23/73), there was no dedicated technician and for 34% (25/73) no neurologist. Access to a neurologist resulted in the highest proportion of EEGs performed per annum. Of the respondents, 77% (56/73) agreed that there was a need for a paediatric apprenticeship in EEG skills. Qualitative data to justify need for paediatric EEG training was grouped into three themes: (1) “professional development”; (2) “better care”; and (3) “help paediatric patients and neurologists”. Significance . There is a lack of paediatric EEG training amongst doctors and technicians working with epilepsy in SSA. Expanding training beyond current capacity in SSA, for technicians and practitioners involved in EEG, is necessary.\n
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\n \n\n \n \n \n \n \n \n Demonstrating the feasibility of digital health to support pediatric patients in \\South\\ \\Africa\\.\n \n \n \n \n\n\n \n Davies, E. H.; Fieggen, K.; Wilmshurst, J.; Anyanwu, O.; Burman, R. J.; and Komarzynski, S.\n\n\n \n\n\n\n Epilepsia Open, 6(4): 653–662. dec 2021.\n \n\n\n\n
\n\n\n\n \n \n \"DemonstratingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{davies_demonstrating_2021,\nabstract = {Abstract\n\nObjective\nResources for management of epilepsy in Africa are extremely limited reinforcing the need to develop innovative strategies for optimizing care. Studies have shown that the prevalence of epilepsy in low‐ and middle‐income countries is substantially greater than in more resourced countries. The objective of this report was to demonstrate that mobile Health (mHealth) technologies have the potential to improve the management of epilepsy in Africa.\n\n\nMethods\nThe feasibility of technology‐based home monitoring was investigated in an observational study of 40 children with refractory epilepsy or epilepsy associated with intellectual disability and/or behavior difficulties in South Africa. Technology‐based home monitoring was implemented for six months. Physical activity, sleep, and heart rate were continuously monitored with a wearable device. Caregivers completed regular mobile Patient Reported Outcomes (mPROs) and reported seizures and ad hoc events using a dedicated app. Feasibility was assessed and descriptively measured for recruitment, retention, and engagement of the participants.\n\n\nResults\nThe mHealth technology was able to capture important information that gives an impression of the overall experience of the children and their caregivers. Thirty‐seven participants (94.9{\\%}) reported at least one clinical event. Seventy‐nine percent of caregivers reported seizure events in their children, which were the primary event anticipated. Median engagement with the wearable device and monthly mPROs was 30.8{\\%} and 57.1{\\%}, respectively. However, most participants (87{\\%}) had to be given smartphones for them to have Bluetooth capabilities and access to the study app. Tolerability to the device was impacted by the difficult living circumstances of caregivers that induced fear of loss or theft.\n\n\nSignificance\nThe study showed how the use of remote patient monitoring in the form of mHealth can benefit epilepsy patients, despite highly variable engagement with the technology. The combination of mPROs and wearable devices generated informative datasets that will allow clinicians but also the children and their caregivers to better understand and manage the disease.},\nauthor = {Davies, Elin Haf and Fieggen, Karen and Wilmshurst, Jo and Anyanwu, Obuchinezia and Burman, Richard Joseph and Komarzynski, Sandra},\ndoi = {10.1002/epi4.12527},\nfile = {:Users/jacquelinebracher/Zotero/storage/9IUQCWQN/Davies et al. - 2021 - Demonstrating the feasibility of digital health to.pdf:pdf},\nissn = {2470-9239, 2470-9239},\njournal = {Epilepsia Open},\nmonth = {dec},\nnumber = {4},\npages = {653--662},\ntitle = {{Demonstrating the feasibility of digital health to support pediatric patients in {\\{}South{\\}} {\\{}Africa{\\}}}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1002/epi4.12527},\nvolume = {6},\nyear = {2021}\n}\n
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\n Abstract Objective Resources for management of epilepsy in Africa are extremely limited reinforcing the need to develop innovative strategies for optimizing care. Studies have shown that the prevalence of epilepsy in low‐ and middle‐income countries is substantially greater than in more resourced countries. The objective of this report was to demonstrate that mobile Health (mHealth) technologies have the potential to improve the management of epilepsy in Africa. Methods The feasibility of technology‐based home monitoring was investigated in an observational study of 40 children with refractory epilepsy or epilepsy associated with intellectual disability and/or behavior difficulties in South Africa. Technology‐based home monitoring was implemented for six months. Physical activity, sleep, and heart rate were continuously monitored with a wearable device. Caregivers completed regular mobile Patient Reported Outcomes (mPROs) and reported seizures and ad hoc events using a dedicated app. Feasibility was assessed and descriptively measured for recruitment, retention, and engagement of the participants. Results The mHealth technology was able to capture important information that gives an impression of the overall experience of the children and their caregivers. Thirty‐seven participants (94.9%) reported at least one clinical event. Seventy‐nine percent of caregivers reported seizure events in their children, which were the primary event anticipated. Median engagement with the wearable device and monthly mPROs was 30.8% and 57.1%, respectively. However, most participants (87%) had to be given smartphones for them to have Bluetooth capabilities and access to the study app. Tolerability to the device was impacted by the difficult living circumstances of caregivers that induced fear of loss or theft. Significance The study showed how the use of remote patient monitoring in the form of mHealth can benefit epilepsy patients, despite highly variable engagement with the technology. The combination of mPROs and wearable devices generated informative datasets that will allow clinicians but also the children and their caregivers to better understand and manage the disease.\n
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\n \n\n \n \n \n \n \n \n Association of Immunosuppression and Viral Load with Subcortical Brain Volume in an International Sample of People Living with HIV.\n \n \n \n \n\n\n \n Nir, T M; Fouche, J.; Ananworanich, J; Ances, B M; Boban, J; Brew, B J; Chaganti, J R; Chang, L; Ching, C R K; Cysique, L A; Ernst, T; Faskowitz, J; Gupta, V; Harezlak, J; Heaps-Woodruff, J M; Hinkin, C H; Hoare, J; Joska, J A; Kallianpur, K J; Kuhn, T; Lam, H Y; Law, M; Lebrun-Frénay, C; Levine, A J; Mondot, L; Nakamoto, B K; Navia, B A; Pennec, X; Porges, E C; Salminen, L E; Shikuma, C M; Surento, W; Thames, A D; Valcour, V; Vassallo, M; Woods, A J; Thompson, P M; Cohen, R A; Paul, R; Stein, D J; and Jahanshad, N\n\n\n \n\n\n\n 2021.\n \n\n\n\n
\n\n\n\n \n \n \"AssociationPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@misc{Nir2021,\nannote = {Export Date: 29 December 2022},\nauthor = {Nir, T M and Fouche, J.-P. and Ananworanich, J and Ances, B M and Boban, J and Brew, B J and Chaganti, J R and Chang, L and Ching, C R K and Cysique, L A and Ernst, T and Faskowitz, J and Gupta, V and Harezlak, J and Heaps-Woodruff, J M and Hinkin, C H and Hoare, J and Joska, J A and Kallianpur, K J and Kuhn, T and Lam, H Y and Law, M and Lebrun-Fr{\\'{e}}nay, C and Levine, A J and Mondot, L and Nakamoto, B K and Navia, B A and Pennec, X and Porges, E C and Salminen, L E and Shikuma, C M and Surento, W and Thames, A D and Valcour, V and Vassallo, M and Woods, A J and Thompson, P M and Cohen, R A and Paul, R and Stein, D J and Jahanshad, N},\ndoi = {10.1001/jamanetworkopen.2020.31190},\nfile = {:Users/jacquelinebracher/Zotero/storage/LPK46P4J/Nir et al. - 2021 - Association of Immunosuppression and Viral Load Wi.pdf:pdf},\nnumber = {1},\ntitle = {{Association of Immunosuppression and Viral Load with Subcortical Brain Volume in an International Sample of People Living with HIV}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85100125045{\\&}doi=10.1001{\\%}2Fjamanetworkopen.2020.31190{\\&}partnerID=40{\\&}md5=33fb0fff32a40a126bc97d5a3716982f},\nvolume = {4},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n The clinical characterization of the adult patient with an anxiety or related disorder aimed at personalization of management.\n \n \n \n \n\n\n \n Stein, D. J; Craske, M. G; Rothbaum, B. O; Chamberlain, S. R; Fineberg, N. A; Choi, K. W; De Jonge, P.; Baldwin, D. S; and Maj, M.\n\n\n \n\n\n\n World Psychiatry, 20(3): 336–356. oct 2021.\n \n\n\n\n
\n\n\n\n \n \n \"ThePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{stein_clinical_2021,\nabstract = {The clinical construct of “anxiety neurosis” was broad and poorly defined, so that the delineation of specific anxiety disorders in the DSM‐III was an important advance. However, anxiety and related disorders are not only frequently comorbid, but each is also quite heterogeneous; thus diagnostic manuals provide only a first step towards formulating a management plan, and the development of additional decision support tools for the treatment of anxiety conditions is needed. This paper aims to describe systematically important domains that are relevant to the personalization of management of anxiety and related disorders in adults. For each domain, we summarize the available research evidence and review the relevant assessment instruments, paying special attention to their suitability for use in routine clinical practice. We emphasize areas where the available evidence allows the clinician to personalize the management of anxiety conditions, and we point out key unmet needs. Overall, the evidence suggests that we are becoming able to move from simply recommending that anxiety and related disorders be treated with selective serotonin reuptake inhibitors, cognitive‐behavioral therapy, or their combination, to a more complex approach which emphasizes that the clinician has a broadening array of management modalities available, and that the treatment of anxiety and related disorders can already be personalized in a number of important respects.},\nauthor = {Stein, Dan J and Craske, Michelle G and Rothbaum, Barbara O and Chamberlain, Samuel R and Fineberg, Naomi A and Choi, Karmel W and {De Jonge}, Peter and Baldwin, David S and Maj, Mario},\ndoi = {10.1002/wps.20919},\nfile = {:Users/jacquelinebracher/Zotero/storage/5LH4RGGF/Stein et al. - 2021 - The clinical characterization of the adult patient.pdf:pdf},\nissn = {1723-8617, 2051-5545},\njournal = {World Psychiatry},\nmonth = {oct},\nnumber = {3},\npages = {336--356},\ntitle = {{The clinical characterization of the adult patient with an anxiety or related disorder aimed at personalization of management}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1002/wps.20919},\nvolume = {20},\nyear = {2021}\n}\n
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\n The clinical construct of “anxiety neurosis” was broad and poorly defined, so that the delineation of specific anxiety disorders in the DSM‐III was an important advance. However, anxiety and related disorders are not only frequently comorbid, but each is also quite heterogeneous; thus diagnostic manuals provide only a first step towards formulating a management plan, and the development of additional decision support tools for the treatment of anxiety conditions is needed. This paper aims to describe systematically important domains that are relevant to the personalization of management of anxiety and related disorders in adults. For each domain, we summarize the available research evidence and review the relevant assessment instruments, paying special attention to their suitability for use in routine clinical practice. We emphasize areas where the available evidence allows the clinician to personalize the management of anxiety conditions, and we point out key unmet needs. Overall, the evidence suggests that we are becoming able to move from simply recommending that anxiety and related disorders be treated with selective serotonin reuptake inhibitors, cognitive‐behavioral therapy, or their combination, to a more complex approach which emphasizes that the clinician has a broadening array of management modalities available, and that the treatment of anxiety and related disorders can already be personalized in a number of important respects.\n
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\n \n\n \n \n \n \n \n \n Generalised \\Anxiety\\ \\Disorder\\ and \\Depression\\: \\Contemporary\\ \\Treatment\\ \\Approaches\\.\n \n \n \n \n\n\n \n Goodwin, G. M; and Stein, D. J\n\n\n \n\n\n\n Advances in Therapy, 38(S2): 45–51. sep 2021.\n \n\n\n\n
\n\n\n\n \n \n \"GeneralisedPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{goodwin_generalised_2021,\nauthor = {Goodwin, Guy M and Stein, Dan J},\ndoi = {10.1007/s12325-021-01859-8},\nfile = {:Users/jacquelinebracher/Zotero/storage/RZYM7CAV/Goodwin and Stein - 2021 - Generalised Anxiety Disorder and Depression Conte.pdf:pdf},\nissn = {0741-238X, 1865-8652},\njournal = {Advances in Therapy},\nmonth = {sep},\nnumber = {S2},\npages = {45--51},\nshorttitle = {Generalised {\\{}Anxiety{\\}} {\\{}Disorder{\\}} and {\\{}Depression{\\}}},\ntitle = {{Generalised {\\{}Anxiety{\\}} {\\{}Disorder{\\}} and {\\{}Depression{\\}}: {\\{}Contemporary{\\}} {\\{}Treatment{\\}} {\\{}Approaches{\\}}}},\nurl = {https://link.springer.com/10.1007/s12325-021-01859-8},\nvolume = {38},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Epigenome-wide meta-analysis of blood DNA methylation and its association with subcortical volumes: findings from the ENIGMA Epigenetics Working Group.\n \n \n \n \n\n\n \n Jia, T; Chu, C; Liu, Y; van Dongen, J; Papastergios, E; Armstrong, N J; Bastin, M E; Carrillo-Roa, T; den Braber, A; Harris, M; Jansen, R; Liu, J; Luciano, M; Ori, A P S; Roiz Santiañez, R; Ruggeri, B; Sarkisyan, D; Shin, J; Sungeun, K; Tordesillas Gutiérrez, D; van't Ent, D; Ames, D; Artiges, E; Bakalkin, G; Banaschewski, T; Bokde, A L W; Brodaty, H; Bromberg, U; Brouwer, R; Büchel, C; Burke Quinlan, E; Cahn, W; de Zubicaray, G I; Ehrlich, S; Ekström, T J; Flor, H; Fröhner, J H; Frouin, V; Garavan, H; Gowland, P; Heinz, A; Hoare, J; Ittermann, B; Jahanshad, N; Jiang, J; Kwok, J B; Martin, N G; Martinot, J.; Mather, K A; McMahon, K L; McRae, A F; Nees, F; Papadopoulos Orfanos, D; Paus, T; Poustka, L; Sämann, P G; Schofield, P R; Smolka, M N; Stein, D J; Strike, L T; Teeuw, J; Thalamuthu, A; Trollor, J; Walter, H; Wardlaw, J M; Wen, W; Whelan, R; Apostolova, L G; Binder, E B; Boomsma, D I; Calhoun, V; Crespo-Facorro, B; Deary, I J; Hulshoff Pol, H; Ophoff, R A; Pausova, Z; Sachdev, P S; Saykin, A; Wright, M J; Thompson, P M; Schumann, G; and Desrivières, S\n\n\n \n\n\n\n 2021.\n \n\n\n\n
\n\n\n\n \n \n \"Epigenome-widePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@misc{Jia2021,\nannote = {Export Date: 29 December 2022},\nauthor = {Jia, T and Chu, C and Liu, Y and van Dongen, J and Papastergios, E and Armstrong, N J and Bastin, M E and Carrillo-Roa, T and den Braber, A and Harris, M and Jansen, R and Liu, J and Luciano, M and Ori, A P S and {Roiz Santia{\\~{n}}ez}, R and Ruggeri, B and Sarkisyan, D and Shin, J and Sungeun, K and {Tordesillas Guti{\\'{e}}rrez}, D and van't Ent, D and Ames, D and Artiges, E and Bakalkin, G and Banaschewski, T and Bokde, A L W and Brodaty, H and Bromberg, U and Brouwer, R and B{\\"{u}}chel, C and {Burke Quinlan}, E and Cahn, W and de Zubicaray, G I and Ehrlich, S and Ekstr{\\"{o}}m, T J and Flor, H and Fr{\\"{o}}hner, J H and Frouin, V and Garavan, H and Gowland, P and Heinz, A and Hoare, J and Ittermann, B and Jahanshad, N and Jiang, J and Kwok, J B and Martin, N G and Martinot, J.-L. and Mather, K A and McMahon, K L and McRae, A F and Nees, F and {Papadopoulos Orfanos}, D and Paus, T and Poustka, L and S{\\"{a}}mann, P G and Schofield, P R and Smolka, M N and Stein, D J and Strike, L T and Teeuw, J and Thalamuthu, A and Trollor, J and Walter, H and Wardlaw, J M and Wen, W and Whelan, R and Apostolova, L G and Binder, E B and Boomsma, D I and Calhoun, V and Crespo-Facorro, B and Deary, I J and {Hulshoff Pol}, H and Ophoff, R A and Pausova, Z and Sachdev, P S and Saykin, A and Wright, M J and Thompson, P M and Schumann, G and Desrivi{\\`{e}}res, S},\ndoi = {10.1038/s41380-019-0605-z},\nfile = {:Users/jacquelinebracher/Zotero/storage/ZT6JS8PW/Jia et al. - 2021 - Epigenome-wide meta-analysis of blood DNA methylat.pdf:pdf},\nnumber = {8},\npages = {3884--3895},\ntitle = {{Epigenome-wide meta-analysis of blood DNA methylation and its association with subcortical volumes: findings from the ENIGMA Epigenetics Working Group}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85076442903{\\&}doi=10.1038{\\%}2Fs41380-019-0605-z{\\&}partnerID=40{\\&}md5=11dc5350d5b6c4aea6451f8f76d41909},\nvolume = {26},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n Molecular and electrophysiological features of spinocerebellar ataxia type seven in induced pluripotent stem cells.\n \n \n \n\n\n \n Burman, R.; Watson, L.; Smith, D.; Raimondo, J.; Ballo, R.; Scholefield, J.; Cowley, S.; Wood, M.; Kidson, S.; and Greenberg, L.\n\n\n \n\n\n\n PLoS ONE, 16(2 February). 2021.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n  \n \n 11 downloads\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{Burman2021,\nabstract = {Spinocerebellar ataxia type 7 (SCA7) is an inherited neurodegenerative disease caused by a polyglutamine repeat expansion in the ATXN7 gene. Patients with this disease suffer from a degeneration of their cerebellar Purkinje neurons and retinal photoreceptors that result in a progressive ataxia and loss of vision. As with many neurodegenerative diseases, studies of pathogenesis have been hindered by a lack of disease-relevant models. To this end, we have generated induced pluripotent stem cells (iPSCs) from a cohort of SCA7 patients in South Africa. First, we differentiated the SCA7 affected iPSCs into neurons which showed evidence of a transcriptional phenotype affecting components of STAGA (ATXN7 and KAT2A) and the heat shock protein pathway (DNAJA1 and HSP70). We then performed electrophysiology on the SCA7 iPSC-derived neurons and found that these cells show features of functional aberrations. Lastly, we were able to differentiate the SCA7 iPSCs into retinal photoreceptors that also showed similar transcriptional aberrations to the SCA7 neurons. Our findings give technical insights on how iPSC-derived neurons and photoreceptors can be derived from SCA7 patients and demonstrate that these cells express molecular and electrophysiological differences that may be indicative of impaired neuronal health. We hope that these findings will contribute towards the ongoing efforts to establish the cell-derived models of neurodegenerative diseases that are needed to develop patient-specific treatments.},\nauthor = {Burman, R.J. and Watson, L.M. and Smith, D.C. and Raimondo, J.V. and Ballo, R. and Scholefield, J. and Cowley, S.A. and Wood, M.J.A. and Kidson, S.H. and Greenberg, L.J.},\ndoi = {10.1371/journal.pone.0247434},\nfile = {:Users/jacquelinebracher/Zotero/storage/B3PHST7W/Burman et al. - 2021 - Molecular and electrophysiological features of spi.pdf:pdf},\njournal = {PLoS ONE},\nnumber = {2 February},\ntitle = {{Molecular and electrophysiological features of spinocerebellar ataxia type seven in induced pluripotent stem cells}},\nvolume = {16},\nyear = {2021}\n}\n
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\n Spinocerebellar ataxia type 7 (SCA7) is an inherited neurodegenerative disease caused by a polyglutamine repeat expansion in the ATXN7 gene. Patients with this disease suffer from a degeneration of their cerebellar Purkinje neurons and retinal photoreceptors that result in a progressive ataxia and loss of vision. As with many neurodegenerative diseases, studies of pathogenesis have been hindered by a lack of disease-relevant models. To this end, we have generated induced pluripotent stem cells (iPSCs) from a cohort of SCA7 patients in South Africa. First, we differentiated the SCA7 affected iPSCs into neurons which showed evidence of a transcriptional phenotype affecting components of STAGA (ATXN7 and KAT2A) and the heat shock protein pathway (DNAJA1 and HSP70). We then performed electrophysiology on the SCA7 iPSC-derived neurons and found that these cells show features of functional aberrations. Lastly, we were able to differentiate the SCA7 iPSCs into retinal photoreceptors that also showed similar transcriptional aberrations to the SCA7 neurons. Our findings give technical insights on how iPSC-derived neurons and photoreceptors can be derived from SCA7 patients and demonstrate that these cells express molecular and electrophysiological differences that may be indicative of impaired neuronal health. We hope that these findings will contribute towards the ongoing efforts to establish the cell-derived models of neurodegenerative diseases that are needed to develop patient-specific treatments.\n
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\n \n\n \n \n \n \n \n De novo variants in CACNA1E found in patients with intellectual disability, developmental regression and social cognition deficit but no seizures.\n \n \n \n\n\n \n Royer-Bertrand, B.; Jequier Gygax, M.; Cisarova, K.; Rosenfeld, J.; Bassetti, J.; Moldovan, O.; O'Heir, E.; Burrage, L.; Allen, J.; Emrick, L.; Donald, K.; and Superti-Furga, A.\n\n\n \n\n\n\n Molecular Autism, 12(1). 2021.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{Royer-Bertrand2021,\nabstract = {Background: De novo variants in the voltage-gated calcium channel subunit $\\alpha$1 E gene (CACNA1E) have been described as causative of epileptic encephalopathy with contractures, macrocephaly and dyskinesias. Methods: Following the observation of an index patient with developmental delay and autism spectrum disorder (ASD) without seizures who had a de novo deleterious CACNA1E variant, we screened GeneMatcher for other individuals with CACNA1E variants and neurodevelopmental phenotypes without epilepsy. The spectrum of pathogenic CACNA1E variants was compared to the mutational landscape of variants in the gnomAD control population database. Results: We identified seven unrelated individuals with intellectual disability, developmental regression and ASD-like behavioral profile, and notably without epilepsy, who had de novo heterozygous putatively pathogenic variants in CACNA1E. Age of onset of clinical manifestation, presence or absence of regression and degree of severity were variable, and no clear-cut genotype–phenotype association could be recognized. The analysis of disease-associated variants and their comparison to benign variants from the control population allowed for the identification of regions in the CACNA1E protein that seem to be intolerant to substitutions and thus more likely to harbor pathogenic variants. As in a few reported cases with CACNA1E variants and epilepsy, one patient showed a positive clinical behavioral response to topiramate, a specific calcium channel modulator. Limitations: The significance of our study is limited by the absence of functional experiments of the effect of identified variants, the small sample size and the lack of systematic ASD assessment in all participants. Moreover, topiramate was given to one patient only and for a short period of time. Conclusions: Our results indicate that CACNA1E variants may result in neurodevelopmental disorders without epilepsy and expand the mutational and phenotypic spectrum of this gene. CACNA1E deserves to be included in gene panels for non-specific developmental disorders, including ASD, and not limited to patients with seizures, to improve diagnostic recognition and explore the possible efficacy of topiramate.},\nauthor = {Royer-Bertrand, B. and {Jequier Gygax}, M. and Cisarova, K. and Rosenfeld, J.A. and Bassetti, J.A. and Moldovan, O. and O'Heir, E. and Burrage, L.C. and Allen, J. and Emrick, L.T. and Donald, K.A. and Superti-Furga, A.},\ndoi = {10.1186/s13229-021-00473-3},\nfile = {:Users/jacquelinebracher/Zotero/storage/A7EUZ6R6/Royer-Bertrand et al. - 2021 - De novo variants in CACNA1E found in patients with.pdf:pdf},\njournal = {Molecular Autism},\nnumber = {1},\ntitle = {{De novo variants in CACNA1E found in patients with intellectual disability, developmental regression and social cognition deficit but no seizures}},\nvolume = {12},\nyear = {2021}\n}\n
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\n Background: De novo variants in the voltage-gated calcium channel subunit $α$1 E gene (CACNA1E) have been described as causative of epileptic encephalopathy with contractures, macrocephaly and dyskinesias. Methods: Following the observation of an index patient with developmental delay and autism spectrum disorder (ASD) without seizures who had a de novo deleterious CACNA1E variant, we screened GeneMatcher for other individuals with CACNA1E variants and neurodevelopmental phenotypes without epilepsy. The spectrum of pathogenic CACNA1E variants was compared to the mutational landscape of variants in the gnomAD control population database. Results: We identified seven unrelated individuals with intellectual disability, developmental regression and ASD-like behavioral profile, and notably without epilepsy, who had de novo heterozygous putatively pathogenic variants in CACNA1E. Age of onset of clinical manifestation, presence or absence of regression and degree of severity were variable, and no clear-cut genotype–phenotype association could be recognized. The analysis of disease-associated variants and their comparison to benign variants from the control population allowed for the identification of regions in the CACNA1E protein that seem to be intolerant to substitutions and thus more likely to harbor pathogenic variants. As in a few reported cases with CACNA1E variants and epilepsy, one patient showed a positive clinical behavioral response to topiramate, a specific calcium channel modulator. Limitations: The significance of our study is limited by the absence of functional experiments of the effect of identified variants, the small sample size and the lack of systematic ASD assessment in all participants. Moreover, topiramate was given to one patient only and for a short period of time. Conclusions: Our results indicate that CACNA1E variants may result in neurodevelopmental disorders without epilepsy and expand the mutational and phenotypic spectrum of this gene. CACNA1E deserves to be included in gene panels for non-specific developmental disorders, including ASD, and not limited to patients with seizures, to improve diagnostic recognition and explore the possible efficacy of topiramate.\n
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\n \n\n \n \n \n \n \n \n Prevalence and clinical correlates of substance use disorders in \\South\\ \\African\\ \\Xhosa\\ patients with schizophrenia.\n \n \n \n \n\n\n \n Temmingh, H.; Susser, E.; Mall, S.; Campbell, M.; Sibeko, G.; and Stein, D. J\n\n\n \n\n\n\n Social Psychiatry and Psychiatric Epidemiology, 56(4): 695–706. apr 2021.\n \n\n\n\n
\n\n\n\n \n \n \"PrevalencePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{temmingh_prevalence_2021,\nauthor = {Temmingh, Henk and Susser, Ezra and Mall, Sumaya and Campbell, Megan and Sibeko, Goodman and Stein, Dan J},\ndoi = {10.1007/s00127-020-01942-5},\nfile = {:Users/jacquelinebracher/Zotero/storage/UC955C3Z/Temmingh et al. - 2021 - Prevalence and clinical correlates of substance us.pdf:pdf},\nissn = {0933-7954, 1433-9285},\njournal = {Social Psychiatry and Psychiatric Epidemiology},\nmonth = {apr},\nnumber = {4},\npages = {695--706},\ntitle = {{Prevalence and clinical correlates of substance use disorders in {\\{}South{\\}} {\\{}African{\\}} {\\{}Xhosa{\\}} patients with schizophrenia}},\nurl = {https://link.springer.com/10.1007/s00127-020-01942-5},\nvolume = {56},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Association between maternal depression during pregnancy and newborn \\DNA\\ methylation.\n \n \n \n \n\n\n \n Drzymalla, E.; Gladish, N.; Koen, N.; Epstein, M. P; Kobor, M. S; Zar, H. J; Stein, D. J; and Hüls, A.\n\n\n \n\n\n\n Translational Psychiatry, 11(1): 572. nov 2021.\n \n\n\n\n
\n\n\n\n \n \n \"AssociationPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{drzymalla_association_2021,\nabstract = {Abstract\n\nAround 15–65{\\%} of women globally experience depression during pregnancy, prevalence being particularly high in low- and middle-income countries. Prenatal depression has been associated with adverse birth and child development outcomes. DNA methylation (DNAm) may aid in understanding this association. In this project, we analyzed associations between prenatal depression and DNAm from cord blood from participants of the South African Drakenstein Child Health Study. We examined DNAm in an epigenome-wide association study (EWAS) of 248 mother-child pairs. DNAm was measured using the Infinium MethylationEPIC (\nN\n= 145) and the Infinium HumanMethylation450 (\nN\n= 103) arrays. Prenatal depression scores, obtained with the Edinburgh Postnatal Depression Scale (EPDS) and the Beck Depression Inventory-II (BDI-II), were analyzed as continuous and dichotomized variables. We used linear robust models to estimate associations between depression and newborn DNAm, adjusted for measured (smoking status, household income, sex, preterm birth, cell type proportions, and genetic principal components) and unmeasured confounding using Cate and Bacon algorithms. Bonferroni correction was used to adjust for multiple testing. DMRcate and dmrff were used to test for differentially methylated regions (DMRs). Differential DNAm was significantly associated with BDI-II variables, in cg16473797 ($\\Delta$ beta = −1.10E-02,\np\n= 6.87E-08), cg23262030 ($\\Delta$ beta per BDI-II total IQR = 1.47E-03,\np\n= 1.18E-07), and cg04859497 ($\\Delta$ beta = −6.42E-02,\np\n= 1.06E-09). Five DMRs were associated with at least two depression variables. Further studies are needed to replicate these findings and investigate their biological impact.},\nauthor = {Drzymalla, Emily and Gladish, Nicole and Koen, Nastassja and Epstein, Michael P and Kobor, Michael S and Zar, Heather J and Stein, Dan J and H{\\"{u}}ls, Anke},\ndoi = {10.1038/s41398-021-01697-w},\nfile = {:Users/jacquelinebracher/Zotero/storage/CYNNXSU5/Drzymalla et al. - 2021 - Association between maternal depression during pre.pdf:pdf},\nissn = {2158-3188},\njournal = {Translational Psychiatry},\nmonth = {nov},\nnumber = {1},\npages = {572},\ntitle = {{Association between maternal depression during pregnancy and newborn {\\{}DNA{\\}} methylation}},\nurl = {https://www.nature.com/articles/s41398-021-01697-w},\nvolume = {11},\nyear = {2021}\n}\n
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\n Abstract Around 15–65% of women globally experience depression during pregnancy, prevalence being particularly high in low- and middle-income countries. Prenatal depression has been associated with adverse birth and child development outcomes. DNA methylation (DNAm) may aid in understanding this association. In this project, we analyzed associations between prenatal depression and DNAm from cord blood from participants of the South African Drakenstein Child Health Study. We examined DNAm in an epigenome-wide association study (EWAS) of 248 mother-child pairs. DNAm was measured using the Infinium MethylationEPIC ( N = 145) and the Infinium HumanMethylation450 ( N = 103) arrays. Prenatal depression scores, obtained with the Edinburgh Postnatal Depression Scale (EPDS) and the Beck Depression Inventory-II (BDI-II), were analyzed as continuous and dichotomized variables. We used linear robust models to estimate associations between depression and newborn DNAm, adjusted for measured (smoking status, household income, sex, preterm birth, cell type proportions, and genetic principal components) and unmeasured confounding using Cate and Bacon algorithms. Bonferroni correction was used to adjust for multiple testing. DMRcate and dmrff were used to test for differentially methylated regions (DMRs). Differential DNAm was significantly associated with BDI-II variables, in cg16473797 ($Δ$ beta = −1.10E-02, p = 6.87E-08), cg23262030 ($Δ$ beta per BDI-II total IQR = 1.47E-03, p = 1.18E-07), and cg04859497 ($Δ$ beta = −6.42E-02, p = 1.06E-09). Five DMRs were associated with at least two depression variables. Further studies are needed to replicate these findings and investigate their biological impact.\n
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\n \n\n \n \n \n \n \n \n A global collaboration to study intimate partner violence-related head trauma: \\The\\ \\ENIGMA\\ consortium \\IPV\\ working group.\n \n \n \n \n\n\n \n Esopenko, C.; Meyer, J.; Wilde, E. A; Marshall, A. D; Tate, D. F; Lin, A. P; Koerte, I. K; Werner, K. B; Dennis, E. L; Ware, A. L; De Souza, N. L; Menefee, D. S; Dams-O'Connor, K.; Stein, D. J; Bigler, E. D; Shenton, M. E; Chiou, K. S; Postmus, J. L; Monahan, K.; Eagan-Johnson, B.; Van Donkelaar, P.; Merkley, T. L; Velez, C.; Hodges, C. B; Lindsey, H. M; Johnson, P.; Irimia, A.; Spruiell, M.; Bennett, E. R; Bridwell, A.; Zieman, G.; and Hillary, F. G\n\n\n \n\n\n\n Brain Imaging and Behavior, 15(2): 475–503. apr 2021.\n \n\n\n\n
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@article{esopenko_global_2021,\nauthor = {Esopenko, Carrie and Meyer, Jessica and Wilde, Elisabeth A and Marshall, Amy D and Tate, David F and Lin, Alexander P and Koerte, Inga K and Werner, Kimberly B and Dennis, Emily L and Ware, Ashley L and {De Souza}, Nicola L and Menefee, Deleene S and Dams-O'Connor, Kristen and Stein, Dan J and Bigler, Erin D and Shenton, Martha E and Chiou, Kathy S and Postmus, Judy L and Monahan, Kathleen and Eagan-Johnson, Brenda and {Van Donkelaar}, Paul and Merkley, Tricia L and Velez, Carmen and Hodges, Cooper B and Lindsey, Hannah M and Johnson, Paula and Irimia, Andrei and Spruiell, Matthew and Bennett, Esther R and Bridwell, Ashley and Zieman, Glynnis and Hillary, Frank G},\ndoi = {10.1007/s11682-020-00417-0},\nfile = {:Users/jacquelinebracher/Zotero/storage/5AI7RSAY/Esopenko et al. - 2021 - A global collaboration to study intimate partner v.pdf:pdf},\nissn = {1931-7557, 1931-7565},\njournal = {Brain Imaging and Behavior},\nmonth = {apr},\nnumber = {2},\npages = {475--503},\nshorttitle = {A global collaboration to study intimate partner v},\ntitle = {{A global collaboration to study intimate partner violence-related head trauma: {\\{}The{\\}} {\\{}ENIGMA{\\}} consortium {\\{}IPV{\\}} working group}},\nurl = {http://link.springer.com/10.1007/s11682-020-00417-0},\nvolume = {15},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n Maternal emotional and physical intimate partner violence and early child development: Investigating mediators in a cross-sectional study in a South African birth cohort.\n \n \n \n\n\n \n Barnett, W.; Halligan, S.; Wedderburn, C.; MacGinty, R.; Hoffman, N.; Zar, H.; Stein, D.; and Donald, K.\n\n\n \n\n\n\n BMJ Open, 11(10). 2021.\n \n\n\n\n
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@article{Barnett2021,\nabstract = {This study investigated associations between recent maternal intimate partner violence (IPV) (emotional, physical and sexual) and child development at 2 years as well as whether maternal depression or alcohol use mediated these relationships. Cross-sectional study nested in a South African birth cohort. Two primary care clinics in Paarl, South Africa. 626 mother–child pairs; inclusion criteria for maternal antenatal enrolment were clinic attendance and remaining in the study area for at least 1 year; women were excluded if a minor. Child cognitive, language and motor development composite scores. These were assessed using the Bayley Scales of Infant and Toddler Development, third edition. Emotional IPV was associated with lower cognitive ($\\beta$=−0.32; 95{\\%} CI −0.60 to –0.04), language ($\\beta$=−0.36; 95{\\%} CI −0.69 to –0.01) or motor composite scores ($\\beta$=−0.58; 95{\\%} CI −0.95 to –0.20) in children at 2 years of age. Physical IPV was associated with lower motor scores ($\\beta$=−0.42; 95{\\%} CI −0.75 to –0.09) at 2 years. Sexual IPV was unrelated to developmental outcomes, possibly due to low prevalence. Neither recent maternal depression nor alcohol use were shown to mediate the relationship between IPV and developmental outcomes. Interventions to reduce maternal physical and emotional IPV and early-life interventions for infants and toddlers are needed to promote optimal child development.},\nauthor = {Barnett, W. and Halligan, S.L. and Wedderburn, C. and MacGinty, R. and Hoffman, N. and Zar, H.J. and Stein, D. and Donald, K.},\ndoi = {10.1136/bmjopen-2020-046829},\nfile = {:Users/jacquelinebracher/Zotero/storage/CHI5EQYY/Barnett et al. - 2021 - Maternal emotional and physical intimate partner v.pdf:pdf},\njournal = {BMJ Open},\nnumber = {10},\ntitle = {{Maternal emotional and physical intimate partner violence and early child development: Investigating mediators in a cross-sectional study in a South African birth cohort}},\nvolume = {11},\nyear = {2021}\n}\n
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\n This study investigated associations between recent maternal intimate partner violence (IPV) (emotional, physical and sexual) and child development at 2 years as well as whether maternal depression or alcohol use mediated these relationships. Cross-sectional study nested in a South African birth cohort. Two primary care clinics in Paarl, South Africa. 626 mother–child pairs; inclusion criteria for maternal antenatal enrolment were clinic attendance and remaining in the study area for at least 1 year; women were excluded if a minor. Child cognitive, language and motor development composite scores. These were assessed using the Bayley Scales of Infant and Toddler Development, third edition. Emotional IPV was associated with lower cognitive ($β$=−0.32; 95% CI −0.60 to –0.04), language ($β$=−0.36; 95% CI −0.69 to –0.01) or motor composite scores ($β$=−0.58; 95% CI −0.95 to –0.20) in children at 2 years of age. Physical IPV was associated with lower motor scores ($β$=−0.42; 95% CI −0.75 to –0.09) at 2 years. Sexual IPV was unrelated to developmental outcomes, possibly due to low prevalence. Neither recent maternal depression nor alcohol use were shown to mediate the relationship between IPV and developmental outcomes. Interventions to reduce maternal physical and emotional IPV and early-life interventions for infants and toddlers are needed to promote optimal child development.\n
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\n \n\n \n \n \n \n \n \n A review of systems biology research of anxiety disorders.\n \n \n \n \n\n\n \n Mufford, M. S; Van Der Meer, D.; Andreassen, O. A; Ramesar, R.; Stein, D. J; and Dalvie, S.\n\n\n \n\n\n\n Brazilian Journal of Psychiatry, 43(4): 414–423. aug 2021.\n \n\n\n\n
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@article{mufford_review_2021,\nauthor = {Mufford, Mary S and {Van Der Meer}, Dennis and Andreassen, Ole A and Ramesar, Raj and Stein, Dan J and Dalvie, Shareefa},\ndoi = {10.1590/1516-4446-2020-1090},\nfile = {:Users/jacquelinebracher/Zotero/storage/GSVH4BRI/Mufford et al. - 2021 - A review of systems biology research of anxiety di.pdf:pdf},\nissn = {1809-452X, 1516-4446},\njournal = {Brazilian Journal of Psychiatry},\nmonth = {aug},\nnumber = {4},\npages = {414--423},\ntitle = {{A review of systems biology research of anxiety disorders}},\nurl = {http://www.scielo.br/scielo.php?script=sci{\\_}arttext{\\&}pid=S1516-44462021000400414{\\&}tlng=en},\nvolume = {43},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Hunger as a driver of depressive symptoms: \\Optimising\\ responses to mental health aspects of the \\COVID\\-19 pandemic.\n \n \n \n \n\n\n \n Hunt, X; Stein, D J; Spaull, N; and Tomlinson, M\n\n\n \n\n\n\n South African Medical Journal, 111(7): 604. may 2021.\n \n\n\n\n
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@article{hunt_hunger_2021,\nauthor = {Hunt, X and Stein, D J and Spaull, N and Tomlinson, M},\ndoi = {10.7196/SAMJ.2021.v111i7.15754},\nfile = {:Users/jacquelinebracher/Zotero/storage/8SGLZV57/Hunt et al. - 2021 - Hunger as a driver of depressive symptoms Optimis.pdf:pdf},\nissn = {2078-5135, 0256-9574},\njournal = {South African Medical Journal},\nmonth = {may},\nnumber = {7},\npages = {604},\nshorttitle = {Hunger as a driver of depressive symptoms},\ntitle = {{Hunger as a driver of depressive symptoms: {\\{}Optimising{\\}} responses to mental health aspects of the {\\{}COVID{\\}}-19 pandemic}},\nurl = {http://www.samj.org.za/index.php/samj/article/view/13298},\nvolume = {111},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n A qualitative study exploring caregivers' experiences, perspectives, and expectations for precision medicine in epilepsy in \\South\\ \\Africa\\.\n \n \n \n \n\n\n \n Muchada, I. F.; Wilmshurst, J. M; Laing, N.; Haf Davies, E.; and Fieggen, K.\n\n\n \n\n\n\n Epilepsy & Behavior, 117: 107873. apr 2021.\n \n\n\n\n
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@article{muchada_qualitative_2021,\nauthor = {Muchada, Irene Farisai and Wilmshurst, Jo M and Laing, Nakita and {Haf Davies}, Elin and Fieggen, Karen},\ndoi = {10.1016/j.yebeh.2021.107873},\nfile = {:Users/jacquelinebracher/Zotero/storage/TXYVKV48/Muchada et al. - 2021 - A qualitative study exploring caregivers' experien.pdf:pdf},\nissn = {15255050},\njournal = {Epilepsy {\\&} Behavior},\nmonth = {apr},\npages = {107873},\ntitle = {{A qualitative study exploring caregivers' experiences, perspectives, and expectations for precision medicine in epilepsy in {\\{}South{\\}} {\\{}Africa{\\}}}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S1525505021001074},\nvolume = {117},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Daily activities, participation, satisfaction, and functional mobility of adults with cerebral palsy more than 25 years after selective dorsal rhizotomy: a long-term follow-up during adulthood.\n \n \n \n \n\n\n \n Veerbeek, B. E; Lamberts, R. P; Fieggen, A G.; Verkoeijen, P. P J L; and Langerak, N. G\n\n\n \n\n\n\n Disability and Rehabilitation, 43(15): 2191–2199. jul 2021.\n \n\n\n\n
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@article{veerbeek_daily_2021,\nauthor = {Veerbeek, Berendina E and Lamberts, Robert P and Fieggen, A Graham and Verkoeijen, Peter P J L and Langerak, Nelleke G},\ndoi = {10.1080/09638288.2019.1695001},\nissn = {0963-8288, 1464-5165},\njournal = {Disability and Rehabilitation},\nmonth = {jul},\nnumber = {15},\npages = {2191--2199},\nshorttitle = {Daily activities, participation, satisfaction, and},\ntitle = {{Daily activities, participation, satisfaction, and functional mobility of adults with cerebral palsy more than 25 years after selective dorsal rhizotomy: a long-term follow-up during adulthood}},\nurl = {https://www.tandfonline.com/doi/full/10.1080/09638288.2019.1695001},\nvolume = {43},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Correction: \\Brain\\ structural abnormalities in obesity: relation to age, genetic risk, and common psychiatric disorders.\n \n \n \n \n\n\n \n Opel, N.; Thalamuthu, A.; Milaneschi, Y.; Grotegerd, D.; Flint, C.; Leenings, R.; Goltermann, J.; Richter, M.; Hahn, T.; Woditsch, G.; Berger, K.; Hermesdorf, M.; McIntosh, A.; Whalley, H. C; Harris, M. A; MacMaster, F. P; Walter, H.; Veer, I. M; Frodl, T.; Carballedo, A.; Krug, A.; Nenadic, I.; Kircher, T.; Aleman, A.; Groenewold, N. A; Stein, D. J; Soares, J. C; Zunta-Soares, G. B; Mwangi, B.; Wu, M.; Walter, M.; Li, M.; Harrison, B. J; Davey, C. G; Cullen, K. R; Klimes-Dougan, B.; Mueller, B. A; Sämann, P. G; Penninx, B.; Nawijn, L.; Veltman, D. J; Aftanas, L.; Brak, I. V; Filimonova, E. A; Osipov, E. A; Reneman, L.; Schrantee, A.; Grabe, H. J; Van Der Auwera, S.; Wittfeld, K.; Hosten, N.; Völzke, H.; Sim, K.; Gotlib, I. H; Sacchet, M. D; Lagopoulos, J.; Hatton, S. N; Hickie, I.; Pozzi, E.; Thompson, P. M; Jahanshad, N.; Schmaal, L.; Baune, B. T; and Dannlowski, U.\n\n\n \n\n\n\n Molecular Psychiatry, 26(12): 7854. dec 2021.\n \n\n\n\n
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@article{opel_correction_2021,\nauthor = {Opel, Nils and Thalamuthu, Anbupalam and Milaneschi, Yuri and Grotegerd, Dominik and Flint, Claas and Leenings, Ramona and Goltermann, Janik and Richter, Maike and Hahn, Tim and Woditsch, Georg and Berger, Klaus and Hermesdorf, Marco and McIntosh, Andrew and Whalley, Heather C and Harris, Mathew A and MacMaster, Frank P and Walter, Henrik and Veer, Ilya M and Frodl, Thomas and Carballedo, Angela and Krug, Axel and Nenadic, Igor and Kircher, Tilo and Aleman, Andre and Groenewold, Nynke A and Stein, Dan J and Soares, Jair C and Zunta-Soares, Giovana B and Mwangi, Benson and Wu, Mon-Ju and Walter, Martin and Li, Meng and Harrison, Ben J and Davey, Christopher G and Cullen, Kathryn R and Klimes-Dougan, Bonnie and Mueller, Bryon A and S{\\"{a}}mann, Philipp G and Penninx, Brenda and Nawijn, Laura and Veltman, Dick J and Aftanas, Lyubomir and Brak, Ivan V and Filimonova, Elena A and Osipov, Evgeniy A and Reneman, Liesbeth and Schrantee, Anouk and Grabe, Hans J and {Van Der Auwera}, Sandra and Wittfeld, Katharina and Hosten, Norbert and V{\\"{o}}lzke, Henry and Sim, Kang and Gotlib, Ian H and Sacchet, Matthew D and Lagopoulos, Jim and Hatton, Sean N and Hickie, Ian and Pozzi, Elena and Thompson, Paul M and Jahanshad, Neda and Schmaal, Lianne and Baune, Bernhard T and Dannlowski, Udo},\ndoi = {10.1038/s41380-021-01191-1},\nfile = {:Users/jacquelinebracher/Zotero/storage/NY4FS7VA/Opel et al. - 2021 - Correction Brain structural abnormalities in obes.pdf:pdf},\nissn = {1359-4184, 1476-5578},\njournal = {Molecular Psychiatry},\nmonth = {dec},\nnumber = {12},\npages = {7854},\nshorttitle = {Correction},\ntitle = {{Correction: {\\{}Brain{\\}} structural abnormalities in obesity: relation to age, genetic risk, and common psychiatric disorders}},\nurl = {https://www.nature.com/articles/s41380-021-01191-1},\nvolume = {26},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Multivariate approach for longitudinal analysis of brain metabolite levels from ages 5-11 years in children with perinatal \\HIV\\ infection.\n \n \n \n \n\n\n \n Van Biljon, N.; Robertson, F.; Holmes, M.; Cotton, M. F; Laughton, B.; Van Der Kouwe, A.; Meintjes, E.; and Little, F.\n\n\n \n\n\n\n NeuroImage, 237: 118101. aug 2021.\n \n\n\n\n
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@article{van_biljon_multivariate_2021,\nauthor = {{Van Biljon}, No{\\"{e}}lle and Robertson, Frances and Holmes, Martha and Cotton, Mark F and Laughton, Barbara and {Van Der Kouwe}, Andre and Meintjes, Ernesta and Little, Francesca},\ndoi = {10.1016/j.neuroimage.2021.118101},\nfile = {:Users/jacquelinebracher/Zotero/storage/W9SIKJGE/Van Biljon et al. - 2021 - Multivariate approach for longitudinal analysis of.pdf:pdf},\nissn = {10538119},\njournal = {NeuroImage},\nmonth = {aug},\npages = {118101},\ntitle = {{Multivariate approach for longitudinal analysis of brain metabolite levels from ages 5-11 years in children with perinatal {\\{}HIV{\\}} infection}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S1053811921003785},\nvolume = {237},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Repeats expansions in \\ATXN2\\, \\NOP56\\, \\NIPA1\\ and \\ATXN1\\ are not associated with \\ALS\\ in \\Africans\\.\n \n \n \n \n\n\n \n Nel, M.; Mavundla, T.; Gultig, K.; Botha, G.; Mulder, N.; Benatar, M.; Wuu, J.; Cooley, A.; Myers, J.; Rampersaud, E.; Wu, G.; and Heckmann, J. M\n\n\n \n\n\n\n IBRO Neuroscience Reports, 10: 130–135. jun 2021.\n \n\n\n\n
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@article{nel_repeats_2021,\nauthor = {Nel, Melissa and Mavundla, Thandeka and Gultig, Kayleigh and Botha, Gerrit and Mulder, Nicola and Benatar, Michael and Wuu, Joanne and Cooley, Anne and Myers, Jason and Rampersaud, Evadnie and Wu, Gang and Heckmann, Jeannine M},\ndoi = {10.1016/j.ibneur.2021.02.002},\nfile = {:Users/jacquelinebracher/Zotero/storage/V37FWXFW/Nel et al. - 2021 - Repeats expansions in ATXN2, NOP56, NIPA1 and ATXN.pdf:pdf},\nissn = {26672421},\njournal = {IBRO Neuroscience Reports},\nmonth = {jun},\npages = {130--135},\ntitle = {{Repeats expansions in {\\{}ATXN2{\\}}, {\\{}NOP56{\\}}, {\\{}NIPA1{\\}} and {\\{}ATXN1{\\}} are not associated with {\\{}ALS{\\}} in {\\{}Africans{\\}}}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S2667242121000117},\nvolume = {10},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Précis of \\The\\ \\Hidden\\ \\Spring\\: \\A\\ \\Journey\\ to the \\Source\\ of \\Consciousness\\.\n \n \n \n \n\n\n \n Solms, M.\n\n\n \n\n\n\n Journal of Consciousness Studies, 28(11): 153–166. nov 2021.\n \n\n\n\n
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@article{solms_precis_2021,\nauthor = {Solms, Mark},\ndoi = {10.53765/20512201.28.11.153},\nissn = {1355-8250},\njournal = {Journal of Consciousness Studies},\nmonth = {nov},\nnumber = {11},\npages = {153--166},\nshorttitle = {Pr{\\'{e}}cis of {\\{}The{\\}} {\\{}Hidden{\\}} {\\{}Spring{\\}}},\ntitle = {{Pr{\\'{e}}cis of {\\{}The{\\}} {\\{}Hidden{\\}} {\\{}Spring{\\}}: {\\{}A{\\}} {\\{}Journey{\\}} to the {\\{}Source{\\}} of {\\{}Consciousness{\\}}}},\nurl = {https://www.ingentaconnect.com/content/10.53765/20512201.28.11.153},\nvolume = {28},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Maternal psychosocial risk factors and child gestational epigenetic age in a South African birth cohort study.\n \n \n \n \n\n\n \n Koen, N; Jones, M J; Nhapi, R T; Lake, M T; Donald, K A; Barnett, W; Hoffman, N; MacIsaac, J L; Morin, A M; Lin, D T S; Kobor, M S; Koenen, K C; Zar, H J; and Stein, D J\n\n\n \n\n\n\n 2021.\n \n\n\n\n
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@misc{Koen2021,\nannote = {Export Date: 29 December 2022},\nauthor = {Koen, N and Jones, M J and Nhapi, R T and Lake, M T and Donald, K A and Barnett, W and Hoffman, N and MacIsaac, J L and Morin, A M and Lin, D T S and Kobor, M S and Koenen, K C and Zar, H J and Stein, D J},\ndoi = {10.1038/s41398-021-01434-3},\nfile = {:Users/jacquelinebracher/Zotero/storage/BWBZR6LJ/Koen et al. - 2021 - Maternal psychosocial risk factors and child gesta.pdf:pdf},\nnumber = {1},\ntitle = {{Maternal psychosocial risk factors and child gestational epigenetic age in a South African birth cohort study}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85109183461{\\&}doi=10.1038{\\%}2Fs41398-021-01434-3{\\&}partnerID=40{\\&}md5=f3f3d6b2ae875fa4c0990d12082be94f},\nvolume = {11},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Toward a neurocircuit-based taxonomy to guide treatment of obsessive–compulsive disorder.\n \n \n \n \n\n\n \n Shephard, E.; Stern, E. R; Van Den Heuvel, O. A; Costa, D. L C; Batistuzzo, M. C; Godoy, P. B G; Lopes, A. C; Brunoni, A. R; Hoexter, M. Q; Shavitt, R. G; Reddy, Y C J.; Lochner, C.; Stein, D. J; Simpson, H B.; and Miguel, E. C\n\n\n \n\n\n\n Molecular Psychiatry, 26(9): 4583–4604. sep 2021.\n \n\n\n\n
\n\n\n\n \n \n \"TowardPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{shephard_toward_2021,\nauthor = {Shephard, Elizabeth and Stern, Emily R and {Van Den Heuvel}, Odile A and Costa, Daniel L C and Batistuzzo, Marcelo C and Godoy, Priscilla B G and Lopes, Antonio C and Brunoni, Andre R and Hoexter, Marcelo Q and Shavitt, Roseli G and Reddy, Y C Janardhan and Lochner, Christine and Stein, Dan J and Simpson, H Blair and Miguel, Euripedes C},\ndoi = {10.1038/s41380-020-01007-8},\nfile = {:Users/jacquelinebracher/Zotero/storage/XPURASKW/Shephard et al. - 2021 - Toward a neurocircuit-based taxonomy to guide trea.pdf:pdf},\nissn = {1359-4184, 1476-5578},\njournal = {Molecular Psychiatry},\nmonth = {sep},\nnumber = {9},\npages = {4583--4604},\ntitle = {{Toward a neurocircuit-based taxonomy to guide treatment of obsessive–compulsive disorder}},\nurl = {https://www.nature.com/articles/s41380-020-01007-8},\nvolume = {26},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n What is a mental disorder? \\An\\ exemplar-focused approach.\n \n \n \n \n\n\n \n Stein, D. J; Palk, A. C; and Kendler, K. S\n\n\n \n\n\n\n Psychological Medicine, 51(6): 894–901. apr 2021.\n \n\n\n\n
\n\n\n\n \n \n \"WhatPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{stein_what_2021,\nabstract = {Abstract\n\nThe question of ‘what is a mental disorder?' is central to the philosophy of psychiatry, and has crucial practical implications for psychiatric nosology. Rather than approaching the problem in terms of abstractions, we review a series of exemplars – real-world examples of problematic cases that emerged during work on and immediately after DSM-5, with the aim of developing practical guidelines for addressing future proposals. We consider cases where (1) there is harm but no clear dysfunction, (2) there is dysfunction but no clear harm, and (3) there is possible dysfunction and/or harm, but this is controversial for various reasons. We found no specific criteria to determine whether future proposals for new entities should be accepted or rejected; any such proposal will need to be assessed on its particular merits, using practical judgment. Nevertheless, several suggestions for the field emerged. First, while harm is useful for defining mental disorder, some proposed entities may require careful consideration of individual\nv.\nsocietal harm, as well as of societal accommodation. Second, while dysfunction is useful for defining mental disorder, the field would benefit from more sharply defined indicators of dysfunction. Third, it would be useful to incorporate evidence of diagnostic validity and clinical utility into the definition of mental disorder, and to further clarify the type and extent of data needed to support such judgments.},\nauthor = {Stein, Dan J and Palk, Andrea C and Kendler, Kenneth S},\ndoi = {10.1017/S0033291721001185},\nfile = {:Users/jacquelinebracher/Zotero/storage/YVGAVVUF/Stein et al. - 2021 - What is a mental disorder An exemplar-focused app.pdf:pdf},\nissn = {0033-2917, 1469-8978},\njournal = {Psychological Medicine},\nmonth = {apr},\nnumber = {6},\npages = {894--901},\nshorttitle = {What is a mental disorder?},\ntitle = {{What is a mental disorder? {\\{}An{\\}} exemplar-focused approach}},\nurl = {https://www.cambridge.org/core/product/identifier/S0033291721001185/type/journal{\\_}article},\nvolume = {51},\nyear = {2021}\n}\n
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\n Abstract The question of ‘what is a mental disorder?' is central to the philosophy of psychiatry, and has crucial practical implications for psychiatric nosology. Rather than approaching the problem in terms of abstractions, we review a series of exemplars – real-world examples of problematic cases that emerged during work on and immediately after DSM-5, with the aim of developing practical guidelines for addressing future proposals. We consider cases where (1) there is harm but no clear dysfunction, (2) there is dysfunction but no clear harm, and (3) there is possible dysfunction and/or harm, but this is controversial for various reasons. We found no specific criteria to determine whether future proposals for new entities should be accepted or rejected; any such proposal will need to be assessed on its particular merits, using practical judgment. Nevertheless, several suggestions for the field emerged. First, while harm is useful for defining mental disorder, some proposed entities may require careful consideration of individual v. societal harm, as well as of societal accommodation. Second, while dysfunction is useful for defining mental disorder, the field would benefit from more sharply defined indicators of dysfunction. Third, it would be useful to incorporate evidence of diagnostic validity and clinical utility into the definition of mental disorder, and to further clarify the type and extent of data needed to support such judgments.\n
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\n \n\n \n \n \n \n \n Evaluating Community Engagement Strategies to Manage Stigma in Two African Genomics Studies Involving People Living with Schizophrenia or Rheumatic Heart Disease.\n \n \n \n\n\n \n Campbell, M.; Matshabane, O.; Mqulwana, S.; Mndini, M.; Nagdee, M.; Stein, D.; and De Vries, J.\n\n\n \n\n\n\n Global health, epidemiology and genomics, 2021: 9926495. 2021.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{Campbell2021,\nabstract = {In global health research and genomics research specifically, community engagement has gained prominence in enhancing ethical conduct, particularly in managing the risk of stigmatization, but there is minimal scientific evidence on how to do this effectively. This article reports on community engagement evaluation strategies in two African genomics studies: the Stigma in African Genomics Research study and the Genomics of Schizophrenia in South African Xhosa People (SAX) study. Within the Stigma in African Genomics Research study, a self-report rating scale and open-ended questions were used to track participant responses to an experiential theatre workshop. The workshop focused on participant experiences of living with schizophrenia or rheumatic heart disease (RHD). While the schizophrenia group reported more alienation and less stigma resistance than the RHD group, both groups demonstrated increased stigma resistance over time, after participating in the workshops. Hearing from others living with and managing the same illness normalised participants' own experiences and encouraged them. Within the SAX study, a short rating scale and qualitative feedback methods were used to evaluate a Mental Health Literacy Day targeting mental health stigma. Information talks about (i) the symptoms of schizophrenia and treatment options and (ii) the illness experiences of a patient in recovery were rated as the most helpful on the day. Audience members reported that these talks challenged negative perceptions about severe mental illness. Three important learnings emerged from these evaluations: firstly, integration of evaluation strategies at the research study planning phase is likely to promote more effective community engagement. Secondly, a combination of quantitative and qualitative methods that draw on simple descriptive statistics and thematic analysis can provide nuanced perspectives about the value of community engagement. Thirdly, such evidence is necessary in establishing and promoting the science of community engagement in genomics research and health research more broadly.},\nauthor = {Campbell, M.M. and Matshabane, O.P. and Mqulwana, S. and Mndini, M. and Nagdee, M. and Stein, D.J. and {De Vries}, J.},\ndoi = {10.1155/2021/9926495},\nfile = {:Users/jacquelinebracher/Zotero/storage/MRBX9A4Q/Campbell et al. - 2021 - Evaluating Community Engagement Strategies to Mana.pdf:pdf},\njournal = {Global health, epidemiology and genomics},\npages = {9926495},\ntitle = {{Evaluating Community Engagement Strategies to Manage Stigma in Two African Genomics Studies Involving People Living with Schizophrenia or Rheumatic Heart Disease}},\nvolume = {2021},\nyear = {2021}\n}\n
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\n\n\n
\n In global health research and genomics research specifically, community engagement has gained prominence in enhancing ethical conduct, particularly in managing the risk of stigmatization, but there is minimal scientific evidence on how to do this effectively. This article reports on community engagement evaluation strategies in two African genomics studies: the Stigma in African Genomics Research study and the Genomics of Schizophrenia in South African Xhosa People (SAX) study. Within the Stigma in African Genomics Research study, a self-report rating scale and open-ended questions were used to track participant responses to an experiential theatre workshop. The workshop focused on participant experiences of living with schizophrenia or rheumatic heart disease (RHD). While the schizophrenia group reported more alienation and less stigma resistance than the RHD group, both groups demonstrated increased stigma resistance over time, after participating in the workshops. Hearing from others living with and managing the same illness normalised participants' own experiences and encouraged them. Within the SAX study, a short rating scale and qualitative feedback methods were used to evaluate a Mental Health Literacy Day targeting mental health stigma. Information talks about (i) the symptoms of schizophrenia and treatment options and (ii) the illness experiences of a patient in recovery were rated as the most helpful on the day. Audience members reported that these talks challenged negative perceptions about severe mental illness. Three important learnings emerged from these evaluations: firstly, integration of evaluation strategies at the research study planning phase is likely to promote more effective community engagement. Secondly, a combination of quantitative and qualitative methods that draw on simple descriptive statistics and thematic analysis can provide nuanced perspectives about the value of community engagement. Thirdly, such evidence is necessary in establishing and promoting the science of community engagement in genomics research and health research more broadly.\n
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\n \n\n \n \n \n \n \n Moving on From HAND: Why We Need New Criteria for Cognitive Impairment in Persons Living With Human Immunodeficiency Virus and a Proposed Way Forward.\n \n \n \n\n\n \n Nightingale, S.; Dreyer, A.; Saylor, D.; Gisslén, M.; Winston, A.; and Joska, J.\n\n\n \n\n\n\n Clinical Infectious Diseases, 73(6): 1113–1118. 2021.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{Nightingale2021,\nabstract = {Human immunodeficiency virus (HIV)-associated neurocognitive disorders (HAND) criteria are frequently used to describe cognitive impairment in persons living with HIV (PLWH) across diverse populations globally. These criteria typically find 20-60{\\%} of PLWH meet criteria for HAND, which does not tally with clinical observations in the modern era that cognitive disorders present relatively infrequently. Most with HAND have asymptomatic neurocognitive impairment; however, the significance of low cognitive test performance without symptoms is uncertain. Methods underlying HAND criteria carry a false-positive rate that can exceed 20{\\%}. Comorbidities, education, and complex socioeconomic factors can influence cognitive test performance, further increasing the potential for misclassification. We propose a new framework to characterize cognitive impairment in PLWH that requires a clinical history and acknowledges the multifactorial nature of low cognitive test performance. This framework is intended to be applicable across diverse populations globally, be more aligned with clinical observations, and more closely represent HIV brain pathology.},\nauthor = {Nightingale, S. and Dreyer, A.J. and Saylor, D. and Gissl{\\'{e}}n, M. and Winston, A. and Joska, J.A.},\ndoi = {10.1093/cid/ciab366},\njournal = {Clinical Infectious Diseases},\nnumber = {6},\npages = {1113--1118},\ntitle = {{Moving on From HAND: Why We Need New Criteria for Cognitive Impairment in Persons Living With Human Immunodeficiency Virus and a Proposed Way Forward}},\nvolume = {73},\nyear = {2021}\n}\n
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\n Human immunodeficiency virus (HIV)-associated neurocognitive disorders (HAND) criteria are frequently used to describe cognitive impairment in persons living with HIV (PLWH) across diverse populations globally. These criteria typically find 20-60% of PLWH meet criteria for HAND, which does not tally with clinical observations in the modern era that cognitive disorders present relatively infrequently. Most with HAND have asymptomatic neurocognitive impairment; however, the significance of low cognitive test performance without symptoms is uncertain. Methods underlying HAND criteria carry a false-positive rate that can exceed 20%. Comorbidities, education, and complex socioeconomic factors can influence cognitive test performance, further increasing the potential for misclassification. We propose a new framework to characterize cognitive impairment in PLWH that requires a clinical history and acknowledges the multifactorial nature of low cognitive test performance. This framework is intended to be applicable across diverse populations globally, be more aligned with clinical observations, and more closely represent HIV brain pathology.\n
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\n \n\n \n \n \n \n \n \n Effects of \\Prenatal\\ \\Alcohol\\ \\Exposure\\ on the \\Volumes\\ of the \\Lateral\\ and \\Medial\\ \\Walls\\ of the \\Intraparietal\\ \\Sulcus\\.\n \n \n \n \n\n\n \n Miles, M.; Warton, F. L; Meintjes, E. M; Molteno, C. D; Jacobson, J. L; Jacobson, S. W; and Warton, C. M R\n\n\n \n\n\n\n Frontiers in Neuroanatomy, 15: 639800. jun 2021.\n \n\n\n\n
\n\n\n\n \n \n \"EffectsPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{miles_effects_2021,\nabstract = {Fetal alcohol spectrum disorders (FASD) continue to be the leading preventable cause of intellectual disability in the U.S., Europe, and in endemic areas, such as the Western Cape region of South Africa. Arithmetic is highly sensitive to prenatal alcohol exposure (PAE). The intraparietal sulcus (IPS) is known to play a critical role in number processing. In this study, we investigate whether smaller IPS volumes play a role in the number-processing deficits observed in children with PAE. Participants were 52 9- to 14-year-old children from a historically disadvantaged community in Cape Town, who are participating in our ongoing studies on the effects of PAE on the brain. The IPS was manually parcellated into its medial (MIPS) and lateral (LIPS) walls on magnetic resonance images. The study aimed to examine: (1) the effects of PAE on IPS regional volumes and asymmetry, (2) whether IPS regional volumes are related to number processing performance and, if so, whether these relations are moderated by PAE and (3) potential mediation by regional IPS volumes of the relation between PAE and number processing performance. Total intracranial volume (TIV) was associated with volumes in all regions except the right LIPS. Both left MIPS and left LIPS volumes were significantly smaller in children in the fetal alcohol syndrome (FAS)/partial FAS (PFAS) group compared to controls. The finding in the left LIPS remained significant after controlling for potential confounders and after adjustment for the smaller overall brain size of the children in the FAS/PFAS group. Smaller left LIPS volumes in the FAS/PFAS group may account for the absence of left-right asymmetry in the LIPS in children with FAS/PFAS compared to controls and nonsyndromal heavily exposed (HE) children. Bilaterally, larger MIPS volumes were associated with better WISC IQ Arithmetic scores. These effects, however, were not moderated by the degree of PAE, and regional IPS volumes did not mediate the effect of PAE on WISC Arithmetic scores. Although we found that certain regions of the IPS were smaller in children with FAS and PFAS, these PAE-induced changes in IPS volume did not mediate the alcohol-related deficits in arithmetic.},\nauthor = {Miles, Marlie and Warton, Fleur L and Meintjes, Ernesta M and Molteno, Christopher D and Jacobson, Joseph L and Jacobson, Sandra W and Warton, Christopher M R},\ndoi = {10.3389/fnana.2021.639800},\nfile = {:Users/jacquelinebracher/Zotero/storage/M2RXWCQX/Miles et al. - 2021 - Effects of Prenatal Alcohol Exposure on the Volume.pdf:pdf},\nissn = {1662-5129},\njournal = {Frontiers in Neuroanatomy},\nmonth = {jun},\npages = {639800},\ntitle = {{Effects of {\\{}Prenatal{\\}} {\\{}Alcohol{\\}} {\\{}Exposure{\\}} on the {\\{}Volumes{\\}} of the {\\{}Lateral{\\}} and {\\{}Medial{\\}} {\\{}Walls{\\}} of the {\\{}Intraparietal{\\}} {\\{}Sulcus{\\}}}},\nurl = {https://www.frontiersin.org/articles/10.3389/fnana.2021.639800/full},\nvolume = {15},\nyear = {2021}\n}\n
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\n Fetal alcohol spectrum disorders (FASD) continue to be the leading preventable cause of intellectual disability in the U.S., Europe, and in endemic areas, such as the Western Cape region of South Africa. Arithmetic is highly sensitive to prenatal alcohol exposure (PAE). The intraparietal sulcus (IPS) is known to play a critical role in number processing. In this study, we investigate whether smaller IPS volumes play a role in the number-processing deficits observed in children with PAE. Participants were 52 9- to 14-year-old children from a historically disadvantaged community in Cape Town, who are participating in our ongoing studies on the effects of PAE on the brain. The IPS was manually parcellated into its medial (MIPS) and lateral (LIPS) walls on magnetic resonance images. The study aimed to examine: (1) the effects of PAE on IPS regional volumes and asymmetry, (2) whether IPS regional volumes are related to number processing performance and, if so, whether these relations are moderated by PAE and (3) potential mediation by regional IPS volumes of the relation between PAE and number processing performance. Total intracranial volume (TIV) was associated with volumes in all regions except the right LIPS. Both left MIPS and left LIPS volumes were significantly smaller in children in the fetal alcohol syndrome (FAS)/partial FAS (PFAS) group compared to controls. The finding in the left LIPS remained significant after controlling for potential confounders and after adjustment for the smaller overall brain size of the children in the FAS/PFAS group. Smaller left LIPS volumes in the FAS/PFAS group may account for the absence of left-right asymmetry in the LIPS in children with FAS/PFAS compared to controls and nonsyndromal heavily exposed (HE) children. Bilaterally, larger MIPS volumes were associated with better WISC IQ Arithmetic scores. These effects, however, were not moderated by the degree of PAE, and regional IPS volumes did not mediate the effect of PAE on WISC Arithmetic scores. Although we found that certain regions of the IPS were smaller in children with FAS and PFAS, these PAE-induced changes in IPS volume did not mediate the alcohol-related deficits in arithmetic.\n
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\n \n\n \n \n \n \n \n \n A pilot study of inflammatory mediators in brain extracellular fluid in paediatric TBM.\n \n \n \n \n\n\n \n Loxton, N W; Rohlwink, U K; Tshavhungwe, M; Dlamini, L; Shey, M; Enslin, N; and Figaji, A\n\n\n \n\n\n\n 2021.\n \n\n\n\n
\n\n\n\n \n \n \"APaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Loxton2021,\nannote = {Export Date: 29 December 2022},\nauthor = {Loxton, N W and Rohlwink, U K and Tshavhungwe, M and Dlamini, L and Shey, M and Enslin, N and Figaji, A},\ndoi = {10.1371/journal.pone.0246997},\nfile = {:Users/jacquelinebracher/Zotero/storage/7Q79YH8V/Loxton et al. - 2021 - A pilot study of inflammatory mediators in brain e.pdf:pdf},\nnumber = {3 March},\ntitle = {{A pilot study of inflammatory mediators in brain extracellular fluid in paediatric TBM}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85102621198{\\&}doi=10.1371{\\%}2Fjournal.pone.0246997{\\&}partnerID=40{\\&}md5=02a940b3ebb48ffa9793e00719726d28},\nvolume = {16},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Specialty knowledge and competency standards for pharmacotherapy for adult obsessive-compulsive disorder.\n \n \n \n \n\n\n \n Pittenger, C.; Brennan, B. P; Koran, L.; Mathews, C. A; Nestadt, G.; Pato, M.; Phillips, K. A; Rodriguez, C. I; Simpson, H B.; Skapinakis, P.; Stein, D. J; and Storch, E. A\n\n\n \n\n\n\n Psychiatry Research, 300: 113853. jun 2021.\n \n\n\n\n
\n\n\n\n \n \n \"SpecialtyPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{pittenger_specialty_2021,\nauthor = {Pittenger, Christopher and Brennan, Brian P and Koran, Lorrin and Mathews, Carol A and Nestadt, Gerald and Pato, Michele and Phillips, Katharine A and Rodriguez, Carolyn I and Simpson, H Blair and Skapinakis, Petros and Stein, Dan J and Storch, Eric A},\ndoi = {10.1016/j.psychres.2021.113853},\nfile = {:Users/jacquelinebracher/Zotero/storage/UAZHS9RJ/Pittenger et al. - 2021 - Specialty knowledge and competency standards for p.pdf:pdf},\nissn = {01651781},\njournal = {Psychiatry Research},\nmonth = {jun},\npages = {113853},\ntitle = {{Specialty knowledge and competency standards for pharmacotherapy for adult obsessive-compulsive disorder}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S0165178121001505},\nvolume = {300},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Maternal choline supplementation mitigates alcohol exposure effects on neonatal brain volumes.\n \n \n \n \n\n\n \n Warton, F. L; Molteno, C. D; Warton, C. M R; Wintermark, P.; Lindinger, N. M; Dodge, N. C; Zöllei, L.; Van Der Kouwe, A. J W; Carter, R C.; Jacobson, J. L; Jacobson, S. W; and Meintjes, E. M\n\n\n \n\n\n\n Alcoholism: Clinical and Experimental Research, 45(9): 1762–1774. sep 2021.\n \n\n\n\n
\n\n\n\n \n \n \"MaternalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{warton_maternal_2021,\nabstract = {Abstract\n\nBackground\nPrenatal alcohol exposure (PAE) is associated with smaller regional and global brain volumes. In rats, gestational choline supplementation mitigates adverse developmental effects of ethanol exposure. Our recent randomized, double‐blind, placebo‐controlled maternal choline supplementation trial showed improved somatic and functional outcomes in infants at 6.5 and 12 months postpartum. Here, we examined whether maternal choline supplementation protected the newborn brain from PAE‐related volume reductions and, if so, whether these volume changes were associated with improved infant recognition memory.\n\n\nMethods\nFifty‐two infants born to heavy‐drinking women who had participated in a choline supplementation trial during pregnancy underwent structural magnetic resonance imaging with a multi‐echo FLASH protocol on a 3T Siemens Allegra MRI (median age = 2.8 weeks postpartum). Subcortical regions were manually segmented. Recognition memory was assessed at 12 months on the Fagan Test of Infant Intelligence (FTII). We examined the effects of choline on regional brain volumes, whether choline‐related volume increases were associated with higher FTII scores, and the degree to which the regional volume increases mediated the effects of choline on the FTII.\n\n\nResults\n\nUsable MRI data were acquired in 50 infants (choline:\nn \n= 27; placebo:\nn \n= 23). Normalized volumes were larger in six of 12 regions in the choline than placebo arm (\nt\n≥ 2.05,\np\n≤ 0.05) and were correlated with the degree of maternal choline adherence ($\\beta$ ≥ 0.28,\np\n≤ 0.04). Larger right putamen and corpus callosum were related to higher FTII scores (\nr\n= 0.36,\np\n= 0.02) with a trend toward partial mediation of the choline effect on recognition memory.\n\n\n\nConclusions\nHigh‐dose choline supplementation during pregnancy mitigated PAE‐related regional volume reductions, with larger volumes associated with improved 12‐month recognition memory. These results provide the first evidence that choline may be neuroprotective against PAE‐related brain structural deficits in humans.},\nauthor = {Warton, Fleur L and Molteno, Christopher D and Warton, Christopher M R and Wintermark, Pia and Lindinger, Nadine M and Dodge, Neil C and Z{\\"{o}}llei, Lilla and {Van Der Kouwe}, Andre J W and Carter, R Colin and Jacobson, Joseph L and Jacobson, Sandra W and Meintjes, Ernesta M},\ndoi = {10.1111/acer.14672},\nfile = {:Users/jacquelinebracher/Zotero/storage/Z5GXY47Q/Warton et al. - 2021 - Maternal choline supplementation mitigates alcohol.pdf:pdf},\nissn = {0145-6008, 1530-0277},\njournal = {Alcoholism: Clinical and Experimental Research},\nmonth = {sep},\nnumber = {9},\npages = {1762--1774},\ntitle = {{Maternal choline supplementation mitigates alcohol exposure effects on neonatal brain volumes}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1111/acer.14672},\nvolume = {45},\nyear = {2021}\n}\n
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\n Abstract Background Prenatal alcohol exposure (PAE) is associated with smaller regional and global brain volumes. In rats, gestational choline supplementation mitigates adverse developmental effects of ethanol exposure. Our recent randomized, double‐blind, placebo‐controlled maternal choline supplementation trial showed improved somatic and functional outcomes in infants at 6.5 and 12 months postpartum. Here, we examined whether maternal choline supplementation protected the newborn brain from PAE‐related volume reductions and, if so, whether these volume changes were associated with improved infant recognition memory. Methods Fifty‐two infants born to heavy‐drinking women who had participated in a choline supplementation trial during pregnancy underwent structural magnetic resonance imaging with a multi‐echo FLASH protocol on a 3T Siemens Allegra MRI (median age = 2.8 weeks postpartum). Subcortical regions were manually segmented. Recognition memory was assessed at 12 months on the Fagan Test of Infant Intelligence (FTII). We examined the effects of choline on regional brain volumes, whether choline‐related volume increases were associated with higher FTII scores, and the degree to which the regional volume increases mediated the effects of choline on the FTII. Results Usable MRI data were acquired in 50 infants (choline: n  = 27; placebo: n  = 23). Normalized volumes were larger in six of 12 regions in the choline than placebo arm ( t ≥ 2.05, p ≤ 0.05) and were correlated with the degree of maternal choline adherence ($β$ ≥ 0.28, p ≤ 0.04). Larger right putamen and corpus callosum were related to higher FTII scores ( r = 0.36, p = 0.02) with a trend toward partial mediation of the choline effect on recognition memory. Conclusions High‐dose choline supplementation during pregnancy mitigated PAE‐related regional volume reductions, with larger volumes associated with improved 12‐month recognition memory. These results provide the first evidence that choline may be neuroprotective against PAE‐related brain structural deficits in humans.\n
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\n \n\n \n \n \n \n \n \n Brain aging in major depressive disorder: results from the \\ENIGMA\\ major depressive disorder working group.\n \n \n \n \n\n\n \n Han, L. K M; Dinga, R.; Hahn, T.; Ching, C. R K; Eyler, L. T; Aftanas, L.; Aghajani, M.; Aleman, A.; Baune, B. T; Berger, K.; Brak, I.; Filho, G. B.; Carballedo, A.; Connolly, C. G; Couvy-Duchesne, B.; Cullen, K. R; Dannlowski, U.; Davey, C. G; Dima, D.; Duran, F. L S; Enneking, V.; Filimonova, E.; Frenzel, S.; Frodl, T.; Fu, C. H Y; Godlewska, B. R; Gotlib, I. H; Grabe, H. J; Groenewold, N. A; Grotegerd, D.; Gruber, O.; Hall, G. B; Harrison, B. J; Hatton, S. N; Hermesdorf, M.; Hickie, I. B; Ho, T. C; Hosten, N.; Jansen, A.; Kähler, C.; Kircher, T.; Klimes-Dougan, B.; Krämer, B.; Krug, A.; Lagopoulos, J.; Leenings, R.; MacMaster, F. P; MacQueen, G.; McIntosh, A.; McLellan, Q.; McMahon, K. L; Medland, S. E; Mueller, B. A; Mwangi, B.; Osipov, E.; Portella, M. J; Pozzi, E.; Reneman, L.; Repple, J.; Rosa, P. G P; Sacchet, M. D; Sämann, P. G; Schnell, K.; Schrantee, A.; Simulionyte, E.; Soares, J. C; Sommer, J.; Stein, D. J; Steinsträter, O.; Strike, L. T; Thomopoulos, S. I; Van Tol, M.; Veer, I. M; Vermeiren, R. R J M; Walter, H.; Van Der Wee, N. J A; Van Der Werff, S. J A; Whalley, H.; Winter, N. R; Wittfeld, K.; Wright, M. J; Wu, M.; Völzke, H.; Yang, T. T; Zannias, V.; De Zubicaray, G. I; Zunta-Soares, G. B; Abé, C.; Alda, M.; Andreassen, O. A; Bøen, E.; Bonnin, C. M; Canales-Rodriguez, E. J; Cannon, D.; Caseras, X.; Chaim-Avancini, T. M; Elvsåshagen, T.; Favre, P.; Foley, S. F; Fullerton, J. M; Goikolea, J. M; Haarman, B. C M; Hajek, T.; Henry, C.; Houenou, J.; Howells, F. M; Ingvar, M.; Kuplicki, R.; Lafer, B.; Landén, M.; Machado-Vieira, R.; Malt, U. F; McDonald, C.; Mitchell, P. B; Nabulsi, L.; Otaduy, M. C. G.; Overs, B. J; Polosan, M.; Pomarol-Clotet, E.; Radua, J.; Rive, M. M; Roberts, G.; Ruhe, H. G; Salvador, R.; Sarró, S.; Satterthwaite, T. D; Savitz, J.; Schene, A. H; Schofield, P. R; Serpa, M. H; Sim, K.; Soeiro-de-Souza, M. G.; Sutherland, A. N; Temmingh, H. S; Timmons, G. M; Uhlmann, A.; Vieta, E.; Wolf, D. H; Zanetti, M. V; Jahanshad, N.; Thompson, P. M; Veltman, D. J; Penninx, B. W J H; Marquand, A. F; Cole, J. H; and Schmaal, L.\n\n\n \n\n\n\n Molecular Psychiatry, 26(9): 5124–5139. sep 2021.\n \n\n\n\n
\n\n\n\n \n \n \"BrainPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{han_brain_2021,\nabstract = {Abstract\n\nMajor depressive disorder (MDD) is associated with an increased risk of brain atrophy, aging-related diseases, and mortality. We examined potential advanced brain aging in adult MDD patients, and whether this process is associated with clinical characteristics in a large multicenter international dataset. We performed a mega-analysis by pooling brain measures derived from T1-weighted MRI scans from 19 samples worldwide. Healthy brain aging was estimated by predicting chronological age (18–75 years) from 7 subcortical volumes, 34 cortical thickness and 34 surface area, lateral ventricles and total intracranial volume measures separately in 952 male and 1236 female controls from the ENIGMA MDD working group. The learned model coefficients were applied to 927 male controls and 986 depressed males, and 1199 female controls and 1689 depressed females to obtain independent unbiased brain-based age predictions. The difference between predicted “brain age” and chronological age was calculated to indicate brain-predicted age difference (brain-PAD). On average, MDD patients showed a higher brain-PAD of +1.08 (SE 0.22) years (Cohen's\nd\n= 0.14, 95{\\%} CI: 0.08–0.20) compared with controls. However, this difference did not seem to be driven by specific clinical characteristics (recurrent status, remission status, antidepressant medication use, age of onset, or symptom severity). This highly powered collaborative effort showed subtle patterns of age-related structural brain abnormalities in MDD. Substantial within-group variance and overlap between groups were observed. Longitudinal studies of MDD and somatic health outcomes are needed to further assess the clinical value of these brain-PAD estimates.},\nauthor = {Han, Laura K M and Dinga, Richard and Hahn, Tim and Ching, Christopher R K and Eyler, Lisa T and Aftanas, Lyubomir and Aghajani, Moji and Aleman, Andr{\\'{e}} and Baune, Bernhard T and Berger, Klaus and Brak, Ivan and Filho, Geraldo Busatto and Carballedo, Angela and Connolly, Colm G and Couvy-Duchesne, Baptiste and Cullen, Kathryn R and Dannlowski, Udo and Davey, Christopher G and Dima, Danai and Duran, Fabio L S and Enneking, Verena and Filimonova, Elena and Frenzel, Stefan and Frodl, Thomas and Fu, Cynthia H Y and Godlewska, Beata R and Gotlib, Ian H and Grabe, Hans J and Groenewold, Nynke A and Grotegerd, Dominik and Gruber, Oliver and Hall, Geoffrey B and Harrison, Ben J and Hatton, Sean N and Hermesdorf, Marco and Hickie, Ian B and Ho, Tiffany C and Hosten, Norbert and Jansen, Andreas and K{\\"{a}}hler, Claas and Kircher, Tilo and Klimes-Dougan, Bonnie and Kr{\\"{a}}mer, Bernd and Krug, Axel and Lagopoulos, Jim and Leenings, Ramona and MacMaster, Frank P and MacQueen, Glenda and McIntosh, Andrew and McLellan, Quinn and McMahon, Katie L and Medland, Sarah E and Mueller, Bryon A and Mwangi, Benson and Osipov, Evgeny and Portella, Maria J and Pozzi, Elena and Reneman, Liesbeth and Repple, Jonathan and Rosa, Pedro G P and Sacchet, Matthew D and S{\\"{a}}mann, Philipp G and Schnell, Knut and Schrantee, Anouk and Simulionyte, Egle and Soares, Jair C and Sommer, Jens and Stein, Dan J and Steinstr{\\"{a}}ter, Olaf and Strike, Lachlan T and Thomopoulos, Sophia I and {Van Tol}, Marie-Jos{\\'{e}} and Veer, Ilya M and Vermeiren, Robert R J M and Walter, Henrik and {Van Der Wee}, Nic J A and {Van Der Werff}, Steven J A and Whalley, Heather and Winter, Nils R and Wittfeld, Katharina and Wright, Margaret J and Wu, Mon-Ju and V{\\"{o}}lzke, Henry and Yang, Tony T and Zannias, Vasileios and {De Zubicaray}, Greig I and Zunta-Soares, Giovana B and Ab{\\'{e}}, Christoph and Alda, Martin and Andreassen, Ole A and B{\\o}en, Erlend and Bonnin, Caterina M and Canales-Rodriguez, Erick J and Cannon, Dara and Caseras, Xavier and Chaim-Avancini, Tiffany M and Elvs{\\aa}shagen, Torbj{\\o}rn and Favre, Pauline and Foley, Sonya F and Fullerton, Janice M and Goikolea, Jose M and Haarman, Bartholomeus C M and Hajek, Tomas and Henry, Chantal and Houenou, Josselin and Howells, Fleur M and Ingvar, Martin and Kuplicki, Rayus and Lafer, Beny and Land{\\'{e}}n, Mikael and Machado-Vieira, Rodrigo and Malt, Ulrik F and McDonald, Colm and Mitchell, Philip B and Nabulsi, Leila and Otaduy, Maria Concepcion Garcia and Overs, Bronwyn J and Polosan, Mircea and Pomarol-Clotet, Edith and Radua, Joaquim and Rive, Maria M and Roberts, Gloria and Ruhe, Henricus G and Salvador, Raymond and Sarr{\\'{o}}, Salvador and Satterthwaite, Theodore D and Savitz, Jonathan and Schene, Aart H and Schofield, Peter R and Serpa, Mauricio H and Sim, Kang and Soeiro-de-Souza, Marcio Gerhardt and Sutherland, Ashley N and Temmingh, Henk S and Timmons, Garrett M and Uhlmann, Anne and Vieta, Eduard and Wolf, Daniel H and Zanetti, Marcus V and Jahanshad, Neda and Thompson, Paul M and Veltman, Dick J and Penninx, Brenda W J H and Marquand, Andre F and Cole, James H and Schmaal, Lianne},\ndoi = {10.1038/s41380-020-0754-0},\nfile = {:Users/jacquelinebracher/Zotero/storage/FSNT4JRW/Han et al. - 2021 - Brain aging in major depressive disorder results .pdf:pdf},\nissn = {1359-4184, 1476-5578},\njournal = {Molecular Psychiatry},\nmonth = {sep},\nnumber = {9},\npages = {5124--5139},\nshorttitle = {Brain aging in major depressive disorder},\ntitle = {{Brain aging in major depressive disorder: results from the {\\{}ENIGMA{\\}} major depressive disorder working group}},\nurl = {https://www.nature.com/articles/s41380-020-0754-0},\nvolume = {26},\nyear = {2021}\n}\n
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\n Abstract Major depressive disorder (MDD) is associated with an increased risk of brain atrophy, aging-related diseases, and mortality. We examined potential advanced brain aging in adult MDD patients, and whether this process is associated with clinical characteristics in a large multicenter international dataset. We performed a mega-analysis by pooling brain measures derived from T1-weighted MRI scans from 19 samples worldwide. Healthy brain aging was estimated by predicting chronological age (18–75 years) from 7 subcortical volumes, 34 cortical thickness and 34 surface area, lateral ventricles and total intracranial volume measures separately in 952 male and 1236 female controls from the ENIGMA MDD working group. The learned model coefficients were applied to 927 male controls and 986 depressed males, and 1199 female controls and 1689 depressed females to obtain independent unbiased brain-based age predictions. The difference between predicted “brain age” and chronological age was calculated to indicate brain-predicted age difference (brain-PAD). On average, MDD patients showed a higher brain-PAD of +1.08 (SE 0.22) years (Cohen's d = 0.14, 95% CI: 0.08–0.20) compared with controls. However, this difference did not seem to be driven by specific clinical characteristics (recurrent status, remission status, antidepressant medication use, age of onset, or symptom severity). This highly powered collaborative effort showed subtle patterns of age-related structural brain abnormalities in MDD. Substantial within-group variance and overlap between groups were observed. Longitudinal studies of MDD and somatic health outcomes are needed to further assess the clinical value of these brain-PAD estimates.\n
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\n \n\n \n \n \n \n \n \n Response to \\Otto\\ \\Kernberg\\.\n \n \n \n \n\n\n \n Solms, M.\n\n\n \n\n\n\n Neuropsychoanalysis, 23(2): 115–119. jul 2021.\n \n\n\n\n
\n\n\n\n \n \n \"ResponsePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{solms_response_2021,\nauthor = {Solms, Mark},\ndoi = {10.1080/15294145.2021.1984284},\nissn = {1529-4145, 2044-3978},\njournal = {Neuropsychoanalysis},\nmonth = {jul},\nnumber = {2},\npages = {115--119},\ntitle = {{Response to {\\{}Otto{\\}} {\\{}Kernberg{\\}}}},\nurl = {https://www.tandfonline.com/doi/full/10.1080/15294145.2021.1984284},\nvolume = {23},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n The role of causal knowledge in stigma considerations in African genomics research: Views of South African Xhosa people.\n \n \n \n\n\n \n Matshabane, O.; Campbell, M.; Faure, M.; Appelbaum, P.; Marshall, P.; Stein, D.; and de Vries, J.\n\n\n \n\n\n\n Social Science and Medicine, 277. 2021.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Matshabane2021,\nabstract = {Introduction: Advances in genomics research have raised several ethical concerns. One concern is the potential impact of genomics research on stigma experienced by people affected by a disease. Studies have found that the type of illness as well as disease causal beliefs impact on the relation between genetic attribution and stigma. This study explored the potential impact of genetic attribution of disease on stigma among Xhosa people with Rheumatic Heart Disease (RHD). Methods: Study participants were 46 Xhosa people with RHD living in the Western Cape Province of South Africa. Using video vignettes in 7 focus group discussions we explored whether and how genetic attribution may impact on disease-stigma. Vignettes introduced participants to non-genetic and genetic causal explanations and were followed-up with a series of open-ended questions eliciting their perceptions of non-genetic disease causes as well as genetic causation and its impact on internalised stigma. Results: This study found that Xhosa people with RHD have a general understanding of genetics and genetic attribution for disease. Additionally, and not withstanding their genetic knowledge, these participants hold multiple disease causal beliefs including genetic, infectious disease, psychosocial, behavioural and cultural explanations. While there was evidence of internalised stigma experiences among participants, these appeared not to be related to a genetic attribution to the disease. Discussion: The findings of this study provide clues as to why it is unlikely that a genetic conceptualisation of disease impacts internalised stigma experiences of Xhosa people. The causal explanations provided by participants reflect their cultural understandings and their context, namely, living in low-income and poverty-stricken environments. Divergence in these findings from much of the evidence from high-income countries emphasises that context matters when considering the impact of genetic attribution on stigma and caution against generalising findings from one part of the globe to another.},\nauthor = {Matshabane, O.P. and Campbell, M.M. and Faure, M.C. and Appelbaum, P.S. and Marshall, P.A. and Stein, D.J. and de Vries, J.},\ndoi = {10.1016/j.socscimed.2021.113902},\nfile = {:Users/jacquelinebracher/Zotero/storage/DJM46PB9/Matshabane et al. - 2021 - The role of causal knowledge in stigma considerati.pdf:pdf},\njournal = {Social Science and Medicine},\ntitle = {{The role of causal knowledge in stigma considerations in African genomics research: Views of South African Xhosa people}},\nvolume = {277},\nyear = {2021}\n}\n
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\n Introduction: Advances in genomics research have raised several ethical concerns. One concern is the potential impact of genomics research on stigma experienced by people affected by a disease. Studies have found that the type of illness as well as disease causal beliefs impact on the relation between genetic attribution and stigma. This study explored the potential impact of genetic attribution of disease on stigma among Xhosa people with Rheumatic Heart Disease (RHD). Methods: Study participants were 46 Xhosa people with RHD living in the Western Cape Province of South Africa. Using video vignettes in 7 focus group discussions we explored whether and how genetic attribution may impact on disease-stigma. Vignettes introduced participants to non-genetic and genetic causal explanations and were followed-up with a series of open-ended questions eliciting their perceptions of non-genetic disease causes as well as genetic causation and its impact on internalised stigma. Results: This study found that Xhosa people with RHD have a general understanding of genetics and genetic attribution for disease. Additionally, and not withstanding their genetic knowledge, these participants hold multiple disease causal beliefs including genetic, infectious disease, psychosocial, behavioural and cultural explanations. While there was evidence of internalised stigma experiences among participants, these appeared not to be related to a genetic attribution to the disease. Discussion: The findings of this study provide clues as to why it is unlikely that a genetic conceptualisation of disease impacts internalised stigma experiences of Xhosa people. The causal explanations provided by participants reflect their cultural understandings and their context, namely, living in low-income and poverty-stricken environments. Divergence in these findings from much of the evidence from high-income countries emphasises that context matters when considering the impact of genetic attribution on stigma and caution against generalising findings from one part of the globe to another.\n
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\n \n\n \n \n \n \n \n \n Perinatal suicidality: prevalence and correlates in a \\South\\ \\African\\ birth cohort.\n \n \n \n \n\n\n \n Maré, K. T; Pellowski, J. A; Koopowitz, S.; Hoffman, N.; Van Der Westhuizen, C.; Workman, L.; Zar, H. J; and Stein, D. J\n\n\n \n\n\n\n Archives of Women's Mental Health, 24(5): 737–748. oct 2021.\n \n\n\n\n
\n\n\n\n \n \n \"PerinatalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{mare_perinatal_2021,\nauthor = {Mar{\\'{e}}, Karen T and Pellowski, Jennifer A and Koopowitz, Sheri-Michelle and Hoffman, Nadia and {Van Der Westhuizen}, Claire and Workman, Lesley and Zar, Heather J and Stein, Dan J},\ndoi = {10.1007/s00737-021-01121-8},\nfile = {:Users/jacquelinebracher/Zotero/storage/U23YU95E/Mar{\\'{e}} et al. - 2021 - Perinatal suicidality prevalence and correlates i.pdf:pdf},\nissn = {1434-1816, 1435-1102},\njournal = {Archives of Women's Mental Health},\nmonth = {oct},\nnumber = {5},\npages = {737--748},\nshorttitle = {Perinatal suicidality},\ntitle = {{Perinatal suicidality: prevalence and correlates in a {\\{}South{\\}} {\\{}African{\\}} birth cohort}},\nurl = {https://link.springer.com/10.1007/s00737-021-01121-8},\nvolume = {24},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Brief psychotherapy administered by non-specialised health workers to address risky substance use in patients with multidrug-resistant tuberculosis: a feasibility and acceptability study.\n \n \n \n \n\n\n \n Calligaro, G. L; De Wit, Z.; Cirota, J.; Orrell, C.; Myers, B.; Decker, S.; Stein, D. J; Sorsdahl, K.; and Dawson, R.\n\n\n \n\n\n\n Pilot and Feasibility Studies, 7(1): 28. dec 2021.\n \n\n\n\n
\n\n\n\n \n \n \"BriefPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{calligaro_brief_2021,\nabstract = {Abstract\n\nBackground\nOnly 55{\\%} of multidrug-resistant tuberculosis (MDR-TB) cases worldwide complete treatment, with problem substance use a risk for default and treatment failure. Nevertheless, there is little research on psychotherapeutic interventions for reducing substance use amongst MDR-TB patients, in general, and on their delivery by non-specialist health workers in particular.\n\n\nObjectives\nTo explore the feasibility and acceptability of a non-specialist health worker-delivered 4-session brief motivational interviewing and relapse prevention (MI-RP) intervention for problem substance use and to obtain preliminary data on the effects of this intervention on substance use severity, depressive symptoms, psychological distress and functional impairment at 3 months after hospital discharge.\n\n\nMethods\n\nBetween December 2015 and October 2016, consenting MDR-TB patients admitted to Brewelskloof Hospital who screened at moderate to severe risk for substance-related problems on the Alcohol, Smoking and Substance Involvement Screening Test (ASSIST) were enrolled, and a baseline questionnaire administered. In the 4 weeks prior to planned discharge, trained counsellors delivered the MI-RP intervention. The baseline questionnaire was re-administered 3 months post-discharge and qualitative interviews were conducted with a randomly selected sample of participants (\nn\n= 10).\n\n\n\nResults\nSixty patients were screened: 40 (66{\\%}) met inclusion criteria of which 39 (98{\\%}) were enrolled. Of the enrolled patients, 26 (67{\\%}) completed the counselling sessions and the final assessment. Qualitative interviews revealed participants' perceptions of the value of the intervention. From baseline to follow-up, patients reported reductions in substance use severity, symptoms of depression, distress and functional impairment.\n\n\nConclusion\nIn this feasibility study, participant retention in the study was moderate. We found preliminary evidence supporting the benefits of the intervention for reducing substance use and symptoms of psychological distress, supported by qualitative reports of patient experiences. Randomised studies are needed to demonstrate efficacy of this intervention before considering potential for wider implementation.\n\n\nTrial registration\n\nSouth African National Clinical Trials Register (\nDOH-27-0315-5007\n) on 01/04/2015 (\nhttp://www.sanctr.gov.za\n)},\nauthor = {Calligaro, Gregory L and {De Wit}, Zani and Cirota, Jacqui and Orrell, Catherine and Myers, Bronwyn and Decker, Sebastian and Stein, Dan J and Sorsdahl, Katherine and Dawson, Rodney},\ndoi = {10.1186/s40814-020-00764-1},\nfile = {:Users/jacquelinebracher/Zotero/storage/UXW9654A/Calligaro et al. - 2021 - Brief psychotherapy administered by non-specialise.pdf:pdf},\nissn = {2055-5784},\njournal = {Pilot and Feasibility Studies},\nmonth = {dec},\nnumber = {1},\npages = {28},\nshorttitle = {Brief psychotherapy administered by non-specialise},\ntitle = {{Brief psychotherapy administered by non-specialised health workers to address risky substance use in patients with multidrug-resistant tuberculosis: a feasibility and acceptability study}},\nurl = {https://pilotfeasibilitystudies.biomedcentral.com/articles/10.1186/s40814-020-00764-1},\nvolume = {7},\nyear = {2021}\n}\n
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\n Abstract Background Only 55% of multidrug-resistant tuberculosis (MDR-TB) cases worldwide complete treatment, with problem substance use a risk for default and treatment failure. Nevertheless, there is little research on psychotherapeutic interventions for reducing substance use amongst MDR-TB patients, in general, and on their delivery by non-specialist health workers in particular. Objectives To explore the feasibility and acceptability of a non-specialist health worker-delivered 4-session brief motivational interviewing and relapse prevention (MI-RP) intervention for problem substance use and to obtain preliminary data on the effects of this intervention on substance use severity, depressive symptoms, psychological distress and functional impairment at 3 months after hospital discharge. Methods Between December 2015 and October 2016, consenting MDR-TB patients admitted to Brewelskloof Hospital who screened at moderate to severe risk for substance-related problems on the Alcohol, Smoking and Substance Involvement Screening Test (ASSIST) were enrolled, and a baseline questionnaire administered. In the 4 weeks prior to planned discharge, trained counsellors delivered the MI-RP intervention. The baseline questionnaire was re-administered 3 months post-discharge and qualitative interviews were conducted with a randomly selected sample of participants ( n = 10). Results Sixty patients were screened: 40 (66%) met inclusion criteria of which 39 (98%) were enrolled. Of the enrolled patients, 26 (67%) completed the counselling sessions and the final assessment. Qualitative interviews revealed participants' perceptions of the value of the intervention. From baseline to follow-up, patients reported reductions in substance use severity, symptoms of depression, distress and functional impairment. Conclusion In this feasibility study, participant retention in the study was moderate. We found preliminary evidence supporting the benefits of the intervention for reducing substance use and symptoms of psychological distress, supported by qualitative reports of patient experiences. Randomised studies are needed to demonstrate efficacy of this intervention before considering potential for wider implementation. Trial registration South African National Clinical Trials Register ( DOH-27-0315-5007 ) on 01/04/2015 ( http://www.sanctr.gov.za )\n
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\n \n\n \n \n \n \n \n \n The role of new medical treatments for the management of developmental and epileptic encephalopathies: \\Novel\\ concepts and results.\n \n \n \n \n\n\n \n Johannessen Landmark, C.; Potschka, H.; Auvin, S.; Wilmshurst, J. M; Johannessen, S. I; Kasteleijn‐Nolst Trenité, D.; and Wirrell, E. C\n\n\n \n\n\n\n Epilepsia, 62(4): 857–873. apr 2021.\n \n\n\n\n
\n\n\n\n \n \n \"ThePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{johannessen_landmark_role_2021,\nabstract = {Abstract\nDevelopmental and epileptic encephalopathies (DEEs) are among the most challenging of all epilepsies to manage, given the exceedingly frequent and often severe seizure types, pharmacoresistance to conventional antiseizure medications, and numerous comorbidities. During the past decade, efforts have focused on development of new treatment options for DEEs, with several recently approved in the United States or Europe, including cannabidiol as an orphan drug in Dravet and Lennox–Gastaut syndromes and everolimus as a possible antiepileptogenic and precision drug for tuberous sclerosis complex, with its impact on the mammalian target of rapamycin pathway. Furthermore, fenfluramine, an old drug, was repurposed as a novel therapy in the treatment of Dravet syndrome. The evolution of new insights into pathophysiological processes of various DEEs provides possibilities to investigate novel and repurposed drugs and to place them into the context of their role in future management of these patients. The purpose of this review is to provide an overview of these new medical treatment options for the DEEs and to discuss the clinical implications of these results for improved treatment.},\nauthor = {{Johannessen Landmark}, Cecilie and Potschka, Heidrun and Auvin, St{\\'{e}}phane and Wilmshurst, Jo M and Johannessen, Svein I and {Kasteleijn‐Nolst Trenit{\\'{e}}}, Doroth{\\'{e}}e and Wirrell, Elaine C},\ndoi = {10.1111/epi.16849},\nissn = {0013-9580, 1528-1167},\njournal = {Epilepsia},\nmonth = {apr},\nnumber = {4},\npages = {857--873},\nshorttitle = {The role of new medical treatments for the managem},\ntitle = {{The role of new medical treatments for the management of developmental and epileptic encephalopathies: {\\{}Novel{\\}} concepts and results}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1111/epi.16849},\nvolume = {62},\nyear = {2021}\n}\n
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\n Abstract Developmental and epileptic encephalopathies (DEEs) are among the most challenging of all epilepsies to manage, given the exceedingly frequent and often severe seizure types, pharmacoresistance to conventional antiseizure medications, and numerous comorbidities. During the past decade, efforts have focused on development of new treatment options for DEEs, with several recently approved in the United States or Europe, including cannabidiol as an orphan drug in Dravet and Lennox–Gastaut syndromes and everolimus as a possible antiepileptogenic and precision drug for tuberous sclerosis complex, with its impact on the mammalian target of rapamycin pathway. Furthermore, fenfluramine, an old drug, was repurposed as a novel therapy in the treatment of Dravet syndrome. The evolution of new insights into pathophysiological processes of various DEEs provides possibilities to investigate novel and repurposed drugs and to place them into the context of their role in future management of these patients. The purpose of this review is to provide an overview of these new medical treatment options for the DEEs and to discuss the clinical implications of these results for improved treatment.\n
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\n \n\n \n \n \n \n \n \n The \\ILAE\\ classification of seizures and the epilepsies: \\Modification\\ for seizures in the neonate. \\Position\\ paper by the \\ILAE\\ \\Task\\ \\Force\\ on \\Neonatal\\ \\Seizures\\.\n \n \n \n \n\n\n \n Pressler, R. M; Cilio, M. R.; Mizrahi, E. M; Moshé, S. L; Nunes, M. L; Plouin, P.; Vanhatalo, S.; Yozawitz, E.; De Vries, L. S; Puthenveettil Vinayan, K.; Triki, C. C; Wilmshurst, J. M; Yamamoto, H.; and Zuberi, S. M\n\n\n \n\n\n\n Epilepsia, 62(3): 615–628. mar 2021.\n \n\n\n\n
\n\n\n\n \n \n \"ThePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{pressler_ilae_2021,\nabstract = {Abstract\nSeizures are the most common neurological emergency in the neonatal period and in contrast to those in infancy and childhood, are often provoked seizures with an acute cause and may be electrographic‐only. Hence, neonatal seizures may not fit easily into classification schemes for seizures and epilepsies primarily developed for older children and adults. A Neonatal Seizures Task Force was established by the International League Against Epilepsy (ILAE) to develop a modification of the 2017 ILAE Classification of Seizures and Epilepsies, relevant to neonates. The neonatal classification framework emphasizes the role of electroencephalography (EEG) in the diagnosis of seizures in the neonate and includes a classification of seizure types relevant to this age group. The seizure type is determined by the predominant clinical feature. Many neonatal seizures are electrographic‐only with no evident clinical features; therefore, these are included in the proposed classification. Clinical events without an EEG correlate are not included. Because seizures in the neonatal period have been shown to have a focal onset, a division into focal and generalized is unnecessary. Seizures can have a motor (automatisms, clonic, epileptic spasms, myoclonic, tonic), non‐motor (autonomic, behavior arrest), or sequential presentation. The classification allows the user to choose the level of detail when classifying seizures in this age group.},\nauthor = {Pressler, Ronit M and Cilio, Maria Roberta and Mizrahi, Eli M and Mosh{\\'{e}}, Solomon L and Nunes, Magda L and Plouin, Perrine and Vanhatalo, Sampsa and Yozawitz, Elissa and {De Vries}, Linda S and {Puthenveettil Vinayan}, Kollencheri and Triki, Chahnez C and Wilmshurst, Jo M and Yamamoto, Hitoshi and Zuberi, Sameer M},\ndoi = {10.1111/epi.16815},\nfile = {:Users/jacquelinebracher/Zotero/storage/CQKKMWGC/Pressler et al. - 2021 - The ILAE classification of seizures and the epilep.pdf:pdf},\nissn = {0013-9580, 1528-1167},\njournal = {Epilepsia},\nmonth = {mar},\nnumber = {3},\npages = {615--628},\nshorttitle = {The {\\{}ILAE{\\}} classification of seizures and the epil},\ntitle = {{The {\\{}ILAE{\\}} classification of seizures and the epilepsies: {\\{}Modification{\\}} for seizures in the neonate. {\\{}Position{\\}} paper by the {\\{}ILAE{\\}} {\\{}Task{\\}} {\\{}Force{\\}} on {\\{}Neonatal{\\}} {\\{}Seizures{\\}}}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1111/epi.16815},\nvolume = {62},\nyear = {2021}\n}\n
\n
\n\n\n
\n Abstract Seizures are the most common neurological emergency in the neonatal period and in contrast to those in infancy and childhood, are often provoked seizures with an acute cause and may be electrographic‐only. Hence, neonatal seizures may not fit easily into classification schemes for seizures and epilepsies primarily developed for older children and adults. A Neonatal Seizures Task Force was established by the International League Against Epilepsy (ILAE) to develop a modification of the 2017 ILAE Classification of Seizures and Epilepsies, relevant to neonates. The neonatal classification framework emphasizes the role of electroencephalography (EEG) in the diagnosis of seizures in the neonate and includes a classification of seizure types relevant to this age group. The seizure type is determined by the predominant clinical feature. Many neonatal seizures are electrographic‐only with no evident clinical features; therefore, these are included in the proposed classification. Clinical events without an EEG correlate are not included. Because seizures in the neonatal period have been shown to have a focal onset, a division into focal and generalized is unnecessary. Seizures can have a motor (automatisms, clonic, epileptic spasms, myoclonic, tonic), non‐motor (autonomic, behavior arrest), or sequential presentation. The classification allows the user to choose the level of detail when classifying seizures in this age group.\n
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\n \n\n \n \n \n \n \n \n Importance of access to epilepsy monitoring units during the \\COVID\\-19 pandemic: \\Consensus\\ statement of the \\International\\ \\League\\ against epilepsy and the \\International\\ \\Federation\\ of \\Clinical\\ \\Neurophysiology\\.\n \n \n \n \n\n\n \n Beniczky, S.; Husain, A.; Ikeda, A.; Alabri, H.; Helen Cross, J; Wilmshurst, J.; Seeck, M.; Focke, N.; Braga, P.; Wiebe, S.; Schuele, S.; and Trinka, E.\n\n\n \n\n\n\n Clinical Neurophysiology, 132(9): 2248–2250. sep 2021.\n \n\n\n\n
\n\n\n\n \n \n \"ImportancePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{beniczky_importance_2021,\nauthor = {Beniczky, S{\\'{a}}ndor and Husain, Aatif and Ikeda, Akio and Alabri, Haifa and {Helen Cross}, J and Wilmshurst, Jo and Seeck, Margitta and Focke, Niels and Braga, Patricia and Wiebe, Samuel and Schuele, Stephan and Trinka, Eugen},\ndoi = {10.1016/j.clinph.2021.05.001},\nfile = {:Users/jacquelinebracher/Zotero/storage/Q2L9B8JW/Beniczky et al. - 2021 - Importance of access to epilepsy monitoring units .pdf:pdf},\nissn = {13882457},\njournal = {Clinical Neurophysiology},\nmonth = {sep},\nnumber = {9},\npages = {2248--2250},\nshorttitle = {Importance of access to epilepsy monitoring units },\ntitle = {{Importance of access to epilepsy monitoring units during the {\\{}COVID{\\}}-19 pandemic: {\\{}Consensus{\\}} statement of the {\\{}International{\\}} {\\{}League{\\}} against epilepsy and the {\\{}International{\\}} {\\{}Federation{\\}} of {\\{}Clinical{\\}} {\\{}Neurophysiology{\\}}}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S1388245721005678},\nvolume = {132},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n White matter microstructure and its relation to clinical features of obsessive–compulsive disorder: findings from the \\ENIGMA\\ \\OCD\\ \\Working\\ \\Group\\.\n \n \n \n \n\n\n \n Piras, F.; Piras, F.; Abe, Y.; Agarwal, S. M.; Anticevic, A.; Ameis, S.; Arnold, P.; Banaj, N.; Bargalló, N.; Batistuzzo, M. C; Benedetti, F.; Beucke, J.; Boedhoe, P. S W; Bollettini, I.; Brem, S.; Calvo, A.; Cho, K. I. K.; Ciullo, V.; Dallaspezia, S.; Dickie, E.; Ely, B. A.; Fan, S.; Fouche, J.; Gruner, P.; Gürsel, D. A; Hauser, T.; Hirano, Y.; Hoexter, M. Q; Iorio, M.; James, A.; Reddy, Y C J.; Kaufmann, C.; Koch, K.; Kochunov, P.; Kwon, J. S.; Lazaro, L.; Lochner, C.; Marsh, R.; Nakagawa, A.; Nakamae, T.; Narayanaswamy, J. C; Sakai, Y.; Shimizu, E.; Simon, D.; Simpson, H. B.; Soreni, N.; Stämpfli, P.; Stern, E. R; Szeszko, P.; Takahashi, J.; Venkatasubramanian, G.; Wang, Z.; Yun, J.; ENIGMA OCD Working Group; Assogna, F.; Calvo, R.; Wit, S. J D.; Hough, M.; Kuno, M.; Miguel, E. C; Morer, A.; Pittenger, C.; Poletti, S.; Smeraldi, E.; Sato, J. R; Tsuchiyagaito, A.; Walitza, S.; Van Der Werf, Y. D; Vecchio, D.; Zarei, M.; Stein, D. J; Jahanshad, N.; Thompson, P. M; Van Den Heuvel, O. A; and Spalletta, G.\n\n\n \n\n\n\n Translational Psychiatry, 11(1): 173. mar 2021.\n \n\n\n\n
\n\n\n\n \n \n \"WhitePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{piras_white_2021,\nabstract = {Abstract\n\nMicrostructural alterations in cortico-subcortical connections are thought to be present in obsessive–compulsive disorder (OCD). However, prior studies have yielded inconsistent findings, perhaps because small sample sizes provided insufficient power to detect subtle abnormalities. Here we investigated microstructural white matter alterations and their relation to clinical features in the largest dataset of adult and pediatric OCD to date. We analyzed diffusion tensor imaging metrics from 700 adult patients and 645 adult controls, as well as 174 pediatric patients and 144 pediatric controls across 19 sites participating in the ENIGMA OCD Working Group, in a cross-sectional case-control magnetic resonance study. We extracted measures of fractional anisotropy (FA) as main outcome, and mean diffusivity, radial diffusivity, and axial diffusivity as secondary outcomes for 25 white matter regions. We meta-analyzed patient-control group differences (Cohen's\nd\n) across sites, after adjusting for age and sex, and investigated associations with clinical characteristics. Adult OCD patients showed significant FA reduction in the sagittal stratum (\nd\n= −0.21,\nz\n= −3.21,\np\n= 0.001) and posterior thalamic radiation (\nd\n= −0.26,\nz\n= −4.57,\np\n{\\textless}0.0001). In the sagittal stratum, lower FA was associated with a younger age of onset (\nz\n= 2.71,\np\n= 0.006), longer duration of illness (\nz\n= −2.086,\np\n= 0.036), and a higher percentage of medicated patients in the cohorts studied (\nz\n= −1.98,\np\n= 0.047). No significant association with symptom severity was found. Pediatric OCD patients did not show any detectable microstructural abnormalities compared to controls. Our findings of microstructural alterations in projection and association fibers to posterior brain regions in OCD are consistent with models emphasizing deficits in connectivity as an important feature of this disorder.},\nauthor = {Piras, Fabrizio and Piras, Federica and Abe, Yoshinari and Agarwal, Sri Mahavir and Anticevic, Alan and Ameis, Stephanie and Arnold, Paul and Banaj, Nerisa and Bargall{\\'{o}}, N{\\'{u}}ria and Batistuzzo, Marcelo C and Benedetti, Francesco and Beucke, Jan-Carl and Boedhoe, Premika S W and Bollettini, Irene and Brem, Silvia and Calvo, Anna and Cho, Kang Ik Kevin and Ciullo, Valentina and Dallaspezia, Sara and Dickie, Erin and Ely, Benjamin Adam and Fan, Siyan and Fouche, Jean-Paul and Gruner, Patricia and G{\\"{u}}rsel, Deniz A and Hauser, Tobias and Hirano, Yoshiyuki and Hoexter, Marcelo Q and Iorio, Mariangela and James, Anthony and Reddy, Y C Janardhan and Kaufmann, Christian and Koch, Kathrin and Kochunov, Peter and Kwon, Jun Soo and Lazaro, Luisa and Lochner, Christine and Marsh, Rachel and Nakagawa, Akiko and Nakamae, Takashi and Narayanaswamy, Janardhanan C and Sakai, Yuki and Shimizu, Eiji and Simon, Daniela and Simpson, Helen Blair and Soreni, Noam and St{\\"{a}}mpfli, Philipp and Stern, Emily R and Szeszko, Philip and Takahashi, Jumpei and Venkatasubramanian, Ganesan and Wang, Zhen and Yun, Je-Yeon and {ENIGMA OCD Working Group} and Assogna, Francesca and Calvo, Rosa and Wit, Stella J De and Hough, Morgan and Kuno, Masaru and Miguel, Euripedes C and Morer, Astrid and Pittenger, Christopher and Poletti, Sara and Smeraldi, Enrico and Sato, Jo{\\~{a}}o R and Tsuchiyagaito, Aki and Walitza, Susanne and {Van Der Werf}, Ysbrand D and Vecchio, Daniela and Zarei, Mojtaba and Stein, Dan J and Jahanshad, Neda and Thompson, Paul M and {Van Den Heuvel}, Odile A and Spalletta, Gianfranco},\ndoi = {10.1038/s41398-021-01276-z},\nfile = {:Users/jacquelinebracher/Zotero/storage/CFDS8PAM/Piras et al. - 2021 - White matter microstructure and its relation to cl.pdf:pdf},\nissn = {2158-3188},\njournal = {Translational Psychiatry},\nmonth = {mar},\nnumber = {1},\npages = {173},\nshorttitle = {White matter microstructure and its relation to cl},\ntitle = {{White matter microstructure and its relation to clinical features of obsessive–compulsive disorder: findings from the {\\{}ENIGMA{\\}} {\\{}OCD{\\}} {\\{}Working{\\}} {\\{}Group{\\}}}},\nurl = {https://www.nature.com/articles/s41398-021-01276-z},\nvolume = {11},\nyear = {2021}\n}\n
\n
\n\n\n
\n Abstract Microstructural alterations in cortico-subcortical connections are thought to be present in obsessive–compulsive disorder (OCD). However, prior studies have yielded inconsistent findings, perhaps because small sample sizes provided insufficient power to detect subtle abnormalities. Here we investigated microstructural white matter alterations and their relation to clinical features in the largest dataset of adult and pediatric OCD to date. We analyzed diffusion tensor imaging metrics from 700 adult patients and 645 adult controls, as well as 174 pediatric patients and 144 pediatric controls across 19 sites participating in the ENIGMA OCD Working Group, in a cross-sectional case-control magnetic resonance study. We extracted measures of fractional anisotropy (FA) as main outcome, and mean diffusivity, radial diffusivity, and axial diffusivity as secondary outcomes for 25 white matter regions. We meta-analyzed patient-control group differences (Cohen's d ) across sites, after adjusting for age and sex, and investigated associations with clinical characteristics. Adult OCD patients showed significant FA reduction in the sagittal stratum ( d = −0.21, z = −3.21, p = 0.001) and posterior thalamic radiation ( d = −0.26, z = −4.57, p \\textless0.0001). In the sagittal stratum, lower FA was associated with a younger age of onset ( z = 2.71, p = 0.006), longer duration of illness ( z = −2.086, p = 0.036), and a higher percentage of medicated patients in the cohorts studied ( z = −1.98, p = 0.047). No significant association with symptom severity was found. Pediatric OCD patients did not show any detectable microstructural abnormalities compared to controls. Our findings of microstructural alterations in projection and association fibers to posterior brain regions in OCD are consistent with models emphasizing deficits in connectivity as an important feature of this disorder.\n
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\n \n\n \n \n \n \n \n \n Clinical \\Studies\\ in \\Neuropsychoanalysis\\ \\Revisited\\.\n \n \n \n \n\n\n \n Salas, C.; Turnbull, O.; and Solms, M.\n\n\n \n\n\n\n Routledge, London, 1 edition, jun 2021.\n \n\n\n\n
\n\n\n\n \n \n \"ClinicalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@book{salas_clinical_2021,\naddress = {London},\nauthor = {Salas, Christian and Turnbull, Oliver and Solms, Mark},\ndoi = {10.4324/9781003188551},\nedition = {1},\nisbn = {978-1-00-318855-1},\nmonth = {jun},\npublisher = {Routledge},\ntitle = {{Clinical {\\{}Studies{\\}} in {\\{}Neuropsychoanalysis{\\}} {\\{}Revisited{\\}}}},\nurl = {https://www.taylorfrancis.com/books/9781003188551},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Association of maternal and infant inflammation with neurodevelopment in HIV-exposed uninfected children in a South African birth cohort.\n \n \n \n \n\n\n \n Sevenoaks, T; Wedderburn, C J; Donald, K A; Barnett, W; Zar, H J; Stein, D J; and Naudé, P J W\n\n\n \n\n\n\n 2021.\n \n\n\n\n
\n\n\n\n \n \n \"AssociationPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@misc{Sevenoaks2021,\nannote = {Export Date: 29 December 2022},\nauthor = {Sevenoaks, T and Wedderburn, C J and Donald, K A and Barnett, W and Zar, H J and Stein, D J and Naud{\\'{e}}, P J W},\ndoi = {10.1016/j.bbi.2020.08.021},\nfile = {:Users/jacquelinebracher/Zotero/storage/7ZL9D7A8/Sevenoaks et al. - 2021 - Association of maternal and infant inflammation wi.pdf:pdf},\npages = {65--73},\ntitle = {{Association of maternal and infant inflammation with neurodevelopment in HIV-exposed uninfected children in a South African birth cohort}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85094907881{\\&}doi=10.1016{\\%}2Fj.bbi.2020.08.021{\\&}partnerID=40{\\&}md5=7cde5eda4273c82a3580a969c0ece4a4},\nvolume = {91},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Immune \\Dysregulation\\ \\Is\\ \\Associated\\ with \\Neurodevelopment\\ and \\Neurocognitive\\ \\Performance\\ in \\HIV\\ \\Pediatric\\ \\Populations\\—\\A\\ \\Scoping\\ \\Review\\.\n \n \n \n \n\n\n \n Williams, M. E; Janse Van Rensburg, A.; Loots, D. T.; Naudé, P. J W; and Mason, S.\n\n\n \n\n\n\n Viruses, 13(12): 2543. dec 2021.\n \n\n\n\n
\n\n\n\n \n \n \"ImmunePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{williams_immune_2021,\nabstract = {HIV-1 is known for its complex interaction with the dysregulated immune system and is responsible for the development of neurocognitive deficits and neurodevelopmental delays in pediatric HIV populations. Considering that HIV-1-induced immune dysregulation and its association with neurodevelopmental and neurocognitive impairments in pediatric populations are not well understood, we conducted a scoping review on this topic. The study aimed to systematically review the association of blood and cerebrospinal fluid (CSF) immune markers with neurocognitive deficits and neurodevelopmental delays in pediatric HIV populations. PubMed, Scopus, and Web of Science databases were searched using a search protocol designed specifically for this study. Studies were selected based on a set eligibility criterion. Titles, abstracts, and full texts were assessed by two independent reviewers. Data from the selected studies were extracted and analyzed by two independent reviewers. Seven studies were considered eligible for use in this context, which included four cross-sectional and three longitudinal studies. An average of 130 (±70.61) children living with HIV, 138 (±65.37) children exposed to HIV but uninfected and 90 (±86.66) HIV-negative participants were included across the seven studies. Results indicate that blood and CSF immune markers are associated with neurocognitive development/performance in pediatric HIV populations. Only seven studies met the inclusion criteria, therefore, these limited the number of significant conclusions which could have been made by using such an approach. All considered, the evidence suggests that immune dysregulation, as in the case of adult HIV populations, also has a significant association with neurocognitive performance in pediatric HIV populations.},\nauthor = {Williams, Monray E and {Janse Van Rensburg}, Anicia and Loots, Du Toit and Naud{\\'{e}}, Petrus J W and Mason, Shayne},\ndoi = {10.3390/v13122543},\nfile = {:Users/jacquelinebracher/Zotero/storage/PC9QB55D/Williams et al. - 2021 - Immune Dysregulation Is Associated with Neurodevel.pdf:pdf},\nissn = {1999-4915},\njournal = {Viruses},\nmonth = {dec},\nnumber = {12},\npages = {2543},\ntitle = {{Immune {\\{}Dysregulation{\\}} {\\{}Is{\\}} {\\{}Associated{\\}} with {\\{}Neurodevelopment{\\}} and {\\{}Neurocognitive{\\}} {\\{}Performance{\\}} in {\\{}HIV{\\}} {\\{}Pediatric{\\}} {\\{}Populations{\\}}—{\\{}A{\\}} {\\{}Scoping{\\}} {\\{}Review{\\}}}},\nurl = {https://www.mdpi.com/1999-4915/13/12/2543},\nvolume = {13},\nyear = {2021}\n}\n
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\n HIV-1 is known for its complex interaction with the dysregulated immune system and is responsible for the development of neurocognitive deficits and neurodevelopmental delays in pediatric HIV populations. Considering that HIV-1-induced immune dysregulation and its association with neurodevelopmental and neurocognitive impairments in pediatric populations are not well understood, we conducted a scoping review on this topic. The study aimed to systematically review the association of blood and cerebrospinal fluid (CSF) immune markers with neurocognitive deficits and neurodevelopmental delays in pediatric HIV populations. PubMed, Scopus, and Web of Science databases were searched using a search protocol designed specifically for this study. Studies were selected based on a set eligibility criterion. Titles, abstracts, and full texts were assessed by two independent reviewers. Data from the selected studies were extracted and analyzed by two independent reviewers. Seven studies were considered eligible for use in this context, which included four cross-sectional and three longitudinal studies. An average of 130 (±70.61) children living with HIV, 138 (±65.37) children exposed to HIV but uninfected and 90 (±86.66) HIV-negative participants were included across the seven studies. Results indicate that blood and CSF immune markers are associated with neurocognitive development/performance in pediatric HIV populations. Only seven studies met the inclusion criteria, therefore, these limited the number of significant conclusions which could have been made by using such an approach. All considered, the evidence suggests that immune dysregulation, as in the case of adult HIV populations, also has a significant association with neurocognitive performance in pediatric HIV populations.\n
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\n \n\n \n \n \n \n \n \n Mechanisms of cognitive impairment in temporal lobe epilepsy: \\A\\ systematic review of resting-state functional connectivity studies.\n \n \n \n \n\n\n \n Ives-Deliperi, V.; and Butler, J. T\n\n\n \n\n\n\n Epilepsy & Behavior, 115: 107686. feb 2021.\n \n\n\n\n
\n\n\n\n \n \n \"MechanismsPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{ives-deliperi_mechanisms_2021,\nauthor = {Ives-Deliperi, Victoria and Butler, James T},\ndoi = {10.1016/j.yebeh.2020.107686},\nissn = {15255050},\njournal = {Epilepsy {\\&} Behavior},\nmonth = {feb},\npages = {107686},\nshorttitle = {Mechanisms of cognitive impairment in temporal lob},\ntitle = {{Mechanisms of cognitive impairment in temporal lobe epilepsy: {\\{}A{\\}} systematic review of resting-state functional connectivity studies}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S1525505020308660},\nvolume = {115},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n The neurocognitive profile of post-traumatic stress disorder (PTSD), major depressive disorder (MDD), and PTSD with comorbid MDD.\n \n \n \n \n\n\n \n Koopowitz, S.; Maré, K T; Zar, H J; Stein, D J; and Ipser, J C\n\n\n \n\n\n\n 2021.\n \n\n\n\n
\n\n\n\n \n \n \"ThePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Koopowitz2021,\nannote = {Export Date: 29 December 2022},\nauthor = {Koopowitz, S.-M. and Mar{\\'{e}}, K T and Zar, H J and Stein, D J and Ipser, J C},\ndoi = {10.1002/brb3.1950},\nfile = {:Users/jacquelinebracher/Zotero/storage/GP5JZ5JM/Koopowitz et al. - 2021 - The neurocognitive profile of post‐traumatic stres.pdf:pdf},\nnumber = {4},\ntitle = {{The neurocognitive profile of post-traumatic stress disorder (PTSD), major depressive disorder (MDD), and PTSD with comorbid MDD}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85101988799{\\&}doi=10.1002{\\%}2Fbrb3.1950{\\&}partnerID=40{\\&}md5=2712b59f4cfa526b69a36444cd24788f},\nvolume = {11},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Managing depression and anxiety in people with epilepsy: A survey of epilepsy health professionals by the ILAE Psychology Task Force.\n \n \n \n \n\n\n \n Gandy, M; Modi, A C; Wagner, J L; LaFrance Jr., W C; Reuber, M; Tang, V; Valente, K D; Goldstein, L H; Donald, K A; Rayner, G; and Michaelis, R\n\n\n \n\n\n\n 2021.\n \n\n\n\n
\n\n\n\n \n \n \"ManagingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Gandy2021,\nannote = {Export Date: 29 December 2022},\nauthor = {Gandy, M and Modi, A C and Wagner, J L and {LaFrance  Jr.}, W C and Reuber, M and Tang, V and Valente, K D and Goldstein, L H and Donald, K A and Rayner, G and Michaelis, R},\ndoi = {10.1002/epi4.12455},\nfile = {:Users/jacquelinebracher/Zotero/storage/IPNW5WHG/Gandy et al. - 2021 - Managing depression and anxiety in people with epi.pdf:pdf},\nnumber = {1},\npages = {127--139},\ntitle = {{Managing depression and anxiety in people with epilepsy: A survey of epilepsy health professionals by the ILAE Psychology Task Force}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85100575534{\\&}doi=10.1002{\\%}2Fepi4.12455{\\&}partnerID=40{\\&}md5=144032479c81a1cb8d350221567149b9},\nvolume = {6},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Prevalence and correlates of metabolic syndrome and its components in adults with psychotic disorders in \\Eldoret\\, \\Kenya\\.\n \n \n \n \n\n\n \n Kwobah, E.; Koen, N.; Mwangi, A.; Atwoli, L.; and Stein, D. J\n\n\n \n\n\n\n PLOS ONE, 16(1): e0245086. jan 2021.\n \n\n\n\n
\n\n\n\n \n \n \"PrevalencePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{kwobah_prevalence_2021,\nabstract = {Background\nA high prevalence of metabolic syndrome and its components in patients with psychotic disorders may increase the risk for cardiovascular diseases. Unfortunately, relatively little work in this field has emerged from low-resourced contexts. This study investigated the prevalence, correlates, and treatment patterns of metabolic disorders in patients with psychotic disorders in Western Kenya.\n\n\nMethods\n300 patients with psychosis and 300 controls were recruited at Moi Teaching and Referral Hospital in Eldoret, Kenya. Data on demographic characteristics, weight, height, abdominal circumference, blood pressure, blood glucose, lipid profile, and treatments were collected. Categorical and continuous data were compared between the patient and control groups using Pearson's chi-squared tests and t-tests, respectively. Variables found to be significantly different between these groups were included in logistic regression models to determine potential predictors of metabolic syndrome.\n\n\nResults\nCompared to controls, patients with psychosis were found to have a higher mean random blood glucose [5.23 vs 4.79, p = 0.003], higher body mass index [5.23 vs 4.79, p = 0.001], higher triglycerides [1.98 vs 1.56, p{\\textless}0.001], larger waist circumference [89.23 vs 86.39, p = 0.009] and lower high density lipoprotein [1.22 vs 1.32, p{\\textless}0.001]. The odds of developing metabolic syndrome were increased with age [OR = 1.05, CI: 1.02–1.07] and presence of a psychotic disorder [OR = 2.09 [CI 1.23–3.55]; and were reduced with female gender [OR 0.41, CI 0.25–0.67], among those who were never married [OR 0.52, CI 0.28–0.94] and among the widowed/separated/ divorced marital status [OR 0.38, CI 0.17–0.81]. While the majority of patients received treatment with olanzapine, there was no association between olanzapine use and metabolic syndrome and its components. More than half of the patients in this study sample were not receiving treatment for the various components of metabolic syndrome.\n\n\nConclusion\nIn the study setting of Eldoret, metabolic syndrome and its components were more prevalent among patients with psychotic disorders than in controls; and a clear treatment gap for these disorders was evident. There is a need for efforts to ensure adequate screening and treatment for these physical disorders in resource-limited settings.},\nauthor = {Kwobah, Edith and Koen, Nastassja and Mwangi, Ann and Atwoli, Lukoye and Stein, Dan J},\ndoi = {10.1371/journal.pone.0245086},\neditor = {Milan, Alberto},\nfile = {:Users/jacquelinebracher/Zotero/storage/7U4UNZUV/Kwobah et al. - 2021 - Prevalence and correlates of metabolic syndrome an.pdf:pdf},\nissn = {1932-6203},\njournal = {PLOS ONE},\nmonth = {jan},\nnumber = {1},\npages = {e0245086},\ntitle = {{Prevalence and correlates of metabolic syndrome and its components in adults with psychotic disorders in {\\{}Eldoret{\\}}, {\\{}Kenya{\\}}}},\nurl = {https://dx.plos.org/10.1371/journal.pone.0245086},\nvolume = {16},\nyear = {2021}\n}\n
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\n Background A high prevalence of metabolic syndrome and its components in patients with psychotic disorders may increase the risk for cardiovascular diseases. Unfortunately, relatively little work in this field has emerged from low-resourced contexts. This study investigated the prevalence, correlates, and treatment patterns of metabolic disorders in patients with psychotic disorders in Western Kenya. Methods 300 patients with psychosis and 300 controls were recruited at Moi Teaching and Referral Hospital in Eldoret, Kenya. Data on demographic characteristics, weight, height, abdominal circumference, blood pressure, blood glucose, lipid profile, and treatments were collected. Categorical and continuous data were compared between the patient and control groups using Pearson's chi-squared tests and t-tests, respectively. Variables found to be significantly different between these groups were included in logistic regression models to determine potential predictors of metabolic syndrome. Results Compared to controls, patients with psychosis were found to have a higher mean random blood glucose [5.23 vs 4.79, p = 0.003], higher body mass index [5.23 vs 4.79, p = 0.001], higher triglycerides [1.98 vs 1.56, p\\textless0.001], larger waist circumference [89.23 vs 86.39, p = 0.009] and lower high density lipoprotein [1.22 vs 1.32, p\\textless0.001]. The odds of developing metabolic syndrome were increased with age [OR = 1.05, CI: 1.02–1.07] and presence of a psychotic disorder [OR = 2.09 [CI 1.23–3.55]; and were reduced with female gender [OR 0.41, CI 0.25–0.67], among those who were never married [OR 0.52, CI 0.28–0.94] and among the widowed/separated/ divorced marital status [OR 0.38, CI 0.17–0.81]. While the majority of patients received treatment with olanzapine, there was no association between olanzapine use and metabolic syndrome and its components. More than half of the patients in this study sample were not receiving treatment for the various components of metabolic syndrome. Conclusion In the study setting of Eldoret, metabolic syndrome and its components were more prevalent among patients with psychotic disorders than in controls; and a clear treatment gap for these disorders was evident. There is a need for efforts to ensure adequate screening and treatment for these physical disorders in resource-limited settings.\n
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\n \n\n \n \n \n \n \n Consensus statement from the international consensus meeting on post-traumatic cranioplasty.\n \n \n \n\n\n \n Iaccarino, C.; Kolias, A.; Adelson, P.; Rubiano, A.; Viaroli, E.; Buki, A.; Cinalli, G.; Fountas, K.; Khan, T.; Signoretti, S.; Hutchinson, P.; and Servadei, F.\n\n\n \n\n\n\n Acta Neurochirurgica, 163(2): 423–440. 2021.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Iaccarino2021,\nabstract = {Background: Due to the lack of high-quality evidence which has hindered the development of evidence-based guidelines, there is a need to provide general guidance on cranioplasty (CP) following traumatic brain injury (TBI), as well as identify areas of ongoing uncertainty via a consensus-based approach. Methods: The international consensus meeting on post-traumatic CP was held during the International Conference on Recent Advances in Neurotraumatology (ICRAN), in Naples, Italy, in June 2018. This meeting was endorsed by the Neurotrauma Committee of the World Federation of Neurosurgical Societies (WFNS), the NIHR Global Health Research Group on Neurotrauma, and several other neurotrauma organizations. Discussions and voting were organized around 5 pre-specified themes: (1) indications and technique, (2) materials, (3) timing, (4) hydrocephalus, and (5) paediatric CP. Results: The participants discussed published evidence on each topic and proposed consensus statements, which were subject to ratification using anonymous real-time voting. Statements required an agreement threshold of more than 70{\\%} for inclusion in the final recommendations. Conclusions: This document is the first set of practical consensus-based clinical recommendations on post-traumatic CP, focusing on timing, materials, complications, and surgical procedures. Future research directions are also presented.},\nauthor = {Iaccarino, C. and Kolias, A. and Adelson, P.D. and Rubiano, A.M. and Viaroli, E. and Buki, A. and Cinalli, G. and Fountas, K. and Khan, T. and Signoretti, S. and Hutchinson, P.J. and Servadei, F.},\ndoi = {10.1007/s00701-020-04663-5},\nfile = {:Users/jacquelinebracher/Zotero/storage/SWL7LG2A/Iaccarino et al. - 2021 - Consensus statement from the international consens.pdf:pdf},\njournal = {Acta Neurochirurgica},\nnumber = {2},\npages = {423--440},\ntitle = {{Consensus statement from the international consensus meeting on post-traumatic cranioplasty}},\nvolume = {163},\nyear = {2021}\n}\n
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\n Background: Due to the lack of high-quality evidence which has hindered the development of evidence-based guidelines, there is a need to provide general guidance on cranioplasty (CP) following traumatic brain injury (TBI), as well as identify areas of ongoing uncertainty via a consensus-based approach. Methods: The international consensus meeting on post-traumatic CP was held during the International Conference on Recent Advances in Neurotraumatology (ICRAN), in Naples, Italy, in June 2018. This meeting was endorsed by the Neurotrauma Committee of the World Federation of Neurosurgical Societies (WFNS), the NIHR Global Health Research Group on Neurotrauma, and several other neurotrauma organizations. Discussions and voting were organized around 5 pre-specified themes: (1) indications and technique, (2) materials, (3) timing, (4) hydrocephalus, and (5) paediatric CP. Results: The participants discussed published evidence on each topic and proposed consensus statements, which were subject to ratification using anonymous real-time voting. Statements required an agreement threshold of more than 70% for inclusion in the final recommendations. Conclusions: This document is the first set of practical consensus-based clinical recommendations on post-traumatic CP, focusing on timing, materials, complications, and surgical procedures. Future research directions are also presented.\n
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\n \n\n \n \n \n \n \n \n Patient outcomes and experience of a task-shared screening and brief intervention service for problem substance use in \\South\\ \\African\\ emergency centres: a mixed methods study.\n \n \n \n \n\n\n \n Van Der Westhuizen, C.; Malan, M.; Naledi, T.; Roelofse, M.; Myers, B.; Stein, D. J; Lahri, S.; and Sorsdahl, K.\n\n\n \n\n\n\n Addiction Science & Clinical Practice, 16(1): 31. dec 2021.\n \n\n\n\n
\n\n\n\n \n \n \"PatientPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{van_der_westhuizen_patient_2021,\nabstract = {Abstract\n\nBackground\nScreening, brief intervention and referral to treatment (SBIRT) programmes have resulted in generally positive outcomes in healthcare settings, particularly for problem alcohol use, yet implementation is hampered by barriers such as concerns regarding the burden on healthcare professionals. In low-resourced settings, task-sharing approaches can reduce this burden by using non-professional healthcare workers, yet data are scarce regarding the outcomes and acceptability to patients within a SBIRT service. This study aims to evaluate patient-reported outcomes, patient acceptability, perceived benefits and recommendations for improving a task-shared SBIRT service in South African emergency centres (ECs).\n\n\nMethods\nThis mixed methods study incorporates quantitative substance use screening and patient satisfaction data collected routinely within the service at three hospitals, and qualitative semi-structured interviews with 18 EC patient beneficiaries of the programme exploring acceptability and perceived benefits of the programme, as well as recommendations to improve the service. Approximately three months after the acute EC visit, a sub-sample of patients were followed up telephonically to assess patient-reported satisfaction and substance use outcomes.\n\n\nResults\nOf the 4847 patients eligible for the brief intervention, 3707 patients (76{\\%}) used alcohol as their primary substance and 794 (16{\\%}) used cannabis. At follow-up (n = 273), significant reductions in substance use frequency and severity were noted and over 95{\\%} of patients were satisfied with the service. In the semi-structured interviews, participants identified the non-judgemental caring approach of the counsellors, and the screening and psychoeducation components of the intervention as being the most valuable, motivating them to decrease substance use and make other positive lifestyle changes. Study participants made recommendations to include group sessions, market the programme in communities and extend the programme's reach to include a broader age group and a variety of settings.\n\n\nConclusions\nThis task-shared SBIRT service was found to be acceptable to patients, who reported several benefits of a single SBIRT contact session delivered during an acute EC visit. These findings add to the SBIRT literature by highlighting the role of non-professional healthcare workers in delivering a low-intensity SBIRT service feasible to implement in low-resourced settings.},\nauthor = {{Van Der Westhuizen}, Claire and Malan, Megan and Naledi, Tracey and Roelofse, Marinda and Myers, Bronwyn and Stein, Dan J and Lahri, Sa'ad and Sorsdahl, Katherine},\ndoi = {10.1186/s13722-021-00239-5},\nfile = {:Users/jacquelinebracher/Zotero/storage/3Q7GBTXC/Van Der Westhuizen et al. - 2021 - Patient outcomes and experience of a task-shared s.pdf:pdf},\nissn = {1940-0640},\njournal = {Addiction Science {\\&} Clinical Practice},\nmonth = {dec},\nnumber = {1},\npages = {31},\nshorttitle = {Patient outcomes and experience of a task-shared s},\ntitle = {{Patient outcomes and experience of a task-shared screening and brief intervention service for problem substance use in {\\{}South{\\}} {\\{}African{\\}} emergency centres: a mixed methods study}},\nurl = {https://ascpjournal.biomedcentral.com/articles/10.1186/s13722-021-00239-5},\nvolume = {16},\nyear = {2021}\n}\n
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\n Abstract Background Screening, brief intervention and referral to treatment (SBIRT) programmes have resulted in generally positive outcomes in healthcare settings, particularly for problem alcohol use, yet implementation is hampered by barriers such as concerns regarding the burden on healthcare professionals. In low-resourced settings, task-sharing approaches can reduce this burden by using non-professional healthcare workers, yet data are scarce regarding the outcomes and acceptability to patients within a SBIRT service. This study aims to evaluate patient-reported outcomes, patient acceptability, perceived benefits and recommendations for improving a task-shared SBIRT service in South African emergency centres (ECs). Methods This mixed methods study incorporates quantitative substance use screening and patient satisfaction data collected routinely within the service at three hospitals, and qualitative semi-structured interviews with 18 EC patient beneficiaries of the programme exploring acceptability and perceived benefits of the programme, as well as recommendations to improve the service. Approximately three months after the acute EC visit, a sub-sample of patients were followed up telephonically to assess patient-reported satisfaction and substance use outcomes. Results Of the 4847 patients eligible for the brief intervention, 3707 patients (76%) used alcohol as their primary substance and 794 (16%) used cannabis. At follow-up (n = 273), significant reductions in substance use frequency and severity were noted and over 95% of patients were satisfied with the service. In the semi-structured interviews, participants identified the non-judgemental caring approach of the counsellors, and the screening and psychoeducation components of the intervention as being the most valuable, motivating them to decrease substance use and make other positive lifestyle changes. Study participants made recommendations to include group sessions, market the programme in communities and extend the programme's reach to include a broader age group and a variety of settings. Conclusions This task-shared SBIRT service was found to be acceptable to patients, who reported several benefits of a single SBIRT contact session delivered during an acute EC visit. These findings add to the SBIRT literature by highlighting the role of non-professional healthcare workers in delivering a low-intensity SBIRT service feasible to implement in low-resourced settings.\n
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\n \n\n \n \n \n \n \n \n Hair-\\Pulling\\ \\Does\\ \\Not\\ \\Necessarily\\ \\Serve\\ an \\Emotion\\ \\Regulation\\ \\Function\\ in \\Adults\\ \\With\\ \\Trichotillomania\\.\n \n \n \n \n\n\n \n Lochner, C.; Demetriou, S.; Kidd, M.; Coetzee, B.; and Stein, D. J\n\n\n \n\n\n\n Frontiers in Psychology, 12: 675468. jul 2021.\n \n\n\n\n
\n\n\n\n \n \n \"Hair-\\Pulling\\Paper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{lochner_hair-pulling_2021,\nabstract = {Background:\nTrichotillomania (TTM) has been associated with childhood trauma and perceived stress. While it has been hypothesized that hair-pulling regulate negative emotions, the relationship between childhood trauma, perceived stress, emotion regulation, and hair-pulling has not been well-studied.\n\n\nMethods:\nFifty-six adults with TTM and 31 healthy controls completed the Childhood Trauma Questionnaire (CTQ), Perceived Stress Scale (PSS), and Difficulties in Emotion Regulation Scale (DERS). Hair-pulling severity was measured with the Massachusetts General Hospital-Hair Pulling Scale. CTQ, PSS, and DERS total scores were compared across groups using ANCOVA and the correlation between hair-pulling severity and emotion dysregulation was determined. Regression analyses were used to estimate the association of CTQ and PSS totals with DERS, and to determine whether associations between predictors and dependent variable (DERS) differed across groups.\n\n\nResults:\nTTM patients reported higher rates of childhood trauma (\np\n{\\textless}= 0.01), perceived stress (\np\n= 0.03), and emotion dysregulation (\np\n{\\textless}= 0.01). There was no association between emotion dysregulation and pulling severity (\nr\n= −0.02,\np\n= 0.89). Perceived stress was associated with emotion dysregulation in both groups (\np\n{\\textless} 0.01), and no association between childhood trauma and emotion dysregulation in either group. Perceived stress was the only significant predictor of emotion dysregulation in both groups (\nF\n= 28.29,\np\n{\\textless} 0.01).\n\n\nConclusion:\nThe association between perceived stress and emotion dysregulation is not specific to TTM, and there is no association between emotion dysregulation and hair-pulling severity, suggesting that key factors other than emotion dysregulation contribute to hair-pulling. Alternative explanatory models are needed.},\nauthor = {Lochner, Christine and Demetriou, Salome and Kidd, Martin and Coetzee, Bronwyn{\\`{e}} and Stein, Dan J},\ndoi = {10.3389/fpsyg.2021.675468},\nfile = {:Users/jacquelinebracher/Zotero/storage/5QTHWUYL/Lochner et al. - 2021 - Hair-Pulling Does Not Necessarily Serve an Emotion.pdf:pdf},\nissn = {1664-1078},\njournal = {Frontiers in Psychology},\nmonth = {jul},\npages = {675468},\ntitle = {{Hair-{\\{}Pulling{\\}} {\\{}Does{\\}} {\\{}Not{\\}} {\\{}Necessarily{\\}} {\\{}Serve{\\}} an {\\{}Emotion{\\}} {\\{}Regulation{\\}} {\\{}Function{\\}} in {\\{}Adults{\\}} {\\{}With{\\}} {\\{}Trichotillomania{\\}}}},\nurl = {https://www.frontiersin.org/articles/10.3389/fpsyg.2021.675468/full},\nvolume = {12},\nyear = {2021}\n}\n
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\n Background: Trichotillomania (TTM) has been associated with childhood trauma and perceived stress. While it has been hypothesized that hair-pulling regulate negative emotions, the relationship between childhood trauma, perceived stress, emotion regulation, and hair-pulling has not been well-studied. Methods: Fifty-six adults with TTM and 31 healthy controls completed the Childhood Trauma Questionnaire (CTQ), Perceived Stress Scale (PSS), and Difficulties in Emotion Regulation Scale (DERS). Hair-pulling severity was measured with the Massachusetts General Hospital-Hair Pulling Scale. CTQ, PSS, and DERS total scores were compared across groups using ANCOVA and the correlation between hair-pulling severity and emotion dysregulation was determined. Regression analyses were used to estimate the association of CTQ and PSS totals with DERS, and to determine whether associations between predictors and dependent variable (DERS) differed across groups. Results: TTM patients reported higher rates of childhood trauma ( p \\textless= 0.01), perceived stress ( p = 0.03), and emotion dysregulation ( p \\textless= 0.01). There was no association between emotion dysregulation and pulling severity ( r = −0.02, p = 0.89). Perceived stress was associated with emotion dysregulation in both groups ( p \\textless 0.01), and no association between childhood trauma and emotion dysregulation in either group. Perceived stress was the only significant predictor of emotion dysregulation in both groups ( F = 28.29, p \\textless 0.01). Conclusion: The association between perceived stress and emotion dysregulation is not specific to TTM, and there is no association between emotion dysregulation and hair-pulling severity, suggesting that key factors other than emotion dysregulation contribute to hair-pulling. Alternative explanatory models are needed.\n
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\n \n\n \n \n \n \n \n \n Dissecting the genetic association of \\C\\-reactive protein with \\PTSD\\, traumatic events, and social support.\n \n \n \n \n\n\n \n Muniz Carvalho, C.; Wendt, F. R; Maihofer, A. X; Stein, D. J; Stein, M. B; Sumner, J. A; Hemmings, S. M J; Nievergelt, C. M; Koenen, K. C; Gelernter, J.; Belangero, S. I; and Polimanti, R.\n\n\n \n\n\n\n Neuropsychopharmacology, 46(6): 1071–1077. may 2021.\n \n\n\n\n
\n\n\n\n \n \n \"DissectingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{muniz_carvalho_dissecting_2021,\nauthor = {{Muniz Carvalho}, Carolina and Wendt, Frank R and Maihofer, Adam X and Stein, Dan J and Stein, Murray B and Sumner, Jennifer A and Hemmings, Sian M J and Nievergelt, Caroline M and Koenen, Karestan C and Gelernter, Joel and Belangero, Sintia I and Polimanti, Renato},\ndoi = {10.1038/s41386-020-0655-6},\nfile = {:Users/jacquelinebracher/Zotero/storage/3SK3W2RY/Muniz Carvalho et al. - 2021 - Dissecting the genetic association of C-reactive p.pdf:pdf},\nissn = {0893-133X, 1740-634X},\njournal = {Neuropsychopharmacology},\nmonth = {may},\nnumber = {6},\npages = {1071--1077},\ntitle = {{Dissecting the genetic association of {\\{}C{\\}}-reactive protein with {\\{}PTSD{\\}}, traumatic events, and social support}},\nurl = {https://www.nature.com/articles/s41386-020-0655-6},\nvolume = {46},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Tuberculosis in \\Myasthenia\\ \\Gravis\\ patients on immunosuppressive therapy in a high-risk area: \\Implications\\ for preventative therapy.\n \n \n \n \n\n\n \n Steyn, E. C; Naidoo, T. M; Marais, S.; and Heckmann, J. M\n\n\n \n\n\n\n Journal of the Neurological Sciences, 425: 117447. jun 2021.\n \n\n\n\n
\n\n\n\n \n \n \"TuberculosisPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{steyn_tuberculosis_2021,\nauthor = {Steyn, Elizabeth C and Naidoo, Tristan M and Marais, Suzaan and Heckmann, Jeannine M},\ndoi = {10.1016/j.jns.2021.117447},\nissn = {0022510X},\njournal = {Journal of the Neurological Sciences},\nmonth = {jun},\npages = {117447},\nshorttitle = {Tuberculosis in {\\{}Myasthenia{\\}} {\\{}Gravis{\\}} patients on },\ntitle = {{Tuberculosis in {\\{}Myasthenia{\\}} {\\{}Gravis{\\}} patients on immunosuppressive therapy in a high-risk area: {\\{}Implications{\\}} for preventative therapy}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S0022510X21001416},\nvolume = {425},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Artificial intelligence for classification of temporal lobe epilepsy with \\ROI\\-level \\MRI\\ data: \\A\\ worldwide \\ENIGMA\\-\\Epilepsy\\ study.\n \n \n \n \n\n\n \n Gleichgerrcht, E.; Munsell, B. C; Alhusaini, S.; Alvim, M. K M; Bargalló, N.; Bender, B.; Bernasconi, A.; Bernasconi, N.; Bernhardt, B.; Blackmon, K.; Caligiuri, M. E.; Cendes, F.; Concha, L.; Desmond, P. M; Devinsky, O.; Doherty, C. P; Domin, M.; Duncan, J. S; Focke, N. K; Gambardella, A.; Gong, B.; Guerrini, R.; Hatton, S. N; Kälviäinen, R.; Keller, S. S; Kochunov, P.; Kotikalapudi, R.; Kreilkamp, B. A K; Labate, A.; Langner, S.; Larivière, S.; Lenge, M.; Lui, E.; Martin, P.; Mascalchi, M.; Meletti, S.; O'Brien, T. J; Pardoe, H. R; Pariente, J. C; Xian Rao, J.; Richardson, M. P; Rodríguez-Cruces, R.; Rüber, T.; Sinclair, B.; Soltanian-Zadeh, H.; Stein, D. J; Striano, P.; Taylor, P. N; Thomas, R. H; Elisabetta Vaudano, A.; Vivash, L.; Von Podewills, F.; Vos, S. B; Weber, B.; Yao, Y.; Lin Yasuda, C.; Zhang, J.; Thompson, P. M; Sisodiya, S. M; McDonald, C. R; Bonilha, L.; Altmann, A.; Depondt, C.; Galovic, M.; Thomopoulos, S. I; and Wiest, R.\n\n\n \n\n\n\n NeuroImage: Clinical, 31: 102765. 2021.\n \n\n\n\n
\n\n\n\n \n \n \"ArtificialPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{gleichgerrcht_artificial_2021,\nauthor = {Gleichgerrcht, Ezequiel and Munsell, Brent C and Alhusaini, Saud and Alvim, Marina K M and Bargall{\\'{o}}, N{\\'{u}}ria and Bender, Benjamin and Bernasconi, Andrea and Bernasconi, Neda and Bernhardt, Boris and Blackmon, Karen and Caligiuri, Maria Eugenia and Cendes, Fernando and Concha, Luis and Desmond, Patricia M and Devinsky, Orrin and Doherty, Colin P and Domin, Martin and Duncan, John S and Focke, Niels K and Gambardella, Antonio and Gong, Bo and Guerrini, Renzo and Hatton, Sean N and K{\\"{a}}lvi{\\"{a}}inen, Reetta and Keller, Simon S and Kochunov, Peter and Kotikalapudi, Raviteja and Kreilkamp, Barbara A K and Labate, Angelo and Langner, Soenke and Larivi{\\`{e}}re, Sara and Lenge, Matteo and Lui, Elaine and Martin, Pascal and Mascalchi, Mario and Meletti, Stefano and O'Brien, Terence J and Pardoe, Heath R and Pariente, Jose C and {Xian Rao}, Jun and Richardson, Mark P and Rodr{\\'{i}}guez-Cruces, Ra{\\'{u}}l and R{\\"{u}}ber, Theodor and Sinclair, Ben and Soltanian-Zadeh, Hamid and Stein, Dan J and Striano, Pasquale and Taylor, Peter N and Thomas, Rhys H and {Elisabetta Vaudano}, Anna and Vivash, Lucy and {Von Podewills}, Felix and Vos, Sjoerd B and Weber, Bernd and Yao, Yi and {Lin Yasuda}, Clarissa and Zhang, Junsong and Thompson, Paul M and Sisodiya, Sanjay M and McDonald, Carrie R and Bonilha, Leonardo and Altmann, Andre and Depondt, Chantal and Galovic, Marian and Thomopoulos, Sophia I and Wiest, Roland},\ndoi = {10.1016/j.nicl.2021.102765},\nfile = {:Users/jacquelinebracher/Zotero/storage/ZLX36JIG/Gleichgerrcht et al. - 2021 - Artificial intelligence for classification of temp.pdf:pdf},\nissn = {22131582},\njournal = {NeuroImage: Clinical},\npages = {102765},\nshorttitle = {Artificial intelligence for classification of temp},\ntitle = {{Artificial intelligence for classification of temporal lobe epilepsy with {\\{}ROI{\\}}-level {\\{}MRI{\\}} data: {\\{}A{\\}} worldwide {\\{}ENIGMA{\\}}-{\\{}Epilepsy{\\}} study}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S2213158221002096},\nvolume = {31},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Peripheral \\Taenia\\ infection increases immunoglobulins in the central nervous system.\n \n \n \n \n\n\n \n Van Belle, S.; De Lange, A.; Tomes, H.; Lucas, R.; Naidoo, V.; and Raimondo, J. V.\n\n\n \n\n\n\n International Journal for Parasitology, 51(8): 685–692. jul 2021.\n \n\n\n\n
\n\n\n\n \n \n \"PeripheralPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{van_belle_peripheral_2021,\nauthor = {{Van Belle}, Sylvia and {De Lange}, Anja and Tomes, Hayley and Lucas, Rodney and Naidoo, Vinogran and Raimondo, Joseph Valentino},\ndoi = {10.1016/j.ijpara.2020.12.008},\nfile = {:Users/jacquelinebracher/Zotero/storage/Q56M3C4F/Van Belle et al. - 2021 - Peripheral Taenia infection increases immunoglobul.pdf:pdf},\nissn = {00207519},\njournal = {International Journal for Parasitology},\nmonth = {jul},\nnumber = {8},\npages = {685--692},\ntitle = {{Peripheral {\\{}Taenia{\\}} infection increases immunoglobulins in the central nervous system}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S0020751921000953},\nvolume = {51},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Randomised controlled trial of naming outcomes in anterior temporal lobectomy versus selective amygdalohippocampectomy.\n \n \n \n \n\n\n \n Ives-Deliperi, V.; and Butler, J. T.\n\n\n \n\n\n\n Journal of Neurology, Neurosurgery & Psychiatry, 92(9): 1020–1021. sep 2021.\n \n\n\n\n
\n\n\n\n \n \n \"RandomisedPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{ives-deliperi_randomised_2021,\nauthor = {Ives-Deliperi, Victoria and Butler, James Thomas},\ndoi = {10.1136/jnnp-2020-324531},\nissn = {0022-3050, 1468-330X},\njournal = {Journal of Neurology, Neurosurgery {\\&} Psychiatry},\nmonth = {sep},\nnumber = {9},\npages = {1020--1021},\ntitle = {{Randomised controlled trial of naming outcomes in anterior temporal lobectomy versus selective amygdalohippocampectomy}},\nurl = {https://jnnp.bmj.com/lookup/doi/10.1136/jnnp-2020-324531},\nvolume = {92},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Evaluation of \\EEG\\ training curricula for non‐specialist clinicians: a systematic qualitative review.\n \n \n \n \n\n\n \n Kander, V.; Hardman, J.; and Wilmshurst, J. M\n\n\n \n\n\n\n Epileptic Disorders, 23(2): 203–217. apr 2021.\n \n\n\n\n
\n\n\n\n \n \n \"EvaluationPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{kander_evaluation_2021,\nabstract = {Abstract\n\n\nObjective\n\n. Neurologists and epileptologists are scarce in sub‐Saharan Africa (SSA). Whilst electroencephalograms (EEGs) are becoming more available in the region, interpretation is typically undertaken by non‐specialist clinicians with limited or no training. This is a systematic review of the peer‐reviewed literature on EEG training of non‐specialist clinicians worldwide, assessing the efficacy of the training methodology and the curricula content.\n\n\n\nMethods\n\n. The published literature was searched for papers relating to EEG training of non‐specialist clinicians worldwide (1/01/1989‐30/06/2020). All regions of the world were included and assessed for content on efficacy of curricula and potential adaptability or applicability to resource‐poor settings. The grey literature was searched using ProQuest and Primo databases and references from review articles. The websites of the International League Against Epilepsy, International Federation of Clinical Neurophysiologist, American Academy of Neurology and World Federation of Neurology were reviewed for reports (non‐peer reviewed) which described roll‐out and impact of novel EEG training curricula.\n\n\n\nResults\n\n. There was limited data. From 2,613 articles, 15 complied with the study question. Ten studies were performed on cross‐speciality clinicians, four on neurology registrars and one on a combination of healthcare workers. There was diversity of curricula models used. The studies themselves lacked consistency and directness. A few training programs were trialled in low‐middle‐income countries (LMICs) and paediatric training was included in only two. An ideal training curriculum was not evident nor evaluated for resource‐poor settings. However, diverse teaching models were reported and set the foundations for further development of EEG training curricula for non‐specialist clinicians.\n\n\n\nSignificance\n\n. There is a lack of access to education in EEG training and interpretation for non‐specialist clinicians in LMICs. Existing models need to be expanded or adapted and evaluated for this population group.},\nauthor = {Kander, Veena and Hardman, Joanne and Wilmshurst, Jo M},\ndoi = {10.1684/epd.2021.1270},\nissn = {1294-9361, 1950-6945},\njournal = {Epileptic Disorders},\nmonth = {apr},\nnumber = {2},\npages = {203--217},\nshorttitle = {Evaluation of {\\{}EEG{\\}} training curricula for non‐spe},\ntitle = {{Evaluation of {\\{}EEG{\\}} training curricula for non‐specialist clinicians: a systematic qualitative review}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1684/epd.2021.1270},\nvolume = {23},\nyear = {2021}\n}\n
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\n Abstract Objective . Neurologists and epileptologists are scarce in sub‐Saharan Africa (SSA). Whilst electroencephalograms (EEGs) are becoming more available in the region, interpretation is typically undertaken by non‐specialist clinicians with limited or no training. This is a systematic review of the peer‐reviewed literature on EEG training of non‐specialist clinicians worldwide, assessing the efficacy of the training methodology and the curricula content. Methods . The published literature was searched for papers relating to EEG training of non‐specialist clinicians worldwide (1/01/1989‐30/06/2020). All regions of the world were included and assessed for content on efficacy of curricula and potential adaptability or applicability to resource‐poor settings. The grey literature was searched using ProQuest and Primo databases and references from review articles. The websites of the International League Against Epilepsy, International Federation of Clinical Neurophysiologist, American Academy of Neurology and World Federation of Neurology were reviewed for reports (non‐peer reviewed) which described roll‐out and impact of novel EEG training curricula. Results . There was limited data. From 2,613 articles, 15 complied with the study question. Ten studies were performed on cross‐speciality clinicians, four on neurology registrars and one on a combination of healthcare workers. There was diversity of curricula models used. The studies themselves lacked consistency and directness. A few training programs were trialled in low‐middle‐income countries (LMICs) and paediatric training was included in only two. An ideal training curriculum was not evident nor evaluated for resource‐poor settings. However, diverse teaching models were reported and set the foundations for further development of EEG training curricula for non‐specialist clinicians. Significance . There is a lack of access to education in EEG training and interpretation for non‐specialist clinicians in LMICs. Existing models need to be expanded or adapted and evaluated for this population group.\n
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\n \n\n \n \n \n \n \n \n Structural brain imaging studies offer clues about the effects of the shared genetic etiology among neuropsychiatric disorders.\n \n \n \n \n\n\n \n Radonjić, N. V; Hess, J. L; Rovira, P.; Andreassen, O.; Buitelaar, J. K; Ching, C. R K; Franke, B.; Hoogman, M.; Jahanshad, N.; McDonald, C.; Schmaal, L.; Sisodiya, S. M; Stein, D. J; Van Den Heuvel, O. A; Van Erp, T. G M; Van Rooij, D.; Veltman, D. J; Thompson, P.; and Faraone, S. V\n\n\n \n\n\n\n Molecular Psychiatry, 26(6): 2101–2110. jun 2021.\n \n\n\n\n
\n\n\n\n \n \n \"StructuralPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{radonjic_structural_2021,\nabstract = {Abstract\n\nGenomewide association studies have found significant genetic correlations among many neuropsychiatric disorders. In contrast, we know much less about the degree to which structural brain alterations are similar among disorders and, if so, the degree to which such similarities have a genetic etiology. From the Enhancing Neuroimaging Genetics through Meta-Analysis (ENIGMA) consortium, we acquired standardized mean differences (SMDs) in regional brain volume and cortical thickness between cases and controls. We had data on 41 brain regions for: attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), bipolar disorder (BD), epilepsy, major depressive disorder (MDD), obsessive compulsive disorder (OCD), and schizophrenia (SCZ). These data had been derived from 24,360 patients and 37,425 controls. The SMDs were significantly correlated between SCZ and BD, OCD, MDD, and ASD. MDD was positively correlated with BD and OCD. BD was positively correlated with OCD and negatively correlated with ADHD. These pairwise correlations among disorders were correlated with the corresponding pairwise correlations among disorders derived from genomewide association studies (\nr\n= 0.494). Our results show substantial similarities in sMRI phenotypes among neuropsychiatric disorders and suggest that these similarities are accounted for, in part, by corresponding similarities in common genetic variant architectures.},\nauthor = {Radonji{\\'{c}}, Nevena V and Hess, Jonathan L and Rovira, Paula and Andreassen, Ole and Buitelaar, Jan K and Ching, Christopher R K and Franke, Barbara and Hoogman, Martine and Jahanshad, Neda and McDonald, Carrie and Schmaal, Lianne and Sisodiya, Sanjay M and Stein, Dan J and {Van Den Heuvel}, Odile A and {Van Erp}, Theo G M and {Van Rooij}, Daan and Veltman, Dick J and Thompson, Paul and Faraone, Stephen V},\ndoi = {10.1038/s41380-020-01002-z},\nfile = {:Users/jacquelinebracher/Zotero/storage/E5X6SNLD/Radonji{\\'{c}} et al. - 2021 - Structural brain imaging studies offer clues about.pdf:pdf},\nissn = {1359-4184, 1476-5578},\njournal = {Molecular Psychiatry},\nmonth = {jun},\nnumber = {6},\npages = {2101--2110},\ntitle = {{Structural brain imaging studies offer clues about the effects of the shared genetic etiology among neuropsychiatric disorders}},\nurl = {https://www.nature.com/articles/s41380-020-01002-z},\nvolume = {26},\nyear = {2021}\n}\n
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\n Abstract Genomewide association studies have found significant genetic correlations among many neuropsychiatric disorders. In contrast, we know much less about the degree to which structural brain alterations are similar among disorders and, if so, the degree to which such similarities have a genetic etiology. From the Enhancing Neuroimaging Genetics through Meta-Analysis (ENIGMA) consortium, we acquired standardized mean differences (SMDs) in regional brain volume and cortical thickness between cases and controls. We had data on 41 brain regions for: attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), bipolar disorder (BD), epilepsy, major depressive disorder (MDD), obsessive compulsive disorder (OCD), and schizophrenia (SCZ). These data had been derived from 24,360 patients and 37,425 controls. The SMDs were significantly correlated between SCZ and BD, OCD, MDD, and ASD. MDD was positively correlated with BD and OCD. BD was positively correlated with OCD and negatively correlated with ADHD. These pairwise correlations among disorders were correlated with the corresponding pairwise correlations among disorders derived from genomewide association studies ( r = 0.494). Our results show substantial similarities in sMRI phenotypes among neuropsychiatric disorders and suggest that these similarities are accounted for, in part, by corresponding similarities in common genetic variant architectures.\n
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\n \n\n \n \n \n \n \n \n Variability in experimental pain studies: nuisance or opportunity?.\n \n \n \n \n\n\n \n Madden, V. J; Kamerman, P. R; Catley, M. J; Bellan, V.; Russek, L. N; Camfferman, D.; and Lorimer Moseley, G\n\n\n \n\n\n\n British Journal of Anaesthesia, 126(2): e61—-e64. feb 2021.\n \n\n\n\n
\n\n\n\n \n \n \"VariabilityPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{madden_variability_2021,\nauthor = {Madden, Victoria J and Kamerman, Peter R and Catley, Mark J and Bellan, Valeria and Russek, Leslie N and Camfferman, Danny and {Lorimer Moseley}, G},\ndoi = {10.1016/j.bja.2020.11.005},\nfile = {:Users/jacquelinebracher/Zotero/storage/5399Y9QE/Madden et al. - 2021 - Variability in experimental pain studies nuisance.pdf:pdf},\nissn = {00070912},\njournal = {British Journal of Anaesthesia},\nmonth = {feb},\nnumber = {2},\npages = {e61----e64},\nshorttitle = {Variability in experimental pain studies},\ntitle = {{Variability in experimental pain studies: nuisance or opportunity?}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S000709122030917X},\nvolume = {126},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Importance of access to epilepsy monitoring units during the \\COVID\\‐19 pandemic: consensus statement of the \\International\\ \\League\\ \\Against\\ \\Epilepsy\\ and the \\International\\ \\Federation\\ of \\Clinical\\ \\Neurophysiology\\∗.\n \n \n \n \n\n\n \n Beniczky, S.; Husain, A.; Ikeda, A.; Alabri, H.; Cross, J H.; Wilmshurst, J.; Seeck, M.; Focke, N.; Braga, P.; Wiebe, S.; Schuele, S.; and Trinka, E.\n\n\n \n\n\n\n Epileptic Disorders, 23(4): 533–536. aug 2021.\n \n\n\n\n
\n\n\n\n \n \n \"ImportancePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{beniczky_importance_2021-1,\nabstract = {Abstract\nRestructuring of healthcare services during the COVID‐19 pandemic has led to lockdown of epilepsy monitoring units (EMUs) in many hospitals. The ad‐hoc taskforce of the International League Against Epilepsy (ILAE) and the International Federation of Clinical Neurophysiology (IFCN) highlights the detrimental effect of postponing video‐EEG monitoring of patients with epilepsy and other paroxysmal events. The taskforce calls for action for continued functioning of EMUs during emergency situations, such as the COVID‐19 pandemic. Long‐term video‐EEG monitoring is an essential diagnostic service. Access to video‐EEG monitoring of the patients in the EMUs must be given high priority. Patients should be screened for COVID‐19, before admission, according to the local regulations. Local policies for COVID‐19 infection control should be adhered to during the video‐EEG monitoring. In cases of differential diagnosis in which reduction of antiseizure medication is not required, home video‐EEG monitoring should be considered as an alternative in selected patients.},\nauthor = {Beniczky, S{\\'{a}}ndor and Husain, Aatif and Ikeda, Akio and Alabri, Haifa and Cross, J Helen and Wilmshurst, Jo and Seeck, Margitta and Focke, Niels and Braga, Patricia and Wiebe, Samuel and Schuele, Stephan and Trinka, Eugen},\ndoi = {10.1684/epd.2021.1292},\nfile = {:Users/jacquelinebracher/Zotero/storage/Q2L9B8JW/Beniczky et al. - 2021 - Importance of access to epilepsy monitoring units .pdf:pdf},\nissn = {1294-9361, 1950-6945},\njournal = {Epileptic Disorders},\nmonth = {aug},\nnumber = {4},\npages = {533--536},\nshorttitle = {Importance of access to epilepsy monitoring units },\ntitle = {{Importance of access to epilepsy monitoring units during the {\\{}COVID{\\}}‐19 pandemic: consensus statement of the {\\{}International{\\}} {\\{}League{\\}} {\\{}Against{\\}} {\\{}Epilepsy{\\}} and the {\\{}International{\\}} {\\{}Federation{\\}} of {\\{}Clinical{\\}} {\\{}Neurophysiology{\\}}∗}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1684/epd.2021.1292},\nvolume = {23},\nyear = {2021}\n}\n
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\n Abstract Restructuring of healthcare services during the COVID‐19 pandemic has led to lockdown of epilepsy monitoring units (EMUs) in many hospitals. The ad‐hoc taskforce of the International League Against Epilepsy (ILAE) and the International Federation of Clinical Neurophysiology (IFCN) highlights the detrimental effect of postponing video‐EEG monitoring of patients with epilepsy and other paroxysmal events. The taskforce calls for action for continued functioning of EMUs during emergency situations, such as the COVID‐19 pandemic. Long‐term video‐EEG monitoring is an essential diagnostic service. Access to video‐EEG monitoring of the patients in the EMUs must be given high priority. Patients should be screened for COVID‐19, before admission, according to the local regulations. Local policies for COVID‐19 infection control should be adhered to during the video‐EEG monitoring. In cases of differential diagnosis in which reduction of antiseizure medication is not required, home video‐EEG monitoring should be considered as an alternative in selected patients.\n
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\n \n\n \n \n \n \n \n \n Microglial Metabolism After Pediatric Traumatic Brain Injury – Overlooked Bystanders or Active Participants?.\n \n \n \n \n\n\n \n Shi, A C; Rohlwink, U; Scafidi, S; and Kannan, S\n\n\n \n\n\n\n 2021.\n \n\n\n\n
\n\n\n\n \n \n \"MicroglialPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Shi2021,\nannote = {Export Date: 29 December 2022},\nauthor = {Shi, A C and Rohlwink, U and Scafidi, S and Kannan, S},\ndoi = {10.3389/fneur.2020.626999},\nfile = {:Users/jacquelinebracher/Zotero/storage/87FY4V3C/Shi et al. - 2021 - Microglial Metabolism After Pediatric Traumatic Br.pdf:pdf},\ntitle = {{Microglial Metabolism After Pediatric Traumatic Brain Injury – Overlooked Bystanders or Active Participants?}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85100612778{\\&}doi=10.3389{\\%}2Ffneur.2020.626999{\\&}partnerID=40{\\&}md5=acece34576d810bdf235a9401c154a79},\nvolume = {11},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Disentangling sex differences in the shared genetic architecture of posttraumatic stress disorder, traumatic experiences, and social support with body size and composition.\n \n \n \n \n\n\n \n Muniz Carvalho, C.; Wendt, F. R; Pathak, G. A; Maihofer, A. X; Stein, D. J; Sumner, J. A; Hemmings, S. M J; Nievergelt, C. M; Koenen, K. C; Gelernter, J.; Belangero, S. I; and Polimanti, R.\n\n\n \n\n\n\n Neurobiology of Stress, 15: 100400. nov 2021.\n \n\n\n\n
\n\n\n\n \n \n \"DisentanglingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{muniz_carvalho_disentangling_2021,\nauthor = {{Muniz Carvalho}, Carolina and Wendt, Frank R and Pathak, Gita A and Maihofer, Adam X and Stein, Dan J and Sumner, Jennifer A and Hemmings, Sian M J and Nievergelt, Caroline M and Koenen, Karestan C and Gelernter, Joel and Belangero, Sintia I and Polimanti, Renato},\ndoi = {10.1016/j.ynstr.2021.100400},\nfile = {:Users/jacquelinebracher/Zotero/storage/8HG2AGYQ/Muniz Carvalho et al. - 2021 - Disentangling sex differences in the shared geneti.pdf:pdf},\nissn = {23522895},\njournal = {Neurobiology of Stress},\nmonth = {nov},\npages = {100400},\ntitle = {{Disentangling sex differences in the shared genetic architecture of posttraumatic stress disorder, traumatic experiences, and social support with body size and composition}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S2352289521001089},\nvolume = {15},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Lipocalin 2 as a link between ageing, risk factor conditions and age-related brain diseases.\n \n \n \n \n\n\n \n Dekens, D. W; Eisel, U. L M; Gouweleeuw, L.; Schoemaker, R. G; De Deyn, P. P; and Naudé, P. J W\n\n\n \n\n\n\n Ageing Research Reviews, 70: 101414. sep 2021.\n \n\n\n\n
\n\n\n\n \n \n \"LipocalinPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{dekens_lipocalin_2021,\nauthor = {Dekens, Doortje W and Eisel, Ulrich L M and Gouweleeuw, Leonie and Schoemaker, Regien G and {De Deyn}, Peter P and Naud{\\'{e}}, Petrus J W},\ndoi = {10.1016/j.arr.2021.101414},\nfile = {:Users/jacquelinebracher/Zotero/storage/WLS8EJPX/Dekens et al. - 2021 - Lipocalin 2 as a link between ageing, risk factor .pdf:pdf},\nissn = {15681637},\njournal = {Ageing Research Reviews},\nmonth = {sep},\npages = {101414},\ntitle = {{Lipocalin 2 as a link between ageing, risk factor conditions and age-related brain diseases}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S1568163721001616},\nvolume = {70},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Identifying subtypes of trichotillomania (hair pulling disorder) and excoriation (skin picking) disorder using mixture modeling in a multicenter sample.\n \n \n \n \n\n\n \n Grant, J. E; Peris, T. S; Ricketts, E. J; Lochner, C.; Stein, D. J; Stochl, J.; Chamberlain, S. R; Scharf, J. M; Dougherty, D. D; Woods, D. W; Piacentini, J.; and Keuthen, N. J\n\n\n \n\n\n\n Journal of Psychiatric Research, 137: 603–612. may 2021.\n \n\n\n\n
\n\n\n\n \n \n \"IdentifyingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{grant_identifying_2021,\nauthor = {Grant, Jon E and Peris, Tara S and Ricketts, Emily J and Lochner, Christine and Stein, Dan J and Stochl, Jan and Chamberlain, Samuel R and Scharf, Jeremiah M and Dougherty, Darin D and Woods, Douglas W and Piacentini, John and Keuthen, Nancy J},\ndoi = {10.1016/j.jpsychires.2020.11.001},\nfile = {:Users/jacquelinebracher/Zotero/storage/TTKIKVE8/Grant et al. - 2021 - Identifying subtypes of trichotillomania (hair pul.pdf:pdf},\nissn = {00223956},\njournal = {Journal of Psychiatric Research},\nmonth = {may},\npages = {603--612},\ntitle = {{Identifying subtypes of trichotillomania (hair pulling disorder) and excoriation (skin picking) disorder using mixture modeling in a multicenter sample}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S0022395620310578},\nvolume = {137},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Traumatic Brain Injury–Related Pediatric Mortality and Morbidity in Low- and Middle-Income Countries: A Systematic Review.\n \n \n \n \n\n\n \n Bandyopadhyay, S; Kawka, M; Marks, K; Richards, G C; Taylor, E H; Sravanam, S; Petrinic, T; Thango, N; Figaji, A; Peter, N; and Lakhoo, K\n\n\n \n\n\n\n 2021.\n \n\n\n\n
\n\n\n\n \n \n \"TraumaticPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Bandyopadhyay2021,\nannote = {Export Date: 29 December 2022},\nauthor = {Bandyopadhyay, S and Kawka, M and Marks, K and Richards, G C and Taylor, E H and Sravanam, S and Petrinic, T and Thango, N and Figaji, A and Peter, N and Lakhoo, K},\ndoi = {10.1016/j.wneu.2021.06.077},\npages = {109--130.e23},\ntitle = {{Traumatic Brain Injury–Related Pediatric Mortality and Morbidity in Low- and Middle-Income Countries: A Systematic Review}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85111594772{\\&}doi=10.1016{\\%}2Fj.wneu.2021.06.077{\\&}partnerID=40{\\&}md5=64c6ed1a5c7641e88b4f0b2d88496823},\nvolume = {153},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Low-coverage sequencing cost-effectively detects known and novel variation in underrepresented populations.\n \n \n \n \n\n\n \n Martin, A. R; Atkinson, E. G; Chapman, S. B; Stevenson, A.; Stroud, R. E; Abebe, T.; Akena, D.; Alemayehu, M.; Ashaba, F. K; Atwoli, L.; Bowers, T.; Chibnik, L. B; Daly, M. J; DeSmet, T.; Dodge, S.; Fekadu, A.; Ferriera, S.; Gelaye, B.; Gichuru, S.; Injera, W. E; James, R.; Kariuki, S. M; Kigen, G.; Koenen, K. C; Kwobah, E.; Kyebuzibwa, J.; Majara, L.; Musinguzi, H.; Mwema, R. M; Neale, B. M; Newman, C. P; Newton, C. R J C; Pickrell, J. K; Ramesar, R.; Shiferaw, W.; Stein, D. J; Teferra, S.; Van Der Merwe, C.; and Zingela, Z.\n\n\n \n\n\n\n The American Journal of Human Genetics, 108(4): 656–668. apr 2021.\n \n\n\n\n
\n\n\n\n \n \n \"Low-coveragePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{martin_low-coverage_2021,\nauthor = {Martin, Alicia R and Atkinson, Elizabeth G and Chapman, Sin{\\'{e}}ad B and Stevenson, Anne and Stroud, Rocky E and Abebe, Tamrat and Akena, Dickens and Alemayehu, Melkam and Ashaba, Fred K and Atwoli, Lukoye and Bowers, Tera and Chibnik, Lori B and Daly, Mark J and DeSmet, Timothy and Dodge, Sheila and Fekadu, Abebaw and Ferriera, Steven and Gelaye, Bizu and Gichuru, Stella and Injera, Wilfred E and James, Roxanne and Kariuki, Symon M and Kigen, Gabriel and Koenen, Karestan C and Kwobah, Edith and Kyebuzibwa, Joseph and Majara, Lerato and Musinguzi, Henry and Mwema, Rehema M and Neale, Benjamin M and Newman, Carter P and Newton, Charles R J C and Pickrell, Joseph K and Ramesar, Raj and Shiferaw, Welelta and Stein, Dan J and Teferra, Solomon and {Van Der Merwe}, Celia and Zingela, Zukiswa},\ndoi = {10.1016/j.ajhg.2021.03.012},\nfile = {:Users/jacquelinebracher/Zotero/storage/29J6MTUC/Martin et al. - 2021 - Low-coverage sequencing cost-effectively detects k.pdf:pdf},\nissn = {00029297},\njournal = {The American Journal of Human Genetics},\nmonth = {apr},\nnumber = {4},\npages = {656--668},\ntitle = {{Low-coverage sequencing cost-effectively detects known and novel variation in underrepresented populations}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S0002929721000963},\nvolume = {108},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Does duration of HIV infection substitute for age as a risk factor for amyloid deposition?.\n \n \n \n \n\n\n \n Ipser, J C; and Vera, J H\n\n\n \n\n\n\n 2021.\n \n\n\n\n
\n\n\n\n \n \n \"DoesPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Ipser2021,\nannote = {Export Date: 29 December 2022},\nauthor = {Ipser, J C and Vera, J H},\ndoi = {10.1097/QAD.0000000000002932},\nfile = {:Users/jacquelinebracher/Zotero/storage/AJBYCASR/Ipser and Vera - 2021 - Does duration of HIV infection substitute for age .pdf:pdf},\nnumber = {9},\npages = {1501--1502},\ntitle = {{Does duration of HIV infection substitute for age as a risk factor for amyloid deposition?}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85109825547{\\&}doi=10.1097{\\%}2FQAD.0000000000002932{\\&}partnerID=40{\\&}md5=8b623813be2058eef4224c9f70aa7783},\nvolume = {35},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Rationale for and usefulness of the inclusion of gaming disorder in the \\ICD\\‐11.\n \n \n \n \n\n\n \n Billieux, J.; Stein, D. J; Castro‐Calvo, J.; Higushi, S.; and King, D. L\n\n\n \n\n\n\n World Psychiatry, 20(2): 198–199. jun 2021.\n \n\n\n\n
\n\n\n\n \n \n \"RationalePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{billieux_rationale_2021,\nauthor = {Billieux, Jo{\\"{e}}l and Stein, Dan J and Castro‐Calvo, Jesus and Higushi, Susumu and King, Daniel L},\ndoi = {10.1002/wps.20848},\nfile = {:Users/jacquelinebracher/Zotero/storage/TBCT3YQK/Billieux et al. - 2021 - Rationale for and usefulness of the inclusion of g.pdf:pdf},\nissn = {1723-8617, 2051-5545},\njournal = {World Psychiatry},\nmonth = {jun},\nnumber = {2},\npages = {198--199},\ntitle = {{Rationale for and usefulness of the inclusion of gaming disorder in the {\\{}ICD{\\}}‐11}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1002/wps.20848},\nvolume = {20},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Brain interstitial glycerol correlates with evolving brain injury in paediatric traumatic brain injury.\n \n \n \n \n\n\n \n Thango, N S; Rohlwink, U K; Dlamini, L; Tshavhungwe, M P; Banderker, E; Salie, S; Enslin, J M N; and Figaji, A A\n\n\n \n\n\n\n 2021.\n \n\n\n\n
\n\n\n\n \n \n \"BrainPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Thango2021,\nannote = {Export Date: 29 December 2022},\nauthor = {Thango, N S and Rohlwink, U K and Dlamini, L and Tshavhungwe, M P and Banderker, E and Salie, S and Enslin, J M N and Figaji, A A},\ndoi = {10.1007/s00381-021-05058-2},\nnumber = {5},\npages = {1713--1721},\ntitle = {{Brain interstitial glycerol correlates with evolving brain injury in paediatric traumatic brain injury}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85100858300{\\&}doi=10.1007{\\%}2Fs00381-021-05058-2{\\&}partnerID=40{\\&}md5=a38f1d163ef9af5b89df0fa4ddac11b2},\nvolume = {37},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n Rates of cognitive impairment in a South African cohort of people with HIV: variation by definitional criteria and lack of association with neuroimaging biomarkers.\n \n \n \n\n\n \n Dreyer, A.; Nightingale, S.; Heaps-Woodruff, J.; Henry, M.; Gouse, H.; Paul, R.; Thomas, K.; and Joska, J.\n\n\n \n\n\n\n Journal of NeuroVirology, 27(4): 579–594. 2021.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Dreyer2021,\nabstract = {There is wide variation in the reported prevalence of cognitive impairment in people with HIV (PWH). Part of this variation may be attributable to different studies using different methods of combining neuropsychological test scores to classify participants as either cognitively impaired or unimpaired. Our aim was to determine, in a South African cohort of PWH (N = 148), (a) how much variation in reported rates was due to method used to define cognitive impairment and (b) which method correlated best with MRI biomarkers of HIV-related brain pathology. Participants completed detailed neuropsychological assessment and underwent 3 T structural MRI and diffusion tensor imaging (DTI). We used the neuropsychological data to investigate 20 different methods of determining HIV-associated cognitive impairment. We used the neuroimaging data to obtain volumes for cortical and subcortical grey matter and total white matter and DTI metrics for several white matter tracts. Applying each of the 20 methods to the cognitive dataset resulted in a wide variation (20–97{\\%}) in estimated rates of impairment. Logistic regression models showed no method was associated with HIV-related neuroimaging abnormalities as measured by structural volumes or DTI metrics. We conclude that for the population from which this sample was drawn, much of the variation in reported rates of cognitive impairment in PWH is due to the method of classification used, and that none of these methods accurately reflects biological effects of HIV in the brain. We suggest that defining HIV-associated cognitive impairment using neuropsychological test performance only is insufficient; pre-morbid functioning, co-morbidities, cognitive symptoms, and functional impairment should always be considered.},\nauthor = {Dreyer, A.J. and Nightingale, S. and Heaps-Woodruff, J.M. and Henry, M. and Gouse, H. and Paul, R.H. and Thomas, K.G.F. and Joska, J.A.},\ndoi = {10.1007/s13365-021-00993-x},\njournal = {Journal of NeuroVirology},\nnumber = {4},\npages = {579--594},\ntitle = {{Rates of cognitive impairment in a South African cohort of people with HIV: variation by definitional criteria and lack of association with neuroimaging biomarkers}},\nvolume = {27},\nyear = {2021}\n}\n
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\n There is wide variation in the reported prevalence of cognitive impairment in people with HIV (PWH). Part of this variation may be attributable to different studies using different methods of combining neuropsychological test scores to classify participants as either cognitively impaired or unimpaired. Our aim was to determine, in a South African cohort of PWH (N = 148), (a) how much variation in reported rates was due to method used to define cognitive impairment and (b) which method correlated best with MRI biomarkers of HIV-related brain pathology. Participants completed detailed neuropsychological assessment and underwent 3 T structural MRI and diffusion tensor imaging (DTI). We used the neuropsychological data to investigate 20 different methods of determining HIV-associated cognitive impairment. We used the neuroimaging data to obtain volumes for cortical and subcortical grey matter and total white matter and DTI metrics for several white matter tracts. Applying each of the 20 methods to the cognitive dataset resulted in a wide variation (20–97%) in estimated rates of impairment. Logistic regression models showed no method was associated with HIV-related neuroimaging abnormalities as measured by structural volumes or DTI metrics. We conclude that for the population from which this sample was drawn, much of the variation in reported rates of cognitive impairment in PWH is due to the method of classification used, and that none of these methods accurately reflects biological effects of HIV in the brain. We suggest that defining HIV-associated cognitive impairment using neuropsychological test performance only is insufficient; pre-morbid functioning, co-morbidities, cognitive symptoms, and functional impairment should always be considered.\n
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\n \n\n \n \n \n \n \n \n Altered white matter microstructural organization in posttraumatic stress disorder across 3047 adults: results from the PGC-ENIGMA PTSD consortium.\n \n \n \n \n\n\n \n Dennis, E L; Disner, S G; Fani, N; Salminen, L E; Logue, M; Clarke, E K; Haswell, C C; Averill, C L; Baugh, L A; Bomyea, J; Bruce, S E; Cha, J; Choi, K; Davenport, N D; Densmore, M; du Plessis, S; Forster, G L; Frijling, J L; Gonenc, A; Gruber, S; Grupe, D W; Guenette, J P; Hayes, J; Hofmann, D; Ipser, J; Jovanovic, T; Kelly, S; Kennis, M; Kinzel, P; Koch, S B J; Koerte, I; Koopowitz, S; Korgaonkar, M; Krystal, J; Lebois, L A M; Li, G; Magnotta, V A; Manthey, A; May, G J; Menefee, D S; Nawijn, L; Nelson, S M; Neufeld, R W J; Nitschke, J B; O'Doherty, D; Peverill, M; Ressler, K J; Roos, A; Sheridan, M A; Sierk, A; Simmons, A; Simons, R M; Simons, J S; Stevens, J; Suarez-Jimenez, B; Sullivan, D R; Théberge, J; Tran, J K; van den Heuvel, L; van der Werff, S J A; van Rooij, S J H; van Zuiden, M; Velez, C; Verfaellie, M; Vermeiren, R.; Wade, B S C; Wager, T; Walter, H; Winternitz, S; Wolff, J; York, G; Zhu, Y; Zhu, X; Abdallah, C G; Bryant, R; Daniels, J K; Davidson, R J; Fercho, K A; Franz, C; Geuze, E; Gordon, E M; Kaufman, M L; Kremen, W S; Lagopoulos, J; Lanius, R A; Lyons, M J; McCauley, S R; McGlinchey, R; McLaughlin, K A; Milberg, W; Neria, Y; Olff, M; Seedat, S; Shenton, M; Sponheim, S R; Stein, D J; Stein, M B; Straube, T; Tate, D F; van der Wee, N J A; Veltman, D J; Wang, L; Wilde, E A; Thompson, P M; Kochunov, P; Jahanshad, N; and Morey, R A\n\n\n \n\n\n\n 2021.\n \n\n\n\n
\n\n\n\n \n \n \"AlteredPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Dennis2021a,\nannote = {Export Date: 29 December 2022},\nauthor = {Dennis, E L and Disner, S G and Fani, N and Salminen, L E and Logue, M and Clarke, E K and Haswell, C C and Averill, C L and Baugh, L A and Bomyea, J and Bruce, S E and Cha, J and Choi, K and Davenport, N D and Densmore, M and du Plessis, S and Forster, G L and Frijling, J L and Gonenc, A and Gruber, S and Grupe, D W and Guenette, J P and Hayes, J and Hofmann, D and Ipser, J and Jovanovic, T and Kelly, S and Kennis, M and Kinzel, P and Koch, S B J and Koerte, I and Koopowitz, S and Korgaonkar, M and Krystal, J and Lebois, L A M and Li, G and Magnotta, V A and Manthey, A and May, G J and Menefee, D S and Nawijn, L and Nelson, S M and Neufeld, R W J and Nitschke, J B and O'Doherty, D and Peverill, M and Ressler, K J and Roos, A and Sheridan, M A and Sierk, A and Simmons, A and Simons, R M and Simons, J S and Stevens, J and Suarez-Jimenez, B and Sullivan, D R and Th{\\'{e}}berge, J and Tran, J K and van den Heuvel, L and van der Werff, S J A and van Rooij, S J H and van Zuiden, M and Velez, C and Verfaellie, M and Vermeiren, R.R.J.M. and Wade, B S C and Wager, T and Walter, H and Winternitz, S and Wolff, J and York, G and Zhu, Y and Zhu, X and Abdallah, C G and Bryant, R and Daniels, J K and Davidson, R J and Fercho, K A and Franz, C and Geuze, E and Gordon, E M and Kaufman, M L and Kremen, W S and Lagopoulos, J and Lanius, R A and Lyons, M J and McCauley, S R and McGlinchey, R and McLaughlin, K A and Milberg, W and Neria, Y and Olff, M and Seedat, S and Shenton, M and Sponheim, S R and Stein, D J and Stein, M B and Straube, T and Tate, D F and van der Wee, N J A and Veltman, D J and Wang, L and Wilde, E A and Thompson, P M and Kochunov, P and Jahanshad, N and Morey, R A},\ndoi = {10.1038/s41380-019-0631-x},\nfile = {:Users/jacquelinebracher/Zotero/storage/FKYCL8T9/Dennis et al. - 2021 - Altered white matter microstructural organization .pdf:pdf},\nnumber = {8},\npages = {4315--4330},\ntitle = {{Altered white matter microstructural organization in posttraumatic stress disorder across 3047 adults: results from the PGC-ENIGMA PTSD consortium}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85077020994{\\&}doi=10.1038{\\%}2Fs41380-019-0631-x{\\&}partnerID=40{\\&}md5=a0577daacf1d6c56c05253d918592906},\nvolume = {26},\nyear = {2021}\n}\n
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\n \n\n \n \n \n \n \n \n Cortical and subcortical brain structure in generalized anxiety disorder: findings from 28 research sites in the \\ENIGMA\\-\\Anxiety\\ \\Working\\ \\Group\\.\n \n \n \n \n\n\n \n Harrewijn, A.; Cardinale, E. M; Groenewold, N. A; Bas-Hoogendam, J. M.; Aghajani, M.; Hilbert, K.; Cardoner, N.; Porta-Casteràs, D.; Gosnell, S.; Salas, R.; Jackowski, A. P; Pan, P. M; Salum, G. A; Blair, K. S; Blair, J. R; Hammoud, M. Z; Milad, M. R; Burkhouse, K. L; Phan, K L.; Schroeder, H. K; Strawn, J. R; Beesdo-Baum, K.; Jahanshad, N.; Thomopoulos, S. I; Buckner, R.; Nielsen, J. A; Smoller, J. W; Soares, J. C; Mwangi, B.; Wu, M.; Zunta-Soares, G. B; Assaf, M.; Diefenbach, G. J; Brambilla, P.; Maggioni, E.; Hofmann, D.; Straube, T.; Andreescu, C.; Berta, R.; Tamburo, E.; Price, R. B; Manfro, G. G; Agosta, F.; Canu, E.; Cividini, C.; Filippi, M.; Kostić, M.; Munjiza Jovanovic, A.; Alberton, B. A V; Benson, B.; Freitag, G. F; Filippi, C. A; Gold, A. L; Leibenluft, E.; Ringlein, G. V; Werwath, K. E; Zwiebel, H.; Zugman, A.; Grabe, H. J; Van Der Auwera, S.; Wittfeld, K.; Völzke, H.; Bülow, R.; Balderston, N. L; Ernst, M.; Grillon, C.; Mujica-Parodi, L. R; Van Nieuwenhuizen, H.; Critchley, H. D; Makovac, E.; Mancini, M.; Meeten, F.; Ottaviani, C.; Ball, T. M; Fonzo, G. A; Paulus, M. P; Stein, M. B; Gur, R. E; Gur, R. C; Kaczkurkin, A. N; Larsen, B.; Satterthwaite, T. D; Harper, J.; Myers, M.; Perino, M. T; Sylvester, C. M; Yu, Q.; Lueken, U.; Veltman, D. J; Thompson, P. M; Stein, D. J; Van Der Wee, N. J A; Winkler, A. M; and Pine, D. S\n\n\n \n\n\n\n Translational Psychiatry, 11(1): 502. oct 2021.\n \n\n\n\n
\n\n\n\n \n \n \"CorticalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{harrewijn_cortical_2021,\nabstract = {Abstract\nThe goal of this study was to compare brain structure between individuals with generalized anxiety disorder (GAD) and healthy controls. Previous studies have generated inconsistent findings, possibly due to small sample sizes, or clinical/analytic heterogeneity. To address these concerns, we combined data from 28 research sites worldwide through the ENIGMA-Anxiety Working Group, using a single, pre-registered mega-analysis. Structural magnetic resonance imaging data from children and adults (5–90 years) were processed using FreeSurfer. The main analysis included the regional and vertex-wise cortical thickness, cortical surface area, and subcortical volume as dependent variables, and GAD, age, age-squared, sex, and their interactions as independent variables. Nuisance variables included IQ, years of education, medication use, comorbidities, and global brain measures. The main analysis (1020 individuals with GAD and 2999 healthy controls) included random slopes per site and random intercepts per scanner. A secondary analysis (1112 individuals with GAD and 3282 healthy controls) included fixed slopes and random intercepts per scanner with the same variables. The main analysis showed no effect of GAD on brain structure, nor interactions involving GAD, age, or sex. The secondary analysis showed increased volume in the right ventral diencephalon in male individuals with GAD compared to male healthy controls, whereas female individuals with GAD did not differ from female healthy controls. This mega-analysis combining worldwide data showed that differences in brain structure related to GAD are small, possibly reflecting heterogeneity or those structural alterations are not a major component of its pathophysiology.},\nauthor = {Harrewijn, Anita and Cardinale, Elise M and Groenewold, Nynke A and Bas-Hoogendam, Janna Marie and Aghajani, Moji and Hilbert, Kevin and Cardoner, Narcis and Porta-Caster{\\`{a}}s, Daniel and Gosnell, Savannah and Salas, Ramiro and Jackowski, Andrea P and Pan, Pedro M and Salum, Giovanni A and Blair, Karina S and Blair, James R and Hammoud, Mira Z and Milad, Mohammed R and Burkhouse, Katie L and Phan, K Luan and Schroeder, Heidi K and Strawn, Jeffrey R and Beesdo-Baum, Katja and Jahanshad, Neda and Thomopoulos, Sophia I and Buckner, Randy and Nielsen, Jared A and Smoller, Jordan W and Soares, Jair C and Mwangi, Benson and Wu, Mon-Ju and Zunta-Soares, Giovana B and Assaf, Michal and Diefenbach, Gretchen J and Brambilla, Paolo and Maggioni, Eleonora and Hofmann, David and Straube, Thomas and Andreescu, Carmen and Berta, Rachel and Tamburo, Erica and Price, Rebecca B and Manfro, Gisele G and Agosta, Federica and Canu, Elisa and Cividini, Camilla and Filippi, Massimo and Kosti{\\'{c}}, Milutin and {Munjiza Jovanovic}, Ana and Alberton, Bianca A V and Benson, Brenda and Freitag, Gabrielle F and Filippi, Courtney A and Gold, Andrea L and Leibenluft, Ellen and Ringlein, Grace V and Werwath, Kathryn E and Zwiebel, Hannah and Zugman, Andr{\\'{e}} and Grabe, Hans J and {Van Der Auwera}, Sandra and Wittfeld, Katharina and V{\\"{o}}lzke, Henry and B{\\"{u}}low, Robin and Balderston, Nicholas L and Ernst, Monique and Grillon, Christian and Mujica-Parodi, Lilianne R and {Van Nieuwenhuizen}, Helena and Critchley, Hugo D and Makovac, Elena and Mancini, Matteo and Meeten, Frances and Ottaviani, Cristina and Ball, Tali M and Fonzo, Gregory A and Paulus, Martin P and Stein, Murray B and Gur, Raquel E and Gur, Ruben C and Kaczkurkin, Antonia N and Larsen, Bart and Satterthwaite, Theodore D and Harper, Jennifer and Myers, Michael and Perino, Michael T and Sylvester, Chad M and Yu, Qiongru and Lueken, Ulrike and Veltman, Dick J and Thompson, Paul M and Stein, Dan J and {Van Der Wee}, Nic J A and Winkler, Anderson M and Pine, Daniel S},\ndoi = {10.1038/s41398-021-01622-1},\nfile = {:Users/jacquelinebracher/Zotero/storage/WX2I7XVD/Harrewijn et al. - 2021 - Cortical and subcortical brain structure in genera.pdf:pdf},\nissn = {2158-3188},\njournal = {Translational Psychiatry},\nmonth = {oct},\nnumber = {1},\npages = {502},\nshorttitle = {Cortical and subcortical brain structure in genera},\ntitle = {{Cortical and subcortical brain structure in generalized anxiety disorder: findings from 28 research sites in the {\\{}ENIGMA{\\}}-{\\{}Anxiety{\\}} {\\{}Working{\\}} {\\{}Group{\\}}}},\nurl = {https://www.nature.com/articles/s41398-021-01622-1},\nvolume = {11},\nyear = {2021}\n}\n
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\n Abstract The goal of this study was to compare brain structure between individuals with generalized anxiety disorder (GAD) and healthy controls. Previous studies have generated inconsistent findings, possibly due to small sample sizes, or clinical/analytic heterogeneity. To address these concerns, we combined data from 28 research sites worldwide through the ENIGMA-Anxiety Working Group, using a single, pre-registered mega-analysis. Structural magnetic resonance imaging data from children and adults (5–90 years) were processed using FreeSurfer. The main analysis included the regional and vertex-wise cortical thickness, cortical surface area, and subcortical volume as dependent variables, and GAD, age, age-squared, sex, and their interactions as independent variables. Nuisance variables included IQ, years of education, medication use, comorbidities, and global brain measures. The main analysis (1020 individuals with GAD and 2999 healthy controls) included random slopes per site and random intercepts per scanner. A secondary analysis (1112 individuals with GAD and 3282 healthy controls) included fixed slopes and random intercepts per scanner with the same variables. The main analysis showed no effect of GAD on brain structure, nor interactions involving GAD, age, or sex. The secondary analysis showed increased volume in the right ventral diencephalon in male individuals with GAD compared to male healthy controls, whereas female individuals with GAD did not differ from female healthy controls. This mega-analysis combining worldwide data showed that differences in brain structure related to GAD are small, possibly reflecting heterogeneity or those structural alterations are not a major component of its pathophysiology.\n
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\n \n\n \n \n \n \n \n \n Using structural \\MRI\\ to identify bipolar disorders – 13 site machine learning study in 3020 individuals from the \\ENIGMA\\ \\Bipolar\\ \\Disorders\\ \\Working\\ \\Group\\.\n \n \n \n \n\n\n \n Nunes, A.; Schnack, H. G; Ching, C. R K; Agartz, I.; Akudjedu, T. N; Alda, M.; Alnæs, D.; Alonso-Lana, S.; Bauer, J.; Baune, B. T; Bøen, E.; Bonnin, C. D. M.; Busatto, G. F; Canales-Rodríguez, E. J; Cannon, D. M; Caseras, X.; Chaim-Avancini, T. M; Dannlowski, U.; Díaz-Zuluaga, A. M; Dietsche, B.; Doan, N. T.; Duchesnay, E.; Elvsåshagen, T.; Emden, D.; Eyler, L. T; Fatjó-Vilas, M.; Favre, P.; Foley, S. F; Fullerton, J. M; Glahn, D. C; Goikolea, J. M; Grotegerd, D.; Hahn, T.; Henry, C.; Hibar, D. P; Houenou, J.; Howells, F. M; Jahanshad, N.; Kaufmann, T.; Kenney, J.; Kircher, T. T J; Krug, A.; Lagerberg, T. V; Lenroot, R. K; López-Jaramillo, C.; Machado-Vieira, R.; Malt, U. F; McDonald, C.; Mitchell, P. B; Mwangi, B.; Nabulsi, L.; Opel, N.; Overs, B. J; Pineda-Zapata, J. A; Pomarol-Clotet, E.; Redlich, R.; Roberts, G.; Rosa, P. G; Salvador, R.; Satterthwaite, T. D; Soares, J. C; Stein, D. J; Temmingh, H. S; Trappenberg, T.; Uhlmann, A.; Van Haren, N. E M; Vieta, E.; Westlye, L. T; Wolf, D. H; Yüksel, D.; Zanetti, M. V; Andreassen, O. A; Thompson, P. M; Hajek, T.; and for the ENIGMA Bipolar Disorders Working Group\n\n\n \n\n\n\n Molecular Psychiatry, 25(9): 2130–2143. sep 2020.\n \n\n\n\n
\n\n\n\n \n \n \"UsingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{nunes_using_2020,\nabstract = {Abstract\nBipolar disorders (BDs) are among the leading causes of morbidity and disability. Objective biological markers, such as those based on brain imaging, could aid in clinical management of BD. Machine learning (ML) brings neuroimaging analyses to individual subject level and may potentially allow for their diagnostic use. However, fair and optimal application of ML requires large, multi-site datasets. We applied ML (support vector machines) to MRI data (regional cortical thickness, surface area, subcortical volumes) from 853 BD and 2167 control participants from 13 cohorts in the ENIGMA consortium. We attempted to differentiate BD from control participants, investigated different data handling strategies and studied the neuroimaging/clinical features most important for classification. Individual site accuracies ranged from 45.23{\\%} to 81.07{\\%}. Aggregate subject-level analyses yielded the highest accuracy (65.23{\\%}, 95{\\%} CI = 63.47–67.00, ROC-AUC = 71.49{\\%}, 95{\\%} CI = 69.39–73.59), followed by leave-one-site-out cross-validation (accuracy = 58.67{\\%}, 95{\\%} CI = 56.70–60.63). Meta-analysis of individual site accuracies did not provide above chance results. There was substantial agreement between the regions that contributed to identification of BD participants in the best performing site and in the aggregate dataset (Cohen's Kappa = 0.83, 95{\\%} CI = 0.829–0.831). Treatment with anticonvulsants and age were associated with greater odds of correct classification. Although short of the 80{\\%} clinically relevant accuracy threshold, the results are promising and provide a fair and realistic estimate of classification performance, which can be achieved in a large, ecologically valid, multi-site sample of BD participants based on regional neurostructural measures. Furthermore, the significant classification in different samples was based on plausible and similar neuroanatomical features. Future multi-site studies should move towards sharing of raw/voxelwise neuroimaging data.},\nauthor = {Nunes, Abraham and Schnack, Hugo G and Ching, Christopher R K and Agartz, Ingrid and Akudjedu, Theophilus N and Alda, Martin and Aln{\\ae}s, Dag and Alonso-Lana, Silvia and Bauer, Jochen and Baune, Bernhard T and B{\\o}en, Erlend and Bonnin, Caterina Del Mar and Busatto, Geraldo F and Canales-Rodr{\\'{i}}guez, Erick J and Cannon, Dara M and Caseras, Xavier and Chaim-Avancini, Tiffany M and Dannlowski, Udo and D{\\'{i}}az-Zuluaga, Ana M and Dietsche, Bruno and Doan, Nhat Trung and Duchesnay, Edouard and Elvs{\\aa}shagen, Torbj{\\o}rn and Emden, Daniel and Eyler, Lisa T and Fatj{\\'{o}}-Vilas, Mar and Favre, Pauline and Foley, Sonya F and Fullerton, Janice M and Glahn, David C and Goikolea, Jose M and Grotegerd, Dominik and Hahn, Tim and Henry, Chantal and Hibar, Derrek P and Houenou, Josselin and Howells, Fleur M and Jahanshad, Neda and Kaufmann, Tobias and Kenney, Joanne and Kircher, Tilo T J and Krug, Axel and Lagerberg, Trine V and Lenroot, Rhoshel K and L{\\'{o}}pez-Jaramillo, Carlos and Machado-Vieira, Rodrigo and Malt, Ulrik F and McDonald, Colm and Mitchell, Philip B and Mwangi, Benson and Nabulsi, Leila and Opel, Nils and Overs, Bronwyn J and Pineda-Zapata, Julian A and Pomarol-Clotet, Edith and Redlich, Ronny and Roberts, Gloria and Rosa, Pedro G and Salvador, Raymond and Satterthwaite, Theodore D and Soares, Jair C and Stein, Dan J and Temmingh, Henk S and Trappenberg, Thomas and Uhlmann, Anne and {Van Haren}, Neeltje E M and Vieta, Eduard and Westlye, Lars T and Wolf, Daniel H and Y{\\"{u}}ksel, Dilara and Zanetti, Marcus V and Andreassen, Ole A and Thompson, Paul M and Hajek, Tomas and {for the ENIGMA Bipolar Disorders Working Group}},\ndoi = {10.1038/s41380-018-0228-9},\nfile = {:Users/jacquelinebracher/Zotero/storage/4JI5V6XT/Nunes et al. - 2020 - Using structural MRI to identify bipolar disorders.pdf:pdf},\nissn = {1359-4184, 1476-5578},\njournal = {Molecular Psychiatry},\nmonth = {sep},\nnumber = {9},\npages = {2130--2143},\ntitle = {{Using structural {\\{}MRI{\\}} to identify bipolar disorders – 13 site machine learning study in 3020 individuals from the {\\{}ENIGMA{\\}} {\\{}Bipolar{\\}} {\\{}Disorders{\\}} {\\{}Working{\\}} {\\{}Group{\\}}}},\nurl = {https://www.nature.com/articles/s41380-018-0228-9},\nvolume = {25},\nyear = {2020}\n}\n
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\n Abstract Bipolar disorders (BDs) are among the leading causes of morbidity and disability. Objective biological markers, such as those based on brain imaging, could aid in clinical management of BD. Machine learning (ML) brings neuroimaging analyses to individual subject level and may potentially allow for their diagnostic use. However, fair and optimal application of ML requires large, multi-site datasets. We applied ML (support vector machines) to MRI data (regional cortical thickness, surface area, subcortical volumes) from 853 BD and 2167 control participants from 13 cohorts in the ENIGMA consortium. We attempted to differentiate BD from control participants, investigated different data handling strategies and studied the neuroimaging/clinical features most important for classification. Individual site accuracies ranged from 45.23% to 81.07%. Aggregate subject-level analyses yielded the highest accuracy (65.23%, 95% CI = 63.47–67.00, ROC-AUC = 71.49%, 95% CI = 69.39–73.59), followed by leave-one-site-out cross-validation (accuracy = 58.67%, 95% CI = 56.70–60.63). Meta-analysis of individual site accuracies did not provide above chance results. There was substantial agreement between the regions that contributed to identification of BD participants in the best performing site and in the aggregate dataset (Cohen's Kappa = 0.83, 95% CI = 0.829–0.831). Treatment with anticonvulsants and age were associated with greater odds of correct classification. Although short of the 80% clinically relevant accuracy threshold, the results are promising and provide a fair and realistic estimate of classification performance, which can be achieved in a large, ecologically valid, multi-site sample of BD participants based on regional neurostructural measures. Furthermore, the significant classification in different samples was based on plausible and similar neuroanatomical features. Future multi-site studies should move towards sharing of raw/voxelwise neuroimaging data.\n
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\n \n\n \n \n \n \n \n \n \\MRS\\ suggests multi-regional inflammation and white matter axonal damage at 11 years following perinatal \\HIV\\ infection.\n \n \n \n \n\n\n \n Graham, A. S; Holmes, M. J; Little, F.; Dobbels, E.; Cotton, M. F; Laughton, B.; Van Der Kouwe, A.; Meintjes, E. M; and Robertson, F. C\n\n\n \n\n\n\n NeuroImage: Clinical, 28: 102505. 2020.\n \n\n\n\n
\n\n\n\n \n \n \"\\MRS\\Paper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{graham_mrs_2020,\nauthor = {Graham, Amy S and Holmes, Martha J and Little, Francesca and Dobbels, Els and Cotton, Mark F and Laughton, Barbara and {Van Der Kouwe}, Andre and Meintjes, Ernesta M and Robertson, Frances C},\ndoi = {10.1016/j.nicl.2020.102505},\nfile = {:Users/jacquelinebracher/Zotero/storage/ISEF3GSK/Graham et al. - 2020 - MRS suggests multi-regional inflammation and white.pdf:pdf},\nissn = {22131582},\njournal = {NeuroImage: Clinical},\npages = {102505},\ntitle = {{{\\{}MRS{\\}} suggests multi-regional inflammation and white matter axonal damage at 11 years following perinatal {\\{}HIV{\\}} infection}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S2213158220303429},\nvolume = {28},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n Establishing criteria for pediatric epilepsy surgery center levels of care: \\Report\\ from the \\ILAE\\ \\Pediatric\\ \\Epilepsy\\ \\Surgery\\ \\Task\\ \\Force\\.\n \n \n \n \n\n\n \n Gaillard, W. D; Jette, N.; Arnold, S. T; Arzimanoglou, A.; Braun, K. P J; Cukiert, A.; Dick, A.; Harvey, A S.; Jacobs, J.; Rydenhag, B.; Udani, V.; Wilmshurst, J. M; Cross, J H.; Jayakar, P.; Task Force for Pediatric Epilepsy Surgery, Commission for Pediatrics,; and the Surgical Commission of the International League Against Epilepsy\n\n\n \n\n\n\n Epilepsia, 61(12): 2629–2642. dec 2020.\n \n\n\n\n
\n\n\n\n \n \n \"EstablishingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{gaillard_establishing_2020,\nabstract = {Abstract\nPresurgical evaluation and surgery in the pediatric age group are unique in challenges related to caring for the very young, range of etiologies, choice of appropriate investigations, and surgical procedures. Accepted standards that define the criteria for levels of presurgical evaluation and epilepsy surgery care do not exist. Through a modified Delphi process involving 61 centers with experience in pediatric epilepsy surgery across 20 countries, including low–middle‐ to high‐income countries, we established consensus for two levels of care. Levels were based on age, etiology, complexity of presurgical evaluation, and surgical procedure. Competencies were assigned to the levels of care relating to personnel, technology, and facilities. Criteria were established when consensus was reached (≥75{\\%} agreement). Level 1 care consists of children age 9 years and older, with discrete lesions including hippocampal sclerosis, undergoing lobectomy or lesionectomy, preferably on the cerebral convexity and not close to eloquent cortex, by a team including a pediatric epileptologist, pediatric neurosurgeon, and pediatric neuroradiologist with access to video‐electroencephalography and 1.5‐T magnetic resonance imaging (MRI). Level 2 care, also encompassing Level 1 care, occurs across the age span and range of etiologies (including tuberous sclerosis complex, Sturge‐Weber syndrome, hypothalamic hamartoma) associated with MRI lesions that may be ill‐defined, multilobar, hemispheric, or multifocal, and includes children with normal MRI or foci in/abutting eloquent cortex. Available Level 2 technologies includes 3‐T MRI, other advanced magnetic resonance technology including functional MRI and diffusion tensor imaging (tractography), positron emission tomography and/or single photon emission computed tomography, source localization with electroencephalography or magnetoencephalography, and the ability to perform intra‐ or extraoperative invasive monitoring and functional mapping, by a large multidisciplinary team with pediatric expertise in epilepsy, neurophysiology, neuroradiology, epilepsy neurosurgery, neuropsychology, anesthesia, neurocritical care, psychiatry, and nursing. Levels of care will improve safety and outcomes for pediatric epilepsy surgery and provide standards for personnel and technology to achieve these levels.},\nauthor = {Gaillard, William D and Jette, Nathalie and Arnold, Susan T and Arzimanoglou, Alexis and Braun, Kees P J and Cukiert, Arthur and Dick, Alexander and Harvey, A Simon and Jacobs, Julia and Rydenhag, Bertil and Udani, Vrajesh and Wilmshurst, Jo M and Cross, J Helen and Jayakar, Prasanna and {Task Force for Pediatric Epilepsy Surgery, Commission for Pediatrics, and the Surgical Commission of the International League Against Epilepsy}},\ndoi = {10.1111/epi.16698},\nfile = {:Users/jacquelinebracher/Zotero/storage/V39G63CW/Gaillard et al. - 2020 - Establishing criteria for pediatric epilepsy surge.pdf:pdf},\nissn = {0013-9580, 1528-1167},\njournal = {Epilepsia},\nmonth = {dec},\nnumber = {12},\npages = {2629--2642},\nshorttitle = {Establishing criteria for pediatric epilepsy surge},\ntitle = {{Establishing criteria for pediatric epilepsy surgery center levels of care: {\\{}Report{\\}} from the {\\{}ILAE{\\}} {\\{}Pediatric{\\}} {\\{}Epilepsy{\\}} {\\{}Surgery{\\}} {\\{}Task{\\}} {\\{}Force{\\}}}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1111/epi.16698},\nvolume = {61},\nyear = {2020}\n}\n
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\n Abstract Presurgical evaluation and surgery in the pediatric age group are unique in challenges related to caring for the very young, range of etiologies, choice of appropriate investigations, and surgical procedures. Accepted standards that define the criteria for levels of presurgical evaluation and epilepsy surgery care do not exist. Through a modified Delphi process involving 61 centers with experience in pediatric epilepsy surgery across 20 countries, including low–middle‐ to high‐income countries, we established consensus for two levels of care. Levels were based on age, etiology, complexity of presurgical evaluation, and surgical procedure. Competencies were assigned to the levels of care relating to personnel, technology, and facilities. Criteria were established when consensus was reached (≥75% agreement). Level 1 care consists of children age 9 years and older, with discrete lesions including hippocampal sclerosis, undergoing lobectomy or lesionectomy, preferably on the cerebral convexity and not close to eloquent cortex, by a team including a pediatric epileptologist, pediatric neurosurgeon, and pediatric neuroradiologist with access to video‐electroencephalography and 1.5‐T magnetic resonance imaging (MRI). Level 2 care, also encompassing Level 1 care, occurs across the age span and range of etiologies (including tuberous sclerosis complex, Sturge‐Weber syndrome, hypothalamic hamartoma) associated with MRI lesions that may be ill‐defined, multilobar, hemispheric, or multifocal, and includes children with normal MRI or foci in/abutting eloquent cortex. Available Level 2 technologies includes 3‐T MRI, other advanced magnetic resonance technology including functional MRI and diffusion tensor imaging (tractography), positron emission tomography and/or single photon emission computed tomography, source localization with electroencephalography or magnetoencephalography, and the ability to perform intra‐ or extraoperative invasive monitoring and functional mapping, by a large multidisciplinary team with pediatric expertise in epilepsy, neurophysiology, neuroradiology, epilepsy neurosurgery, neuropsychology, anesthesia, neurocritical care, psychiatry, and nursing. Levels of care will improve safety and outcomes for pediatric epilepsy surgery and provide standards for personnel and technology to achieve these levels.\n
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\n \n\n \n \n \n \n \n \n Association between maternal psychological adversity and lung function in South African infants: A birth cohort study.\n \n \n \n \n\n\n \n Kariuki, S M; Gray, D M; Newton, C.; Vanker, A; MacGinty, R P; Koen, N; Barnett, W; Chibnik, L; Koenen, K C; Stein, D J; and Zar, H J\n\n\n \n\n\n\n Pediatric Pulmonology, 55(1): 236–244. 2020.\n \n\n\n\n
\n\n\n\n \n \n \"AssociationPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n\n\n\n
\n 
@article{Kariuki2020236,\nannote = {cited By 0},\nauthor = {Kariuki, S M and Gray, D M and Newton, C.R.J.C. and Vanker, A and MacGinty, R P and Koen, N and Barnett, W and Chibnik, L and Koenen, K C and Stein, D J and Zar, H J},\ndoi = {10.1002/ppul.24532},\nfile = {:Users/jacquelinebracher/Zotero/storage/6IBHG9K5/Kariuki et al. - 2020 - Association between maternal psychological adversi.pdf:pdf},\nissn = {87556863},\njournal = {Pediatric Pulmonology},\nkeywords = {adult; antenatal depression; Article; birth; breat},\nnumber = {1},\npages = {236--244},\npublisher = {John Wiley and Sons Inc.},\ntitle = {{Association between maternal psychological adversity and lung function in South African infants: A birth cohort study}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85073936981{\\&}doi=10.1002{\\%}2Fppul.24532{\\&}partnerID=40{\\&}md5=087b9ab967ebc2485bddb5cafd3f794d},\nvolume = {55},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n Ethical issues in global neuroimaging genetics collaborations.\n \n \n \n \n\n\n \n Palk, A.; Illes, J.; Thompson, P. M; and Stein, D. J\n\n\n \n\n\n\n NeuroImage, 221: 117208. nov 2020.\n \n\n\n\n
\n\n\n\n \n \n \"EthicalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{palk_ethical_2020,\nauthor = {Palk, Andrea and Illes, Judy and Thompson, Paul M and Stein, Dan J},\ndoi = {10.1016/j.neuroimage.2020.117208},\nfile = {:Users/jacquelinebracher/Zotero/storage/PMTUDPPF/Palk et al. - 2020 - Ethical issues in global neuroimaging genetics col.pdf:pdf},\nissn = {10538119},\njournal = {NeuroImage},\nmonth = {nov},\npages = {117208},\ntitle = {{Ethical issues in global neuroimaging genetics collaborations}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S1053811920306947},\nvolume = {221},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n The association of peripheral immune markers with brain cortical thickness and surface area in South African people living with HIV.\n \n \n \n\n\n \n Williams, M.; Joska, J.; Amod, A.; Paul, R.; Stein, D.; Ipser, J.; and Naudé, P.\n\n\n \n\n\n\n Journal of NeuroVirology, 26(6): 908–919. 2020.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Williams2020c,\nabstract = {A spectrum of cognitive impairments known as HIV-associated neurocognitive disorders (HAND) are consequences of the effects of HIV-1 within the central nervous system. Regardless of treatment status, an aberrant chronic neuro-immune regulation is a crucial contributor to the development of HAND. However, the extent to which inflammation affects brain structures critical for cognitive status remains unclear. The present study aimed to determine associations of peripheral immune markers with cortical thickness and surface area. Participants included 65 treatment-na{\\"{i}}ve HIV-positive individuals and 26 HIV-negative controls. Thickness and surface area of all cortical regions were derived using automated parcellation of T1-weighted images acquired at 3 T. Peripheral immune markers included C-C motif ligand 2 (CCL2), matrix metalloproteinase 9 (MMP9), neutrophil gelatinase-associated lipocalin (NGAL), thymidine phosphorylase (TYMP), transforming growth factor (TGF)-$\\beta$1, and vascular endothelial growth factor (VEGF), which were measured using enzyme-linked immunosorbent assays. Associations of these markers with thickness and surface area of cortical regions were evaluated. A mediation analysis examined whether associations of inflammatory markers with cognitive functioning were mediated by brain cortical thickness and surface area. After controlling for multiple comparisons, higher NGAL was associated with reduced thickness of the bilateral orbitofrontal cortex in HIV-positive participants. The association of NGAL with worse motor function was mediated by cortical thickness of the bilateral orbitofrontal region. Taken together, this study suggests that NGAL plays a potential role in the neuropathophysiology of neurocognitive impairments of HIV.},\nauthor = {Williams, M.E. and Joska, J.A. and Amod, A.R. and Paul, R.H. and Stein, D.J. and Ipser, J.C. and Naud{\\'{e}}, P.J.W.},\ndoi = {10.1007/s13365-020-00873-w},\njournal = {Journal of NeuroVirology},\nnumber = {6},\npages = {908--919},\ntitle = {{The association of peripheral immune markers with brain cortical thickness and surface area in South African people living with HIV}},\nvolume = {26},\nyear = {2020}\n}\n
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\n A spectrum of cognitive impairments known as HIV-associated neurocognitive disorders (HAND) are consequences of the effects of HIV-1 within the central nervous system. Regardless of treatment status, an aberrant chronic neuro-immune regulation is a crucial contributor to the development of HAND. However, the extent to which inflammation affects brain structures critical for cognitive status remains unclear. The present study aimed to determine associations of peripheral immune markers with cortical thickness and surface area. Participants included 65 treatment-naïve HIV-positive individuals and 26 HIV-negative controls. Thickness and surface area of all cortical regions were derived using automated parcellation of T1-weighted images acquired at 3 T. Peripheral immune markers included C-C motif ligand 2 (CCL2), matrix metalloproteinase 9 (MMP9), neutrophil gelatinase-associated lipocalin (NGAL), thymidine phosphorylase (TYMP), transforming growth factor (TGF)-$β$1, and vascular endothelial growth factor (VEGF), which were measured using enzyme-linked immunosorbent assays. Associations of these markers with thickness and surface area of cortical regions were evaluated. A mediation analysis examined whether associations of inflammatory markers with cognitive functioning were mediated by brain cortical thickness and surface area. After controlling for multiple comparisons, higher NGAL was associated with reduced thickness of the bilateral orbitofrontal cortex in HIV-positive participants. The association of NGAL with worse motor function was mediated by cortical thickness of the bilateral orbitofrontal region. Taken together, this study suggests that NGAL plays a potential role in the neuropathophysiology of neurocognitive impairments of HIV.\n
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\n \n\n \n \n \n \n \n \n COVID-19: Increased Risk to the Mental Health and Safety of Women Living with HIV in South Africa.\n \n \n \n \n\n\n \n Joska, J A; Andersen, L; Rabie, S; Marais, A; Ndwandwa, E.; Wilson, P; King, A; and Sikkema, K J\n\n\n \n\n\n\n AIDS and Behavior. 2020.\n \n\n\n\n
\n\n\n\n \n \n \"COVID-19:Paper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Joska2020,\nannote = {cited By 1},\nauthor = {Joska, J A and Andersen, L and Rabie, S and Marais, A and Ndwandwa, E.-S. and Wilson, P and King, A and Sikkema, K J},\ndoi = {10.1007/s10461-020-02897-z},\nfile = {:Users/jacquelinebracher/Zotero/storage/3LPPXMCJ/Joska et al. - 2020 - COVID-19 Increased Risk to the Mental Health and .pdf:pdf},\nissn = {10907165},\njournal = {AIDS and Behavior},\npublisher = {Springer},\ntitle = {{COVID-19: Increased Risk to the Mental Health and Safety of Women Living with HIV in South Africa}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85083987047{\\&}doi=10.1007{\\%}2Fs10461-020-02897-z{\\&}partnerID=40{\\&}md5=9c9eeeabe2b8610acd7becf74f59a973},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n Management of intracranial tuberculous mass lesions: How long should we treat for?.\n \n \n \n\n\n \n Marais, S.; Van Toorn, R.; Chow, F.; Manesh, A.; Siddiqi, O.; Figaji, A.; Schoeman, J.; Meintjes, G.; Aarnoutse, R.; Anderson, S.; Wasserman, S.; and Wilkinson, R.\n\n\n \n\n\n\n Wellcome Open Research, 4. 2020.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Marais2020,\nabstract = {Tuberculous intracranial mass lesions are common in settings with high tuberculosis (TB) incidence and HIV prevalence. The diagnosis of such lesions, which include tuberculoma and tuberculous abscesses, is often presumptive and based on radiological features, supportive evidence of TB elsewhere and response to TB treatment. However, the treatment response is unpredictable, with lesions frequently enlarging paradoxically or persisting for many years despite appropriate TB treatment and corticosteroid therapy. Most international guidelines recommend a 9-12 month course of TB treatment for central nervous system TB when the infecting Mycobacterium tuberculosis ( M.tb) strain is sensitive to first-line drugs. However, there is variation in opinion and practice with respect to the duration of TB treatment in patients with tuberculomas or tuberculous abscesses. A major reason for this is the lack of prospective clinical trial evidence. Some experts suggest continuing treatment until radiological resolution of enhancing lesions has been achieved, but this may unnecessarily expose patients to prolonged periods of potentially toxic drugs. It is currently unknown whether persistent radiological enhancement of intracranial tuberculomas after 9-12 months of treatment represents active disease, inflammatory response in a sterilized lesion or merely revascularization. The consequences of stopping TB treatment prior to resolution of lesional enhancement have rarely been explored. These important issues were discussed at the 3 rd International Tuberculous Meningitis Consortium meeting. Most clinicians were of the opinion that continued enhancement does not necessarily represent treatment failure and that prolonged TB therapy was not warranted in patients presumably infected with M.tb strains susceptible to first-line drugs. In this manuscript we highlight current medical treatment practices, benefits and disadvantages of different TB treatment durations and the need for evidence-based guidelines regarding the treatment duration of patients with intracranial tuberculous mass lesions.},\nauthor = {Marais, S. and {Van Toorn}, R. and Chow, F.C. and Manesh, A. and Siddiqi, O.K. and Figaji, A. and Schoeman, J.F. and Meintjes, G. and Aarnoutse, R.E. and Anderson, S.T.B. and Wasserman, S.A. and Wilkinson, R.J.},\ndoi = {10.12688/wellcomeopenres.15501.3},\nfile = {:Users/jacquelinebracher/Zotero/storage/Y6Y9Q2TS/Marais et al. - 2020 - Management of intracranial tuberculous mass lesion.pdf:pdf},\njournal = {Wellcome Open Research},\ntitle = {{Management of intracranial tuberculous mass lesions: How long should we treat for?}},\nvolume = {4},\nyear = {2020}\n}\n
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\n Tuberculous intracranial mass lesions are common in settings with high tuberculosis (TB) incidence and HIV prevalence. The diagnosis of such lesions, which include tuberculoma and tuberculous abscesses, is often presumptive and based on radiological features, supportive evidence of TB elsewhere and response to TB treatment. However, the treatment response is unpredictable, with lesions frequently enlarging paradoxically or persisting for many years despite appropriate TB treatment and corticosteroid therapy. Most international guidelines recommend a 9-12 month course of TB treatment for central nervous system TB when the infecting Mycobacterium tuberculosis ( M.tb) strain is sensitive to first-line drugs. However, there is variation in opinion and practice with respect to the duration of TB treatment in patients with tuberculomas or tuberculous abscesses. A major reason for this is the lack of prospective clinical trial evidence. Some experts suggest continuing treatment until radiological resolution of enhancing lesions has been achieved, but this may unnecessarily expose patients to prolonged periods of potentially toxic drugs. It is currently unknown whether persistent radiological enhancement of intracranial tuberculomas after 9-12 months of treatment represents active disease, inflammatory response in a sterilized lesion or merely revascularization. The consequences of stopping TB treatment prior to resolution of lesional enhancement have rarely been explored. These important issues were discussed at the 3 rd International Tuberculous Meningitis Consortium meeting. Most clinicians were of the opinion that continued enhancement does not necessarily represent treatment failure and that prolonged TB therapy was not warranted in patients presumably infected with M.tb strains susceptible to first-line drugs. In this manuscript we highlight current medical treatment practices, benefits and disadvantages of different TB treatment durations and the need for evidence-based guidelines regarding the treatment duration of patients with intracranial tuberculous mass lesions.\n
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\n \n\n \n \n \n \n \n \n The effects of acute serotonin challenge on executive planning in patients with obsessive–compulsive disorder (OCD), their first-degree relatives, and healthy controls.\n \n \n \n \n\n\n \n Lochner, C; Chamberlain, S R; Kidd, M; Taljaard, L; Fineberg, N A; Robbins, T W; and Stein, D J\n\n\n \n\n\n\n Psychopharmacology. 2020.\n \n\n\n\n
\n\n\n\n \n \n \"ThePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Lochner2020,\nannote = {cited By 0},\nauthor = {Lochner, C and Chamberlain, S R and Kidd, M and Taljaard, L and Fineberg, N A and Robbins, T W and Stein, D J},\ndoi = {10.1007/s00213-020-05597-7},\nfile = {:Users/jacquelinebracher/Zotero/storage/D4367DPY/Lochner et al. - 2020 - The effects of acute serotonin challenge on execut.pdf:pdf},\nissn = {00333158},\njournal = {Psychopharmacology},\npublisher = {Springer},\ntitle = {{The effects of acute serotonin challenge on executive planning in patients with obsessive–compulsive disorder (OCD), their first-degree relatives, and healthy controls}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85087647578{\\&}doi=10.1007{\\%}2Fs00213-020-05597-7{\\&}partnerID=40{\\&}md5=a1594501da4a2834fd0b98667adabe3d},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n Clinical advances in obsessive-compulsive disorder: A position statement by the International College of Obsessive-Compulsive Spectrum Disorders.\n \n \n \n \n\n\n \n Fineberg, N A; Hollander, E; Pallanti, S; Walitza, S; Grünblatt, E; Dell'Osso, B M; Albert, U; Geller, D A; Brakoulias, V; Janardhan Reddy, Y C; Arumugham, S S; Shavitt, R G; Drummond, L; Grancini, B; De Carlo, V; Cinosi, E; Chamberlain, S R; Ioannidis, K; Rodriguez, C I; Garg, K; Castle, D; Van Ameringen, M; Stein, D J; Carmi, L; Zohar, J; and Menchon, J M\n\n\n \n\n\n\n International Clinical Psychopharmacology,173–193. 2020.\n \n\n\n\n
\n\n\n\n \n \n \"ClinicalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Fineberg2020173,\nannote = {cited By 1},\nauthor = {Fineberg, N A and Hollander, E and Pallanti, S and Walitza, S and Gr{\\"{u}}nblatt, E and Dell'Osso, B M and Albert, U and Geller, D A and Brakoulias, V and {Janardhan Reddy}, Y C and Arumugham, S S and Shavitt, R G and Drummond, L and Grancini, B and {De Carlo}, V and Cinosi, E and Chamberlain, S R and Ioannidis, K and Rodriguez, C I and Garg, K and Castle, D and {Van Ameringen}, M and Stein, D J and Carmi, L and Zohar, J and Menchon, J M},\ndoi = {10.1097/YIC.0000000000000314},\nfile = {:Users/jacquelinebracher/Zotero/storage/2FYQXYYD/Fineberg et al. - 2020 - Clinical advances in obsessive-compulsive disorder.pdf:pdf},\nissn = {02681315},\njournal = {International Clinical Psychopharmacology},\npages = {173--193},\npublisher = {Lippincott Williams and Wilkins},\ntitle = {{Clinical advances in obsessive-compulsive disorder: A position statement by the International College of Obsessive-Compulsive Spectrum Disorders}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85085883572{\\&}doi=10.1097{\\%}2FYIC.0000000000000314{\\&}partnerID=40{\\&}md5=64431366e15dce4133355e92a15a5ca0},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n Taenia larvae possess distinct acetylcholinesterase profiles with implications for host cholinergic signalling.\n \n \n \n \n\n\n \n De Lange, A.; Prodjinotho, U. F.; Tomes, H.; Hagen, J.; Jacobs, B.; Smith, K.; Horsnell, W.; Sikasunge, C.; Hockman, D.; Selkirk, M. E; Prazeres Da Costa, C.; and Raimondo, J. V.\n\n\n \n\n\n\n PLOS Neglected Tropical Diseases, 14(12): e0008966. dec 2020.\n \n\n\n\n
\n\n\n\n \n \n \"TaeniaPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{de_lange_taenia_2020,\nabstract = {Larvae of the cestodes\nTaenia solium\nand\nTaenia crassiceps\ninfect the central nervous system of humans.\nTaenia solium\nlarvae in the brain cause neurocysticercosis, the leading cause of adult-acquired epilepsy worldwide. Relatively little is understood about how cestode-derived products modulate host neural and immune signalling. Acetylcholinesterases, a class of enzyme that breaks down acetylcholine, are produced by a host of parasitic worms to aid their survival in the host. Acetylcholine is an important signalling molecule in both the human nervous and immune systems, with powerful modulatory effects on the excitability of cortical networks. Therefore, it is important to establish whether cestode derived acetylcholinesterases may alter host neuronal cholinergic signalling. Here we make use of multiple techniques to profile acetylcholinesterase activity in different extracts of both\nTaenia crassiceps\nand\nTaenia solium\nlarvae. We find that the larvae of both species contain substantial acetylcholinesterase activity. However, acetylcholinesterase activity is lower in\nTaenia solium\nas compared to\nTaenia crassiceps\nlarvae. Further, whilst we observed acetylcholinesterase activity in all fractions of\nTaenia crassiceps\nlarvae, including on the membrane surface and in the excreted/secreted extracts, we could not identify acetylcholinesterases on the membrane surface or in the excreted/secreted extracts of\nTaenia solium\nlarvae. Bioinformatic analysis revealed conservation of the functional protein domains in the\nTaenia solium\nacetylcholinesterases, when compared to the homologous human sequence. Finally, using whole-cell patch clamp recordings in rat hippocampal brain slice cultures, we demonstrate that\nTaenia\nlarval derived acetylcholinesterases can break down acetylcholine at a concentration which induces changes in neuronal signalling. Together, these findings highlight the possibility that\nTaenia\nlarval acetylcholinesterases can interfere with cholinergic signalling in the host, potentially contributing to pathogenesis in neurocysticercosis.},\nauthor = {{De Lange}, Anja and Prodjinotho, Ulrich Fabien and Tomes, Hayley and Hagen, Jana and Jacobs, Brittany-Amber and Smith, Katherine and Horsnell, William and Sikasunge, Chummy and Hockman, Dorit and Selkirk, Murray E and {Prazeres Da Costa}, Clarissa and Raimondo, Joseph Valentino},\ndoi = {10.1371/journal.pntd.0008966},\neditor = {Mitre, Edward},\nfile = {:Users/jacquelinebracher/Zotero/storage/GR23EQTD/De Lange et al. - 2020 - Taenia larvae possess distinct acetylcholinesteras.pdf:pdf},\nissn = {1935-2735},\njournal = {PLOS Neglected Tropical Diseases},\nmonth = {dec},\nnumber = {12},\npages = {e0008966},\ntitle = {{Taenia larvae possess distinct acetylcholinesterase profiles with implications for host cholinergic signalling}},\nurl = {https://dx.plos.org/10.1371/journal.pntd.0008966},\nvolume = {14},\nyear = {2020}\n}\n
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\n Larvae of the cestodes Taenia solium and Taenia crassiceps infect the central nervous system of humans. Taenia solium larvae in the brain cause neurocysticercosis, the leading cause of adult-acquired epilepsy worldwide. Relatively little is understood about how cestode-derived products modulate host neural and immune signalling. Acetylcholinesterases, a class of enzyme that breaks down acetylcholine, are produced by a host of parasitic worms to aid their survival in the host. Acetylcholine is an important signalling molecule in both the human nervous and immune systems, with powerful modulatory effects on the excitability of cortical networks. Therefore, it is important to establish whether cestode derived acetylcholinesterases may alter host neuronal cholinergic signalling. Here we make use of multiple techniques to profile acetylcholinesterase activity in different extracts of both Taenia crassiceps and Taenia solium larvae. We find that the larvae of both species contain substantial acetylcholinesterase activity. However, acetylcholinesterase activity is lower in Taenia solium as compared to Taenia crassiceps larvae. Further, whilst we observed acetylcholinesterase activity in all fractions of Taenia crassiceps larvae, including on the membrane surface and in the excreted/secreted extracts, we could not identify acetylcholinesterases on the membrane surface or in the excreted/secreted extracts of Taenia solium larvae. Bioinformatic analysis revealed conservation of the functional protein domains in the Taenia solium acetylcholinesterases, when compared to the homologous human sequence. Finally, using whole-cell patch clamp recordings in rat hippocampal brain slice cultures, we demonstrate that Taenia larval derived acetylcholinesterases can break down acetylcholine at a concentration which induces changes in neuronal signalling. Together, these findings highlight the possibility that Taenia larval acetylcholinesterases can interfere with cholinergic signalling in the host, potentially contributing to pathogenesis in neurocysticercosis.\n
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\n \n\n \n \n \n \n \n \n Common \\Childhood\\ \\Epilepsy\\ \\Mimics\\.\n \n \n \n \n\n\n \n Samia, P.; and Wilmshurst, J. M\n\n\n \n\n\n\n In Salih, M. A M, editor(s), Clinical \\Child\\ \\Neurology\\, pages 743–765. Springer International Publishing, Cham, 2020.\n \n\n\n\n
\n\n\n\n \n \n \"CommonPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@incollection{salih_common_2020,\naddress = {Cham},\nauthor = {Samia, Pauline and Wilmshurst, Jo M},\nbooktitle = {Clinical {\\{}Child{\\}} {\\{}Neurology{\\}}},\ndoi = {10.1007/978-3-319-43153-6_23},\neditor = {Salih, Mustafa A M},\nisbn = {978-3-319-43152-9 978-3-319-43153-6},\npages = {743--765},\npublisher = {Springer International Publishing},\ntitle = {{Common {\\{}Childhood{\\}} {\\{}Epilepsy{\\}} {\\{}Mimics{\\}}}},\nurl = {http://link.springer.com/10.1007/978-3-319-43153-6{\\_}23},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n Differential effects of social isolation rearing on glutamate- and GABA-stimulated noradrenaline release in the rat prefrontal cortex and hippocampus.\n \n \n \n \n\n\n \n Atmore, K H; Stein, D J; Harvey, B H; Russell, V A; and Howells, F M\n\n\n \n\n\n\n European Neuropsychopharmacology. 2020.\n \n\n\n\n
\n\n\n\n \n \n \"DifferentialPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Atmore2020,\nannote = {cited By 0},\nauthor = {Atmore, K H and Stein, D J and Harvey, B H and Russell, V A and Howells, F M},\ndoi = {10.1016/j.euroneuro.2020.05.007},\nissn = {0924977X},\njournal = {European Neuropsychopharmacology},\npublisher = {Elsevier B.V.},\ntitle = {{Differential effects of social isolation rearing on glutamate- and GABA-stimulated noradrenaline release in the rat prefrontal cortex and hippocampus}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85086475456{\\&}doi=10.1016{\\%}2Fj.euroneuro.2020.05.007{\\&}partnerID=40{\\&}md5=8bec876d6f496bf1a489ca8d5ba20ecf},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n The relationship between measurement of in vivo brain glutamate and markers of iron metabolism: A proton magnetic resonance spectroscopy study in healthy adults.\n \n \n \n \n\n\n \n Burger, A; Kotze, M J; Stein, D J; van Rensburg, S; and Howells, F M\n\n\n \n\n\n\n European Journal of Neuroscience, 51(4): 984–990. 2020.\n \n\n\n\n
\n\n\n\n \n \n \"ThePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n\n\n\n
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@article{Burger2020984,\nannote = {cited By 0},\nauthor = {Burger, A and Kotze, M J and Stein, D J and van Rensburg, S and Howells, F M},\ndoi = {10.1111/ejn.14583},\nissn = {0953816X},\njournal = {European Journal of Neuroscience},\nkeywords = {anterior cingulate; Article; brain region; concen,creatine; glutamic acid; glutamine; transferrin},\nnumber = {4},\npages = {984--990},\npublisher = {Blackwell Publishing Ltd},\ntitle = {{The relationship between measurement of in vivo brain glutamate and markers of iron metabolism: A proton magnetic resonance spectroscopy study in healthy adults}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85074711693{\\&}doi=10.1111{\\%}2Fejn.14583{\\&}partnerID=40{\\&}md5=122523e3e157d4b2146bf63b20c9f771},\nvolume = {51},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n The relationship between white matter microstructure and general cognitive ability in patients with schizophrenia and healthy participants in the ENIGMA consortium.\n \n \n \n \n\n\n \n Holleran, L; Kelly, S; Alloza, C; Agartz, I; Andreassen, O A; Arango, C; Banaj, N; Calhoun, V; Cannon, D; Carr, V; Corvin, A; Glahn, D C; Gur, R; Hong, E; Hoschl, C; Howells, F M; James, A; Janssen, J; Kochunov, P; Lawrie, S M; Liu, J; Martinez, C; McDonald, C; Morris, D; Mothersill, D; Pantelis, C; Piras, F; Potkin, S; Rasser, P E; Roalf, D; Rowland, L; Satterthwaite, T; Schall, U; Spalletta, G; Spaniel, F; Stein, D J; Uhlmann, A; Voineskos, A; Zalesky, A; van Erp, T G M; Turner, J A; Deary, I J; Thompson, P M; Jahanshad, N; and Donohoe, G\n\n\n \n\n\n\n American Journal of Psychiatry, 177(6): 537–547. 2020.\n \n\n\n\n
\n\n\n\n \n \n \"ThePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Holleran2020537,\nannote = {cited By 3},\nauthor = {Holleran, L and Kelly, S and Alloza, C and Agartz, I and Andreassen, O A and Arango, C and Banaj, N and Calhoun, V and Cannon, D and Carr, V and Corvin, A and Glahn, D C and Gur, R and Hong, E and Hoschl, C and Howells, F M and James, A and Janssen, J and Kochunov, P and Lawrie, S M and Liu, J and Martinez, C and McDonald, C and Morris, D and Mothersill, D and Pantelis, C and Piras, F and Potkin, S and Rasser, P E and Roalf, D and Rowland, L and Satterthwaite, T and Schall, U and Spalletta, G and Spaniel, F and Stein, D J and Uhlmann, A and Voineskos, A and Zalesky, A and van Erp, T G M and Turner, J A and Deary, I J and Thompson, P M and Jahanshad, N and Donohoe, G},\ndoi = {10.1176/appi.ajp.2019.19030225},\nfile = {:Users/jacquelinebracher/Zotero/storage/HLJH6XHC/Holleran et al. - 2020 - The Relationship Between White Matter Microstructu.pdf:pdf},\nissn = {0002953X},\njournal = {American Journal of Psychiatry},\nnumber = {6},\npages = {537--547},\npublisher = {American Psychiatric Association},\ntitle = {{The relationship between white matter microstructure and general cognitive ability in patients with schizophrenia and healthy participants in the ENIGMA consortium}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85083781754{\\&}doi=10.1176{\\%}2Fappi.ajp.2019.19030225{\\&}partnerID=40{\\&}md5=bef31062a5972f976cc22a2e0112e6e0},\nvolume = {177},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n Brain Network Connectivity from Matching Cortical Feature Densities.\n \n \n \n \n\n\n \n Lee, D; Donald, K A; Dalal, T; Wedderburn, C J; Roos, A; Ipser, J; Subramoney, S; Zar, H J; Stein, D J; Narr, K L; Hellemann, G; Woods, R P; and Joshi, S H\n\n\n \n\n\n\n 2020.\n \n\n\n\n
\n\n\n\n \n \n \"BrainPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n\n\n\n
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@conference{Lee2020995,\nannote = {cited By 0},\nauthor = {Lee, D and Donald, K A and Dalal, T and Wedderburn, C J and Roos, A and Ipser, J and Subramoney, S and Zar, H J and Stein, D J and Narr, K L and Hellemann, G and Woods, R P and Joshi, S H},\nbooktitle = {Proceedings - International Symposium on Biomedical Imaging},\ndoi = {10.1109/ISBI45749.2020.9098689},\nfile = {:Users/jacquelinebracher/Zotero/storage/PPL67XF8/Lee et al. - 2020 - Brain Network Connectivity from Matching Cortical .pdf:pdf},\nisbn = {9781538693308},\nissn = {19457928},\nkeywords = {Brain,Brain connectivity; Brain networks; Feature densi,Medical imaging},\npages = {995--998},\npublisher = {IEEE Computer Society},\ntitle = {{Brain Network Connectivity from Matching Cortical Feature Densities}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85085861688{\\&}doi=10.1109{\\%}2FISBI45749.2020.9098689{\\&}partnerID=40{\\&}md5=1e8c0b4a32e81702c837ca0d465e0714},\nvolume = {2020-April},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n Management of Spasticity After Traumatic Brain Injury in Children.\n \n \n \n \n\n\n \n Enslin, J M N; Rohlwink, U K; and Figaji, A\n\n\n \n\n\n\n Frontiers in Neurology, 11. 2020.\n \n\n\n\n
\n\n\n\n \n \n \"ManagementPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n\n\n\n
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@article{Enslin2020,\nannote = {cited By 0},\nauthor = {Enslin, J M N and Rohlwink, U K and Figaji, A},\ndoi = {10.3389/fneur.2020.00126},\nfile = {:Users/jacquelinebracher/Zotero/storage/VCKIJZJ7/Enslin et al. - 2020 - Management of Spasticity After Traumatic Brain Inj.pdf:pdf},\nissn = {16642295},\njournal = {Frontiers in Neurology},\nkeywords = {alpha 2 adrenergic receptor stimulating agent; bac,child; clinical effectiveness; clinical feature;},\npublisher = {Frontiers Media S.A.},\ntitle = {{Management of Spasticity After Traumatic Brain Injury in Children}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85081674379{\\&}doi=10.3389{\\%}2Ffneur.2020.00126{\\&}partnerID=40{\\&}md5=24617679bc259e9fe201dd1ee7233e9f},\nvolume = {11},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n Checklists to guide the supportive and critical care of tuberculous meningitis.\n \n \n \n\n\n \n Donovan, J.; Rohlwink, U.; Tucker, E.; Hiep, N.; Thwaites, G.; Figaji, A.; Aarnoutse, R.; Anderson, S.; Bahr, N.; Bang, N.; Wasserman, S.; and Wilkinson, R.\n\n\n \n\n\n\n Wellcome Open Research, 4. 2020.\n \n\n\n\n
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@article{Donovan2020,\nabstract = {The assessment and management of tuberculous meningitis (TBM) is often complex, yet no standardised approach exists, and evidence for the clinical care of patients, including those with critical illness, is limited. The roles of proformas and checklists are increasing in medicine; proformas provide a framework for a thorough approach to patient care, whereas checklists offer a priority-based approach that may be applied to deteriorating patients in time-critical situations. We aimed to develop a comprehensive assessment proforma and an accompanying 'priorities' checklist for patients with TBM, with the overriding goal being to improve patient outcomes. The proforma outlines what should be asked, checked, or tested at initial evaluation and daily inpatient review to assist supportive clinical care for patients, with an adapted list for patients in critical care. It is accompanied by a supporting document describing why these points are relevant to TBM. Our priorities checklist offers a useful and easy reminder of important issues to review during a time-critical period of acute patient deterioration. The benefit of these documents to patient outcomes would require investigation; however, we hope they will promote standardisation of patient assessment and care, particularly of critically unwell individuals, in whom morbidity and mortality remains unacceptably high.},\nauthor = {Donovan, J. and Rohlwink, U.K. and Tucker, E.W. and Hiep, N.T.T. and Thwaites, G.E. and Figaji, A.A. and Aarnoutse, R.E. and Anderson, S.T.B. and Bahr, N.C. and Bang, N.D. and Wasserman, S.A. and Wilkinson, R.J.},\ndoi = {10.12688/wellcomeopenres.15512.2},\nfile = {:Users/jacquelinebracher/Zotero/storage/TD97XEB5/Donovan et al. - 2020 - Checklists to guide the supportive and critical ca.pdf:pdf},\njournal = {Wellcome Open Research},\ntitle = {{Checklists to guide the supportive and critical care of tuberculous meningitis}},\nvolume = {4},\nyear = {2020}\n}\n
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\n The assessment and management of tuberculous meningitis (TBM) is often complex, yet no standardised approach exists, and evidence for the clinical care of patients, including those with critical illness, is limited. The roles of proformas and checklists are increasing in medicine; proformas provide a framework for a thorough approach to patient care, whereas checklists offer a priority-based approach that may be applied to deteriorating patients in time-critical situations. We aimed to develop a comprehensive assessment proforma and an accompanying 'priorities' checklist for patients with TBM, with the overriding goal being to improve patient outcomes. The proforma outlines what should be asked, checked, or tested at initial evaluation and daily inpatient review to assist supportive clinical care for patients, with an adapted list for patients in critical care. It is accompanied by a supporting document describing why these points are relevant to TBM. Our priorities checklist offers a useful and easy reminder of important issues to review during a time-critical period of acute patient deterioration. The benefit of these documents to patient outcomes would require investigation; however, we hope they will promote standardisation of patient assessment and care, particularly of critically unwell individuals, in whom morbidity and mortality remains unacceptably high.\n
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\n \n\n \n \n \n \n \n \n Duration of illness and cortical thickness in trichotillomania: Preliminary evidence for illness change over time.\n \n \n \n \n\n\n \n Grant, J E; Keuthen, N J; Stein, D J; Lochner, C; and Chamberlain, S R\n\n\n \n\n\n\n European Neuropsychopharmacology, 32: 88–93. 2020.\n \n\n\n\n
\n\n\n\n \n \n \"DurationPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n\n\n\n
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@article{Grant202088,\nannote = {cited By 0},\nauthor = {Grant, J E and Keuthen, N J and Stein, D J and Lochner, C and Chamberlain, S R},\ndoi = {10.1016/j.euroneuro.2020.01.002},\nfile = {:Users/jacquelinebracher/Zotero/storage/ZW8N2UBB/Grant et al. - 2020 - Duration of illness and cortical thickness in tric.pdf:pdf},\nissn = {0924977X},\njournal = {European Neuropsychopharmacology},\nkeywords = {adult; Article; brain size; chronicity; clinical a},\npages = {88--93},\npublisher = {Elsevier B.V.},\ntitle = {{Duration of illness and cortical thickness in trichotillomania: Preliminary evidence for illness change over time}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85077926610{\\&}doi=10.1016{\\%}2Fj.euroneuro.2020.01.002{\\&}partnerID=40{\\&}md5=5549394e4bacf77db6b952c683466518},\nvolume = {32},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n Methamphetamine Use and Antipsychotic-related Extrapyramidal Side-effects in Patients with Psychotic Disorders.\n \n \n \n \n\n\n \n Temmingh, H S; van den Brink, W; Howells, F; Sibeko, G; and Stein, D J\n\n\n \n\n\n\n Journal of Dual Diagnosis, 16(2): 208–217. 2020.\n \n\n\n\n
\n\n\n\n \n \n \"MethamphetaminePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n\n\n\n
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@article{Temmingh2020208,\nannote = {cited By 1},\nauthor = {Temmingh, H S and van den Brink, W and Howells, F and Sibeko, G and Stein, D J},\ndoi = {10.1080/15504263.2020.1714099},\nissn = {15504263},\njournal = {Journal of Dual Diagnosis},\nkeywords = {Abnormal Involuntary Movement Scale; adult; aged;,alcohol; amisulpride; aripiprazole; cannabis; chlo},\nnumber = {2},\npages = {208--217},\npublisher = {Routledge},\ntitle = {{Methamphetamine Use and Antipsychotic-related Extrapyramidal Side-effects in Patients with Psychotic Disorders}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85078411816{\\&}doi=10.1080{\\%}2F15504263.2020.1714099{\\&}partnerID=40{\\&}md5=7e161595cbadb99042a32526faae27f1},\nvolume = {16},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n Towards a cross-cultural assessment of binge-watching: Psychometric evaluation of the “watching TV series motives” and “binge-watching engagement and symptoms” questionnaires across nine languages.\n \n \n \n \n\n\n \n Flayelle, M; Castro-Calvo, J; Vögele, C; Astur, R; Ballester-Arnal, R; Challet-Bouju, G; Brand, M; Cárdenas, G; Devos, G; Elkholy, H; Grall-Bronnec, M; James, R J E; Jiménez-Martínez, M; Khazaal, Y; Valizadeh-Haghi, S; King, D L; Liu, Y; Lochner, C; Steins-Loeber, S; Long, J; Potenza, M N; Rahmatizadeh, S; Schimmenti, A; Stein, D J; Tóth-Király, I; Tunney, R; Wang, Y; Zhai, Z W; Maurage, P; and Billieux, J\n\n\n \n\n\n\n Computers in Human Behavior, 111. 2020.\n \n\n\n\n
\n\n\n\n \n \n \"TowardsPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n\n\n\n
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@article{Flayelle2020,\nannote = {cited By 0},\nauthor = {Flayelle, M and Castro-Calvo, J and V{\\"{o}}gele, C and Astur, R and Ballester-Arnal, R and Challet-Bouju, G and Brand, M and C{\\'{a}}rdenas, G and Devos, G and Elkholy, H and Grall-Bronnec, M and James, R J E and Jim{\\'{e}}nez-Mart{\\'{i}}nez, M and Khazaal, Y and Valizadeh-Haghi, S and King, D L and Liu, Y and Lochner, C and Steins-Loeber, S and Long, J and Potenza, M N and Rahmatizadeh, S and Schimmenti, A and Stein, D J and T{\\'{o}}th-Kir{\\'{a}}ly, I and Tunney, R and Wang, Y and Zhai, Z W and Maurage, P and Billieux, J},\ndoi = {10.1016/j.chb.2020.106410},\nfile = {:Users/jacquelinebracher/Zotero/storage/LPG23YB9/Flayelle et al. - 2020 - Towards a cross-cultural assessment of binge-watch.pdf:pdf},\nissn = {07475632},\njournal = {Computers in Human Behavior},\nkeywords = {Construct validity; Correlational analysis; Cross,Students,Surveys},\npublisher = {Elsevier Ltd},\ntitle = {{Towards a cross-cultural assessment of binge-watching: Psychometric evaluation of the “watching TV series motives” and “binge-watching engagement and symptoms” questionnaires across nine languages}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85085469865{\\&}doi=10.1016{\\%}2Fj.chb.2020.106410{\\&}partnerID=40{\\&}md5=d0938c15b826b15a6754a130a7cd4e83},\nvolume = {111},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n Association of \\Copy\\ \\Number\\ \\Variation\\ of the 15q11.2 \\BP1\\-\\BP2\\ \\Region\\ \\With\\ \\Cortical\\ and \\Subcortical\\ \\Morphology\\ and \\Cognition\\.\n \n \n \n \n\n\n \n Writing Committee for the ENIGMA-CNV Working Group; Van Der Meer, D.; Sønderby, I. E; Kaufmann, T.; Walters, G B.; Abdellaoui, A.; Ames, D.; Amunts, K.; Andersson, M.; Armstrong, N. J; Bernard, M.; Blackburn, N. B; Blangero, J.; Boomsma, D. I; Brodaty, H.; Brouwer, R. M; Bülow, R.; Cahn, W.; Calhoun, V. D; Caspers, S.; Cavalleri, G. L; Ching, C. R K; Cichon, S.; Ciufolini, S.; Corvin, A.; Crespo-Facorro, B.; Curran, J. E; Dalvie, S.; Dazzan, P.; De Geus, E. J C; De Zubicaray, G. I; De Zwarte, S. M C; Delanty, N.; Den Braber, A.; Desrivieres, S.; Di Forti, M.; Doherty, J. L; Donohoe, G.; Ehrlich, S.; Eising, E.; Espeseth, T.; Fisher, S. E; Fladby, T.; Frei, O.; Frouin, V.; Fukunaga, M.; Gareau, T.; Glahn, D. C; Grabe, H. J; Groenewold, N. A; Gústafsson, Ó.; Haavik, J.; Haberg, A. K; Hashimoto, R.; Hehir-Kwa, J. Y; Hibar, D. P; Hillegers, M. H J; Hoffmann, P.; Holleran, L.; Hottenga, J.; Hulshoff Pol, H. E; Ikeda, M.; Jacquemont, S.; Jahanshad, N.; Jockwitz, C.; Johansson, S.; Jönsson, E. G; Kikuchi, M.; Knowles, E. E M; Kwok, J. B; Le Hellard, S.; Linden, D. E J; Liu, J.; Lundervold, A.; Lundervold, A. J; Martin, N. G; Mather, K. A; Mathias, S. R; McMahon, K. L; McRae, A. F; Medland, S. E; Moberget, T.; Moreau, C.; Morris, D. W; Mühleisen, T. W; Murray, R. M; Nordvik, J. E; Nyberg, L.; Olde Loohuis, L. M; Ophoff, R. A; Owen, M. J; Paus, T.; Pausova, Z.; Peralta, J. M; Pike, B.; Prieto, C.; Quinlan, E. B.; Reinbold, C. S; Reis Marques, T.; Rucker, J. J H; Sachdev, P. S; Sando, S. B; Schofield, P. R; Schork, A. J; Schumann, G.; Shin, J.; Shumskaya, E.; Silva, A. I; Sisodiya, S. M; Steen, V. M; Stein, D. J; Strike, L. T; Tamnes, C. K; Teumer, A.; Thalamuthu, A.; Tordesillas-Gutiérrez, D.; Uhlmann, A.; Úlfarsson, M. Ö; Van 'T Ent, D.; Van Den Bree, M. B M; Vassos, E.; Wen, W.; Wittfeld, K.; Wright, M. J; Zayats, T.; Dale, A. M; Djurovic, S.; Agartz, I.; Westlye, L. T; Stefánsson, H.; Stefánsson, K.; Thompson, P. M; and Andreassen, O. A\n\n\n \n\n\n\n JAMA Psychiatry, 77(4): 420. apr 2020.\n \n\n\n\n
\n\n\n\n \n \n \"AssociationPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{writing_committee_for_the_enigma-cnv_working_group_association_2020,\nauthor = {{Writing Committee for the ENIGMA-CNV Working Group} and {Van Der Meer}, Dennis and S{\\o}nderby, Ida E and Kaufmann, Tobias and Walters, G Bragi and Abdellaoui, Abdel and Ames, David and Amunts, Katrin and Andersson, Micael and Armstrong, Nicola J and Bernard, Manon and Blackburn, Nicholas B and Blangero, John and Boomsma, Dorret I and Brodaty, Henry and Brouwer, Rachel M and B{\\"{u}}low, Robin and Cahn, Wiepke and Calhoun, Vince D and Caspers, Svenja and Cavalleri, Gianpiero L and Ching, Christopher R K and Cichon, Sven and Ciufolini, Simone and Corvin, Aiden and Crespo-Facorro, Benedicto and Curran, Joanne E and Dalvie, Shareefa and Dazzan, Paola and {De Geus}, Eco J C and {De Zubicaray}, Greig I and {De Zwarte}, Sonja M C and Delanty, Norman and {Den Braber}, Anouk and Desrivieres, Sylvane and {Di Forti}, Marta and Doherty, Joanne L and Donohoe, Gary and Ehrlich, Stefan and Eising, Else and Espeseth, Thomas and Fisher, Simon E and Fladby, Tormod and Frei, Oleksandr and Frouin, Vincent and Fukunaga, Masaki and Gareau, Thomas and Glahn, David C and Grabe, Hans J and Groenewold, Nynke A and G{\\'{u}}stafsson, {\\'{O}}mar and Haavik, Jan and Haberg, Asta K and Hashimoto, Ryota and Hehir-Kwa, Jayne Y and Hibar, Derrek P and Hillegers, Manon H J and Hoffmann, Per and Holleran, Laurena and Hottenga, Jouke-Jan and {Hulshoff Pol}, Hilleke E and Ikeda, Masashi and Jacquemont, S{\\'{e}}bastien and Jahanshad, Neda and Jockwitz, Christiane and Johansson, Stefan and J{\\"{o}}nsson, Erik G and Kikuchi, Masataka and Knowles, Emma E M and Kwok, John B and {Le Hellard}, Stephanie and Linden, David E J and Liu, Jingyu and Lundervold, Arvid and Lundervold, Astri J and Martin, Nicholas G and Mather, Karen A and Mathias, Samuel R and McMahon, Katie L and McRae, Allan F and Medland, Sarah E and Moberget, Torgeir and Moreau, Clara and Morris, Derek W and M{\\"{u}}hleisen, Thomas W and Murray, Robin M and Nordvik, Jan E and Nyberg, Lars and {Olde Loohuis}, Loes M and Ophoff, Roel A and Owen, Michael J and Paus, Tomas and Pausova, Zdenka and Peralta, Juan M and Pike, Bruce and Prieto, Carlos and Quinlan, Erin Burke and Reinbold, C{\\'{e}}line S and {Reis Marques}, Tiago and Rucker, James J H and Sachdev, Perminder S and Sando, Sigrid B and Schofield, Peter R and Schork, Andrew J and Schumann, Gunter and Shin, Jean and Shumskaya, Elena and Silva, Ana I and Sisodiya, Sanjay M and Steen, Vidar M and Stein, Dan J and Strike, Lachlan T and Tamnes, Christian K and Teumer, Alexander and Thalamuthu, Anbupalam and Tordesillas-Guti{\\'{e}}rrez, Diana and Uhlmann, Anne and {\\'{U}}lfarsson, Magn{\\'{u}}s {\\"{O}} and {Van 'T Ent}, Dennis and {Van Den Bree}, Marianne B M and Vassos, Evangelos and Wen, Wei and Wittfeld, Katharina and Wright, Margaret J and Zayats, Tetyana and Dale, Anders M and Djurovic, Srdjan and Agartz, Ingrid and Westlye, Lars T and Stef{\\'{a}}nsson, Hreinn and Stef{\\'{a}}nsson, K{\\'{a}}ri and Thompson, Paul M and Andreassen, Ole A},\ndoi = {10.1001/jamapsychiatry.2019.3779},\nfile = {:Users/jacquelinebracher/Zotero/storage/QJAVS4Y4/Writing Committee for the ENIGMA-CNV Working Group et al. - 2020 - Association of Copy Number Variation of the 15q11..pdf:pdf},\nissn = {2168-622X},\njournal = {JAMA Psychiatry},\nmonth = {apr},\nnumber = {4},\npages = {420},\ntitle = {{Association of {\\{}Copy{\\}} {\\{}Number{\\}} {\\{}Variation{\\}} of the 15q11.2 {\\{}BP1{\\}}-{\\{}BP2{\\}} {\\{}Region{\\}} {\\{}With{\\}} {\\{}Cortical{\\}} and {\\{}Subcortical{\\}} {\\{}Morphology{\\}} and {\\{}Cognition{\\}}}},\nurl = {https://jamanetwork.com/journals/jamapsychiatry/fullarticle/2753864},\nvolume = {77},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n Age-\\Dependent\\ \\Changes\\ in \\Synaptic\\ \\NMDA\\ \\Receptor\\ \\Composition\\ in \\Adult\\ \\Human\\ \\Cortical\\ \\Neurons\\.\n \n \n \n \n\n\n \n Pegasiou, C. M; Zolnourian, A.; Gomez-Nicola, D.; Deinhardt, K.; Nicoll, J. A R; Ahmed, A. I; Vajramani, G.; Grundy, P.; Verhoog, M. B; Mansvelder, H. D; Perry, V H; Bulters, D.; and Vargas-Caballero, M.\n\n\n \n\n\n\n Cerebral Cortex, 30(7): 4246–4256. jun 2020.\n \n\n\n\n
\n\n\n\n \n \n \"Age-\\Dependent\\Paper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{pegasiou_age-dependent_2020,\nabstract = {Abstract\nThe molecular processes underlying the aging-related decline in cognitive performance and memory observed in humans are poorly understood. Studies in rodents have shown a decrease in N-methyl-D-aspartate receptors (NMDARs) that contain the GluN2B subunit in aging synapses, and this decrease is correlated with impaired memory functions. However, the age-dependent contribution of GluN2B-containing receptors to synaptic transmission in human cortical synapses has not been previously studied. We investigated the synaptic contribution of GluN2A and GluN2B-containing NMDARs in adult human neurons using fresh nonpathological temporal cortical tissue resected during neurosurgical procedures. The tissue we obtained fulfilled quality criteria by the absence of inflammation markers and proteomic degradation. We show an age-dependent decline in the NMDA/AMPA receptor ratio in adult human temporal cortical synapses. We demonstrate that GluN2B-containing NMDA receptors contribute to synaptic responses in the adult human brain with a reduced contribution in older individuals. With previous evidence demonstrating the critical role of synaptic GluN2B in regulating synaptic strength and memory storage in mice, this progressive reduction of GluN2B in the human brain during aging may underlie a molecular mechanism in the age-related decline in cognitive abilities and memory observed in humans.},\nauthor = {Pegasiou, Chrysia M and Zolnourian, Ardalan and Gomez-Nicola, Diego and Deinhardt, Katrin and Nicoll, James A R and Ahmed, Aminul I and Vajramani, Girish and Grundy, Paul and Verhoog, Matthijs B and Mansvelder, Huibert D and Perry, V H and Bulters, Diederik and Vargas-Caballero, Mariana},\ndoi = {10.1093/cercor/bhaa052},\nfile = {:Users/jacquelinebracher/Zotero/storage/DPM3HSP6/Pegasiou et al. - 2020 - Age-Dependent Changes in Synaptic NMDA Receptor Co.pdf:pdf},\nissn = {1047-3211, 1460-2199},\njournal = {Cerebral Cortex},\nmonth = {jun},\nnumber = {7},\npages = {4246--4256},\ntitle = {{Age-{\\{}Dependent{\\}} {\\{}Changes{\\}} in {\\{}Synaptic{\\}} {\\{}NMDA{\\}} {\\{}Receptor{\\}} {\\{}Composition{\\}} in {\\{}Adult{\\}} {\\{}Human{\\}} {\\{}Cortical{\\}} {\\{}Neurons{\\}}}},\nurl = {https://academic.oup.com/cercor/article/30/7/4246/5805352},\nvolume = {30},\nyear = {2020}\n}\n
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\n Abstract The molecular processes underlying the aging-related decline in cognitive performance and memory observed in humans are poorly understood. Studies in rodents have shown a decrease in N-methyl-D-aspartate receptors (NMDARs) that contain the GluN2B subunit in aging synapses, and this decrease is correlated with impaired memory functions. However, the age-dependent contribution of GluN2B-containing receptors to synaptic transmission in human cortical synapses has not been previously studied. We investigated the synaptic contribution of GluN2A and GluN2B-containing NMDARs in adult human neurons using fresh nonpathological temporal cortical tissue resected during neurosurgical procedures. The tissue we obtained fulfilled quality criteria by the absence of inflammation markers and proteomic degradation. We show an age-dependent decline in the NMDA/AMPA receptor ratio in adult human temporal cortical synapses. We demonstrate that GluN2B-containing NMDA receptors contribute to synaptic responses in the adult human brain with a reduced contribution in older individuals. With previous evidence demonstrating the critical role of synaptic GluN2B in regulating synaptic strength and memory storage in mice, this progressive reduction of GluN2B in the human brain during aging may underlie a molecular mechanism in the age-related decline in cognitive abilities and memory observed in humans.\n
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\n \n\n \n \n \n \n \n Pharmacological treatments for social anxiety disorder in adults: A systematic review and network meta-analysis.\n \n \n \n\n\n \n Williams, T.; McCaul, M.; Schwarzer, G.; Cipriani, A.; Stein, D.; and Ipser, J.\n\n\n \n\n\n\n Acta Neuropsychiatrica. 2020.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Williams2020b,\nabstract = {Objective:The aim of this paper was to provide a systematic review and update on the pharmacotherapy of social anxiety disorder (SAD), including the efficacy and tolerability of these agents, the ranking of interventions, and the grading of results by quality of evidence.Methods:The Common Mental Disorder Controlled Trial Register and two trial registries were searched for RCTs comparing any pharmacological intervention or placebo in the treatment of SAD. We performed a standard pairwise meta-analysis using a random effects model and carried out a network meta-analysis using the statistical package, R. Quality of evidence was also assessed.Results:We included 67 RCTs in the review and 21 to 45 interventions in the network meta-analysis. Paroxetine was most effective in the reduction of symptom severity as compared to placebo. Superior response to treatment was also observed for paroxetine, brofaromine, bromazepam, clonazepam, escitalopram, fluvoxamine, phenelzine, and sertraline. Higher dropout rates were found for fluvoxamine. Brofaromine, escitalopram, fluvoxamine, paroxetine, pregabalin, sertraline, and venlafaxine performed worse in comparison to placebo for the outcome of dropouts due to adverse events. Olanzapine yielded a relatively high rank for treatment efficacy and buspirone the worse rank for dropouts due to any cause.Conclusion:The differences between drugs and placebo were small, apart from a significant reduction in symptom severity and response for paroxetine. We suggest paroxetine as a first line treatment of SAD, with the consideration of future research on the drug olanzapine as well as brofaromine, bromazepam, clonazepam, escitalopram, fluvoxamine, phenelzine, and sertraline because we observed a response to treatment.},\nauthor = {Williams, T. and McCaul, M. and Schwarzer, G. and Cipriani, A. and Stein, D.J. and Ipser, J.},\ndoi = {10.1017/neu.2020.6},\njournal = {Acta Neuropsychiatrica},\ntitle = {{Pharmacological treatments for social anxiety disorder in adults: A systematic review and network meta-analysis}},\nyear = {2020}\n}\n
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\n Objective:The aim of this paper was to provide a systematic review and update on the pharmacotherapy of social anxiety disorder (SAD), including the efficacy and tolerability of these agents, the ranking of interventions, and the grading of results by quality of evidence.Methods:The Common Mental Disorder Controlled Trial Register and two trial registries were searched for RCTs comparing any pharmacological intervention or placebo in the treatment of SAD. We performed a standard pairwise meta-analysis using a random effects model and carried out a network meta-analysis using the statistical package, R. Quality of evidence was also assessed.Results:We included 67 RCTs in the review and 21 to 45 interventions in the network meta-analysis. Paroxetine was most effective in the reduction of symptom severity as compared to placebo. Superior response to treatment was also observed for paroxetine, brofaromine, bromazepam, clonazepam, escitalopram, fluvoxamine, phenelzine, and sertraline. Higher dropout rates were found for fluvoxamine. Brofaromine, escitalopram, fluvoxamine, paroxetine, pregabalin, sertraline, and venlafaxine performed worse in comparison to placebo for the outcome of dropouts due to adverse events. Olanzapine yielded a relatively high rank for treatment efficacy and buspirone the worse rank for dropouts due to any cause.Conclusion:The differences between drugs and placebo were small, apart from a significant reduction in symptom severity and response for paroxetine. We suggest paroxetine as a first line treatment of SAD, with the consideration of future research on the drug olanzapine as well as brofaromine, bromazepam, clonazepam, escitalopram, fluvoxamine, phenelzine, and sertraline because we observed a response to treatment.\n
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\n \n\n \n \n \n \n \n \n Febrile \\Seizures\\.\n \n \n \n \n\n\n \n Quvile, T.; and Wilmshurst, J. M\n\n\n \n\n\n\n In Salih, M. A M, editor(s), Clinical \\Child\\ \\Neurology\\, pages 767–776. Springer International Publishing, Cham, 2020.\n \n\n\n\n
\n\n\n\n \n \n \"FebrilePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@incollection{salih_febrile_2020,\naddress = {Cham},\nauthor = {Quvile, Tandokazi and Wilmshurst, Jo M},\nbooktitle = {Clinical {\\{}Child{\\}} {\\{}Neurology{\\}}},\ndoi = {10.1007/978-3-319-43153-6_24},\neditor = {Salih, Mustafa A M},\nisbn = {978-3-319-43152-9 978-3-319-43153-6},\npages = {767--776},\npublisher = {Springer International Publishing},\ntitle = {{Febrile {\\{}Seizures{\\}}}},\nurl = {http://link.springer.com/10.1007/978-3-319-43153-6{\\_}24},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n The \\Potential\\ \\Therapeutic\\ \\Value\\ of \\Medicinal\\ \\Plants\\ in the \\Management\\ of \\Metabolic\\ \\Disorders\\.\n \n \n \n \n\n\n \n Nyakudya, T. T; Tshabalala, T.; Dangarembizi, R.; Erlwanger, K. H; and Ndhlala, A. R\n\n\n \n\n\n\n Molecules, 25(11): 2669. jun 2020.\n \n\n\n\n
\n\n\n\n \n \n \"ThePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{nyakudya_potential_2020,\nabstract = {Metabolic syndrome (MetS) is a prevalent, multifactorial and complex disease that is associated with an increased risk of developing diabetes and other major cardiovascular complications. The rise in the global prevalence of MetS has been attributed to genetic, epigenetic, and environmental factors. The adoption of sedentary lifestyles that are characterized by low physical activity and the consumption of high-energy diets contributes to MetS development. Current management criteria for MetS risk factors involve changes in lifestyle and the use of pharmacological agents that target specific biochemical pathways involved in the metabolism of nutrients. Pharmaceutical drugs are usually expensive and are associated with several undesirable side effects. Alternative management strategies of MetS risk factors involve the use of medicinal plants that are considered to have multiple therapeutic targets and are easily accessible. Medicinal plants contain several different biologically active compounds that provide health benefits. The impact of phytochemicals present in local medicinal plants on sustainable health and well-being of individuals has been studied for many years and found to involve a plethora of complex biochemical, metabolic, and physiological mechanisms. While some of these phytochemicals are the basis of mainstream prescribed drugs (e.g., metformin, reserpine, quinine, and salicin), there is a need to identify more medicinal plants that can be used for the management of components of MetS and to describe their possible mechanisms of action. In this review, we assess the potential health benefits of South African ethnomedicinal plants in protecting against the development of health outcomes associated with MetS. We aim to provide the state of the current knowledge on the use of medicinal plants and their therapeutically important phytochemicals by discussing the current trends, with critical examples from recent primary references of how medicinal plants are being used in South African rural and urban communities.},\nauthor = {Nyakudya, Trevor T and Tshabalala, Thulani and Dangarembizi, Rachael and Erlwanger, Kennedy H and Ndhlala, Ashwell R},\ndoi = {10.3390/molecules25112669},\nfile = {:Users/jacquelinebracher/Zotero/storage/255ADIFK/Nyakudya et al. - 2020 - The Potential Therapeutic Value of Medicinal Plant.pdf:pdf},\nissn = {1420-3049},\njournal = {Molecules},\nmonth = {jun},\nnumber = {11},\npages = {2669},\ntitle = {{The {\\{}Potential{\\}} {\\{}Therapeutic{\\}} {\\{}Value{\\}} of {\\{}Medicinal{\\}} {\\{}Plants{\\}} in the {\\{}Management{\\}} of {\\{}Metabolic{\\}} {\\{}Disorders{\\}}}},\nurl = {https://www.mdpi.com/1420-3049/25/11/2669},\nvolume = {25},\nyear = {2020}\n}\n
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\n Metabolic syndrome (MetS) is a prevalent, multifactorial and complex disease that is associated with an increased risk of developing diabetes and other major cardiovascular complications. The rise in the global prevalence of MetS has been attributed to genetic, epigenetic, and environmental factors. The adoption of sedentary lifestyles that are characterized by low physical activity and the consumption of high-energy diets contributes to MetS development. Current management criteria for MetS risk factors involve changes in lifestyle and the use of pharmacological agents that target specific biochemical pathways involved in the metabolism of nutrients. Pharmaceutical drugs are usually expensive and are associated with several undesirable side effects. Alternative management strategies of MetS risk factors involve the use of medicinal plants that are considered to have multiple therapeutic targets and are easily accessible. Medicinal plants contain several different biologically active compounds that provide health benefits. The impact of phytochemicals present in local medicinal plants on sustainable health and well-being of individuals has been studied for many years and found to involve a plethora of complex biochemical, metabolic, and physiological mechanisms. While some of these phytochemicals are the basis of mainstream prescribed drugs (e.g., metformin, reserpine, quinine, and salicin), there is a need to identify more medicinal plants that can be used for the management of components of MetS and to describe their possible mechanisms of action. In this review, we assess the potential health benefits of South African ethnomedicinal plants in protecting against the development of health outcomes associated with MetS. We aim to provide the state of the current knowledge on the use of medicinal plants and their therapeutically important phytochemicals by discussing the current trends, with critical examples from recent primary references of how medicinal plants are being used in South African rural and urban communities.\n
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\n \n\n \n \n \n \n \n \n Mental, behavioral and neurodevelopmental disorders in the ICD-11: An international perspective on key changes and controversies.\n \n \n \n \n\n\n \n Stein, D J; Szatmari, P; Gaebel, W; Berk, M; Vieta, E; Maj, M; De Vries, Y A; Roest, A M; De Jonge, P; Maercker, A; Brewin, C R; Pike, K M; Grilo, C M; Fineberg, N A; Briken, P; Cohen-Kettenis, P T; and Reed, G M\n\n\n \n\n\n\n BMC Medicine, 18(1). 2020.\n \n\n\n\n
\n\n\n\n \n \n \"Mental,Paper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n\n\n\n
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@article{Stein2020,\nannote = {cited By 5},\nauthor = {Stein, D J and Szatmari, P and Gaebel, W and Berk, M and Vieta, E and Maj, M and {De Vries}, Y A and Roest, A M and {De Jonge}, P and Maercker, A and Brewin, C R and Pike, K M and Grilo, C M and Fineberg, N A and Briken, P and Cohen-Kettenis, P T and Reed, G M},\ndoi = {10.1186/s12916-020-1495-2},\nfile = {:Users/jacquelinebracher/Zotero/storage/Z5AC43RD/Stein et al. - 2020 - Mental, behavioral and neurodevelopmental disorder.pdf:pdf},\nissn = {17417015},\njournal = {BMC Medicine},\nkeywords = {addiction; adjustment disorder; anxiety disorder;},\nnumber = {1},\npublisher = {BioMed Central Ltd.},\ntitle = {{Mental, behavioral and neurodevelopmental disorders in the ICD-11: An international perspective on key changes and controversies}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85078321818{\\&}doi=10.1186{\\%}2Fs12916-020-1495-2{\\&}partnerID=40{\\&}md5=5fd8e9c954c1b37c6c84e647ee58e07c},\nvolume = {18},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n Whole-exome sequencing in an \\Afrikaner\\ family with bipolar disorder.\n \n \n \n \n\n\n \n Engelbrecht, H.; Dalvie, S.; Agenbag, G.; Stein, D. J; and Ramesar, R. S\n\n\n \n\n\n\n Journal of Affective Disorders, 276: 69–75. nov 2020.\n \n\n\n\n
\n\n\n\n \n \n \"Whole-exomePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{engelbrecht_whole-exome_2020,\nauthor = {Engelbrecht, Hannah-Ruth and Dalvie, Shareefa and Agenbag, Gloudi and Stein, Dan J and Ramesar, Raj S},\ndoi = {10.1016/j.jad.2020.06.045},\nissn = {01650327},\njournal = {Journal of Affective Disorders},\nmonth = {nov},\npages = {69--75},\ntitle = {{Whole-exome sequencing in an {\\{}Afrikaner{\\}} family with bipolar disorder}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S0165032720324344},\nvolume = {276},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n Structural brain differences between ultra-endurance athletes and sedentary persons.\n \n \n \n \n\n\n \n Paruk, T; Rauch, L; Jankiewicz, M; Van Breda, K; Stein, D J; and King, M\n\n\n \n\n\n\n Sports Medicine and Health Science, 2(2): 89–94. jun 2020.\n \n\n\n\n
\n\n\n\n \n \n \"StructuralPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{paruk_structural_2020,\nauthor = {Paruk, T and Rauch, L and Jankiewicz, M and {Van Breda}, K and Stein, D J and King, M},\ndoi = {10.1016/j.smhs.2020.05.004},\nfile = {:Users/jacquelinebracher/Zotero/storage/8LN8HBDN/Paruk et al. - 2020 - Structural brain differences between ultra-enduran.pdf:pdf},\nissn = {26663376},\njournal = {Sports Medicine and Health Science},\nmonth = {jun},\nnumber = {2},\npages = {89--94},\ntitle = {{Structural brain differences between ultra-endurance athletes and sedentary persons}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S2666337620300238},\nvolume = {2},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n White matter disturbances in major depressive disorder: a coordinated analysis across 20 international cohorts in the ENIGMA MDD working group.\n \n \n \n \n\n\n \n van Velzen, L S; Kelly, S; Isaev, D; Aleman, A; Aftanas, L I; Bauer, J; Baune, B T; Brak, I V; Carballedo, A; Connolly, C G; Couvy-Duchesne, B; Cullen, K R; Danilenko, K V; Dannlowski, U; Enneking, V; Filimonova, E; Förster, K; Frodl, T; Gotlib, I H; Groenewold, N A; Grotegerd, D; Harris, M A; Hatton, S N; Hawkins, E L; Hickie, I B; Ho, T C; Jansen, A; Kircher, T; Klimes-Dougan, B; Kochunov, P; Krug, A; Lagopoulos, J; Lee, R; Lett, T A; Li, M; MacMaster, F P; Martin, N G; McIntosh, A M; McLellan, Q; Meinert, S; Nenadić, I; Osipov, E; Penninx, B.; Portella, M J; Repple, J; Roos, A; Sacchet, M D; Sämann, P G; Schnell, K; Shen, X; Sim, K; Stein, D J; van Tol, M.; Tomyshev, A S; Tozzi, L; Veer, I M; Vermeiren, R; Vives-Gilabert, Y; Walter, H; Walter, M; van der Wee, N J A; van der Werff, S J A; Schreiner, M W; Whalley, H C; Wright, M J; Yang, T T; Zhu, A; Veltman, D J; Thompson, P M; Jahanshad, N; and Schmaal, L\n\n\n \n\n\n\n Molecular Psychiatry, 25(7): 1511–1525. 2020.\n \n\n\n\n
\n\n\n\n \n \n \"WhitePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n\n\n\n
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@article{vanVelzen20201511,\nannote = {cited By 17},\nauthor = {van Velzen, L S and Kelly, S and Isaev, D and Aleman, A and Aftanas, L I and Bauer, J and Baune, B T and Brak, I V and Carballedo, A and Connolly, C G and Couvy-Duchesne, B and Cullen, K R and Danilenko, K V and Dannlowski, U and Enneking, V and Filimonova, E and F{\\"{o}}rster, K and Frodl, T and Gotlib, I H and Groenewold, N A and Grotegerd, D and Harris, M A and Hatton, S N and Hawkins, E L and Hickie, I B and Ho, T C and Jansen, A and Kircher, T and Klimes-Dougan, B and Kochunov, P and Krug, A and Lagopoulos, J and Lee, R and Lett, T A and Li, M and MacMaster, F P and Martin, N G and McIntosh, A M and McLellan, Q and Meinert, S and Nenadi{\\'{c}}, I and Osipov, E and Penninx, B.W.J.H. and Portella, M J and Repple, J and Roos, A and Sacchet, M D and S{\\"{a}}mann, P G and Schnell, K and Shen, X and Sim, K and Stein, D J and van Tol, M.-J. and Tomyshev, A S and Tozzi, L and Veer, I M and Vermeiren, R and Vives-Gilabert, Y and Walter, H and Walter, M and van der Wee, N J A and van der Werff, S J A and Schreiner, M W and Whalley, H C and Wright, M J and Yang, T T and Zhu, A and Veltman, D J and Thompson, P M and Jahanshad, N and Schmaal, L},\ndoi = {10.1038/s41380-019-0477-2},\nfile = {:Users/jacquelinebracher/Zotero/storage/J8I2A4LT/Van Velzen et al. - 2020 - White matter disturbances in major depressive diso.pdf:pdf},\nissn = {13594184},\njournal = {Molecular Psychiatry},\nkeywords = {adult; age distribution; aged; Article; capsula i,antidepressant agent},\nnumber = {7},\npages = {1511--1525},\npublisher = {Springer Nature},\ntitle = {{White matter disturbances in major depressive disorder: a coordinated analysis across 20 international cohorts in the ENIGMA MDD working group}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85072031087{\\&}doi=10.1038{\\%}2Fs41380-019-0477-2{\\&}partnerID=40{\\&}md5=886d9e2f4b0d7a92e4a5c1bc2e0a589b},\nvolume = {25},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n Gene expression profiling of orbital muscles in treatment-resistant ophthalmoplegic myasthenia gravis.\n \n \n \n \n\n\n \n Europa, T. A; Nel, M.; and Heckmann, J. M\n\n\n \n\n\n\n Orphanet Journal of Rare Diseases, 15(1): 346. dec 2020.\n \n\n\n\n
\n\n\n\n \n \n \"GenePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{europa_gene_2020,\nabstract = {Abstract\n\nBackground\nUnbiased in silico approaches applied to genome-wide data prioritized putative functional gene variants associating with treatment-resistant ophthalmoplegic myasthenia gravis (OP-MG). Although altered expression of genes harbouring these variants, or associated pathways, were shown in patient-derived transdifferentiated-myocyte models, gene expression in orbital-derived muscle was required to test the validity of the predictions.\n\n\nMethods\nWe sampled orbicularis oculi muscle (OOM) and one paralysed extraocular muscle (EOM) from six individuals with OP-MG during blepharoptosis and re-alignment surgeries, respectively. For controls, the OOMs were sampled from four individuals without myasthenia undergoing surgery for non-muscle causes of ptosis, and one non-paralysed EOM. Using a qPCR array, expression of 120 genes was compared between OP-MG and control OOMs, profiling putative “OP-MG” genes, genes in related biological pathways and genes reported to be dysregulated in MG cases or experimental MG models, and in EOMs of cases with strabismus. Normalization was performed with two stable reference genes. Differential gene expression was compared between OP-MG and control samples using the $\\Delta$$\\Delta$CT method. Co-expression was analysed by pairwise correlation of gene transcripts to infer expression networks.\n\n\nResults\n\nOverall, transcript levels were similar in OOMs and EOMs (\np\n= 0.72). In OOMs, significant downregulated expression of eight genes was observed in OP-MG cases compared with controls ({\\textgreater}twofold;\np\n≤ 0.016), including\nTFAM\n, a mitochondrial transcription factor, and genes related to the following pathways: atrophy signalling; muscle regeneration and contraction; glycogen synthesis; and extracellular matrix remodelling. Several microRNAs, known to be highly expressed in EOMs, are predicted to regulate some of these genes. Co-expression analyses of gene-pairs suggested high interconnectedness of gene expression networks in OP-MG muscle, but not controls (r {\\textgreater}0.96,\np\n{\\textless}0.01). Significant inverse directions of gene-pair correlations were noted in OP-MG versus controls OOM networks (r ≥ 0.92,\np\n{\\textless}0.001) involving most OP-MG genes overlapping prominently with muscle atrophy/contractility and oxidative metabolism genes.\n\n\n\nConclusions\nThe gene expression in orbital muscles derived from OP-MG individuals compared with normal controls, support the pathogenic hypothesis previously generated from whole genome sequence analyses. Repression of gene transcripts in OP-MG orbital muscle implicate tissue-specific regulatory mechanisms, which may inform future biomarker discovery approaches.},\nauthor = {Europa, Tarin A and Nel, Melissa and Heckmann, Jeannine M},\ndoi = {10.1186/s13023-020-01629-9},\nfile = {:Users/jacquelinebracher/Zotero/storage/TU68KBNG/Europa et al. - 2020 - Gene expression profiling of orbital muscles in tr.pdf:pdf},\nissn = {1750-1172},\njournal = {Orphanet Journal of Rare Diseases},\nmonth = {dec},\nnumber = {1},\npages = {346},\ntitle = {{Gene expression profiling of orbital muscles in treatment-resistant ophthalmoplegic myasthenia gravis}},\nurl = {https://ojrd.biomedcentral.com/articles/10.1186/s13023-020-01629-9},\nvolume = {15},\nyear = {2020}\n}\n
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\n Abstract Background Unbiased in silico approaches applied to genome-wide data prioritized putative functional gene variants associating with treatment-resistant ophthalmoplegic myasthenia gravis (OP-MG). Although altered expression of genes harbouring these variants, or associated pathways, were shown in patient-derived transdifferentiated-myocyte models, gene expression in orbital-derived muscle was required to test the validity of the predictions. Methods We sampled orbicularis oculi muscle (OOM) and one paralysed extraocular muscle (EOM) from six individuals with OP-MG during blepharoptosis and re-alignment surgeries, respectively. For controls, the OOMs were sampled from four individuals without myasthenia undergoing surgery for non-muscle causes of ptosis, and one non-paralysed EOM. Using a qPCR array, expression of 120 genes was compared between OP-MG and control OOMs, profiling putative “OP-MG” genes, genes in related biological pathways and genes reported to be dysregulated in MG cases or experimental MG models, and in EOMs of cases with strabismus. Normalization was performed with two stable reference genes. Differential gene expression was compared between OP-MG and control samples using the $Δ$$Δ$CT method. Co-expression was analysed by pairwise correlation of gene transcripts to infer expression networks. Results Overall, transcript levels were similar in OOMs and EOMs ( p = 0.72). In OOMs, significant downregulated expression of eight genes was observed in OP-MG cases compared with controls (\\textgreatertwofold; p ≤ 0.016), including TFAM , a mitochondrial transcription factor, and genes related to the following pathways: atrophy signalling; muscle regeneration and contraction; glycogen synthesis; and extracellular matrix remodelling. Several microRNAs, known to be highly expressed in EOMs, are predicted to regulate some of these genes. Co-expression analyses of gene-pairs suggested high interconnectedness of gene expression networks in OP-MG muscle, but not controls (r \\textgreater0.96, p \\textless0.01). Significant inverse directions of gene-pair correlations were noted in OP-MG versus controls OOM networks (r ≥ 0.92, p \\textless0.001) involving most OP-MG genes overlapping prominently with muscle atrophy/contractility and oxidative metabolism genes. Conclusions The gene expression in orbital muscles derived from OP-MG individuals compared with normal controls, support the pathogenic hypothesis previously generated from whole genome sequence analyses. Repression of gene transcripts in OP-MG orbital muscle implicate tissue-specific regulatory mechanisms, which may inform future biomarker discovery approaches.\n
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\n \n\n \n \n \n \n \n \n The prevalence and risk factors for phantom limb pain in people with amputations: \\A\\ systematic review and meta-analysis.\n \n \n \n \n\n\n \n Limakatso, K.; Bedwell, G. J; Madden, V. J; and Parker, R.\n\n\n \n\n\n\n PLOS ONE, 15(10): e0240431. oct 2020.\n \n\n\n\n
\n\n\n\n \n \n \"ThePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{limakatso_prevalence_2020,\nauthor = {Limakatso, Katleho and Bedwell, Gillian J and Madden, Victoria J and Parker, Romy},\ndoi = {10.1371/journal.pone.0240431},\neditor = {Eshraghi, Arezoo},\nfile = {:Users/jacquelinebracher/Zotero/storage/Y8DXLALZ/Limakatso et al. - 2020 - The prevalence and risk factors for phantom limb p.pdf:pdf},\nissn = {1932-6203},\njournal = {PLOS ONE},\nmonth = {oct},\nnumber = {10},\npages = {e0240431},\nshorttitle = {The prevalence and risk factors for phantom limb p},\ntitle = {{The prevalence and risk factors for phantom limb pain in people with amputations: {\\{}A{\\}} systematic review and meta-analysis}},\nurl = {https://dx.plos.org/10.1371/journal.pone.0240431},\nvolume = {15},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n Signatures of HIV-1 subtype B and C Tat proteins and their effects in the neuropathogenesis of HIV-associated neurocognitive impairments.\n \n \n \n\n\n \n Williams, M.; Zulu, S.; Stein, D.; Joska, J.; and Naudé, P.\n\n\n \n\n\n\n Neurobiology of Disease, 136. 2020.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Williams2020a,\nabstract = {HIV-associated neurocognitive impairments (HANI) are a spectrum of neurological disorders due to the effects of HIV-1 on the central nervous system (CNS). The HIV-1 subtypes; HIV-1 subtype B (HIV-1B) and HIV-1 subtype C (HIV-1C) are responsible for the highest prevalence of HANI and HIV infections respectively. The HIV transactivator of transcription (Tat) protein is a major contributor to the neuropathogenesis of HIV. The effects of the Tat protein on cells of the CNS is determined by the subtype-associated amino acid sequence variations. The extent to which the sequence variation between Tat-subtypes contribute to underlying mechanisms and neurological outcomes are not clear. In this review of the literature, we discuss how amino acid variations between HIV-1B Tat (Tat[sbnd]B) and HIV-1C Tat (Tat[sbnd]C) proteins contribute to the potential underlying neurobiological mechanisms of HANI. Tat-C is considered to be a more effective transactivator, whereas Tat-B may exert increased neurovirulence, including neuronal apoptosis, monocyte infiltration into the brain, (neuro)inflammation, oxidative stress and blood-brain barrier damage. These findings support the premise that Tat variants from different HIV-1 subtypes may direct neurovirulence and neurological outcomes in HANI.},\nauthor = {Williams, M.E. and Zulu, S.S. and Stein, D.J. and Joska, J.A. and Naud{\\'{e}}, P.J.W.},\ndoi = {10.1016/j.nbd.2019.104701},\njournal = {Neurobiology of Disease},\ntitle = {{Signatures of HIV-1 subtype B and C Tat proteins and their effects in the neuropathogenesis of HIV-associated neurocognitive impairments}},\nvolume = {136},\nyear = {2020}\n}\n
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\n HIV-associated neurocognitive impairments (HANI) are a spectrum of neurological disorders due to the effects of HIV-1 on the central nervous system (CNS). The HIV-1 subtypes; HIV-1 subtype B (HIV-1B) and HIV-1 subtype C (HIV-1C) are responsible for the highest prevalence of HANI and HIV infections respectively. The HIV transactivator of transcription (Tat) protein is a major contributor to the neuropathogenesis of HIV. The effects of the Tat protein on cells of the CNS is determined by the subtype-associated amino acid sequence variations. The extent to which the sequence variation between Tat-subtypes contribute to underlying mechanisms and neurological outcomes are not clear. In this review of the literature, we discuss how amino acid variations between HIV-1B Tat (Tat[sbnd]B) and HIV-1C Tat (Tat[sbnd]C) proteins contribute to the potential underlying neurobiological mechanisms of HANI. Tat-C is considered to be a more effective transactivator, whereas Tat-B may exert increased neurovirulence, including neuronal apoptosis, monocyte infiltration into the brain, (neuro)inflammation, oxidative stress and blood-brain barrier damage. These findings support the premise that Tat variants from different HIV-1 subtypes may direct neurovirulence and neurological outcomes in HANI.\n
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\n \n\n \n \n \n \n \n \n Peripheral immune dysregulation in the ART era of HIV-associated neurocognitive impairments: A systematic review.\n \n \n \n \n\n\n \n Williams, M E; Ipser, J C; Stein, D J; Joska, J A; and Naudé, P J W\n\n\n \n\n\n\n Psychoneuroendocrinology, 118. 2020.\n \n\n\n\n
\n\n\n\n \n \n \"PeripheralPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n\n\n\n
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@article{Williams2020,\nannote = {cited By 0},\nauthor = {Williams, M E and Ipser, J C and Stein, D J and Joska, J A and Naud{\\'{e}}, P J W},\ndoi = {10.1016/j.psyneuen.2020.104689},\nissn = {03064530},\njournal = {Psychoneuroendocrinology},\nkeywords = {alpha interferon; antiretrovirus agent; C reactive,antiretroviral therapy; cell activation; electroc},\npublisher = {Elsevier Ltd},\ntitle = {{Peripheral immune dysregulation in the ART era of HIV-associated neurocognitive impairments: A systematic review}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85085486367{\\&}doi=10.1016{\\%}2Fj.psyneuen.2020.104689{\\&}partnerID=40{\\&}md5=be301f93c4128bcf4fef7256038ffa4c},\nvolume = {118},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n Recreational Use of HIV Antiretroviral Medication and Implications for HIV Pre-exposure Prophylaxis and Treatment.\n \n \n \n\n\n \n Kuo, C.; Giovenco, D.; DeAtley, T.; Hoare, J.; Underhill, K.; Atujuna, M.; Mathews, C.; Stein, D.; Brown, L.; and Operario, D.\n\n\n \n\n\n\n AIDS and Behavior, 24(9): 2650–2655. 2020.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Kuo2020,\nabstract = {Diversion of antiretroviral therapy (ART) for recreational use is concerning for countries with high HIV prevalence. This paper presents reports of recreational use of ART among adolescents from two HIV prevention studies in South Africa: (1) a cross-sectional survey of N = 200 adolescents and (2) a qualitative study of pre-exposure prophylaxis with N = 57 adolescents and N = 25 clinicians. Among adolescents, 3{\\%} used and 14{\\%} knew someone who used non-prescribed ART for recreational purposes. Administration included smoking (71{\\%}), snorting (15{\\%}), injecting (15{\\%}), ingesting (15{\\%}), and inserting (3{\\%}). Participants predicted increased crime as recreational use of ART increased. Future studies should investigate prevalence, composition, and diversion of ART from HIV prevention and treatment.},\nauthor = {Kuo, C. and Giovenco, D. and DeAtley, T. and Hoare, J. and Underhill, K. and Atujuna, M. and Mathews, C. and Stein, D.J. and Brown, L.K. and Operario, D.},\ndoi = {10.1007/s10461-020-02821-5},\nfile = {:Users/jacquelinebracher/Zotero/storage/JILCTG5Y/Kuo et al. - 2020 - Recreational Use of HIV Antiretroviral Medication .pdf:pdf},\njournal = {AIDS and Behavior},\nnumber = {9},\npages = {2650--2655},\ntitle = {{Recreational Use of HIV Antiretroviral Medication and Implications for HIV Pre-exposure Prophylaxis and Treatment}},\nvolume = {24},\nyear = {2020}\n}\n
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\n Diversion of antiretroviral therapy (ART) for recreational use is concerning for countries with high HIV prevalence. This paper presents reports of recreational use of ART among adolescents from two HIV prevention studies in South Africa: (1) a cross-sectional survey of N = 200 adolescents and (2) a qualitative study of pre-exposure prophylaxis with N = 57 adolescents and N = 25 clinicians. Among adolescents, 3% used and 14% knew someone who used non-prescribed ART for recreational purposes. Administration included smoking (71%), snorting (15%), injecting (15%), ingesting (15%), and inserting (3%). Participants predicted increased crime as recreational use of ART increased. Future studies should investigate prevalence, composition, and diversion of ART from HIV prevention and treatment.\n
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\n \n\n \n \n \n \n \n Cognition, Structural Brain Changes, and Systemic Inflammation in Adolescents Living with HIV on Antiretroviral Therapy.\n \n \n \n\n\n \n Hoare, J.; Myer, L.; Heany, S.; Fouche, J.; Phillips, N.; Zar, H.; and Stein, D.\n\n\n \n\n\n\n Journal of Acquired Immune Deficiency Syndromes, 84(1): 114–121. 2020.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Hoare2020,\nabstract = {Objective:To investigate the association between neurocognitive impairment, neuroimaging, and systemic inflammation in perinatally infected adolescents living with HIV (PHIV) on antiretroviral therapy (ART). Systemic inflammation may be one mechanism driving neurocognitive impairment despite ART, but this has not been investigated in adolescence when the brain is undergoing rapid development.Setting:Cape Town, South Africa.Methods:Baseline data were drawn from the Cape Town Adolescent Antiretroviral Cohort. PHIV on ART {\\textgreater}6 months completed a comprehensive neurocognitive test battery. Diffusion tensor imaging and structural brain magnetic resonance imaging was done to determine whole brain fractional anisotropy, mean diffusion (MD), grey and white matter volumes, and cortical thickness. We examined how neurocognitive and neurostructural measures were associated with a concurrently measured marker of systemic inflammation, high-sensitive C-reactive protein (hs-CRP).Results:One hundred sixty-eight PHIV ages 9-12 years (mean CD4 980 cells/µL; 85.3{\\%} viral load {\\textless}50 copies/mL) and 43 controls were included in the analysis. PHIV had similar hs-CRP (P = 0.17) to controls, after participants with hs-CRP {\\textgreater}10 were excluded from the analysis. Forty-eight percent of the PHIV in this analysis have a neurocognitive disorder. Whole brain grey (P = 0.049) and white matter volumes (P = 0.044) were lowest in PHIV with a major neurocognitive disorder. Higher MD, was found in PHIV with a major neurocognitive disorder (P = 0.002). Among PHIV with a neurocognitive disorder, hs-CRP negatively correlated with general intelligence, visual spatial acuity, and executive function (all P = {\\textless} 0.05). Whole brain MD correlated with higher hs-CRP values (P = {\\textless} 0.01) in PHIV.Conclusions:A marker of systemic inflammation was associated with both neurocognitive impairment and MD increases in PHIV.},\nauthor = {Hoare, J. and Myer, L. and Heany, S. and Fouche, J.-P. and Phillips, N. and Zar, H.J. and Stein, D.J.},\ndoi = {10.1097/QAI.0000000000002314},\nfile = {:Users/jacquelinebracher/Zotero/storage/TD99HRV7/Hoare et al. - 2020 - Cognition, Structural Brain Changes, and Systemic .pdf:pdf},\njournal = {Journal of Acquired Immune Deficiency Syndromes},\nnumber = {1},\npages = {114--121},\ntitle = {{Cognition, Structural Brain Changes, and Systemic Inflammation in Adolescents Living with HIV on Antiretroviral Therapy}},\nvolume = {84},\nyear = {2020}\n}\n
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\n Objective:To investigate the association between neurocognitive impairment, neuroimaging, and systemic inflammation in perinatally infected adolescents living with HIV (PHIV) on antiretroviral therapy (ART). Systemic inflammation may be one mechanism driving neurocognitive impairment despite ART, but this has not been investigated in adolescence when the brain is undergoing rapid development.Setting:Cape Town, South Africa.Methods:Baseline data were drawn from the Cape Town Adolescent Antiretroviral Cohort. PHIV on ART \\textgreater6 months completed a comprehensive neurocognitive test battery. Diffusion tensor imaging and structural brain magnetic resonance imaging was done to determine whole brain fractional anisotropy, mean diffusion (MD), grey and white matter volumes, and cortical thickness. We examined how neurocognitive and neurostructural measures were associated with a concurrently measured marker of systemic inflammation, high-sensitive C-reactive protein (hs-CRP).Results:One hundred sixty-eight PHIV ages 9-12 years (mean CD4 980 cells/µL; 85.3% viral load \\textless50 copies/mL) and 43 controls were included in the analysis. PHIV had similar hs-CRP (P = 0.17) to controls, after participants with hs-CRP \\textgreater10 were excluded from the analysis. Forty-eight percent of the PHIV in this analysis have a neurocognitive disorder. Whole brain grey (P = 0.049) and white matter volumes (P = 0.044) were lowest in PHIV with a major neurocognitive disorder. Higher MD, was found in PHIV with a major neurocognitive disorder (P = 0.002). Among PHIV with a neurocognitive disorder, hs-CRP negatively correlated with general intelligence, visual spatial acuity, and executive function (all P = \\textless 0.05). Whole brain MD correlated with higher hs-CRP values (P = \\textless 0.01) in PHIV.Conclusions:A marker of systemic inflammation was associated with both neurocognitive impairment and MD increases in PHIV.\n
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\n \n\n \n \n \n \n \n \n Neuroimaging young children and associations with neurocognitive development in a South African birth cohort study.\n \n \n \n \n\n\n \n Wedderburn, C J; Subramoney, S; Yeung, S; Fouche, J.; Joshi, S H; Narr, K L; Rehman, A M; Roos, A; Ipser, J; Robertson, F C; Groenewold, N A; Gibb, D M; Zar, H J; Stein, D J; and Donald, K A\n\n\n \n\n\n\n NeuroImage, 219. 2020.\n \n\n\n\n
\n\n\n\n \n \n \"NeuroimagingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n\n\n\n
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@article{Wedderburn2020,\nannote = {cited By 0},\nauthor = {Wedderburn, C J and Subramoney, S and Yeung, S and Fouche, J.-P. and Joshi, S H and Narr, K L and Rehman, A M and Roos, A and Ipser, J and Robertson, F C and Groenewold, N A and Gibb, D M and Zar, H J and Stein, D J and Donald, K A},\ndoi = {10.1016/j.neuroimage.2020.116846},\nfile = {:Users/jacquelinebracher/Zotero/storage/CUUXW9R2/Wedderburn et al. - 2020 - Neuroimaging young children and associations with .pdf:pdf},\nissn = {10538119},\njournal = {NeuroImage},\nkeywords = {Africa south of the Sahara; anesthesia; article; B},\npublisher = {Academic Press Inc.},\ntitle = {{Neuroimaging young children and associations with neurocognitive development in a South African birth cohort study}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85086501333{\\&}doi=10.1016{\\%}2Fj.neuroimage.2020.116846{\\&}partnerID=40{\\&}md5=b7bda161a46afe22cb895c4a6fbe475d},\nvolume = {219},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n Accelerated Immunodeficiency-associated Vaccine-derived Poliovirus Serotype 3 Sequence Evolution Rate in an 11-week-old Boy with X-linked Agammaglobulinemia and Perinatal Human Immunodeficiency Virus Exposure.\n \n \n \n \n\n\n \n Jallow, S; Wilmshurst, J M; Howard, W; Copelyn, J; Seakamela, L; Chan, K.; Sebunya, R; Sibiya, R; Du Plessis, H; Jacobs, C; Berkowitz, N; Blumberg, L; McCarthy, K; Maseti, E; Kamupira, M; Dlamini, N; Gumede, N; Diop, O M; Lau, Y L; Moonsamy, S; Eley, B; and Suchard, M\n\n\n \n\n\n\n Clinical Infectious Diseases, 70(1): 132–135. 2020.\n \n\n\n\n
\n\n\n\n \n \n \"AcceleratedPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n\n\n\n
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@article{Jallow2020132,\nannote = {cited By 1},\nauthor = {Jallow, S and Wilmshurst, J M and Howard, W and Copelyn, J and Seakamela, L and Chan, K.-W. and Sebunya, R and Sibiya, R and {Du Plessis}, H and Jacobs, C and Berkowitz, N and Blumberg, L and McCarthy, K and Maseti, E and Kamupira, M and Dlamini, N and Gumede, N and Diop, O M and Lau, Y L and Moonsamy, S and Eley, B and Suchard, M},\ndoi = {10.1093/cid/ciz361},\nfile = {:Users/jacquelinebracher/Zotero/storage/8IEB6CZV/Jallow et al. - 2020 - Accelerated Immunodeficiency-associated Vaccine-de.pdf:pdf},\nissn = {10584838},\njournal = {Clinical Infectious Diseases},\nkeywords = {Article; birth weight; case report; cerebrospinal,aciclovir; cefotaxime; immunoglobulin G; nevirapin},\nnumber = {1},\npages = {132--135},\npublisher = {Oxford University Press},\ntitle = {{Accelerated Immunodeficiency-associated Vaccine-derived Poliovirus Serotype 3 Sequence Evolution Rate in an 11-week-old Boy with X-linked Agammaglobulinemia and Perinatal Human Immunodeficiency Virus Exposure}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85076585306{\\&}doi=10.1093{\\%}2Fcid{\\%}2Fciz361{\\&}partnerID=40{\\&}md5=34b7a857b9ddf97a261fd410986977ec},\nvolume = {70},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n Interleukin-4 and Anxiety in Adults with Atopic Dermatitis.\n \n \n \n \n\n\n \n Gray, N A; Naude, P J; Esterhuizen, T M; Khumalo, N P; and Stein, D J\n\n\n \n\n\n\n Acta Neuropsychiatrica. 2020.\n \n\n\n\n
\n\n\n\n \n \n \"Interleukin-4Paper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Gray2020,\nannote = {cited By 0},\nauthor = {Gray, N A and Naude, P J and Esterhuizen, T M and Khumalo, N P and Stein, D J},\ndoi = {10.1017/neu.2020.23},\nissn = {09242708},\njournal = {Acta Neuropsychiatrica},\npublisher = {Cambridge University Press},\ntitle = {{Interleukin-4 and Anxiety in Adults with Atopic Dermatitis}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85084858345{\\&}doi=10.1017{\\%}2Fneu.2020.23{\\&}partnerID=40{\\&}md5=907662a04581fcf23a15d29d24fc9ff7},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n Decision-Making by Patients With Methamphetamine Use Disorder Receiving Contingency Management Treatment: Magnitude and Frequency Effects.\n \n \n \n\n\n \n Lake, M.; Shoptaw, S.; Ipser, J.; Takada, S.; van Nunen, L.; Lipinska, G.; Stein, D.; and London, E.\n\n\n \n\n\n\n Frontiers in Psychiatry, 11. 2020.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Lake2020,\nabstract = {Background: Individuals with substance use disorders exhibit maladaptive decision-making on the Iowa Gambling Task (IGT), which involves selecting from card decks differing in the magnitudes of rewards, and the frequency and magnitude of losses. We investigated whether baseline IGT performance could predict responses to contingency management (CM) by treatment-seeking individuals with methamphetamine use disorder (MA Use Disorder) in Cape Town, South Africa. Methods: Twenty-nine individuals with MA Use Disorder underwent an 8-week, escalating reinforcement, voucher-based CM treatment in a study on the suitability of CM therapy for the South African context. Along with 20 healthy control participants, they performed a computerized version of the IGT before starting CM treatment. Seventeen participants maintained abstinence from methamphetamine throughout the trial (full responders), and 12 had an incomplete response (partial responders). Performance on the IGT was scored for magnitude effect (selection of large immediate rewards with high long-term loss) and for frequency effect (preference for frequent rewards and avoidance of frequent losses). Group differences were investigated using linear mixed-effect modeling. Results: Partial responders made more selections from decks providing large, immediate rewards and long-term losses than healthy controls [p = 0.038, g = -0.77 (-1.09: -0.44)]. Full responders showed a greater, nonsignificant preference for frequent rewards and aversion to frequent losses than partial responders [p = 0.054, g = -0.63 (-0.95: -0.29)]. Conclusions: A predilection for choices based on the size and immediacy of reward may reflect a cognitive strategy that works against CM. Pretesting with a decision-making task, such as the IGT, may help in matching cognitive therapies to clients with MA Use Disorder.},\nauthor = {Lake, M.T. and Shoptaw, S. and Ipser, J.C. and Takada, S. and van Nunen, L.J. and Lipinska, G. and Stein, D.J. and London, E.D.},\ndoi = {10.3389/fpsyt.2020.00022},\nfile = {:Users/jacquelinebracher/Zotero/storage/X8E9K48Z/Lake et al. - 2020 - Decision-Making by Patients With Methamphetamine U.pdf:pdf},\njournal = {Frontiers in Psychiatry},\ntitle = {{Decision-Making by Patients With Methamphetamine Use Disorder Receiving Contingency Management Treatment: Magnitude and Frequency Effects}},\nvolume = {11},\nyear = {2020}\n}\n
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\n Background: Individuals with substance use disorders exhibit maladaptive decision-making on the Iowa Gambling Task (IGT), which involves selecting from card decks differing in the magnitudes of rewards, and the frequency and magnitude of losses. We investigated whether baseline IGT performance could predict responses to contingency management (CM) by treatment-seeking individuals with methamphetamine use disorder (MA Use Disorder) in Cape Town, South Africa. Methods: Twenty-nine individuals with MA Use Disorder underwent an 8-week, escalating reinforcement, voucher-based CM treatment in a study on the suitability of CM therapy for the South African context. Along with 20 healthy control participants, they performed a computerized version of the IGT before starting CM treatment. Seventeen participants maintained abstinence from methamphetamine throughout the trial (full responders), and 12 had an incomplete response (partial responders). Performance on the IGT was scored for magnitude effect (selection of large immediate rewards with high long-term loss) and for frequency effect (preference for frequent rewards and avoidance of frequent losses). Group differences were investigated using linear mixed-effect modeling. Results: Partial responders made more selections from decks providing large, immediate rewards and long-term losses than healthy controls [p = 0.038, g = -0.77 (-1.09: -0.44)]. Full responders showed a greater, nonsignificant preference for frequent rewards and aversion to frequent losses than partial responders [p = 0.054, g = -0.63 (-0.95: -0.29)]. Conclusions: A predilection for choices based on the size and immediacy of reward may reflect a cognitive strategy that works against CM. Pretesting with a decision-making task, such as the IGT, may help in matching cognitive therapies to clients with MA Use Disorder.\n
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\n \n\n \n \n \n \n \n \n Schizophrenia \\Polygenic\\ \\Risk\\ and \\Brain\\ \\Structural\\ \\Changes\\ in \\Methamphetamine\\-\\Associated\\ \\Psychosis\\ in a \\South\\ \\African\\ \\Population\\.\n \n \n \n \n\n\n \n Passchier, R. V; Stein, D. J; Uhlmann, A.; Van Der Merwe, C.; and Dalvie, S.\n\n\n \n\n\n\n Frontiers in Genetics, 11: 1018. oct 2020.\n \n\n\n\n
\n\n\n\n \n \n \"SchizophreniaPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{passchier_schizophrenia_2020,\nauthor = {Passchier, Ruth V and Stein, Dan J and Uhlmann, Anne and {Van Der Merwe}, Celia and Dalvie, Shareefa},\ndoi = {10.3389/fgene.2020.01018},\nfile = {:Users/jacquelinebracher/Zotero/storage/XWZ9FSFW/Passchier et al. - 2020 - Schizophrenia Polygenic Risk and Brain Structural .pdf:pdf},\nissn = {1664-8021},\njournal = {Frontiers in Genetics},\nmonth = {oct},\npages = {1018},\ntitle = {{Schizophrenia {\\{}Polygenic{\\}} {\\{}Risk{\\}} and {\\{}Brain{\\}} {\\{}Structural{\\}} {\\{}Changes{\\}} in {\\{}Methamphetamine{\\}}-{\\{}Associated{\\}} {\\{}Psychosis{\\}} in a {\\{}South{\\}} {\\{}African{\\}} {\\{}Population{\\}}}},\nurl = {https://www.frontiersin.org/article/10.3389/fgene.2020.01018/full},\nvolume = {11},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n Mental health delivery and neurogenetics discovery in Africa.\n \n \n \n \n\n\n \n Stein, D J; Lehner, T; Lombard, Z; Pringle, B; Senthil, G; and Uddin, M\n\n\n \n\n\n\n The Lancet Psychiatry, 7(6): 473–474. 2020.\n \n\n\n\n
\n\n\n\n \n \n \"MentalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n\n\n\n
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@article{Stein2020473,\nannote = {cited By 0},\nauthor = {Stein, D J and Lehner, T and Lombard, Z and Pringle, B and Senthil, G and Uddin, M},\ndoi = {10.1016/S2215-0366(20)30085-7},\nfile = {:Users/jacquelinebracher/Zotero/storage/VYBYLP5G/Stein et al. - 2020 - Mental health delivery and neurogenetics discovery.pdf:pdf},\nissn = {22150366},\njournal = {The Lancet Psychiatry},\nkeywords = {Africa; Comorbidity; Delivery of Health Care; Dep,Africa; comorbidity; depression; genotype environm},\nnumber = {6},\npages = {473--474},\npublisher = {Elsevier Ltd},\ntitle = {{Mental health delivery and neurogenetics discovery in Africa}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85084704285{\\&}doi=10.1016{\\%}2FS2215-0366{\\%}2820{\\%}2930085-7{\\&}partnerID=40{\\&}md5=98b957afd78917c52e565fe5cec657b6},\nvolume = {7},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n International Survey Reveals Opportunities to Improve Tuberculous Meningitis Management and the Need for Standardized Guidelines.\n \n \n \n \n\n\n \n Tucker, E W; Marais, S; Seddon, J A; van Crevel, R; Ganiem, A R; Ruslami, R; Zhang, W; Sun, F; Zhou, X; Solomons, R S; Cresswell, F V; Wilmshurst, J; and Rohlwink, U\n\n\n \n\n\n\n 2020.\n \n\n\n\n
\n\n\n\n \n \n \"InternationalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@misc{Tucker2020,\nannote = {Export Date: 29 December 2022},\nauthor = {Tucker, E W and Marais, S and Seddon, J A and van Crevel, R and Ganiem, A R and Ruslami, R and Zhang, W and Sun, F and Zhou, X and Solomons, R S and Cresswell, F V and Wilmshurst, J and Rohlwink, U},\ndoi = {10.1093/ofid/ofaa445},\nfile = {:Users/jacquelinebracher/Zotero/storage/ESM89Q3S/Tucker et al. - 2020 - International Survey Reveals Opportunities to Impr.pdf:pdf},\nnumber = {11},\ntitle = {{International Survey Reveals Opportunities to Improve Tuberculous Meningitis Management and the Need for Standardized Guidelines}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85096802944{\\&}doi=10.1093{\\%}2Fofid{\\%}2Fofaa445{\\&}partnerID=40{\\&}md5=71006311bfaa69ca34dc33d406f64744},\nvolume = {7},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n The prevalence and clinical correlates of substance use disorders in patients with psychotic disorders from an \\Upper\\-\\Middle\\-\\Income\\ \\Country\\.\n \n \n \n \n\n\n \n Temmingh, H. S; Mall, S.; Howells, F. M; Sibeko, G.; and Stein, D. J\n\n\n \n\n\n\n South African Journal of Psychiatry, 26. jul 2020.\n \n\n\n\n
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@article{temmingh_prevalence_2020,\nauthor = {Temmingh, Henk S and Mall, Sumaya and Howells, Fleur M and Sibeko, Goodman and Stein, Dan J},\ndoi = {10.4102/sajpsychiatry.v26i0.1473},\nfile = {:Users/jacquelinebracher/Zotero/storage/MNZIVY3W/Temmingh et al. - 2020 - The prevalence and clinical correlates of substanc.pdf:pdf},\nissn = {2078-6786, 1608-9685},\njournal = {South African Journal of Psychiatry},\nmonth = {jul},\ntitle = {{The prevalence and clinical correlates of substance use disorders in patients with psychotic disorders from an {\\{}Upper{\\}}-{\\{}Middle{\\}}-{\\{}Income{\\}} {\\{}Country{\\}}}},\nurl = {http://www.sajpsychiatry.org/index.php/sajp/article/view/1473},\nvolume = {26},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n \\ENIGMA\\ \\MDD\\: seven years of global neuroimaging studies of major depression through worldwide data sharing.\n \n \n \n \n\n\n \n Schmaal, L.; Pozzi, E.; C. Ho, T.; Van Velzen, L. S; Veer, I. M; Opel, N.; Van Someren, E. J W; Han, L. K M; Aftanas, L.; Aleman, A.; Baune, B. T; Berger, K.; Blanken, T. F; Capitão, L.; Couvy-Duchesne, B.; R. Cullen, K.; Dannlowski, U.; Davey, C.; Erwin-Grabner, T.; Evans, J.; Frodl, T.; Fu, C. H Y; Godlewska, B.; Gotlib, I. H; Goya-Maldonado, R.; Grabe, H. J; Groenewold, N. A; Grotegerd, D.; Gruber, O.; Gutman, B. A; Hall, G. B; Harrison, B. J; Hatton, S. N; Hermesdorf, M.; Hickie, I. B; Hilland, E.; Irungu, B.; Jonassen, R.; Kelly, S.; Kircher, T.; Klimes-Dougan, B.; Krug, A.; Landrø, N. I.; Lagopoulos, J.; Leerssen, J.; Li, M.; Linden, D. E J; MacMaster, F. P; M. McIntosh, A.; Mehler, D. M A; Nenadić, I.; Penninx, B. W J H; Portella, M. J; Reneman, L.; Rentería, M. E; Sacchet, M. D; G. Sämann, P.; Schrantee, A.; Sim, K.; Soares, J. C; Stein, D. J; Tozzi, L.; Van Der Wee, N. J A; Van Tol, M.; Vermeiren, R.; Vives-Gilabert, Y.; Walter, H.; Walter, M.; Whalley, H. C; Wittfeld, K.; Whittle, S.; Wright, M. J; Yang, T. T; Zarate, C.; Thomopoulos, S. I; Jahanshad, N.; Thompson, P. M; and Veltman, D. J\n\n\n \n\n\n\n Translational Psychiatry, 10(1): 172. may 2020.\n \n\n\n\n
\n\n\n\n \n \n \"\\ENIGMA\\Paper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{schmaal_enigma_2020,\nabstract = {Abstract\nA key objective in the field of translational psychiatry over the past few decades has been to identify the brain correlates of major depressive disorder (MDD). Identifying measurable indicators of brain processes associated with MDD could facilitate the detection of individuals at risk, and the development of novel treatments, the monitoring of treatment effects, and predicting who might benefit most from treatments that target specific brain mechanisms. However, despite intensive neuroimaging research towards this effort, underpowered studies and a lack of reproducible findings have hindered progress. Here, we discuss the work of the ENIGMA Major Depressive Disorder (MDD) Consortium, which was established to address issues of poor replication, unreliable results, and overestimation of effect sizes in previous studies. The ENIGMA MDD Consortium currently includes data from 45 MDD study cohorts from 14 countries across six continents. The primary aim of ENIGMA MDD is to identify structural and functional brain alterations associated with MDD that can be reliably detected and replicated across cohorts worldwide. A secondary goal is to investigate how demographic, genetic, clinical, psychological, and environmental factors affect these associations. In this review, we summarize findings of the ENIGMA MDD disease working group to date and discuss future directions. We also highlight the challenges and benefits of large-scale data sharing for mental health research.},\nauthor = {Schmaal, Lianne and Pozzi, Elena and {C. Ho}, Tiffany and {Van Velzen}, Laura S and Veer, Ilya M and Opel, Nils and {Van Someren}, Eus J W and Han, Laura K M and Aftanas, Lybomir and Aleman, Andr{\\'{e}} and Baune, Bernhard T and Berger, Klaus and Blanken, Tessa F and Capit{\\~{a}}o, Liliana and Couvy-Duchesne, Baptiste and {R. Cullen}, Kathryn and Dannlowski, Udo and Davey, Christopher and Erwin-Grabner, Tracy and Evans, Jennifer and Frodl, Thomas and Fu, Cynthia H Y and Godlewska, Beata and Gotlib, Ian H and Goya-Maldonado, Roberto and Grabe, Hans J and Groenewold, Nynke A and Grotegerd, Dominik and Gruber, Oliver and Gutman, Boris A and Hall, Geoffrey B and Harrison, Ben J and Hatton, Sean N and Hermesdorf, Marco and Hickie, Ian B and Hilland, Eva and Irungu, Benson and Jonassen, Rune and Kelly, Sinead and Kircher, Tilo and Klimes-Dougan, Bonnie and Krug, Axel and Landr{\\o}, Nils Inge and Lagopoulos, Jim and Leerssen, Jeanne and Li, Meng and Linden, David E J and MacMaster, Frank P and {M. McIntosh}, Andrew and Mehler, David M A and Nenadi{\\'{c}}, Igor and Penninx, Brenda W J H and Portella, Maria J and Reneman, Liesbeth and Renter{\\'{i}}a, Miguel E and Sacchet, Matthew D and {G. S{\\"{a}}mann}, Philipp and Schrantee, Anouk and Sim, Kang and Soares, Jair C and Stein, Dan J and Tozzi, Leonardo and {Van Der Wee}, Nic J A and {Van Tol}, Marie-Jos{\\'{e}} and Vermeiren, Robert and Vives-Gilabert, Yolanda and Walter, Henrik and Walter, Martin and Whalley, Heather C and Wittfeld, Katharina and Whittle, Sarah and Wright, Margaret J and Yang, Tony T and Zarate, Carlos and Thomopoulos, Sophia I and Jahanshad, Neda and Thompson, Paul M and Veltman, Dick J},\ndoi = {10.1038/s41398-020-0842-6},\nfile = {:Users/jacquelinebracher/Zotero/storage/WNCHVHIA/Schmaal et al. - 2020 - ENIGMA MDD seven years of global neuroimaging stu.pdf:pdf},\nissn = {2158-3188},\njournal = {Translational Psychiatry},\nmonth = {may},\nnumber = {1},\npages = {172},\nshorttitle = {{\\{}ENIGMA{\\}} {\\{}MDD{\\}}},\ntitle = {{{\\{}ENIGMA{\\}} {\\{}MDD{\\}}: seven years of global neuroimaging studies of major depression through worldwide data sharing}},\nurl = {https://www.nature.com/articles/s41398-020-0842-6},\nvolume = {10},\nyear = {2020}\n}\n
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\n Abstract A key objective in the field of translational psychiatry over the past few decades has been to identify the brain correlates of major depressive disorder (MDD). Identifying measurable indicators of brain processes associated with MDD could facilitate the detection of individuals at risk, and the development of novel treatments, the monitoring of treatment effects, and predicting who might benefit most from treatments that target specific brain mechanisms. However, despite intensive neuroimaging research towards this effort, underpowered studies and a lack of reproducible findings have hindered progress. Here, we discuss the work of the ENIGMA Major Depressive Disorder (MDD) Consortium, which was established to address issues of poor replication, unreliable results, and overestimation of effect sizes in previous studies. The ENIGMA MDD Consortium currently includes data from 45 MDD study cohorts from 14 countries across six continents. The primary aim of ENIGMA MDD is to identify structural and functional brain alterations associated with MDD that can be reliably detected and replicated across cohorts worldwide. A secondary goal is to investigate how demographic, genetic, clinical, psychological, and environmental factors affect these associations. In this review, we summarize findings of the ENIGMA MDD disease working group to date and discuss future directions. We also highlight the challenges and benefits of large-scale data sharing for mental health research.\n
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\n \n\n \n \n \n \n \n \n Clearance of immunodeficiency-associated vaccine-derived poliovirus infection with pocapavir.\n \n \n \n \n\n\n \n Copelyn, J; Hincks, J R; Wilmshurst, J M; Petersen, W; Howard, W; Jallow, S; Moonsamy, S; Seakamela, L; Suchard, M; Collett, M S; and Eley, B\n\n\n \n\n\n\n Pediatric Infectious Disease Journal,435–437. 2020.\n \n\n\n\n
\n\n\n\n \n \n \"ClearancePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Copelyn2020435,\nannote = {cited By 0},\nauthor = {Copelyn, J and Hincks, J R and Wilmshurst, J M and Petersen, W and Howard, W and Jallow, S and Moonsamy, S and Seakamela, L and Suchard, M and Collett, M S and Eley, B},\ndoi = {10.1097/INF.0000000000002584},\nissn = {08913668},\njournal = {Pediatric Infectious Disease Journal},\npages = {435--437},\npublisher = {Lippincott Williams and Wilkins},\ntitle = {{Clearance of immunodeficiency-associated vaccine-derived poliovirus infection with pocapavir}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85083773159{\\&}doi=10.1097{\\%}2FINF.0000000000002584{\\&}partnerID=40{\\&}md5=0d1123b936f0c4171998c05aac3ac0eb},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n Accuracy of diagnostic judgments using \\ICD\\-11 vs. \\ICD\\-10 diagnostic guidelines for obsessive-compulsive and related disorders.\n \n \n \n \n\n\n \n Kogan, C. S; Stein, D. J; Rebello, T. J; Keeley, J. W; Chan, K J.; Fineberg, N. A; Fontenelle, L. F; Grant, J. E; Matsunaga, H.; Simpson, H B.; Thomsen, P. H.; Van Den Heuvel, O. A; Veale, D.; Grenier, J.; Kulygina, M.; Matsumoto, C.; Domínguez-Martínez, T.; Stona, A.; Wang, Z.; and Reed, G. M\n\n\n \n\n\n\n Journal of Affective Disorders, 273: 328–340. aug 2020.\n \n\n\n\n
\n\n\n\n \n \n \"AccuracyPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n 
@article{kogan_accuracy_2020,\nauthor = {Kogan, Cary S and Stein, Dan J and Rebello, Tahilia J and Keeley, Jared W and Chan, K Jacky and Fineberg, Naomi A and Fontenelle, Leonardo F and Grant, Jon E and Matsunaga, Hisato and Simpson, H Blair and Thomsen, Per Hove and {Van Den Heuvel}, Odile A and Veale, David and Grenier, Jean and Kulygina, Mayya and Matsumoto, Chihiro and Dom{\\'{i}}nguez-Mart{\\'{i}}nez, Tecelli and Stona, Anne-Claire and Wang, Zhen and Reed, Geoffrey M},\ndoi = {10.1016/j.jad.2020.03.103},\nfile = {:Users/jacquelinebracher/Zotero/storage/I6NMQHFD/Kogan et al. - 2020 - Accuracy of diagnostic judgments using ICD-11 vs. .pdf:pdf},\nissn = {01650327},\njournal = {Journal of Affective Disorders},\nmonth = {aug},\npages = {328--340},\ntitle = {{Accuracy of diagnostic judgments using {\\{}ICD{\\}}-11 vs. {\\{}ICD{\\}}-10 diagnostic guidelines for obsessive-compulsive and related disorders}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S0165032719327181},\nvolume = {273},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n A South African cerebral palsy registry is needed.\n \n \n \n\n\n \n Katangwe, T.; van Toorn, R.; Solomons, R.; Donald, K.; Steel, S.; Springer, P.; and Kruger, M.\n\n\n \n\n\n\n South African Medical Journal, 110(5): 353–354. 2020.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Katangwe2020,\nauthor = {Katangwe, T.J. and van Toorn, R. and Solomons, R.S. and Donald, K. and Steel, S. and Springer, P.E. and Kruger, M.},\ndoi = {10.7196/SAMJ.2020.v110i5.14504},\nfile = {:Users/jacquelinebracher/Zotero/storage/4YVYXTS5/Katangwe et al. - 2020 - A South African cerebral palsy registry is needed.pdf:pdf},\njournal = {South African Medical Journal},\nnumber = {5},\npages = {353--354},\ntitle = {{A South African cerebral palsy registry is needed}},\nvolume = {110},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n The clinical characterization of the adult patient with depression aimed at personalization of management.\n \n \n \n \n\n\n \n Maj, M.; Stein, D. J; Parker, G.; Zimmerman, M.; Fava, G. A; De Hert, M.; Demyttenaere, K.; McIntyre, R. S; Widiger, T.; and Wittchen, H.\n\n\n \n\n\n\n World Psychiatry, 19(3): 269–293. oct 2020.\n \n\n\n\n
\n\n\n\n \n \n \"ThePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{maj_clinical_2020,\nabstract = {Depression is widely acknowledged to be a heterogeneous entity, and the need to further characterize the individual patient who has received this diagnosis in order to personalize the management plan has been repeatedly emphasized. However, the research evidence that should guide this personalization is at present fragmentary, and the selection of treatment is usually based on the clinician's and/or the patient's preference and on safety issues, in a trial‐and‐error fashion, paying little attention to the particular features of the specific case. This may be one of the reasons why the majority of patients with a diagnosis of depression do not achieve remission with the first treatment they receive. The predominant pessimism about the actual feasibility of the personalization of treatment of depression in routine clinical practice has recently been tempered by some secondary analyses of databases from clinical trials, using approaches such as individual patient data meta‐analysis and machine learning, which indicate that some variables may indeed contribute to the identification of patients who are likely to respond differently to various antidepressant drugs or to antidepressant medication vs. specific psychotherapies. The need to develop decision support tools guiding the personalization of treatment of depression has been recently reaffirmed, and the point made that these tools should be developed through large observational studies using a comprehensive battery of self‐report and clinical measures. The present paper aims to describe systematically the salient domains that should be considered in this effort to personalize depression treatment. For each domain, the available research evidence is summarized, and the relevant assessment instruments are reviewed, with special attention to their suitability for use in routine clinical practice, also in view of their possible inclusion in the above‐mentioned comprehensive battery of measures. The main unmet needs that research should address in this area are emphasized. Where the available evidence allows providing the clinician with specific advice that can already be used today to make the management of depression more personalized, this advice is highlighted. Indeed, some sections of the paper, such as those on neurocognition and on physical comorbidities, indicate that the modern management of depression is becoming increasingly complex, with several components other than simply the choice of an antidepressant and/or a psychotherapy, some of which can already be reliably personalized.},\nauthor = {Maj, Mario and Stein, Dan J and Parker, Gordon and Zimmerman, Mark and Fava, Giovanni A and {De Hert}, Marc and Demyttenaere, Koen and McIntyre, Roger S and Widiger, Thomas and Wittchen, Hans‐Ulrich},\ndoi = {10.1002/wps.20771},\nfile = {:Users/jacquelinebracher/Zotero/storage/MQ62AK4V/Maj et al. - 2020 - The clinical characterization of the adult patient.pdf:pdf},\nissn = {1723-8617, 2051-5545},\njournal = {World Psychiatry},\nmonth = {oct},\nnumber = {3},\npages = {269--293},\ntitle = {{The clinical characterization of the adult patient with depression aimed at personalization of management}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1002/wps.20771},\nvolume = {19},\nyear = {2020}\n}\n
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\n Depression is widely acknowledged to be a heterogeneous entity, and the need to further characterize the individual patient who has received this diagnosis in order to personalize the management plan has been repeatedly emphasized. However, the research evidence that should guide this personalization is at present fragmentary, and the selection of treatment is usually based on the clinician's and/or the patient's preference and on safety issues, in a trial‐and‐error fashion, paying little attention to the particular features of the specific case. This may be one of the reasons why the majority of patients with a diagnosis of depression do not achieve remission with the first treatment they receive. The predominant pessimism about the actual feasibility of the personalization of treatment of depression in routine clinical practice has recently been tempered by some secondary analyses of databases from clinical trials, using approaches such as individual patient data meta‐analysis and machine learning, which indicate that some variables may indeed contribute to the identification of patients who are likely to respond differently to various antidepressant drugs or to antidepressant medication vs. specific psychotherapies. The need to develop decision support tools guiding the personalization of treatment of depression has been recently reaffirmed, and the point made that these tools should be developed through large observational studies using a comprehensive battery of self‐report and clinical measures. The present paper aims to describe systematically the salient domains that should be considered in this effort to personalize depression treatment. For each domain, the available research evidence is summarized, and the relevant assessment instruments are reviewed, with special attention to their suitability for use in routine clinical practice, also in view of their possible inclusion in the above‐mentioned comprehensive battery of measures. The main unmet needs that research should address in this area are emphasized. Where the available evidence allows providing the clinician with specific advice that can already be used today to make the management of depression more personalized, this advice is highlighted. Indeed, some sections of the paper, such as those on neurocognition and on physical comorbidities, indicate that the modern management of depression is becoming increasingly complex, with several components other than simply the choice of an antidepressant and/or a psychotherapy, some of which can already be reliably personalized.\n
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\n \n\n \n \n \n \n \n \n Pediatric \\Status\\ \\Epilepticus\\.\n \n \n \n \n\n\n \n Mekki, M. S.; Ibekwe, R.; and Wilmshurst, J. M\n\n\n \n\n\n\n In Salih, M. A M, editor(s), Clinical \\Child\\ \\Neurology\\, pages 777–794. Springer International Publishing, Cham, 2020.\n \n\n\n\n
\n\n\n\n \n \n \"PediatricPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@incollection{salih_pediatric_2020,\naddress = {Cham},\nauthor = {Mekki, Mohammed Siddig and Ibekwe, Roland and Wilmshurst, Jo M},\nbooktitle = {Clinical {\\{}Child{\\}} {\\{}Neurology{\\}}},\ndoi = {10.1007/978-3-319-43153-6_25},\neditor = {Salih, Mustafa A M},\nisbn = {978-3-319-43152-9 978-3-319-43153-6},\npages = {777--794},\npublisher = {Springer International Publishing},\ntitle = {{Pediatric {\\{}Status{\\}} {\\{}Epilepticus{\\}}}},\nurl = {http://link.springer.com/10.1007/978-3-319-43153-6{\\_}25},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n Approach to a \\Child\\ with \\Epilepsy\\.\n \n \n \n \n\n\n \n Kija, E.; and Wilmshurst, J. M\n\n\n \n\n\n\n In Salih, M. A M, editor(s), Clinical \\Child\\ \\Neurology\\, pages 795–808. Springer International Publishing, Cham, 2020.\n \n\n\n\n
\n\n\n\n \n \n \"ApproachPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@incollection{salih_approach_2020,\naddress = {Cham},\nauthor = {Kija, Edward and Wilmshurst, Jo M},\nbooktitle = {Clinical {\\{}Child{\\}} {\\{}Neurology{\\}}},\ndoi = {10.1007/978-3-319-43153-6_26},\neditor = {Salih, Mustafa A M},\nisbn = {978-3-319-43152-9 978-3-319-43153-6},\npages = {795--808},\npublisher = {Springer International Publishing},\ntitle = {{Approach to a {\\{}Child{\\}} with {\\{}Epilepsy{\\}}}},\nurl = {https://link.springer.com/10.1007/978-3-319-43153-6{\\_}26},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n Incidence of spinal deformities and the relationship with physical status and back pain in ambulant adults with cerebral palsy and spastic diplegia.\n \n \n \n \n\n\n \n Langerak, N G; Britz, E; Dix-Peek, S; du Toit, J; Fieggen, A G; and Lamberts, R P\n\n\n \n\n\n\n European Spine Journal, 29(6): 1416–1423. 2020.\n \n\n\n\n
\n\n\n\n \n \n \"IncidencePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n\n\n\n
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@article{Langerak20201416,\nannote = {cited By 0},\nauthor = {Langerak, N G and Britz, E and Dix-Peek, S and du Toit, J and Fieggen, A G and Lamberts, R P},\ndoi = {10.1007/s00586-019-06235-3},\nfile = {:Users/jacquelinebracher/Zotero/storage/PPFG4PER/Langerak et al. - 2020 - Incidence of spinal deformities and the relationsh.pdf:pdf},\nissn = {09406719},\njournal = {European Spine Journal},\nkeywords = {abduction; adduction; adult; ankle; Article; backa},\nnumber = {6},\npages = {1416--1423},\npublisher = {Springer},\ntitle = {{Incidence of spinal deformities and the relationship with physical status and back pain in ambulant adults with cerebral palsy and spastic diplegia}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85076138761{\\&}doi=10.1007{\\%}2Fs00586-019-06235-3{\\&}partnerID=40{\\&}md5=f12a21155afd289ea7ee418ff03f9f15},\nvolume = {29},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n Toward identifying reproducible brain signatures of obsessive-compulsive profiles: Rationale and methods for a new global initiative.\n \n \n \n \n\n\n \n Simpson, H B; Van Den Heuvel, O A; Miguel, E C; Reddy, Y C J; Stein, D J; Lewis-Fernández, R; Shavitt, R G; Lochner, C; Pouwels, P J W; Narayanawamy, J C; Venkatasubramanian, G; Hezel, D M; Vriend, C; Batistuzzo, M C; Hoexter, M Q; De Joode, N T; Costa, D L; De Mathis, M A; Sheshachala, K; Narayan, M; Van Balkom, A.; Batelaan, N M; Venkataram, S; Cherian, A; Marincowitz, C; Pannekoek, N; Stovezky, Y R; Mare, K; Liu, F; Otaduy, M C G; Pastorello, B; Rao, R; Katechis, M; Van Meter, P; and Wall, M\n\n\n \n\n\n\n BMC Psychiatry, 20(1). 2020.\n \n\n\n\n
\n\n\n\n \n \n \"TowardPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n\n\n\n
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@article{Simpson2020,\nannote = {cited By 1},\nauthor = {Simpson, H B and {Van Den Heuvel}, O A and Miguel, E C and Reddy, Y C J and Stein, D J and Lewis-Fern{\\'{a}}ndez, R and Shavitt, R G and Lochner, C and Pouwels, P J W and Narayanawamy, J C and Venkatasubramanian, G and Hezel, D M and Vriend, C and Batistuzzo, M C and Hoexter, M Q and {De Joode}, N T and Costa, D L and {De Mathis}, M A and Sheshachala, K and Narayan, M and {Van Balkom}, A.J.L.M. and Batelaan, N M and Venkataram, S and Cherian, A and Marincowitz, C and Pannekoek, N and Stovezky, Y R and Mare, K and Liu, F and Otaduy, M C G and Pastorello, B and Rao, R and Katechis, M and {Van Meter}, P and Wall, M},\ndoi = {10.1186/s12888-020-2439-2},\nfile = {:Users/jacquelinebracher/Zotero/storage/M7UR484F/Simpson et al. - 2020 - Toward identifying reproducible brain signatures o.pdf:pdf},\nissn = {1471244X},\njournal = {BMC Psychiatry},\nkeywords = {adult; Article; behavior; Brazil; childhood trauma},\nnumber = {1},\npublisher = {BioMed Central Ltd.},\ntitle = {{Toward identifying reproducible brain signatures of obsessive-compulsive profiles: Rationale and methods for a new global initiative}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85079359493{\\&}doi=10.1186{\\%}2Fs12888-020-2439-2{\\&}partnerID=40{\\&}md5=2be7655e13b4d456191d8715dba86321},\nvolume = {20},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n Keeping people with epilepsy safe during the \\COVID\\-19 pandemic.\n \n \n \n \n\n\n \n French, J. A; Brodie, M. J; Caraballo, R.; Devinsky, O.; Ding, D.; Jehi, L.; Jette, N.; Kanner, A.; Modi, A. C; Newton, C. R; Patel, A. A; Pennell, P. B; Perucca, E.; Sander, J. W; Scheffer, I. E; Singh, G.; Williams, E.; Wilmshurst, J.; and Cross, J H.\n\n\n \n\n\n\n Neurology, 94(23): 1032–1037. jun 2020.\n \n\n\n\n
\n\n\n\n \n \n \"KeepingPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{french_keeping_2020,\nabstract = {Objectives\nTo provide information on the effect of the coronavirus disease of 2019 (COVID-19) pandemic on people with epilepsy and provide consensus recommendations on how to provide the best possible care for people with epilepsy while avoiding visits to urgent care facilities and hospitalizations during the novel coronavirus pandemic.\n\n\nMethods\nThe authors developed consensus statements in 2 sections. The first was “How should we/clinicians modify our clinical care pathway for people with epilepsy during the COVID-19 pandemic?” The second was “What general advice should we give to people with epilepsy during this crisis? The authors individually scored statements on a scale of −10 (strongly disagree) to +10 (strongly agree). Five of 11 recommendations for physicians and 3/5 recommendations for individuals/families were rated by all the authors as 7 or above (strongly agree) on the first round of rating. Subsequently, a teleconference was held where statements for which there was a lack of strong consensus were revised.\n\n\nResults\nAfter revision, all consensus recommendations received a score of 7 or above. The recommendations focus on administration of as much care as possible at home to keep people with epilepsy out of health care facilities, where they are likely to encounter COVID-19 (including strategies for rescue therapy), as well as minimization of risk of seizure exacerbation through adherence, and through ensuring a regular supply of medication. We also provide helpful links to additional helpful information for people with epilepsy and health providers.\n\n\nConclusion\nThese recommendations may help health care professionals provide optimal care to people with epilepsy during the coronavirus pandemic.},\nauthor = {French, Jacqueline A and Brodie, Martin J and Caraballo, Roberto and Devinsky, Orrin and Ding, Ding and Jehi, Lara and Jette, Nathalie and Kanner, Andres and Modi, Avani C and Newton, Charles R and Patel, Archana A and Pennell, Page B and Perucca, Emilio and Sander, Josemir W and Scheffer, Ingrid E and Singh, Gagandeep and Williams, Emma and Wilmshurst, Jo and Cross, J Helen},\ndoi = {10.1212/WNL.0000000000009632},\nfile = {:Users/jacquelinebracher/Zotero/storage/N7XR23QY/French et al. - 2020 - Keeping people with epilepsy safe during the COVID.pdf:pdf},\nissn = {0028-3878, 1526-632X},\njournal = {Neurology},\nmonth = {jun},\nnumber = {23},\npages = {1032--1037},\ntitle = {{Keeping people with epilepsy safe during the {\\{}COVID{\\}}-19 pandemic}},\nurl = {https://www.neurology.org/lookup/doi/10.1212/WNL.0000000000009632},\nvolume = {94},\nyear = {2020}\n}\n
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\n Objectives To provide information on the effect of the coronavirus disease of 2019 (COVID-19) pandemic on people with epilepsy and provide consensus recommendations on how to provide the best possible care for people with epilepsy while avoiding visits to urgent care facilities and hospitalizations during the novel coronavirus pandemic. Methods The authors developed consensus statements in 2 sections. The first was “How should we/clinicians modify our clinical care pathway for people with epilepsy during the COVID-19 pandemic?” The second was “What general advice should we give to people with epilepsy during this crisis? The authors individually scored statements on a scale of −10 (strongly disagree) to +10 (strongly agree). Five of 11 recommendations for physicians and 3/5 recommendations for individuals/families were rated by all the authors as 7 or above (strongly agree) on the first round of rating. Subsequently, a teleconference was held where statements for which there was a lack of strong consensus were revised. Results After revision, all consensus recommendations received a score of 7 or above. The recommendations focus on administration of as much care as possible at home to keep people with epilepsy out of health care facilities, where they are likely to encounter COVID-19 (including strategies for rescue therapy), as well as minimization of risk of seizure exacerbation through adherence, and through ensuring a regular supply of medication. We also provide helpful links to additional helpful information for people with epilepsy and health providers. Conclusion These recommendations may help health care professionals provide optimal care to people with epilepsy during the coronavirus pandemic.\n
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\n \n\n \n \n \n \n \n \n Classification of \\Childhood\\ \\Epileptic\\ \\Seizures\\.\n \n \n \n \n\n\n \n Hammond, C. K; and Wilmshurst, J. M\n\n\n \n\n\n\n In Salih, M. A M, editor(s), Clinical \\Child\\ \\Neurology\\, pages 731–741. Springer International Publishing, Cham, 2020.\n \n\n\n\n
\n\n\n\n \n \n \"ClassificationPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@incollection{salih_classification_2020,\naddress = {Cham},\nauthor = {Hammond, Charles K and Wilmshurst, Jo M},\nbooktitle = {Clinical {\\{}Child{\\}} {\\{}Neurology{\\}}},\ndoi = {10.1007/978-3-319-43153-6_22},\neditor = {Salih, Mustafa A M},\nisbn = {978-3-319-43152-9 978-3-319-43153-6},\npages = {731--741},\npublisher = {Springer International Publishing},\ntitle = {{Classification of {\\{}Childhood{\\}} {\\{}Epileptic{\\}} {\\{}Seizures{\\}}}},\nurl = {http://link.springer.com/10.1007/978-3-319-43153-6{\\_}22},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n Chloride dynamics alter the input-output properties of neurons.\n \n \n \n \n\n\n \n Currin, C B; Trevelyan, A J; Akerman, C J; and Raimondo, J V\n\n\n \n\n\n\n PLoS Computational Biology, 16(5). 2020.\n \n\n\n\n
\n\n\n\n \n \n \"ChloridePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n  \n \n 13 downloads\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n\n\n\n
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@article{Currin2020,\nannote = {cited By 0},\nauthor = {Currin, C B and Trevelyan, A J and Akerman, C J and Raimondo, J V},\ndoi = {10.1371/journal.pcbi.1007932},\nfile = {:Users/jacquelinebracher/Zotero/storage/HZTQ2BEE/Currin et al. - 2020 - Chloride dynamics alter the input-output propertie.pdf:pdf},\nissn = {1553734X},\njournal = {PLoS Computational Biology},\nkeywords = {4 aminobutyric acid; chloride,animal cell; animal tissue; Article; chloride tra},\nnumber = {5},\npublisher = {Public Library of Science},\ntitle = {{Chloride dynamics alter the input-output properties of neurons}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85086083197{\\&}doi=10.1371{\\%}2Fjournal.pcbi.1007932{\\&}partnerID=40{\\&}md5=b81f863b4459d7ebfacc34899980744a},\nvolume = {16},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n An accelerated shift in the use of remote systems in epilepsy due to the \\COVID\\-19 pandemic.\n \n \n \n \n\n\n \n Kuchenbuch, M.; D'Onofrio, G.; Wirrell, E.; Jiang, Y.; Dupont, S.; Grinspan, Z. M; Auvin, S.; Wilmshurst, J. M; Arzimanoglou, A.; Cross, J H.; Specchio, N.; and Nabbout, R.\n\n\n \n\n\n\n Epilepsy & Behavior, 112: 107376. nov 2020.\n \n\n\n\n
\n\n\n\n \n \n \"AnPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{kuchenbuch_accelerated_2020,\nauthor = {Kuchenbuch, Mathieu and D'Onofrio, Gianluca and Wirrell, Elaine and Jiang, Yuwu and Dupont, Sophie and Grinspan, Zachary M and Auvin, Stephane and Wilmshurst, Jo M and Arzimanoglou, Alexis and Cross, J Helen and Specchio, Nicola and Nabbout, Rima},\ndoi = {10.1016/j.yebeh.2020.107376},\nfile = {:Users/jacquelinebracher/Zotero/storage/7TNY9HGN/Kuchenbuch et al. - 2020 - An accelerated shift in the use of remote systems .pdf:pdf},\nissn = {15255050},\njournal = {Epilepsy {\\&} Behavior},\nmonth = {nov},\npages = {107376},\ntitle = {{An accelerated shift in the use of remote systems in epilepsy due to the {\\{}COVID{\\}}-19 pandemic}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S1525505020305552},\nvolume = {112},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n Screening and assessment tools for gaming disorder: A comprehensive systematic review.\n \n \n \n \n\n\n \n King, D L; Chamberlain, S R; Carragher, N; Billieux, J; Stein, D; Mueller, K; Potenza, M N; Rumpf, H J; Saunders, J; Starcevic, V; Demetrovics, Z; Brand, M; Lee, H K; Spada, M; Lindenberg, K; Wu, A M S; Lemenager, T; Pallesen, S; Achab, S; Kyrios, M; Higuchi, S; Fineberg, N A; and Delfabbro, P H\n\n\n \n\n\n\n Clinical Psychology Review, 77. 2020.\n \n\n\n\n
\n\n\n\n \n \n \"ScreeningPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n\n\n\n
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@article{King2020,\nannote = {cited By 12},\nauthor = {King, D L and Chamberlain, S R and Carragher, N and Billieux, J and Stein, D and Mueller, K and Potenza, M N and Rumpf, H J and Saunders, J and Starcevic, V and Demetrovics, Z and Brand, M and Lee, H K and Spada, M and Lindenberg, K and Wu, A M S and Lemenager, T and Pallesen, S and Achab, S and Kyrios, M and Higuchi, S and Fineberg, N A and Delfabbro, P H},\ndoi = {10.1016/j.cpr.2020.101831},\nfile = {:Users/jacquelinebracher/Zotero/storage/I57SHN92/King et al. - 2020 - Screening and assessment tools for gaming disorder.pdf:pdf},\nissn = {02727358},\njournal = {Clinical Psychology Review},\nkeywords = {Article; clinical assessment tool; criterion varia},\npublisher = {Elsevier Inc.},\ntitle = {{Screening and assessment tools for gaming disorder: A comprehensive systematic review}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85080107889{\\&}doi=10.1016{\\%}2Fj.cpr.2020.101831{\\&}partnerID=40{\\&}md5=d4b34e6b4ec754fcefdeb52e6839ae3e},\nvolume = {77},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n New project for a scientific psychology: \\General\\ scheme.\n \n \n \n \n\n\n \n Solms, M.\n\n\n \n\n\n\n Neuropsychoanalysis, 22(1-2): 5–35. jul 2020.\n \n\n\n\n
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@article{solms_new_2020,\nauthor = {Solms, Mark},\ndoi = {10.1080/15294145.2020.1833361},\nissn = {1529-4145, 2044-3978},\njournal = {Neuropsychoanalysis},\nmonth = {jul},\nnumber = {1-2},\npages = {5--35},\nshorttitle = {New project for a scientific psychology},\ntitle = {{New project for a scientific psychology: {\\{}General{\\}} scheme}},\nurl = {https://www.tandfonline.com/doi/full/10.1080/15294145.2020.1833361},\nvolume = {22},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n Structural brain network development in children following prenatal methamphetamine exposure.\n \n \n \n\n\n \n Roos, A.; Fouche, J.; du Toit, S.; du Plessis, S.; Stein, D.; and Donald, K.\n\n\n \n\n\n\n Journal of Comparative Neurology, 528(11): 1856–1863. 2020.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Roos2020,\nabstract = {Brain imaging studies in children with prenatal methamphetamine exposure (PME) suggest structural and functional alterations of striatal, frontal, parietal, and limbic regions. However, no longitudinal studies have investigated changes in structural connectivity during the first 2 years of formal schooling. The aim of this study was to explore the effects of PME on structural connectivity of brain networks in children over the critical first 2 years of formal schooling when foundational learning takes place. Networks are expected to gradually increase in global connectedness while segregating into defined systems. Graph theoretical analysis was used to investigate changes in structural connectivity at age 6 and 8 years in children with and without PME. While healthy control children showed increased connectivity in frontal and limbic hubs over time, children with PME showed increased connectivity in the superior parietal cortex and striatum in their global network. Furthermore, compared to control children, those with PME were characterized by less change in segregation of structural networks over time. These findings are consistent with previous work on regions implicated in children with PME, but they additionally demonstrate alterations in structural connectivity between regions that underlie primary cognitive, behavioral, and emotional development. Understanding patterns of network development during critical periods in at-risk children may inform strategies for supporting this group of children in these developmental tasks important for lifelong brain health and development.},\nauthor = {Roos, A. and Fouche, J.-P. and du Toit, S. and du Plessis, S. and Stein, D.J. and Donald, K.A.},\ndoi = {10.1002/cne.24858},\njournal = {Journal of Comparative Neurology},\nnumber = {11},\npages = {1856--1863},\ntitle = {{Structural brain network development in children following prenatal methamphetamine exposure}},\nvolume = {528},\nyear = {2020}\n}\n
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\n Brain imaging studies in children with prenatal methamphetamine exposure (PME) suggest structural and functional alterations of striatal, frontal, parietal, and limbic regions. However, no longitudinal studies have investigated changes in structural connectivity during the first 2 years of formal schooling. The aim of this study was to explore the effects of PME on structural connectivity of brain networks in children over the critical first 2 years of formal schooling when foundational learning takes place. Networks are expected to gradually increase in global connectedness while segregating into defined systems. Graph theoretical analysis was used to investigate changes in structural connectivity at age 6 and 8 years in children with and without PME. While healthy control children showed increased connectivity in frontal and limbic hubs over time, children with PME showed increased connectivity in the superior parietal cortex and striatum in their global network. Furthermore, compared to control children, those with PME were characterized by less change in segregation of structural networks over time. These findings are consistent with previous work on regions implicated in children with PME, but they additionally demonstrate alterations in structural connectivity between regions that underlie primary cognitive, behavioral, and emotional development. Understanding patterns of network development during critical periods in at-risk children may inform strategies for supporting this group of children in these developmental tasks important for lifelong brain health and development.\n
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\n \n\n \n \n \n \n \n \n Correction: \\Nurse\\-\\Delivered\\ \\Cognitive\\ \\Behavioral\\ \\Therapy\\ for \\Adherence\\ and \\Depression\\ \\Among\\ \\People\\ \\Living\\ \\With\\ \\HIV\\ (the \\Ziphamandla\\ \\Study\\): \\Protocol\\ for a \\Randomized\\ \\Controlled\\ \\Trial\\.\n \n \n \n \n\n\n \n Joska, J. A; Andersen, L. S; Smith-Alvarez, R.; Magidson, J.; Lee, J. S; O'Cleirigh, C.; and Safren, S. A\n\n\n \n\n\n\n JMIR Research Protocols, 9(9): e24074. sep 2020.\n \n\n\n\n
\n\n\n\n \n \n \"Correction:Paper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{joska_correction_2020,\nabstract = {There is an unmet need to develop effective, feasible, and scalable interventions for poor adherence and depression in persons living with HIV in low- and middle-income countries (LMIC). This study aims to investigate the effectiveness of a nurse-delivered cognitive behavioral therapy (CBT) intervention for adherence and depression (CBT-AD) among persons living with HIV who are failing first-line antiretroviral therapy (ART) in Cape Town, South Africa. This study is a 2-arm randomized controlled trial of CBT-AD integrated into the HIV primary care setting in South Africa. A total of 160 participants who did not achieve viral suppression from their first-line ART and have a unipolar depressive mood disorder will be randomized to receive either 8 sessions of CBT-AD or enhanced treatment as usual. Participants will be assessed for major depressive disorder using the Mini International Neuropsychiatric Interview at baseline and 4, 8, and 12 months. The primary outcomes are depression on the Hamilton Depression Scale (HAM-D; as assessed by a blinded assessor) at the 4-month assessment and changes in ART adherence (assessed via real-time, electronic monitoring with Wisepill) between baseline and the 4-month assessment. Secondary outcomes are HIV viral load and CD4 cell count at the 12-month assessment as well as ART adherence (Wisepill) and depression (HAM-D) over follow-up (4-, 8-, and 12-month assessments). The trial commenced in August 2015 and recruitment began in July 2016. Enrollment was completed in June 2019. Results of this study will inform whether an existing intervention (CBT-AD) can be effectively administered in LMIC by nurses with training and ongoing supervision. This will present unique opportunities to further explore the scale-up of a behavioral intervention to enhance ART adherence among persons living with HIV with major depression in a high-prevalence setting, to move toward achieving The Joint United Nations Programme on HIV/AIDS 90-90-90 goals. ClincialTrials.gov NCT02696824; https://clinicaltrials.gov/ct2/show/NCT02696824},\nauthor = {Joska, John A and Andersen, Lena S and Smith-Alvarez, Rosana and Magidson, Jessica and Lee, Jasper S and O'Cleirigh, Conall and Safren, Steven A},\ndoi = {10.2196/24074},\nfile = {:Users/jacquelinebracher/Zotero/storage/Z7TR4I6Q/Joska et al. - 2020 - Correction Nurse-Delivered Cognitive Behavioral T.pdf:pdf},\nissn = {1929-0748},\njournal = {JMIR Research Protocols},\nmonth = {sep},\nnumber = {9},\npages = {e24074},\nshorttitle = {Correction},\ntitle = {{Correction: {\\{}Nurse{\\}}-{\\{}Delivered{\\}} {\\{}Cognitive{\\}} {\\{}Behavioral{\\}} {\\{}Therapy{\\}} for {\\{}Adherence{\\}} and {\\{}Depression{\\}} {\\{}Among{\\}} {\\{}People{\\}} {\\{}Living{\\}} {\\{}With{\\}} {\\{}HIV{\\}} (the {\\{}Ziphamandla{\\}} {\\{}Study{\\}}): {\\{}Protocol{\\}} for a {\\{}Randomized{\\}} {\\{}Controlled{\\}} {\\{}Trial{\\}}}},\nurl = {http://www.researchprotocols.org/2020/9/e24074/},\nvolume = {9},\nyear = {2020}\n}\n
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\n There is an unmet need to develop effective, feasible, and scalable interventions for poor adherence and depression in persons living with HIV in low- and middle-income countries (LMIC). This study aims to investigate the effectiveness of a nurse-delivered cognitive behavioral therapy (CBT) intervention for adherence and depression (CBT-AD) among persons living with HIV who are failing first-line antiretroviral therapy (ART) in Cape Town, South Africa. This study is a 2-arm randomized controlled trial of CBT-AD integrated into the HIV primary care setting in South Africa. A total of 160 participants who did not achieve viral suppression from their first-line ART and have a unipolar depressive mood disorder will be randomized to receive either 8 sessions of CBT-AD or enhanced treatment as usual. Participants will be assessed for major depressive disorder using the Mini International Neuropsychiatric Interview at baseline and 4, 8, and 12 months. The primary outcomes are depression on the Hamilton Depression Scale (HAM-D; as assessed by a blinded assessor) at the 4-month assessment and changes in ART adherence (assessed via real-time, electronic monitoring with Wisepill) between baseline and the 4-month assessment. Secondary outcomes are HIV viral load and CD4 cell count at the 12-month assessment as well as ART adherence (Wisepill) and depression (HAM-D) over follow-up (4-, 8-, and 12-month assessments). The trial commenced in August 2015 and recruitment began in July 2016. Enrollment was completed in June 2019. Results of this study will inform whether an existing intervention (CBT-AD) can be effectively administered in LMIC by nurses with training and ongoing supervision. This will present unique opportunities to further explore the scale-up of a behavioral intervention to enhance ART adherence among persons living with HIV with major depression in a high-prevalence setting, to move toward achieving The Joint United Nations Programme on HIV/AIDS 90-90-90 goals. ClincialTrials.gov NCT02696824; https://clinicaltrials.gov/ct2/show/NCT02696824\n
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\n \n\n \n \n \n \n \n \n Antimicrobial effects of craniopharyngioma cystic fluid.\n \n \n \n \n\n\n \n Jokonya, L.; Reid, T.; Kasambala, M.; Mduluza-Jokonya, T. L.; Fieggen, G.; Mduluza, T.; Kalangu, K. K N; and Naicker, T.\n\n\n \n\n\n\n Child's Nervous System, 36(11): 2641–2646. nov 2020.\n \n\n\n\n
\n\n\n\n \n \n \"AntimicrobialPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{jokonya_antimicrobial_2020,\nauthor = {Jokonya, Luxwell and Reid, Tsungai and Kasambala, Maritha and Mduluza-Jokonya, Tariro Lavender and Fieggen, Graham and Mduluza, Takafira and Kalangu, Kazadi K N and Naicker, Thajasvarie},\ndoi = {10.1007/s00381-020-04825-x},\nfile = {:Users/jacquelinebracher/Zotero/storage/6Q3G642F/Jokonya et al. - 2020 - Antimicrobial effects of craniopharyngioma cystic .pdf:pdf},\nissn = {0256-7040, 1433-0350},\njournal = {Child's Nervous System},\nmonth = {nov},\nnumber = {11},\npages = {2641--2646},\ntitle = {{Antimicrobial effects of craniopharyngioma cystic fluid}},\nurl = {https://link.springer.com/10.1007/s00381-020-04825-x},\nvolume = {36},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n Chronic pain in people with \\HIV\\: a common comorbidity and threat to quality of life.\n \n \n \n \n\n\n \n Madden, V. J; Parker, R.; and Goodin, B. R\n\n\n \n\n\n\n Pain Management, 10(4): 253–260. jul 2020.\n \n\n\n\n
\n\n\n\n \n \n \"ChronicPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{madden_chronic_2020,\nabstract = {Evidence indicates that over half of all people with HIV (PWH) will experience nonmalignant chronic pain throughout their lifetimes, with increasing prevalence as they age. Peripheral neuropathy resulting from the neurotoxic effects of HIV itself and the medications used to treat HIV were widely considered the primary cause of acute and chronic pain early on in the antiretroviral treatment era. However, recent studies suggest a predominance of non-neuropathic (e.g., musculoskeletal) pain in PWH with uncertain etiology. Chronic pain is often widespread in PWH, affecting multiple body locations. Additional research is needed to better understand contributors to chronic pain in PWH, which is likely to include biological (e.g., immune dysregulation), psychological (e.g., substance abuse) and social (e.g., stigma) factors.},\nauthor = {Madden, Victoria J and Parker, Romy and Goodin, Burel R},\ndoi = {10.2217/pmt-2020-0004},\nfile = {:Users/jacquelinebracher/Zotero/storage/4BI7IFYK/Madden et al. - 2020 - Chronic pain in people with HIV a common comorbid.pdf:pdf},\nissn = {1758-1869, 1758-1877},\njournal = {Pain Management},\nmonth = {jul},\nnumber = {4},\npages = {253--260},\nshorttitle = {Chronic pain in people with {\\{}HIV{\\}}},\ntitle = {{Chronic pain in people with {\\{}HIV{\\}}: a common comorbidity and threat to quality of life}},\nurl = {https://www.futuremedicine.com/doi/10.2217/pmt-2020-0004},\nvolume = {10},\nyear = {2020}\n}\n
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\n Evidence indicates that over half of all people with HIV (PWH) will experience nonmalignant chronic pain throughout their lifetimes, with increasing prevalence as they age. Peripheral neuropathy resulting from the neurotoxic effects of HIV itself and the medications used to treat HIV were widely considered the primary cause of acute and chronic pain early on in the antiretroviral treatment era. However, recent studies suggest a predominance of non-neuropathic (e.g., musculoskeletal) pain in PWH with uncertain etiology. Chronic pain is often widespread in PWH, affecting multiple body locations. Additional research is needed to better understand contributors to chronic pain in PWH, which is likely to include biological (e.g., immune dysregulation), psychological (e.g., substance abuse) and social (e.g., stigma) factors.\n
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\n \n\n \n \n \n \n \n \n A systematic review of research on neuropsychological measures in psychotic disorders from low and middle-income countries: \\The\\ question of clinical utility.\n \n \n \n \n\n\n \n Mwesiga, E. K; Akena, D.; Koen, N.; Senono, R.; Obuku, E. A; Gumikiriza, J. L.; Robbins, R. N; Nakasujja, N.; and Stein, D. J\n\n\n \n\n\n\n Schizophrenia Research: Cognition, 22: 100187. dec 2020.\n \n\n\n\n
\n\n\n\n \n \n \"APaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{mwesiga_systematic_2020,\nauthor = {Mwesiga, Emmanuel K and Akena, Dickens and Koen, Nastassja and Senono, Richard and Obuku, Ekwaro A and Gumikiriza, Joy Louise and Robbins, Reuben N and Nakasujja, Noeline and Stein, Dan J},\ndoi = {10.1016/j.scog.2020.100187},\nfile = {:Users/jacquelinebracher/Zotero/storage/XW437CAG/Mwesiga et al. - 2020 - A systematic review of research on neuropsychologi.pdf:pdf},\nissn = {22150013},\njournal = {Schizophrenia Research: Cognition},\nmonth = {dec},\npages = {100187},\nshorttitle = {A systematic review of research on neuropsychologi},\ntitle = {{A systematic review of research on neuropsychological measures in psychotic disorders from low and middle-income countries: {\\{}The{\\}} question of clinical utility}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S2215001320300081},\nvolume = {22},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n Infectious morbidity of breastfed, HIV-exposed uninfected infants under conditions of universal antiretroviral therapy in South Africa: a prospective cohort study.\n \n \n \n \n\n\n \n le Roux, S M; Abrams, E J; Donald, K A; Brittain, K; Phillips, T K; Zerbe, A; le Roux, D M; Kroon, M; and Myer, L\n\n\n \n\n\n\n The Lancet Child and Adolescent Health, 4(3): 220–231. 2020.\n \n\n\n\n
\n\n\n\n \n \n \"InfectiousPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n\n\n\n
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@article{leRoux2020220,\nannote = {cited By 3},\nauthor = {le Roux, S M and Abrams, E J and Donald, K A and Brittain, K and Phillips, T K and Zerbe, A and le Roux, D M and Kroon, M and Myer, L},\ndoi = {10.1016/S2352-4642(19)30375-X},\nfile = {:Users/jacquelinebracher/Zotero/storage/AXYX8J4J/Le Roux et al. - 2020 - Infectious morbidity of breastfed, HIV-exposed uni.pdf:pdf},\nissn = {23524642},\njournal = {The Lancet Child and Adolescent Health},\nkeywords = {adult; antiretroviral therapy; Article; breast fee},\nnumber = {3},\npages = {220--231},\npublisher = {Elsevier B.V.},\ntitle = {{Infectious morbidity of breastfed, HIV-exposed uninfected infants under conditions of universal antiretroviral therapy in South Africa: a prospective cohort study}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85079555590{\\&}doi=10.1016{\\%}2FS2352-4642{\\%}2819{\\%}2930375-X{\\&}partnerID=40{\\&}md5=010b4dc3f69a1f7c0ac1b21ec5ce9111},\nvolume = {4},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n Nurse-delivered cognitive behavioral therapy for adherence and depression among people living with HIV (the ziphamandla study): Protocol for a randomized controlled trial.\n \n \n \n \n\n\n \n Joska, J A; Andersen, L S; Smith-Alvarez, R; Magidson, J; Lee, J S; O'Cleirigh, C; and Safren, S A\n\n\n \n\n\n\n JMIR Research Protocols, 9(2). 2020.\n \n\n\n\n
\n\n\n\n \n \n \"Nurse-deliveredPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Joska2020,\nannote = {cited By 1},\nauthor = {Joska, J A and Andersen, L S and Smith-Alvarez, R and Magidson, J and Lee, J S and O'Cleirigh, C and Safren, S A},\ndoi = {10.2196/14200},\nfile = {:Users/jacquelinebracher/Zotero/storage/Y3L65PY7/Joska et al. - 2020 - Nurse-Delivered Cognitive Behavioral Therapy for A.pdf:pdf},\nissn = {19290748},\njournal = {JMIR Research Protocols},\nnumber = {2},\npublisher = {JMIR Publications},\ntitle = {{Nurse-delivered cognitive behavioral therapy for adherence and depression among people living with HIV (the ziphamandla study): Protocol for a randomized controlled trial}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85083369611{\\&}doi=10.2196{\\%}2F14200{\\&}partnerID=40{\\&}md5=b9742ea8a78a2e9fa815aabd8ac14004},\nvolume = {9},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n Response to the commentaries on the “\\New\\ \\Project\\”.\n \n \n \n \n\n\n \n Solms, M.\n\n\n \n\n\n\n Neuropsychoanalysis, 22(1-2): 97–107. jul 2020.\n \n\n\n\n
\n\n\n\n \n \n \"ResponsePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{solms_response_2020,\nauthor = {Solms, Mark},\ndoi = {10.1080/15294145.2020.1843215},\nissn = {1529-4145, 2044-3978},\njournal = {Neuropsychoanalysis},\nmonth = {jul},\nnumber = {1-2},\npages = {97--107},\ntitle = {{Response to the commentaries on the “{\\{}New{\\}} {\\{}Project{\\}}”}},\nurl = {https://www.tandfonline.com/doi/full/10.1080/15294145.2020.1843215},\nvolume = {22},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n Serology testing in the \\COVID\\-19 pandemic response.\n \n \n \n \n\n\n \n Peeling, R. W; Wedderburn, C. J; Garcia, P. J; Boeras, D.; Fongwen, N.; Nkengasong, J.; Sall, A.; Tanuri, A.; and Heymann, D. L\n\n\n \n\n\n\n The Lancet Infectious Diseases, 20(9): e245—-e249. sep 2020.\n \n\n\n\n
\n\n\n\n \n \n \"SerologyPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{peeling_serology_2020,\nauthor = {Peeling, Rosanna W and Wedderburn, Catherine J and Garcia, Patricia J and Boeras, Debrah and Fongwen, Noah and Nkengasong, John and Sall, Amadou and Tanuri, Amilcar and Heymann, David L},\ndoi = {10.1016/S1473-3099(20)30517-X},\nfile = {:Users/jacquelinebracher/Zotero/storage/NIFM3442/Peeling et al. - 2020 - Serology testing in the COVID-19 pandemic response.pdf:pdf},\nissn = {14733099},\njournal = {The Lancet Infectious Diseases},\nmonth = {sep},\nnumber = {9},\npages = {e245----e249},\ntitle = {{Serology testing in the {\\{}COVID{\\}}-19 pandemic response}},\nurl = {https://linkinghub.elsevier.com/retrieve/pii/S147330992030517X},\nvolume = {20},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n Subcortical surface morphometry in substance dependence: \\An\\ \\ENIGMA\\ addiction working group study.\n \n \n \n \n\n\n \n Chye, Y.; Mackey, S.; Gutman, B. A; Ching, C. R K; Batalla, A.; Blaine, S.; Brooks, S.; Caparelli, E. C; Cousijn, J.; Dagher, A.; Foxe, J. J; Goudriaan, A. E; Hester, R.; Hutchison, K.; Jahanshad, N.; Kaag, A. M; Korucuoglu, O.; Li, C. R; London, E. D; Lorenzetti, V.; Luijten, M.; Martin‐Santos, R.; Meda, S. A; Momenan, R.; Morales, A.; Orr, C.; Paulus, M. P; Pearlson, G.; Reneman, L.; Schmaal, L.; Sinha, R.; Solowij, N.; Stein, D. J; Stein, E. A; Tang, D.; Uhlmann, A.; Van Holst, R.; Veltman, D. J; Verdejo‐Garcia, A.; Wiers, R. W; Yücel, M.; Thompson, P. M; Conrod, P.; and Garavan, H.\n\n\n \n\n\n\n Addiction Biology, 25(6): e12830. nov 2020.\n \n\n\n\n
\n\n\n\n \n \n \"SubcorticalPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{chye_subcortical_2020,\nabstract = {Abstract\nWhile imaging studies have demonstrated volumetric differences in subcortical structures associated with dependence on various abused substances, findings to date have not been wholly consistent. Moreover, most studies have not compared brain morphology across those dependent on different substances of abuse to identify substance‐specific and substance‐general dependence effects. By pooling large multinational datasets from 33 imaging sites, this study examined subcortical surface morphology in 1628 nondependent controls and 2277 individuals with dependence on alcohol, nicotine, cocaine, methamphetamine, and/or cannabis. Subcortical structures were defined by FreeSurfer segmentation and converted to a mesh surface to extract two vertex‐level metrics—the radial distance (RD) of the structure surface from a medial curve and the log of the Jacobian determinant (JD)—that, respectively, describe local thickness and surface area dilation/contraction. Mega‐analyses were performed on measures of RD and JD to test for the main effect of substance dependence, controlling for age, sex, intracranial volume, and imaging site. Widespread differences between dependent users and nondependent controls were found across subcortical structures, driven primarily by users dependent on alcohol. Alcohol dependence was associated with localized lower RD and JD across most structures, with the strongest effects in the hippocampus, thalamus, putamen, and amygdala. Meanwhile, nicotine use was associated with greater RD and JD relative to nonsmokers in multiple regions, with the strongest effects in the bilateral hippocampus and right nucleus accumbens. By demonstrating subcortical morphological differences unique to alcohol and nicotine use, rather than dependence across all substances, results suggest substance‐specific relationships with subcortical brain structures.},\nauthor = {Chye, Yann and Mackey, Scott and Gutman, Boris A and Ching, Christopher R K and Batalla, Albert and Blaine, Sara and Brooks, Samantha and Caparelli, Elisabeth C and Cousijn, Janna and Dagher, Alain and Foxe, John J and Goudriaan, Anna E and Hester, Robert and Hutchison, Kent and Jahanshad, Neda and Kaag, Anne M and Korucuoglu, Ozlem and Li, Chiang‐Shan R and London, Edythe D and Lorenzetti, Valentina and Luijten, Maartje and Martin‐Santos, Rocio and Meda, Shashwath A and Momenan, Reza and Morales, Angelica and Orr, Catherine and Paulus, Martin P and Pearlson, Godfrey and Reneman, Liesbeth and Schmaal, Lianne and Sinha, Rajita and Solowij, Nadia and Stein, Dan J and Stein, Elliot A and Tang, Deborah and Uhlmann, Anne and {Van Holst}, Ruth and Veltman, Dick J and Verdejo‐Garcia, Antonio and Wiers, Reinout W and Y{\\"{u}}cel, Murat and Thompson, Paul M and Conrod, Patricia and Garavan, Hugh},\ndoi = {10.1111/adb.12830},\nfile = {:Users/jacquelinebracher/Zotero/storage/XD23ECDE/Chye et al. - 2020 - Subcortical surface morphometry in substance depen.pdf:pdf},\nissn = {1355-6215, 1369-1600},\njournal = {Addiction Biology},\nmonth = {nov},\nnumber = {6},\npages = {e12830},\nshorttitle = {Subcortical surface morphometry in substance depen},\ntitle = {{Subcortical surface morphometry in substance dependence: {\\{}An{\\}} {\\{}ENIGMA{\\}} addiction working group study}},\nurl = {https://onlinelibrary.wiley.com/doi/10.1111/adb.12830},\nvolume = {25},\nyear = {2020}\n}\n
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\n Abstract While imaging studies have demonstrated volumetric differences in subcortical structures associated with dependence on various abused substances, findings to date have not been wholly consistent. Moreover, most studies have not compared brain morphology across those dependent on different substances of abuse to identify substance‐specific and substance‐general dependence effects. By pooling large multinational datasets from 33 imaging sites, this study examined subcortical surface morphology in 1628 nondependent controls and 2277 individuals with dependence on alcohol, nicotine, cocaine, methamphetamine, and/or cannabis. Subcortical structures were defined by FreeSurfer segmentation and converted to a mesh surface to extract two vertex‐level metrics—the radial distance (RD) of the structure surface from a medial curve and the log of the Jacobian determinant (JD)—that, respectively, describe local thickness and surface area dilation/contraction. Mega‐analyses were performed on measures of RD and JD to test for the main effect of substance dependence, controlling for age, sex, intracranial volume, and imaging site. Widespread differences between dependent users and nondependent controls were found across subcortical structures, driven primarily by users dependent on alcohol. Alcohol dependence was associated with localized lower RD and JD across most structures, with the strongest effects in the hippocampus, thalamus, putamen, and amygdala. Meanwhile, nicotine use was associated with greater RD and JD relative to nonsmokers in multiple regions, with the strongest effects in the bilateral hippocampus and right nucleus accumbens. By demonstrating subcortical morphological differences unique to alcohol and nicotine use, rather than dependence across all substances, results suggest substance‐specific relationships with subcortical brain structures.\n
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\n \n\n \n \n \n \n \n \n A management algorithm for adult patients with both brain oxygen and intracranial pressure monitoring: the Seattle International Severe Traumatic Brain Injury Consensus Conference (SIBICC).\n \n \n \n \n\n\n \n Chesnut, R; Aguilera, S; Buki, A; Bulger, E; Citerio, G; Cooper, D J; Arrastia, R D; Diringer, M; Figaji, A; Gao, G; Geocadin, R; Ghajar, J; Harris, O; Hoffer, A; Hutchinson, P; Joseph, M; Kitagawa, R; Manley, G; Mayer, S; Menon, D K; Meyfroidt, G; Michael, D B; Oddo, M; Okonkwo, D; Patel, M; Robertson, C; Rosenfeld, J V; Rubiano, A M; Sahuquillo, J; Servadei, F; Shutter, L; Stein, D; Stocchetti, N; Taccone, F S; Timmons, S; Tsai, E; Ullman, J S; Vespa, P; Videtta, W; Wright, D W; Zammit, C; and Hawryluk, G W J\n\n\n \n\n\n\n Intensive Care Medicine, 46(5): 919–929. 2020.\n \n\n\n\n
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@article{Chesnut2020919,\nannote = {cited By 4},\nauthor = {Chesnut, R and Aguilera, S and Buki, A and Bulger, E and Citerio, G and Cooper, D J and Arrastia, R D and Diringer, M and Figaji, A and Gao, G and Geocadin, R and Ghajar, J and Harris, O and Hoffer, A and Hutchinson, P and Joseph, M and Kitagawa, R and Manley, G and Mayer, S and Menon, D K and Meyfroidt, G and Michael, D B and Oddo, M and Okonkwo, D and Patel, M and Robertson, C and Rosenfeld, J V and Rubiano, A M and Sahuquillo, J and Servadei, F and Shutter, L and Stein, D and Stocchetti, N and Taccone, F S and Timmons, S and Tsai, E and Ullman, J S and Vespa, P and Videtta, W and Wright, D W and Zammit, C and Hawryluk, G W J},\ndoi = {10.1007/s00134-019-05900-x},\nfile = {:Users/jacquelinebracher/Zotero/storage/BDASUK4Q/Chesnut et al. - 2020 - A management algorithm for adult patients with bot.pdf:pdf},\nissn = {03424642},\njournal = {Intensive Care Medicine},\nkeywords = {adult; algorithm; Article; blood transfusion; brai},\nnumber = {5},\npages = {919--929},\npublisher = {Springer},\ntitle = {{A management algorithm for adult patients with both brain oxygen and intracranial pressure monitoring: the Seattle International Severe Traumatic Brain Injury Consensus Conference (SIBICC)}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85078140804{\\&}doi=10.1007{\\%}2Fs00134-019-05900-x{\\&}partnerID=40{\\&}md5=80ddc0187d858ce2339f1a7ff3cc3727},\nvolume = {46},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n \n The transition to status epilepticus: how the brain meets the demands of perpetual seizure activity.\n \n \n \n \n\n\n \n Burman, R J; Raimondo, J V; Jefferys, J G R; Sen, A; and Akerman, C J\n\n\n \n\n\n\n Seizure, 75: 137–144. 2020.\n \n\n\n\n
\n\n\n\n \n \n \"ThePaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n\n\n\n
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@article{Burman2020137,\nannote = {cited By 1},\nauthor = {Burman, R J and Raimondo, J V and Jefferys, J G R and Sen, A and Akerman, C J},\ndoi = {10.1016/j.seizure.2019.09.012},\nfile = {:Users/jacquelinebracher/Zotero/storage/LZBXHSK2/Burman et al. - 2020 - The transition to status epilepticus how the brai.pdf:pdf},\nissn = {10591311},\njournal = {Seizure},\nkeywords = {bicuculline; dyflos; homocysteine; kainic acid rec,biological model; cortical excitability; disease},\npages = {137--144},\npublisher = {W.B. Saunders Ltd},\ntitle = {{The transition to status epilepticus: how the brain meets the demands of perpetual seizure activity}},\nurl = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85076851135{\\&}doi=10.1016{\\%}2Fj.seizure.2019.09.012{\\&}partnerID=40{\\&}md5=124f970d8a73141e975ef65c02563537},\nvolume = {75},\nyear = {2020}\n}\n
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\n \n\n \n \n \n \n \n Exploring how a genetic attribution to disease relates to stigma experiences of Xhosa patients with schizophrenia in South Africa.\n \n \n \n\n\n \n Matshabane, O.; Campbell, M.; Faure, M.; Marshall, P.; Mayosi, B.; Stein, D.; Appelbaum, P.; and de Vries, J.\n\n\n \n\n\n\n Social Psychiatry and Psychiatric Epidemiology, 55(12): 1679–1686. 2020.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{Matshabane2020,\nabstract = {Background: Over the past three decades, a range of international stakeholders have highlighted the possibility that genomic research may impact stigma associated with psychiatric disorders. Limited research has been conducted in Africa to investigate this relation. Method: In the present study, using focus group discussions, we explored the relation between genetic attribution and stigma among 36 Xhosa people with schizophrenia. We addressed three main questions: (1) What causal beliefs do Xhosa people with schizophrenia use to explain their illness and to what extent do genetic explanations play a role in these beliefs? (2) What are the internalised stigma experiences of Xhosa people with schizophrenia? (3) How do genetic explanations relate to stigma experiences, if at all? Results: Most participants were able to define genetics and some linked genetics to disease causation. Despite adequate knowledge of genetics and an emphasis on genetic explanations of schizophrenia in the study, most participants held a multitude of causal explanations including: psychosocial, environmental, and cultural. Moreover, participants rarely mentioned disease cause when describing their stigma experiences. Discussion: For this population group, there was no straight-forward relation between a genetic attribution and stigma. Therefore, we did not find evidence that genetic attribution may significantly increase stigma. Although North American and European literature provides conflicting evidence regarding this relation, there is increased consensus that biomedical explanations for psychiatric disorders may reduce blame. This study found evidence supporting that consensus. This study provides an empirical foundation to inform ongoing work on the psychosocial implications of psychiatric genomics research in non-Western contexts.},\nauthor = {Matshabane, O.P. and Campbell, M.M. and Faure, M.C. and Marshall, P.A. and Mayosi, B.M. and Stein, D.J. and Appelbaum, P.S. and de Vries, J.},\ndoi = {10.1007/s00127-020-01875-z},\njournal = {Social Psychiatry and Psychiatric Epidemiology},\nnumber = {12},\npages = {1679--1686},\ntitle = {{Exploring how a genetic attribution to disease relates to stigma experiences of Xhosa patients with schizophrenia in South Africa}},\nvolume = {55},\nyear = {2020}\n}\n
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\n Background: Over the past three decades, a range of international stakeholders have highlighted the possibility that genomic research may impact stigma associated with psychiatric disorders. Limited research has been conducted in Africa to investigate this relation. Method: In the present study, using focus group discussions, we explored the relation between genetic attribution and stigma among 36 Xhosa people with schizophrenia. We addressed three main questions: (1) What causal beliefs do Xhosa people with schizophrenia use to explain their illness and to what extent do genetic explanations play a role in these beliefs? (2) What are the internalised stigma experiences of Xhosa people with schizophrenia? (3) How do genetic explanations relate to stigma experiences, if at all? Results: Most participants were able to define genetics and some linked genetics to disease causation. Despite adequate knowledge of genetics and an emphasis on genetic explanations of schizophrenia in the study, most participants held a multitude of causal explanations including: psychosocial, environmental, and cultural. Moreover, participants rarely mentioned disease cause when describing their stigma experiences. Discussion: For this population group, there was no straight-forward relation between a genetic attribution and stigma. Therefore, we did not find evidence that genetic attribution may significantly increase stigma. Although North American and European literature provides conflicting evidence regarding this relation, there is increased consensus that biomedical explanations for psychiatric disorders may reduce blame. This study found evidence supporting that consensus. This study provides an empirical foundation to inform ongoing work on the psychosocial implications of psychiatric genomics research in non-Western contexts.\n
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\n  \n\n  \n  \n  \n  \n  \n  .\n  \n  \n  \n\n\n  \n  Heckmann, J. M; Europa, T. A; Soni, A. J;  and Nel, M.\n\n\n  \n\n\n\n  Frontiers in Neurology,834212. feb .\n  \n\n\n\n
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@article{heckmann_epidemiology_2022,\nabstract = {Myasthenia gravis (MG) appears to have a similar incidence among adult populations worldwide. However, epidemiological and phenotypic differences have been noted among children and juveniles with MG. We reviewed the literature on childhood- and juvenile-onset MG among different populations, with the focus on ocular involvement, antibody profiles, the genetic susceptibility to juvenile MG phenotypes, the use of immune treatments, and the reported responses of extraocular muscles to therapies. Although epidemiological studies used different methodologies, reports from Asia, compared to Europe, showed more than two-fold higher proportions of prepubertal onset (before 12 years) vs. postpubertal-onset juveniles with MG. Compared to European children, ocular MG was 4-fold more frequent among Asian children, and 2–3-fold more frequent among children with African ancestry both in prepubertal and postpubertal ages at onset. These results suggest genetic influences. In Asia,\nHLA-B\n*\n46\nand\nDRB1\n*\n09\nappeared overrepresented in children with ocular MG. In Europe, children with MG had a significantly higher rate of transforming from ocular to generalized disease and with an overrepresentation of\nHLADRB1\n*\n04\n. Although treatment regimens vary widely and the responses to immune therapies of the ocular muscles involved in MG were generally poorly described, there were indications that earlier use of steroid therapy may have better outcomes. Reports of treatment-resistant ophthalmoplegia may be more frequent in African and Asian juvenile MG cohorts compared to Europeans. Genetic and muscle gene expression studies point to dysregulated muscle atrophy signaling and mitochondrial metabolism pathways as pathogenetic mechanisms underpinning treatment-resistant ophthalmoplegia in susceptible individuals. In conclusion, phenotypic differences in juveniles with ocular manifestations of MG were evident in different populations suggesting pathogenetic influences. Treatment responses in MG-associated ocular disease should attract more careful descriptive reports. In MG, extraocular muscles may be vulnerable to critical periods of poor force generation and certain individuals may be particularly susceptible to developing treatment-resistant ophthalmoplegia. The development of prognostic biomarkers to identify these susceptible individuals is an unmet need.},\nauthor = {Heckmann, Jeannine M and Europa, Tarin A and Soni, Aayesha J and Nel, Melissa},\ndoi = {10.3389/fneur.2022.834212},\nfile = {:Users/jacquelinebracher/Zotero/storage/H9ECV634/Heckmann et al. - 2022 - The Epidemiology and Phenotypes of Ocular Manifest.pdf:pdf},\nissn = {1664-2295},\njournal = {Frontiers in Neurology},\nmonth = {feb},\npages = {834212},\nshorttitle = {The {\\{}Epidemiology{\\}} and {\\{}Phenotypes{\\}} of {\\{}Ocular{\\}} {\\{}M}}
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\n  Myasthenia gravis (MG) appears to have a similar incidence among adult populations worldwide. However, epidemiological and phenotypic differences have been noted among children and juveniles with MG. We reviewed the literature on childhood- and juvenile-onset MG among different populations, with the focus on ocular involvement, antibody profiles, the genetic susceptibility to juvenile MG phenotypes, the use of immune treatments, and the reported responses of extraocular muscles to therapies. Although epidemiological studies used different methodologies, reports from Asia, compared to Europe, showed more than two-fold higher proportions of prepubertal onset (before 12 years) vs. postpubertal-onset juveniles with MG. Compared to European children, ocular MG was 4-fold more frequent among Asian children, and 2–3-fold more frequent among children with African ancestry both in prepubertal and postpubertal ages at onset. These results suggest genetic influences. In Asia, HLA-B * 46 and DRB1 * 09 appeared overrepresented in children with ocular MG. In Europe, children with MG had a significantly higher rate of transforming from ocular to generalized disease and with an overrepresentation of HLADRB1 * 04 . Although treatment regimens vary widely and the responses to immune therapies of the ocular muscles involved in MG were generally poorly described, there were indications that earlier use of steroid therapy may have better outcomes. Reports of treatment-resistant ophthalmoplegia may be more frequent in African and Asian juvenile MG cohorts compared to Europeans. Genetic and muscle gene expression studies point to dysregulated muscle atrophy signaling and mitochondrial metabolism pathways as pathogenetic mechanisms underpinning treatment-resistant ophthalmoplegia in susceptible individuals. In conclusion, phenotypic differences in juveniles with ocular manifestations of MG were evident in different populations suggesting pathogenetic influences. Treatment responses in MG-associated ocular disease should attract more careful descriptive reports. In MG, extraocular muscles may be vulnerable to critical periods of poor force generation and certain individuals may be particularly susceptible to developing treatment-resistant ophthalmoplegia. The development of prognostic biomarkers to identify these susceptible individuals is an unmet need.\n
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\n  \n\n  \n  \n  \n  \n  \n  How to manage obsessive-compulsive disorder (\\OCD\\) under \\COVID\\-19: \\A\\ clinician's guide from the \\International\\ \\College\\ of \\Obsessive\\ \\Compulsive\\ \\Spectrum\\ \\Disorders\\ (\\ICOCS\\) and the \\Obsessive\\-\\Compulsive\\ and \\Related\\ \\Disorders\\ \\Researc.\n  \n  \n  \n\n\n  \n  Fineberg, N A; Van Ameringen, M; Drummond, L; Hollander, E; Stein, D J; Geller, D; Walitza, S; Pallanti, S; Pellegrini, L; Zohar, J; Rodriguez, C I; Menchon, J M; Morgado, P; Mpavaenda, D; Fontenelle, L F; Feusner, J D; Grassi, G; Lochner, C; Veltman, D J; Sireau, N; Carmi, L; Adam, D; Nicolini, H;  and Dell'Osso, B\n\n\n  \n\n\n\n  Comprehensive Psychiatry,152174. jul .\n  \n\n\n\n
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@article{fineberg_how_2020,\nauthor = {Fineberg, N A and {Van Ameringen}, M and Drummond, L and Hollander, E and Stein, D J and Geller, D and Walitza, S and Pallanti, S and Pellegrini, L and Zohar, J and Rodriguez, C I and Menchon, J M and Morgado, P and Mpavaenda, D and Fontenelle, L F and Feusner, J D and Grassi, G and Lochner, C and Veltman, D J and Sireau, N and Carmi, L and Adam, D and Nicolini, H and Dell'Osso, B},\ndoi = {10.1016/j.comppsych.2020.152174},\nfile = {:Users/jacquelinebracher/Zotero/storage/Q4JSPDHZ/Fineberg et al. - 2020 - How to manage obsessive-compulsive disorder (OCD) .pdf:pdf},\nissn = {0010440X},\njournal = {Comprehensive Psychiatry},\nmonth = {jul},\npages = {152174},\nshorttitle = {How to manage obsessive-compulsive disorder ({\\{}OCD{\\}}},\ntitle = {{How to manage obsessive-compulsive disorder ({\\{}OCD{\\}}) under {\\{}COVID{\\}}-19: {\\{}A{\\}} clinician's guide from the {\\{}International{\\}} {\\{}College{\\}} of {\\{}Obsessive{\\}} {\\{}Compulsive{\\}} {\\{}Spectrum{\\}} {\\{}Disorders{\\}} ({\\{}ICOCS{\\}}) and the {\\{}Obsessive{\\}}-{\\{}Compulsive{\\}} and {\\{}Related{\\}} {\\{}Disorders{\\}} {\\{}Researc}}}
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\n  \n\n  \n  \n  \n  \n  \n  .\n  \n  \n  \n\n\n  \n  Montag, C.; Solms, M.; Stelzel, C.;  and Davis, K. L\n\n\n  \n\n\n\n  Personality Neuroscience,e10.  .\n  \n\n\n\n
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@article{montag_future_2022,\nabstract = {Abstract\nThe Affective Neuroscience Personality Scales (ANPS) were designed to provide researchers in the mental sciences with an inventory to assess primary emotional systems according to Pankseppian Affective Neuroscience Theory (ANT). The original ANPS, providing researchers with such a tool, was published in 2003. In the present brief communication, about 20 years later, we reflect upon some pressing matters regarding the further development of the ANPS. We touch upon problems related to disentangling traits and states of the primary emotional systems with the currently available versions of the ANPS and upon its psychometric properties and its length. We reflect also on problems such as the large overlap between the SADNESS and FEAR dimensions, the disentangling of PANIC and GRIEF in the context of SADNESS, and the absence of a LUST scale. Lastly, we want to encourage scientists with the present brief communication to engage in further biological validation of the ANPS.},\nauthor = {Montag, Christian and Solms, Mark and Stelzel, Christine and Davis, Kenneth L},\ndoi = {10.1017/pen.2022.2},\nfile = {:Users/jacquelinebracher/Zotero/storage/GHQZ9BGU/Montag et al. - 2022 - The future of the Affective Neuroscience Personali.pdf:pdf},\nissn = {2513-9886},\njournal = {Personality Neuroscience},\npages = {e10},\nshorttitle = {The future of the {\\{}Affective{\\}} {\\{}Neuroscience{\\}} {\\{}Pers}}
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\n  Abstract The Affective Neuroscience Personality Scales (ANPS) were designed to provide researchers in the mental sciences with an inventory to assess primary emotional systems according to Pankseppian Affective Neuroscience Theory (ANT). The original ANPS, providing researchers with such a tool, was published in 2003. In the present brief communication, about 20 years later, we reflect upon some pressing matters regarding the further development of the ANPS. We touch upon problems related to disentangling traits and states of the primary emotional systems with the currently available versions of the ANPS and upon its psychometric properties and its length. We reflect also on problems such as the large overlap between the SADNESS and FEAR dimensions, the disentangling of PANIC and GRIEF in the context of SADNESS, and the absence of a LUST scale. Lastly, we want to encourage scientists with the present brief communication to engage in further biological validation of the ANPS.\n
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\n  \n\n  \n  \n  \n  \n  \n  .\n  \n  \n  \n\n\n  \n  Kanmounye, U. S; Robertson, F. C; Thango, N. S; Doe, A. N.; Bankole, N. D. A.; Ginette, P. A.; Ondoma, S.; Balogun, J. A; Opoku, I.; Jokonya, L.; Mbaye, T.; Shabhay, Z. A; Ashour, A. M; Silva, A. C. V.; Cheserem, B.; Karekezi, C.; Hassani, F. D.; Mentri, N.; Laeke, T.; Aklilu, A. T.; Sanoussi, S.; Musara, A.; Ntalaja, J.; Ssenyonga, P.; Bakhti, S.; El Abbadi, N.; Mahmud, M. R.; El-Ghandour, N. M F; Al-Habib, A.; Kolias, A. G; Servadei, F.; Fieggen, G.; Qureshi, M.; Esene, I.; CAANS Young Neurosurgeons Committee;  and Committee, W. Y. N.\n\n\n  \n\n\n\n  Frontiers in Surgery,647279. may .\n  \n\n\n\n
\n\n\n\n  \n\n  \n  \n    doi\n   \n  \n\n  \n  link\n   \n  \n\n  bibtex\n    \n\n  \n   \n  \n    abstract \n  \n\n  \n\n  \n  \n  \n  \n  \n  \n  \n\n   \n  \n  \n\n\n\n
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@article{kanmounye_needs_2021,\nabstract = {Introduction:\nAfrica has many untreated neurosurgical cases due to limited access to safe, affordable, and timely care. In this study, we surveyed young African neurosurgeons and trainees to identify challenges to training and practice.\n\n\nMethods:\nAfrican trainees and residents were surveyed online by the Young Neurosurgeons Forum from April 25th to November 30th, 2018. The survey link was distributed via social media platforms and through professional society mailing lists. Univariate and bivariate data analyses were run and a\nP\n-value {\\textless} 0.05 was considered to be statistically significant.\n\n\nResults:\n112 respondents from 20 countries participated in this study. 98 (87.5{\\%}) were male, 63 (56.3{\\%}) were from sub-Saharan Africa, and 52 (46.4{\\%}) were residents. 39 (34.8{\\%}) had regular journal club sessions at their hospital, 100 (89.3{\\%}) did not have access to cadaver dissection labs, and 62 (55.4{\\%}) had never attended a WFNS-endorsed conference. 67.0{\\%} of respondents reported limited research opportunities and 58.9{\\%} reported limited education opportunities. Lack of mentorship (\nP\n= 0.023, Phi = 0.26), lack of access to journals (\nP\n= 0.002, Phi = 0.332), and limited access to conferences (\nP\n= 0.019, Phi = 0.369) were associated with the country income category.\n\n\nConclusion:\nThis survey identified barriers to education, research, and practice among African trainees and young neurosurgeons. The findings of this study should inform future initiatives aimed at reducing the barriers faced by this group.},\nauthor = {Kanmounye, Ulrick S and Robertson, Faith C and Thango, Nqobile S and Doe, Alvin Nah and Bankole, Nourou Dine Adeniran and Ginette, Pape Aicha and Ondoma, Solomon and Balogun, James A and Opoku, Isabella and Jokonya, Luxwell and Mbaye, Thioub and Shabhay, Zarina A and Ashour, Ahmed M and Silva, Ana Cristina Veiga and Cheserem, Beverly and Karekezi, Claire and Hassani, Fahd Derkaoui and Mentri, Nesrine and Laeke, Tsegazeab and Aklilu, Abenezer Tirsit and Sanoussi, Samuila and Musara, Aaron and Ntalaja, Jeff and Ssenyonga, Peter and Bakhti, Souad and {El Abbadi}, Najia and Mahmud, Muhammad Raji and El-Ghandour, Nasser M F and Al-Habib, Amro and Kolias, Angelos G and Servadei, Franco and Fieggen, Graham and Qureshi, Mahmood and Esene, Ignatius and {CAANS Young Neurosurgeons Committee and WFNS Young Neurosurgeons Committee}},\ndoi = {10.3389/fsurg.2021.647279},\nfile = {:Users/jacquelinebracher/Zotero/storage/XLKI4TRP/Kanmounye et al. - 2021 - Needs of Young African Neurosurgeons and Residents.pdf:pdf},\nissn = {2296-875X},\njournal = {Frontiers in Surgery},\nmonth = {may},\npages = {647279},\nshorttitle = {Needs of {\\{}Young{\\}} {\\{}African{\\}} {\\{}Neurosurgeons{\\}} and {\\{}Re}}
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\n  Introduction: Africa has many untreated neurosurgical cases due to limited access to safe, affordable, and timely care. In this study, we surveyed young African neurosurgeons and trainees to identify challenges to training and practice. Methods: African trainees and residents were surveyed online by the Young Neurosurgeons Forum from April 25th to November 30th, 2018. The survey link was distributed via social media platforms and through professional society mailing lists. Univariate and bivariate data analyses were run and a P -value \\textless 0.05 was considered to be statistically significant. Results: 112 respondents from 20 countries participated in this study. 98 (87.5%) were male, 63 (56.3%) were from sub-Saharan Africa, and 52 (46.4%) were residents. 39 (34.8%) had regular journal club sessions at their hospital, 100 (89.3%) did not have access to cadaver dissection labs, and 62 (55.4%) had never attended a WFNS-endorsed conference. 67.0% of respondents reported limited research opportunities and 58.9% reported limited education opportunities. Lack of mentorship ( P = 0.023, Phi = 0.26), lack of access to journals ( P = 0.002, Phi = 0.332), and limited access to conferences ( P = 0.019, Phi = 0.369) were associated with the country income category. Conclusion: This survey identified barriers to education, research, and practice among African trainees and young neurosurgeons. The findings of this study should inform future initiatives aimed at reducing the barriers faced by this group.\n
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\n  \n\n  \n  \n  \n  \n  \n  .\n  \n  \n  \n\n\n  \n  Stein, D. J\n\n\n  \n\n\n\n  Neurology and Therapy, (S1): 13–19. apr .\n  \n\n\n\n
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@article{stein_evidence-based_2023,\nauthor = {Stein, Dan J},\ndoi = {10.1007/s40120-023-00470-z},\nfile = {:Users/jacquelinebracher/Zotero/storage/ZK2RI36V/Stein - 2023 - Evidence-Based Pharmacotherapy of Anxiety Symptoms.pdf:pdf},\nissn = {2193-8253, 2193-6536},\njournal = {Neurology and Therapy},\nmonth = {apr},\nnumber = {S1},\npages = {13--19},\nshorttitle = {Evidence-{\\{}Based{\\}} {\\{}Pharmacotherapy{\\}} of {\\{}Anxiety{\\}} {\\{}S}}
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\n  \n\n  \n  \n  \n  \n  \n  .\n  \n  \n  \n\n\n  \n  Jörns-Presentati, A.; Napp, A.; Dessauvagie, A. S; Stein, D. J; Jonker, D.; Breet, E.; Charles, W.; Swart, R. L; Lahti, M.; Suliman, S.; Jansen, R.; Van Den Heuvel, L. L; Seedat, S.;  and Groen, G.\n\n\n  \n\n\n\n  PLOS ONE, (5): e0251689. may .\n  \n\n\n\n
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@article{jorns-presentati_prevalence_2021,\nabstract = {Background and purpose\nMost research regarding child and adolescent mental health prevention and promotion in low-and middle-income countries is undertaken in high-income countries. This systematic review set out to synthesise findings from epidemiological studies, published between 2008 and 2020, documenting the prevalence of mental health problems in adolescents from across sub-Saharan Africa.\n\n\nMethods\nA systematic search of multiple databases (MEDLINE, PsycINFO, Scopus) and Google Scholar was conducted guided by the Joanna Briggs Institute (JBI) Reviewer's manual for systematic reviews of observational epidemiological studies. Studies included reported prevalence outcomes for adolescents aged 10–19 using either clinical interviews or standardized questionnaires to assess psychopathology. Clinical samples were excluded.\n\n\nResults\nThe search yielded 1 549 records of which 316 studies were assessed for eligibility and 51 met the inclusion criteria. We present a qualitative synthesis of 37 of these 51 included articles. The other 14 studies reporting prevalence rates for adolescents living with HIV are published elsewhere. The prevalence of depression, anxiety disorders, emotional and behavioural difficulties, posttraumatic stress and suicidal behaviour in the general adolescent population and selected at-risk groups in 16 sub-Saharan countries (with a total population of 97 616 adolescents) are reported.},\nauthor = {J{\\"{o}}rns-Presentati, Astrid and Napp, Ann-Kathrin and Dessauvagie, Anja S and Stein, Dan J and Jonker, Deborah and Breet, Elsie and Charles, Weslin and Swart, Renier L and Lahti, Mari and Suliman, Sharain and Jansen, Ronelle and {Van Den Heuvel}, Leigh L and Seedat, Soraya and Groen, Gunter},\ndoi = {10.1371/journal.pone.0251689},\neditor = {Sar, Vedat},\nfile = {:Users/jacquelinebracher/Zotero/storage/V6KE7IXZ/J{\\"{o}}rns-Presentati et al. - 2021 - The prevalence of mental health problems in sub-Sa.pdf:pdf},\nissn = {1932-6203},\njournal = {PLOS ONE},\nmonth = {may},\nnumber = {5},\npages = {e0251689},\nshorttitle = {The prevalence of mental health problems in sub-{\\{}S}}
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\n  Background and purpose Most research regarding child and adolescent mental health prevention and promotion in low-and middle-income countries is undertaken in high-income countries. This systematic review set out to synthesise findings from epidemiological studies, published between 2008 and 2020, documenting the prevalence of mental health problems in adolescents from across sub-Saharan Africa. Methods A systematic search of multiple databases (MEDLINE, PsycINFO, Scopus) and Google Scholar was conducted guided by the Joanna Briggs Institute (JBI) Reviewer's manual for systematic reviews of observational epidemiological studies. Studies included reported prevalence outcomes for adolescents aged 10–19 using either clinical interviews or standardized questionnaires to assess psychopathology. Clinical samples were excluded. Results The search yielded 1 549 records of which 316 studies were assessed for eligibility and 51 met the inclusion criteria. We present a qualitative synthesis of 37 of these 51 included articles. The other 14 studies reporting prevalence rates for adolescents living with HIV are published elsewhere. The prevalence of depression, anxiety disorders, emotional and behavioural difficulties, posttraumatic stress and suicidal behaviour in the general adolescent population and selected at-risk groups in 16 sub-Saharan countries (with a total population of 97 616 adolescents) are reported.\n
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\n  \n\n  \n  \n  \n  \n  \n  .\n  \n  \n  \n\n\n  \n  Oosthuizen, K.; Steyn, E. C.; Tucker, L.; Ncube, I. V.; Hardie, D.;  and Marais, S.\n\n\n  \n\n\n\n  Neurology, (1): 27–29. jul .\n  \n\n\n\n
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@article{oosthuizen_sars-cov-2_2021,\nauthor = {Oosthuizen, Katryn and Steyn, Elizabeth Christina and Tucker, Lawrence and Ncube, Innocent Vusumusi and Hardie, Diana and Marais, Suzaan},\ndoi = {10.1212/WNL.0000000000012051},\nissn = {0028-3878, 1526-632X},\njournal = {Neurology},\nmonth = {jul},\nnumber = {1},\npages = {27--29},\nshorttitle = {{\\{}SARS{\\}}-{\\{}CoV{\\}}-2 {\\{}Encephalitis{\\}} {\\{}Presenting{\\}} as a {\\{}C}}
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\n  \n\n  \n  \n  \n  \n  \n  .\n  \n  \n  \n\n\n  \n  Stein, D. J\n\n\n  \n\n\n\n  Advances in Therapy, (S2): 52–60. sep .\n  \n\n\n\n
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@article{stein_evidence-based_2021,\nauthor = {Stein, Dan J},\ndoi = {10.1007/s12325-021-01860-1},\nfile = {:Users/jacquelinebracher/Zotero/storage/4KGA7IFR/Stein - 2021 - Evidence-Based Pharmacotherapy of Generalised Anxi.pdf:pdf},\nissn = {0741-238X, 1865-8652},\njournal = {Advances in Therapy},\nmonth = {sep},\nnumber = {S2},\npages = {52--60},\nshorttitle = {Evidence-{\\{}Based{\\}} {\\{}Pharmacotherapy{\\}} of {\\{}Generalised}}
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\n  \n\n  \n  \n  \n  \n  \n  .\n  \n  \n  \n\n\n  \n  Kasule, M.; Matshaba, M.; Wonkam, A.;  and De Vries, J.\n\n\n  \n\n\n\n  BMC Medical Ethics, (1): 37. jun .\n  \n\n\n\n
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@article{kasule_feeding_2023,\nabstract = {Abstract\n\nPurpose\nWe explored the views of Botswana stakeholders involved in developing, implementing and applying ethical standards for return of individual study results from genomic research. This allowed for mapping opportunities and challenges regarding actionability requirements that determine whether individual genomic research results should be fed back.\n\n\nMethods\nUsing in-depth interviews, this study explored the views of sixteen (16) stakeholders about the extent, nature and timing of feedback of individual genomic research findings, including incidental findings that arise in the context of African genomics research. Coded data was analyzed through an iterative process of analytic induction to document and interpret themes.\n\n\nResults\nOverall, respondents were of the view that feedback of actionable individual genomic results was an important outcome that could benefit participants. However, a number of themes surfaced that pointed to opportunities and challenges that exist in Botswana that could help in planning for feeding back of individual genomic results that were mapped. Some of the opportunities cited by the respondents included the existence of good governance; democracy and humanitarianism; universal healthcare system; national commitment to science; research and innovation to transform Botswana into a knowledge-based economy; and applicable standard of care which could promote actionability. On the other hand, contextual issues like the requirement for validation of genomic research results in accredited laboratories, high cost of validation of genomic results, and linkage to care, as well as lack of experts like genomic scientists and counselors were considered as challenges for return of individual results.\n\n\nConclusion\nWe propose that decisions whether and which genomic results to return take into consideration contextual opportunities and challenges for actionability for return of results in a research setting. This is likely to avoid or minimize ethical issues of justice, equity and harm regarding actionability decisions.},\nauthor = {Kasule, Mary and Matshaba, Mogomotsi and Wonkam, Ambroise and {De Vries}, Jantina},\ndoi = {10.1186/s12910-023-00912-1},\nfile = {:Users/jacquelinebracher/Zotero/storage/R7T2553B/Kasule et al. - 2023 - Feeding back of individual genetic results in Bots.pdf:pdf},\nissn = {1472-6939},\njournal = {BMC Medical Ethics},\nmonth = {jun},\nnumber = {1},\npages = {37},\nshorttitle = {Feeding back of individual genetic results in {\\{}Bot}}
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\n  Abstract Purpose We explored the views of Botswana stakeholders involved in developing, implementing and applying ethical standards for return of individual study results from genomic research. This allowed for mapping opportunities and challenges regarding actionability requirements that determine whether individual genomic research results should be fed back. Methods Using in-depth interviews, this study explored the views of sixteen (16) stakeholders about the extent, nature and timing of feedback of individual genomic research findings, including incidental findings that arise in the context of African genomics research. Coded data was analyzed through an iterative process of analytic induction to document and interpret themes. Results Overall, respondents were of the view that feedback of actionable individual genomic results was an important outcome that could benefit participants. However, a number of themes surfaced that pointed to opportunities and challenges that exist in Botswana that could help in planning for feeding back of individual genomic results that were mapped. Some of the opportunities cited by the respondents included the existence of good governance; democracy and humanitarianism; universal healthcare system; national commitment to science; research and innovation to transform Botswana into a knowledge-based economy; and applicable standard of care which could promote actionability. On the other hand, contextual issues like the requirement for validation of genomic research results in accredited laboratories, high cost of validation of genomic results, and linkage to care, as well as lack of experts like genomic scientists and counselors were considered as challenges for return of individual results. Conclusion We propose that decisions whether and which genomic results to return take into consideration contextual opportunities and challenges for actionability for return of results in a research setting. This is likely to avoid or minimize ethical issues of justice, equity and harm regarding actionability decisions.\n
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\n  \n\n  \n  \n  \n  \n  \n  .\n  \n  \n  \n\n\n  \n  Hirsch, E.; French, J.; Scheffer, I. E; Bogacz, A.; Alsaadi, T.; Sperling, M. R; Abdulla, F.; Zuberi, S. M; Trinka, E.; Specchio, N.; Somerville, E.; Samia, P.; Riney, K.; Nabbout, R.; Jain, S.; Wilmshurst, J. M; Auvin, S.; Wiebe, S.; Perucca, E.; Moshé, S. L; Tinuper, P.;  and Wirrell, E. C\n\n\n  \n\n\n\n  Epilepsia, (6): 1475–1499. jun .\n  \n\n\n\n
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@article{hirsch_ilae_2022,\nabstract = {Abstract\nIn 2017, the International League Against Epilepsy (ILAE) Classification of Epilepsies described the “genetic generalized epilepsies” (GGEs), which contained the “idiopathic generalized epilepsies” (IGEs). The goal of this paper is to delineate the four syndromes comprising the IGEs, namely childhood absence epilepsy, juvenile absence epilepsy, juvenile myoclonic epilepsy, and epilepsy with generalized tonic–clonic seizures alone. We provide updated diagnostic criteria for these IGE syndromes determined by the expert consensus opinion of the ILAE's Task Force on Nosology and Definitions (2017–2021) and international external experts outside our Task Force. We incorporate current knowledge from recent advances in genetic, imaging, and electroencephalographic studies, together with current terminology and classification of seizures and epilepsies. Patients that do not fulfill criteria for one of these syndromes, but that have one, or a combination, of the following generalized seizure types: absence, myoclonic, tonic‐clonic and myoclonic‐tonic‐clonic seizures, with 2.5–5.5 Hz generalized spike‐wave should be classified as having GGE. Recognizing these four IGE syndromes as a special grouping among the GGEs is helpful, as they carry prognostic and therapeutic implications.},\nauthor = {Hirsch, Edouard and French, Jacqueline and Scheffer, Ingrid E and Bogacz, Alicia and Alsaadi, Taoufik and Sperling, Michael R and Abdulla, Fatema and Zuberi, Sameer M and Trinka, Eugen and Specchio, Nicola and Somerville, Ernest and Samia, Pauline and Riney, Kate and Nabbout, Rima and Jain, Satish and Wilmshurst, Jo M and Auvin, Stephane and Wiebe, Samuel and Perucca, Emilio and Mosh{\\'{e}}, Solomon L and Tinuper, Paolo and Wirrell, Elaine C},\ndoi = {10.1111/epi.17236},\nfile = {:Users/jacquelinebracher/Zotero/storage/IFKGLMEK/Hirsch et al. - 2022 - ILAE definition of the Idiopathic Generalized Epil.pdf:pdf},\nissn = {0013-9580, 1528-1167},\njournal = {Epilepsia},\nmonth = {jun},\nnumber = {6},\npages = {1475--1499},\nshorttitle = {{\\{}ILAE{\\}} definition of the {\\{}Idiopathic{\\}} {\\{}Generalized}}
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\n  Abstract In 2017, the International League Against Epilepsy (ILAE) Classification of Epilepsies described the “genetic generalized epilepsies” (GGEs), which contained the “idiopathic generalized epilepsies” (IGEs). The goal of this paper is to delineate the four syndromes comprising the IGEs, namely childhood absence epilepsy, juvenile absence epilepsy, juvenile myoclonic epilepsy, and epilepsy with generalized tonic–clonic seizures alone. We provide updated diagnostic criteria for these IGE syndromes determined by the expert consensus opinion of the ILAE's Task Force on Nosology and Definitions (2017–2021) and international external experts outside our Task Force. We incorporate current knowledge from recent advances in genetic, imaging, and electroencephalographic studies, together with current terminology and classification of seizures and epilepsies. Patients that do not fulfill criteria for one of these syndromes, but that have one, or a combination, of the following generalized seizure types: absence, myoclonic, tonic‐clonic and myoclonic‐tonic‐clonic seizures, with 2.5–5.5 Hz generalized spike‐wave should be classified as having GGE. Recognizing these four IGE syndromes as a special grouping among the GGEs is helpful, as they carry prognostic and therapeutic implications.\n
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\n  \n\n  \n  \n  \n  \n  \n  .\n  \n  \n  \n\n\n  \n  Stein, D. J; Khoo, J.; Picarel-Blanchot, F.; Olivier, V.;  and Van Ameringen, M.\n\n\n  \n\n\n\n  Advances in Therapy, (3): 1567–1583. mar .\n  \n\n\n\n
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@article{stein_efficacy_2021,\nauthor = {Stein, Dan J and Khoo, Jon-Paul and Picarel-Blanchot, Fran{\\c{c}}oise and Olivier, Val{\\'{e}}rie and {Van Ameringen}, Michael},\ndoi = {10.1007/s12325-020-01583-9},\nfile = {:Users/jacquelinebracher/Zotero/storage/CFGN8BD2/Stein et al. - 2021 - Efficacy of Agomelatine 25–50 mg for the Treatment.pdf:pdf},\nissn = {0741-238X, 1865-8652},\njournal = {Advances in Therapy},\nmonth = {mar},\nnumber = {3},\npages = {1567--1583},\nshorttitle = {Efficacy of {\\{}Agomelatine{\\}} 25–50 mg for the {\\{}Treatm}}
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\n  \n\n  \n  \n  \n  \n  \n  .\n  \n  \n  \n\n\n  \n  Wedderburn, C. J; Evans, C.; Slogrove, A. L; Rehman, A. M; Gibb, D. M; Prendergast, A. J;  and Penazzato, M.\n\n\n  \n\n\n\n  Journal of the International AIDS Society, (6): e26079. jun .\n  \n\n\n\n
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@article{wedderburn_cotrimoxazole_2023,\nabstract = {Abstract\n\nIntroduction\nCo‐trimoxazole prophylaxis is recommended for children born to women with HIV to protect those who acquire HIV from opportunistic infections, severe bacterial infections and malaria. With scale‐up of maternal antiretroviral therapy, most children remain HIV‐exposed uninfected (HEU) and the benefits of universal co‐trimoxazole are uncertain. We assessed the effect of co‐trimoxazole on mortality and morbidity of children who are HEU.\n\n\nMethods\nWe performed a systematic review (PROSPERO number: CRD42021215059). We systematically searched MEDLINE, Embase, Cochrane CENTRAL, Global Health, CINAHL Plus, Africa‐Wide Information, SciELO and WHO Global Index Medicus for peer‐reviewed articles from inception to 4th January 2022 without limits. Ongoing randomized controlled trials (RCTs) were identified through registries. We included RCTs reporting mortality or morbidity in children who are HEU receiving co‐trimoxazole versus no prophylaxis/placebo. The risk of bias was assessed using the Cochrane 2.0 tool. Data were summarized using narrative synthesis and findings were stratified by malaria endemicity.\n\n\nResults\nWe screened 1257 records and included seven reports from four RCTs. Two trials from Botswana and South Africa of 4067 children who are HEU found no difference in mortality or infectious morbidity in children randomized to co‐trimoxazole prophylaxis started at 2–6 weeks of age compared to those randomized to placebo or no treatment, although event rates were low. Sub‐studies found that antimicrobial resistance was higher in infants receiving co‐trimoxazole. Two trials in Uganda investigating prolonged co‐trimoxazole after breastfeeding cessation showed protection against malaria but no other morbidity or mortality differences. All trials had some concerns or a high risk of bias, which limited the certainty of evidence.\n\n\nDiscussion\nStudies show no clinical benefit of co‐trimoxazole prophylaxis in children who are HEU, except to prevent malaria. Potential harms were identified for co‐trimoxazole prophylaxis leading to antimicrobial resistance. The trials in non‐malarial regions were conducted in populations with low mortality potentially reducing generalizability to other settings.\n\n\nConclusions\nIn low‐mortality settings with few HIV transmissions and well‐performing early infant diagnosis and treatment programmes, universal co‐trimoxazole may not be required.},\nauthor = {Wedderburn, Catherine J and Evans, Ceri and Slogrove, Amy L and Rehman, Andrea M and Gibb, Diana M and Prendergast, Andrew J and Penazzato, Martina},\ndoi = {10.1002/jia2.26079},\nfile = {:Users/jacquelinebracher/Zotero/storage/SUDRTH7M/Wedderburn et al. - 2023 - Co‐trimoxazole prophylaxis for children who are HI.pdf:pdf},\nissn = {1758-2652, 1758-2652},\njournal = {Journal of the International AIDS Society},\nmonth = {jun},\nnumber = {6},\npages = {e26079},\nshorttitle = {Co‐trimoxazole prophylaxis for children who are {\\{}H}}
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\n  Abstract Introduction Co‐trimoxazole prophylaxis is recommended for children born to women with HIV to protect those who acquire HIV from opportunistic infections, severe bacterial infections and malaria. With scale‐up of maternal antiretroviral therapy, most children remain HIV‐exposed uninfected (HEU) and the benefits of universal co‐trimoxazole are uncertain. We assessed the effect of co‐trimoxazole on mortality and morbidity of children who are HEU. Methods We performed a systematic review (PROSPERO number: CRD42021215059). We systematically searched MEDLINE, Embase, Cochrane CENTRAL, Global Health, CINAHL Plus, Africa‐Wide Information, SciELO and WHO Global Index Medicus for peer‐reviewed articles from inception to 4th January 2022 without limits. Ongoing randomized controlled trials (RCTs) were identified through registries. We included RCTs reporting mortality or morbidity in children who are HEU receiving co‐trimoxazole versus no prophylaxis/placebo. The risk of bias was assessed using the Cochrane 2.0 tool. Data were summarized using narrative synthesis and findings were stratified by malaria endemicity. Results We screened 1257 records and included seven reports from four RCTs. Two trials from Botswana and South Africa of 4067 children who are HEU found no difference in mortality or infectious morbidity in children randomized to co‐trimoxazole prophylaxis started at 2–6 weeks of age compared to those randomized to placebo or no treatment, although event rates were low. Sub‐studies found that antimicrobial resistance was higher in infants receiving co‐trimoxazole. Two trials in Uganda investigating prolonged co‐trimoxazole after breastfeeding cessation showed protection against malaria but no other morbidity or mortality differences. All trials had some concerns or a high risk of bias, which limited the certainty of evidence. Discussion Studies show no clinical benefit of co‐trimoxazole prophylaxis in children who are HEU, except to prevent malaria. Potential harms were identified for co‐trimoxazole prophylaxis leading to antimicrobial resistance. The trials in non‐malarial regions were conducted in populations with low mortality potentially reducing generalizability to other settings. Conclusions In low‐mortality settings with few HIV transmissions and well‐performing early infant diagnosis and treatment programmes, universal co‐trimoxazole may not be required.\n
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\n  \n\n  \n  \n  \n  \n  \n  .\n  \n  \n  \n\n\n  \n  Chesnut, R. M; Aguilera, S.; Buki, A.; Bulger, E. M; Citerio, G.; Cooper, D J.; Arrastia, R. D.; Diringer, M.; Figaji, A.; Gao, G.; Geocadin, R. G; Ghajar, J.; Harris, O.; Hawryluk, G. W J; Hoffer, A.; Hutchinson, P.; Joseph, M.; Kitagawa, R.; Manley, G.; Mayer, S.; Menon, D. K; Meyfroidt, G.; Michael, D. B; Oddo, M.; Okonkwo, D. O; Patel, M. B; Robertson, C.; Rosenfeld, J. V; Rubiano, A. M; Sahuquillo, J.; Servadei, F.; Shutter, L.; Stein, D. M; Stocchetti, N.; Taccone, F. S.; Timmons, S. D; Tsai, E. C; Ullman, J. S; Videtta, W.; Wright, D. W;  and Zammit, C.\n\n\n  \n\n\n\n  Neurosurgery, (2): 399–408. aug .\n  \n\n\n\n
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@article{chesnut_perceived_2023,\nabstract = {BACKGROUND:\nIntracranial pressure (ICP) monitoring is widely practiced, but the indications are incompletely developed, and guidelines are poorly followed.\n\n\nOBJECTIVE:\nTo study the monitoring practices of an established expert panel (the clinical working group from the Seattle International Brain Injury Consensus Conference effort) to examine the match between monitoring guidelines and their clinical decision-making and offer guidance for clinicians considering monitor insertion.\n\n\nMETHODS:\nWe polled the 42 Seattle International Brain Injury Consensus Conference panel members' ICP monitoring decisions for virtual patients, using matrices of presenting signs (Glasgow Coma Scale [GCS] total or GCS motor, pupillary examination, and computed tomography diagnosis). Monitor insertion decisions were yes, no, or unsure (traffic light approach). We analyzed their responses for weighting of the presenting signs in decision-making using univariate regression.\n\n\nRESULTS:\nHeatmaps constructed from the choices of 41 panel members revealed wider ICP monitor use than predicted by guidelines. Clinical examination (GCS) was by far the most important characteristic and differed from guidelines in being nonlinear. The modified Marshall computed tomography classification was second and pupils third. We constructed a heatmap and listed the main clinical determinants representing 80{\\%} ICP monitor insertion consensus for our recommendations.\n\n\nCONCLUSION:\nCandidacy for ICP monitoring exceeds published indicators for monitor insertion, suggesting the clinical perception that the value of ICP data is greater than simply detecting and monitoring severe intracranial hypertension. Monitor insertion heatmaps are offered as potential guidance for ICP monitor insertion and to stimulate research into what actually drives monitor insertion in unconstrained, real-world conditions.},\nauthor = {Chesnut, Randall M and Aguilera, Sergio and Buki, Andras and Bulger, Eileen M and Citerio, Giuseppe and Cooper, D Jamie and Arrastia, Ramon Diaz and Diringer, Michael and Figaji, Anthony and Gao, Guoyi and Geocadin, Romergryko G and Ghajar, Jamshid and Harris, Odette and Hawryluk, Gregory W J and Hoffer, Alan and Hutchinson, Peter and Joseph, Mathew and Kitagawa, Ryan and Manley, Geoffrey and Mayer, Stephan and Menon, David K and Meyfroidt, Geert and Michael, Daniel B and Oddo, Mauro and Okonkwo, David O and Patel, Mayur B and Robertson, Claudia and Rosenfeld, Jeffrey V and Rubiano, Andres M and Sahuquillo, Juain and Servadei, Franco and Shutter, Lori and Stein, Deborah M and Stocchetti, Nino and Taccone, Fabio Silvio and Timmons, Shelly D and Tsai, Eve C and Ullman, Jamie S and Videtta, Walter and Wright, David W and Zammit, Christopher},\ndoi = {10.1227/neu.0000000000002516},\nfile = {:Users/jacquelinebracher/Zotero/storage/5Q2WFPB4/Chesnut et al. - 2023 - Perceived Utility of Intracranial Pressure Monitor.pdf:pdf},\nissn = {0148-396X, 1524-4040},\njournal = {Neurosurgery},\nmonth = {aug},\nnumber = {2},\npages = {399--408},\nshorttitle = {Perceived {\\{}Utility{\\}} of {\\{}Intracranial{\\}} {\\{}Pressure{\\}} {\\{}}}
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\n  BACKGROUND: Intracranial pressure (ICP) monitoring is widely practiced, but the indications are incompletely developed, and guidelines are poorly followed. OBJECTIVE: To study the monitoring practices of an established expert panel (the clinical working group from the Seattle International Brain Injury Consensus Conference effort) to examine the match between monitoring guidelines and their clinical decision-making and offer guidance for clinicians considering monitor insertion. METHODS: We polled the 42 Seattle International Brain Injury Consensus Conference panel members' ICP monitoring decisions for virtual patients, using matrices of presenting signs (Glasgow Coma Scale [GCS] total or GCS motor, pupillary examination, and computed tomography diagnosis). Monitor insertion decisions were yes, no, or unsure (traffic light approach). We analyzed their responses for weighting of the presenting signs in decision-making using univariate regression. RESULTS: Heatmaps constructed from the choices of 41 panel members revealed wider ICP monitor use than predicted by guidelines. Clinical examination (GCS) was by far the most important characteristic and differed from guidelines in being nonlinear. The modified Marshall computed tomography classification was second and pupils third. We constructed a heatmap and listed the main clinical determinants representing 80% ICP monitor insertion consensus for our recommendations. CONCLUSION: Candidacy for ICP monitoring exceeds published indicators for monitor insertion, suggesting the clinical perception that the value of ICP data is greater than simply detecting and monitoring severe intracranial hypertension. Monitor insertion heatmaps are offered as potential guidance for ICP monitor insertion and to stimulate research into what actually drives monitor insertion in unconstrained, real-world conditions.\n
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\n  \n\n  \n  \n  \n  \n  \n  .\n  \n  \n  \n\n\n  \n  Lee, C.; Lin, C.; Koós, M.; Nagy, L.; Kraus, S. W; Demetrovics, Z.; Potenza, M. N; Ballester-Arnal, R.; Batthyány, D.; Bergeron, S.; Billieux, J.; Burkauskas, J.; Cárdenas-López, G.; Carvalho, J.; Castro-Calvo, J.; Chen, L.; Ciocca, G.; Corazza, O.; Csako, R. I; Fernandez, D. P; Fernandez, E. F; Fujiwara, H.; Fuss, J.; Gabrhelík, R.; Gewirtz-Meydan, A.; Gjoneska, B.; Gola, M.; Grubbs, J. B; Hashim, H. T; Islam, M. S.; Ismail, M.; Jiménez-Martínez, M.; Jurin, T.; Kalina, O.; Klein, V.; Költő, A.; Lee, S.; Lewczuk, K.; Lochner, C.; López-Alvarado, S.; Lukavská, K.; Mayta-Tristán, P.; Milea, I.; Miller, D. J; Orosová, O.; Orosz, G.; Ponce, F. P; Quintana, G. R; Garzola, G. C.; Ramos-Diaz, J.; Rigaud, K.; Rousseau, A.; Scanavino, M. D. T.; Schulmeyer, M. K; Sharan, P.; Shibata, M.; Shoib, S.; Sigre-Leirós, V.; Sniewski, L.; Spasovski, O.; Steibliene, V.; Stein, D. J; Strizek, J.; Ünsal, B. C; Vaillancourt-Morel, M.; Van Hout, M. C.;  and Bőthe, B.\n\n\n  \n\n\n\n  Journal of Psychiatric Research,16–27. sep .\n  \n\n\n\n
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@article{lee_eleven-item_2023,\nauthor = {Lee, Chih-Ting and Lin, Chung-Ying and Ko{\\'{o}}s, M{\\'{o}}nika and Nagy, L{\\'{e}}na and Kraus, Shane W and Demetrovics, Zsolt and Potenza, Marc N and Ballester-Arnal, Rafael and Batthy{\\'{a}}ny, Dominik and Bergeron, Sophie and Billieux, Jo{\\"{e}}l and Burkauskas, Julius and C{\\'{a}}rdenas-L{\\'{o}}pez, Georgina and Carvalho, Joana and Castro-Calvo, Jes{\\'{u}}s and Chen, Lijun and Ciocca, Giacomo and Corazza, Ornella and Csako, Rita I and Fernandez, David P and Fernandez, Elaine F and Fujiwara, Hironobu and Fuss, Johannes and Gabrhel{\\'{i}}k, Roman and Gewirtz-Meydan, Ateret and Gjoneska, Biljana and Gola, Mateusz and Grubbs, Joshua B and Hashim, Hashim T and Islam, Md. Saiful and Ismail, Mustafa and Jim{\\'{e}}nez-Mart{\\'{i}}nez, Martha and Jurin, Tanja and Kalina, Ondrej and Klein, Verena and K{\\"{o}}ltő, Andr{\\'{a}}s and Lee, Sang-Kyu and Lewczuk, Karol and Lochner, Christine and L{\\'{o}}pez-Alvarado, Silvia and Lukavsk{\\'{a}}, Kateřina and Mayta-Trist{\\'{a}}n, Percy and Milea, Ionut and Miller, Dan J and Orosov{\\'{a}}, Oľga and Orosz, G{\\'{a}}bor and Ponce, Fernando P and Quintana, Gonzalo R and Garzola, Gabriel C.Quintero and Ramos-Diaz, Jano and Rigaud, K{\\'{e}}vin and Rousseau, Ann and Scanavino, Marco De Tubino and Schulmeyer, Marion K and Sharan, Pratap and Shibata, Mami and Shoib, Sheikh and Sigre-Leir{\\'{o}}s, Vera and Sniewski, Luke and Spasovski, Ognen and Steibliene, Vesta and Stein, Dan J and Strizek, Julian and {\\"{U}}nsal, Berk C and Vaillancourt-Morel, Marie-Pier and {Van Hout}, Marie Claire and Bőthe, Be{\\'{a}}ta},\ndoi = {10.1016/j.jpsychires.2023.06.033},\nissn = {00223956},\njournal = {Journal of Psychiatric Research},\nmonth = {sep},\npages = {16--27},\nshorttitle = {The eleven-item {\\{}Alcohol{\\}}, {\\{}Smoking{\\}} and {\\{}Substanc}}
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\n  \n\n  \n  \n  \n  \n  \n  .\n  \n  \n  \n\n\n  \n  Haas, A. D; Lienhard, R.; Didden, C.; Cornell, M.; Folb, N.; Boshomane, T. M G; Salazar-Vizcaya, L.; Ruffieux, Y.; Nyakato, P.; Wettstein, A. E; Tlali, M.; Davies, M.; Von Groote, P.; Wainberg, M.; Egger, M.; Maartens, G.;  and Joska, J. A\n\n\n  \n\n\n\n  AIDS and Behavior, (6): 1849–1861. jun .\n  \n\n\n\n
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@article{haas_mental_2023,\nabstract = {Abstract\nWe followed adolescents and adults living with HIV aged older than 15 years who enrolled in a South African private-sector HIV programme to examine adherence and viral non-suppression (viral load {\\textgreater}400 copies/mL) of participants with (20,743, 38{\\%}) and without (33,635, 62{\\%}) mental health diagnoses. Mental health diagnoses were associated with unfavourable adherence patterns. The risk of viral non-suppression was higher among patients with organic mental disorders [adjusted risk ratio (aRR) 1.55, 95{\\%} confidence interval (CI) 1.22–1.96], substance use disorders (aRR 1.53, 95{\\%} CI 1.19–1.97), serious mental disorders (aRR 1.30, 95{\\%} CI 1.09–1.54), and depression (aRR 1.19, 95{\\%} CI 1.10–1.28) when compared with patients without mental health diagnoses. The risk of viral non-suppression was also higher among males, adolescents (15–19 years), and young adults (20–24 years). Our study highlights the need for psychosocial interventions to improve HIV treatment outcomes—particularly of adolescents and young adults—and supports strengthening mental health services in HIV treatment programmes.\n, \nResumen\nMonitoreamos adolescentes y adultos mayores de 15 a{\\~{n}}os que viven con VIH y que est{\\'{a}}n registrados en un programa privado Surafricano para el tratamiento del VIH. Nuestro prop{\\'{o}}sito fue examinar adherencia a los medicamentos y supresi{\\'{o}}n viral (carga viral {\\textless}400 copias/mL) en los participantes con (20,743, 38{\\%}) y sin (33,635, 62{\\%}) diagn{\\'{o}}sticos de salud mental. Los diagn{\\'{o}}sticos de salud mental estuvieron asociados con patrones de adherencia desfavorables. Comparados con pacientes sin diagn{\\'{o}}sticos de salud mental, el riesgo de no supresi{\\'{o}}n viral fue m{\\'{a}}s alto entre pacientes con des{\\'{o}}rdenes mentales org{\\'{a}}nicos [riesgo relativo ajustado (aRR) 1.55, 95{\\%} intervalo de confidencia (CI) 1.22–1.96], des{\\'{o}}rdenes en el uso de sustancias (aRR 1.53, 95{\\%} CI 1.19–1.97), des{\\'{o}}rdenes mentales serios (aRR 1.30, 95{\\%} CI 1.09–1.54), y depresi{\\'{o}}n (aRR 1.19, 95{\\%} CI 1.10–1.28). El riesgo de no supresi{\\'{o}}n viral tambi{\\'{e}}n fue m{\\'{a}}s alto en hombres que en mujeres, en adolescentes (15–19 a{\\~{n}}os), y en adultos j{\\'{o}}venes. Nuestro estudio resalta la necesidad de intervenciones psicosociales para mejorar los resultados del tratamiento contra el VIH –particularmente en adolescentes y adultos j{\\'{o}}venes—, y respalda el fortalecimiento de servicios de salud mental como parte de los programas para el tratamiento del VIH.},\nauthor = {Haas, Andreas D and Lienhard, Raphael and Didden, Christiane and Cornell, Morna and Folb, Naomi and Boshomane, Tebatso M G and Salazar-Vizcaya, Luisa and Ruffieux, Yann and Nyakato, Patience and Wettstein, Anja E and Tlali, Mpho and Davies, Mary-Ann and {Von Groote}, Per and Wainberg, Milton and Egger, Matthias and Maartens, Gary and Joska, John A},\ndoi = {10.1007/s10461-022-03916-x},\nfile = {:Users/jacquelinebracher/Zotero/storage/RNA79P3F/Haas et al. - 2023 - Mental Health, ART Adherence, and Viral Suppressio.pdf:pdf},\nissn = {1090-7165, 1573-3254},\njournal = {AIDS and Behavior},\nmonth = {jun},\nnumber = {6},\npages = {1849--1861},\nshorttitle = {Mental {\\{}Health{\\}}, {\\{}ART{\\}} {\\{}Adherence{\\}}, and {\\{}Viral{\\}} {\\{}S}}
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\n  Abstract We followed adolescents and adults living with HIV aged older than 15 years who enrolled in a South African private-sector HIV programme to examine adherence and viral non-suppression (viral load \\textgreater400 copies/mL) of participants with (20,743, 38%) and without (33,635, 62%) mental health diagnoses. Mental health diagnoses were associated with unfavourable adherence patterns. The risk of viral non-suppression was higher among patients with organic mental disorders [adjusted risk ratio (aRR) 1.55, 95% confidence interval (CI) 1.22–1.96], substance use disorders (aRR 1.53, 95% CI 1.19–1.97), serious mental disorders (aRR 1.30, 95% CI 1.09–1.54), and depression (aRR 1.19, 95% CI 1.10–1.28) when compared with patients without mental health diagnoses. The risk of viral non-suppression was also higher among males, adolescents (15–19 years), and young adults (20–24 years). Our study highlights the need for psychosocial interventions to improve HIV treatment outcomes—particularly of adolescents and young adults—and supports strengthening mental health services in HIV treatment programmes. , Resumen Monitoreamos adolescentes y adultos mayores de 15 años que viven con VIH y que están registrados en un programa privado Surafricano para el tratamiento del VIH. Nuestro propósito fue examinar adherencia a los medicamentos y supresión viral (carga viral \\textless400 copias/mL) en los participantes con (20,743, 38%) y sin (33,635, 62%) diagnósticos de salud mental. Los diagnósticos de salud mental estuvieron asociados con patrones de adherencia desfavorables. Comparados con pacientes sin diagnósticos de salud mental, el riesgo de no supresión viral fue más alto entre pacientes con desórdenes mentales orgánicos [riesgo relativo ajustado (aRR) 1.55, 95% intervalo de confidencia (CI) 1.22–1.96], desórdenes en el uso de sustancias (aRR 1.53, 95% CI 1.19–1.97), desórdenes mentales serios (aRR 1.30, 95% CI 1.09–1.54), y depresión (aRR 1.19, 95% CI 1.10–1.28). El riesgo de no supresión viral también fue más alto en hombres que en mujeres, en adolescentes (15–19 años), y en adultos jóvenes. Nuestro estudio resalta la necesidad de intervenciones psicosociales para mejorar los resultados del tratamiento contra el VIH –particularmente en adolescentes y adultos jóvenes—, y respalda el fortalecimiento de servicios de salud mental como parte de los programas para el tratamiento del VIH.\n
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\n  \n\n  \n  \n  \n  \n  \n  .\n  \n  \n  \n\n\n  \n  Roach, J. T; Qaddoumi, I.; Baticulon, R. E; Figaji, A.; Campos, D. A; Arredondo, L.; Boop, F. A;  and Moreira, D. C\n\n\n  \n\n\n\n  JCO Global Oncology, (9): e2200402. jan .\n  \n\n\n\n
\n\n\n\n  \n\n  \n  \n    doi\n   \n  \n\n  \n  link\n   \n  \n\n  bibtex\n    \n\n  \n   \n  \n    abstract \n  \n\n  \n\n  \n  \n  \n  \n  \n  \n  \n\n   \n  \n  \n\n\n\n
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@article{roach_pediatric_2023,\nabstract = {PURPOSE\nEfforts to address inequities in the treatment of pediatric CNS tumors and the burden of childhood cancer globally have prompted the designation of low-grade glioma as one of six index cancers for the World Health Organization Global Initiative for Childhood Cancer. Understanding the importance of neurosurgical interventions and evaluating pediatric neurosurgical capacity may identify critical interventions to improve outcomes for children with low-grade glioma and other CNS tumors.\n\n\nMETHODS\nAn online, cross-sectional survey assessing pediatric neurosurgical practice and capacity was distributed to members of the International Society of Pediatric Neurosurgery. The survey included 36 items covering domains including patient volume, available infrastructure, scope of practice, case distribution, and multidisciplinary care.\n\n\nRESULTS\nResponses from 196 individuals from 61 countries, spanning all WHO regions, were included. Ninety-six (49.0{\\%}) were from high-income countries, 57 (29.1{\\%}) were from upper-middle–income countries, 42 (21.4{\\%}) were from lower-middle–income countries (LMICs), and 1 was (0.5{\\%}) from a low-income country. Most respondents had a catchment population of ≥ 1 million and indicated the availability of basic neurosurgical resources such as a dedicated neurosurgical operating theater and surgical microscope. The presence of a neurosurgical intensive care unit, inpatient rehabilitation services, and infection monitoring showed similar availability across country groups. Quantitative scoring of 13 infrastructure and service items established that fewer resources were available in low-income countries/LMICs and upper-middle–income countries compared with high-income countries. The volume of pediatric CNS tumor cases and case distribution did not vary according to World Bank country groups.\n\n\nCONCLUSION\nThis study provides a comprehensive evaluation of pediatric neurosurgical capacity across the globe, establishing variability of resources on the basis of the country income level. Our findings suggest that pediatric neurosurgeons in LMICs may benefit from key neurosurgical instrumentation and increased support for multidisciplinary brain tumor programs and childhood cancer research efforts.},\nauthor = {Roach, Jordan T and Qaddoumi, Ibrahim and Baticulon, Ronnie E and Figaji, Anthony and Campos, Danny A and Arredondo, Luis and Boop, Frederick A and Moreira, Daniel C},\ndoi = {10.1200/GO.22.00402},\nissn = {2687-8941},\njournal = {JCO Global Oncology},\nmonth = {jan},\nnumber = {9},\npages = {e2200402},\nshorttitle = {Pediatric {\\{}Neurosurgical{\\}} {\\{}Capacity{\\}} for the {\\{}Care}}
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\n  PURPOSE Efforts to address inequities in the treatment of pediatric CNS tumors and the burden of childhood cancer globally have prompted the designation of low-grade glioma as one of six index cancers for the World Health Organization Global Initiative for Childhood Cancer. Understanding the importance of neurosurgical interventions and evaluating pediatric neurosurgical capacity may identify critical interventions to improve outcomes for children with low-grade glioma and other CNS tumors. METHODS An online, cross-sectional survey assessing pediatric neurosurgical practice and capacity was distributed to members of the International Society of Pediatric Neurosurgery. The survey included 36 items covering domains including patient volume, available infrastructure, scope of practice, case distribution, and multidisciplinary care. RESULTS Responses from 196 individuals from 61 countries, spanning all WHO regions, were included. Ninety-six (49.0%) were from high-income countries, 57 (29.1%) were from upper-middle–income countries, 42 (21.4%) were from lower-middle–income countries (LMICs), and 1 was (0.5%) from a low-income country. Most respondents had a catchment population of ≥ 1 million and indicated the availability of basic neurosurgical resources such as a dedicated neurosurgical operating theater and surgical microscope. The presence of a neurosurgical intensive care unit, inpatient rehabilitation services, and infection monitoring showed similar availability across country groups. Quantitative scoring of 13 infrastructure and service items established that fewer resources were available in low-income countries/LMICs and upper-middle–income countries compared with high-income countries. The volume of pediatric CNS tumor cases and case distribution did not vary according to World Bank country groups. CONCLUSION This study provides a comprehensive evaluation of pediatric neurosurgical capacity across the globe, establishing variability of resources on the basis of the country income level. Our findings suggest that pediatric neurosurgeons in LMICs may benefit from key neurosurgical instrumentation and increased support for multidisciplinary brain tumor programs and childhood cancer research efforts.\n
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\n  \n\n  \n  \n  \n  \n  \n  .\n  \n  \n  \n\n\n  \n  Stein, D. J;  and Hartford, A.\n\n\n  \n\n\n\n  Current Opinion in Behavioral Sciences,101151. aug .\n  \n\n\n\n
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@article{stein_health-policy_2022,\nauthor = {Stein, Dan J and Hartford, Anna},\ndoi = {10.1016/j.cobeha.2022.101151},\nissn = {23521546},\njournal = {Current Opinion in Behavioral Sciences},\nmonth = {aug},\npages = {101151},\nshorttitle = {Health-policy approaches for problematic {\\{}Internet}}
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\n  \n\n  \n  \n  \n  \n  \n  .\n  \n  \n  \n\n\n  \n  Treder, M. S; Shock, J. P; Stein, D. J; Du Plessis, S.; Seedat, S.;  and Tsvetanov, K. A\n\n\n  \n\n\n\n  Frontiers in Psychiatry,615754. feb .\n  \n\n\n\n
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@article{treder_correlation_2021,\nabstract = {In neuroimaging, the difference between chronological age and predicted brain age, also known as\nbrain age delta\n, has been proposed as a pathology marker linked to a range of phenotypes. Brain age delta is estimated using regression, which involves a frequently observed bias due to a negative correlation between chronological age and brain age delta. In brain age prediction models, this correlation can manifest as an overprediction of the age of young brains and an underprediction for elderly ones. We show that this bias can be controlled for by adding correlation constraints to the model training procedure. We develop an analytical solution to this constrained optimization problem for Linear, Ridge, and Kernel Ridge regression. The solution is optimal in the least-squares sense i.e., there is no other model that satisfies the correlation constraints and has a better fit. Analyses on the PAC2019 competition data demonstrate that this approach produces optimal unbiased predictive models with a number of advantages over existing approaches. Finally, we introduce regression toolboxes for Python and MATLAB that implement our algorithm.},\nauthor = {Treder, Matthias S and Shock, Jonathan P and Stein, Dan J and {Du Plessis}, St{\\'{e}}fan and Seedat, Soraya and Tsvetanov, Kamen A},\ndoi = {10.3389/fpsyt.2021.615754},\nfile = {:Users/jacquelinebracher/Zotero/storage/8VRPBWXU/Treder et al. - 2021 - Correlation Constraints for Regression Models Con.pdf:pdf},\nissn = {1664-0640},\njournal = {Frontiers in Psychiatry},\nmonth = {feb},\npages = {615754},\nshorttitle = {Correlation {\\{}Constraints{\\}} for {\\{}Regression{\\}} {\\{}Models}}
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\n  In neuroimaging, the difference between chronological age and predicted brain age, also known as brain age delta , has been proposed as a pathology marker linked to a range of phenotypes. Brain age delta is estimated using regression, which involves a frequently observed bias due to a negative correlation between chronological age and brain age delta. In brain age prediction models, this correlation can manifest as an overprediction of the age of young brains and an underprediction for elderly ones. We show that this bias can be controlled for by adding correlation constraints to the model training procedure. We develop an analytical solution to this constrained optimization problem for Linear, Ridge, and Kernel Ridge regression. The solution is optimal in the least-squares sense i.e., there is no other model that satisfies the correlation constraints and has a better fit. Analyses on the PAC2019 competition data demonstrate that this approach produces optimal unbiased predictive models with a number of advantages over existing approaches. Finally, we introduce regression toolboxes for Python and MATLAB that implement our algorithm.\n
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\n  \n\n  \n  \n  \n  \n  \n  .\n  \n  \n  \n\n\n  \n  Rabie, S.; Tomlinson, M.; Almirol, E.; Stewart, J.; Skiti, Z.; Weiss, R. E; Vogel, L.;  and Rotheram-Borus, M. J.\n\n\n  \n\n\n\n  AIDS and Behavior, (3): 842–854. mar .\n  \n\n\n\n
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@article{rabie_utilizing_2023,\nabstract = {Abstract\nYoung men in South Africa face the intersecting epidemics of HIV, substance use and endemic poverty. We tested the effectiveness of a behavioral intervention using soccer training to reduce the cluster of risks associated with HIV and substance use. This cluster randomized controlled trial was conducted with men aged 18–29 years old in 27 neighborhoods in the townships of Cape Town, South Africa. Neighborhoods were randomized to receive for 6 months either: (1) Soccer League (SL; n = 18 neighborhoods, n = 778 men) who attended soccer three times weekly (72 sessions; 94{\\%} uptake, 45.5{\\%} weekly attendance rate), combined with an HIV/substance use, cognitive-behavioral intervention; or (2) a Control Condition (CC; n = 9; 415 men) who received educational materials and referrals at 3 month intervals. The primary outcome was the number of significant changes in a cluster of outcomes including HIV-related risks, substance abuse, employment/income, mental health, violence, and community engagement. There was only one significant difference on the rapid diagnostic tests for mandrax at 6 months, an insufficient number of changes to indicate a successful intervention. A group-based behavioral intervention was ineffective in addressing multiple risk behaviors among at-risk young men, similar to the findings of several recent soccer-related interventions. Early adulthood may be too late to alter well-established patterns of risk behaviors.\n\nClinical Trial Registration\nThis trial was prospectively registered on 24 November 2014 with ClinicalTrials.gov NCT02358226.},\nauthor = {Rabie, Stephan and Tomlinson, Mark and Almirol, Ellen and Stewart, Jackie and Skiti, Zwelibanzi and Weiss, Robert E and Vogel, Lodewyk and Rotheram-Borus, Mary Jane},\ndoi = {10.1007/s10461-022-03819-x},\nfile = {:Users/jacquelinebracher/Zotero/storage/74ZAZT3Y/Rabie et al. - 2023 - Utilizing Soccer for Delivery of HIV and Substance.pdf:pdf},\nissn = {1090-7165, 1573-3254},\njournal = {AIDS and Behavior},\nmonth = {mar},\nnumber = {3},\npages = {842--854},\nshorttitle = {Utilizing {\\{}Soccer{\\}} for {\\{}Delivery{\\}} of {\\{}HIV{\\}} and {\\{}Su}}
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\n  Abstract Young men in South Africa face the intersecting epidemics of HIV, substance use and endemic poverty. We tested the effectiveness of a behavioral intervention using soccer training to reduce the cluster of risks associated with HIV and substance use. This cluster randomized controlled trial was conducted with men aged 18–29 years old in 27 neighborhoods in the townships of Cape Town, South Africa. Neighborhoods were randomized to receive for 6 months either: (1) Soccer League (SL; n = 18 neighborhoods, n = 778 men) who attended soccer three times weekly (72 sessions; 94% uptake, 45.5% weekly attendance rate), combined with an HIV/substance use, cognitive-behavioral intervention; or (2) a Control Condition (CC; n = 9; 415 men) who received educational materials and referrals at 3 month intervals. The primary outcome was the number of significant changes in a cluster of outcomes including HIV-related risks, substance abuse, employment/income, mental health, violence, and community engagement. There was only one significant difference on the rapid diagnostic tests for mandrax at 6 months, an insufficient number of changes to indicate a successful intervention. A group-based behavioral intervention was ineffective in addressing multiple risk behaviors among at-risk young men, similar to the findings of several recent soccer-related interventions. Early adulthood may be too late to alter well-established patterns of risk behaviors. Clinical Trial Registration This trial was prospectively registered on 24 November 2014 with ClinicalTrials.gov NCT02358226.\n
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\n  \n\n  \n  \n  \n  \n  \n  .\n  \n  \n  \n\n\n  \n  Dennis, E. L; Caeyenberghs, K.; Hoskinson, K. R; Merkley, T. L; Suskauer, S. J; Asarnow, R. F; Babikian, T.; Bartnik-Olson, B.; Bickart, K.; Bigler, E. D; Ewing-Cobbs, L.; Figaji, A.; Giza, C. C; Goodrich-Hunsaker, N. J; Hodges, C. B; Hovenden, E. S; Irimia, A.; Königs, M.; Levin, H. S; Lindsey, H. M; Max, J. E; Newsome, M. R; Olsen, A.; Ryan, N. P; Schmidt, A. T; Spruiell, M. S; Wade, B. S C; Ware, A. L; Watson, C. G; Wheeler, A. L; Yeates, K. O.; Zielinski, B. A; Kochunov, P.; Jahanshad, N.; Thompson, P. M; Tate, D. F;  and Wilde, E. A\n\n\n  \n\n\n\n  Neurology, (3): e298—-e309. jul .\n  \n\n\n\n
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@article{dennis_white_2021,\nabstract = {Objective\nOur study addressed aims (1) to test the hypothesis that moderate-severe traumatic brain injury (TBI) in pediatric patients is associated with widespread white matter (WM) disruption, (2) to test the hypothesis that age and sex affect WM organization after injury, and (3) to examine associations between WM organization and neurobehavioral outcomes.\n\n\nMethods\nData from 10 previously enrolled, existing cohorts recruited from local hospitals and clinics were shared with the Enhancing NeuroImaging Genetics Through Meta-Analysis (ENIGMA) Pediatric Moderate/Severe TBI (msTBI) working group. We conducted a coordinated analysis of diffusion MRI (dMRI) data using the ENIGMA dMRI processing pipeline.\n\n\nResults\nFive hundred seven children and adolescents (244 with complicated msTBI and 263 controls) were included. Patients were clustered into 3 postinjury intervals: acute/subacute, {\\textless}2 months; postacute, 2 to 6 months; and chronic, ≥6 months. Outcomes were dMRI metrics and postinjury behavioral problems as indexed by the Child Behavior Checklist. Our analyses revealed altered WM diffusion metrics across multiple tracts and all postinjury intervals (effect sizes range d = −0.5 to −1.3). Injury severity is a significant contributor to the extent of WM alterations but explained less variance in dMRI measures with increasing time after injury. We observed a sex-by-group interaction: female patients with TBI had significantly lower fractional anisotropy in the uncinate fasciculus than controls ($\\beta$ = 0.043), which coincided with more parent-reported behavioral problems ($\\beta$ = −0.0027).\n\n\nConclusions\nWM disruption after msTBI is widespread, persistent, and influenced by demographic and clinical variables. Future work will test techniques for harmonizing neurocognitive data, enabling more advanced analyses to identify symptom clusters and clinically meaningful patient subtypes.},\nauthor = {Dennis, Emily L and Caeyenberghs, Karen and Hoskinson, Kristen R and Merkley, Tricia L and Suskauer, Stacy J and Asarnow, Robert F and Babikian, Talin and Bartnik-Olson, Brenda and Bickart, Kevin and Bigler, Erin D and Ewing-Cobbs, Linda and Figaji, Anthony and Giza, Christopher C and Goodrich-Hunsaker, Naomi J and Hodges, Cooper B and Hovenden, Elizabeth S and Irimia, Andrei and K{\\"{o}}nigs, Marsh and Levin, Harvey S and Lindsey, Hannah M and Max, Jeffrey E and Newsome, Mary R and Olsen, Alexander and Ryan, Nicholas P and Schmidt, Adam T and Spruiell, Matthew S and Wade, Benjamin S C and Ware, Ashley L and Watson, Christopher G and Wheeler, Anne L and Yeates, Keith Owen and Zielinski, Brandon A and Kochunov, Peter and Jahanshad, Neda and Thompson, Paul M and Tate, David F and Wilde, Elisabeth A},\ndoi = {10.1212/WNL.0000000000012222},\nfile = {:Users/jacquelinebracher/Zotero/storage/S6ME3ZWC/Dennis et al. - 2021 - White Matter Disruption in Pediatric Traumatic Bra.pdf:pdf},\nissn = {0028-3878, 1526-632X},\njournal = {Neurology},\nmonth = {jul},\nnumber = {3},\npages = {e298----e309},\nshorttitle = {White {\\{}Matter{\\}} {\\{}Disruption{\\}} in {\\{}Pediatric{\\}} {\\{}Trauma}}
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\n  Objective Our study addressed aims (1) to test the hypothesis that moderate-severe traumatic brain injury (TBI) in pediatric patients is associated with widespread white matter (WM) disruption, (2) to test the hypothesis that age and sex affect WM organization after injury, and (3) to examine associations between WM organization and neurobehavioral outcomes. Methods Data from 10 previously enrolled, existing cohorts recruited from local hospitals and clinics were shared with the Enhancing NeuroImaging Genetics Through Meta-Analysis (ENIGMA) Pediatric Moderate/Severe TBI (msTBI) working group. We conducted a coordinated analysis of diffusion MRI (dMRI) data using the ENIGMA dMRI processing pipeline. Results Five hundred seven children and adolescents (244 with complicated msTBI and 263 controls) were included. Patients were clustered into 3 postinjury intervals: acute/subacute, \\textless2 months; postacute, 2 to 6 months; and chronic, ≥6 months. Outcomes were dMRI metrics and postinjury behavioral problems as indexed by the Child Behavior Checklist. Our analyses revealed altered WM diffusion metrics across multiple tracts and all postinjury intervals (effect sizes range d = −0.5 to −1.3). Injury severity is a significant contributor to the extent of WM alterations but explained less variance in dMRI measures with increasing time after injury. We observed a sex-by-group interaction: female patients with TBI had significantly lower fractional anisotropy in the uncinate fasciculus than controls ($β$ = 0.043), which coincided with more parent-reported behavioral problems ($β$ = −0.0027). Conclusions WM disruption after msTBI is widespread, persistent, and influenced by demographic and clinical variables. Future work will test techniques for harmonizing neurocognitive data, enabling more advanced analyses to identify symptom clusters and clinically meaningful patient subtypes.\n
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\n  \n\n  \n  \n  \n  \n  \n  .\n  \n  \n  \n\n\n  \n  Gecaite-Stonciene, J.; Lochner, C.; Marincowitz, C.; Fineberg, N. A;  and Stein, D. J\n\n\n  \n\n\n\n  Frontiers in Psychiatry,646030. mar .\n  \n\n\n\n
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@article{gecaite-stonciene_obsessive-compulsive_2021,\nabstract = {Introduction:\nWith the shift from a categorical to a dimensional model, ICD-11 has made substantial changes to the diagnosis of personality disorders (PDs), including obsessive-compulsive (anankastic) personality disorder (OCPD). The ICD-11 PD model proposes a single diagnosis of PD with specifications regarding severity and domains. However, a systematic overview of ICD-11 anankastia is lacking. In this review we address the reformulation of the OCPD diagnosis in the ICD-11, and draw comparisons with the DSM-5, with a particular focus on diagnostic validity and clinical utility. We hypothesized that the ICD-11 PD model provides a diagnostically valid and clinically useful approach to OCPD, with specific emphasis on the anankastia domain as the primary trait qualifier.\n\n\nMethods:\nLiterature published from 2010 to 2020 was systematically searched using the PubMed/MEDLINE, PsychInfo, Cochrane, and Web of Sciences search engines, in order to find all articles that addressed ICD-11 anankastia. Relevant articles were collated, and themes of these articles subsequently extracted.\n\n\nResults:\nOut of the 264 publications identified, 19 articles were included in this review. Four themes were identified, namely (a) overlap of DSM-5 OCPD with the ICD-11 PD model, (b) the factorial structure of the ICD-11 PD model with respect to the anankastia domain, (c) the clinical utility of the ICD-11 PD model, and (d) comparison of the ICD-11 PD model of anankastia with the DSM-5 alternative model for OCPD.\n\n\nConclusions:\nThe ICD-11 anankastia domain overlaps with DSM-5 OCPD traits, and the factor analyses of the ICD-11 PD model further support the diagnostic validity of this domain. There is some support for the clinical utility of the ICD-11 PD model of anankastia but further studies are needed, including of its relationship to obsessive-compulsive and related disorders.},\nauthor = {Gecaite-Stonciene, Julija and Lochner, Christine and Marincowitz, Clara and Fineberg, Naomi A and Stein, Dan J},\ndoi = {10.3389/fpsyt.2021.646030},\nfile = {:Users/jacquelinebracher/Zotero/storage/D9UAU96M/Gecaite-Stonciene et al. - 2021 - Obsessive-Compulsive (Anankastic) Personality Diso.pdf:pdf},\nissn = {1664-0640},\njournal = {Frontiers in Psychiatry},\nmonth = {mar},\npages = {646030},\nshorttitle = {Obsessive-{\\{}Compulsive{\\}} ({\\{}Anankastic{\\}}) {\\{}Personality}}
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\n  Introduction: With the shift from a categorical to a dimensional model, ICD-11 has made substantial changes to the diagnosis of personality disorders (PDs), including obsessive-compulsive (anankastic) personality disorder (OCPD). The ICD-11 PD model proposes a single diagnosis of PD with specifications regarding severity and domains. However, a systematic overview of ICD-11 anankastia is lacking. In this review we address the reformulation of the OCPD diagnosis in the ICD-11, and draw comparisons with the DSM-5, with a particular focus on diagnostic validity and clinical utility. We hypothesized that the ICD-11 PD model provides a diagnostically valid and clinically useful approach to OCPD, with specific emphasis on the anankastia domain as the primary trait qualifier. Methods: Literature published from 2010 to 2020 was systematically searched using the PubMed/MEDLINE, PsychInfo, Cochrane, and Web of Sciences search engines, in order to find all articles that addressed ICD-11 anankastia. Relevant articles were collated, and themes of these articles subsequently extracted. Results: Out of the 264 publications identified, 19 articles were included in this review. Four themes were identified, namely (a) overlap of DSM-5 OCPD with the ICD-11 PD model, (b) the factorial structure of the ICD-11 PD model with respect to the anankastia domain, (c) the clinical utility of the ICD-11 PD model, and (d) comparison of the ICD-11 PD model of anankastia with the DSM-5 alternative model for OCPD. Conclusions: The ICD-11 anankastia domain overlaps with DSM-5 OCPD traits, and the factor analyses of the ICD-11 PD model further support the diagnostic validity of this domain. There is some support for the clinical utility of the ICD-11 PD model of anankastia but further studies are needed, including of its relationship to obsessive-compulsive and related disorders.\n
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\n  \n\n  \n  \n  \n  \n  \n  .\n  \n  \n  \n\n\n  \n  Yahya, I.; Hockman, D.; Brand-Saberi, B.;  and Morosan-Puopolo, G.\n\n\n  \n\n\n\n  Biology, (8): 1245. aug .\n  \n\n\n\n
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@article{yahya_new_2022,\nabstract = {Branchiomeric skeletal muscles are a subset of head muscles originating from skeletal muscle progenitor cells in the mesodermal core of pharyngeal arches. These muscles are involved in facial expression, mastication, and function of the larynx and pharynx. Branchiomeric muscles have been the focus of many studies over the years due to their distinct developmental programs and common origin with the heart muscle. A prerequisite for investigating these muscles' properties and therapeutic potential is understanding their genetic program and differentiation. In contrast to our understanding of how branchiomeric muscles are formed, less is known about their differentiation. This review focuses on the differentiation of branchiomeric muscles in mouse embryos. Furthermore, the relationship between branchiomeric muscle progenitor and neural crest cells in the pharyngeal arches of chicken embryos is also discussed. Additionally, we summarize recent studies into the genetic networks that distinguish between first arch-derived muscles and other pharyngeal arch muscles.},\nauthor = {Yahya, Imadeldin and Hockman, Dorit and Brand-Saberi, Beate and Morosan-Puopolo, Gabriela},\ndoi = {10.3390/biology11081245},\nfile = {:Users/jacquelinebracher/Zotero/storage/EG74QKHH/Yahya et al. - 2022 - New Insights into the Diversity of Branchiomeric M.pdf:pdf},\nissn = {2079-7737},\njournal = {Biology},\nmonth = {aug},\nnumber = {8},\npages = {1245},\nshorttitle = {New {\\{}Insights{\\}} into the {\\{}Diversity{\\}} of {\\{}Branchiome}}
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\n  Branchiomeric skeletal muscles are a subset of head muscles originating from skeletal muscle progenitor cells in the mesodermal core of pharyngeal arches. These muscles are involved in facial expression, mastication, and function of the larynx and pharynx. Branchiomeric muscles have been the focus of many studies over the years due to their distinct developmental programs and common origin with the heart muscle. A prerequisite for investigating these muscles' properties and therapeutic potential is understanding their genetic program and differentiation. In contrast to our understanding of how branchiomeric muscles are formed, less is known about their differentiation. This review focuses on the differentiation of branchiomeric muscles in mouse embryos. Furthermore, the relationship between branchiomeric muscle progenitor and neural crest cells in the pharyngeal arches of chicken embryos is also discussed. Additionally, we summarize recent studies into the genetic networks that distinguish between first arch-derived muscles and other pharyngeal arch muscles.\n
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\n  \n\n  \n  \n  \n  \n  \n  .\n  \n  \n  \n\n\n  \n  Hathorn, S. K.; Lochner, C.; Stein, D. J;  and Bantjes, J.\n\n\n  \n\n\n\n  Frontiers in Psychiatry,733773. sep .\n  \n\n\n\n
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@article{hathorn_help-seeking_2021,\nabstract = {Introduction:\nMany individuals with obsessive-compulsive disorder (OCD) delay seeking help, leading to greater illness severity, additional comorbidity, and increased functional impairment. Patterns of help-seeking for OCD have however not yet been described in South Africa, a low-and middle-income country with many health service challenges. Using the health belief model as a conceptual framework, study aims were to identify predictors of and barriers to help-seeking among South Africans with OCD.\n\n\nMethods:\nFifty adults with OCD completed an online survey to assess (1) socio-demographic characteristics, (2) OCD symptom severity, (3) treatment barriers, (4) perceived treatment benefits, (5) self-efficacy, and (6) help-seeking intention. Multiple linear regression analysis was used to establish predictors of help-seeking intention. Descriptive statistics were used to determine the most endorsed help-seeking barriers.\n\n\nResults:\n42.6{\\%} of the variance in help-seeking intention was explained by the investigated constructs (\nR\n2\n= 0.426,\nF\n= 4.45 and\np\n{\\textless} 0.01). Perceived treatment benefits were the only significant predictor of help-seeking intention (\nB\n= 1.37,\nt\n= 5.16, and\np\n{\\textless} 0.01). More than a third (36{\\%}) of the sample endorsed wanting to handle the problem independently as a significant barrier, followed by treatment concerns (26{\\%}), affordability (22{\\%}), and shame (20{\\%}).\n\n\nConclusion:\nAn innovative analysis of help-seeking patterns suggested that perceived treatment benefits were the only significant predictor of help-seeking intention among South African adults with OCD. Psychoeducation and mental health literacy programmes may be useful in increasing public appreciation of the benefits of OCD treatment, and in mitigating key help-seeking barriers.},\nauthor = {Hathorn, Sarah Kate and Lochner, Christine and Stein, Dan J and Bantjes, Jason},\ndoi = {10.3389/fpsyt.2021.733773},\nfile = {:Users/jacquelinebracher/Zotero/storage/ZMYY4TAV/Hathorn et al. - 2021 - Help-Seeking Intention in Obsessive-Compulsive Dis.pdf:pdf},\nissn = {1664-0640},\njournal = {Frontiers in Psychiatry},\nmonth = {sep},\npages = {733773},\nshorttitle = {Help-{\\{}Seeking{\\}} {\\{}Intention{\\}} in {\\{}Obsessive{\\}}-{\\{}Compuls}}
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\n  Introduction: Many individuals with obsessive-compulsive disorder (OCD) delay seeking help, leading to greater illness severity, additional comorbidity, and increased functional impairment. Patterns of help-seeking for OCD have however not yet been described in South Africa, a low-and middle-income country with many health service challenges. Using the health belief model as a conceptual framework, study aims were to identify predictors of and barriers to help-seeking among South Africans with OCD. Methods: Fifty adults with OCD completed an online survey to assess (1) socio-demographic characteristics, (2) OCD symptom severity, (3) treatment barriers, (4) perceived treatment benefits, (5) self-efficacy, and (6) help-seeking intention. Multiple linear regression analysis was used to establish predictors of help-seeking intention. Descriptive statistics were used to determine the most endorsed help-seeking barriers. Results: 42.6% of the variance in help-seeking intention was explained by the investigated constructs ( R 2 = 0.426, F = 4.45 and p \\textless 0.01). Perceived treatment benefits were the only significant predictor of help-seeking intention ( B = 1.37, t = 5.16, and p \\textless 0.01). More than a third (36%) of the sample endorsed wanting to handle the problem independently as a significant barrier, followed by treatment concerns (26%), affordability (22%), and shame (20%). Conclusion: An innovative analysis of help-seeking patterns suggested that perceived treatment benefits were the only significant predictor of help-seeking intention among South African adults with OCD. Psychoeducation and mental health literacy programmes may be useful in increasing public appreciation of the benefits of OCD treatment, and in mitigating key help-seeking barriers.\n
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\n  \n\n  \n  \n  \n  \n  \n  .\n  \n  \n  \n\n\n  \n  Giovenco, D.; Pettifor, A.; Bekker, L.; Filiatreau, L. M; Liu, T.; Akande, M.; Gill, K.; Atujuna, M.; Stein, D. J;  and Kuo, C.\n\n\n  \n\n\n\n  AIDS and Behavior, (6): 1906–1913. jun .\n  \n\n\n\n
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@article{giovenco_understanding_2023,\nauthor = {Giovenco, Danielle and Pettifor, Audrey and Bekker, Linda-Gail and Filiatreau, Lindsey M and Liu, Tao and Akande, Morayo and Gill, Katherine and Atujuna, Millicent and Stein, Dan J and Kuo, Caroline},\ndoi = {10.1007/s10461-022-03924-x},\nfile = {:Users/jacquelinebracher/Zotero/storage/77L9B35A/Giovenco et al. - 2023 - Understanding Oral Prep Interest Among South Afric.pdf:pdf},\nissn = {1090-7165, 1573-3254},\njournal = {AIDS and Behavior},\nmonth = {jun},\nnumber = {6},\npages = {1906--1913},\nshorttitle = {Understanding {\\{}Oral{\\}} {\\{}Prep{\\}} {\\{}Interest{\\}} {\\{}Among{\\}} {\\{}So}}
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