@article{achtyes_ulotaront_2023,
	title = {Ulotaront: review of preliminary evidence for the efficacy and safety of a {TAAR1} agonist in schizophrenia},
	issn = {1433-8491},
	shorttitle = {Ulotaront},
	url = {https://doi.org/10.1007/s00406-023-01580-3},
	doi = {10.1007/s00406-023-01580-3},
	abstract = {Ulotaront is a trace amine-associated receptor 1 (TAAR1) agonist in Phase 3 clinical development for the treatment of schizophrenia. Ulotaront was discovered through a unique, target-agnostic approach optimized to identify drug candidates lacking D2 and 5-HT2A receptor antagonism, while demonstrating an antipsychotic-like phenotypic profile in vivo. The mechanism of action (MOA) of ulotaront is thought to be mediated by agonism at TAAR1 and serotonin 5-HT1A receptors. Ulotaront has completed two Phase 2 trials (4-week acute study and 26-week open-label extension) which led to Breakthrough Therapy Designation from the US Food and Drug Administration for the treatment of schizophrenia. In the double-blind, placebo-controlled, acute study, ulotaront was associated with significant (p {\textless} 0.001) improvement in Positive and Negative Syndrome Scale (PANSS) total score (effect size [ES]: 0.45), with improvements vs. placebo also observed across secondary endpoints. Post-hoc analyses of the acute trial revealed additional evidence to support the effect of ulotaront on negative symptoms. In the 4-week study, ulotaront was well-tolerated, with an incidence of adverse events (AEs) numerically lower compared to placebo (45.8\% vs. 50.4\%; with a number needed to harm [NNH] for individual ulotaront AEs all {\textgreater} 40). The open-label extension demonstrated further improvement across schizophrenia symptoms and confirmed the tolerability of ulotaront, with a 6-month completion rate of 67\%. Based on current data, ulotaront shows potential to be a first-in-class TAAR1 agonist for the treatment of schizophrenia with a safety and efficacy profile distinct from current antipsychotics.},
	language = {en},
	urldate = {2023-07-19},
	journal = {European Archives of Psychiatry and Clinical Neuroscience},
	author = {Achtyes, Eric D. and Hopkins, Seth C. and Dedic, Nina and Dworak, Heather and Zeni, Courtney and Koblan, Kenneth},
	month = may,
	year = {2023},
	keywords = {Schizophrenia, Serotonin 5-HT1A, Trace amine-associated receptor 1},
}

Ulotaront is a trace amine-associated receptor 1 (TAAR1) agonist in Phase 3 clinical development for the treatment of schizophrenia. Ulotaront was discovered through a unique, target-agnostic approach optimized to identify drug candidates lacking D2 and 5-HT2A receptor antagonism, while demonstrating an antipsychotic-like phenotypic profile in vivo. The mechanism of action (MOA) of ulotaront is thought to be mediated by agonism at TAAR1 and serotonin 5-HT1A receptors. Ulotaront has completed two Phase 2 trials (4-week acute study and 26-week open-label extension) which led to Breakthrough Therapy Designation from the US Food and Drug Administration for the treatment of schizophrenia. In the double-blind, placebo-controlled, acute study, ulotaront was associated with significant (p \textless 0.001) improvement in Positive and Negative Syndrome Scale (PANSS) total score (effect size [ES]: 0.45), with improvements vs. placebo also observed across secondary endpoints. Post-hoc analyses of the acute trial revealed additional evidence to support the effect of ulotaront on negative symptoms. In the 4-week study, ulotaront was well-tolerated, with an incidence of adverse events (AEs) numerically lower compared to placebo (45.8% vs. 50.4%; with a number needed to harm [NNH] for individual ulotaront AEs all \textgreater 40). The open-label extension demonstrated further improvement across schizophrenia symptoms and confirmed the tolerability of ulotaront, with a 6-month completion rate of 67%. Based on current data, ulotaront shows potential to be a first-in-class TAAR1 agonist for the treatment of schizophrenia with a safety and efficacy profile distinct from current antipsychotics.

@misc{wells_important_2023,
	title = {Important information --- next week's {Virtual} {Becoming} a {Next}-{Gen} {Science} {Teacher} session},
	author = {Wells, Andrea},
	collaborator = {{"Walker} and {Britny"} and Morley, Heather and Boutiette, Kirsten and {saracat23@gmail.com}},
	month = jun,
	year = {2023},
}

@misc{noauthor_two_2022,
	title = {Two large studies reveal genes and genome regions that influence schizophrenia risk},
	url = {https://www.broadinstitute.org/news/two-large-studies-reveal-genes-and-genome-regions-influence-schizophrenia-risk},
	abstract = {International collaborations analyze common and rare DNA variants in hundreds of thousands of people, further elucidating genetic roots of psychiatric disorder},
	language = {en},
	urldate = {2022-04-09},
	journal = {Broad Institute},
	month = apr,
	year = {2022},
	note = {Section: Research News},
}

International collaborations analyze common and rare DNA variants in hundreds of thousands of people, further elucidating genetic roots of psychiatric disorder

@misc{noauthor_results_2022,
	title = {Results {\textbar} {SCHEMA} browser},
	url = {https://schema.broadinstitute.org/results},
	urldate = {2022-05-05},
	month = may,
	year = {2022},
}

@article{barron_doors_2022,
	title = {The doors of precision: {Reenergizing} psychiatric drug development with psychedelics and open access computational tools},
	volume = {8},
	issn = {2375-2548},
	shorttitle = {The doors of precision},
	url = {https://www.science.org/doi/10.1126/sciadv.abp8283},
	doi = {10.1126/sciadv.abp8283},
	abstract = {Psychedelics paired with new applications of computational tools might help bypass the imprecision of psychiatric diagnosis and connect measures of behavior to specific physiologic targets.},
	language = {en},
	number = {11},
	urldate = {2022-05-25},
	journal = {Science Advances},
	author = {Barron, Daniel S. and Friedman, Richard A.},
	month = mar,
	year = {2022},
	note = {Number: 11},
	pages = {eabp8283},
}

Psychedelics paired with new applications of computational tools might help bypass the imprecision of psychiatric diagnosis and connect measures of behavior to specific physiologic targets.

@article{lago_druggable_2022,
	title = {The druggable schizophrenia genome: from repurposing opportunities to unexplored drug targets},
	volume = {7},
	copyright = {2022 The Author(s)},
	issn = {2056-7944},
	shorttitle = {The druggable schizophrenia genome},
	url = {https://www.nature.com/articles/s41525-022-00290-4},
	doi = {10.1038/s41525-022-00290-4},
	abstract = {There have been no new drugs for the treatment of schizophrenia in several decades and treatment resistance represents a major unmet clinical need. The drugs that exist are based on serendipitous clinical observations rather than an evidence-based understanding of disease pathophysiology. In the present review, we address these bottlenecks by integrating common, rare, and expression-related schizophrenia risk genes with knowledge of the druggability of the human genome as a whole. We highlight novel drug repurposing opportunities, clinical trial candidates which are supported by genetic evidence, and unexplored therapeutic opportunities in the lesser-known regions of the schizophrenia genome. By identifying translational gaps and opportunities across the schizophrenia disease space, we discuss a framework for translating increasingly well-powered genetic association studies into personalized treatments for schizophrenia and initiating the vital task of characterizing clinically relevant drug targets in underexplored regions of the human genome.},
	language = {en},
	number = {1},
	urldate = {2022-05-27},
	journal = {npj Genomic Medicine},
	author = {Lago, Santiago G. and Bahn, Sabine},
	month = mar,
	year = {2022},
	note = {Number: 1
Publisher: Nature Publishing Group},
	keywords = {Genome, Pharmaceutics, Schizophrenia, Target identification},
	pages = {1--13},
}

There have been no new drugs for the treatment of schizophrenia in several decades and treatment resistance represents a major unmet clinical need. The drugs that exist are based on serendipitous clinical observations rather than an evidence-based understanding of disease pathophysiology. In the present review, we address these bottlenecks by integrating common, rare, and expression-related schizophrenia risk genes with knowledge of the druggability of the human genome as a whole. We highlight novel drug repurposing opportunities, clinical trial candidates which are supported by genetic evidence, and unexplored therapeutic opportunities in the lesser-known regions of the schizophrenia genome. By identifying translational gaps and opportunities across the schizophrenia disease space, we discuss a framework for translating increasingly well-powered genetic association studies into personalized treatments for schizophrenia and initiating the vital task of characterizing clinically relevant drug targets in underexplored regions of the human genome.

@article{barron_doors_2022-1,
	title = {The doors of precision: {Reenergizing} psychiatric drug development with psychedelics and open access computational tools},
	volume = {8},
	issn = {2375-2548},
	shorttitle = {The doors of precision},
	url = {https://www.science.org/doi/10.1126/sciadv.abp8283},
	doi = {10.1126/sciadv.abp8283},
	abstract = {Psychedelics paired with new applications of computational tools might help bypass the imprecision of psychiatric diagnosis and connect measures of behavior to specific physiologic targets.},
	language = {en},
	number = {11},
	urldate = {2022-05-29},
	journal = {Science Advances},
	author = {Barron, Daniel S. and Friedman, Richard A.},
	month = mar,
	year = {2022},
	note = {Number: 11},
	pages = {eabp8283},
}

Psychedelics paired with new applications of computational tools might help bypass the imprecision of psychiatric diagnosis and connect measures of behavior to specific physiologic targets.

@misc{noauthor_candidates_2022,
	title = {Candidates for {Drug} {Repurposing} to {Address} the {Cognitive} {Symptoms} in {Schizophrenia} {\textbar} {bioRxiv}},
	url = {https://www.biorxiv.org/content/10.1101/2022.03.07.483231v1},
	urldate = {2022-05-29},
	month = may,
	year = {2022},
}

@incollection{talevi_drug_2022,
	address = {Cham},
	series = {Computer-{Aided} {Drug} {Discovery} and {Design}},
	title = {Drug {Discovery} {Paradigms}: {Phenotypic}-{Based} {Drug} {Discovery}},
	isbn = {978-3-030-95895-4},
	shorttitle = {Drug {Discovery} {Paradigms}},
	url = {https://doi.org/10.1007/978-3-030-95895-4_2},
	abstract = {A drug discovery and development project typically starts with the identification of novel active scaffolds, i.e., core chemical structures with a desired biological effect. Beyond serendipitous discoveries and findings based on ethnopharmacology/traditional medicine, drug discovery in the modern age has been guided by two fundamental screening philosophies (implemented whether through in silico, in vitro or less often, in vivo approximations). Occasionally, novel chemotypes can be designed de novo by searching for complementary features to a binding site in a predefined drug target. Historically, systematic screening for new active compounds comprised phenotypic screening assays (e.g., against a collection of microorganisms, animal models of disease, or cellular models). Later, the interest of the pharmaceutical companies experienced a substantial shift toward target-focused approximations in which exquisitely selective compounds were sought, usually through high-throughput screening. There, the test compounds were typically confronted with some biological entity, usually a protein, to identify those which could modulate such biomolecule. Nevertheless, as target-focused approximation failed to deliver the expectations, especially when pursuing therapies for complex disorders, renewed interest in phenotypic screening was observed in the pharmaceutical community, supported by a network pharmacology paradigm, high-content screening, small animal models, and organoids and other advanced cell culture platforms.},
	language = {en},
	urldate = {2022-05-29},
	booktitle = {Drug {Target} {Selection} and {Validation}},
	publisher = {Springer International Publishing},
	author = {Talevi, Alan and Bellera, Carolina L.},
	editor = {Scotti, Marcus T. and Bellera, Carolina L.},
	year = {2022},
	doi = {10.1007/978-3-030-95895-4_2},
	keywords = {Drug discovery, High-content analysis, High-content screening (HCS), High-throughput screening, Hit identification, Phenotypic screening, Target deconvolution, Target-focused approximations},
	pages = {25--40},
}

A drug discovery and development project typically starts with the identification of novel active scaffolds, i.e., core chemical structures with a desired biological effect. Beyond serendipitous discoveries and findings based on ethnopharmacology/traditional medicine, drug discovery in the modern age has been guided by two fundamental screening philosophies (implemented whether through in silico, in vitro or less often, in vivo approximations). Occasionally, novel chemotypes can be designed de novo by searching for complementary features to a binding site in a predefined drug target. Historically, systematic screening for new active compounds comprised phenotypic screening assays (e.g., against a collection of microorganisms, animal models of disease, or cellular models). Later, the interest of the pharmaceutical companies experienced a substantial shift toward target-focused approximations in which exquisitely selective compounds were sought, usually through high-throughput screening. There, the test compounds were typically confronted with some biological entity, usually a protein, to identify those which could modulate such biomolecule. Nevertheless, as target-focused approximation failed to deliver the expectations, especially when pursuing therapies for complex disorders, renewed interest in phenotypic screening was observed in the pharmaceutical community, supported by a network pharmacology paradigm, high-content screening, small animal models, and organoids and other advanced cell culture platforms.

@techreport{koch_candidates_2022,
	type = {preprint},
	title = {Candidates for {Drug} {Repurposing} to {Address} the {Cognitive} {Symptoms} in {Schizophrenia}},
	url = {http://biorxiv.org/lookup/doi/10.1101/2022.03.07.483231},
	abstract = {In the protein-protein interactome, we have previously identified a significant overlap between schizophrenia risk genes and genes associated with cognitive performance. Here, we further studied this overlap to identify potential candidate drugs for repurposing to treat the cognitive symptoms in schizophrenia. We first defined a cognition-related schizophrenia interactome from network propagation analyses, and identified drugs known to target more than one protein within this network. Thereafter, we used gene expression data to further select drugs that could counteract schizophrenia-associated gene expression perturbations. Additionally, we stratified these analyses by sex to identify sex-specific pharmacological treatment options for the cognitive symptoms in schizophrenia. After excluding drugs contraindicated in schizophrenia, we identified eight drug candidates, most of which have anti-inflammatory and neuroprotective effects. Due to gene expression differences in male and female patients, four of those drugs were also selected in our male-specific analyses, and the other four in the female-specific analyses. Based on our bioinformatics analyses of disease genetics, we suggest eight candidate drugs that warrant further examination for repurposing to treat the cognitive symptoms in schizophrenia, and suggest that these symptoms could be addressed by sex-specific pharmacological treatment options.},
	language = {en},
	urldate = {2022-05-31},
	institution = {Genetics},
	author = {Koch, Elise and Kauppi, Karolina and Chen, Chi-Hua},
	month = mar,
	year = {2022},
	doi = {10.1101/2022.03.07.483231},
}

In the protein-protein interactome, we have previously identified a significant overlap between schizophrenia risk genes and genes associated with cognitive performance. Here, we further studied this overlap to identify potential candidate drugs for repurposing to treat the cognitive symptoms in schizophrenia. We first defined a cognition-related schizophrenia interactome from network propagation analyses, and identified drugs known to target more than one protein within this network. Thereafter, we used gene expression data to further select drugs that could counteract schizophrenia-associated gene expression perturbations. Additionally, we stratified these analyses by sex to identify sex-specific pharmacological treatment options for the cognitive symptoms in schizophrenia. After excluding drugs contraindicated in schizophrenia, we identified eight drug candidates, most of which have anti-inflammatory and neuroprotective effects. Due to gene expression differences in male and female patients, four of those drugs were also selected in our male-specific analyses, and the other four in the female-specific analyses. Based on our bioinformatics analyses of disease genetics, we suggest eight candidate drugs that warrant further examination for repurposing to treat the cognitive symptoms in schizophrenia, and suggest that these symptoms could be addressed by sex-specific pharmacological treatment options.

@article{xiao_vitro_2022,
	title = {In {Vitro} {ADME} and {Preclinical} {Pharmacokinetics} of {Ulotaront}, a {TAAR1}/5-{HT1A} {Receptor} {Agonist} for the {Treatment} of {Schizophrenia}},
	volume = {39},
	issn = {1573-904X},
	doi = {10.1007/s11095-022-03267-1},
	abstract = {PURPOSE: Ulotaront (SEP-363856) is a TAAR1 agonist with 5-HT1A agonist activity currently in clinical development for the treatment of schizophrenia. The objectives of the current study were to characterize the in vitro ADME properties, preclinical PK, and to evaluate the DDI potential of ulotaront and its major metabolite SEP-383103.
METHODS: Solubility, permeability, plasma protein binding, CYP inhibition and induction, transporter inhibition and uptake studies were conducted in vitro. Phenotyping studies were conducted using recombinant human CYPs and FMOs, human liver microsomes and human liver homogenates. Preclinical plasma and brain pharmacokinetics were determined after a single intraperitoneal, intravenous, and oral administration of ulotaront.
RESULTS: Ulotaront is a compound of high solubility, high permeability, and low binding to plasma proteins. Ulotaront metabolism is mediated via both NADPH-dependent and NADPH-independent pathways, with CYP2D6 as the major metabolizing enzyme. Ulotaront is an inducer of CYP2B6, and an inhibitor of CYP2D6, OCT1 and OCT2, while SEP-383103 is neither a CYP inducer nor a potent inhibitor of CYPs and human transporters. Ulotaront exhibits rapid absorption, greater than 70\% bioavailability, approximately 3.5 L/kg volume of distribution, 1.5-4 h half-life, 12-43 ml/min/kg clearance, and good penetration across the blood-brain barrier in preclinical species.
CONCLUSIONS: Ulotaront has been designated as a BCS1 compound by US FDA. The ability of ulotaront to penetrate the blood-brain barrier for CNS targeting has been demonstrated in mice and rats. The potential for ulotaront and SEP-383103 to act as perpetrators of CYP and transporter-mediated DDIs is predicted to be remote.},
	language = {eng},
	number = {5},
	journal = {Pharmaceutical Research},
	author = {Xiao, Guangqing and Chen, Yu-Luan and Dedic, Nina and Xie, Linghong and Koblan, Kenneth S. and Galluppi, Gerald R.},
	month = may,
	year = {2022},
	pmid = {35484370},
	note = {Number: 5},
	keywords = {Animals, CYP2D6, Cytochrome P-450 CYP2D6, Cytochrome P-450 Enzyme System, Mice, Microsomes, Liver, NADP, Pharmaceutical Preparations, Rats, Receptor, Serotonin, 5-HT1A, Schizophrenia, TAAR1, blood–brain barrier, drug-drug interactions, phenotyping, ulotaront},
	pages = {837--850},
}

PURPOSE: Ulotaront (SEP-363856) is a TAAR1 agonist with 5-HT1A agonist activity currently in clinical development for the treatment of schizophrenia. The objectives of the current study were to characterize the in vitro ADME properties, preclinical PK, and to evaluate the DDI potential of ulotaront and its major metabolite SEP-383103. METHODS: Solubility, permeability, plasma protein binding, CYP inhibition and induction, transporter inhibition and uptake studies were conducted in vitro. Phenotyping studies were conducted using recombinant human CYPs and FMOs, human liver microsomes and human liver homogenates. Preclinical plasma and brain pharmacokinetics were determined after a single intraperitoneal, intravenous, and oral administration of ulotaront. RESULTS: Ulotaront is a compound of high solubility, high permeability, and low binding to plasma proteins. Ulotaront metabolism is mediated via both NADPH-dependent and NADPH-independent pathways, with CYP2D6 as the major metabolizing enzyme. Ulotaront is an inducer of CYP2B6, and an inhibitor of CYP2D6, OCT1 and OCT2, while SEP-383103 is neither a CYP inducer nor a potent inhibitor of CYPs and human transporters. Ulotaront exhibits rapid absorption, greater than 70% bioavailability, approximately 3.5 L/kg volume of distribution, 1.5-4 h half-life, 12-43 ml/min/kg clearance, and good penetration across the blood-brain barrier in preclinical species. CONCLUSIONS: Ulotaront has been designated as a BCS1 compound by US FDA. The ability of ulotaront to penetrate the blood-brain barrier for CNS targeting has been demonstrated in mice and rats. The potential for ulotaront and SEP-383103 to act as perpetrators of CYP and transporter-mediated DDIs is predicted to be remote.

@article{nair_trace_2022,
	title = {Trace {Amine}-{Associated} {Receptor} 1 ({TAAR1}): {Molecular} and {Clinical} {Insights} for the {Treatment} of {Schizophrenia} and {Related} {Comorbidities}},
	volume = {5},
	shorttitle = {Trace {Amine}-{Associated} {Receptor} 1 ({TAAR1})},
	url = {https://doi.org/10.1021/acsptsci.2c00016},
	doi = {10.1021/acsptsci.2c00016},
	abstract = {Schizophrenia is a complex and severe mental illness. Current treatments for schizophrenia typically modulate dopaminergic neurotransmission by D2-receptor blockade. While reducing positive symptoms of schizophrenia, current antipsychotic drugs have little clinical effect on negative symptoms and cognitive impairments. For the last few decades, discovery efforts have sought nondopaminergic compounds with the aim to effectively treat the broad symptoms of schizophrenia. In this viewpoint, we provide an overview on trace-amine associated receptor-1 (TAAR1), which presents a clinically validated nondopaminergic target for treating schizophrenia and related disorders, with significantly less overall side-effect burden. TAAR1 agonists may also be specifically beneficial for the substance abuse comorbidity and metabolic syndrome that is often present in patients with schizophrenia.},
	number = {3},
	urldate = {2022-07-11},
	journal = {ACS Pharmacology \& Translational Science},
	author = {Nair, Pramod C. and Chalker, Justin M. and McKinnon, Ross A. and Langmead, Christopher J and Gregory, Karen J. and Bastiampillai, Tarun},
	month = mar,
	year = {2022},
	note = {Number: 3
Publisher: American Chemical Society},
	pages = {183--188},
}

Schizophrenia is a complex and severe mental illness. Current treatments for schizophrenia typically modulate dopaminergic neurotransmission by D2-receptor blockade. While reducing positive symptoms of schizophrenia, current antipsychotic drugs have little clinical effect on negative symptoms and cognitive impairments. For the last few decades, discovery efforts have sought nondopaminergic compounds with the aim to effectively treat the broad symptoms of schizophrenia. In this viewpoint, we provide an overview on trace-amine associated receptor-1 (TAAR1), which presents a clinically validated nondopaminergic target for treating schizophrenia and related disorders, with significantly less overall side-effect burden. TAAR1 agonists may also be specifically beneficial for the substance abuse comorbidity and metabolic syndrome that is often present in patients with schizophrenia.

@misc{noauthor_redefining_2022,
	title = {Redefining the standard of care for brain disorders {\textbar} {MapLight} {Therapeutics}},
	url = {https://maplightrx.com/},
	abstract = {Targeted treatment for Autism Spectrum Disorder, Parkinson’s Disease and Schizophrenia.},
	language = {en-US},
	urldate = {2022-07-11},
	journal = {MapLight},
	month = jul,
	year = {2022},
}

Targeted treatment for Autism Spectrum Disorder, Parkinson’s Disease and Schizophrenia.

@article{arnovitz_mdma_2022,
	title = {{MDMA} for the {Treatment} of {Negative} {Symptoms} in {Schizophrenia}},
	volume = {11},
	copyright = {http://creativecommons.org/licenses/by/3.0/},
	issn = {2077-0383},
	url = {https://www.mdpi.com/2077-0383/11/12/3255},
	doi = {10.3390/jcm11123255},
	abstract = {The profound economic burden of schizophrenia is due, in part, to the negative symptoms of the disease, which can severely limit daily functioning. There is much debate in the field regarding their measurement and classification and there are no FDA-approved treatments for negative symptoms despite an abundance of research. 3,4-Methylenedioxy methamphetamine (MDMA) is a schedule I substance that has emerged as a novel therapeutic given its ability to enhance social interactions, generate empathy, and induce a state of metaplasticity in the brain. This review provides a rationale for the use of MDMA in the treatment of negative symptoms by reviewing the literature on negative symptoms, their treatment, MDMA, and MDMA-assisted therapy. It reviews recent evidence that supports the safe and potentially effective use of MDMA to treat negative symptoms and concludes with considerations regarding safety and possible mechanisms of action.},
	language = {en},
	number = {12},
	urldate = {2022-07-12},
	journal = {Journal of Clinical Medicine},
	author = {Arnovitz, Mitchell D. and Spitzberg, Andrew J. and Davani, Ashkhan J. and Vadhan, Nehal P. and Holland, Julie and Kane, John M. and Michaels, Timothy I.},
	month = jan,
	year = {2022},
	note = {Number: 12},
	keywords = {MDMA, negative symptoms, psychedelic-assisted therapy, psychosis, schizophrenia},
	pages = {3255},
}

The profound economic burden of schizophrenia is due, in part, to the negative symptoms of the disease, which can severely limit daily functioning. There is much debate in the field regarding their measurement and classification and there are no FDA-approved treatments for negative symptoms despite an abundance of research. 3,4-Methylenedioxy methamphetamine (MDMA) is a schedule I substance that has emerged as a novel therapeutic given its ability to enhance social interactions, generate empathy, and induce a state of metaplasticity in the brain. This review provides a rationale for the use of MDMA in the treatment of negative symptoms by reviewing the literature on negative symptoms, their treatment, MDMA, and MDMA-assisted therapy. It reviews recent evidence that supports the safe and potentially effective use of MDMA to treat negative symptoms and concludes with considerations regarding safety and possible mechanisms of action.

@misc{noauthor_dysconnection_2022,
	title = {The dysconnection hypothesis (2016) {\textbar} {Elsevier} {Enhanced} {Reader}},
	url = {https://reader.elsevier.com/reader/sd/pii/S0920996416303310?token=3C3ADD40DC9C8F4000D822B8662E2D2DEEE4C390849A44CAE342B4DDD5C1EFDDFB034F4124C352B1BD3815573AA0C902&originRegion=us-east-1&originCreation=20220724184006},
	language = {en},
	urldate = {2022-07-24},
	month = jul,
	year = {2022},
	doi = {10.1016/j.schres.2016.07.014},
}

@article{spark_beyond_2022,
	title = {Beyond antipsychotics: a twenty-first century update for preclinical development of schizophrenia therapeutics},
	volume = {12},
	copyright = {2022 The Author(s)},
	issn = {2158-3188},
	shorttitle = {Beyond antipsychotics},
	url = {https://www.nature.com/articles/s41398-022-01904-2},
	doi = {10.1038/s41398-022-01904-2},
	abstract = {Despite 50+ years of drug discovery, current antipsychotics have limited efficacy against negative and cognitive symptoms of schizophrenia, and are ineffective—with the exception of clozapine—against any symptom domain for patients who are treatment resistant. Novel therapeutics with diverse non-dopamine D2 receptor targets have been explored extensively in clinical trials, yet often fail due to a lack of efficacy despite showing promise in preclinical development. This lack of translation between preclinical and clinical efficacy suggests a systematic failure in current methods that determine efficacy in preclinical rodent models. In this review, we critically evaluate rodent models and behavioural tests used to determine preclinical efficacy, and look to clinical research to provide a roadmap for developing improved translational measures. We highlight the dependence of preclinical models and tests on dopamine-centric theories of dysfunction and how this has contributed towards a self-reinforcing loop away from clinically meaningful predictions of efficacy. We review recent clinical findings of distinct dopamine-mediated dysfunction of corticostriatal circuits in patients with treatment-resistant vs. non-treatment-resistant schizophrenia and suggest criteria for establishing rodent models to reflect such differences, with a focus on objective, translational measures. Finally, we review current schizophrenia drug discovery and propose a framework where preclinical models are validated against objective, clinically informed measures and preclinical tests of efficacy map onto those used clinically.},
	language = {en},
	number = {1},
	urldate = {2022-07-24},
	journal = {Translational Psychiatry},
	author = {Spark, Daisy L. and Fornito, Alex and Langmead, Christopher J. and Stewart, Gregory D.},
	month = apr,
	year = {2022},
	note = {Number: 1
Publisher: Nature Publishing Group},
	keywords = {Molecular neuroscience, Predictive markers},
	pages = {1--11},
}

Despite 50+ years of drug discovery, current antipsychotics have limited efficacy against negative and cognitive symptoms of schizophrenia, and are ineffective—with the exception of clozapine—against any symptom domain for patients who are treatment resistant. Novel therapeutics with diverse non-dopamine D2 receptor targets have been explored extensively in clinical trials, yet often fail due to a lack of efficacy despite showing promise in preclinical development. This lack of translation between preclinical and clinical efficacy suggests a systematic failure in current methods that determine efficacy in preclinical rodent models. In this review, we critically evaluate rodent models and behavioural tests used to determine preclinical efficacy, and look to clinical research to provide a roadmap for developing improved translational measures. We highlight the dependence of preclinical models and tests on dopamine-centric theories of dysfunction and how this has contributed towards a self-reinforcing loop away from clinically meaningful predictions of efficacy. We review recent clinical findings of distinct dopamine-mediated dysfunction of corticostriatal circuits in patients with treatment-resistant vs. non-treatment-resistant schizophrenia and suggest criteria for establishing rodent models to reflect such differences, with a focus on objective, translational measures. Finally, we review current schizophrenia drug discovery and propose a framework where preclinical models are validated against objective, clinically informed measures and preclinical tests of efficacy map onto those used clinically.

@misc{noauthor_impact_2022,
	title = {Impact of {GPCR} {Structures} on {Drug} {Discovery} - {ScienceDirect}},
	url = {https://www.sciencedirect.com/science/article/pii/S0092867420302658#mmc4},
	urldate = {2022-07-25},
	month = jul,
	year = {2022},
}

@article{arnovitz_mdma_2022-1,
	title = {{MDMA} for the {Treatment} of {Negative} {Symptoms} in {Schizophrenia}},
	volume = {11},
	copyright = {http://creativecommons.org/licenses/by/3.0/},
	issn = {2077-0383},
	url = {https://www.mdpi.com/2077-0383/11/12/3255},
	doi = {10.3390/jcm11123255},
	abstract = {The profound economic burden of schizophrenia is due, in part, to the negative symptoms of the disease, which can severely limit daily functioning. There is much debate in the field regarding their measurement and classification and there are no FDA-approved treatments for negative symptoms despite an abundance of research. 3,4-Methylenedioxy methamphetamine (MDMA) is a schedule I substance that has emerged as a novel therapeutic given its ability to enhance social interactions, generate empathy, and induce a state of metaplasticity in the brain. This review provides a rationale for the use of MDMA in the treatment of negative symptoms by reviewing the literature on negative symptoms, their treatment, MDMA, and MDMA-assisted therapy. It reviews recent evidence that supports the safe and potentially effective use of MDMA to treat negative symptoms and concludes with considerations regarding safety and possible mechanisms of action.},
	language = {en},
	number = {12},
	urldate = {2022-08-10},
	journal = {Journal of Clinical Medicine},
	author = {Arnovitz, Mitchell D. and Spitzberg, Andrew J. and Davani, Ashkhan J. and Vadhan, Nehal P. and Holland, Julie and Kane, John M. and Michaels, Timothy I.},
	month = jan,
	year = {2022},
	note = {Number: 12
Publisher: Multidisciplinary Digital Publishing Institute},
	keywords = {MDMA, negative symptoms, psychedelic-assisted therapy, psychosis, schizophrenia},
	pages = {3255},
}

The profound economic burden of schizophrenia is due, in part, to the negative symptoms of the disease, which can severely limit daily functioning. There is much debate in the field regarding their measurement and classification and there are no FDA-approved treatments for negative symptoms despite an abundance of research. 3,4-Methylenedioxy methamphetamine (MDMA) is a schedule I substance that has emerged as a novel therapeutic given its ability to enhance social interactions, generate empathy, and induce a state of metaplasticity in the brain. This review provides a rationale for the use of MDMA in the treatment of negative symptoms by reviewing the literature on negative symptoms, their treatment, MDMA, and MDMA-assisted therapy. It reviews recent evidence that supports the safe and potentially effective use of MDMA to treat negative symptoms and concludes with considerations regarding safety and possible mechanisms of action.

@article{spark_beyond_2022-1,
	title = {Beyond antipsychotics: a twenty-first century update for preclinical development of schizophrenia therapeutics},
	volume = {12},
	copyright = {2022 The Author(s)},
	issn = {2158-3188},
	shorttitle = {Beyond antipsychotics},
	url = {https://www.nature.com/articles/s41398-022-01904-2},
	doi = {10.1038/s41398-022-01904-2},
	abstract = {Despite 50+ years of drug discovery, current antipsychotics have limited efficacy against negative and cognitive symptoms of schizophrenia, and are ineffective—with the exception of clozapine—against any symptom domain for patients who are treatment resistant. Novel therapeutics with diverse non-dopamine D2 receptor targets have been explored extensively in clinical trials, yet often fail due to a lack of efficacy despite showing promise in preclinical development. This lack of translation between preclinical and clinical efficacy suggests a systematic failure in current methods that determine efficacy in preclinical rodent models. In this review, we critically evaluate rodent models and behavioural tests used to determine preclinical efficacy, and look to clinical research to provide a roadmap for developing improved translational measures. We highlight the dependence of preclinical models and tests on dopamine-centric theories of dysfunction and how this has contributed towards a self-reinforcing loop away from clinically meaningful predictions of efficacy. We review recent clinical findings of distinct dopamine-mediated dysfunction of corticostriatal circuits in patients with treatment-resistant vs. non-treatment-resistant schizophrenia and suggest criteria for establishing rodent models to reflect such differences, with a focus on objective, translational measures. Finally, we review current schizophrenia drug discovery and propose a framework where preclinical models are validated against objective, clinically informed measures and preclinical tests of efficacy map onto those used clinically.},
	language = {en},
	number = {1},
	urldate = {2022-08-10},
	journal = {Translational Psychiatry},
	author = {Spark, Daisy L. and Fornito, Alex and Langmead, Christopher J. and Stewart, Gregory D.},
	month = apr,
	year = {2022},
	note = {Number: 1
Publisher: Nature Publishing Group},
	keywords = {Molecular neuroscience, Predictive markers},
	pages = {1--11},
}

Despite 50+ years of drug discovery, current antipsychotics have limited efficacy against negative and cognitive symptoms of schizophrenia, and are ineffective—with the exception of clozapine—against any symptom domain for patients who are treatment resistant. Novel therapeutics with diverse non-dopamine D2 receptor targets have been explored extensively in clinical trials, yet often fail due to a lack of efficacy despite showing promise in preclinical development. This lack of translation between preclinical and clinical efficacy suggests a systematic failure in current methods that determine efficacy in preclinical rodent models. In this review, we critically evaluate rodent models and behavioural tests used to determine preclinical efficacy, and look to clinical research to provide a roadmap for developing improved translational measures. We highlight the dependence of preclinical models and tests on dopamine-centric theories of dysfunction and how this has contributed towards a self-reinforcing loop away from clinically meaningful predictions of efficacy. We review recent clinical findings of distinct dopamine-mediated dysfunction of corticostriatal circuits in patients with treatment-resistant vs. non-treatment-resistant schizophrenia and suggest criteria for establishing rodent models to reflect such differences, with a focus on objective, translational measures. Finally, we review current schizophrenia drug discovery and propose a framework where preclinical models are validated against objective, clinically informed measures and preclinical tests of efficacy map onto those used clinically.

@misc{noauthor_inflammatory_2022,
	title = {Inflammatory bowel disease-associated gene set projecte {\textbar} {Open}-i},
	url = {https://openi.nlm.nih.gov/detailedresult?img=PMC4251289_fphar-05-00252-g003&query=multiscale%20neuron&it=xg&req=4&npos=52},
	urldate = {2022-08-16},
	month = aug,
	year = {2022},
}

@misc{noauthor_manual_2022,
	title = {Manual {\textbar} {ApiNATOMY} {Lyph} {Viewer}},
	url = {http://open-physiology-viewer-docs.surge.sh/},
	urldate = {2022-09-12},
	month = sep,
	year = {2022},
}

@article{sapienza_schizophrenia_2022,
	title = {Schizophrenia and psychedelic state: {Dysconnection} versus hyper-connection. {A} perspective on two different models of psychosis stemming from dysfunctional integration processes},
	issn = {1476-5578},
	shorttitle = {Schizophrenia and psychedelic state},
	doi = {10.1038/s41380-022-01721-5},
	abstract = {Psychotic symptoms are a cross-sectional dimension affecting multiple diagnostic categories, despite schizophrenia represents the prototype of psychoses. Initially, dopamine was considered the most involved molecule in the neurobiology of schizophrenia. Over the next years, several biological factors were added to the discussion helping to constitute the concept of schizophrenia as a disease marked by a deficit of functional integration, contributing to the formulation of the Dysconnection Hypothesis in 1995. Nowadays the notion of dysconnection persists in the conceptualization of schizophrenia enriched by neuroimaging findings which corroborate the hypothesis. At the same time, in recent years, psychedelics received a lot of attention by the scientific community and astonishing findings emerged about the rearrangement of brain networks under the effect of these compounds. Specifically, a global decrease in functional connectivity was found, highlighting the disintegration of preserved and functional circuits and an increase of overall connectivity in the brain. The aim of this paper is to compare the biological bases of dysconnection in schizophrenia with the alterations of neuronal cyto-architecture induced by psychedelics and the consequent state of cerebral hyper-connection. These two models of psychosis, despite diametrically opposed, imply a substantial deficit of integration of neural signaling reached through two opposite paths.},
	language = {eng},
	journal = {Molecular Psychiatry},
	author = {Sapienza, Jacopo and Bosia, Marta and Spangaro, Marco and Martini, Francesca and Agostoni, Giulia and Cuoco, Federica and Cocchi, Federica and Cavallaro, Roberto},
	month = aug,
	year = {2022},
	pmid = {35931756},
	note = {1 citations (Semantic Scholar/DOI) [2023-01-12]},
}

Psychotic symptoms are a cross-sectional dimension affecting multiple diagnostic categories, despite schizophrenia represents the prototype of psychoses. Initially, dopamine was considered the most involved molecule in the neurobiology of schizophrenia. Over the next years, several biological factors were added to the discussion helping to constitute the concept of schizophrenia as a disease marked by a deficit of functional integration, contributing to the formulation of the Dysconnection Hypothesis in 1995. Nowadays the notion of dysconnection persists in the conceptualization of schizophrenia enriched by neuroimaging findings which corroborate the hypothesis. At the same time, in recent years, psychedelics received a lot of attention by the scientific community and astonishing findings emerged about the rearrangement of brain networks under the effect of these compounds. Specifically, a global decrease in functional connectivity was found, highlighting the disintegration of preserved and functional circuits and an increase of overall connectivity in the brain. The aim of this paper is to compare the biological bases of dysconnection in schizophrenia with the alterations of neuronal cyto-architecture induced by psychedelics and the consequent state of cerebral hyper-connection. These two models of psychosis, despite diametrically opposed, imply a substantial deficit of integration of neural signaling reached through two opposite paths.

@article{sapienza_schizophrenia_2022,
	title = {Schizophrenia and psychedelic state: {Dysconnection} versus hyper-connection. {A} perspective on two different models of psychosis stemming from dysfunctional integration processes},
	issn = {1476-5578},
	shorttitle = {Schizophrenia and psychedelic state},
	doi = {10.1038/s41380-022-01721-5},
	abstract = {Psychotic symptoms are a cross-sectional dimension affecting multiple diagnostic categories, despite schizophrenia represents the prototype of psychoses. Initially, dopamine was considered the most involved molecule in the neurobiology of schizophrenia. Over the next years, several biological factors were added to the discussion helping to constitute the concept of schizophrenia as a disease marked by a deficit of functional integration, contributing to the formulation of the Dysconnection Hypothesis in 1995. Nowadays the notion of dysconnection persists in the conceptualization of schizophrenia enriched by neuroimaging findings which corroborate the hypothesis. At the same time, in recent years, psychedelics received a lot of attention by the scientific community and astonishing findings emerged about the rearrangement of brain networks under the effect of these compounds. Specifically, a global decrease in functional connectivity was found, highlighting the disintegration of preserved and functional circuits and an increase of overall connectivity in the brain. The aim of this paper is to compare the biological bases of dysconnection in schizophrenia with the alterations of neuronal cyto-architecture induced by psychedelics and the consequent state of cerebral hyper-connection. These two models of psychosis, despite diametrically opposed, imply a substantial deficit of integration of neural signaling reached through two opposite paths.},
	language = {eng},
	journal = {Molecular Psychiatry},
	author = {Sapienza, Jacopo and Bosia, Marta and Spangaro, Marco and Martini, Francesca and Agostoni, Giulia and Cuoco, Federica and Cocchi, Federica and Cavallaro, Roberto},
	month = aug,
	year = {2022},
	pmid = {35931756},
	note = {1 citations (Semantic Scholar/DOI) [2023-01-12]},
}

Psychotic symptoms are a cross-sectional dimension affecting multiple diagnostic categories, despite schizophrenia represents the prototype of psychoses. Initially, dopamine was considered the most involved molecule in the neurobiology of schizophrenia. Over the next years, several biological factors were added to the discussion helping to constitute the concept of schizophrenia as a disease marked by a deficit of functional integration, contributing to the formulation of the Dysconnection Hypothesis in 1995. Nowadays the notion of dysconnection persists in the conceptualization of schizophrenia enriched by neuroimaging findings which corroborate the hypothesis. At the same time, in recent years, psychedelics received a lot of attention by the scientific community and astonishing findings emerged about the rearrangement of brain networks under the effect of these compounds. Specifically, a global decrease in functional connectivity was found, highlighting the disintegration of preserved and functional circuits and an increase of overall connectivity in the brain. The aim of this paper is to compare the biological bases of dysconnection in schizophrenia with the alterations of neuronal cyto-architecture induced by psychedelics and the consequent state of cerebral hyper-connection. These two models of psychosis, despite diametrically opposed, imply a substantial deficit of integration of neural signaling reached through two opposite paths.

@article{turkia_self-treatment_2022,
	title = {Self-treatment of psychosis and complex post-traumatic stress disorder with {LSD} and {DMT}—{A} retrospective case study},
	volume = {1},
	issn = {2773-0212},
	url = {https://www.sciencedirect.com/science/article/pii/S2773021222000232},
	doi = {10.1016/j.psycr.2022.100029},
	abstract = {This article describes a case of a teenager with early complex trauma due to chronic domestic violence. Cannabis use triggered auditory hallucinations, after which the teenager was diagnosed with an acute schizophrenia-like psychotic disorder. Antipsychotic medication did not fully resolve symptoms. Eventually the teenager chose to self-medicate with LSD in order to resolve a suicidal condition. The teenager carried out six unsupervised LSD sessions, followed by an extended period of almost daily use of inhaled low-dose DMT. Psychotic symptoms were mostly resolved after approximately one year. Subsequent cannabis use caused a transient relapse. While his psychosis may have been due to cannabis use in the presence of a genetic predisposition, LSD and DMT did not promote psychotic symptoms in this case, and resolved the suicidal condition in one session. Additional high-dose LSD sessions and low-dose DMT sessions appeared to resolve the symptoms related to the early complex trauma. Alternatively, if psychosis is understood as a massive defense system resulting from early complex trauma, and if his psychotic symptoms were partially due to such trauma, psychedelics appeared to transcend this defense system, providing access to traumatic memories in order to allow for an integrative treatment effect. Information was acquired from medical record excerpts provided by the patient, a semi-structured retrospective video interview, and follow-up interviews a year later. The present case suggests a need for further studies on the relationship between psychedelics and psychotic disorders, the feasibility of supervised vs unsupervised settings for various situations, and alternative therapeutic models for utilizing the hyperaware-hypersensitive state induced by psychedelics. With regard to self-treatment, a harm reduction approach should be adopted. Low-risk psycholytic self-treatment protocols could be developed for future use in public health care systems.},
	language = {en},
	number = {2},
	urldate = {2023-01-02},
	journal = {Psychiatry Research Case Reports},
	author = {Turkia, Mika},
	month = dec,
	year = {2022},
	note = {1 citations (Semantic Scholar/DOI) [2023-01-12]},
	keywords = {25B-NBOMe, C-PTSD, DMT, LSD, Psychedelic therapy, Psychedelics, Psychosis},
	pages = {100029},
}

This article describes a case of a teenager with early complex trauma due to chronic domestic violence. Cannabis use triggered auditory hallucinations, after which the teenager was diagnosed with an acute schizophrenia-like psychotic disorder. Antipsychotic medication did not fully resolve symptoms. Eventually the teenager chose to self-medicate with LSD in order to resolve a suicidal condition. The teenager carried out six unsupervised LSD sessions, followed by an extended period of almost daily use of inhaled low-dose DMT. Psychotic symptoms were mostly resolved after approximately one year. Subsequent cannabis use caused a transient relapse. While his psychosis may have been due to cannabis use in the presence of a genetic predisposition, LSD and DMT did not promote psychotic symptoms in this case, and resolved the suicidal condition in one session. Additional high-dose LSD sessions and low-dose DMT sessions appeared to resolve the symptoms related to the early complex trauma. Alternatively, if psychosis is understood as a massive defense system resulting from early complex trauma, and if his psychotic symptoms were partially due to such trauma, psychedelics appeared to transcend this defense system, providing access to traumatic memories in order to allow for an integrative treatment effect. Information was acquired from medical record excerpts provided by the patient, a semi-structured retrospective video interview, and follow-up interviews a year later. The present case suggests a need for further studies on the relationship between psychedelics and psychotic disorders, the feasibility of supervised vs unsupervised settings for various situations, and alternative therapeutic models for utilizing the hyperaware-hypersensitive state induced by psychedelics. With regard to self-treatment, a harm reduction approach should be adopted. Low-risk psycholytic self-treatment protocols could be developed for future use in public health care systems.

@article{spark_beyond_2022,
	title = {Beyond antipsychotics: a twenty-first century update for preclinical development of schizophrenia therapeutics},
	volume = {12},
	copyright = {2022 The Author(s)},
	issn = {2158-3188},
	shorttitle = {Beyond antipsychotics},
	url = {https://www.nature.com/articles/s41398-022-01904-2},
	doi = {10.1038/s41398-022-01904-2},
	abstract = {Despite 50+ years of drug discovery, current antipsychotics have limited efficacy against negative and cognitive symptoms of schizophrenia, and are ineffective—with the exception of clozapine—against any symptom domain for patients who are treatment resistant. Novel therapeutics with diverse non-dopamine D2 receptor targets have been explored extensively in clinical trials, yet often fail due to a lack of efficacy despite showing promise in preclinical development. This lack of translation between preclinical and clinical efficacy suggests a systematic failure in current methods that determine efficacy in preclinical rodent models. In this review, we critically evaluate rodent models and behavioural tests used to determine preclinical efficacy, and look to clinical research to provide a roadmap for developing improved translational measures. We highlight the dependence of preclinical models and tests on dopamine-centric theories of dysfunction and how this has contributed towards a self-reinforcing loop away from clinically meaningful predictions of efficacy. We review recent clinical findings of distinct dopamine-mediated dysfunction of corticostriatal circuits in patients with treatment-resistant vs. non-treatment-resistant schizophrenia and suggest criteria for establishing rodent models to reflect such differences, with a focus on objective, translational measures. Finally, we review current schizophrenia drug discovery and propose a framework where preclinical models are validated against objective, clinically informed measures and preclinical tests of efficacy map onto those used clinically.},
	language = {en},
	number = {1},
	urldate = {2022-08-10},
	journal = {Translational Psychiatry},
	author = {Spark, Daisy L. and Fornito, Alex and Langmead, Christopher J. and Stewart, Gregory D.},
	month = apr,
	year = {2022},
	note = {Number: 1
Publisher: Nature Publishing Group},
	keywords = {Molecular neuroscience, Predictive markers},
	pages = {1--11},
}

Despite 50+ years of drug discovery, current antipsychotics have limited efficacy against negative and cognitive symptoms of schizophrenia, and are ineffective—with the exception of clozapine—against any symptom domain for patients who are treatment resistant. Novel therapeutics with diverse non-dopamine D2 receptor targets have been explored extensively in clinical trials, yet often fail due to a lack of efficacy despite showing promise in preclinical development. This lack of translation between preclinical and clinical efficacy suggests a systematic failure in current methods that determine efficacy in preclinical rodent models. In this review, we critically evaluate rodent models and behavioural tests used to determine preclinical efficacy, and look to clinical research to provide a roadmap for developing improved translational measures. We highlight the dependence of preclinical models and tests on dopamine-centric theories of dysfunction and how this has contributed towards a self-reinforcing loop away from clinically meaningful predictions of efficacy. We review recent clinical findings of distinct dopamine-mediated dysfunction of corticostriatal circuits in patients with treatment-resistant vs. non-treatment-resistant schizophrenia and suggest criteria for establishing rodent models to reflect such differences, with a focus on objective, translational measures. Finally, we review current schizophrenia drug discovery and propose a framework where preclinical models are validated against objective, clinically informed measures and preclinical tests of efficacy map onto those used clinically.

@article{arnovitz_mdma_2022,
	title = {{MDMA} for the {Treatment} of {Negative} {Symptoms} in {Schizophrenia}},
	volume = {11},
	copyright = {http://creativecommons.org/licenses/by/3.0/},
	issn = {2077-0383},
	url = {https://www.mdpi.com/2077-0383/11/12/3255},
	doi = {10.3390/jcm11123255},
	abstract = {The profound economic burden of schizophrenia is due, in part, to the negative symptoms of the disease, which can severely limit daily functioning. There is much debate in the field regarding their measurement and classification and there are no FDA-approved treatments for negative symptoms despite an abundance of research. 3,4-Methylenedioxy methamphetamine (MDMA) is a schedule I substance that has emerged as a novel therapeutic given its ability to enhance social interactions, generate empathy, and induce a state of metaplasticity in the brain. This review provides a rationale for the use of MDMA in the treatment of negative symptoms by reviewing the literature on negative symptoms, their treatment, MDMA, and MDMA-assisted therapy. It reviews recent evidence that supports the safe and potentially effective use of MDMA to treat negative symptoms and concludes with considerations regarding safety and possible mechanisms of action.},
	language = {en},
	number = {12},
	urldate = {2022-08-10},
	journal = {Journal of Clinical Medicine},
	author = {Arnovitz, Mitchell D. and Spitzberg, Andrew J. and Davani, Ashkhan J. and Vadhan, Nehal P. and Holland, Julie and Kane, John M. and Michaels, Timothy I.},
	month = jan,
	year = {2022},
	note = {Number: 12
Publisher: Multidisciplinary Digital Publishing Institute},
	keywords = {MDMA, negative symptoms, psychedelic-assisted therapy, psychosis, schizophrenia},
	pages = {3255},
}

The profound economic burden of schizophrenia is due, in part, to the negative symptoms of the disease, which can severely limit daily functioning. There is much debate in the field regarding their measurement and classification and there are no FDA-approved treatments for negative symptoms despite an abundance of research. 3,4-Methylenedioxy methamphetamine (MDMA) is a schedule I substance that has emerged as a novel therapeutic given its ability to enhance social interactions, generate empathy, and induce a state of metaplasticity in the brain. This review provides a rationale for the use of MDMA in the treatment of negative symptoms by reviewing the literature on negative symptoms, their treatment, MDMA, and MDMA-assisted therapy. It reviews recent evidence that supports the safe and potentially effective use of MDMA to treat negative symptoms and concludes with considerations regarding safety and possible mechanisms of action.

@article{spark_beyond_2022-1,
	title = {Beyond antipsychotics: a twenty-first century update for preclinical development of schizophrenia therapeutics},
	volume = {12},
	copyright = {2022 The Author(s)},
	issn = {2158-3188},
	shorttitle = {Beyond antipsychotics},
	url = {https://www.nature.com/articles/s41398-022-01904-2},
	doi = {10.1038/s41398-022-01904-2},
	abstract = {Despite 50+ years of drug discovery, current antipsychotics have limited efficacy against negative and cognitive symptoms of schizophrenia, and are ineffective—with the exception of clozapine—against any symptom domain for patients who are treatment resistant. Novel therapeutics with diverse non-dopamine D2 receptor targets have been explored extensively in clinical trials, yet often fail due to a lack of efficacy despite showing promise in preclinical development. This lack of translation between preclinical and clinical efficacy suggests a systematic failure in current methods that determine efficacy in preclinical rodent models. In this review, we critically evaluate rodent models and behavioural tests used to determine preclinical efficacy, and look to clinical research to provide a roadmap for developing improved translational measures. We highlight the dependence of preclinical models and tests on dopamine-centric theories of dysfunction and how this has contributed towards a self-reinforcing loop away from clinically meaningful predictions of efficacy. We review recent clinical findings of distinct dopamine-mediated dysfunction of corticostriatal circuits in patients with treatment-resistant vs. non-treatment-resistant schizophrenia and suggest criteria for establishing rodent models to reflect such differences, with a focus on objective, translational measures. Finally, we review current schizophrenia drug discovery and propose a framework where preclinical models are validated against objective, clinically informed measures and preclinical tests of efficacy map onto those used clinically.},
	language = {en},
	number = {1},
	urldate = {2022-07-24},
	journal = {Translational Psychiatry},
	author = {Spark, Daisy L. and Fornito, Alex and Langmead, Christopher J. and Stewart, Gregory D.},
	month = apr,
	year = {2022},
	note = {Number: 1
Publisher: Nature Publishing Group},
	keywords = {Molecular neuroscience, Predictive markers},
	pages = {1--11},
}

Despite 50+ years of drug discovery, current antipsychotics have limited efficacy against negative and cognitive symptoms of schizophrenia, and are ineffective—with the exception of clozapine—against any symptom domain for patients who are treatment resistant. Novel therapeutics with diverse non-dopamine D2 receptor targets have been explored extensively in clinical trials, yet often fail due to a lack of efficacy despite showing promise in preclinical development. This lack of translation between preclinical and clinical efficacy suggests a systematic failure in current methods that determine efficacy in preclinical rodent models. In this review, we critically evaluate rodent models and behavioural tests used to determine preclinical efficacy, and look to clinical research to provide a roadmap for developing improved translational measures. We highlight the dependence of preclinical models and tests on dopamine-centric theories of dysfunction and how this has contributed towards a self-reinforcing loop away from clinically meaningful predictions of efficacy. We review recent clinical findings of distinct dopamine-mediated dysfunction of corticostriatal circuits in patients with treatment-resistant vs. non-treatment-resistant schizophrenia and suggest criteria for establishing rodent models to reflect such differences, with a focus on objective, translational measures. Finally, we review current schizophrenia drug discovery and propose a framework where preclinical models are validated against objective, clinically informed measures and preclinical tests of efficacy map onto those used clinically.

@article{xiong_ddinter_2022,
	title = {{DDInter}: an online drug–drug interaction database towards improving clinical decision-making and patient safety},
	volume = {50},
	issn = {0305-1048},
	shorttitle = {{DDInter}},
	url = {https://doi.org/10.1093/nar/gkab880},
	doi = {10.1093/nar/gkab880},
	abstract = {Drug-drug interaction (DDI) can trigger many adverse effects in patients and has emerged as a threat to medicine and public health. Despite the continuous information accumulation of clinically significant DDIs, there are few open-access knowledge systems dedicated to the curation of DDI associations. To facilitate the clinicians to screen for dangerous drug combinations and improve health systems, we present DDInter, a curated DDI database with comprehensive data, practical medication guidance, intuitive function interface, and powerful visualization to the scientific community. Currently, DDInter contains about 0.24M DDI associations connecting 1833 approved drugs (1972 entities). Each drug is annotated with basic chemical and pharmacological information and its interaction network. For DDI associations, abundant and professional annotations are provided, including severity, mechanism description, strategies for managing potential side effects, alternative medications, etc. The drug entities and interaction entities are efficiently cross-linked. In addition to basic query and browsing, the prescription checking function is developed to facilitate clinicians to decide whether drugs combinations can be used safely. It can also be used for informatics-based DDI investigation and evaluation of other prediction frameworks. We hope that DDInter will prove useful in improving clinical decision-making and patient safety. DDInter is freely available, without registration, at http://ddinter.scbdd.com/.},
	number = {D1},
	urldate = {2022-07-20},
	journal = {Nucleic Acids Research},
	author = {Xiong, Guoli and Yang, Zhijiang and Yi, Jiacai and Wang, Ningning and Wang, Lei and Zhu, Huimin and Wu, Chengkun and Lu, Aiping and Chen, Xiang and Liu, Shao and Hou, Tingjun and Cao, Dongsheng},
	month = jan,
	year = {2022},
	pages = {D1200--D1207},
}

Drug-drug interaction (DDI) can trigger many adverse effects in patients and has emerged as a threat to medicine and public health. Despite the continuous information accumulation of clinically significant DDIs, there are few open-access knowledge systems dedicated to the curation of DDI associations. To facilitate the clinicians to screen for dangerous drug combinations and improve health systems, we present DDInter, a curated DDI database with comprehensive data, practical medication guidance, intuitive function interface, and powerful visualization to the scientific community. Currently, DDInter contains about 0.24M DDI associations connecting 1833 approved drugs (1972 entities). Each drug is annotated with basic chemical and pharmacological information and its interaction network. For DDI associations, abundant and professional annotations are provided, including severity, mechanism description, strategies for managing potential side effects, alternative medications, etc. The drug entities and interaction entities are efficiently cross-linked. In addition to basic query and browsing, the prescription checking function is developed to facilitate clinicians to decide whether drugs combinations can be used safely. It can also be used for informatics-based DDI investigation and evaluation of other prediction frameworks. We hope that DDInter will prove useful in improving clinical decision-making and patient safety. DDInter is freely available, without registration, at http://ddinter.scbdd.com/.

@article{arnovitz_mdma_2022-1,
	title = {{MDMA} for the {Treatment} of {Negative} {Symptoms} in {Schizophrenia}},
	volume = {11},
	copyright = {http://creativecommons.org/licenses/by/3.0/},
	issn = {2077-0383},
	url = {https://www.mdpi.com/2077-0383/11/12/3255},
	doi = {10.3390/jcm11123255},
	abstract = {The profound economic burden of schizophrenia is due, in part, to the negative symptoms of the disease, which can severely limit daily functioning. There is much debate in the field regarding their measurement and classification and there are no FDA-approved treatments for negative symptoms despite an abundance of research. 3,4-Methylenedioxy methamphetamine (MDMA) is a schedule I substance that has emerged as a novel therapeutic given its ability to enhance social interactions, generate empathy, and induce a state of metaplasticity in the brain. This review provides a rationale for the use of MDMA in the treatment of negative symptoms by reviewing the literature on negative symptoms, their treatment, MDMA, and MDMA-assisted therapy. It reviews recent evidence that supports the safe and potentially effective use of MDMA to treat negative symptoms and concludes with considerations regarding safety and possible mechanisms of action.},
	language = {en},
	number = {12},
	urldate = {2022-07-12},
	journal = {Journal of Clinical Medicine},
	author = {Arnovitz, Mitchell D. and Spitzberg, Andrew J. and Davani, Ashkhan J. and Vadhan, Nehal P. and Holland, Julie and Kane, John M. and Michaels, Timothy I.},
	month = jan,
	year = {2022},
	keywords = {MDMA, negative symptoms, psychedelic-assisted therapy, psychosis, schizophrenia},
	pages = {3255},
}

The profound economic burden of schizophrenia is due, in part, to the negative symptoms of the disease, which can severely limit daily functioning. There is much debate in the field regarding their measurement and classification and there are no FDA-approved treatments for negative symptoms despite an abundance of research. 3,4-Methylenedioxy methamphetamine (MDMA) is a schedule I substance that has emerged as a novel therapeutic given its ability to enhance social interactions, generate empathy, and induce a state of metaplasticity in the brain. This review provides a rationale for the use of MDMA in the treatment of negative symptoms by reviewing the literature on negative symptoms, their treatment, MDMA, and MDMA-assisted therapy. It reviews recent evidence that supports the safe and potentially effective use of MDMA to treat negative symptoms and concludes with considerations regarding safety and possible mechanisms of action.

@article{nair_trace_2022,
	title = {Trace {Amine}-{Associated} {Receptor} 1 ({TAAR1}): {Molecular} and {Clinical} {Insights} for the {Treatment} of {Schizophrenia} and {Related} {Comorbidities}},
	volume = {5},
	shorttitle = {Trace {Amine}-{Associated} {Receptor} 1 ({TAAR1})},
	url = {https://doi.org/10.1021/acsptsci.2c00016},
	doi = {10.1021/acsptsci.2c00016},
	abstract = {Schizophrenia is a complex and severe mental illness. Current treatments for schizophrenia typically modulate dopaminergic neurotransmission by D2-receptor blockade. While reducing positive symptoms of schizophrenia, current antipsychotic drugs have little clinical effect on negative symptoms and cognitive impairments. For the last few decades, discovery efforts have sought nondopaminergic compounds with the aim to effectively treat the broad symptoms of schizophrenia. In this viewpoint, we provide an overview on trace-amine associated receptor-1 (TAAR1), which presents a clinically validated nondopaminergic target for treating schizophrenia and related disorders, with significantly less overall side-effect burden. TAAR1 agonists may also be specifically beneficial for the substance abuse comorbidity and metabolic syndrome that is often present in patients with schizophrenia.},
	number = {3},
	urldate = {2022-07-11},
	journal = {ACS Pharmacology \& Translational Science},
	author = {Nair, Pramod C. and Chalker, Justin M. and McKinnon, Ross A. and Langmead, Christopher J and Gregory, Karen J. and Bastiampillai, Tarun},
	month = mar,
	year = {2022},
	note = {Publisher: American Chemical Society},
	pages = {183--188},
}

Schizophrenia is a complex and severe mental illness. Current treatments for schizophrenia typically modulate dopaminergic neurotransmission by D2-receptor blockade. While reducing positive symptoms of schizophrenia, current antipsychotic drugs have little clinical effect on negative symptoms and cognitive impairments. For the last few decades, discovery efforts have sought nondopaminergic compounds with the aim to effectively treat the broad symptoms of schizophrenia. In this viewpoint, we provide an overview on trace-amine associated receptor-1 (TAAR1), which presents a clinically validated nondopaminergic target for treating schizophrenia and related disorders, with significantly less overall side-effect burden. TAAR1 agonists may also be specifically beneficial for the substance abuse comorbidity and metabolic syndrome that is often present in patients with schizophrenia.

@article{xiao_vitro_2022,
	title = {In {Vitro} {ADME} and {Preclinical} {Pharmacokinetics} of {Ulotaront}, a {TAAR1}/5-{HT1A} {Receptor} {Agonist} for the {Treatment} of {Schizophrenia}},
	volume = {39},
	issn = {1573-904X},
	doi = {10.1007/s11095-022-03267-1},
	abstract = {PURPOSE: Ulotaront (SEP-363856) is a TAAR1 agonist with 5-HT1A agonist activity currently in clinical development for the treatment of schizophrenia. The objectives of the current study were to characterize the in vitro ADME properties, preclinical PK, and to evaluate the DDI potential of ulotaront and its major metabolite SEP-383103.
METHODS: Solubility, permeability, plasma protein binding, CYP inhibition and induction, transporter inhibition and uptake studies were conducted in vitro. Phenotyping studies were conducted using recombinant human CYPs and FMOs, human liver microsomes and human liver homogenates. Preclinical plasma and brain pharmacokinetics were determined after a single intraperitoneal, intravenous, and oral administration of ulotaront.
RESULTS: Ulotaront is a compound of high solubility, high permeability, and low binding to plasma proteins. Ulotaront metabolism is mediated via both NADPH-dependent and NADPH-independent pathways, with CYP2D6 as the major metabolizing enzyme. Ulotaront is an inducer of CYP2B6, and an inhibitor of CYP2D6, OCT1 and OCT2, while SEP-383103 is neither a CYP inducer nor a potent inhibitor of CYPs and human transporters. Ulotaront exhibits rapid absorption, greater than 70\% bioavailability, approximately 3.5 L/kg volume of distribution, 1.5-4 h half-life, 12-43 ml/min/kg clearance, and good penetration across the blood-brain barrier in preclinical species.
CONCLUSIONS: Ulotaront has been designated as a BCS1 compound by US FDA. The ability of ulotaront to penetrate the blood-brain barrier for CNS targeting has been demonstrated in mice and rats. The potential for ulotaront and SEP-383103 to act as perpetrators of CYP and transporter-mediated DDIs is predicted to be remote.},
	language = {eng},
	number = {5},
	journal = {Pharmaceutical Research},
	author = {Xiao, Guangqing and Chen, Yu-Luan and Dedic, Nina and Xie, Linghong and Koblan, Kenneth S. and Galluppi, Gerald R.},
	month = may,
	year = {2022},
	pmid = {35484370},
	keywords = {Animals, CYP2D6, Cytochrome P-450 CYP2D6, Cytochrome P-450 Enzyme System, Mice, Microsomes, Liver, NADP, Pharmaceutical Preparations, Rats, Receptor, Serotonin, 5-HT1A, Schizophrenia, TAAR1, blood–brain barrier, drug-drug interactions, phenotyping, ulotaront},
	pages = {837--850},
}

PURPOSE: Ulotaront (SEP-363856) is a TAAR1 agonist with 5-HT1A agonist activity currently in clinical development for the treatment of schizophrenia. The objectives of the current study were to characterize the in vitro ADME properties, preclinical PK, and to evaluate the DDI potential of ulotaront and its major metabolite SEP-383103. METHODS: Solubility, permeability, plasma protein binding, CYP inhibition and induction, transporter inhibition and uptake studies were conducted in vitro. Phenotyping studies were conducted using recombinant human CYPs and FMOs, human liver microsomes and human liver homogenates. Preclinical plasma and brain pharmacokinetics were determined after a single intraperitoneal, intravenous, and oral administration of ulotaront. RESULTS: Ulotaront is a compound of high solubility, high permeability, and low binding to plasma proteins. Ulotaront metabolism is mediated via both NADPH-dependent and NADPH-independent pathways, with CYP2D6 as the major metabolizing enzyme. Ulotaront is an inducer of CYP2B6, and an inhibitor of CYP2D6, OCT1 and OCT2, while SEP-383103 is neither a CYP inducer nor a potent inhibitor of CYPs and human transporters. Ulotaront exhibits rapid absorption, greater than 70% bioavailability, approximately 3.5 L/kg volume of distribution, 1.5-4 h half-life, 12-43 ml/min/kg clearance, and good penetration across the blood-brain barrier in preclinical species. CONCLUSIONS: Ulotaront has been designated as a BCS1 compound by US FDA. The ability of ulotaront to penetrate the blood-brain barrier for CNS targeting has been demonstrated in mice and rats. The potential for ulotaront and SEP-383103 to act as perpetrators of CYP and transporter-mediated DDIs is predicted to be remote.

@techreport{koch_candidates_2022,
	type = {preprint},
	title = {Candidates for {Drug} {Repurposing} to {Address} the {Cognitive} {Symptoms} in {Schizophrenia}},
	url = {http://biorxiv.org/lookup/doi/10.1101/2022.03.07.483231},
	abstract = {In the protein-protein interactome, we have previously identified a significant overlap between schizophrenia risk genes and genes associated with cognitive performance. Here, we further studied this overlap to identify potential candidate drugs for repurposing to treat the cognitive symptoms in schizophrenia. We first defined a cognition-related schizophrenia interactome from network propagation analyses, and identified drugs known to target more than one protein within this network. Thereafter, we used gene expression data to further select drugs that could counteract schizophrenia-associated gene expression perturbations. Additionally, we stratified these analyses by sex to identify sex-specific pharmacological treatment options for the cognitive symptoms in schizophrenia. After excluding drugs contraindicated in schizophrenia, we identified eight drug candidates, most of which have anti-inflammatory and neuroprotective effects. Due to gene expression differences in male and female patients, four of those drugs were also selected in our male-specific analyses, and the other four in the female-specific analyses. Based on our bioinformatics analyses of disease genetics, we suggest eight candidate drugs that warrant further examination for repurposing to treat the cognitive symptoms in schizophrenia, and suggest that these symptoms could be addressed by sex-specific pharmacological treatment options.},
	language = {en},
	urldate = {2022-05-31},
	institution = {Genetics},
	author = {Koch, Elise and Kauppi, Karolina and Chen, Chi-Hua},
	month = mar,
	year = {2022},
	doi = {10.1101/2022.03.07.483231},
}

In the protein-protein interactome, we have previously identified a significant overlap between schizophrenia risk genes and genes associated with cognitive performance. Here, we further studied this overlap to identify potential candidate drugs for repurposing to treat the cognitive symptoms in schizophrenia. We first defined a cognition-related schizophrenia interactome from network propagation analyses, and identified drugs known to target more than one protein within this network. Thereafter, we used gene expression data to further select drugs that could counteract schizophrenia-associated gene expression perturbations. Additionally, we stratified these analyses by sex to identify sex-specific pharmacological treatment options for the cognitive symptoms in schizophrenia. After excluding drugs contraindicated in schizophrenia, we identified eight drug candidates, most of which have anti-inflammatory and neuroprotective effects. Due to gene expression differences in male and female patients, four of those drugs were also selected in our male-specific analyses, and the other four in the female-specific analyses. Based on our bioinformatics analyses of disease genetics, we suggest eight candidate drugs that warrant further examination for repurposing to treat the cognitive symptoms in schizophrenia, and suggest that these symptoms could be addressed by sex-specific pharmacological treatment options.

@incollection{talevi_drug_2022,
	address = {Cham},
	series = {Computer-{Aided} {Drug} {Discovery} and {Design}},
	title = {Drug {Discovery} {Paradigms}: {Phenotypic}-{Based} {Drug} {Discovery}},
	isbn = {978-3-030-95895-4},
	shorttitle = {Drug {Discovery} {Paradigms}},
	url = {https://doi.org/10.1007/978-3-030-95895-4_2},
	abstract = {A drug discovery and development project typically starts with the identification of novel active scaffolds, i.e., core chemical structures with a desired biological effect. Beyond serendipitous discoveries and findings based on ethnopharmacology/traditional medicine, drug discovery in the modern age has been guided by two fundamental screening philosophies (implemented whether through in silico, in vitro or less often, in vivo approximations). Occasionally, novel chemotypes can be designed de novo by searching for complementary features to a binding site in a predefined drug target. Historically, systematic screening for new active compounds comprised phenotypic screening assays (e.g., against a collection of microorganisms, animal models of disease, or cellular models). Later, the interest of the pharmaceutical companies experienced a substantial shift toward target-focused approximations in which exquisitely selective compounds were sought, usually through high-throughput screening. There, the test compounds were typically confronted with some biological entity, usually a protein, to identify those which could modulate such biomolecule. Nevertheless, as target-focused approximation failed to deliver the expectations, especially when pursuing therapies for complex disorders, renewed interest in phenotypic screening was observed in the pharmaceutical community, supported by a network pharmacology paradigm, high-content screening, small animal models, and organoids and other advanced cell culture platforms.},
	language = {en},
	urldate = {2022-05-29},
	booktitle = {Drug {Target} {Selection} and {Validation}},
	publisher = {Springer International Publishing},
	author = {Talevi, Alan and Bellera, Carolina L.},
	editor = {Scotti, Marcus T. and Bellera, Carolina L.},
	year = {2022},
	doi = {10.1007/978-3-030-95895-4_2},
	keywords = {Drug discovery, High-content analysis, High-content screening (HCS), High-throughput screening, Hit identification, Phenotypic screening, Target deconvolution, Target-focused approximations},
	pages = {25--40},
}

A drug discovery and development project typically starts with the identification of novel active scaffolds, i.e., core chemical structures with a desired biological effect. Beyond serendipitous discoveries and findings based on ethnopharmacology/traditional medicine, drug discovery in the modern age has been guided by two fundamental screening philosophies (implemented whether through in silico, in vitro or less often, in vivo approximations). Occasionally, novel chemotypes can be designed de novo by searching for complementary features to a binding site in a predefined drug target. Historically, systematic screening for new active compounds comprised phenotypic screening assays (e.g., against a collection of microorganisms, animal models of disease, or cellular models). Later, the interest of the pharmaceutical companies experienced a substantial shift toward target-focused approximations in which exquisitely selective compounds were sought, usually through high-throughput screening. There, the test compounds were typically confronted with some biological entity, usually a protein, to identify those which could modulate such biomolecule. Nevertheless, as target-focused approximation failed to deliver the expectations, especially when pursuing therapies for complex disorders, renewed interest in phenotypic screening was observed in the pharmaceutical community, supported by a network pharmacology paradigm, high-content screening, small animal models, and organoids and other advanced cell culture platforms.

@article{barron_doors_2022,
	title = {The doors of precision: {Reenergizing} psychiatric drug development with psychedelics and open access computational tools},
	volume = {8},
	issn = {2375-2548},
	shorttitle = {The doors of precision},
	url = {https://www.science.org/doi/10.1126/sciadv.abp8283},
	doi = {10.1126/sciadv.abp8283},
	abstract = {Psychedelics paired with new applications of computational tools might help bypass the imprecision of psychiatric diagnosis and connect measures of behavior to specific physiologic targets.},
	language = {en},
	number = {11},
	urldate = {2022-05-29},
	journal = {Science Advances},
	author = {Barron, Daniel S. and Friedman, Richard A.},
	month = mar,
	year = {2022},
	pages = {eabp8283},
}

Psychedelics paired with new applications of computational tools might help bypass the imprecision of psychiatric diagnosis and connect measures of behavior to specific physiologic targets.

@article{lago_druggable_2022,
	title = {The druggable schizophrenia genome: from repurposing opportunities to unexplored drug targets},
	volume = {7},
	copyright = {2022 The Author(s)},
	issn = {2056-7944},
	shorttitle = {The druggable schizophrenia genome},
	url = {https://www.nature.com/articles/s41525-022-00290-4},
	doi = {10.1038/s41525-022-00290-4},
	abstract = {There have been no new drugs for the treatment of schizophrenia in several decades and treatment resistance represents a major unmet clinical need. The drugs that exist are based on serendipitous clinical observations rather than an evidence-based understanding of disease pathophysiology. In the present review, we address these bottlenecks by integrating common, rare, and expression-related schizophrenia risk genes with knowledge of the druggability of the human genome as a whole. We highlight novel drug repurposing opportunities, clinical trial candidates which are supported by genetic evidence, and unexplored therapeutic opportunities in the lesser-known regions of the schizophrenia genome. By identifying translational gaps and opportunities across the schizophrenia disease space, we discuss a framework for translating increasingly well-powered genetic association studies into personalized treatments for schizophrenia and initiating the vital task of characterizing clinically relevant drug targets in underexplored regions of the human genome.},
	language = {en},
	number = {1},
	urldate = {2022-05-27},
	journal = {npj Genomic Medicine},
	author = {Lago, Santiago G. and Bahn, Sabine},
	month = mar,
	year = {2022},
	note = {Number: 1
Publisher: Nature Publishing Group},
	keywords = {Genome, Pharmaceutics, Schizophrenia, Target identification},
	pages = {1--13},
}

There have been no new drugs for the treatment of schizophrenia in several decades and treatment resistance represents a major unmet clinical need. The drugs that exist are based on serendipitous clinical observations rather than an evidence-based understanding of disease pathophysiology. In the present review, we address these bottlenecks by integrating common, rare, and expression-related schizophrenia risk genes with knowledge of the druggability of the human genome as a whole. We highlight novel drug repurposing opportunities, clinical trial candidates which are supported by genetic evidence, and unexplored therapeutic opportunities in the lesser-known regions of the schizophrenia genome. By identifying translational gaps and opportunities across the schizophrenia disease space, we discuss a framework for translating increasingly well-powered genetic association studies into personalized treatments for schizophrenia and initiating the vital task of characterizing clinically relevant drug targets in underexplored regions of the human genome.

@article{barron_doors_2022-1,
	title = {The doors of precision: {Reenergizing} psychiatric drug development with psychedelics and open access computational tools},
	volume = {8},
	issn = {2375-2548},
	shorttitle = {The doors of precision},
	url = {https://www.science.org/doi/10.1126/sciadv.abp8283},
	doi = {10.1126/sciadv.abp8283},
	abstract = {Psychedelics paired with new applications of computational tools might help bypass the imprecision of psychiatric diagnosis and connect measures of behavior to specific physiologic targets.},
	language = {en},
	number = {11},
	urldate = {2022-05-25},
	journal = {Science Advances},
	author = {Barron, Daniel S. and Friedman, Richard A.},
	month = mar,
	year = {2022},
	pages = {eabp8283},
}

Psychedelics paired with new applications of computational tools might help bypass the imprecision of psychiatric diagnosis and connect measures of behavior to specific physiologic targets.

@article{saleem_alternative_2022,
	title = {Alternative {Therapy} of {Psychosis}: {Potential} {Phytochemicals} and {Drug} {Targets} in the {Management} of {Schizophrenia}},
	volume = {13},
	issn = {1663-9812},
	shorttitle = {Alternative {Therapy} of {Psychosis}},
	url = {https://www.frontiersin.org/article/10.3389/fphar.2022.895668},
	abstract = {Schizophrenia is a chronic mental and behavioral disorder characterized by clusters of symptoms including hallucinations, delusions, disorganized thoughts and social withdrawal. It is mainly contributed by defects in dopamine, glutamate, cholinergic and serotonergic pathways, genetic and environmental factors, prenatal infections, oxidative stress, immune system activation and inflammation. Management of schizophrenia is usually carried out with typical and atypical antipsychotics, but it yields modest benefits with a diversity of side effects. Therefore, the current study was designed to determine the phytochemicals as new drug candidates for treatment and management of schizophrenia. These phytochemicals alter and affect neurotransmission, cell signaling pathways, endocannabinoid receptors, neuro-inflammation, activation of immune system and status of oxidative stress. Phytochemicals exhibiting anti-schizophrenic activity are mostly flavonoids, polyphenols, alkaloids, terpenoids, terpenes, polypropanoids, lactones and glycosides. However, well-designed clinical trials are consequently required to investigate potential protective effect and therapeutic benefits of these phytochemicals against schizophrenia.},
	urldate = {2022-05-25},
	journal = {Frontiers in Pharmacology},
	author = {Saleem, Ammara and {Qurat-ul-Ain} and Akhtar, Muhammad Furqan},
	year = {2022},
}

Schizophrenia is a chronic mental and behavioral disorder characterized by clusters of symptoms including hallucinations, delusions, disorganized thoughts and social withdrawal. It is mainly contributed by defects in dopamine, glutamate, cholinergic and serotonergic pathways, genetic and environmental factors, prenatal infections, oxidative stress, immune system activation and inflammation. Management of schizophrenia is usually carried out with typical and atypical antipsychotics, but it yields modest benefits with a diversity of side effects. Therefore, the current study was designed to determine the phytochemicals as new drug candidates for treatment and management of schizophrenia. These phytochemicals alter and affect neurotransmission, cell signaling pathways, endocannabinoid receptors, neuro-inflammation, activation of immune system and status of oxidative stress. Phytochemicals exhibiting anti-schizophrenic activity are mostly flavonoids, polyphenols, alkaloids, terpenoids, terpenes, polypropanoids, lactones and glycosides. However, well-designed clinical trials are consequently required to investigate potential protective effect and therapeutic benefits of these phytochemicals against schizophrenia.

@article{baptista_protein_2022,
	title = {Protein {Interaction} {Network} for {Identifying} {Vascular} {Response} of {Metformin} ({Oral} {Antidiabetic})},
	volume = {2},
	copyright = {http://creativecommons.org/licenses/by/3.0/},
	issn = {2673-7426},
	url = {https://www.mdpi.com/2673-7426/2/2/14},
	doi = {10.3390/biomedinformatics2020014},
	abstract = {Metformin is the most used oral anti-diabetic drug in the world and consequently is commonly found in the aquatic environment. Some studies demonstrated that metformin may act as an endocrine-disrupting-chemical (EDC) in fish, although it does not have a classic EDC structure. In this sense, the aim of this work was to evaluate the potential disrupting effect of metformin in the cardiovascular system through in vitro, ex vivo, and in silico studies. For this purpose, human umbilical artery (HUA) and rat aorta artery (RAA) were used. The toxic concentrations of metformin were determined by a cytotoxicity assay and in silico simulations were performed to analyze the interactions of metformin with hormonal receptors. Our results show that metformin decreases viability of the smooth muscle cells. Moreover, metformin induces a vasorelaxant effect in rat aorta and human models by an endothelium-dependent and -independent pathways. Furthermore, docking simulations showed that metformin binds to androgen receptors (AR) and estrogen receptors (ERα and ERβ). In conclusion, the in silico assays suggested that metformin has the potential to be an endocrine disruptor, acting mainly on ERα. Further studies are needed to use metformin in pregnant women without impairing the cardiovascular health of the future generation.},
	language = {en},
	number = {2},
	urldate = {2022-05-10},
	journal = {BioMedInformatics},
	author = {Baptista, Margarida and Lorigo, Margarida and Cairrao, Elisa},
	month = jun,
	year = {2022},
	note = {Number: 2
Publisher: Multidisciplinary Digital Publishing Institute},
	keywords = {A7r5 cell line, endocrine-disrupting chemical, endothelium, human umbilical artery, metformin, molecular docking, rat aorta artery, vasorelaxation},
	pages = {217--233},
}

Metformin is the most used oral anti-diabetic drug in the world and consequently is commonly found in the aquatic environment. Some studies demonstrated that metformin may act as an endocrine-disrupting-chemical (EDC) in fish, although it does not have a classic EDC structure. In this sense, the aim of this work was to evaluate the potential disrupting effect of metformin in the cardiovascular system through in vitro, ex vivo, and in silico studies. For this purpose, human umbilical artery (HUA) and rat aorta artery (RAA) were used. The toxic concentrations of metformin were determined by a cytotoxicity assay and in silico simulations were performed to analyze the interactions of metformin with hormonal receptors. Our results show that metformin decreases viability of the smooth muscle cells. Moreover, metformin induces a vasorelaxant effect in rat aorta and human models by an endothelium-dependent and -independent pathways. Furthermore, docking simulations showed that metformin binds to androgen receptors (AR) and estrogen receptors (ERα and ERβ). In conclusion, the in silico assays suggested that metformin has the potential to be an endocrine disruptor, acting mainly on ERα. Further studies are needed to use metformin in pregnant women without impairing the cardiovascular health of the future generation.

@article{kim_metformin_2022,
	title = {Metformin and its therapeutic applications in autoimmune inflammatory rheumatic disease},
	volume = {37},
	issn = {1226-3303},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8747910/},
	doi = {10.3904/kjim.2021.363},
	abstract = {Metformin is a first-line therapeutic agent for type 2 diabetes. Apart from its glucose-lowering effect, metformin is attracting interest regarding possible therapeutic benefits in various other conditions. As metformin regulates cell metabolism, proliferation, growth, and autophagy, it may also modulate immune cell functions. Given that metformin acts on multiple intracellular signaling pathways, including adenosine monophosphate (AMP)-activated protein kinase (AMPK) activation, and that AMPK and its downstream intracellular signaling control the activation and differentiation of T and B cells and inflammatory responses, metformin may exert immunomodulatory and anti-inflammatory effects. The efficacy of metformin has been investigated in preclinical and clinical studies on rheumatoid arthritis, osteoarthritis, systemic lupus erythematosus, Sjögren’s syndrome, scleroderma, ankylosing spondylitis, and gout. In this review, we discuss the potential mechanisms through which metformin exerts its therapeutic effects in these diseases, focusing particularly on rheumatoid arthritis and osteoarthritis.},
	number = {1},
	urldate = {2022-05-10},
	journal = {The Korean Journal of Internal Medicine},
	author = {Kim, Ji-Won and Choe, Jung-Yoon and Park, Sung-Hwan},
	month = jan,
	year = {2022},
	pmid = {34879473},
	pmcid = {PMC8747910},
	pages = {13--26},
}

Metformin is a first-line therapeutic agent for type 2 diabetes. Apart from its glucose-lowering effect, metformin is attracting interest regarding possible therapeutic benefits in various other conditions. As metformin regulates cell metabolism, proliferation, growth, and autophagy, it may also modulate immune cell functions. Given that metformin acts on multiple intracellular signaling pathways, including adenosine monophosphate (AMP)-activated protein kinase (AMPK) activation, and that AMPK and its downstream intracellular signaling control the activation and differentiation of T and B cells and inflammatory responses, metformin may exert immunomodulatory and anti-inflammatory effects. The efficacy of metformin has been investigated in preclinical and clinical studies on rheumatoid arthritis, osteoarthritis, systemic lupus erythematosus, Sjögren’s syndrome, scleroderma, ankylosing spondylitis, and gout. In this review, we discuss the potential mechanisms through which metformin exerts its therapeutic effects in these diseases, focusing particularly on rheumatoid arthritis and osteoarthritis.

@article{kim_metformin_2022-1,
	title = {Metformin and its therapeutic applications in autoimmune inflammatory rheumatic disease},
	volume = {37},
	issn = {2005-6648},
	doi = {10.3904/kjim.2021.363},
	abstract = {Metformin is a first-line therapeutic agent for type 2 diabetes. Apart from its glucose-lowering effect, metformin is attracting interest regarding possible therapeutic benefits in various other conditions. As metformin regulates cell metabolism, proliferation, growth, and autophagy, it may also modulate immune cell functions. Given that metformin acts on multiple intracellular signaling pathways, including adenosine monophosphate (AMP)-activated protein kinase (AMPK) activation, and that AMPK and its downstream intracellular signaling control the activation and differentiation of T and B cells and inflammatory responses, metformin may exert immunomodulatory and anti- inflammatory effects. The efficacy of metformin has been investigated in preclinical and clinical studies on rheumatoid arthritis, osteoarthritis, systemic lupus erythematosus, Sjögren's syndrome, scleroderma, ankylosing spondylitis, and gout. In this review, we discuss the potential mechanisms through which metformin exerts its therapeutic effects in these diseases, focusing particularly on rheumatoid arthritis and osteoarthritis.},
	language = {eng},
	number = {1},
	journal = {The Korean Journal of Internal Medicine},
	author = {Kim, Ji-Won and Choe, Jung-Yoon and Park, Sung-Hwan},
	month = jan,
	year = {2022},
	pmid = {34879473},
	pmcid = {PMC8747910},
	keywords = {AMP-Activated Protein Kinases, AMP-activated protein kinases, Arthritis, Rheumatoid, Arthritis, rheumatoid, Connective tissue diseases, Diabetes Mellitus, Type 2, Humans, Metformin, Osteoarthritis},
	pages = {13--26},
}

Metformin is a first-line therapeutic agent for type 2 diabetes. Apart from its glucose-lowering effect, metformin is attracting interest regarding possible therapeutic benefits in various other conditions. As metformin regulates cell metabolism, proliferation, growth, and autophagy, it may also modulate immune cell functions. Given that metformin acts on multiple intracellular signaling pathways, including adenosine monophosphate (AMP)-activated protein kinase (AMPK) activation, and that AMPK and its downstream intracellular signaling control the activation and differentiation of T and B cells and inflammatory responses, metformin may exert immunomodulatory and anti- inflammatory effects. The efficacy of metformin has been investigated in preclinical and clinical studies on rheumatoid arthritis, osteoarthritis, systemic lupus erythematosus, Sjögren's syndrome, scleroderma, ankylosing spondylitis, and gout. In this review, we discuss the potential mechanisms through which metformin exerts its therapeutic effects in these diseases, focusing particularly on rheumatoid arthritis and osteoarthritis.

@misc{noauthor_two_2022,
	title = {Two large studies reveal genes and genome regions that influence schizophrenia risk},
	url = {https://www.broadinstitute.org/news/two-large-studies-reveal-genes-and-genome-regions-influence-schizophrenia-risk},
	abstract = {International collaborations analyze common and rare DNA variants in hundreds of thousands of people, further elucidating genetic roots of psychiatric disorder},
	language = {en},
	urldate = {2022-04-09},
	journal = {Broad Institute},
	month = apr,
	year = {2022},
	note = {Section: Research News},
}

International collaborations analyze common and rare DNA variants in hundreds of thousands of people, further elucidating genetic roots of psychiatric disorder

@article{lam_identifying_2021,
	title = {Identifying nootropic drug targets via large-scale cognitive {GWAS} and transcriptomics.},
	volume = {46},
	issn = {0893-133X},
	url = {https://escholarship.org/uc/item/338966jd},
	doi = {10.1038/s41386-021-01023-4},
	abstract = {Broad-based cognitive deficits are an enduring and disabling symptom for many patients with severe mental illness, and these impairments are inadequately addressed by current medications. While novel drug targets for schizophrenia and depression have emerged from recent large-scale genome-wide association studies (GWAS) of these psychiatric disorders, GWAS of general cognitive ability can suggest potential targets for nootropic drug repurposing. Here, we (1) meta-analyze results from two recent cognitive GWAS to further enhance power for locus discovery; (2) employ several complementary transcriptomic methods to identify genes in these loci that are credibly associated with cognition; and (3) further annotate the resulting genes using multiple chemoinformatic databases to identify "druggable" targets. Using our meta-analytic data set (N = 373,617), we identified 241 independent cognition-associated loci (29 novel), and 76 genes were identified by 2 or more methods of gene identification. Actin and chromatin binding gene sets were identified as novel pathways that could be targeted via drug repurposing. Leveraging our transcriptomic and chemoinformatic databases, we identified 16 putative genes targeted by existing drugs potentially available for cognitive repurposing.},
	language = {en},
	number = {10},
	urldate = {2022-05-08},
	journal = {Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology},
	author = {Lam, Max and Chen, Chia-Yen and Ge, Tian and Xia, Yan and Hill, David W. and Trampush, Joey W. and Yu, Jin and Knowles, Emma and Davies, Gail and Stahl, Eli A. and Huckins, Laura and Liewald, David C. and Djurovic, Srdjan and Melle, Ingrid and Christoforou, Andrea and Reinvang, Ivar and DeRosse, Pamela and Lundervold, Astri J. and Steen, Vidar M. and Espeseth, Thomas and Räikkönen, Katri and Widen, Elisabeth and Palotie, Aarno and Eriksson, Johan G. and Giegling, Ina and Konte, Bettina and Hartmann, Annette M. and Roussos, Panos and Giakoumaki, Stella and Burdick, Katherine E. and Payton, Antony and Ollier, William and Chiba-Falek, Ornit and Koltai, Deborah C. and Need, Anna C. and Cirulli, Elizabeth T. and Voineskos, Aristotle N. and Stefanis, Nikos C. and Avramopoulos, Dimitrios and Hatzimanolis, Alex and Smyrnis, Nikolaos and Bilder, Robert M. and Freimer, Nelson B. and Cannon, Tyrone D. and London, Edythe and Poldrack, Russell A. and Sabb, Fred W. and Congdon, Eliza and Conley, Emily Drabant and Scult, Matthew A. and Dickinson, Dwight and Straub, Richard E. and Donohoe, Gary and Morris, Derek and Corvin, Aiden and Gill, Michael and Hariri, Ahmad R. and Weinberger, Daniel R. and Pendleton, Neil and Bitsios, Panos and Rujescu, Dan and Lahti, Jari and Le Hellard, Stephanie and Keller, Matthew C. and Andreassen, Ole A. and Deary, Ian J. and Glahn, David C. and Huang, Hailiang and Liu, Chunyu and Malhotra, Anil K. and Lencz, Todd},
	month = sep,
	year = {2021},
	note = {Number: 10},
	pages = {1788--1801},
}

Broad-based cognitive deficits are an enduring and disabling symptom for many patients with severe mental illness, and these impairments are inadequately addressed by current medications. While novel drug targets for schizophrenia and depression have emerged from recent large-scale genome-wide association studies (GWAS) of these psychiatric disorders, GWAS of general cognitive ability can suggest potential targets for nootropic drug repurposing. Here, we (1) meta-analyze results from two recent cognitive GWAS to further enhance power for locus discovery; (2) employ several complementary transcriptomic methods to identify genes in these loci that are credibly associated with cognition; and (3) further annotate the resulting genes using multiple chemoinformatic databases to identify "druggable" targets. Using our meta-analytic data set (N = 373,617), we identified 241 independent cognition-associated loci (29 novel), and 76 genes were identified by 2 or more methods of gene identification. Actin and chromatin binding gene sets were identified as novel pathways that could be targeted via drug repurposing. Leveraging our transcriptomic and chemoinformatic databases, we identified 16 putative genes targeted by existing drugs potentially available for cognitive repurposing.

@article{mejia-gutierrez_silico_2021,
	title = {In {Silico} {Repositioning} of {Dopamine} {Modulators} with {Possible} {Application} to {Schizophrenia}: {Pharmacophore} {Mapping}, {Molecular} {Docking} and {Molecular} {Dynamics} {Analysis}},
	volume = {6},
	shorttitle = {In {Silico} {Repositioning} of {Dopamine} {Modulators} with {Possible} {Application} to {Schizophrenia}},
	url = {https://doi.org/10.1021/acsomega.0c05984},
	doi = {10.1021/acsomega.0c05984},
	abstract = {We have performed theoretical calculations with 70 drugs that have been considered in 231 clinical trials as possible candidates to repurpose drugs for schizophrenia based on their interactions with the dopaminergic system. A hypothesis of shared pharmacophore features was formulated to support our calculations. To do so, we have used the crystal structure of the D2-like dopamine receptor in complex with risperidone, eticlopride, and nemonapride. Linagliptin, citalopram, flunarizine, sildenafil, minocycline, and duloxetine were the drugs that best fit with our model. Molecular docking calculations, molecular dynamics outcomes, blood-brain barrier penetration, and human intestinal absorption were studied and compared with the results. From the six drugs selected in the shared pharmacophore features input, flunarizine showed the best docking score with D2, D3, and D4 dopamine receptors and had high stability during molecular dynamics simulations. Flunarizine is a frequently used medication to treat migraines and vertigo. However, its antipsychotic properties have been previously hypothesized, particularly because of its possible ability to block the D2 dopamine receptors.},
	number = {23},
	urldate = {2022-05-25},
	journal = {ACS Omega},
	author = {Mejia-Gutierrez, Melissa and Vásquez-Paz, Bryan D. and Fierro, Leonardo and Maza, Julio R.},
	month = jun,
	year = {2021},
	note = {Number: 23
Publisher: American Chemical Society},
	pages = {14748--14764},
}

We have performed theoretical calculations with 70 drugs that have been considered in 231 clinical trials as possible candidates to repurpose drugs for schizophrenia based on their interactions with the dopaminergic system. A hypothesis of shared pharmacophore features was formulated to support our calculations. To do so, we have used the crystal structure of the D2-like dopamine receptor in complex with risperidone, eticlopride, and nemonapride. Linagliptin, citalopram, flunarizine, sildenafil, minocycline, and duloxetine were the drugs that best fit with our model. Molecular docking calculations, molecular dynamics outcomes, blood-brain barrier penetration, and human intestinal absorption were studied and compared with the results. From the six drugs selected in the shared pharmacophore features input, flunarizine showed the best docking score with D2, D3, and D4 dopamine receptors and had high stability during molecular dynamics simulations. Flunarizine is a frequently used medication to treat migraines and vertigo. However, its antipsychotic properties have been previously hypothesized, particularly because of its possible ability to block the D2 dopamine receptors.

@article{shukla_signature-based_2021,
	title = {Signature-based approaches for informed drug repurposing: targeting {CNS} disorders},
	volume = {46},
	issn = {0893-133X},
	shorttitle = {Signature-based approaches for informed drug repurposing},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7688959/},
	doi = {10.1038/s41386-020-0752-6},
	abstract = {CNS disorders, and in particular psychiatric illnesses, lack definitive disease-altering therapeutics. The limited understanding of the mechanisms driving these illnesses with the slow pace and high cost of drug development exacerbates this issue. For these reasons, drug repurposing – both a less expensive and time-efficient practice compared to de novo drug development – has been a promising strategy to overcome the paucity of treatments available for these debilitating disorders. While empirical drug-repurposing has been a routine practice in clinical psychiatry, innovative, informed, and cost-effective repurposing efforts using big data (“omics”) have been designed to characterize drugs by structural and transcriptomic signatures. These strategies, in conjunction with ontological integration, provide an important opportunity to address knowledge-based challenges associated with drug development for CNS disorders. In this review, we discuss various signature-based in silico approaches to drug repurposing, its integration with multiple omics platforms, and how this data can be used for clinically relevant, evidence-based drug repurposing. These tools provide an exciting translational avenue to merge omics-based drug discovery platforms with patient-specific disease signatures, ultimately facilitating the identification of new therapies for numerous psychiatric disorders.},
	number = {1},
	urldate = {2022-05-27},
	journal = {Neuropsychopharmacology},
	author = {Shukla, Rammohan and Henkel, Nicholas D. and Alganem, Khaled and Hamoud, Abdul-rizaq and Reigle, James and Alnafisah, Rawan S. and Eby, Hunter M. and Imami, Ali S. and Creeden, Justin F and Miruzzi, Scott A. and Meller, Jaroslaw and Mccullumsmith, Robert E.},
	month = jan,
	year = {2021},
	pmid = {32604402},
	pmcid = {PMC7688959},
	note = {Number: 1},
	pages = {116--130},
}

CNS disorders, and in particular psychiatric illnesses, lack definitive disease-altering therapeutics. The limited understanding of the mechanisms driving these illnesses with the slow pace and high cost of drug development exacerbates this issue. For these reasons, drug repurposing – both a less expensive and time-efficient practice compared to de novo drug development – has been a promising strategy to overcome the paucity of treatments available for these debilitating disorders. While empirical drug-repurposing has been a routine practice in clinical psychiatry, innovative, informed, and cost-effective repurposing efforts using big data (“omics”) have been designed to characterize drugs by structural and transcriptomic signatures. These strategies, in conjunction with ontological integration, provide an important opportunity to address knowledge-based challenges associated with drug development for CNS disorders. In this review, we discuss various signature-based in silico approaches to drug repurposing, its integration with multiple omics platforms, and how this data can be used for clinically relevant, evidence-based drug repurposing. These tools provide an exciting translational avenue to merge omics-based drug discovery platforms with patient-specific disease signatures, ultimately facilitating the identification of new therapies for numerous psychiatric disorders.

@article{shukla_signature-based_2021-1,
	title = {Signature-based approaches for informed drug repurposing: targeting {CNS} disorders},
	volume = {46},
	issn = {0893-133X},
	shorttitle = {Signature-based approaches for informed drug repurposing},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7688959/},
	doi = {10.1038/s41386-020-0752-6},
	abstract = {CNS disorders, and in particular psychiatric illnesses, lack definitive disease-altering therapeutics. The limited understanding of the mechanisms driving these illnesses with the slow pace and high cost of drug development exacerbates this issue. For these reasons, drug repurposing – both a less expensive and time-efficient practice compared to de novo drug development – has been a promising strategy to overcome the paucity of treatments available for these debilitating disorders. While empirical drug-repurposing has been a routine practice in clinical psychiatry, innovative, informed, and cost-effective repurposing efforts using big data (“omics”) have been designed to characterize drugs by structural and transcriptomic signatures. These strategies, in conjunction with ontological integration, provide an important opportunity to address knowledge-based challenges associated with drug development for CNS disorders. In this review, we discuss various signature-based in silico approaches to drug repurposing, its integration with multiple omics platforms, and how this data can be used for clinically relevant, evidence-based drug repurposing. These tools provide an exciting translational avenue to merge omics-based drug discovery platforms with patient-specific disease signatures, ultimately facilitating the identification of new therapies for numerous psychiatric disorders.},
	number = {1},
	urldate = {2022-05-29},
	journal = {Neuropsychopharmacology},
	author = {Shukla, Rammohan and Henkel, Nicholas D. and Alganem, Khaled and Hamoud, Abdul-rizaq and Reigle, James and Alnafisah, Rawan S. and Eby, Hunter M. and Imami, Ali S. and Creeden, Justin F and Miruzzi, Scott A. and Meller, Jaroslaw and Mccullumsmith, Robert E.},
	month = jan,
	year = {2021},
	pmid = {32604402},
	pmcid = {PMC7688959},
	note = {Number: 1},
	pages = {116--130},
}

CNS disorders, and in particular psychiatric illnesses, lack definitive disease-altering therapeutics. The limited understanding of the mechanisms driving these illnesses with the slow pace and high cost of drug development exacerbates this issue. For these reasons, drug repurposing – both a less expensive and time-efficient practice compared to de novo drug development – has been a promising strategy to overcome the paucity of treatments available for these debilitating disorders. While empirical drug-repurposing has been a routine practice in clinical psychiatry, innovative, informed, and cost-effective repurposing efforts using big data (“omics”) have been designed to characterize drugs by structural and transcriptomic signatures. These strategies, in conjunction with ontological integration, provide an important opportunity to address knowledge-based challenges associated with drug development for CNS disorders. In this review, we discuss various signature-based in silico approaches to drug repurposing, its integration with multiple omics platforms, and how this data can be used for clinically relevant, evidence-based drug repurposing. These tools provide an exciting translational avenue to merge omics-based drug discovery platforms with patient-specific disease signatures, ultimately facilitating the identification of new therapies for numerous psychiatric disorders.

@article{zanin_early_2021,
	title = {An {Early} {Stage} {Researcher}'s {Primer} on {Systems} {Medicine} {Terminology}},
	volume = {4},
	url = {https://www.liebertpub.com/doi/10.1089/nsm.2020.0003},
	doi = {10.1089/nsm.2020.0003},
	abstract = {Background: Systems Medicine is a novel approach to medicine, that is, an interdisciplinary field that considers the human body as a system, composed of multiple parts and of complex relationships at multiple levels, and further integrated into an environment. Exploring Systems Medicine implies understanding and combining concepts coming from diametral different fields, including medicine, biology, statistics, modeling and simulation, and data science. Such heterogeneity leads to semantic issues, which may slow down implementation and fruitful interaction between these highly diverse fields.

Methods: In this review, we collect and explain more than100 terms related to Systems Medicine. These include both modeling and data science terms and basic systems medicine terms, along with some synthetic definitions, examples of applications, and lists of relevant references.

Results: This glossary aims at being a first aid kit for the Systems Medicine researcher facing an unfamiliar term, where he/she can get a first understanding of them, and, more importantly, examples and references for digging into the topic.},
	number = {1},
	urldate = {2022-06-05},
	journal = {Network and Systems Medicine},
	author = {Zanin, Massimiliano and Aitya, Nadim A.A. and Basilio, José and Baumbach, Jan and Benis, Arriel and Behera, Chandan K. and Bucholc, Magda and Castiglione, Filippo and Chouvarda, Ioanna and Comte, Blandine and Dao, Tien-Tuan and Ding, Xuemei and Pujos-Guillot, Estelle and Filipovic, Nenad and Finn, David P. and Glass, David H. and Harel, Nissim and Iesmantas, Tomas and Ivanoska, Ilinka and Joshi, Alok and Boudjeltia, Karim Zouaoui and Kaoui, Badr and Kaur, Daman and Maguire, Liam P. and McClean, Paula L. and McCombe, Niamh and de Miranda, João Luís and Moisescu, Mihnea Alexandru and Pappalardo, Francesco and Polster, Annikka and Prasad, Girijesh and Rozman, Damjana and Sacala, Ioan and Sanchez-Bornot, Jose M. and Schmid, Johannes A. and Sharp, Trevor and Solé-Casals, Jordi and Spiwok, Vojtěch and Spyrou, George M. and Stalidzans, Egils and Stres, Blaž and Sustersic, Tijana and Symeonidis, Ioannis and Tieri, Paolo and Todd, Stephen and Van Steen, Kristel and Veneva, Milena and Wang, Da-Hui and Wang, Haiying and Wang, Hui and Watterson, Steven and Wong-Lin, KongFatt and Yang, Su and Zou, Xin and Schmidt, Harald H.H.W.},
	month = mar,
	year = {2021},
	note = {Number: 1
Publisher: Mary Ann Liebert, Inc., publishers},
	keywords = {multiscale data science, multiscale modeling, systems medicine},
	pages = {2--50},
}

Background: Systems Medicine is a novel approach to medicine, that is, an interdisciplinary field that considers the human body as a system, composed of multiple parts and of complex relationships at multiple levels, and further integrated into an environment. Exploring Systems Medicine implies understanding and combining concepts coming from diametral different fields, including medicine, biology, statistics, modeling and simulation, and data science. Such heterogeneity leads to semantic issues, which may slow down implementation and fruitful interaction between these highly diverse fields. Methods: In this review, we collect and explain more than100 terms related to Systems Medicine. These include both modeling and data science terms and basic systems medicine terms, along with some synthetic definitions, examples of applications, and lists of relevant references. Results: This glossary aims at being a first aid kit for the Systems Medicine researcher facing an unfamiliar term, where he/she can get a first understanding of them, and, more importantly, examples and references for digging into the topic.

@article{lam_identifying_2021-1,
	title = {Identifying nootropic drug targets via large-scale cognitive {GWAS} and transcriptomics.},
	volume = {46},
	issn = {0893-133X},
	url = {https://escholarship.org/uc/item/338966jd},
	doi = {10.1038/s41386-021-01023-4},
	abstract = {Broad-based cognitive deficits are an enduring and disabling symptom for many patients with severe mental illness, and these impairments are inadequately addressed by current medications. While novel drug targets for schizophrenia and depression have emerged from recent large-scale genome-wide association studies (GWAS) of these psychiatric disorders, GWAS of general cognitive ability can suggest potential targets for nootropic drug repurposing. Here, we (1) meta-analyze results from two recent cognitive GWAS to further enhance power for locus discovery; (2) employ several complementary transcriptomic methods to identify genes in these loci that are credibly associated with cognition; and (3) further annotate the resulting genes using multiple chemoinformatic databases to identify "druggable" targets. Using our meta-analytic data set (N = 373,617), we identified 241 independent cognition-associated loci (29 novel), and 76 genes were identified by 2 or more methods of gene identification. Actin and chromatin binding gene sets were identified as novel pathways that could be targeted via drug repurposing. Leveraging our transcriptomic and chemoinformatic databases, we identified 16 putative genes targeted by existing drugs potentially available for cognitive repurposing.},
	language = {en},
	number = {10},
	urldate = {2022-06-28},
	journal = {Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology},
	author = {Lam, Max and Chen, Chia-Yen and Ge, Tian and Xia, Yan and Hill, David W. and Trampush, Joey W. and Yu, Jin and Knowles, Emma and Davies, Gail and Stahl, Eli A. and Huckins, Laura and Liewald, David C. and Djurovic, Srdjan and Melle, Ingrid and Christoforou, Andrea and Reinvang, Ivar and DeRosse, Pamela and Lundervold, Astri J. and Steen, Vidar M. and Espeseth, Thomas and Räikkönen, Katri and Widen, Elisabeth and Palotie, Aarno and Eriksson, Johan G. and Giegling, Ina and Konte, Bettina and Hartmann, Annette M. and Roussos, Panos and Giakoumaki, Stella and Burdick, Katherine E. and Payton, Antony and Ollier, William and Chiba-Falek, Ornit and Koltai, Deborah C. and Need, Anna C. and Cirulli, Elizabeth T. and Voineskos, Aristotle N. and Stefanis, Nikos C. and Avramopoulos, Dimitrios and Hatzimanolis, Alex and Smyrnis, Nikolaos and Bilder, Robert M. and Freimer, Nelson B. and Cannon, Tyrone D. and London, Edythe and Poldrack, Russell A. and Sabb, Fred W. and Congdon, Eliza and Conley, Emily Drabant and Scult, Matthew A. and Dickinson, Dwight and Straub, Richard E. and Donohoe, Gary and Morris, Derek and Corvin, Aiden and Gill, Michael and Hariri, Ahmad R. and Weinberger, Daniel R. and Pendleton, Neil and Bitsios, Panos and Rujescu, Dan and Lahti, Jari and Le Hellard, Stephanie and Keller, Matthew C. and Andreassen, Ole A. and Deary, Ian J. and Glahn, David C. and Huang, Hailiang and Liu, Chunyu and Malhotra, Anil K. and Lencz, Todd},
	month = sep,
	year = {2021},
	note = {Number: 10},
	pages = {1788--1801},
}

Broad-based cognitive deficits are an enduring and disabling symptom for many patients with severe mental illness, and these impairments are inadequately addressed by current medications. While novel drug targets for schizophrenia and depression have emerged from recent large-scale genome-wide association studies (GWAS) of these psychiatric disorders, GWAS of general cognitive ability can suggest potential targets for nootropic drug repurposing. Here, we (1) meta-analyze results from two recent cognitive GWAS to further enhance power for locus discovery; (2) employ several complementary transcriptomic methods to identify genes in these loci that are credibly associated with cognition; and (3) further annotate the resulting genes using multiple chemoinformatic databases to identify "druggable" targets. Using our meta-analytic data set (N = 373,617), we identified 241 independent cognition-associated loci (29 novel), and 76 genes were identified by 2 or more methods of gene identification. Actin and chromatin binding gene sets were identified as novel pathways that could be targeted via drug repurposing. Leveraging our transcriptomic and chemoinformatic databases, we identified 16 putative genes targeted by existing drugs potentially available for cognitive repurposing.

@article{zanin_early_2021-1,
	title = {An {Early} {Stage} {Researcher}'s {Primer} on {Systems} {Medicine} {Terminology}},
	volume = {4},
	url = {https://www.liebertpub.com/doi/10.1089/nsm.2020.0003},
	doi = {10.1089/nsm.2020.0003},
	abstract = {Background: Systems Medicine is a novel approach to medicine, that is, an interdisciplinary field that considers the human body as a system, composed of multiple parts and of complex relationships at multiple levels, and further integrated into an environment. Exploring Systems Medicine implies understanding and combining concepts coming from diametral different fields, including medicine, biology, statistics, modeling and simulation, and data science. Such heterogeneity leads to semantic issues, which may slow down implementation and fruitful interaction between these highly diverse fields.

Methods: In this review, we collect and explain more than100 terms related to Systems Medicine. These include both modeling and data science terms and basic systems medicine terms, along with some synthetic definitions, examples of applications, and lists of relevant references.

Results: This glossary aims at being a first aid kit for the Systems Medicine researcher facing an unfamiliar term, where he/she can get a first understanding of them, and, more importantly, examples and references for digging into the topic.},
	number = {1},
	urldate = {2022-07-18},
	journal = {Network and Systems Medicine},
	author = {Zanin, Massimiliano and Aitya, Nadim A.A. and Basilio, José and Baumbach, Jan and Benis, Arriel and Behera, Chandan K. and Bucholc, Magda and Castiglione, Filippo and Chouvarda, Ioanna and Comte, Blandine and Dao, Tien-Tuan and Ding, Xuemei and Pujos-Guillot, Estelle and Filipovic, Nenad and Finn, David P. and Glass, David H. and Harel, Nissim and Iesmantas, Tomas and Ivanoska, Ilinka and Joshi, Alok and Boudjeltia, Karim Zouaoui and Kaoui, Badr and Kaur, Daman and Maguire, Liam P. and McClean, Paula L. and McCombe, Niamh and de Miranda, João Luís and Moisescu, Mihnea Alexandru and Pappalardo, Francesco and Polster, Annikka and Prasad, Girijesh and Rozman, Damjana and Sacala, Ioan and Sanchez-Bornot, Jose M. and Schmid, Johannes A. and Sharp, Trevor and Solé-Casals, Jordi and Spiwok, Vojtěch and Spyrou, George M. and Stalidzans, Egils and Stres, Blaž and Sustersic, Tijana and Symeonidis, Ioannis and Tieri, Paolo and Todd, Stephen and Van Steen, Kristel and Veneva, Milena and Wang, Da-Hui and Wang, Haiying and Wang, Hui and Watterson, Steven and Wong-Lin, KongFatt and Yang, Su and Zou, Xin and Schmidt, Harald H.H.W.},
	month = mar,
	year = {2021},
	note = {Number: 1
Publisher: Mary Ann Liebert, Inc., publishers},
	keywords = {multiscale data science, multiscale modeling, systems medicine},
	pages = {2--50},
}

Background: Systems Medicine is a novel approach to medicine, that is, an interdisciplinary field that considers the human body as a system, composed of multiple parts and of complex relationships at multiple levels, and further integrated into an environment. Exploring Systems Medicine implies understanding and combining concepts coming from diametral different fields, including medicine, biology, statistics, modeling and simulation, and data science. Such heterogeneity leads to semantic issues, which may slow down implementation and fruitful interaction between these highly diverse fields. Methods: In this review, we collect and explain more than100 terms related to Systems Medicine. These include both modeling and data science terms and basic systems medicine terms, along with some synthetic definitions, examples of applications, and lists of relevant references. Results: This glossary aims at being a first aid kit for the Systems Medicine researcher facing an unfamiliar term, where he/she can get a first understanding of them, and, more importantly, examples and references for digging into the topic.

@article{gomes_beyond_2021,
	title = {Beyond {Dopamine} {Receptor} {Antagonism}: {New} {Targets} for {Schizophrenia} {Treatment} and {Prevention}},
	volume = {22},
	issn = {1422-0067},
	shorttitle = {Beyond {Dopamine} {Receptor} {Antagonism}},
	doi = {10.3390/ijms22094467},
	abstract = {Treatment of schizophrenia (SCZ) historically relies on the use of antipsychotic drugs to treat psychosis, with all of the currently available antipsychotics acting through the antagonism of dopamine D2 receptors. Although antipsychotics reduce psychotic symptoms in many patients, they induce numerous undesirable effects and are not effective against negative and cognitive symptoms. These highlight the need to develop new drugs to treat SCZ. An advanced understanding of the circuitry of SCZ has pointed to pathological origins in the excitation/inhibition balance in regions such as the hippocampus, and restoring function in this region, particularly as a means to compensate for parvalbumin (PV) interneuron loss and resultant hippocampal hyperactivity, may be a more efficacious approach to relieve a broad range of SCZ symptoms. Other targets, such as cholinergic receptors and the trace amine-associated receptor 1 (TAAR1), have also shown some promise for the treatment of SCZ. Importantly, assessing efficacy of novel compounds must take into consideration treatment history of the patient, as preclinical studies suggest prior antipsychotic treatment may interfere with the efficacy of these novel agents. However, while novel therapeutic targets may be more effective in treating SCZ, a more effective approach would be to prevent the transition to SCZ in susceptible individuals. A focus on stress, which has been shown to be a predisposing factor in risk for SCZ, is a possible avenue that has shown promise in preclinical studies. Therefore, therapeutic approaches based on our current understanding of the circuitry of SCZ and its etiology are likely to enable development of more effective therapeutic interventions for this complex disorder.},
	language = {eng},
	number = {9},
	journal = {International Journal of Molecular Sciences},
	author = {Gomes, Felipe V. and Grace, Anthony A.},
	month = apr,
	year = {2021},
	pmid = {33922888},
	pmcid = {PMC8123139},
	note = {Number: 9},
	keywords = {Animals, Antipsychotic Agents, D-Amino-Acid Oxidase, Dopamine Antagonists, Glutamic Acid, Humans, Molecular Targeted Therapy, Receptors, Cholinergic, Receptors, G-Protein-Coupled, Schizophrenia, Sodium Benzoate, antipsychotics, dopamine, gamma-Aminobutyric Acid, glutamate, hippocampus, parvalbumin, psychosis, stress},
	pages = {4467},
}

Treatment of schizophrenia (SCZ) historically relies on the use of antipsychotic drugs to treat psychosis, with all of the currently available antipsychotics acting through the antagonism of dopamine D2 receptors. Although antipsychotics reduce psychotic symptoms in many patients, they induce numerous undesirable effects and are not effective against negative and cognitive symptoms. These highlight the need to develop new drugs to treat SCZ. An advanced understanding of the circuitry of SCZ has pointed to pathological origins in the excitation/inhibition balance in regions such as the hippocampus, and restoring function in this region, particularly as a means to compensate for parvalbumin (PV) interneuron loss and resultant hippocampal hyperactivity, may be a more efficacious approach to relieve a broad range of SCZ symptoms. Other targets, such as cholinergic receptors and the trace amine-associated receptor 1 (TAAR1), have also shown some promise for the treatment of SCZ. Importantly, assessing efficacy of novel compounds must take into consideration treatment history of the patient, as preclinical studies suggest prior antipsychotic treatment may interfere with the efficacy of these novel agents. However, while novel therapeutic targets may be more effective in treating SCZ, a more effective approach would be to prevent the transition to SCZ in susceptible individuals. A focus on stress, which has been shown to be a predisposing factor in risk for SCZ, is a possible avenue that has shown promise in preclinical studies. Therefore, therapeutic approaches based on our current understanding of the circuitry of SCZ and its etiology are likely to enable development of more effective therapeutic interventions for this complex disorder.

@article{alnefeesi_trace_2021,
	title = {Trace amine-associated receptor 1 ({TAAR1}): {Potential} application in mood disorders: {A} systematic review},
	volume = {131},
	issn = {0149-7634},
	shorttitle = {Trace amine-associated receptor 1 ({TAAR1})},
	url = {https://www.sciencedirect.com/science/article/pii/S0149763421004024},
	doi = {10.1016/j.neubiorev.2021.09.020},
	abstract = {There is a need for innovation with respect to therapeutics in psychiatry. Available evidence indicates that the trace amine-associated receptor 1 (TAAR1) agonist SEP-363856 is promising, as it improves measures of cognitive and reward function in schizophrenia. Hedonic and cognitive impairments are transdiagnostic and constitute major burdens in mood disorders. Herein, we systematically review the behavioural and genetic literature documenting the role of TAAR1 in reward and cognitive function, and propose a mechanistic model of TAAR1’s functions in the brain. Notably, TAAR1 activity confers antidepressant-like effects, enhances attention and response inhibition, and reduces compulsive reward seeking without impairing normal function. Further characterization of the responsible mechanisms suggests ion-homeostatic, metabolic, neurotrophic, and anti-inflammatory enhancements in the limbic system. Multiple lines of evidence establish the viability of TAAR1 as a biological target for the treatment of mood disorders. Furthermore, the evidence suggests a role for TAAR1 in reward and cognitive function, which is attributed to a cascade of events that are relevant to the cellular integrity and function of the central nervous system.},
	language = {en},
	urldate = {2022-07-21},
	journal = {Neuroscience \& Biobehavioral Reviews},
	author = {Alnefeesi, Yazen and Tamura, Jocelyn K. and Lui, Leanna M. W. and Jawad, Muhammad Youshay and Ceban, Felicia and Ling, Susan and Nasri, Flora and Rosenblat, Joshua D. and McIntyre, Roger S.},
	month = dec,
	year = {2021},
	keywords = {Arousal, Attention, Bipolar disorder, Brain derived neurotrophic factor (BDNF), Cognitive control, Cognitive function, Depression, Mammalian target of rapamycin (mTOR), Medial prefrontal cortex (mPFC), Reward function, Trace amine-associated receptor 1 (TAAR1), Ventral tegmental area (VTA)},
	pages = {192--210},
}

There is a need for innovation with respect to therapeutics in psychiatry. Available evidence indicates that the trace amine-associated receptor 1 (TAAR1) agonist SEP-363856 is promising, as it improves measures of cognitive and reward function in schizophrenia. Hedonic and cognitive impairments are transdiagnostic and constitute major burdens in mood disorders. Herein, we systematically review the behavioural and genetic literature documenting the role of TAAR1 in reward and cognitive function, and propose a mechanistic model of TAAR1’s functions in the brain. Notably, TAAR1 activity confers antidepressant-like effects, enhances attention and response inhibition, and reduces compulsive reward seeking without impairing normal function. Further characterization of the responsible mechanisms suggests ion-homeostatic, metabolic, neurotrophic, and anti-inflammatory enhancements in the limbic system. Multiple lines of evidence establish the viability of TAAR1 as a biological target for the treatment of mood disorders. Furthermore, the evidence suggests a role for TAAR1 in reward and cognitive function, which is attributed to a cascade of events that are relevant to the cellular integrity and function of the central nervous system.

@article{wu_potential_2021,
	title = {Potential of {Ligands} for {Trace} {Amine}-{Associated} {Receptor} 1 ({TAAR1}) in the {Management} of {Substance} {Use} {Disorders}},
	volume = {35},
	issn = {1172-7047},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8787759/},
	doi = {10.1007/s40263-021-00871-4},
	abstract = {Trace amines, including β-phenylethylamine (β-PEA), p-tyramine (TYR), tryptamine (TRP) and p-octopamine (OCT), represent a group of amines expressed at low levels in the mammalian brain. Given the close structural similarities to traditional monoamines, the links between trace amines and the monoaminergic system have long been established. Trace amine associated receptor 1 (TAAR1), the most well characterized receptor in the TAARs family, has been shown to be potently activated by trace amines like TYR and PEA. Meanwhile, catecholamine metabolites and amphetamine analogs are also potent agonists of TAAR1, implicating its role in mediating the monoaminergic system and substance use disorders. In the central nervous system, TAAR1 is expressed in brain regions involved in dopaminergic, serotonergic and glutamatergic transmission. Genetic animal models and electrophysiological studies have revealed that TAAR1 is a potent modulator of the monoaminergic system, and TAAR1 agonists may be potential pharmacotherapies for the treatment of substance use disorders. Selective and potent engineered TAAR1 ligands, including full (RO5166017 and RO5256390) and partial (RO5203648, RO5263397 and RO5073012) agonists and the antagonist EPPTB (N-(3-ethoxyphenyl)-4-(1-pyrrolidinyl)-3-(trifluoromethyl)benzamide, RO5212773), serve as invaluable tools for the investigation of TAAR1 functions and display high potential for the development of TAAR1-based pharmacotherapies for the treatment of substance use disorders. Despite a number of advances that have been made, more clinical studies are warranted in order to test the potential and efficacy of TAAR1 ligands in the treatment of psychiatric disorders, especially substance use disorders.},
	number = {12},
	urldate = {2022-07-23},
	journal = {CNS drugs},
	author = {Wu, Ruyan and Li, Jun-Xu},
	month = dec,
	year = {2021},
	pmid = {34766253},
	pmcid = {PMC8787759},
	note = {Number: 12},
	pages = {1239--1248},
}

Trace amines, including β-phenylethylamine (β-PEA), p-tyramine (TYR), tryptamine (TRP) and p-octopamine (OCT), represent a group of amines expressed at low levels in the mammalian brain. Given the close structural similarities to traditional monoamines, the links between trace amines and the monoaminergic system have long been established. Trace amine associated receptor 1 (TAAR1), the most well characterized receptor in the TAARs family, has been shown to be potently activated by trace amines like TYR and PEA. Meanwhile, catecholamine metabolites and amphetamine analogs are also potent agonists of TAAR1, implicating its role in mediating the monoaminergic system and substance use disorders. In the central nervous system, TAAR1 is expressed in brain regions involved in dopaminergic, serotonergic and glutamatergic transmission. Genetic animal models and electrophysiological studies have revealed that TAAR1 is a potent modulator of the monoaminergic system, and TAAR1 agonists may be potential pharmacotherapies for the treatment of substance use disorders. Selective and potent engineered TAAR1 ligands, including full (RO5166017 and RO5256390) and partial (RO5203648, RO5263397 and RO5073012) agonists and the antagonist EPPTB (N-(3-ethoxyphenyl)-4-(1-pyrrolidinyl)-3-(trifluoromethyl)benzamide, RO5212773), serve as invaluable tools for the investigation of TAAR1 functions and display high potential for the development of TAAR1-based pharmacotherapies for the treatment of substance use disorders. Despite a number of advances that have been made, more clinical studies are warranted in order to test the potential and efficacy of TAAR1 ligands in the treatment of psychiatric disorders, especially substance use disorders.

@article{olson_promise_2021,
	title = {The {Promise} of {Psychedelic} {Science}},
	volume = {4},
	url = {https://doi.org/10.1021/acsptsci.1c00071},
	doi = {10.1021/acsptsci.1c00071},
	number = {2},
	journal = {ACS Pharmacology \& Translational Science},
	author = {Olson, David E.},
	month = apr,
	year = {2021},
	note = {Number: 2
Publisher: American Chemical Society},
	pages = {413--415},
}

@article{yang_physical_2021,
	title = {Physical bioenergetics: {Energy} fluxes, budgets, and constraints in cells},
	volume = {118},
	copyright = {© 2021 . https://www.pnas.org/site/aboutpnas/licenses.xhtmlPublished under the PNAS license.},
	issn = {0027-8424, 1091-6490},
	shorttitle = {Physical bioenergetics},
	url = {https://www.pnas.org/content/118/26/e2026786118},
	doi = {10.1073/pnas.2026786118},
	abstract = {\<p\>Cells are the basic units of all living matter which harness the flow of energy to drive the processes of life. While the biochemical networks involved in energy transduction are well-characterized, the energetic costs and constraints for specific cellular processes remain largely unknown. In particular, what are the energy budgets of cells? What are the constraints and limits energy flows impose on cellular processes? Do cells operate near these limits, and if so how do energetic constraints impact cellular functions? Physics has provided many tools to study nonequilibrium systems and to define physical limits, but applying these tools to cell biology remains a challenge. Physical bioenergetics, which resides at the interface of nonequilibrium physics, energy metabolism, and cell biology, seeks to understand how much energy cells are using, how they partition this energy between different cellular processes, and the associated energetic constraints. Here we review recent advances and discuss open questions and challenges in physical bioenergetics.\</p\>},
	language = {en},
	number = {26},
	urldate = {2021-07-01},
	journal = {Proceedings of the National Academy of Sciences},
	author = {Yang, Xingbo and Heinemann, Matthias and Howard, Jonathon and Huber, Greg and Iyer-Biswas, Srividya and Treut, Guillaume Le and Lynch, Michael and Montooth, Kristi L. and Needleman, Daniel J. and Pigolotti, Simone and Rodenfels, Jonathan and Ronceray, Pierre and Shankar, Sadasivan and Tavassoly, Iman and Thutupalli, Shashi and Titov, Denis V. and Wang, Jin and Foster, Peter J.},
	month = jun,
	year = {2021},
	pmid = {34140336},
}

<p>Cells are the basic units of all living matter which harness the flow of energy to drive the processes of life. While the biochemical networks involved in energy transduction are well-characterized, the energetic costs and constraints for specific cellular processes remain largely unknown. In particular, what are the energy budgets of cells? What are the constraints and limits energy flows impose on cellular processes? Do cells operate near these limits, and if so how do energetic constraints impact cellular functions? Physics has provided many tools to study nonequilibrium systems and to define physical limits, but applying these tools to cell biology remains a challenge. Physical bioenergetics, which resides at the interface of nonequilibrium physics, energy metabolism, and cell biology, seeks to understand how much energy cells are using, how they partition this energy between different cellular processes, and the associated energetic constraints. Here we review recent advances and discuss open questions and challenges in physical bioenergetics.</p>

@article{vargas_psychedelics_2021,
	title = {Psychedelics and {Other} {Psychoplastogens} for {Treating} {Mental} {Illness}},
	volume = {12},
	issn = {1664-0640},
	url = {https://www.frontiersin.org/articles/10.3389/fpsyt.2021.727117},
	abstract = {Psychedelics have inspired new hope for treating brain disorders, as they seem to be unlike any treatments currently available. Not only do they produce sustained therapeutic effects following a single administration, they also appear to have broad therapeutic potential, demonstrating efficacy for treating depression, post-traumatic stress disorder (PTSD), anxiety disorders, substance abuse disorder, and alcohol use disorder, among others. Psychedelics belong to a more general class of compounds known as psychoplastogens, which robustly promote structural and functional neural plasticity in key circuits relevant to brain health. Here we discuss the importance of structural plasticity in the treatment of neuropsychiatric diseases, as well as the evidence demonstrating that psychedelics are among the most effective chemical modulators of neural plasticity studied to date. Furthermore, we provide a theoretical framework with the potential to explain why psychedelic compounds produce long-lasting therapeutic effects across a wide range of brain disorders. Despite their promise as broadly efficacious neurotherapeutics, there are several issues associated with psychedelic-based medicines that drastically limit their clinical scalability. We discuss these challenges and how they might be overcome through the development of non-hallucinogenic psychoplastogens. The clinical use of psychedelics and other psychoplastogenic compounds marks a paradigm shift in neuropsychiatry toward therapeutic approaches relying on the selective modulation of neural circuits with small molecule drugs. Psychoplastogen research brings us one step closer to actually curing mental illness by rectifying the underlying pathophysiology of disorders like depression, moving beyond simply treating disease symptoms. However, determining how to most effectively deploy psychoplastogenic medicines at scale will be an important consideration as the field moves forward.},
	urldate = {2022-11-25},
	journal = {Frontiers in Psychiatry},
	author = {Vargas, Maxemiliano V. and Meyer, Retsina and Avanes, Arabo A. and Rus, Mark and Olson, David E.},
	year = {2021},
}

Psychedelics have inspired new hope for treating brain disorders, as they seem to be unlike any treatments currently available. Not only do they produce sustained therapeutic effects following a single administration, they also appear to have broad therapeutic potential, demonstrating efficacy for treating depression, post-traumatic stress disorder (PTSD), anxiety disorders, substance abuse disorder, and alcohol use disorder, among others. Psychedelics belong to a more general class of compounds known as psychoplastogens, which robustly promote structural and functional neural plasticity in key circuits relevant to brain health. Here we discuss the importance of structural plasticity in the treatment of neuropsychiatric diseases, as well as the evidence demonstrating that psychedelics are among the most effective chemical modulators of neural plasticity studied to date. Furthermore, we provide a theoretical framework with the potential to explain why psychedelic compounds produce long-lasting therapeutic effects across a wide range of brain disorders. Despite their promise as broadly efficacious neurotherapeutics, there are several issues associated with psychedelic-based medicines that drastically limit their clinical scalability. We discuss these challenges and how they might be overcome through the development of non-hallucinogenic psychoplastogens. The clinical use of psychedelics and other psychoplastogenic compounds marks a paradigm shift in neuropsychiatry toward therapeutic approaches relying on the selective modulation of neural circuits with small molecule drugs. Psychoplastogen research brings us one step closer to actually curing mental illness by rectifying the underlying pathophysiology of disorders like depression, moving beyond simply treating disease symptoms. However, determining how to most effectively deploy psychoplastogenic medicines at scale will be an important consideration as the field moves forward.

@article{olson_promise_2021,
	title = {The {Promise} of {Psychedelic} {Science}},
	volume = {4},
	url = {https://doi.org/10.1021/acsptsci.1c00071},
	doi = {10.1021/acsptsci.1c00071},
	number = {2},
	journal = {ACS Pharmacology \& Translational Science},
	author = {Olson, David E.},
	month = apr,
	year = {2021},
	note = {Publisher: American Chemical Society},
	pages = {413--415},
}

@article{wu_potential_2021,
	title = {Potential of {Ligands} for {Trace} {Amine}-{Associated} {Receptor} 1 ({TAAR1}) in the {Management} of {Substance} {Use} {Disorders}},
	volume = {35},
	issn = {1172-7047},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8787759/},
	doi = {10.1007/s40263-021-00871-4},
	abstract = {Trace amines, including β-phenylethylamine (β-PEA), p-tyramine (TYR), tryptamine (TRP) and p-octopamine (OCT), represent a group of amines expressed at low levels in the mammalian brain. Given the close structural similarities to traditional monoamines, the links between trace amines and the monoaminergic system have long been established. Trace amine associated receptor 1 (TAAR1), the most well characterized receptor in the TAARs family, has been shown to be potently activated by trace amines like TYR and PEA. Meanwhile, catecholamine metabolites and amphetamine analogs are also potent agonists of TAAR1, implicating its role in mediating the monoaminergic system and substance use disorders. In the central nervous system, TAAR1 is expressed in brain regions involved in dopaminergic, serotonergic and glutamatergic transmission. Genetic animal models and electrophysiological studies have revealed that TAAR1 is a potent modulator of the monoaminergic system, and TAAR1 agonists may be potential pharmacotherapies for the treatment of substance use disorders. Selective and potent engineered TAAR1 ligands, including full (RO5166017 and RO5256390) and partial (RO5203648, RO5263397 and RO5073012) agonists and the antagonist EPPTB (N-(3-ethoxyphenyl)-4-(1-pyrrolidinyl)-3-(trifluoromethyl)benzamide, RO5212773), serve as invaluable tools for the investigation of TAAR1 functions and display high potential for the development of TAAR1-based pharmacotherapies for the treatment of substance use disorders. Despite a number of advances that have been made, more clinical studies are warranted in order to test the potential and efficacy of TAAR1 ligands in the treatment of psychiatric disorders, especially substance use disorders.},
	number = {12},
	urldate = {2022-07-23},
	journal = {CNS drugs},
	author = {Wu, Ruyan and Li, Jun-Xu},
	month = dec,
	year = {2021},
	pmid = {34766253},
	pmcid = {PMC8787759},
	pages = {1239--1248},
}

Trace amines, including β-phenylethylamine (β-PEA), p-tyramine (TYR), tryptamine (TRP) and p-octopamine (OCT), represent a group of amines expressed at low levels in the mammalian brain. Given the close structural similarities to traditional monoamines, the links between trace amines and the monoaminergic system have long been established. Trace amine associated receptor 1 (TAAR1), the most well characterized receptor in the TAARs family, has been shown to be potently activated by trace amines like TYR and PEA. Meanwhile, catecholamine metabolites and amphetamine analogs are also potent agonists of TAAR1, implicating its role in mediating the monoaminergic system and substance use disorders. In the central nervous system, TAAR1 is expressed in brain regions involved in dopaminergic, serotonergic and glutamatergic transmission. Genetic animal models and electrophysiological studies have revealed that TAAR1 is a potent modulator of the monoaminergic system, and TAAR1 agonists may be potential pharmacotherapies for the treatment of substance use disorders. Selective and potent engineered TAAR1 ligands, including full (RO5166017 and RO5256390) and partial (RO5203648, RO5263397 and RO5073012) agonists and the antagonist EPPTB (N-(3-ethoxyphenyl)-4-(1-pyrrolidinyl)-3-(trifluoromethyl)benzamide, RO5212773), serve as invaluable tools for the investigation of TAAR1 functions and display high potential for the development of TAAR1-based pharmacotherapies for the treatment of substance use disorders. Despite a number of advances that have been made, more clinical studies are warranted in order to test the potential and efficacy of TAAR1 ligands in the treatment of psychiatric disorders, especially substance use disorders.

@article{alnefeesi_trace_2021,
	title = {Trace amine-associated receptor 1 ({TAAR1}): {Potential} application in mood disorders: {A} systematic review},
	volume = {131},
	issn = {0149-7634},
	shorttitle = {Trace amine-associated receptor 1 ({TAAR1})},
	url = {https://www.sciencedirect.com/science/article/pii/S0149763421004024},
	doi = {10.1016/j.neubiorev.2021.09.020},
	abstract = {There is a need for innovation with respect to therapeutics in psychiatry. Available evidence indicates that the trace amine-associated receptor 1 (TAAR1) agonist SEP-363856 is promising, as it improves measures of cognitive and reward function in schizophrenia. Hedonic and cognitive impairments are transdiagnostic and constitute major burdens in mood disorders. Herein, we systematically review the behavioural and genetic literature documenting the role of TAAR1 in reward and cognitive function, and propose a mechanistic model of TAAR1’s functions in the brain. Notably, TAAR1 activity confers antidepressant-like effects, enhances attention and response inhibition, and reduces compulsive reward seeking without impairing normal function. Further characterization of the responsible mechanisms suggests ion-homeostatic, metabolic, neurotrophic, and anti-inflammatory enhancements in the limbic system. Multiple lines of evidence establish the viability of TAAR1 as a biological target for the treatment of mood disorders. Furthermore, the evidence suggests a role for TAAR1 in reward and cognitive function, which is attributed to a cascade of events that are relevant to the cellular integrity and function of the central nervous system.},
	language = {en},
	urldate = {2022-07-21},
	journal = {Neuroscience \& Biobehavioral Reviews},
	author = {Alnefeesi, Yazen and Tamura, Jocelyn K. and Lui, Leanna M. W. and Jawad, Muhammad Youshay and Ceban, Felicia and Ling, Susan and Nasri, Flora and Rosenblat, Joshua D. and McIntyre, Roger S.},
	month = dec,
	year = {2021},
	keywords = {Arousal, Attention, Bipolar disorder, Brain derived neurotrophic factor (BDNF), Cognitive control, Cognitive function, Depression, Mammalian target of rapamycin (mTOR), Medial prefrontal cortex (mPFC), Reward function, Trace amine-associated receptor 1 (TAAR1), Ventral tegmental area (VTA)},
	pages = {192--210},
}

There is a need for innovation with respect to therapeutics in psychiatry. Available evidence indicates that the trace amine-associated receptor 1 (TAAR1) agonist SEP-363856 is promising, as it improves measures of cognitive and reward function in schizophrenia. Hedonic and cognitive impairments are transdiagnostic and constitute major burdens in mood disorders. Herein, we systematically review the behavioural and genetic literature documenting the role of TAAR1 in reward and cognitive function, and propose a mechanistic model of TAAR1’s functions in the brain. Notably, TAAR1 activity confers antidepressant-like effects, enhances attention and response inhibition, and reduces compulsive reward seeking without impairing normal function. Further characterization of the responsible mechanisms suggests ion-homeostatic, metabolic, neurotrophic, and anti-inflammatory enhancements in the limbic system. Multiple lines of evidence establish the viability of TAAR1 as a biological target for the treatment of mood disorders. Furthermore, the evidence suggests a role for TAAR1 in reward and cognitive function, which is attributed to a cascade of events that are relevant to the cellular integrity and function of the central nervous system.

@article{gomes_beyond_2021,
	title = {Beyond {Dopamine} {Receptor} {Antagonism}: {New} {Targets} for {Schizophrenia} {Treatment} and {Prevention}},
	volume = {22},
	issn = {1422-0067},
	shorttitle = {Beyond {Dopamine} {Receptor} {Antagonism}},
	doi = {10.3390/ijms22094467},
	abstract = {Treatment of schizophrenia (SCZ) historically relies on the use of antipsychotic drugs to treat psychosis, with all of the currently available antipsychotics acting through the antagonism of dopamine D2 receptors. Although antipsychotics reduce psychotic symptoms in many patients, they induce numerous undesirable effects and are not effective against negative and cognitive symptoms. These highlight the need to develop new drugs to treat SCZ. An advanced understanding of the circuitry of SCZ has pointed to pathological origins in the excitation/inhibition balance in regions such as the hippocampus, and restoring function in this region, particularly as a means to compensate for parvalbumin (PV) interneuron loss and resultant hippocampal hyperactivity, may be a more efficacious approach to relieve a broad range of SCZ symptoms. Other targets, such as cholinergic receptors and the trace amine-associated receptor 1 (TAAR1), have also shown some promise for the treatment of SCZ. Importantly, assessing efficacy of novel compounds must take into consideration treatment history of the patient, as preclinical studies suggest prior antipsychotic treatment may interfere with the efficacy of these novel agents. However, while novel therapeutic targets may be more effective in treating SCZ, a more effective approach would be to prevent the transition to SCZ in susceptible individuals. A focus on stress, which has been shown to be a predisposing factor in risk for SCZ, is a possible avenue that has shown promise in preclinical studies. Therefore, therapeutic approaches based on our current understanding of the circuitry of SCZ and its etiology are likely to enable development of more effective therapeutic interventions for this complex disorder.},
	language = {eng},
	number = {9},
	journal = {International Journal of Molecular Sciences},
	author = {Gomes, Felipe V. and Grace, Anthony A.},
	month = apr,
	year = {2021},
	pmid = {33922888},
	pmcid = {PMC8123139},
	keywords = {Animals, Antipsychotic Agents, D-Amino-Acid Oxidase, Dopamine Antagonists, Glutamic Acid, Humans, Molecular Targeted Therapy, Receptors, Cholinergic, Receptors, G-Protein-Coupled, Schizophrenia, Sodium Benzoate, antipsychotics, dopamine, gamma-Aminobutyric Acid, glutamate, hippocampus, parvalbumin, psychosis, stress},
	pages = {4467},
}

Treatment of schizophrenia (SCZ) historically relies on the use of antipsychotic drugs to treat psychosis, with all of the currently available antipsychotics acting through the antagonism of dopamine D2 receptors. Although antipsychotics reduce psychotic symptoms in many patients, they induce numerous undesirable effects and are not effective against negative and cognitive symptoms. These highlight the need to develop new drugs to treat SCZ. An advanced understanding of the circuitry of SCZ has pointed to pathological origins in the excitation/inhibition balance in regions such as the hippocampus, and restoring function in this region, particularly as a means to compensate for parvalbumin (PV) interneuron loss and resultant hippocampal hyperactivity, may be a more efficacious approach to relieve a broad range of SCZ symptoms. Other targets, such as cholinergic receptors and the trace amine-associated receptor 1 (TAAR1), have also shown some promise for the treatment of SCZ. Importantly, assessing efficacy of novel compounds must take into consideration treatment history of the patient, as preclinical studies suggest prior antipsychotic treatment may interfere with the efficacy of these novel agents. However, while novel therapeutic targets may be more effective in treating SCZ, a more effective approach would be to prevent the transition to SCZ in susceptible individuals. A focus on stress, which has been shown to be a predisposing factor in risk for SCZ, is a possible avenue that has shown promise in preclinical studies. Therefore, therapeutic approaches based on our current understanding of the circuitry of SCZ and its etiology are likely to enable development of more effective therapeutic interventions for this complex disorder.

@article{zanin_early_2021,
	title = {An {Early} {Stage} {Researcher}'s {Primer} on {Systems} {Medicine} {Terminology}},
	volume = {4},
	url = {https://www.liebertpub.com/doi/10.1089/nsm.2020.0003},
	doi = {10.1089/nsm.2020.0003},
	abstract = {Background: Systems Medicine is a novel approach to medicine, that is, an interdisciplinary field that considers the human body as a system, composed of multiple parts and of complex relationships at multiple levels, and further integrated into an environment. Exploring Systems Medicine implies understanding and combining concepts coming from diametral different fields, including medicine, biology, statistics, modeling and simulation, and data science. Such heterogeneity leads to semantic issues, which may slow down implementation and fruitful interaction between these highly diverse fields.

Methods: In this review, we collect and explain more than100 terms related to Systems Medicine. These include both modeling and data science terms and basic systems medicine terms, along with some synthetic definitions, examples of applications, and lists of relevant references.

Results: This glossary aims at being a first aid kit for the Systems Medicine researcher facing an unfamiliar term, where he/she can get a first understanding of them, and, more importantly, examples and references for digging into the topic.},
	number = {1},
	urldate = {2022-07-18},
	journal = {Network and Systems Medicine},
	author = {Zanin, Massimiliano and Aitya, Nadim A.A. and Basilio, José and Baumbach, Jan and Benis, Arriel and Behera, Chandan K. and Bucholc, Magda and Castiglione, Filippo and Chouvarda, Ioanna and Comte, Blandine and Dao, Tien-Tuan and Ding, Xuemei and Pujos-Guillot, Estelle and Filipovic, Nenad and Finn, David P. and Glass, David H. and Harel, Nissim and Iesmantas, Tomas and Ivanoska, Ilinka and Joshi, Alok and Boudjeltia, Karim Zouaoui and Kaoui, Badr and Kaur, Daman and Maguire, Liam P. and McClean, Paula L. and McCombe, Niamh and de Miranda, João Luís and Moisescu, Mihnea Alexandru and Pappalardo, Francesco and Polster, Annikka and Prasad, Girijesh and Rozman, Damjana and Sacala, Ioan and Sanchez-Bornot, Jose M. and Schmid, Johannes A. and Sharp, Trevor and Solé-Casals, Jordi and Spiwok, Vojtěch and Spyrou, George M. and Stalidzans, Egils and Stres, Blaž and Sustersic, Tijana and Symeonidis, Ioannis and Tieri, Paolo and Todd, Stephen and Van Steen, Kristel and Veneva, Milena and Wang, Da-Hui and Wang, Haiying and Wang, Hui and Watterson, Steven and Wong-Lin, KongFatt and Yang, Su and Zou, Xin and Schmidt, Harald H.H.W.},
	month = mar,
	year = {2021},
	note = {Publisher: Mary Ann Liebert, Inc., publishers},
	keywords = {multiscale data science, multiscale modeling, systems medicine},
	pages = {2--50},
}

Background: Systems Medicine is a novel approach to medicine, that is, an interdisciplinary field that considers the human body as a system, composed of multiple parts and of complex relationships at multiple levels, and further integrated into an environment. Exploring Systems Medicine implies understanding and combining concepts coming from diametral different fields, including medicine, biology, statistics, modeling and simulation, and data science. Such heterogeneity leads to semantic issues, which may slow down implementation and fruitful interaction between these highly diverse fields. Methods: In this review, we collect and explain more than100 terms related to Systems Medicine. These include both modeling and data science terms and basic systems medicine terms, along with some synthetic definitions, examples of applications, and lists of relevant references. Results: This glossary aims at being a first aid kit for the Systems Medicine researcher facing an unfamiliar term, where he/she can get a first understanding of them, and, more importantly, examples and references for digging into the topic.

@article{lam_identifying_2021,
	title = {Identifying nootropic drug targets via large-scale cognitive {GWAS} and transcriptomics.},
	volume = {46},
	issn = {0893-133X},
	url = {https://escholarship.org/uc/item/338966jd},
	doi = {10.1038/s41386-021-01023-4},
	abstract = {Broad-based cognitive deficits are an enduring and disabling symptom for many patients with severe mental illness, and these impairments are inadequately addressed by current medications. While novel drug targets for schizophrenia and depression have emerged from recent large-scale genome-wide association studies (GWAS) of these psychiatric disorders, GWAS of general cognitive ability can suggest potential targets for nootropic drug repurposing. Here, we (1) meta-analyze results from two recent cognitive GWAS to further enhance power for locus discovery; (2) employ several complementary transcriptomic methods to identify genes in these loci that are credibly associated with cognition; and (3) further annotate the resulting genes using multiple chemoinformatic databases to identify "druggable" targets. Using our meta-analytic data set (N = 373,617), we identified 241 independent cognition-associated loci (29 novel), and 76 genes were identified by 2 or more methods of gene identification. Actin and chromatin binding gene sets were identified as novel pathways that could be targeted via drug repurposing. Leveraging our transcriptomic and chemoinformatic databases, we identified 16 putative genes targeted by existing drugs potentially available for cognitive repurposing.},
	language = {en},
	number = {10},
	urldate = {2022-06-28},
	journal = {Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology},
	author = {Lam, Max and Chen, Chia-Yen and Ge, Tian and Xia, Yan and Hill, David W. and Trampush, Joey W. and Yu, Jin and Knowles, Emma and Davies, Gail and Stahl, Eli A. and Huckins, Laura and Liewald, David C. and Djurovic, Srdjan and Melle, Ingrid and Christoforou, Andrea and Reinvang, Ivar and DeRosse, Pamela and Lundervold, Astri J. and Steen, Vidar M. and Espeseth, Thomas and Räikkönen, Katri and Widen, Elisabeth and Palotie, Aarno and Eriksson, Johan G. and Giegling, Ina and Konte, Bettina and Hartmann, Annette M. and Roussos, Panos and Giakoumaki, Stella and Burdick, Katherine E. and Payton, Antony and Ollier, William and Chiba-Falek, Ornit and Koltai, Deborah C. and Need, Anna C. and Cirulli, Elizabeth T. and Voineskos, Aristotle N. and Stefanis, Nikos C. and Avramopoulos, Dimitrios and Hatzimanolis, Alex and Smyrnis, Nikolaos and Bilder, Robert M. and Freimer, Nelson B. and Cannon, Tyrone D. and London, Edythe and Poldrack, Russell A. and Sabb, Fred W. and Congdon, Eliza and Conley, Emily Drabant and Scult, Matthew A. and Dickinson, Dwight and Straub, Richard E. and Donohoe, Gary and Morris, Derek and Corvin, Aiden and Gill, Michael and Hariri, Ahmad R. and Weinberger, Daniel R. and Pendleton, Neil and Bitsios, Panos and Rujescu, Dan and Lahti, Jari and Le Hellard, Stephanie and Keller, Matthew C. and Andreassen, Ole A. and Deary, Ian J. and Glahn, David C. and Huang, Hailiang and Liu, Chunyu and Malhotra, Anil K. and Lencz, Todd},
	month = sep,
	year = {2021},
	pages = {1788--1801},
}

Broad-based cognitive deficits are an enduring and disabling symptom for many patients with severe mental illness, and these impairments are inadequately addressed by current medications. While novel drug targets for schizophrenia and depression have emerged from recent large-scale genome-wide association studies (GWAS) of these psychiatric disorders, GWAS of general cognitive ability can suggest potential targets for nootropic drug repurposing. Here, we (1) meta-analyze results from two recent cognitive GWAS to further enhance power for locus discovery; (2) employ several complementary transcriptomic methods to identify genes in these loci that are credibly associated with cognition; and (3) further annotate the resulting genes using multiple chemoinformatic databases to identify "druggable" targets. Using our meta-analytic data set (N = 373,617), we identified 241 independent cognition-associated loci (29 novel), and 76 genes were identified by 2 or more methods of gene identification. Actin and chromatin binding gene sets were identified as novel pathways that could be targeted via drug repurposing. Leveraging our transcriptomic and chemoinformatic databases, we identified 16 putative genes targeted by existing drugs potentially available for cognitive repurposing.

@article{barnett_analysis_2021,
	title = {The {Analysis} of {Knowledge}},
	url = {https://press.rebus.community/intro-to-phil-epistemology/chapter/the-analysis-of-knowledge/},
	language = {en},
	urldate = {2022-06-27},
	author = {Barnett, Brian C.},
	month = aug,
	year = {2021},
	note = {Book Title: Introduction to Philosophy: Epistemology
Publisher: The Rebus Community},
}

@article{zanin_early_2021,
	title = {An {Early} {Stage} {Researcher}'s {Primer} on {Systems} {Medicine} {Terminology}},
	volume = {4},
	url = {https://www.liebertpub.com/doi/10.1089/nsm.2020.0003},
	doi = {10.1089/nsm.2020.0003},
	abstract = {Background: Systems Medicine is a novel approach to medicine, that is, an interdisciplinary field that considers the human body as a system, composed of multiple parts and of complex relationships at multiple levels, and further integrated into an environment. Exploring Systems Medicine implies understanding and combining concepts coming from diametral different fields, including medicine, biology, statistics, modeling and simulation, and data science. Such heterogeneity leads to semantic issues, which may slow down implementation and fruitful interaction between these highly diverse fields.

Methods: In this review, we collect and explain more than100 terms related to Systems Medicine. These include both modeling and data science terms and basic systems medicine terms, along with some synthetic definitions, examples of applications, and lists of relevant references.

Results: This glossary aims at being a first aid kit for the Systems Medicine researcher facing an unfamiliar term, where he/she can get a first understanding of them, and, more importantly, examples and references for digging into the topic.},
	number = {1},
	urldate = {2022-06-05},
	journal = {Network and Systems Medicine},
	author = {Zanin, Massimiliano and Aitya, Nadim A.A. and Basilio, José and Baumbach, Jan and Benis, Arriel and Behera, Chandan K. and Bucholc, Magda and Castiglione, Filippo and Chouvarda, Ioanna and Comte, Blandine and Dao, Tien-Tuan and Ding, Xuemei and Pujos-Guillot, Estelle and Filipovic, Nenad and Finn, David P. and Glass, David H. and Harel, Nissim and Iesmantas, Tomas and Ivanoska, Ilinka and Joshi, Alok and Boudjeltia, Karim Zouaoui and Kaoui, Badr and Kaur, Daman and Maguire, Liam P. and McClean, Paula L. and McCombe, Niamh and de Miranda, João Luís and Moisescu, Mihnea Alexandru and Pappalardo, Francesco and Polster, Annikka and Prasad, Girijesh and Rozman, Damjana and Sacala, Ioan and Sanchez-Bornot, Jose M. and Schmid, Johannes A. and Sharp, Trevor and Solé-Casals, Jordi and Spiwok, Vojtěch and Spyrou, George M. and Stalidzans, Egils and Stres, Blaž and Sustersic, Tijana and Symeonidis, Ioannis and Tieri, Paolo and Todd, Stephen and Van Steen, Kristel and Veneva, Milena and Wang, Da-Hui and Wang, Haiying and Wang, Hui and Watterson, Steven and Wong-Lin, KongFatt and Yang, Su and Zou, Xin and Schmidt, Harald H.H.W.},
	month = mar,
	year = {2021},
	note = {Publisher: Mary Ann Liebert, Inc., publishers},
	keywords = {multiscale data science, multiscale modeling, systems medicine},
	pages = {2--50},
}

Background: Systems Medicine is a novel approach to medicine, that is, an interdisciplinary field that considers the human body as a system, composed of multiple parts and of complex relationships at multiple levels, and further integrated into an environment. Exploring Systems Medicine implies understanding and combining concepts coming from diametral different fields, including medicine, biology, statistics, modeling and simulation, and data science. Such heterogeneity leads to semantic issues, which may slow down implementation and fruitful interaction between these highly diverse fields. Methods: In this review, we collect and explain more than100 terms related to Systems Medicine. These include both modeling and data science terms and basic systems medicine terms, along with some synthetic definitions, examples of applications, and lists of relevant references. Results: This glossary aims at being a first aid kit for the Systems Medicine researcher facing an unfamiliar term, where he/she can get a first understanding of them, and, more importantly, examples and references for digging into the topic.

@article{shukla_signature-based_2021,
	title = {Signature-based approaches for informed drug repurposing: targeting {CNS} disorders},
	volume = {46},
	issn = {0893-133X},
	shorttitle = {Signature-based approaches for informed drug repurposing},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7688959/},
	doi = {10.1038/s41386-020-0752-6},
	abstract = {CNS disorders, and in particular psychiatric illnesses, lack definitive disease-altering therapeutics. The limited understanding of the mechanisms driving these illnesses with the slow pace and high cost of drug development exacerbates this issue. For these reasons, drug repurposing – both a less expensive and time-efficient practice compared to de novo drug development – has been a promising strategy to overcome the paucity of treatments available for these debilitating disorders. While empirical drug-repurposing has been a routine practice in clinical psychiatry, innovative, informed, and cost-effective repurposing efforts using big data (“omics”) have been designed to characterize drugs by structural and transcriptomic signatures. These strategies, in conjunction with ontological integration, provide an important opportunity to address knowledge-based challenges associated with drug development for CNS disorders. In this review, we discuss various signature-based in silico approaches to drug repurposing, its integration with multiple omics platforms, and how this data can be used for clinically relevant, evidence-based drug repurposing. These tools provide an exciting translational avenue to merge omics-based drug discovery platforms with patient-specific disease signatures, ultimately facilitating the identification of new therapies for numerous psychiatric disorders.},
	number = {1},
	urldate = {2022-05-29},
	journal = {Neuropsychopharmacology},
	author = {Shukla, Rammohan and Henkel, Nicholas D. and Alganem, Khaled and Hamoud, Abdul-rizaq and Reigle, James and Alnafisah, Rawan S. and Eby, Hunter M. and Imami, Ali S. and Creeden, Justin F and Miruzzi, Scott A. and Meller, Jaroslaw and Mccullumsmith, Robert E.},
	month = jan,
	year = {2021},
	pmid = {32604402},
	pmcid = {PMC7688959},
	pages = {116--130},
}

CNS disorders, and in particular psychiatric illnesses, lack definitive disease-altering therapeutics. The limited understanding of the mechanisms driving these illnesses with the slow pace and high cost of drug development exacerbates this issue. For these reasons, drug repurposing – both a less expensive and time-efficient practice compared to de novo drug development – has been a promising strategy to overcome the paucity of treatments available for these debilitating disorders. While empirical drug-repurposing has been a routine practice in clinical psychiatry, innovative, informed, and cost-effective repurposing efforts using big data (“omics”) have been designed to characterize drugs by structural and transcriptomic signatures. These strategies, in conjunction with ontological integration, provide an important opportunity to address knowledge-based challenges associated with drug development for CNS disorders. In this review, we discuss various signature-based in silico approaches to drug repurposing, its integration with multiple omics platforms, and how this data can be used for clinically relevant, evidence-based drug repurposing. These tools provide an exciting translational avenue to merge omics-based drug discovery platforms with patient-specific disease signatures, ultimately facilitating the identification of new therapies for numerous psychiatric disorders.

@article{shukla_signature-based_2021-1,
	title = {Signature-based approaches for informed drug repurposing: targeting {CNS} disorders},
	volume = {46},
	issn = {0893-133X},
	shorttitle = {Signature-based approaches for informed drug repurposing},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7688959/},
	doi = {10.1038/s41386-020-0752-6},
	abstract = {CNS disorders, and in particular psychiatric illnesses, lack definitive disease-altering therapeutics. The limited understanding of the mechanisms driving these illnesses with the slow pace and high cost of drug development exacerbates this issue. For these reasons, drug repurposing – both a less expensive and time-efficient practice compared to de novo drug development – has been a promising strategy to overcome the paucity of treatments available for these debilitating disorders. While empirical drug-repurposing has been a routine practice in clinical psychiatry, innovative, informed, and cost-effective repurposing efforts using big data (“omics”) have been designed to characterize drugs by structural and transcriptomic signatures. These strategies, in conjunction with ontological integration, provide an important opportunity to address knowledge-based challenges associated with drug development for CNS disorders. In this review, we discuss various signature-based in silico approaches to drug repurposing, its integration with multiple omics platforms, and how this data can be used for clinically relevant, evidence-based drug repurposing. These tools provide an exciting translational avenue to merge omics-based drug discovery platforms with patient-specific disease signatures, ultimately facilitating the identification of new therapies for numerous psychiatric disorders.},
	number = {1},
	urldate = {2022-05-27},
	journal = {Neuropsychopharmacology},
	author = {Shukla, Rammohan and Henkel, Nicholas D. and Alganem, Khaled and Hamoud, Abdul-rizaq and Reigle, James and Alnafisah, Rawan S. and Eby, Hunter M. and Imami, Ali S. and Creeden, Justin F and Miruzzi, Scott A. and Meller, Jaroslaw and Mccullumsmith, Robert E.},
	month = jan,
	year = {2021},
	pmid = {32604402},
	pmcid = {PMC7688959},
	pages = {116--130},
}

CNS disorders, and in particular psychiatric illnesses, lack definitive disease-altering therapeutics. The limited understanding of the mechanisms driving these illnesses with the slow pace and high cost of drug development exacerbates this issue. For these reasons, drug repurposing – both a less expensive and time-efficient practice compared to de novo drug development – has been a promising strategy to overcome the paucity of treatments available for these debilitating disorders. While empirical drug-repurposing has been a routine practice in clinical psychiatry, innovative, informed, and cost-effective repurposing efforts using big data (“omics”) have been designed to characterize drugs by structural and transcriptomic signatures. These strategies, in conjunction with ontological integration, provide an important opportunity to address knowledge-based challenges associated with drug development for CNS disorders. In this review, we discuss various signature-based in silico approaches to drug repurposing, its integration with multiple omics platforms, and how this data can be used for clinically relevant, evidence-based drug repurposing. These tools provide an exciting translational avenue to merge omics-based drug discovery platforms with patient-specific disease signatures, ultimately facilitating the identification of new therapies for numerous psychiatric disorders.

@article{shukla_signature-based_2021-2,
	title = {Signature-based approaches for informed drug repurposing: targeting {CNS} disorders},
	volume = {46},
	issn = {0893-133X},
	shorttitle = {Signature-based approaches for informed drug repurposing},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7688959/},
	doi = {10.1038/s41386-020-0752-6},
	abstract = {CNS disorders, and in particular psychiatric illnesses, lack definitive disease-altering therapeutics. The limited understanding of the mechanisms driving these illnesses with the slow pace and high cost of drug development exacerbates this issue. For these reasons, drug repurposing – both a less expensive and time-efficient practice compared to de novo drug development – has been a promising strategy to overcome the paucity of treatments available for these debilitating disorders. While empirical drug-repurposing has been a routine practice in clinical psychiatry, innovative, informed, and cost-effective repurposing efforts using big data (“omics”) have been designed to characterize drugs by structural and transcriptomic signatures. These strategies, in conjunction with ontological integration, provide an important opportunity to address knowledge-based challenges associated with drug development for CNS disorders. In this review, we discuss various signature-based in silico approaches to drug repurposing, its integration with multiple omics platforms, and how this data can be used for clinically relevant, evidence-based drug repurposing. These tools provide an exciting translational avenue to merge omics-based drug discovery platforms with patient-specific disease signatures, ultimately facilitating the identification of new therapies for numerous psychiatric disorders.},
	number = {1},
	urldate = {2022-05-27},
	journal = {Neuropsychopharmacology},
	author = {Shukla, Rammohan and Henkel, Nicholas D. and Alganem, Khaled and Hamoud, Abdul-rizaq and Reigle, James and Alnafisah, Rawan S. and Eby, Hunter M. and Imami, Ali S. and Creeden, Justin F and Miruzzi, Scott A. and Meller, Jaroslaw and Mccullumsmith, Robert E.},
	month = jan,
	year = {2021},
	pmid = {32604402},
	pmcid = {PMC7688959},
	pages = {116--130},
}

CNS disorders, and in particular psychiatric illnesses, lack definitive disease-altering therapeutics. The limited understanding of the mechanisms driving these illnesses with the slow pace and high cost of drug development exacerbates this issue. For these reasons, drug repurposing – both a less expensive and time-efficient practice compared to de novo drug development – has been a promising strategy to overcome the paucity of treatments available for these debilitating disorders. While empirical drug-repurposing has been a routine practice in clinical psychiatry, innovative, informed, and cost-effective repurposing efforts using big data (“omics”) have been designed to characterize drugs by structural and transcriptomic signatures. These strategies, in conjunction with ontological integration, provide an important opportunity to address knowledge-based challenges associated with drug development for CNS disorders. In this review, we discuss various signature-based in silico approaches to drug repurposing, its integration with multiple omics platforms, and how this data can be used for clinically relevant, evidence-based drug repurposing. These tools provide an exciting translational avenue to merge omics-based drug discovery platforms with patient-specific disease signatures, ultimately facilitating the identification of new therapies for numerous psychiatric disorders.

@article{mejia-gutierrez_silico_2021,
	title = {In {Silico} {Repositioning} of {Dopamine} {Modulators} with {Possible} {Application} to {Schizophrenia}: {Pharmacophore} {Mapping}, {Molecular} {Docking} and {Molecular} {Dynamics} {Analysis}},
	volume = {6},
	shorttitle = {In {Silico} {Repositioning} of {Dopamine} {Modulators} with {Possible} {Application} to {Schizophrenia}},
	url = {https://doi.org/10.1021/acsomega.0c05984},
	doi = {10.1021/acsomega.0c05984},
	abstract = {We have performed theoretical calculations with 70 drugs that have been considered in 231 clinical trials as possible candidates to repurpose drugs for schizophrenia based on their interactions with the dopaminergic system. A hypothesis of shared pharmacophore features was formulated to support our calculations. To do so, we have used the crystal structure of the D2-like dopamine receptor in complex with risperidone, eticlopride, and nemonapride. Linagliptin, citalopram, flunarizine, sildenafil, minocycline, and duloxetine were the drugs that best fit with our model. Molecular docking calculations, molecular dynamics outcomes, blood-brain barrier penetration, and human intestinal absorption were studied and compared with the results. From the six drugs selected in the shared pharmacophore features input, flunarizine showed the best docking score with D2, D3, and D4 dopamine receptors and had high stability during molecular dynamics simulations. Flunarizine is a frequently used medication to treat migraines and vertigo. However, its antipsychotic properties have been previously hypothesized, particularly because of its possible ability to block the D2 dopamine receptors.},
	number = {23},
	urldate = {2022-05-25},
	journal = {ACS Omega},
	author = {Mejia-Gutierrez, Melissa and Vásquez-Paz, Bryan D. and Fierro, Leonardo and Maza, Julio R.},
	month = jun,
	year = {2021},
	note = {Publisher: American Chemical Society},
	pages = {14748--14764},
}

We have performed theoretical calculations with 70 drugs that have been considered in 231 clinical trials as possible candidates to repurpose drugs for schizophrenia based on their interactions with the dopaminergic system. A hypothesis of shared pharmacophore features was formulated to support our calculations. To do so, we have used the crystal structure of the D2-like dopamine receptor in complex with risperidone, eticlopride, and nemonapride. Linagliptin, citalopram, flunarizine, sildenafil, minocycline, and duloxetine were the drugs that best fit with our model. Molecular docking calculations, molecular dynamics outcomes, blood-brain barrier penetration, and human intestinal absorption were studied and compared with the results. From the six drugs selected in the shared pharmacophore features input, flunarizine showed the best docking score with D2, D3, and D4 dopamine receptors and had high stability during molecular dynamics simulations. Flunarizine is a frequently used medication to treat migraines and vertigo. However, its antipsychotic properties have been previously hypothesized, particularly because of its possible ability to block the D2 dopamine receptors.

@article{lin_reduced_2021,
	title = {Reduced {Mortality} {Associated} {With} the {Use} of {Metformin} {Among} {Patients} {With} {Autoimmune} {Diseases}},
	volume = {12},
	issn = {1664-2392},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8104028/},
	doi = {10.3389/fendo.2021.641635},
	abstract = {Objective
Metformin has been linked to anti-proliferative and anti-inflammatory mechanisms. In this study, we aimed to examine the long-term impact of metformin on mortality and organ damage in patients with autoimmune diseases and type 2 diabetes mellitus (T2DM).

Methods
We conducted a cohort study using the National Health Insurance Research Database in Taiwan between 1997 and 2013. Based on metformin and other anti-diabetic agent prescriptions, we categorized all patients with autoimmune diseases into either the metformin group (metformin administration for at least 28 days) or the non-metformin group. The primary outcomes were all-cause mortality and annual admission rate, while the secondary outcome was target organ damage. We followed patients from the index date to the date on which the event of interest occurred, death, or the end of this study.

Results
Our cohort study included 3,359 subjects for analysis. During a mean follow up of 5.2 ± 3.8 years, the event rate of all-cause mortality was 228 (33.6\%) in the metformin group and 125 (36.9\%) in the non-metformin group. The risk of both all-cause mortality and annual number of admissions for autoimmune diseases was significantly lower in the metformin group than in the non-metformin group [hazard ratio (HR) 0.77; 95\% CI 0.62–0.96 and risk ratio (RR) 0.81; 95\% CI 0.73–0.90, respectively].

Conclusion
Metformin may add benefits beyond T2DM control with regard to reducing all-cause mortality and admission rate, as well as minimizing end-organ injury in lungs and kidneys among patients with autoimmune diseases.},
	urldate = {2022-05-10},
	journal = {Frontiers in Endocrinology},
	author = {Lin, Chun-Yu and Wu, Chun-Hsin and Hsu, Chung-Yuan and Chen, Tien-Hsing and Lin, Ming-Shyan and Lin, Yu-Sheng and Su, Yu-Jih},
	month = apr,
	year = {2021},
	pmid = {33967957},
	pmcid = {PMC8104028},
	pages = {641635},
}

Objective Metformin has been linked to anti-proliferative and anti-inflammatory mechanisms. In this study, we aimed to examine the long-term impact of metformin on mortality and organ damage in patients with autoimmune diseases and type 2 diabetes mellitus (T2DM). Methods We conducted a cohort study using the National Health Insurance Research Database in Taiwan between 1997 and 2013. Based on metformin and other anti-diabetic agent prescriptions, we categorized all patients with autoimmune diseases into either the metformin group (metformin administration for at least 28 days) or the non-metformin group. The primary outcomes were all-cause mortality and annual admission rate, while the secondary outcome was target organ damage. We followed patients from the index date to the date on which the event of interest occurred, death, or the end of this study. Results Our cohort study included 3,359 subjects for analysis. During a mean follow up of 5.2 ± 3.8 years, the event rate of all-cause mortality was 228 (33.6%) in the metformin group and 125 (36.9%) in the non-metformin group. The risk of both all-cause mortality and annual number of admissions for autoimmune diseases was significantly lower in the metformin group than in the non-metformin group [hazard ratio (HR) 0.77; 95% CI 0.62–0.96 and risk ratio (RR) 0.81; 95% CI 0.73–0.90, respectively]. Conclusion Metformin may add benefits beyond T2DM control with regard to reducing all-cause mortality and admission rate, as well as minimizing end-organ injury in lungs and kidneys among patients with autoimmune diseases.

@article{clayton_mitochondria_2021,
	title = {Mitochondria as {Key} {Players} in the {Pathogenesis} and {Treatment} of {Rheumatoid} {Arthritis}},
	volume = {12},
	issn = {1664-3224},
	doi = {10.3389/fimmu.2021.673916},
	abstract = {Mitochondria are major energy-producing organelles that have central roles in cellular metabolism. They also act as important signalling hubs, and their dynamic regulation in response to stress signals helps to dictate the stress response of the cell. Rheumatoid arthritis is an inflammatory and autoimmune disease with high prevalence and complex aetiology. Mitochondrial activity affects differentiation, activation and survival of immune and non-immune cells that contribute to the pathogenesis of this disease. This review outlines what is known about the role of mitochondria in rheumatoid arthritis pathogenesis, and how current and future therapeutic strategies can function through modulation of mitochondrial activity. We also highlight areas of this topic that warrant further study. As producers of energy and of metabolites such as succinate and citrate, mitochondria help to shape the inflammatory phenotype of leukocytes during disease. Mitochondrial components can directly stimulate immune receptors by acting as damage-associated molecular patterns, which could represent an initiating factor for the development of sterile inflammation. Mitochondria are also an important source of intracellular reactive oxygen species, and facilitate the activation of the NLRP3 inflammasome, which produces cytokines linked to disease symptoms in rheumatoid arthritis. The fact that mitochondria contain their own genetic material renders them susceptible to mutation, which can propagate their dysfunction and immunostimulatory potential. Several drugs currently used for the treatment of rheumatoid arthritis regulate mitochondrial function either directly or indirectly. These actions contribute to their immunomodulatory functions, but can also lead to adverse effects. Metabolic and mitochondrial pathways are attractive targets for future anti-rheumatic drugs, however many questions still remain about the precise role of mitochondrial activity in different cell types in rheumatoid arthritis.},
	language = {eng},
	journal = {Frontiers in Immunology},
	author = {Clayton, Sally A. and MacDonald, Lucy and Kurowska-Stolarska, Mariola and Clark, Andrew R.},
	year = {2021},
	pmid = {33995417},
	pmcid = {PMC8118696},
	keywords = {Animals, Arthritis, Rheumatoid, DAMP, DMARD (disease modifying anti-rheumatic drug), Humans, Mitochondria, NLRP3, metabolism, mitochondria, oxidative phosphorylation, rheumatoid arthritis},
	pages = {673916},
}

Mitochondria are major energy-producing organelles that have central roles in cellular metabolism. They also act as important signalling hubs, and their dynamic regulation in response to stress signals helps to dictate the stress response of the cell. Rheumatoid arthritis is an inflammatory and autoimmune disease with high prevalence and complex aetiology. Mitochondrial activity affects differentiation, activation and survival of immune and non-immune cells that contribute to the pathogenesis of this disease. This review outlines what is known about the role of mitochondria in rheumatoid arthritis pathogenesis, and how current and future therapeutic strategies can function through modulation of mitochondrial activity. We also highlight areas of this topic that warrant further study. As producers of energy and of metabolites such as succinate and citrate, mitochondria help to shape the inflammatory phenotype of leukocytes during disease. Mitochondrial components can directly stimulate immune receptors by acting as damage-associated molecular patterns, which could represent an initiating factor for the development of sterile inflammation. Mitochondria are also an important source of intracellular reactive oxygen species, and facilitate the activation of the NLRP3 inflammasome, which produces cytokines linked to disease symptoms in rheumatoid arthritis. The fact that mitochondria contain their own genetic material renders them susceptible to mutation, which can propagate their dysfunction and immunostimulatory potential. Several drugs currently used for the treatment of rheumatoid arthritis regulate mitochondrial function either directly or indirectly. These actions contribute to their immunomodulatory functions, but can also lead to adverse effects. Metabolic and mitochondrial pathways are attractive targets for future anti-rheumatic drugs, however many questions still remain about the precise role of mitochondrial activity in different cell types in rheumatoid arthritis.

@article{kim_metformin_2021,
	title = {Metformin as a {Treatment} {Strategy} for {Sjögren}’s {Syndrome}},
	volume = {22},
	issn = {1422-0067},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8269365/},
	doi = {10.3390/ijms22137231},
	abstract = {Sjögren’s syndrome (SS), a chronic inflammatory disease involving the salivary and lacrimal glands, presents symptoms of sicca as well as systemic manifestations such as fatigue and musculoskeletal pain. Only a few treatments have been successful in management of SS; thus treatment of the disease is challenging. Metformin is the first-line agent for type 2 diabetes and has anti-inflammatory potential. Its immunomodulatory capacity is exerted via activation of 5’ adenosine monophosphate-activated protein kinase (AMPK). Metformin inhibits mitochondrial respiratory chain complex I which leads to change in adenosine mono-phosphate (AMP) to adenosine tri-phosphate (ATP) ratio. This results in AMPK activation and causes inhibition of mammalian target of rapamycin (mTOR). mTOR plays an important role in T cell differentiation and mTOR deficient T cells differentiate into regulatory T cells. In this manner, metformin enhances immunoregulatory response in an individual. mTOR is responsible for B cell proliferation and germinal center (GC) differentiation. Thus, reduction of B cell differentiation into antibody-producing plasma cells occurs via downregulation of mTOR. Due to the lack of suggested treatment for SS, metformin has been considered as a treatment strategy and is expected to ameliorate salivary gland function.},
	number = {13},
	urldate = {2022-05-10},
	journal = {International Journal of Molecular Sciences},
	author = {Kim, Joa and Kim, Yun-Sung and Park, Sung-Hwan},
	month = jul,
	year = {2021},
	pmid = {34281285},
	pmcid = {PMC8269365},
	pages = {7231},
}

Sjögren’s syndrome (SS), a chronic inflammatory disease involving the salivary and lacrimal glands, presents symptoms of sicca as well as systemic manifestations such as fatigue and musculoskeletal pain. Only a few treatments have been successful in management of SS; thus treatment of the disease is challenging. Metformin is the first-line agent for type 2 diabetes and has anti-inflammatory potential. Its immunomodulatory capacity is exerted via activation of 5’ adenosine monophosphate-activated protein kinase (AMPK). Metformin inhibits mitochondrial respiratory chain complex I which leads to change in adenosine mono-phosphate (AMP) to adenosine tri-phosphate (ATP) ratio. This results in AMPK activation and causes inhibition of mammalian target of rapamycin (mTOR). mTOR plays an important role in T cell differentiation and mTOR deficient T cells differentiate into regulatory T cells. In this manner, metformin enhances immunoregulatory response in an individual. mTOR is responsible for B cell proliferation and germinal center (GC) differentiation. Thus, reduction of B cell differentiation into antibody-producing plasma cells occurs via downregulation of mTOR. Due to the lack of suggested treatment for SS, metformin has been considered as a treatment strategy and is expected to ameliorate salivary gland function.

@article{lam_identifying_2021,
	title = {Identifying nootropic drug targets via large-scale cognitive {GWAS} and transcriptomics.},
	volume = {46},
	issn = {0893-133X},
	url = {https://escholarship.org/uc/item/338966jd},
	doi = {10.1038/s41386-021-01023-4},
	abstract = {Broad-based cognitive deficits are an enduring and disabling symptom for many patients with severe mental illness, and these impairments are inadequately addressed by current medications. While novel drug targets for schizophrenia and depression have emerged from recent large-scale genome-wide association studies (GWAS) of these psychiatric disorders, GWAS of general cognitive ability can suggest potential targets for nootropic drug repurposing. Here, we (1) meta-analyze results from two recent cognitive GWAS to further enhance power for locus discovery; (2) employ several complementary transcriptomic methods to identify genes in these loci that are credibly associated with cognition; and (3) further annotate the resulting genes using multiple chemoinformatic databases to identify "druggable" targets. Using our meta-analytic data set (N = 373,617), we identified 241 independent cognition-associated loci (29 novel), and 76 genes were identified by 2 or more methods of gene identification. Actin and chromatin binding gene sets were identified as novel pathways that could be targeted via drug repurposing. Leveraging our transcriptomic and chemoinformatic databases, we identified 16 putative genes targeted by existing drugs potentially available for cognitive repurposing.},
	language = {en},
	number = {10},
	urldate = {2022-05-08},
	journal = {Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology},
	author = {Lam, Max and Chen, Chia-Yen and Ge, Tian and Xia, Yan and Hill, David W. and Trampush, Joey W. and Yu, Jin and Knowles, Emma and Davies, Gail and Stahl, Eli A. and Huckins, Laura and Liewald, David C. and Djurovic, Srdjan and Melle, Ingrid and Christoforou, Andrea and Reinvang, Ivar and DeRosse, Pamela and Lundervold, Astri J. and Steen, Vidar M. and Espeseth, Thomas and Räikkönen, Katri and Widen, Elisabeth and Palotie, Aarno and Eriksson, Johan G. and Giegling, Ina and Konte, Bettina and Hartmann, Annette M. and Roussos, Panos and Giakoumaki, Stella and Burdick, Katherine E. and Payton, Antony and Ollier, William and Chiba-Falek, Ornit and Koltai, Deborah C. and Need, Anna C. and Cirulli, Elizabeth T. and Voineskos, Aristotle N. and Stefanis, Nikos C. and Avramopoulos, Dimitrios and Hatzimanolis, Alex and Smyrnis, Nikolaos and Bilder, Robert M. and Freimer, Nelson B. and Cannon, Tyrone D. and London, Edythe and Poldrack, Russell A. and Sabb, Fred W. and Congdon, Eliza and Conley, Emily Drabant and Scult, Matthew A. and Dickinson, Dwight and Straub, Richard E. and Donohoe, Gary and Morris, Derek and Corvin, Aiden and Gill, Michael and Hariri, Ahmad R. and Weinberger, Daniel R. and Pendleton, Neil and Bitsios, Panos and Rujescu, Dan and Lahti, Jari and Le Hellard, Stephanie and Keller, Matthew C. and Andreassen, Ole A. and Deary, Ian J. and Glahn, David C. and Huang, Hailiang and Liu, Chunyu and Malhotra, Anil K. and Lencz, Todd},
	month = sep,
	year = {2021},
	pages = {1788--1801},
}

Broad-based cognitive deficits are an enduring and disabling symptom for many patients with severe mental illness, and these impairments are inadequately addressed by current medications. While novel drug targets for schizophrenia and depression have emerged from recent large-scale genome-wide association studies (GWAS) of these psychiatric disorders, GWAS of general cognitive ability can suggest potential targets for nootropic drug repurposing. Here, we (1) meta-analyze results from two recent cognitive GWAS to further enhance power for locus discovery; (2) employ several complementary transcriptomic methods to identify genes in these loci that are credibly associated with cognition; and (3) further annotate the resulting genes using multiple chemoinformatic databases to identify "druggable" targets. Using our meta-analytic data set (N = 373,617), we identified 241 independent cognition-associated loci (29 novel), and 76 genes were identified by 2 or more methods of gene identification. Actin and chromatin binding gene sets were identified as novel pathways that could be targeted via drug repurposing. Leveraging our transcriptomic and chemoinformatic databases, we identified 16 putative genes targeted by existing drugs potentially available for cognitive repurposing.

@misc{toasterbathparty_r-cpd_2021,
	type = {Reddit {Post}},
	title = {R-{CPD} {Doctor} in {Connecticut} ({USA})!},
	url = {www.reddit.com/r/noburp/comments/nuoy1t/rcpd_doctor_in_connecticut_usa/},
	urldate = {2022-04-09},
	journal = {r/noburp},
	author = {toasterbathparty},
	month = jun,
	year = {2021},
}

@article{moon_metformin_2021,
	title = {Metformin ameliorates scleroderma via inhibiting {Th17} cells and reducing {mTOR}-{STAT3} signaling in skin fibroblasts},
	volume = {19},
	issn = {1479-5876},
	url = {https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-021-02860-z},
	doi = {10.1186/s12967-021-02860-z},
	abstract = {Scleroderma is an autoimmune disease that causes dermal fibrosis. It occurs when collagen accumulates in tissue as a result of persistent inflammation. Th17 cells and pro-inflammatory cytokines such as IL-1β, IL-6, IL-17, and TNF-α play important roles in the pathogenesis of scleroderma. Because metformin, a medication used to treat diabetes, has effective immunoregulatory functions, we investigated its therapeutic function in scleroderma. Mice in a model of bleomycin-induced scleroderma were treated with metformin for 2 weeks. Histological assessment demonstrated protective effects of metformin against scleroderma. Metformin decreased the expression of pro-inflammatory factors in dermal tissue and lymphocytes. It also decreased mRNA expression of pro-inflammatory cytokines (IL-1β, IL-6, IL-17, and TNF-α) and fibrosis-inducing molecules both in vivo and in vitro. These results suggest that metformin treatment has anti-inflammatory effects on lymphocytes via the inhibition of IL-17 and cytokines related to Th17 differentiation, such as IL-1β, IL-6, and TNF-α. To investigate how metformin modulates the inflammatory process in skin fibroblasts, we measured mTOR-STAT3 signaling in skin fibroblasts and found that phosphorylated mTOR and phosphorylated STAT3 protein expression were decreased by metformin treatment. These results suggest that metformin has potential to treat scleroderma by inhibiting pro-inflammatory cytokines and anti-inflammatory activity mediated by mTORSTAT3 signaling.},
	language = {en},
	number = {1},
	urldate = {2022-01-08},
	journal = {Journal of Translational Medicine},
	author = {Moon, Jeonghyeon and Lee, Seon-yeong and Choi, Jeong Won and Lee, A Ram and Yoo, Jin Hee and Moon, Su-Jin and Park, Sung-Hwan and Cho, Mi-La},
	month = dec,
	year = {2021},
	pages = {192},
}

Scleroderma is an autoimmune disease that causes dermal fibrosis. It occurs when collagen accumulates in tissue as a result of persistent inflammation. Th17 cells and pro-inflammatory cytokines such as IL-1β, IL-6, IL-17, and TNF-α play important roles in the pathogenesis of scleroderma. Because metformin, a medication used to treat diabetes, has effective immunoregulatory functions, we investigated its therapeutic function in scleroderma. Mice in a model of bleomycin-induced scleroderma were treated with metformin for 2 weeks. Histological assessment demonstrated protective effects of metformin against scleroderma. Metformin decreased the expression of pro-inflammatory factors in dermal tissue and lymphocytes. It also decreased mRNA expression of pro-inflammatory cytokines (IL-1β, IL-6, IL-17, and TNF-α) and fibrosis-inducing molecules both in vivo and in vitro. These results suggest that metformin treatment has anti-inflammatory effects on lymphocytes via the inhibition of IL-17 and cytokines related to Th17 differentiation, such as IL-1β, IL-6, and TNF-α. To investigate how metformin modulates the inflammatory process in skin fibroblasts, we measured mTOR-STAT3 signaling in skin fibroblasts and found that phosphorylated mTOR and phosphorylated STAT3 protein expression were decreased by metformin treatment. These results suggest that metformin has potential to treat scleroderma by inhibiting pro-inflammatory cytokines and anti-inflammatory activity mediated by mTORSTAT3 signaling.

@article{rootman_adults_2021,
	title = {Adults who microdose psychedelics report health related motivations and lower levels of anxiety and depression compared to non-microdosers},
	volume = {11},
	copyright = {2021 The Author(s)},
	issn = {2045-2322},
	url = {https://www.nature.com/articles/s41598-021-01811-4},
	doi = {10.1038/s41598-021-01811-4},
	abstract = {The use of psychedelic substances at sub-sensorium ‘microdoses’, has gained popular academic interest for reported positive effects on wellness and cognition. The present study describes microdosing practices, motivations and mental health among a sample of self-selected microdosers (n = 4050) and non-microdosers (n = 4653) via a mobile application. Psilocybin was the most commonly used microdose substances in our sample (85\%) and we identified diverse microdose practices with regard to dosage, frequency, and the practice of stacking which involves combining psilocybin with non-psychedelic substances such as Lion’s Mane mushrooms, chocolate, and niacin. Microdosers were generally similar to non-microdosing controls with regard to demographics, but were more likely to report a history of mental health concerns. Among individuals reporting mental health concerns, microdosers exhibited lower levels of depression, anxiety, and stress across gender. Health and wellness-related motives were the most prominent motives across microdosers in general, and were more prominent among females and among individuals who reported mental health concerns. Our results indicate health and wellness motives and perceived mental health benefits among microdosers, and highlight the need for further research into the mental health consequences of microdosing including studies with rigorous longitudinal designs.},
	language = {en},
	number = {1},
	urldate = {2021-12-28},
	journal = {Scientific Reports},
	author = {Rootman, Joseph M. and Kryskow, Pamela and Harvey, Kalin and Stamets, Paul and Santos-Brault, Eesmyal and Kuypers, Kim P. C. and Polito, Vince and Bourzat, Francoise and Walsh, Zach},
	month = nov,
	year = {2021},
	keywords = {ADHD, Addiction, Anxiety, Autism spectrum disorders, Bipolar disorder, Depression, Human behaviour, Obsessive compulsive disorder, Post-traumatic stress disorder, Psychiatric disorders, Psychology, Psychosis, Schizophrenia},
	pages = {22479},
}

The use of psychedelic substances at sub-sensorium ‘microdoses’, has gained popular academic interest for reported positive effects on wellness and cognition. The present study describes microdosing practices, motivations and mental health among a sample of self-selected microdosers (n = 4050) and non-microdosers (n = 4653) via a mobile application. Psilocybin was the most commonly used microdose substances in our sample (85%) and we identified diverse microdose practices with regard to dosage, frequency, and the practice of stacking which involves combining psilocybin with non-psychedelic substances such as Lion’s Mane mushrooms, chocolate, and niacin. Microdosers were generally similar to non-microdosing controls with regard to demographics, but were more likely to report a history of mental health concerns. Among individuals reporting mental health concerns, microdosers exhibited lower levels of depression, anxiety, and stress across gender. Health and wellness-related motives were the most prominent motives across microdosers in general, and were more prominent among females and among individuals who reported mental health concerns. Our results indicate health and wellness motives and perceived mental health benefits among microdosers, and highlight the need for further research into the mental health consequences of microdosing including studies with rigorous longitudinal designs.

@article{heffernan_ulotaront_2021,
	title = {Ulotaront: {A} {TAAR1} {Agonist} for the {Treatment} of {Schizophrenia}},
	shorttitle = {Ulotaront},
	url = {https://doi.org/10.1021/acsmedchemlett.1c00527},
	doi = {10.1021/acsmedchemlett.1c00527},
	abstract = {Ulotaront (SEP-363856) is a trace-amine associated receptor 1 (TAAR1) agonist with 5-HT1A receptor agonist activity in Phase 3 clinical development, with FDA Breakthrough Therapy Designation, for the treatment of schizophrenia. TAAR1 is a G-protein-coupled receptor (GPCR) that is expressed in cortical, limbic, and midbrain monoaminergic regions. It is activated by endogenous trace amines, and is believed to play an important role in modulating dopaminergic, serotonergic, and glutamatergic circuitry. TAAR1 agonism data are reported herein for ulotaront and its analogues in comparison to endogenous TAAR1 agonists. In addition, a human TAAR1 homology model was built around ulotaront to identify key interactions and attempt to better understand the scaffold-specific TAAR1 agonism structure–activity relationships.},
	urldate = {2021-12-27},
	journal = {ACS Medicinal Chemistry Letters},
	author = {Heffernan, Michele L. R. and Herman, Lee W. and Brown, Scott and Jones, Philip G. and Shao, Liming and Hewitt, Michael C. and Campbell, John E. and Dedic, Nina and Hopkins, Seth C. and Koblan, Kenneth S. and Xie, Linghong},
	month = dec,
	year = {2021},
	note = {Publisher: American Chemical Society},
}

Ulotaront (SEP-363856) is a trace-amine associated receptor 1 (TAAR1) agonist with 5-HT1A receptor agonist activity in Phase 3 clinical development, with FDA Breakthrough Therapy Designation, for the treatment of schizophrenia. TAAR1 is a G-protein-coupled receptor (GPCR) that is expressed in cortical, limbic, and midbrain monoaminergic regions. It is activated by endogenous trace amines, and is believed to play an important role in modulating dopaminergic, serotonergic, and glutamatergic circuitry. TAAR1 agonism data are reported herein for ulotaront and its analogues in comparison to endogenous TAAR1 agonists. In addition, a human TAAR1 homology model was built around ulotaront to identify key interactions and attempt to better understand the scaffold-specific TAAR1 agonism structure–activity relationships.

@article{underhill_amphetamines_2021,
	title = {Amphetamines signal through intracellular {TAAR1} receptors coupled to {Gα13} and {GαS} in discrete subcellular domains},
	volume = {26},
	copyright = {2019 This is a U.S. government work and not under copyright protection in the U.S.; foreign copyright protection may apply},
	issn = {1476-5578},
	url = {https://www.nature.com/articles/s41380-019-0469-2},
	doi = {10.1038/s41380-019-0469-2},
	abstract = {The extensive use of amphetamines to treat attention deficit hyperactivity disorders in children provides a compelling rationale for understanding the mechanisms of action of amphetamines and amphetamine-related drugs. We have previously shown that acute amphetamine (AMPH) regulates the trafficking of both dopamine and glutamate transporters in dopamine neurons by increasing activation of the small GTPase RhoA and of protein kinase A. Here we demonstrate that these downstream signaling events depend upon the direct activation of a trace amine-associated receptor, TAAR1, an intracellular G-protein coupled receptor (GPCR) that can be activated by amphetamines, trace amines, and biogenic amine metabolites. Using cell lines and mouse lines in which TAAR1 expression has been disrupted, we demonstrate that TAAR1 mediates the effects of AMPH on both RhoA and cAMP signaling. Inhibition of different Gα signaling pathways in cell lines and in vivo using small cell-permeable peptides confirms that the endogenous intracellular TAAR1 couples to G13 and to GS α-subunits to increase RhoA and PKA activity, respectively. Results from experiments with RhoA- and PKA-FRET sensors targeted to different subcellular compartments indicate that AMPH-elicited PKA activation occurs throughout the cell, whereas G13-mediated RhoA activation is concentrated near the endoplasmic reticulum. These observations define TAAR1 as an obligate intracellular target for amphetamines in dopamine neurons and support a model in which distinct pools of TAAR1 mediate the activation of signaling pathways in different compartments to regulate excitatory and dopaminergic neurotransmission.},
	language = {en},
	number = {4},
	urldate = {2021-12-27},
	journal = {Molecular Psychiatry},
	author = {Underhill, Suzanne M. and Hullihen, Patrick D. and Chen, Jingshan and Fenollar-Ferrer, Cristina and Rizzo, M. A. and Ingram, Susan L. and Amara, Susan G.},
	month = apr,
	year = {2021},
	note = {Bandiera\_abtest: a
Cc\_license\_type: cc\_by
Cg\_type: Nature Research Journals
Number: 4
Primary\_atype: Research
Publisher: Nature Publishing Group
Subject\_term: Cell biology;Neuroscience
Subject\_term\_id: cell-biology;neuroscience},
	keywords = {Cell biology, Neuroscience},
	pages = {1208--1223},
}

The extensive use of amphetamines to treat attention deficit hyperactivity disorders in children provides a compelling rationale for understanding the mechanisms of action of amphetamines and amphetamine-related drugs. We have previously shown that acute amphetamine (AMPH) regulates the trafficking of both dopamine and glutamate transporters in dopamine neurons by increasing activation of the small GTPase RhoA and of protein kinase A. Here we demonstrate that these downstream signaling events depend upon the direct activation of a trace amine-associated receptor, TAAR1, an intracellular G-protein coupled receptor (GPCR) that can be activated by amphetamines, trace amines, and biogenic amine metabolites. Using cell lines and mouse lines in which TAAR1 expression has been disrupted, we demonstrate that TAAR1 mediates the effects of AMPH on both RhoA and cAMP signaling. Inhibition of different Gα signaling pathways in cell lines and in vivo using small cell-permeable peptides confirms that the endogenous intracellular TAAR1 couples to G13 and to GS α-subunits to increase RhoA and PKA activity, respectively. Results from experiments with RhoA- and PKA-FRET sensors targeted to different subcellular compartments indicate that AMPH-elicited PKA activation occurs throughout the cell, whereas G13-mediated RhoA activation is concentrated near the endoplasmic reticulum. These observations define TAAR1 as an obligate intracellular target for amphetamines in dopamine neurons and support a model in which distinct pools of TAAR1 mediate the activation of signaling pathways in different compartments to regulate excitatory and dopaminergic neurotransmission.

@article{bloomingdale_quantitative_2021,
	title = {Quantitative systems pharmacology in neuroscience: {Novel} methodologies and technologies},
	volume = {10},
	issn = {2163-8306},
	shorttitle = {Quantitative systems pharmacology in neuroscience},
	url = {https://onlinelibrary.wiley.com/doi/abs/10.1002/psp4.12607},
	doi = {10.1002/psp4.12607},
	abstract = {The development and application of quantitative systems pharmacology models in neuroscience have been modest relative to other fields, such as oncology and immunology, which may reflect the complexity of the brain. Technological and methodological advancements have enhanced the quantitative understanding of brain physiology and pathophysiology and the effects of pharmacological interventions. To maximize the knowledge gained from these novel data types, pharmacometrics modelers may need to expand their toolbox to include additional mathematical and statistical frameworks. A session was held at the 10th annual American Conference on Pharmacometrics (ACoP10) to highlight several recent advancements in quantitative and systems neuroscience. In this mini-review, we provide a brief overview of technological and methodological advancements in the neuroscience therapeutic area that were discussed during the session and how these can be leveraged with quantitative systems pharmacology modeling to enhance our understanding of neurological diseases. Microphysiological systems using human induced pluripotent stem cells (IPSCs), digital biomarkers, and large-scale imaging offer more clinically relevant experimental datasets, enhanced granularity, and a plethora of data to potentially improve the preclinical-to-clinical translation of therapeutics. Network neuroscience methodologies combined with quantitative systems models of neurodegenerative disease could help bridge the gap between cellular and molecular alterations and clinical end points through the integration of information on neural connectomics. Additional topics, such as the neuroimmune system, microbiome, single-cell transcriptomic technologies, and digital device biomarkers, are discussed in brief.},
	language = {en},
	number = {5},
	urldate = {2021-12-27},
	journal = {CPT: Pharmacometrics \& Systems Pharmacology},
	author = {Bloomingdale, Peter and Karelina, Tatiana and Cirit, Murat and Muldoon, Sarah F. and Baker, Justin and McCarty, William J. and Geerts, Hugo and Macha, Sreeraj},
	year = {2021},
	note = {\_eprint: https://onlinelibrary.wiley.com/doi/pdf/10.1002/psp4.12607},
	pages = {412--419},
}

The development and application of quantitative systems pharmacology models in neuroscience have been modest relative to other fields, such as oncology and immunology, which may reflect the complexity of the brain. Technological and methodological advancements have enhanced the quantitative understanding of brain physiology and pathophysiology and the effects of pharmacological interventions. To maximize the knowledge gained from these novel data types, pharmacometrics modelers may need to expand their toolbox to include additional mathematical and statistical frameworks. A session was held at the 10th annual American Conference on Pharmacometrics (ACoP10) to highlight several recent advancements in quantitative and systems neuroscience. In this mini-review, we provide a brief overview of technological and methodological advancements in the neuroscience therapeutic area that were discussed during the session and how these can be leveraged with quantitative systems pharmacology modeling to enhance our understanding of neurological diseases. Microphysiological systems using human induced pluripotent stem cells (IPSCs), digital biomarkers, and large-scale imaging offer more clinically relevant experimental datasets, enhanced granularity, and a plethora of data to potentially improve the preclinical-to-clinical translation of therapeutics. Network neuroscience methodologies combined with quantitative systems models of neurodegenerative disease could help bridge the gap between cellular and molecular alterations and clinical end points through the integration of information on neural connectomics. Additional topics, such as the neuroimmune system, microbiome, single-cell transcriptomic technologies, and digital device biomarkers, are discussed in brief.

@article{guynn_optogenetics_2021,
	title = {Optogenetics and {Controlling} the {Human} {Mind}},
	url = {https://curiosity.scholasticahq.com/article/28096-optogenetics-and-controlling-the-human-mind},
	doi = {10.36898/001c.28096},
	abstract = {From the dawn of history to modern times humans have been using knowledge of neural structures to alter behavior (Faria, 2013). In modern times brain stimulation experiments have been conducted on animals and even humans to control the mind (Marzullo, 2017; Bishop et al., 1963). Behavioral psychologist B.F. Skinner proposed that all behavior can be controlled using rewards and punishments (Schultz \& Schultz, 2019). A new technology in neural engineering known as optogenetics uses CRISPR Cas-9 to genetically modify human neurons to express photosensitive opsins and thus fire when stimulated by certain light wavelengths (Boyden, 2011). Optogenetics offers greater spatial and temporal control of brain activity than current technologies like transcranial magnetic stimulation or psychopharmacological drugs (Williams and Entcheva, 2015; Deisseroth et al., 2006; Shao et al., 2018). The ethics of potential side effects, invasiveness, and abuse should be taken into consideration before human trials begin in the near future (Mathews, 2011; Gilbert, Harris, \& Kidd, 2021).},
	language = {en},
	urldate = {2021-12-23},
	journal = {Curiosity: Interdisciplinary Journal of Research and Innovation},
	author = {Guynn, Michael},
	month = sep,
	year = {2021},
	note = {Publisher: Dixie State University},
	pages = {28096},
}

From the dawn of history to modern times humans have been using knowledge of neural structures to alter behavior (Faria, 2013). In modern times brain stimulation experiments have been conducted on animals and even humans to control the mind (Marzullo, 2017; Bishop et al., 1963). Behavioral psychologist B.F. Skinner proposed that all behavior can be controlled using rewards and punishments (Schultz & Schultz, 2019). A new technology in neural engineering known as optogenetics uses CRISPR Cas-9 to genetically modify human neurons to express photosensitive opsins and thus fire when stimulated by certain light wavelengths (Boyden, 2011). Optogenetics offers greater spatial and temporal control of brain activity than current technologies like transcranial magnetic stimulation or psychopharmacological drugs (Williams and Entcheva, 2015; Deisseroth et al., 2006; Shao et al., 2018). The ethics of potential side effects, invasiveness, and abuse should be taken into consideration before human trials begin in the near future (Mathews, 2011; Gilbert, Harris, & Kidd, 2021).

@article{kantrowitz_trace_2021,
	title = {Trace {Amine}-{Associated} {Receptor} 1 as a {Target} for the {Development} of {New} {Antipsychotics}: {Current} {Status} of {Research} and {Future} {Directions}},
	volume = {35},
	issn = {1179-1934},
	shorttitle = {Trace {Amine}-{Associated} {Receptor} 1 as a {Target} for the {Development} of {New} {Antipsychotics}},
	doi = {10.1007/s40263-021-00864-3},
	abstract = {Schizophrenia is a mental illness associated with an array of symptoms that often result in disability. The primary treatments for schizophrenia are termed antipsychotics. Although antipsychotics modulate a number of different receptor types and subtypes, all currently regulatory agency-approved antipsychotics share in common direct or functional antagonism at the dopamine type 2 receptor (D2R). The majority of people with schizophrenia do not achieve full resolution of their symptoms with antipsychotics, suggesting the need for alternative or complementary approaches. The primary focus of this review is to assess the evidence for the role of the trace amine-associated receptor 1 (TAAR-1) in schizophrenia and the role of TAAR-1 modulators as novel-mechanism antipsychotics. Topics include an overview of TAAR-1 physiology and pathophysiology in schizophrenia, interaction with other neurotransmitter systems, including the dopaminergic, glutamatergic and serotonergic system, and finally, a review of investigational TAAR-1 compounds that have reached Phase II clinical studies in schizophrenia: SEP-363856 (ulotaront) and RO6889450 (ralmitaront). Thus far, results are publicly available only for ulotaront in a relatively young (18-40 years) and acutely exacerbated cohort. These results showed positive effects for overall schizophrenia symptoms without significant tolerability concerns. An ongoing study of ralmitaront will assess specific efficacy in patients with persistent negative symptoms. If trials of TAAR-1 modulators, and other novel-mechanism targets for schizophrenia that are under active study, continue to show positive results, the definition of an antipsychotic may need to be expanded beyond the D2R target in the near future.},
	language = {eng},
	number = {11},
	journal = {CNS drugs},
	author = {Kantrowitz, Joshua T.},
	month = nov,
	year = {2021},
	pmid = {34655036},
	pages = {1153--1161},
}

Schizophrenia is a mental illness associated with an array of symptoms that often result in disability. The primary treatments for schizophrenia are termed antipsychotics. Although antipsychotics modulate a number of different receptor types and subtypes, all currently regulatory agency-approved antipsychotics share in common direct or functional antagonism at the dopamine type 2 receptor (D2R). The majority of people with schizophrenia do not achieve full resolution of their symptoms with antipsychotics, suggesting the need for alternative or complementary approaches. The primary focus of this review is to assess the evidence for the role of the trace amine-associated receptor 1 (TAAR-1) in schizophrenia and the role of TAAR-1 modulators as novel-mechanism antipsychotics. Topics include an overview of TAAR-1 physiology and pathophysiology in schizophrenia, interaction with other neurotransmitter systems, including the dopaminergic, glutamatergic and serotonergic system, and finally, a review of investigational TAAR-1 compounds that have reached Phase II clinical studies in schizophrenia: SEP-363856 (ulotaront) and RO6889450 (ralmitaront). Thus far, results are publicly available only for ulotaront in a relatively young (18-40 years) and acutely exacerbated cohort. These results showed positive effects for overall schizophrenia symptoms without significant tolerability concerns. An ongoing study of ralmitaront will assess specific efficacy in patients with persistent negative symptoms. If trials of TAAR-1 modulators, and other novel-mechanism targets for schizophrenia that are under active study, continue to show positive results, the definition of an antipsychotic may need to be expanded beyond the D2R target in the near future.

@article{olson_promise_2021,
	title = {The {Promise} of {Psychedelic} {Science}},
	volume = {4},
	url = {https://doi.org/10.1021/acsptsci.1c00071},
	doi = {10.1021/acsptsci.1c00071},
	number = {2},
	urldate = {2021-12-20},
	journal = {ACS Pharmacology \& Translational Science},
	author = {Olson, David E.},
	month = apr,
	year = {2021},
	note = {Publisher: American Chemical Society},
	pages = {413--415},
}

@article{upmeier_zu_belzen_modeling_2021,
	title = {Modeling as {Scientific} {Reasoning}—{The} {Role} of {Abductive} {Reasoning} for {Modeling} {Competence}},
	volume = {11},
	doi = {10.3390/educsci11090495},
	number = {9},
	journal = {Education Sciences},
	author = {Upmeier zu Belzen, Annette and Engelschalt, Paul and Krüger, Dirk},
	year = {2021},
	pages = {495},
}

@article{correll_safety_2021,
	title = {Safety and {Effectiveness} of {SEP}−363856 in {Schizophrenia}: {Results} of a 6-{Month}, {Open}-{Label} {Extension} {Study}},
	volume = {26},
	issn = {1092-8529, 2165-6509},
	shorttitle = {Safety and {Effectiveness} of {SEP}−363856 in {Schizophrenia}},
	url = {https://www.cambridge.org/core/product/identifier/S1092852920002357/type/journal_article},
	doi = {10.1017/S1092852920002357},
	abstract = {Method. Patients 10–17 years with bipolar I depression who completed a 6-week double-blind (DB) study of lurasidone vs. placebo were eligible to enroll in a two-year, open-label (OL) extension study in which patients were continued on flexibly-dosed lurasidone (20–80 mg/d) or switched from placebo to lurasidone. Efficacy measures included the Children’s Depression Rating Scale, Revised (CDRS-R) and the Clinical Global Impression, Bipolar Depression Severity scale (CGI-BP-S). Functioning was evaluated utilizing the Clinician-rated Children’s Global Assessment Scale (CGAS) score, with a score {\textgreater}70 indicating no clinically meaningful functional impairment. Responder criteria were met if a patient achieved criteria = 50\% reduction from DB baseline in the CDRS-R total score: remission criteria were met if a patient achieved a CDRS-R Total Score =28 and a YMRS total score =8 and CGI-BP-S depression score =3, and a patient was considered to have met recovery criteria if they achieved remission with a CGAS score {\textgreater}70. In addition, a more stringent outcome, sustained remission, was also analyzed, which required a patient to meet remission criteria for =24 consecutive weeks.
Results. A total of 306 patients completed the 6-week DB study and entered the extension study; 195 (63.7\%) patients completed one year of treatment and 168 (54.9\%) patients completed two years of treatment. Responder rates at OL baseline, one year, and two years were: 51.0\%, 88.4\% and 91.1\%, respectively; remission rates were 24.3\%, 61.3\%, and 75.6\%, respectively; and recovery rates were 17.7\%, 53.8\%, and 73.8\%. On a Pearson correlation analysis, there was a strong inverse relationship (r = À0.71) between CDRS-R total score, and global functioning as measured by the CGAS. Sustained remission was achieved by 37.2\% of patients at one year and 57\% of patients after two years.
Conclusions. In children and adolescents with bipolar depression, up to 2 years of treatment with lurasidone was associated with continued improvement in depressive symptoms, resulting in progressively higher rates of response, remission, recovery, and the more rigorously calculated outcome of sustained remission.},
	language = {en},
	number = {2},
	urldate = {2021-11-28},
	journal = {CNS Spectrums},
	author = {Correll, Christoph U. and Koblan, Kenneth S. and Hopkins, Seth C. and Kent, Justine and Cheng, Hailong and Goldman, Robert and Loebel, Antony},
	month = apr,
	year = {2021},
	pages = {148--149},
}

Method. Patients 10–17 years with bipolar I depression who completed a 6-week double-blind (DB) study of lurasidone vs. placebo were eligible to enroll in a two-year, open-label (OL) extension study in which patients were continued on flexibly-dosed lurasidone (20–80 mg/d) or switched from placebo to lurasidone. Efficacy measures included the Children’s Depression Rating Scale, Revised (CDRS-R) and the Clinical Global Impression, Bipolar Depression Severity scale (CGI-BP-S). Functioning was evaluated utilizing the Clinician-rated Children’s Global Assessment Scale (CGAS) score, with a score \textgreater70 indicating no clinically meaningful functional impairment. Responder criteria were met if a patient achieved criteria = 50% reduction from DB baseline in the CDRS-R total score: remission criteria were met if a patient achieved a CDRS-R Total Score =28 and a YMRS total score =8 and CGI-BP-S depression score =3, and a patient was considered to have met recovery criteria if they achieved remission with a CGAS score \textgreater70. In addition, a more stringent outcome, sustained remission, was also analyzed, which required a patient to meet remission criteria for =24 consecutive weeks. Results. A total of 306 patients completed the 6-week DB study and entered the extension study; 195 (63.7%) patients completed one year of treatment and 168 (54.9%) patients completed two years of treatment. Responder rates at OL baseline, one year, and two years were: 51.0%, 88.4% and 91.1%, respectively; remission rates were 24.3%, 61.3%, and 75.6%, respectively; and recovery rates were 17.7%, 53.8%, and 73.8%. On a Pearson correlation analysis, there was a strong inverse relationship (r = À0.71) between CDRS-R total score, and global functioning as measured by the CGAS. Sustained remission was achieved by 37.2% of patients at one year and 57% of patients after two years. Conclusions. In children and adolescents with bipolar depression, up to 2 years of treatment with lurasidone was associated with continued improvement in depressive symptoms, resulting in progressively higher rates of response, remission, recovery, and the more rigorously calculated outcome of sustained remission.

@article{luptak_novel_2021,
	title = {Novel approaches in schizophrenia-from risk factors and hypotheses to novel drug targets},
	volume = {11},
	issn = {2220-3206},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8311514/},
	doi = {10.5498/wjp.v11.i7.277},
	abstract = {Schizophrenia is a severe psychiatric disorder characterized by emotional, behavioral and cognitive disturbances, and the treatment of schizophrenia is often complicated by noncompliance and pharmacoresistance. The search for the pathophysiological mechanisms underlying schizophrenia has resulted in the proposal of several hypotheses to explain the impacts of environmental, genetic, neurodevelopmental, immune and inflammatory factors on disease onset and progression. This review discusses the newest insights into the pathophysiology of and risk factors for schizophrenia and notes novel approaches in antipsychotic treatment and potential diagnostic and theranostic biomarkers. The current hypotheses focusing on neuromediators (dopamine, glutamate, and serotonin), neuroinflammation, the cannabinoid hypothesis, the gut-brain axis model, and oxidative stress are summarized. Key genetic features, including small nucleotide polymorphisms, copy number variations, microdeletions, mutations and epigenetic changes, are highlighted. Current pharmacotherapy of schizophrenia relies mostly on dopaminergic and serotonergic antagonists/partial agonists, but new findings in the pathophysiology of schizophrenia have allowed the expansion of novel approaches in pharmacotherapy and the establishment of more reliable biomarkers. Substances with promising results in preclinical and clinical studies include lumateperone, pimavanserin, xanomeline, roluperidone, agonists of trace amine-associated receptor 1, inhibitors of glycine transporters, AMPA allosteric modulators, mGLUR2-3 agonists, D-amino acid oxidase inhibitors and cannabidiol. The use of anti-inflammatory agents as an add-on therapy is mentioned.},
	number = {7},
	urldate = {2021-11-28},
	journal = {World Journal of Psychiatry},
	author = {Ľupták, Matej and Michaličková, Danica and Fišar, Zdeněk and Kitzlerová, Eva and Hroudová, Jana},
	month = jul,
	year = {2021},
	pmid = {34327122},
	pmcid = {PMC8311514},
	pages = {277--296},
}

Schizophrenia is a severe psychiatric disorder characterized by emotional, behavioral and cognitive disturbances, and the treatment of schizophrenia is often complicated by noncompliance and pharmacoresistance. The search for the pathophysiological mechanisms underlying schizophrenia has resulted in the proposal of several hypotheses to explain the impacts of environmental, genetic, neurodevelopmental, immune and inflammatory factors on disease onset and progression. This review discusses the newest insights into the pathophysiology of and risk factors for schizophrenia and notes novel approaches in antipsychotic treatment and potential diagnostic and theranostic biomarkers. The current hypotheses focusing on neuromediators (dopamine, glutamate, and serotonin), neuroinflammation, the cannabinoid hypothesis, the gut-brain axis model, and oxidative stress are summarized. Key genetic features, including small nucleotide polymorphisms, copy number variations, microdeletions, mutations and epigenetic changes, are highlighted. Current pharmacotherapy of schizophrenia relies mostly on dopaminergic and serotonergic antagonists/partial agonists, but new findings in the pathophysiology of schizophrenia have allowed the expansion of novel approaches in pharmacotherapy and the establishment of more reliable biomarkers. Substances with promising results in preclinical and clinical studies include lumateperone, pimavanserin, xanomeline, roluperidone, agonists of trace amine-associated receptor 1, inhibitors of glycine transporters, AMPA allosteric modulators, mGLUR2-3 agonists, D-amino acid oxidase inhibitors and cannabidiol. The use of anti-inflammatory agents as an add-on therapy is mentioned.

@article{kantrowitz_trace_2021-1,
	title = {Trace {Amine}-{Associated} {Receptor} 1 as a {Target} for the {Development} of {New} {Antipsychotics}: {Current} {Status} of {Research} and {Future} {Directions}},
	volume = {35},
	issn = {1179-1934},
	shorttitle = {Trace {Amine}-{Associated} {Receptor} 1 as a {Target} for the {Development} of {New} {Antipsychotics}},
	url = {https://doi.org/10.1007/s40263-021-00864-3},
	doi = {10.1007/s40263-021-00864-3},
	abstract = {Schizophrenia is a mental illness associated with an array of symptoms that often result in disability. The primary treatments for schizophrenia are termed antipsychotics. Although antipsychotics modulate a number of different receptor types and subtypes, all currently regulatory agency-approved antipsychotics share in common direct or functional antagonism at the dopamine type 2 receptor (D2R). The majority of people with schizophrenia do not achieve full resolution of their symptoms with antipsychotics, suggesting the need for alternative or complementary approaches. The primary focus of this review is to assess the evidence for the role of the trace amine-associated receptor 1 (TAAR-1) in schizophrenia and the role of TAAR-1 modulators as novel-mechanism antipsychotics. Topics include an overview of TAAR-1 physiology and pathophysiology in schizophrenia, interaction with other neurotransmitter systems, including the dopaminergic, glutamatergic and serotonergic system, and finally, a review of investigational TAAR-1 compounds that have reached Phase II clinical studies in schizophrenia: SEP-363856 (ulotaront) and RO6889450 (ralmitaront). Thus far, results are publicly available only for ulotaront in a relatively young (18–40 years) and acutely exacerbated cohort. These results showed positive effects for overall schizophrenia symptoms without significant tolerability concerns. An ongoing study of ralmitaront will assess specific efficacy in patients with persistent negative symptoms. If trials of TAAR-1 modulators, and other novel-mechanism targets for schizophrenia that are under active study, continue to show positive results, the definition of an antipsychotic may need to be expanded beyond the D2R target in the near future.},
	language = {en},
	number = {11},
	urldate = {2021-11-28},
	journal = {CNS Drugs},
	author = {Kantrowitz, Joshua T.},
	month = nov,
	year = {2021},
	pages = {1153--1161},
}

Schizophrenia is a mental illness associated with an array of symptoms that often result in disability. The primary treatments for schizophrenia are termed antipsychotics. Although antipsychotics modulate a number of different receptor types and subtypes, all currently regulatory agency-approved antipsychotics share in common direct or functional antagonism at the dopamine type 2 receptor (D2R). The majority of people with schizophrenia do not achieve full resolution of their symptoms with antipsychotics, suggesting the need for alternative or complementary approaches. The primary focus of this review is to assess the evidence for the role of the trace amine-associated receptor 1 (TAAR-1) in schizophrenia and the role of TAAR-1 modulators as novel-mechanism antipsychotics. Topics include an overview of TAAR-1 physiology and pathophysiology in schizophrenia, interaction with other neurotransmitter systems, including the dopaminergic, glutamatergic and serotonergic system, and finally, a review of investigational TAAR-1 compounds that have reached Phase II clinical studies in schizophrenia: SEP-363856 (ulotaront) and RO6889450 (ralmitaront). Thus far, results are publicly available only for ulotaront in a relatively young (18–40 years) and acutely exacerbated cohort. These results showed positive effects for overall schizophrenia symptoms without significant tolerability concerns. An ongoing study of ralmitaront will assess specific efficacy in patients with persistent negative symptoms. If trials of TAAR-1 modulators, and other novel-mechanism targets for schizophrenia that are under active study, continue to show positive results, the definition of an antipsychotic may need to be expanded beyond the D2R target in the near future.

@book{larraz-rabanos_development_2021,
	title = {Development of {Creative} {Thinking} {Skills} in the {Teaching}-{Learning} {Process}},
	isbn = {978-1-83969-289-5},
	url = {https://www.intechopen.com/chapters/76737},
	abstract = {Creativity is one of the most appreciated learning skills current the XXI century. The development of creativity has been considered essential in order to achieve an effective and a high-level learning. As different approaches to its study, creativity has been defined as a result, as a process, as a construct derived from the influence of the context and of the experience and as a personality feature of human nature. The aim of this contribution is to explain the study of creativity from the mentioned approaches to achieve a comprehension of such construct. In addition, the focus has been centred on highlight the development of creativity from an educational approach, starting from the description, implication of the use and application of creative strategies in the teaching and learning processes. Finally, a brief description is made of the most important or relevant strategies found in the literature, with emphasis on the incorporation of these strategies in the problem-solving process.},
	language = {en},
	urldate = {2021-11-27},
	publisher = {IntechOpen},
	author = {Larraz-Rábanos, Natalia},
	month = may,
	year = {2021},
	doi = {10.5772/intechopen.97780},
	note = {Publication Title: Teacher Education - New Perspectives},
}

Creativity is one of the most appreciated learning skills current the XXI century. The development of creativity has been considered essential in order to achieve an effective and a high-level learning. As different approaches to its study, creativity has been defined as a result, as a process, as a construct derived from the influence of the context and of the experience and as a personality feature of human nature. The aim of this contribution is to explain the study of creativity from the mentioned approaches to achieve a comprehension of such construct. In addition, the focus has been centred on highlight the development of creativity from an educational approach, starting from the description, implication of the use and application of creative strategies in the teaching and learning processes. Finally, a brief description is made of the most important or relevant strategies found in the literature, with emphasis on the incorporation of these strategies in the problem-solving process.

@article{dickson-gomez_effects_2021,
	title = {Effects of {Implementation} and {Enforcement} {Differences} in {Prescription} {Drug} {Monitoring} {Programs} in 3 {States}: {Connecticut}, {Kentucky}, and {Wisconsin}},
	volume = {15},
	issn = {1178-2218},
	shorttitle = {Effects of {Implementation} and {Enforcement} {Differences} in {Prescription} {Drug} {Monitoring} {Programs} in 3 {States}},
	url = {https://doi.org/10.1177/1178221821992349},
	doi = {10.1177/1178221821992349},
	abstract = {Background and aims:Prescription Drug Monitoring Programs (PDMPs) were designed to curb opioid misuse and diversion by tracking scheduled medications prescribed by medical providers and dispensed by pharmacies. The effects of PDMPs on opioid prescription, misuse and overdose rates have been mixed due in part to variability in states? PDMPs and difficulties measuring this complexity, and a lack of attention to implementation and enforcement of PDMP components. The current study uses qualitative interviews with key informants from 3 states with different PDMPs, Connecticut, Kentucky and Wisconsin to explore differences in the characteristics of the PDMPs in each state; how they are implemented, monitored and enforced; and unintended negative consequences of these programs.Methods:We conducted in-depth interviews with key informants from each state representing the following sectors: PDMP and pain clinic regulation agencies, Medicaid programs, state licensing boards, pharmacies, emergency medicine departments, pain management clinics, first responders, drug courts, drug treatment programs, medication assisted treatment (MAT) providers, and harm reduction organizations. Interview guides explored participants? experiences with and opinions of PDMPs according to their roles. Data analysis was conducted using a collaborative, constant comparison method.Results:While all 3 states had mandated registration and reporting requirements, the states differed in the implementation and enforcement of these and the extent to which provider prescribing was monitored. These, in turn, influenced how medical providers perceived the PDMP and changed how providers prescribed opioids. Unintended consequences of state PDMPs included under-prescribing for pain and ?dumping? patients who were long term users of opioids or who had developed opioid use disorders and may explain the increase in illicit heroin or opioid use.Conclusion:State PDMPs with similar mandates may differ greatly in implementation and enforcement. These differences are important to consider when determining the effects of PDMPs on opioid misuse and overdose.},
	language = {en},
	urldate = {2021-07-18},
	journal = {Substance Abuse: Research and Treatment},
	author = {Dickson-Gomez, Julia and Christenson, Erika and Weeks, Margaret and Galletly, Carol and Wogen, Jennifer and Spector, Antoinette and McDonald, Madelyn and Ohlrich, Jessica},
	month = jan,
	year = {2021},
	keywords = {Opioids, enforcement, implementation, overdose, prescription drug monitoring programs},
	pages = {1178221821992349},
}

Background and aims:Prescription Drug Monitoring Programs (PDMPs) were designed to curb opioid misuse and diversion by tracking scheduled medications prescribed by medical providers and dispensed by pharmacies. The effects of PDMPs on opioid prescription, misuse and overdose rates have been mixed due in part to variability in states? PDMPs and difficulties measuring this complexity, and a lack of attention to implementation and enforcement of PDMP components. The current study uses qualitative interviews with key informants from 3 states with different PDMPs, Connecticut, Kentucky and Wisconsin to explore differences in the characteristics of the PDMPs in each state; how they are implemented, monitored and enforced; and unintended negative consequences of these programs.Methods:We conducted in-depth interviews with key informants from each state representing the following sectors: PDMP and pain clinic regulation agencies, Medicaid programs, state licensing boards, pharmacies, emergency medicine departments, pain management clinics, first responders, drug courts, drug treatment programs, medication assisted treatment (MAT) providers, and harm reduction organizations. Interview guides explored participants? experiences with and opinions of PDMPs according to their roles. Data analysis was conducted using a collaborative, constant comparison method.Results:While all 3 states had mandated registration and reporting requirements, the states differed in the implementation and enforcement of these and the extent to which provider prescribing was monitored. These, in turn, influenced how medical providers perceived the PDMP and changed how providers prescribed opioids. Unintended consequences of state PDMPs included under-prescribing for pain and ?dumping? patients who were long term users of opioids or who had developed opioid use disorders and may explain the increase in illicit heroin or opioid use.Conclusion:State PDMPs with similar mandates may differ greatly in implementation and enforcement. These differences are important to consider when determining the effects of PDMPs on opioid misuse and overdose.

@article{bayer_national_2021,
	title = {A {National} {Mental} {Health} {Profile} of {Parents} of {Children} {With} {Medical} {Complexity}},
	url = {http://pediatrics.aappublications.org/content/early/2021/06/18/peds.2020-023358.abstract},
	doi = {10.1542/peds.2020-023358},
	abstract = {OBJECTIVES The mental health of parents of children with medical complexity (CMC) is poorly understood, yet it drives child and family health outcomes. For parents of CMC, compared with parents of noncomplex children with special health care needs (CSHCN) and children without special health care needs (non-CSHCN), we examined self-reported mental health, knowledge of community sources for help, and emotional support.METHODS Using parent-reported data from the combined 2016–2017 National Survey of Children’s Health, we divided the population into 3 groups: households with CMC, noncomplex CSHCN, and non-CSHCN. We compared these groups regarding the following: (1) parents’ risks for poor or fair mental health and knowledge of where to go for community help and (2) parent-reported sources of emotional support.RESULTS Of 63c955c588 parent-child dyads (weighted from a sample of 65c204), parents of CMC had greater adjusted odds of reporting poor or fair mental health compared with parents of noncomplex CSHCN (adjusted odds ratio [aOR] 2.0; 95\% confidence interval [CI] 1.1–3.8) and non-CSHCN (aOR 4.6; 95\% CI 2.5–8.6). Parents of CMC had greater odds of not knowing where to find community help compared with parents of noncomplex CSHCN (aOR 2.1; 95\% CI 1.4–3.1) and non-CSHCN (aOR 2.9; 95\% CI 2.0–4.3). However, parents of CMC were most likely to report receiving emotional support from health care providers and advocacy groups (P \< .001).CONCLUSIONS Among all parents, those with CMC are at the highest risk to report suboptimal mental health. They more often report that they do not know where to find community help, but they do say that they receive emotional support from health care providers and advocacy groups. Future researchers should identify ways to directly support the emotional wellness of parents of CMC.},
	journal = {Pediatrics},
	author = {Bayer, Nathaniel D. and Wang, Hongyue and Yu, Justin A. and Kuo, Dennis Z. and Halterman, Jill S. and Li, Yue},
	month = jun,
	year = {2021},
	pages = {e2020023358},
}

OBJECTIVES The mental health of parents of children with medical complexity (CMC) is poorly understood, yet it drives child and family health outcomes. For parents of CMC, compared with parents of noncomplex children with special health care needs (CSHCN) and children without special health care needs (non-CSHCN), we examined self-reported mental health, knowledge of community sources for help, and emotional support.METHODS Using parent-reported data from the combined 2016–2017 National Survey of Children’s Health, we divided the population into 3 groups: households with CMC, noncomplex CSHCN, and non-CSHCN. We compared these groups regarding the following: (1) parents’ risks for poor or fair mental health and knowledge of where to go for community help and (2) parent-reported sources of emotional support.RESULTS Of 63c955c588 parent-child dyads (weighted from a sample of 65c204), parents of CMC had greater adjusted odds of reporting poor or fair mental health compared with parents of noncomplex CSHCN (adjusted odds ratio [aOR] 2.0; 95% confidence interval [CI] 1.1–3.8) and non-CSHCN (aOR 4.6; 95% CI 2.5–8.6). Parents of CMC had greater odds of not knowing where to find community help compared with parents of noncomplex CSHCN (aOR 2.1; 95% CI 1.4–3.1) and non-CSHCN (aOR 2.9; 95% CI 2.0–4.3). However, parents of CMC were most likely to report receiving emotional support from health care providers and advocacy groups (P < .001).CONCLUSIONS Among all parents, those with CMC are at the highest risk to report suboptimal mental health. They more often report that they do not know where to find community help, but they do say that they receive emotional support from health care providers and advocacy groups. Future researchers should identify ways to directly support the emotional wellness of parents of CMC.

@techreport{singh_enhancing_2021,
	type = {Clinical trial registration},
	title = {Enhancing {Gamma} {Band} {Response} in {Schizophrenia} to {Improve} {Working}},
	shorttitle = {A {Neurofeedback} {Intervention} to {Improve} {Working} {Memory} in {Schizophrenia}},
	url = {https://clinicaltrials.gov/ct2/show/NCT03260257},
	abstract = {Schizophrenia affects 2.4 million Americans and causes significant individual and societal costs. Cognitive deficits including poor working memory arise early in the course of illness, account for poor long-term outcomes and have been difficult to treat with available treatments. The investigators are proposing to develop a novel, computer-based brain training to improve working memory in schizophrenia patients, which, if successful could have significant personal, societal, and economic impact.},
	number = {NCT03260257},
	urldate = {2021-04-08},
	institution = {clinicaltrials.gov},
	author = {Singh, Fiza},
	collaborator = {{University of California, San Diego} and {National Institutes of Health (NIH)}},
	month = feb,
	year = {2021},
	note = {ZSCC: NoCitationData[s0] 
ubmitted: August 17, 2017},
}

Schizophrenia affects 2.4 million Americans and causes significant individual and societal costs. Cognitive deficits including poor working memory arise early in the course of illness, account for poor long-term outcomes and have been difficult to treat with available treatments. The investigators are proposing to develop a novel, computer-based brain training to improve working memory in schizophrenia patients, which, if successful could have significant personal, societal, and economic impact.

@book{corrigan_health_2021,
	title = {Health and wellness in people living with serious mental illness},
	isbn = {978-1-61537-379-6 1-61537-379-9},
	abstract = {"People with serious mental illness get sick and die 10-20 years younger, compared to others in their same age cohort. The reasons, and possible interventions, are many, but further research is necessary for the continued development and evaluation of strategies to combat the health challenges faced by these patients. In thoroughly describing community-based participatory research (CBPR)-an approach that includes people in a community as partners in all facets of research, rather than just the subjects of that research-Health and Wellness in People Living With Serious Mental Illness provides a template for continued study. It is through this lens that this volume examines the health and concerns of people with mental illness, as well as possible solutions to these health problems. Through multiple case vignettes, the book delves into the challenges of health and wellness for people with mental illness, summarizing the research on mortality and morbidity in this group, as well as information about the status quo on wellness, and offers a grounded, real-world illustration of CBPR in practice"--},
	language = {English},
	author = {Corrigan, , Patrick W. and Ballentine, , Sonya L. and {American Psychiatric Association}},
	year = {2021},
}

"People with serious mental illness get sick and die 10-20 years younger, compared to others in their same age cohort. The reasons, and possible interventions, are many, but further research is necessary for the continued development and evaluation of strategies to combat the health challenges faced by these patients. In thoroughly describing community-based participatory research (CBPR)-an approach that includes people in a community as partners in all facets of research, rather than just the subjects of that research-Health and Wellness in People Living With Serious Mental Illness provides a template for continued study. It is through this lens that this volume examines the health and concerns of people with mental illness, as well as possible solutions to these health problems. Through multiple case vignettes, the book delves into the challenges of health and wellness for people with mental illness, summarizing the research on mortality and morbidity in this group, as well as information about the status quo on wellness, and offers a grounded, real-world illustration of CBPR in practice"–

@techreport{national_institute_of_allergy_and_infectious_diseases_niaid_elotuzumab_2021,
	type = {Clinical trial registration},
	title = {Elotuzumab in {Immunoglobulin} {G4}-{Related} {Disease} ({IgG4}-{RD})},
	url = {https://clinicaltrials.gov/ct2/show/NCT04918147},
	abstract = {This is a two-part multi-center clinical trial in participants with active IgG4-RD.

Part 1 (Cohort 1a and Cohort 1B) is an open-label, dose escalation phase to determine the safety of elotuzumab for investigation in IgG4-RD.

Part 2 (Cohort 2) is a randomized, placebo-controlled, double-blinded (masked) trial phase to compare the effects of elotuzumab and prednisone to elotuzumab placebo and prednisone in participants with IgG4 RD.

Approximately 75 participants with active IgG4-RD will be enrolled in the overall program, 12 in Part 1 and 63 in Part 2. Randomization in Part 2: 2 to 1, with approximately forty-two participants randomized to elotuzumab plus prednisone taper, and twenty-one participants randomized to placebo for elotuzumab plus prednisone taper.

The total duration of participant follow-up in this trial will be 48 weeks (11 months).},
	number = {NCT04918147},
	urldate = {2021-06-22},
	institution = {clinicaltrials.gov},
	author = {{National Institute of Allergy and Infectious Diseases (NIAID)}},
	collaborator = {{Autoimmunity Centers of Excellence} and {Bristol-Myers Squibb} and {Rho Federal Systems Division, Inc.}},
	month = jun,
	year = {2021},
	note = {ZSCC: NoCitationData[s0] 
ubmitted: June 4, 2021},
}

This is a two-part multi-center clinical trial in participants with active IgG4-RD. Part 1 (Cohort 1a and Cohort 1B) is an open-label, dose escalation phase to determine the safety of elotuzumab for investigation in IgG4-RD. Part 2 (Cohort 2) is a randomized, placebo-controlled, double-blinded (masked) trial phase to compare the effects of elotuzumab and prednisone to elotuzumab placebo and prednisone in participants with IgG4 RD. Approximately 75 participants with active IgG4-RD will be enrolled in the overall program, 12 in Part 1 and 63 in Part 2. Randomization in Part 2: 2 to 1, with approximately forty-two participants randomized to elotuzumab plus prednisone taper, and twenty-one participants randomized to placebo for elotuzumab plus prednisone taper. The total duration of participant follow-up in this trial will be 48 weeks (11 months).

@article{muthesius_preserved_2021,
	title = {Preserved metacognition despite impaired perception of intentionality cues in schizophrenia},
	copyright = {© 2021, Posted by Cold Spring Harbor Laboratory. This pre-print is available under a Creative Commons License (Attribution-NonCommercial-NoDerivs 4.0 International), CC BY-NC-ND 4.0, as described at http://creativecommons.org/licenses/by-nc-nd/4.0/},
	url = {https://www.medrxiv.org/content/10.1101/2021.05.18.21257368v1},
	doi = {10.1101/2021.05.18.21257368},
	abstract = {{\textless}h3{\textgreater}Abstract{\textless}/h3{\textgreater} {\textless}p{\textgreater}Social cognition and metacognition are frequently impaired in schizophrenia, and these impairments complicate recovery. Recent work suggests that different aspects of metacognition may not be impaired to the same degree. Furthermore, metacognition and the cognitive capacity being monitored need not be similarly impaired. Here, we assessed performance in detecting cues of intentional behaviour as well as metacognition about detecting those cues in schizophrenia. Thirty patients and controls categorized animations of moving dots into those displaying a dyadic interaction demonstrating a chase or no chase and indicated their confidence in these judgments. Perception and metacognition were assessed using signal detection theoretic measures, which were analysed using frequentist and Bayesian statistics. Patients showed a deficit compared to controls in detecting intentionality cues, but showed preserved metacognitive performance into this task. Our study reveals a selective deficit in the perception of intentionality cues, but preserved metacognitive insight into the validity of this perception. It thus appears that impairment of metacognition in schizophrenia varies across cognitive domains - metacognition should not be considered a monolithic stone that is either impaired or unimpaired.{\textless}/p{\textgreater}},
	language = {en},
	urldate = {2021-06-23},
	journal = {medRxiv},
	author = {Muthesius, Ana and Grothey, Farina and Cunningham, Carter and Hölzer, Susanne and Vogeley, Kai and Schultz, Johannes},
	month = may,
	year = {2021},
	note = {ZSCC: NoCitationData[s0]},
	pages = {2021.05.18.21257368},
}

\textlessh3\textgreaterAbstract\textless/h3\textgreater \textlessp\textgreaterSocial cognition and metacognition are frequently impaired in schizophrenia, and these impairments complicate recovery. Recent work suggests that different aspects of metacognition may not be impaired to the same degree. Furthermore, metacognition and the cognitive capacity being monitored need not be similarly impaired. Here, we assessed performance in detecting cues of intentional behaviour as well as metacognition about detecting those cues in schizophrenia. Thirty patients and controls categorized animations of moving dots into those displaying a dyadic interaction demonstrating a chase or no chase and indicated their confidence in these judgments. Perception and metacognition were assessed using signal detection theoretic measures, which were analysed using frequentist and Bayesian statistics. Patients showed a deficit compared to controls in detecting intentionality cues, but showed preserved metacognitive performance into this task. Our study reveals a selective deficit in the perception of intentionality cues, but preserved metacognitive insight into the validity of this perception. It thus appears that impairment of metacognition in schizophrenia varies across cognitive domains - metacognition should not be considered a monolithic stone that is either impaired or unimpaired.\textless/p\textgreater

@article{perugi_there_2021,
	title = {There are no patients without comorbidity},
	volume = {50},
	issn = {0924977X},
	url = {https://linkinghub.elsevier.com/retrieve/pii/S0924977X21002236},
	doi = {10.1016/j.euroneuro.2021.05.002},
	language = {en},
	urldate = {2021-06-16},
	journal = {European Neuropsychopharmacology},
	author = {Perugi, Giulio and Barbuti, Margherita},
	month = sep,
	year = {2021},
	note = {ZSCC: 0000000},
	pages = {104--106},
}

@article{trejo_cohort_2021,
	title = {“{A} {Cohort} of {Pirate} {Ships}”: {Biomedical} {Citizen} {Scientists}’ {Attitudes} {Toward} {Ethical} {Oversight}},
	volume = {6},
	copyright = {Authors who publish with this journal agree to the following terms:    Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a  Creative Commons Attribution License  that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.  Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgement of its initial publication in this journal.  Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) prior to and during the submission process, as it can lead to productive exchanges, as well as earlier and greater citation of published work (See  The Effect of Open Access ).  All third-party images reproduced on this journal are shared under Educational Fair Use. For more information on  Educational Fair Use , please see  this useful checklist prepared by Columbia University Libraries .   All copyright  of third-party content posted here for research purposes belongs to its original owners.  Unless otherwise stated all references to characters and comic art presented on this journal are ©, ® or ™ of their respective owners. No challenge to any owner’s rights is intended or should be inferred.},
	issn = {2057-4991},
	shorttitle = {“{A} {Cohort} of {Pirate} {Ships}”},
	url = {http://theoryandpractice.citizenscienceassociation.org/articles/10.5334/cstp.360/},
	doi = {10.5334/cstp.360},
	abstract = {As biomedical citizen science initiatives become more prevalent, the unique ethical issues that they raise are attracting policy attention. One issue identified as a significant concern is the ethical oversight of bottom-up biomedical citizen science projects that are designed and executed primarily or solely by members of the public. That is because the federal rules that require ethical oversight of research by institutional review boards generally do not apply to such projects, creating what has been called an ethics gap.

Working to close this gap, practitioners and scholars have considered new mechanisms of ethical oversight for biomedical citizen science. To date, however, participants’ attitudes about ethics and oversight preferences have not been systematically examined. This information is useful to efforts to develop ethical oversight mechanisms because it provides a basis for evaluating the likely effectiveness of specific features of such mechanisms and their acceptability from the perspective of biomedical citizen scientists.

Here, we report data from qualitative interviews with 35 stakeholders in bottom-up biomedical citizen science about their general ethics attitudes and preferences regarding ethical oversight. Interviewees described ten ethical priorities and endorsed oversight mechanisms that are voluntary, community-driven, and offer guidance. Conversely, interviewees rejected mechanisms that are mandatory, hierarchical, and inflexible. Applying these findings, we conclude that expert consultation and community review models appear to align well with ethical priorities and oversight preferences of many biomedical citizen scientists, although local conditions should guide the development and use of mechanisms in specific communities.},
	language = {en},
	number = {1},
	urldate = {2021-06-04},
	journal = {Citizen Science: Theory and Practice},
	author = {Trejo, Meredith and Canfield, Isabel and Brooks, Whitney Bash and Pearlman, Alex and Guerrini, Christi},
	month = may,
	year = {2021},
	note = {ZSCC: 0000000},
	keywords = {DIY biology, Institutional Review Board, biohacking, citizen science, community biology, research ethics},
	pages = {15},
}

As biomedical citizen science initiatives become more prevalent, the unique ethical issues that they raise are attracting policy attention. One issue identified as a significant concern is the ethical oversight of bottom-up biomedical citizen science projects that are designed and executed primarily or solely by members of the public. That is because the federal rules that require ethical oversight of research by institutional review boards generally do not apply to such projects, creating what has been called an ethics gap. Working to close this gap, practitioners and scholars have considered new mechanisms of ethical oversight for biomedical citizen science. To date, however, participants’ attitudes about ethics and oversight preferences have not been systematically examined. This information is useful to efforts to develop ethical oversight mechanisms because it provides a basis for evaluating the likely effectiveness of specific features of such mechanisms and their acceptability from the perspective of biomedical citizen scientists. Here, we report data from qualitative interviews with 35 stakeholders in bottom-up biomedical citizen science about their general ethics attitudes and preferences regarding ethical oversight. Interviewees described ten ethical priorities and endorsed oversight mechanisms that are voluntary, community-driven, and offer guidance. Conversely, interviewees rejected mechanisms that are mandatory, hierarchical, and inflexible. Applying these findings, we conclude that expert consultation and community review models appear to align well with ethical priorities and oversight preferences of many biomedical citizen scientists, although local conditions should guide the development and use of mechanisms in specific communities.

@article{mazzoleni_modelling_2021,
	title = {Modelling {Lobbying} {Behaviour} and {Interdisciplinarity} {Dynamics} in {Academia}},
	volume = {385},
	issn = {03770427},
	url = {http://arxiv.org/abs/1802.01002},
	doi = {10.1016/j.cam.2020.113194},
	abstract = {Disciplinary diversity is being recognized today as the key to establish a vibrant academic environment with bigger potential for breakthroughs in research and technology. However, the interaction of several factors including policies, and behavioral attitudes put significant barriers on advancing interdisciplinarity. A "cognitive rigidity" may rise due to reactive academic lobbying favouring inbreeding. Here, we address, analyse and discuss a mathematical model of lobbying and interdisciplinarity dynamics in Academia. The model consists of four coupled non-linear Ordinary Differential Equations simulating the interaction between three types of academic individuals and a state reflecting the rate of knowledge advancement which is related to the level of disciplinary diversity. Our model predicts a rich nonlinear behaviour including multiplicity of states and sustained periodic oscillations resembling the everlasting struggle between the "new" and the "old". The effect of a control policy that inhibits lobbying is also studied. By appropriate adjustment of the model parameters we approximated the jump/phase transitions in breakthroughs in mathematical and molecular biological sciences resulted by the increased flow of Russian scientists in the USA after the dissolution of the Soviet Union starting in 1989, the launch of the Human Genome Project in 1992 and the Internet diffusion starting in 2000.},
	urldate = {2021-04-21},
	journal = {Journal of Computational and Applied Mathematics},
	author = {Mazzoleni, Stefano and Russo, Lucia and Giannino, Francesco and Toraldo, Gerardo and Siettos, Constantinos},
	month = mar,
	year = {2021},
	note = {ZSCC: NoCitationData[s0] 
arXiv: 1802.01002},
	keywords = {Physics - Physics and Society},
	pages = {113194},
}

Disciplinary diversity is being recognized today as the key to establish a vibrant academic environment with bigger potential for breakthroughs in research and technology. However, the interaction of several factors including policies, and behavioral attitudes put significant barriers on advancing interdisciplinarity. A "cognitive rigidity" may rise due to reactive academic lobbying favouring inbreeding. Here, we address, analyse and discuss a mathematical model of lobbying and interdisciplinarity dynamics in Academia. The model consists of four coupled non-linear Ordinary Differential Equations simulating the interaction between three types of academic individuals and a state reflecting the rate of knowledge advancement which is related to the level of disciplinary diversity. Our model predicts a rich nonlinear behaviour including multiplicity of states and sustained periodic oscillations resembling the everlasting struggle between the "new" and the "old". The effect of a control policy that inhibits lobbying is also studied. By appropriate adjustment of the model parameters we approximated the jump/phase transitions in breakthroughs in mathematical and molecular biological sciences resulted by the increased flow of Russian scientists in the USA after the dissolution of the Soviet Union starting in 1989, the launch of the Human Genome Project in 1992 and the Internet diffusion starting in 2000.

@book{noauthor_antifragility_2021,
	title = {Antifragility},
	copyright = {Creative Commons Attribution-ShareAlike License},
	url = {https://en.wikipedia.org/w/index.php?title=Antifragility&oldid=1013667270},
	abstract = {Antifragility is a property of systems in which they increase in capability to thrive as a result of stressors, shocks, volatility, noise, mistakes, faults, attacks, or failures. The concept was developed by Nassim Nicholas Taleb in his book, Antifragile, and in technical papers. As Taleb explains in his book, antifragility is fundamentally different from the concepts of resiliency (i.e. the ability to recover from failure) and robustness (that is, the ability to resist failure). The concept has been applied in risk analysis, physics, molecular biology, transportation planning, engineering, Aerospace (NASA), and computer science.Taleb defines it as follows in a letter to Nature responding to an earlier review of his book in that journal: Simply, antifragility is defined as a convex response to a stressor or source of harm (for some range of variation), leading to a positive sensitivity to increase in volatility (or variability, stress, dispersion of outcomes, or uncertainty, what is grouped under the designation "disorder cluster"). Likewise fragility is defined as a concave sensitivity to stressors, leading to a negative sensitivity to increase in volatility. The relation between fragility, convexity, and sensitivity to disorder is mathematical, obtained by theorem, not derived from empirical data mining or some historical narrative. It is a priori.},
	language = {en},
	urldate = {2021-04-09},
	month = mar,
	year = {2021},
	note = {Publication Title: Wikipedia},
}

Antifragility is a property of systems in which they increase in capability to thrive as a result of stressors, shocks, volatility, noise, mistakes, faults, attacks, or failures. The concept was developed by Nassim Nicholas Taleb in his book, Antifragile, and in technical papers. As Taleb explains in his book, antifragility is fundamentally different from the concepts of resiliency (i.e. the ability to recover from failure) and robustness (that is, the ability to resist failure). The concept has been applied in risk analysis, physics, molecular biology, transportation planning, engineering, Aerospace (NASA), and computer science.Taleb defines it as follows in a letter to Nature responding to an earlier review of his book in that journal: Simply, antifragility is defined as a convex response to a stressor or source of harm (for some range of variation), leading to a positive sensitivity to increase in volatility (or variability, stress, dispersion of outcomes, or uncertainty, what is grouped under the designation "disorder cluster"). Likewise fragility is defined as a concave sensitivity to stressors, leading to a negative sensitivity to increase in volatility. The relation between fragility, convexity, and sensitivity to disorder is mathematical, obtained by theorem, not derived from empirical data mining or some historical narrative. It is a priori.

@misc{noauthor_antifragility_2021,
	title = {Antifragility},
	copyright = {Creative Commons Attribution-ShareAlike License},
	url = {https://en.wikipedia.org/w/index.php?title=Antifragility&oldid=1013667270},
	abstract = {Antifragility is a property of systems in which they increase in capability to thrive as a result of stressors, shocks, volatility, noise, mistakes, faults, attacks, or failures. The concept was developed by Nassim Nicholas Taleb in his  book, Antifragile, and in technical papers. As Taleb explains in his book, antifragility is fundamentally different from the concepts of resiliency (i.e. the ability to recover from failure) and robustness (that is, the ability to resist failure). The concept has been applied in risk analysis, physics, molecular biology, transportation planning, engineering, Aerospace (NASA), and computer science.Taleb defines it as follows in a letter to Nature responding to an earlier review of his book in that journal:

Simply, antifragility is defined as a convex response to a stressor or source of harm (for some range of variation), leading to a positive sensitivity to increase in volatility (or variability, stress, dispersion of outcomes, or uncertainty, what is grouped under the designation "disorder cluster"). Likewise fragility is defined as a concave sensitivity to stressors, leading to a negative sensitivity to increase in volatility. The relation between fragility, convexity, and sensitivity to disorder is mathematical, obtained by theorem, not derived from empirical data mining or some historical narrative. It is a priori.},
	language = {en},
	urldate = {2021-04-09},
	journal = {Wikipedia},
	month = mar,
	year = {2021},
	note = {Page Version ID: 1013667270},
}

Antifragility is a property of systems in which they increase in capability to thrive as a result of stressors, shocks, volatility, noise, mistakes, faults, attacks, or failures. The concept was developed by Nassim Nicholas Taleb in his book, Antifragile, and in technical papers. As Taleb explains in his book, antifragility is fundamentally different from the concepts of resiliency (i.e. the ability to recover from failure) and robustness (that is, the ability to resist failure). The concept has been applied in risk analysis, physics, molecular biology, transportation planning, engineering, Aerospace (NASA), and computer science.Taleb defines it as follows in a letter to Nature responding to an earlier review of his book in that journal: Simply, antifragility is defined as a convex response to a stressor or source of harm (for some range of variation), leading to a positive sensitivity to increase in volatility (or variability, stress, dispersion of outcomes, or uncertainty, what is grouped under the designation "disorder cluster"). Likewise fragility is defined as a concave sensitivity to stressors, leading to a negative sensitivity to increase in volatility. The relation between fragility, convexity, and sensitivity to disorder is mathematical, obtained by theorem, not derived from empirical data mining or some historical narrative. It is a priori.

@article{cuthbert_evolving_2021,
	title = {Evolving {Concepts} of the {Schizophrenia} {Spectrum}: {A} {Research} {Domain} {Criteria} {Perspective}},
	volume = {12},
	issn = {1664-0640},
	shorttitle = {Evolving {Concepts} of the {Schizophrenia} {Spectrum}},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7947312/},
	doi = {10.3389/fpsyt.2021.641319},
	abstract = {Several trends intersecting over the past two decades have generated increasing debate as to how the concepts of schizophrenia, the schizophrenia spectrum, and the psychotic disorders spectrum should be regarded. These trends are reflected in various areas of research such as genomics, neuroimaging, and data-driven computational studies of multiple response systems. Growing evidence suggests that schizophrenia represents a broad and heterogenous syndrome, rather than a specific disease entity, that is part of a multi-faceted psychosis spectrum. Progress in explicating these various developments has been hampered by the dependence upon sets of symptoms and signs for determining a diagnosis, and by the reliance on traditional diagnostic categories in reviewing clinical research grants. To address these concerns, the U.S. National Institute of Mental Health initiated the Research Domain Criteria (RDoC) project, a translational research program that calls for studies designed in terms of empirically-based functions (such as cognitive control or reward learning) rather than diagnostic groups. RDoC is a research framework rather than an alternative diagnostic system, intended to provide data that can inform future nosological manuals. This commentary includes a brief summary of RDoC as it pertains to schizophrenia and psychotic spectra, examples of recent data that highlight the utility of the approach, and conclusions regarding the implications for evolving conceptualizations of serious mental illness.},
	urldate = {2021-04-09},
	journal = {Frontiers in Psychiatry},
	author = {Cuthbert, Bruce N. and Morris, Sarah E.},
	month = feb,
	year = {2021},
	pmid = {33716834},
	pmcid = {PMC7947312},
	note = {ZSCC: 0000000 },
}

Several trends intersecting over the past two decades have generated increasing debate as to how the concepts of schizophrenia, the schizophrenia spectrum, and the psychotic disorders spectrum should be regarded. These trends are reflected in various areas of research such as genomics, neuroimaging, and data-driven computational studies of multiple response systems. Growing evidence suggests that schizophrenia represents a broad and heterogenous syndrome, rather than a specific disease entity, that is part of a multi-faceted psychosis spectrum. Progress in explicating these various developments has been hampered by the dependence upon sets of symptoms and signs for determining a diagnosis, and by the reliance on traditional diagnostic categories in reviewing clinical research grants. To address these concerns, the U.S. National Institute of Mental Health initiated the Research Domain Criteria (RDoC) project, a translational research program that calls for studies designed in terms of empirically-based functions (such as cognitive control or reward learning) rather than diagnostic groups. RDoC is a research framework rather than an alternative diagnostic system, intended to provide data that can inform future nosological manuals. This commentary includes a brief summary of RDoC as it pertains to schizophrenia and psychotic spectra, examples of recent data that highlight the utility of the approach, and conclusions regarding the implications for evolving conceptualizations of serious mental illness.

@book{psyd_health_2021,
	title = {Health and {Wellness} in {People} {Living} {With} {Serious} {Mental} {Illness}},
	isbn = {978-1-61537-379-6},
	abstract = {People with serious mental illness get sick and die 10--20 years earlier than their same age cohort. The social determinants are many: stigma associated with mental illness, poverty, ethnicity-based discrimination, higher rates of smoking and alcohol and drug use, and poor diet and exercise patterns, to name a few. Although multiple interventions have emerged as ways to combat these health challenges, additional research is necessary for the continued development and evaluation of strategies. This context serves as the springboard for Health and Wellness in People Living With Serious Mental Illness. Through multiple case vignettes, the book delves into the challenges of health and wellness for people with mental illness -- including those listed above -- summarizing the research on mortality and morbidity in this group as well as information about the status quo on wellness. It also provides a thorough description of community-based participatory research (CBPR), an approach that includes people in a community as partners in all facets of research, rather than just the subjects of that research. CBPR acts as the lens through which this guide considers solutions to these health problems, including integrated services and patient-centered medical homes; medical practices that diminish the iatrogenic effects of psychiatry; psychoeducation; interpersonal supports; and shared decision-making. Co-edited by Patrick Corrigan, with a 30-year history in services research, and Sonya Ballentine, a community-based member of a CBPR team, this volume offers a grounded, real-world illustration of CBPR in practice. Students of psychiatry, practicing clinicians, primary care providers, allied health professionals, policy makers -- all will find, in the pages of this book, a nuanced portrait of the health challenges patients with mental illness face, possible treatment options, and future directions for the field.},
	language = {en},
	publisher = {American Psychiatric Pub},
	author = {Psy.D, Patrick W. Corrigan and Ballentine, Sonya L.},
	month = mar,
	year = {2021},
	note = {ZSCC: NoCitationData[s0] 
Google-Books-ID: 7IIiEAAAQBAJ},
	keywords = {Medical / Psychiatry / General},
}

People with serious mental illness get sick and die 10–20 years earlier than their same age cohort. The social determinants are many: stigma associated with mental illness, poverty, ethnicity-based discrimination, higher rates of smoking and alcohol and drug use, and poor diet and exercise patterns, to name a few. Although multiple interventions have emerged as ways to combat these health challenges, additional research is necessary for the continued development and evaluation of strategies. This context serves as the springboard for Health and Wellness in People Living With Serious Mental Illness. Through multiple case vignettes, the book delves into the challenges of health and wellness for people with mental illness – including those listed above – summarizing the research on mortality and morbidity in this group as well as information about the status quo on wellness. It also provides a thorough description of community-based participatory research (CBPR), an approach that includes people in a community as partners in all facets of research, rather than just the subjects of that research. CBPR acts as the lens through which this guide considers solutions to these health problems, including integrated services and patient-centered medical homes; medical practices that diminish the iatrogenic effects of psychiatry; psychoeducation; interpersonal supports; and shared decision-making. Co-edited by Patrick Corrigan, with a 30-year history in services research, and Sonya Ballentine, a community-based member of a CBPR team, this volume offers a grounded, real-world illustration of CBPR in practice. Students of psychiatry, practicing clinicians, primary care providers, allied health professionals, policy makers – all will find, in the pages of this book, a nuanced portrait of the health challenges patients with mental illness face, possible treatment options, and future directions for the field.

@techreport{singh_exome_2020,
	title = {Exome sequencing identifies rare coding variants in 10 genes which confer substantial risk for schizophrenia},
	copyright = {© 2020, Posted by Cold Spring Harbor Laboratory. This pre-print is available under a Creative Commons License (Attribution 4.0 International), CC BY 4.0, as described at http://creativecommons.org/licenses/by/4.0/},
	url = {https://www.medrxiv.org/content/10.1101/2020.09.18.20192815v1},
	abstract = {By meta-analyzing the whole-exomes of 24,248 cases and 97,322 controls, we implicate ultra-rare coding variants (URVs) in ten genes as conferring substantial risk for schizophrenia (odds ratios 3 - 50, P {\textless} 2.14 × 10-6), and 32 genes at a FDR {\textless} 5\%. These genes have the greatest expression in central nervous system neurons and have diverse molecular functions that include the formation, structure, and function of the synapse. The associations of NMDA receptor subunit GRIN2A and AMPA receptor subunit GRIA3 provide support for the dysfunction of the glutamatergic system as a mechanistic hypothesis in the pathogenesis of schizophrenia. We find significant evidence for an overlap of rare variant risk between schizophrenia, autism spectrum disorders (ASD), and severe neurodevelopmental disorders (DD/ID), supporting a neurodevelopmental etiology for schizophrenia. We show that protein-truncating variants in GRIN2A, TRIO, and CACNA1G confer risk for schizophrenia whereas specific missense mutations in these genes confer risk for DD/ID. Nevertheless, few of the strongly associated schizophrenia genes appear to confer risk for DD/ID. We demonstrate that genes prioritized from common variant analyses of schizophrenia are enriched in rare variant risk, suggesting that common and rare genetic risk factors at least partially converge on the same underlying pathogenic biological processes. Even after excluding significantly associated genes, schizophrenia cases still carry a substantial excess of URVs, implying that more schizophrenia risk genes await discovery using this approach.},
	language = {en},
	urldate = {2022-05-05},
	institution = {medRxiv},
	author = {Singh, Tarjinder and Neale, Benjamin M. and Daly, Mark J. and Consortium, on behalf of the Schizophrenia Exome Meta-Analysis (SCHEMA)},
	month = sep,
	year = {2020},
	doi = {10.1101/2020.09.18.20192815},
	note = {Type: article},
	pages = {2020.09.18.20192815},
}

By meta-analyzing the whole-exomes of 24,248 cases and 97,322 controls, we implicate ultra-rare coding variants (URVs) in ten genes as conferring substantial risk for schizophrenia (odds ratios 3 - 50, P \textless 2.14 × 10-6), and 32 genes at a FDR \textless 5%. These genes have the greatest expression in central nervous system neurons and have diverse molecular functions that include the formation, structure, and function of the synapse. The associations of NMDA receptor subunit GRIN2A and AMPA receptor subunit GRIA3 provide support for the dysfunction of the glutamatergic system as a mechanistic hypothesis in the pathogenesis of schizophrenia. We find significant evidence for an overlap of rare variant risk between schizophrenia, autism spectrum disorders (ASD), and severe neurodevelopmental disorders (DD/ID), supporting a neurodevelopmental etiology for schizophrenia. We show that protein-truncating variants in GRIN2A, TRIO, and CACNA1G confer risk for schizophrenia whereas specific missense mutations in these genes confer risk for DD/ID. Nevertheless, few of the strongly associated schizophrenia genes appear to confer risk for DD/ID. We demonstrate that genes prioritized from common variant analyses of schizophrenia are enriched in rare variant risk, suggesting that common and rare genetic risk factors at least partially converge on the same underlying pathogenic biological processes. Even after excluding significantly associated genes, schizophrenia cases still carry a substantial excess of URVs, implying that more schizophrenia risk genes await discovery using this approach.

@article{rutigliano_molecular_2020,
	title = {Molecular {Variants} in {Human} {Trace} {Amine}-{Associated} {Receptors} and {Their} {Implications} in {Mental} and {Metabolic} {Disorders}},
	volume = {40},
	issn = {1573-6830},
	url = {https://doi.org/10.1007/s10571-019-00743-y},
	doi = {10.1007/s10571-019-00743-y},
	abstract = {We provide a comprehensive review of the available evidence on the pathophysiological implications of genetic variants in the human trace amine-associated receptor (TAAR) superfamily. Genes coding for trace amine-associated receptors (taars) represent a multigene family of G-protein-coupled receptors, clustered to a small genomic region of 108 kb located in chromosome 6q23, which has been consistently identified by linkage analyses as a susceptibility locus for schizophrenia and affective disorders. Most TAARs are expressed in brain areas involved in emotions, reward and cognition. TAARs are activated by endogenous trace amines and thyronamines, and evidence for a modulatory action on other monaminergic systems has been reported. Therefore, linkage analyses were followed by fine mapping association studies in schizophrenia and affective disorders. However, none of these reports has received sufficient universal replication, so their status remains uncertain. Single nucleotide polymorphisms in taars have emerged as susceptibility loci from genome-wide association studies investigating migraine and brain development, but none of the detected variants reached the threshold for genome-wide significance. In the last decade, technological advances enabled single-gene or whole-exome sequencing, thus allowing the detection of rare genetic variants, which may have a greater impact on the risk of complex disorders. Using these approaches, several taars (especially taar1) variants have been detected in patients with mental and metabolic disorders, and in some cases, defective receptor function has been demonstrated in vitro. Finally, with the use of transcriptomic and peptidomic techniques, dysregulations of TAARs (especially TAAR6) have been identified in brain disorders characterized by cognitive impairment.},
	language = {en},
	number = {2},
	urldate = {2022-06-29},
	journal = {Cellular and Molecular Neurobiology},
	author = {Rutigliano, Grazia and Zucchi, Riccardo},
	month = mar,
	year = {2020},
	note = {Number: 2},
	keywords = {Bipolar disorder, Genetics, Schizophrenia, Single nucletide polymorphism, Trace amine-associated receptors},
	pages = {239--255},
}

We provide a comprehensive review of the available evidence on the pathophysiological implications of genetic variants in the human trace amine-associated receptor (TAAR) superfamily. Genes coding for trace amine-associated receptors (taars) represent a multigene family of G-protein-coupled receptors, clustered to a small genomic region of 108 kb located in chromosome 6q23, which has been consistently identified by linkage analyses as a susceptibility locus for schizophrenia and affective disorders. Most TAARs are expressed in brain areas involved in emotions, reward and cognition. TAARs are activated by endogenous trace amines and thyronamines, and evidence for a modulatory action on other monaminergic systems has been reported. Therefore, linkage analyses were followed by fine mapping association studies in schizophrenia and affective disorders. However, none of these reports has received sufficient universal replication, so their status remains uncertain. Single nucleotide polymorphisms in taars have emerged as susceptibility loci from genome-wide association studies investigating migraine and brain development, but none of the detected variants reached the threshold for genome-wide significance. In the last decade, technological advances enabled single-gene or whole-exome sequencing, thus allowing the detection of rare genetic variants, which may have a greater impact on the risk of complex disorders. Using these approaches, several taars (especially taar1) variants have been detected in patients with mental and metabolic disorders, and in some cases, defective receptor function has been demonstrated in vitro. Finally, with the use of transcriptomic and peptidomic techniques, dysregulations of TAARs (especially TAAR6) have been identified in brain disorders characterized by cognitive impairment.

@article{xu_taar_2020,
	title = {{TAAR} {Agonists}},
	volume = {40},
	issn = {1573-6830},
	doi = {10.1007/s10571-019-00774-5},
	abstract = {Trace amine-associated receptors (TAARs) are a family of G protein-coupled receptors (GPCRs) that are evolutionarily conserved in vertebrates. The first discovered TAAR1 is mainly expressed in the brain, and is able to detect low abundant trace amines. TAAR1 is also activated by several synthetic compounds and psychostimulant drugs like amphetamine. Activation of TAAR1 by specific agonists can regulate the classical monoaminergic systems in the brain. Further studies have revealed that other TAAR family members are highly expressed in the olfactory system which are termed olfactory TAARs. In vertebrates, olfactory TAARs can specifically recognize volatile or water-soluble amines. Some of these TAAR agonists are produced by decarboxylation of amino acids. In addition, some TAAR agonists are ethological odors that mediate animal innate behaviors. In this study, we provide a comprehensive review of TAAR agonists, including their structures, biosynthesis pathways, and functions.},
	language = {eng},
	number = {2},
	journal = {Cellular and Molecular Neurobiology},
	author = {Xu, Zhengrong and Li, Qian},
	month = mar,
	year = {2020},
	pmid = {31848873},
	note = {Number: 2},
	keywords = {Agonist, Animals, Biogenic Amines, Central Nervous System Stimulants, G protein-coupled receptor (GPCR), Humans, Olfactory receptor, Receptors, G-Protein-Coupled, Signal Transduction, Trace amine-associated receptor (TAAR), Trace amines, Volatile amines},
	pages = {257--272},
}

Trace amine-associated receptors (TAARs) are a family of G protein-coupled receptors (GPCRs) that are evolutionarily conserved in vertebrates. The first discovered TAAR1 is mainly expressed in the brain, and is able to detect low abundant trace amines. TAAR1 is also activated by several synthetic compounds and psychostimulant drugs like amphetamine. Activation of TAAR1 by specific agonists can regulate the classical monoaminergic systems in the brain. Further studies have revealed that other TAAR family members are highly expressed in the olfactory system which are termed olfactory TAARs. In vertebrates, olfactory TAARs can specifically recognize volatile or water-soluble amines. Some of these TAAR agonists are produced by decarboxylation of amino acids. In addition, some TAAR agonists are ethological odors that mediate animal innate behaviors. In this study, we provide a comprehensive review of TAAR agonists, including their structures, biosynthesis pathways, and functions.

@article{pretorius_trace_2020,
	title = {The trace aminergic system: a gender-sensitive therapeutic target for {IBS}?},
	volume = {27},
	issn = {1423-0127},
	shorttitle = {The trace aminergic system},
	url = {https://doi.org/10.1186/s12929-020-00688-1},
	doi = {10.1186/s12929-020-00688-1},
	abstract = {Due to a lack of specific or sensitive biomarkers, drug discovery advances have been limited for individuals suffering from irritable bowel syndrome (IBS). While current therapies provide symptomatic relief, inflammation itself is relatively neglected, despite the presence of chronic immune activation and innate immune system dysfunction. Moreover, considering the microgenderome concept, gender is a significant aetiological risk factor. We believe that we have pinpointed a “missing link” that connects gender, dysbiosis, diet, and inflammation in the context of IBS, which may be manipulated as therapeutic target. The trace aminergic system is conveniently positioned at the interface of the gut microbiome, dietary nutrients and by-products, and mucosal immunity. Almost all leukocyte populations express trace amine associated receptors and significant amounts of trace amines originate from both food and the gut microbiota. Additionally, although IBS-specific data are sparse, existing data supports an interpretation in favour of a gender dependence in trace aminergic signalling. As such, trace aminergic signalling may be altered by fluctuations of especially female reproductive hormones. Utilizing a multidisciplinary approach, this review discusses potential mechanisms of actions, which include hyperreactivity of the immune system and aberrant serotonin signalling, and links outcomes to the symptomology clinically prevalent in IBS. Taken together, it is feasible that the additional level of regulation by the trace aminergic system in IBS has been overlooked, until now. As such, we suggest that components of the trace aminergic system be considered targets for future therapeutic action, with the specific focus of reducing oxidative stress and inflammation.},
	number = {1},
	urldate = {2022-07-19},
	journal = {Journal of Biomedical Science},
	author = {Pretorius, Lesha and Smith, Carine},
	month = sep,
	year = {2020},
	keywords = {Drug discovery, Gut microbiome, Inflammation, Oxidative stress, Trace amine},
	pages = {95},
}

Due to a lack of specific or sensitive biomarkers, drug discovery advances have been limited for individuals suffering from irritable bowel syndrome (IBS). While current therapies provide symptomatic relief, inflammation itself is relatively neglected, despite the presence of chronic immune activation and innate immune system dysfunction. Moreover, considering the microgenderome concept, gender is a significant aetiological risk factor. We believe that we have pinpointed a “missing link” that connects gender, dysbiosis, diet, and inflammation in the context of IBS, which may be manipulated as therapeutic target. The trace aminergic system is conveniently positioned at the interface of the gut microbiome, dietary nutrients and by-products, and mucosal immunity. Almost all leukocyte populations express trace amine associated receptors and significant amounts of trace amines originate from both food and the gut microbiota. Additionally, although IBS-specific data are sparse, existing data supports an interpretation in favour of a gender dependence in trace aminergic signalling. As such, trace aminergic signalling may be altered by fluctuations of especially female reproductive hormones. Utilizing a multidisciplinary approach, this review discusses potential mechanisms of actions, which include hyperreactivity of the immune system and aberrant serotonin signalling, and links outcomes to the symptomology clinically prevalent in IBS. Taken together, it is feasible that the additional level of regulation by the trace aminergic system in IBS has been overlooked, until now. As such, we suggest that components of the trace aminergic system be considered targets for future therapeutic action, with the specific focus of reducing oxidative stress and inflammation.

@article{xu_taar_2020,
	title = {{TAAR} {Agonists}},
	volume = {40},
	issn = {1573-6830},
	doi = {10.1007/s10571-019-00774-5},
	abstract = {Trace amine-associated receptors (TAARs) are a family of G protein-coupled receptors (GPCRs) that are evolutionarily conserved in vertebrates. The first discovered TAAR1 is mainly expressed in the brain, and is able to detect low abundant trace amines. TAAR1 is also activated by several synthetic compounds and psychostimulant drugs like amphetamine. Activation of TAAR1 by specific agonists can regulate the classical monoaminergic systems in the brain. Further studies have revealed that other TAAR family members are highly expressed in the olfactory system which are termed olfactory TAARs. In vertebrates, olfactory TAARs can specifically recognize volatile or water-soluble amines. Some of these TAAR agonists are produced by decarboxylation of amino acids. In addition, some TAAR agonists are ethological odors that mediate animal innate behaviors. In this study, we provide a comprehensive review of TAAR agonists, including their structures, biosynthesis pathways, and functions.},
	language = {eng},
	number = {2},
	journal = {Cellular and Molecular Neurobiology},
	author = {Xu, Zhengrong and Li, Qian},
	month = mar,
	year = {2020},
	pmid = {31848873},
	keywords = {Agonist, Animals, Biogenic Amines, Central Nervous System Stimulants, G protein-coupled receptor (GPCR), Humans, Olfactory receptor, Receptors, G-Protein-Coupled, Signal Transduction, Trace amine-associated receptor (TAAR), Trace amines, Volatile amines},
	pages = {257--272},
}

Trace amine-associated receptors (TAARs) are a family of G protein-coupled receptors (GPCRs) that are evolutionarily conserved in vertebrates. The first discovered TAAR1 is mainly expressed in the brain, and is able to detect low abundant trace amines. TAAR1 is also activated by several synthetic compounds and psychostimulant drugs like amphetamine. Activation of TAAR1 by specific agonists can regulate the classical monoaminergic systems in the brain. Further studies have revealed that other TAAR family members are highly expressed in the olfactory system which are termed olfactory TAARs. In vertebrates, olfactory TAARs can specifically recognize volatile or water-soluble amines. Some of these TAAR agonists are produced by decarboxylation of amino acids. In addition, some TAAR agonists are ethological odors that mediate animal innate behaviors. In this study, we provide a comprehensive review of TAAR agonists, including their structures, biosynthesis pathways, and functions.

@article{rutigliano_molecular_2020,
	title = {Molecular {Variants} in {Human} {Trace} {Amine}-{Associated} {Receptors} and {Their} {Implications} in {Mental} and {Metabolic} {Disorders}},
	volume = {40},
	issn = {1573-6830},
	url = {https://doi.org/10.1007/s10571-019-00743-y},
	doi = {10.1007/s10571-019-00743-y},
	abstract = {We provide a comprehensive review of the available evidence on the pathophysiological implications of genetic variants in the human trace amine-associated receptor (TAAR) superfamily. Genes coding for trace amine-associated receptors (taars) represent a multigene family of G-protein-coupled receptors, clustered to a small genomic region of 108 kb located in chromosome 6q23, which has been consistently identified by linkage analyses as a susceptibility locus for schizophrenia and affective disorders. Most TAARs are expressed in brain areas involved in emotions, reward and cognition. TAARs are activated by endogenous trace amines and thyronamines, and evidence for a modulatory action on other monaminergic systems has been reported. Therefore, linkage analyses were followed by fine mapping association studies in schizophrenia and affective disorders. However, none of these reports has received sufficient universal replication, so their status remains uncertain. Single nucleotide polymorphisms in taars have emerged as susceptibility loci from genome-wide association studies investigating migraine and brain development, but none of the detected variants reached the threshold for genome-wide significance. In the last decade, technological advances enabled single-gene or whole-exome sequencing, thus allowing the detection of rare genetic variants, which may have a greater impact on the risk of complex disorders. Using these approaches, several taars (especially taar1) variants have been detected in patients with mental and metabolic disorders, and in some cases, defective receptor function has been demonstrated in vitro. Finally, with the use of transcriptomic and peptidomic techniques, dysregulations of TAARs (especially TAAR6) have been identified in brain disorders characterized by cognitive impairment.},
	language = {en},
	number = {2},
	urldate = {2022-06-29},
	journal = {Cellular and Molecular Neurobiology},
	author = {Rutigliano, Grazia and Zucchi, Riccardo},
	month = mar,
	year = {2020},
	keywords = {Bipolar disorder, Genetics, Schizophrenia, Single nucletide polymorphism, Trace amine-associated receptors},
	pages = {239--255},
}

We provide a comprehensive review of the available evidence on the pathophysiological implications of genetic variants in the human trace amine-associated receptor (TAAR) superfamily. Genes coding for trace amine-associated receptors (taars) represent a multigene family of G-protein-coupled receptors, clustered to a small genomic region of 108 kb located in chromosome 6q23, which has been consistently identified by linkage analyses as a susceptibility locus for schizophrenia and affective disorders. Most TAARs are expressed in brain areas involved in emotions, reward and cognition. TAARs are activated by endogenous trace amines and thyronamines, and evidence for a modulatory action on other monaminergic systems has been reported. Therefore, linkage analyses were followed by fine mapping association studies in schizophrenia and affective disorders. However, none of these reports has received sufficient universal replication, so their status remains uncertain. Single nucleotide polymorphisms in taars have emerged as susceptibility loci from genome-wide association studies investigating migraine and brain development, but none of the detected variants reached the threshold for genome-wide significance. In the last decade, technological advances enabled single-gene or whole-exome sequencing, thus allowing the detection of rare genetic variants, which may have a greater impact on the risk of complex disorders. Using these approaches, several taars (especially taar1) variants have been detected in patients with mental and metabolic disorders, and in some cases, defective receptor function has been demonstrated in vitro. Finally, with the use of transcriptomic and peptidomic techniques, dysregulations of TAARs (especially TAAR6) have been identified in brain disorders characterized by cognitive impairment.

@article{montastruc_new_2020,
	title = {A {New} {Drug}–{Drug} {Interaction} {Between} {Hydroxychloroquine} and {Metformin}? {A} {Signal} {Detection} {Study}},
	volume = {43},
	issn = {1179-1942},
	shorttitle = {A {New} {Drug}–{Drug} {Interaction} {Between} {Hydroxychloroquine} and {Metformin}?},
	url = {https://doi.org/10.1007/s40264-020-00955-y},
	doi = {10.1007/s40264-020-00955-y},
	abstract = {Hydroxychloroquine was recently promoted in patients infected with COVID-19 infection. A recent experimental study has suggested an increased toxicity of hydroxychloroquine in association with metformin in mice.},
	language = {en},
	number = {7},
	urldate = {2022-05-10},
	journal = {Drug Safety},
	author = {Montastruc, Jean-Louis and Toutain, Pierre-Louis},
	month = jul,
	year = {2020},
	pages = {657--660},
}

Hydroxychloroquine was recently promoted in patients infected with COVID-19 infection. A recent experimental study has suggested an increased toxicity of hydroxychloroquine in association with metformin in mice.

@techreport{singh_exome_2020,
	title = {Exome sequencing identifies rare coding variants in 10 genes which confer substantial risk for schizophrenia},
	copyright = {© 2020, Posted by Cold Spring Harbor Laboratory. This pre-print is available under a Creative Commons License (Attribution 4.0 International), CC BY 4.0, as described at http://creativecommons.org/licenses/by/4.0/},
	url = {https://www.medrxiv.org/content/10.1101/2020.09.18.20192815v1},
	abstract = {By meta-analyzing the whole-exomes of 24,248 cases and 97,322 controls, we implicate ultra-rare coding variants (URVs) in ten genes as conferring substantial risk for schizophrenia (odds ratios 3 - 50, P {\textless} 2.14 × 10-6), and 32 genes at a FDR {\textless} 5\%. These genes have the greatest expression in central nervous system neurons and have diverse molecular functions that include the formation, structure, and function of the synapse. The associations of NMDA receptor subunit GRIN2A and AMPA receptor subunit GRIA3 provide support for the dysfunction of the glutamatergic system as a mechanistic hypothesis in the pathogenesis of schizophrenia. We find significant evidence for an overlap of rare variant risk between schizophrenia, autism spectrum disorders (ASD), and severe neurodevelopmental disorders (DD/ID), supporting a neurodevelopmental etiology for schizophrenia. We show that protein-truncating variants in GRIN2A, TRIO, and CACNA1G confer risk for schizophrenia whereas specific missense mutations in these genes confer risk for DD/ID. Nevertheless, few of the strongly associated schizophrenia genes appear to confer risk for DD/ID. We demonstrate that genes prioritized from common variant analyses of schizophrenia are enriched in rare variant risk, suggesting that common and rare genetic risk factors at least partially converge on the same underlying pathogenic biological processes. Even after excluding significantly associated genes, schizophrenia cases still carry a substantial excess of URVs, implying that more schizophrenia risk genes await discovery using this approach.},
	language = {en},
	urldate = {2022-05-05},
	institution = {medRxiv},
	author = {Singh, Tarjinder and Neale, Benjamin M. and Daly, Mark J. and Consortium, on behalf of the Schizophrenia Exome Meta-Analysis (SCHEMA)},
	month = sep,
	year = {2020},
	doi = {10.1101/2020.09.18.20192815},
	note = {Type: article},
	pages = {2020.09.18.20192815},
}

By meta-analyzing the whole-exomes of 24,248 cases and 97,322 controls, we implicate ultra-rare coding variants (URVs) in ten genes as conferring substantial risk for schizophrenia (odds ratios 3 - 50, P \textless 2.14 × 10-6), and 32 genes at a FDR \textless 5%. These genes have the greatest expression in central nervous system neurons and have diverse molecular functions that include the formation, structure, and function of the synapse. The associations of NMDA receptor subunit GRIN2A and AMPA receptor subunit GRIA3 provide support for the dysfunction of the glutamatergic system as a mechanistic hypothesis in the pathogenesis of schizophrenia. We find significant evidence for an overlap of rare variant risk between schizophrenia, autism spectrum disorders (ASD), and severe neurodevelopmental disorders (DD/ID), supporting a neurodevelopmental etiology for schizophrenia. We show that protein-truncating variants in GRIN2A, TRIO, and CACNA1G confer risk for schizophrenia whereas specific missense mutations in these genes confer risk for DD/ID. Nevertheless, few of the strongly associated schizophrenia genes appear to confer risk for DD/ID. We demonstrate that genes prioritized from common variant analyses of schizophrenia are enriched in rare variant risk, suggesting that common and rare genetic risk factors at least partially converge on the same underlying pathogenic biological processes. Even after excluding significantly associated genes, schizophrenia cases still carry a substantial excess of URVs, implying that more schizophrenia risk genes await discovery using this approach.

@article{apryatin_neurodegenerative_2020,
	title = {Neurodegenerative and metabolic disorders, mediated by the trace amines and their receptors},
	volume = {20},
	issn = {2687-1378},
	url = {https://doi.org/10.17816/MAJ25746},
	doi = {10.17816/MAJ25746},
	abstract = {The aim of the study is the modern scientific literature estimation in the field of the investigation of neurodegenerative and metabolic disorders mediated by the trace amines and their receptors. The analysis of modern ideas about the “feedback” of neurodegenerative and metabolic diseases in which the trace amines and their receptors are involved was carried out. The important role of trace amines and their receptors in the regulation of the dopamine system, in connection with metabolic and neurodegenerative diseases, including Parkinson's disease, ADHD, schizophrenia, obesity, metabolic syndrome and other pathological conditions, has been shown. Trace amines and their receptors have a direct effect on dopamine systems, being regulators of various metabolic and neurodegenerative processes, participating in energy metabolism, neurogenesis,and other vital processes.},
	language = {ru},
	number = {1},
	urldate = {2021-12-23},
	journal = {Medical academic journal},
	author = {Apryatin, Sergey A. and Алексеевич, Апрятин Сергей and Karpenko, Marina N. and Николаевна, Карпенко Марина and Muruzheva, Zamira M. and Магомедовна, Муружева Замира and Bolshakova, Maria V. and Валерьевна, Большакова Мария and Magazenkova, Daria N. and Николаевна, Магазенкова Дарья and Klimenko, Victor M. and Матвеевич, Клименко Виктор},
	month = jun,
	year = {2020},
	keywords = {neurodegenerative and metabolic diseases, trace amines, trace amines receptors, нейродегенеративные и метаболические заболевания, рецепторы следовых аминов, следовые амины},
	pages = {9--22},
}

The aim of the study is the modern scientific literature estimation in the field of the investigation of neurodegenerative and metabolic disorders mediated by the trace amines and their receptors. The analysis of modern ideas about the “feedback” of neurodegenerative and metabolic diseases in which the trace amines and their receptors are involved was carried out. The important role of trace amines and their receptors in the regulation of the dopamine system, in connection with metabolic and neurodegenerative diseases, including Parkinson's disease, ADHD, schizophrenia, obesity, metabolic syndrome and other pathological conditions, has been shown. Trace amines and their receptors have a direct effect on dopamine systems, being regulators of various metabolic and neurodegenerative processes, participating in energy metabolism, neurogenesis,and other vital processes.

@article{rutigliano_molecular_2020,
	title = {Molecular {Variants} in {Human} {Trace} {Amine}-{Associated} {Receptors} and {Their} {Implications} in {Mental} and {Metabolic} {Disorders}},
	volume = {40},
	issn = {0272-4340, 1573-6830},
	url = {http://link.springer.com/10.1007/s10571-019-00743-y},
	doi = {10.1007/s10571-019-00743-y},
	abstract = {We provide a comprehensive review of the available evidence on the pathophysiological implications of genetic variants in the human trace amine-associated receptor (TAAR) superfamily. Genes coding for trace amine-associated receptors (taars) represent a multigene family of G-protein-coupled receptors, clustered to a small genomic region of 108 kb located in chromosome 6q23, which has been consistently identified by linkage analyses as a susceptibility locus for schizophrenia and affective disorders. Most TAARs are expressed in brain areas involved in emotions, reward and cognition. TAARs are activated by endogenous trace amines and thyronamines, and evidence for a modulatory action on other monaminergic systems has been reported. Therefore, linkage analyses were followed by fine mapping association studies in schizophrenia and affective disorders. However, none of these reports has received sufficient universal replication, so their status remains uncertain. Single nucleotide polymorphisms in taars have emerged as susceptibility loci from genome-wide association studies investigating migraine and brain development, but none of the detected variants reached the threshold for genome-wide significance. In the last decade, technological advances enabled single-gene or whole-exome sequencing, thus allowing the detection of rare genetic variants, which may have a greater impact on the risk of complex disorders. Using these approaches, several taars (especially taar1) variants have been detected in patients with mental and metabolic disorders, and in some cases, defective receptor function has been demonstrated in vitro. Finally, with the use of transcriptomic and peptidomic techniques, dysregulations of TAARs (especially TAAR6) have been identified in brain disorders characterized by cognitive impairment.},
	language = {en},
	number = {2},
	urldate = {2021-11-28},
	journal = {Cellular and Molecular Neurobiology},
	author = {Rutigliano, Grazia and Zucchi, Riccardo},
	month = mar,
	year = {2020},
	pages = {239--255},
}

We provide a comprehensive review of the available evidence on the pathophysiological implications of genetic variants in the human trace amine-associated receptor (TAAR) superfamily. Genes coding for trace amine-associated receptors (taars) represent a multigene family of G-protein-coupled receptors, clustered to a small genomic region of 108 kb located in chromosome 6q23, which has been consistently identified by linkage analyses as a susceptibility locus for schizophrenia and affective disorders. Most TAARs are expressed in brain areas involved in emotions, reward and cognition. TAARs are activated by endogenous trace amines and thyronamines, and evidence for a modulatory action on other monaminergic systems has been reported. Therefore, linkage analyses were followed by fine mapping association studies in schizophrenia and affective disorders. However, none of these reports has received sufficient universal replication, so their status remains uncertain. Single nucleotide polymorphisms in taars have emerged as susceptibility loci from genome-wide association studies investigating migraine and brain development, but none of the detected variants reached the threshold for genome-wide significance. In the last decade, technological advances enabled single-gene or whole-exome sequencing, thus allowing the detection of rare genetic variants, which may have a greater impact on the risk of complex disorders. Using these approaches, several taars (especially taar1) variants have been detected in patients with mental and metabolic disorders, and in some cases, defective receptor function has been demonstrated in vitro. Finally, with the use of transcriptomic and peptidomic techniques, dysregulations of TAARs (especially TAAR6) have been identified in brain disorders characterized by cognitive impairment.

@article{feinberg_phenomenal_2020,
	title = {Phenomenal {Consciousness} and {Emergence}: {Eliminating} the {Explanatory} {Gap}},
	volume = {11},
	shorttitle = {Phenomenal {Consciousness} and {Emergence}},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7304239/},
	doi = {10.3389/fpsyg.2020.01041},
	abstract = {The role of emergence in the creation of consciousness has been debated for over a century, but it remains unresolved. In particular there is controversy over the claim that a “strong” or radical form of emergence is required to explain ...},
	language = {en},
	urldate = {2021-08-10},
	journal = {Frontiers in Psychology},
	author = {Feinberg, Todd E. and Mallatt, Jon},
	year = {2020},
	pmid = {32595555},
	note = {Publisher: Frontiers Media SA},
}

The role of emergence in the creation of consciousness has been debated for over a century, but it remains unresolved. In particular there is controversy over the claim that a “strong” or radical form of emergence is required to explain ...

@article{fisk_elevating_2020,
	title = {Elevating the human experience ({HX}) through service research collaborations: introducing {ServCollab}},
	volume = {31},
	issn = {1757-5818},
	shorttitle = {Elevating the human experience ({HX}) through service research collaborations},
	url = {https://www.emerald.com/insight/content/doi/10.1108/JOSM-10-2019-0325/full/html},
	doi = {10.1108/JOSM-10-2019-0325},
	abstract = {Purpose
              Elevating the human experience (HX) through research collaborations is the purpose of this article. ServCollab facilitates and supports service research collaborations that seek to reduce human suffering and improve human well-being.
            
            
              Design/methodology/approach
              To catalyze this initiative, the authors introduce ServCollab's three human rights goals (serve, enable and transform), standards of justice for serving humanity (distributive, procedural and interactional justice) and research approaches for serving humanity (service design and community action research).
            
            
              Research implications
              ServCollab seeks to advance the service research field via large-scale service research projects that pursue theory building, research and action. Service inclusion is the first focus of ServCollab and is illustrated through two projects (transformative refugee services and virtual assistants in social care). This paper seeks to encourage collaboration in more large-scale service research projects that elevate the HX.
            
            
              Practical implications
              ServCollab seeks to raise the aspirations of service researchers, expand the skills of service research teams and build mutually collaborative service research approaches that transform human lives.
            
            
              Originality/value
              ServCollab is a unique organization within the burgeoning service research community. By collaborating with service researchers, with service research centers, with universities, with nonprofit agencies and with foundations, ServCollab will build research capacity to address large-scale human service system problems. ServCollab takes a broad perspective for serving humanity by focusing on the HX. Current business research focuses on the interactive roles of customer experience and employee experience. From the perspective of HX, such role labels are insufficient concepts for the full spectrum of human life.},
	language = {en},
	number = {4},
	urldate = {2021-06-21},
	journal = {Journal of Service Management},
	author = {Fisk, Raymond P. and Alkire (née Nasr), Linda and Anderson, Laurel and Bowen, David E. and Gruber, Thorsten and Ostrom, Amy L. and Patrício, Lia},
	month = may,
	year = {2020},
	note = {ZSCC: NoCitationData[s0]},
	pages = {615--635},
}

Purpose Elevating the human experience (HX) through research collaborations is the purpose of this article. ServCollab facilitates and supports service research collaborations that seek to reduce human suffering and improve human well-being. Design/methodology/approach To catalyze this initiative, the authors introduce ServCollab's three human rights goals (serve, enable and transform), standards of justice for serving humanity (distributive, procedural and interactional justice) and research approaches for serving humanity (service design and community action research). Research implications ServCollab seeks to advance the service research field via large-scale service research projects that pursue theory building, research and action. Service inclusion is the first focus of ServCollab and is illustrated through two projects (transformative refugee services and virtual assistants in social care). This paper seeks to encourage collaboration in more large-scale service research projects that elevate the HX. Practical implications ServCollab seeks to raise the aspirations of service researchers, expand the skills of service research teams and build mutually collaborative service research approaches that transform human lives. Originality/value ServCollab is a unique organization within the burgeoning service research community. By collaborating with service researchers, with service research centers, with universities, with nonprofit agencies and with foundations, ServCollab will build research capacity to address large-scale human service system problems. ServCollab takes a broad perspective for serving humanity by focusing on the HX. Current business research focuses on the interactive roles of customer experience and employee experience. From the perspective of HX, such role labels are insufficient concepts for the full spectrum of human life.

@article{tost_targeting_2020,
	title = {Targeting {Hormones} for {Improving} {Cognition} in {Major} {Mood} {Disorders} and {Schizophrenia}: {Thyroid} {Hormones} and {Prolactin}},
	volume = {40},
	issn = {1179-1918},
	shorttitle = {Targeting {Hormones} for {Improving} {Cognition} in {Major} {Mood} {Disorders} and {Schizophrenia}},
	doi = {10.1007/s40261-019-00854-w},
	abstract = {Cognitive deficits are a core feature of serious mental illnesses such as major depression, bipolar disorder and schizophrenia and are a common cause of functional disability. However, the efficacy of pharmacological interventions for improving the cognitive deficits in these disorders is limited. As pro-cognitive pharmacological treatments are lacking, we aimed to review whether thyroid hormones or drugs that target prolactin may become potential candidates for 'repurposing' trials aiming to improve cognition. We conducted a narrative review focused on thyroid hormones and prolactin as potential targets for improving cognition in major mood disorders or schizophrenia. The role of thyroid hormones and prolactin on cognitive processes in non-psychiatric populations was also reviewed. Although clinical trials regarding these hormones are lacking, particularly in patients with schizophrenia, bipolar disorder or major depression, there is evidence from observational studies for the contribution of these hormones to cognitive processes. Patients with bipolar disorder and subclinical hypothyroidism show poorer cognitive function than euthyroid patients. In patients with early psychosis, lower free thyroxine concentrations have been associated with poorer attention whereas increased prolactin levels have been associated with poorer speed of processing. Only two small clinical trials tested the potential pro-cognitive effects of thyroid hormones, with positive findings for triiodothyronine (T3) treatment in patients receiving lithium or electroconvulsive therapy. In sum, thyroid hormones and prolactin might contribute to the cognitive performance of patients with major mood disorders and psychotic disorders. Thyroid hormones and prolactin-lowering drugs (e.g. cabergoline, aripiprazole) are candidate drugs to be tested in repurposing clinical trials aiming to improve the cognitive abilities of patients with major mood disorder and schizophrenia.},
	language = {eng},
	number = {1},
	journal = {Clinical Drug Investigation},
	author = {Tost, Meritxell and Monreal, José Antonio and Armario, Antonio and Barbero, Juan David and Cobo, Jesús and García-Rizo, Clemente and Bioque, Miquel and Usall, Judith and Huerta-Ramos, Elena and Soria, Virginia and {PNECAT Group} and Labad, Javier},
	month = jan,
	year = {2020},
	pmid = {31612424},
	note = {ZSCC: NoCitationData[s0] },
	keywords = {Bipolar Disorder, Cognition Disorders, Depressive Disorder, Major, Humans, Hypothyroidism, Mood Disorders, Prolactin, Psychotic Disorders, Schizophrenia, Thyroid Hormones, Triiodothyronine},
	pages = {1--14},
}

Cognitive deficits are a core feature of serious mental illnesses such as major depression, bipolar disorder and schizophrenia and are a common cause of functional disability. However, the efficacy of pharmacological interventions for improving the cognitive deficits in these disorders is limited. As pro-cognitive pharmacological treatments are lacking, we aimed to review whether thyroid hormones or drugs that target prolactin may become potential candidates for 'repurposing' trials aiming to improve cognition. We conducted a narrative review focused on thyroid hormones and prolactin as potential targets for improving cognition in major mood disorders or schizophrenia. The role of thyroid hormones and prolactin on cognitive processes in non-psychiatric populations was also reviewed. Although clinical trials regarding these hormones are lacking, particularly in patients with schizophrenia, bipolar disorder or major depression, there is evidence from observational studies for the contribution of these hormones to cognitive processes. Patients with bipolar disorder and subclinical hypothyroidism show poorer cognitive function than euthyroid patients. In patients with early psychosis, lower free thyroxine concentrations have been associated with poorer attention whereas increased prolactin levels have been associated with poorer speed of processing. Only two small clinical trials tested the potential pro-cognitive effects of thyroid hormones, with positive findings for triiodothyronine (T3) treatment in patients receiving lithium or electroconvulsive therapy. In sum, thyroid hormones and prolactin might contribute to the cognitive performance of patients with major mood disorders and psychotic disorders. Thyroid hormones and prolactin-lowering drugs (e.g. cabergoline, aripiprazole) are candidate drugs to be tested in repurposing clinical trials aiming to improve the cognitive abilities of patients with major mood disorder and schizophrenia.

@article{zhou_combining_2020,
	title = {Combining phenome-driven drug-target interaction prediction with patients' electronic health records-based clinical corroboration toward drug discovery},
	volume = {36},
	issn = {1367-4811},
	doi = {10.1093/bioinformatics/btaa451},
	abstract = {MOTIVATION: Predicting drug-target interactions (DTIs) using human phenotypic data have the potential in eliminating the translational gap between animal experiments and clinical outcomes in humans. One challenge in human phenome-driven DTI predictions is integrating and modeling diverse drug and disease phenotypic relationships. Leveraging large amounts of clinical observed phenotypes of drugs and diseases and electronic health records (EHRs) of 72 million patients, we developed a novel integrated computational drug discovery approach by seamlessly combining DTI prediction and clinical corroboration.
RESULTS: We developed a network-based DTI prediction system (TargetPredict) by modeling 855 904 phenotypic and genetic relationships among 1430 drugs, 4251 side effects, 1059 diseases and 17 860 genes. We systematically evaluated TargetPredict in de novo cross-validation and compared it to a state-of-the-art phenome-driven DTI prediction approach. We applied TargetPredict in identifying novel repositioned candidate drugs for Alzheimer's disease (AD), a disease affecting over 5.8 million people in the United States. We evaluated the clinical efficiency of top repositioned drug candidates using EHRs of over 72 million patients. The area under the receiver operating characteristic (ROC) curve was 0.97 in the de novo cross-validation when evaluated using 910 drugs. TargetPredict outperformed a state-of-the-art phenome-driven DTI prediction system as measured by precision-recall curves [measured by average precision (MAP): 0.28 versus 0.23, P-value {\textless} 0.0001]. The EHR-based case-control studies identified that the prescriptions top-ranked repositioned drugs are significantly associated with lower odds of AD diagnosis. For example, we showed that the prescription of liraglutide, a type 2 diabetes drug, is significantly associated with decreased risk of AD diagnosis [adjusted odds ratios (AORs): 0.76; 95\% confidence intervals (CI) (0.70, 0.82), P-value {\textless} 0.0001]. In summary, our integrated approach that seamlessly combines computational DTI prediction and large-scale patients' EHRs-based clinical corroboration has high potential in rapidly identifying novel drug targets and drug candidates for complex diseases.
AVAILABILITY AND IMPLEMENTATION: nlp.case.edu/public/data/TargetPredict.},
	language = {eng},
	number = {Suppl\_1},
	journal = {Bioinformatics (Oxford, England)},
	author = {Zhou, Mengshi and Zheng, Chunlei and Xu, Rong},
	month = jul,
	year = {2020},
	pmid = {32657406},
	pmcid = {PMC7355254},
	note = {ZSCC: 0000006 },
	keywords = {Diabetes Mellitus, Type 2, Drug Development, Drug Discovery, Electronic Health Records, Humans, Pharmaceutical Preparations},
	pages = {i436--i444},
}

MOTIVATION: Predicting drug-target interactions (DTIs) using human phenotypic data have the potential in eliminating the translational gap between animal experiments and clinical outcomes in humans. One challenge in human phenome-driven DTI predictions is integrating and modeling diverse drug and disease phenotypic relationships. Leveraging large amounts of clinical observed phenotypes of drugs and diseases and electronic health records (EHRs) of 72 million patients, we developed a novel integrated computational drug discovery approach by seamlessly combining DTI prediction and clinical corroboration. RESULTS: We developed a network-based DTI prediction system (TargetPredict) by modeling 855 904 phenotypic and genetic relationships among 1430 drugs, 4251 side effects, 1059 diseases and 17 860 genes. We systematically evaluated TargetPredict in de novo cross-validation and compared it to a state-of-the-art phenome-driven DTI prediction approach. We applied TargetPredict in identifying novel repositioned candidate drugs for Alzheimer's disease (AD), a disease affecting over 5.8 million people in the United States. We evaluated the clinical efficiency of top repositioned drug candidates using EHRs of over 72 million patients. The area under the receiver operating characteristic (ROC) curve was 0.97 in the de novo cross-validation when evaluated using 910 drugs. TargetPredict outperformed a state-of-the-art phenome-driven DTI prediction system as measured by precision-recall curves [measured by average precision (MAP): 0.28 versus 0.23, P-value \textless 0.0001]. The EHR-based case-control studies identified that the prescriptions top-ranked repositioned drugs are significantly associated with lower odds of AD diagnosis. For example, we showed that the prescription of liraglutide, a type 2 diabetes drug, is significantly associated with decreased risk of AD diagnosis [adjusted odds ratios (AORs): 0.76; 95% confidence intervals (CI) (0.70, 0.82), P-value \textless 0.0001]. In summary, our integrated approach that seamlessly combines computational DTI prediction and large-scale patients' EHRs-based clinical corroboration has high potential in rapidly identifying novel drug targets and drug candidates for complex diseases. AVAILABILITY AND IMPLEMENTATION: nlp.case.edu/public/data/TargetPredict.

@article{geerts_quantitative_2020,
	title = {Quantitative {Systems} {Pharmacology} for {Neuroscience} {Drug} {Discovery} and {Development}: {Current} {Status}, {Opportunities}, and {Challenges}},
	volume = {9},
	copyright = {© 2019 The Authors. CPT: Pharmacometrics \& Systems Pharmacology published by Wiley Periodicals, Inc. on behalf of the American Society for Clinical Pharmacology and Therapeutics},
	issn = {2163-8306},
	shorttitle = {Quantitative {Systems} {Pharmacology} for {Neuroscience} {Drug} {Discovery} and {Development}},
	url = {https://ascpt.onlinelibrary.wiley.com/doi/abs/10.1002/psp4.12478},
	doi = {https://doi.org/10.1002/psp4.12478},
	abstract = {The substantial progress made in the basic sciences of the brain has yet to be adequately translated to successful clinical therapeutics to treat central nervous system (CNS) diseases. Possible explanations include the lack of quantitative and validated biomarkers, the subjective nature of many clinical endpoints, and complex pharmacokinetic/pharmacodynamic relationships, but also the possibility that highly selective drugs in the CNS do not reflect the complex interactions of different brain circuits. Although computational systems pharmacology modeling designed to capture essential components of complex biological systems has been increasingly accepted in pharmaceutical research and development for oncology, inflammation, and metabolic disorders, the uptake in the CNS field has been very modest. In this article, a cross-disciplinary group with representatives from academia, pharma, regulatory, and funding agencies make the case that the identification and exploitation of CNS therapeutic targets for drug discovery and development can benefit greatly from a system and network approach that can span the gap between molecular pathways and the neuronal circuits that ultimately regulate brain activity and behavior. The National Institute of Neurological Disorders and Stroke (NINDS), in collaboration with the National Institute on Aging (NIA), National Institute of Mental Health (NIMH), National Institute on Drug Abuse (NIDA), and National Center for Advancing Translational Sciences (NCATS), convened a workshop to explore and evaluate the potential of a quantitative systems pharmacology (QSP) approach to CNS drug discovery and development. The objective of the workshop was to identify the challenges and opportunities of QSP as an approach to accelerate drug discovery and development in the field of CNS disorders. In particular, the workshop examined the potential for computational neuroscience to perform QSP-based interrogation of the mechanism of action for CNS diseases, along with a more accurate and comprehensive method for evaluating drug effects and optimizing the design of clinical trials. Following up on an earlier white paper on the use of QSP in general disease mechanism of action and drug discovery, this report focuses on new applications, opportunities, and the accompanying limitations of QSP as an approach to drug development in the CNS therapeutic area based on the discussions in the workshop with various stakeholders.},
	language = {en},
	number = {1},
	urldate = {2021-04-22},
	journal = {CPT: Pharmacometrics \& Systems Pharmacology},
	author = {Geerts, Hugo and Wikswo, John and Graaf, Piet H. van der and Bai, Jane P. F. and Gaiteri, Chris and Bennett, David and Swalley, Susanne E. and Schuck, Edgar and Kaddurah‐Daouk, Rima and Tsaioun, Katya and Pelleymounter, Mary},
	year = {2020},
	note = {ZSCC: NoCitationData[s0] 
\_eprint: https://ascpt.onlinelibrary.wiley.com/doi/pdf/10.1002/psp4.12478},
	pages = {5--20},
}

The substantial progress made in the basic sciences of the brain has yet to be adequately translated to successful clinical therapeutics to treat central nervous system (CNS) diseases. Possible explanations include the lack of quantitative and validated biomarkers, the subjective nature of many clinical endpoints, and complex pharmacokinetic/pharmacodynamic relationships, but also the possibility that highly selective drugs in the CNS do not reflect the complex interactions of different brain circuits. Although computational systems pharmacology modeling designed to capture essential components of complex biological systems has been increasingly accepted in pharmaceutical research and development for oncology, inflammation, and metabolic disorders, the uptake in the CNS field has been very modest. In this article, a cross-disciplinary group with representatives from academia, pharma, regulatory, and funding agencies make the case that the identification and exploitation of CNS therapeutic targets for drug discovery and development can benefit greatly from a system and network approach that can span the gap between molecular pathways and the neuronal circuits that ultimately regulate brain activity and behavior. The National Institute of Neurological Disorders and Stroke (NINDS), in collaboration with the National Institute on Aging (NIA), National Institute of Mental Health (NIMH), National Institute on Drug Abuse (NIDA), and National Center for Advancing Translational Sciences (NCATS), convened a workshop to explore and evaluate the potential of a quantitative systems pharmacology (QSP) approach to CNS drug discovery and development. The objective of the workshop was to identify the challenges and opportunities of QSP as an approach to accelerate drug discovery and development in the field of CNS disorders. In particular, the workshop examined the potential for computational neuroscience to perform QSP-based interrogation of the mechanism of action for CNS diseases, along with a more accurate and comprehensive method for evaluating drug effects and optimizing the design of clinical trials. Following up on an earlier white paper on the use of QSP in general disease mechanism of action and drug discovery, this report focuses on new applications, opportunities, and the accompanying limitations of QSP as an approach to drug development in the CNS therapeutic area based on the discussions in the workshop with various stakeholders.

@article{aftab_conceptual_2020,
	title = {Conceptual {Competence} in {Psychiatry}: {Recommendations} for {Education} and {Training}},
	issn = {1545-7230},
	shorttitle = {Conceptual {Competence} in {Psychiatry}},
	url = {https://doi.org/10.1007/s40596-020-01183-3},
	doi = {10.1007/s40596-020-01183-3},
	language = {en},
	urldate = {2020-03-23},
	journal = {Academic Psychiatry},
	author = {Aftab, Awais and Waterman, G. Scott},
	month = jan,
	year = {2020},
	note = {ZSCC: 0000005},
}

@article{brodrick_free_2020,
	title = {Free to {Choose}: {A} {Moral} {Defense} of the {Right}-to-{Try} {Movement}},
	volume = {45},
	issn = {0360-5310},
	shorttitle = {Free to {Choose}},
	url = {https://academic.oup.com/jmp/article/45/1/61/5700356},
	doi = {10.1093/jmp/jhz028},
	abstract = {Abstract. The claim that individuals legitimately differ with respect to their values seems to be uncontroversial among bioethicists, yet many bioethicists nev},
	language = {en},
	number = {1},
	urldate = {2020-08-12},
	journal = {The Journal of Medicine and Philosophy: A Forum for Bioethics and Philosophy of Medicine},
	author = {Brodrick, Michael},
	month = jan,
	year = {2020},
	note = {ZSCC: 0000005},
	pages = {61--85},
}

Abstract. The claim that individuals legitimately differ with respect to their values seems to be uncontroversial among bioethicists, yet many bioethicists nev

@article{roberts_how_2020,
	title = {How to {Regulate} the {Right} to {Self}-{Medicate}},
	issn = {0956-2737, 1572-8498},
	url = {http://link.springer.com/10.1007/s10730-020-09415-7},
	doi = {10.1007/s10730-020-09415-7},
	abstract = {In Pharmaceutical Freedom Professor Flanigan argues we ought to grant people self-medication rights for the same reasons we respect people’s right to give (or refuse to give) informed consent to treatment. Despite being the most comprehensive argument in favour of self-medication written to date, Flanigan’s Pharmaceutical Freedom leaves a number of questions unanswered, making it unclear how the safe-guards Flanigan incorporates to protect people from harming themselves would work in practice. In this paper, I extend Professor Flanigan’s account by discussing a hypothetical case to illustrate how these safe-guards could work together to protect people from harms caused by their own ignorance or incompetence.},
	language = {en},
	urldate = {2021-04-10},
	journal = {HEC Forum},
	author = {Roberts, Joseph T. F.},
	month = jun,
	year = {2020},
	note = {ZSCC: 0000001},
}

In Pharmaceutical Freedom Professor Flanigan argues we ought to grant people self-medication rights for the same reasons we respect people’s right to give (or refuse to give) informed consent to treatment. Despite being the most comprehensive argument in favour of self-medication written to date, Flanigan’s Pharmaceutical Freedom leaves a number of questions unanswered, making it unclear how the safe-guards Flanigan incorporates to protect people from harming themselves would work in practice. In this paper, I extend Professor Flanigan’s account by discussing a hypothetical case to illustrate how these safe-guards could work together to protect people from harms caused by their own ignorance or incompetence.

@article{roberts_how_2020,
	title = {How to {Regulate} the {Right} to {Self}-{Medicate}},
	issn = {0956-2737, 1572-8498},
	url = {http://link.springer.com/10.1007/s10730-020-09415-7},
	doi = {10.1007/s10730-020-09415-7},
	abstract = {In Pharmaceutical Freedom Professor Flanigan argues we ought to grant people self-medication rights for the same reasons we respect people’s right to give (or refuse to give) informed consent to treatment. Despite being the most comprehensive argument in favour of self-medication written to date, Flanigan’s Pharmaceutical Freedom leaves a number of questions unanswered, making it unclear how the safe-guards Flanigan incorporates to protect people from harming themselves would work in practice. In this paper, I extend Professor Flanigan’s account by discussing a hypothetical case to illustrate how these safe-guards could work together to protect people from harms caused by their own ignorance or incompetence.},
	language = {en},
	urldate = {2021-04-10},
	journal = {HEC Forum},
	author = {Roberts, Joseph T. F.},
	month = jun,
	year = {2020},
	note = {ZSCC: 0000000},
}

In Pharmaceutical Freedom Professor Flanigan argues we ought to grant people self-medication rights for the same reasons we respect people’s right to give (or refuse to give) informed consent to treatment. Despite being the most comprehensive argument in favour of self-medication written to date, Flanigan’s Pharmaceutical Freedom leaves a number of questions unanswered, making it unclear how the safe-guards Flanigan incorporates to protect people from harming themselves would work in practice. In this paper, I extend Professor Flanigan’s account by discussing a hypothetical case to illustrate how these safe-guards could work together to protect people from harms caused by their own ignorance or incompetence.

@article{ingegnoli_link_2020,
	title = {The {Link} {Between} {Autonomic} {Nervous} {System} and {Rheumatoid} {Arthritis}: {From} {Bench} to {Bedside}},
	volume = {7},
	issn = {2296-858X},
	shorttitle = {The {Link} {Between} {Autonomic} {Nervous} {System} and {Rheumatoid} {Arthritis}},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7750536/},
	doi = {10.3389/fmed.2020.589079},
	abstract = {Neuronal stimulation is an emerging field of research focused on the management and treatment of various diseases through the reestablishment of physiological homeostasis. Electrical vagus nerve stimulation has recently been proposed as a revolutionary therapeutic option for rheumatoid arthritis (RA) in combination with or even as a replacement for conventional and biological drugs. In the past few years, disruption of the autonomic system has been linked to RA onset and activity. Novel research on the link between the autonomic nervous system and the immune system (immune-autonomics) has paved the way for the development of innovative RA management strategies. Clinical evidence supports this approach. Cardiovascular involvement, in terms of reduced baroreflex sensitivity and heart rate variability-derived indices, and mood disorders, common comorbidities in patients with RA, have been linked to autonomic nervous system dysfunction, which in turn is influenced by increased levels of circulating pro-inflammatory cytokines. This narrative review provides an overview of the autonomic nervous system and RA connection, discussing most of the common cardiac and mental health-related RA comorbidities and their potential relationships to systemic and joint inflammation.},
	urldate = {2021-04-08},
	journal = {Frontiers in Medicine},
	author = {Ingegnoli, Francesca and Buoli, Massimiliano and Antonucci, Flavia and Coletto, Lavinia Agra and Esposito, Cecilia Maria and Caporali, Roberto},
	month = dec,
	year = {2020},
	pmid = {33365319},
	pmcid = {PMC7750536},
	note = {ZSCC: 0000000 },
}

Neuronal stimulation is an emerging field of research focused on the management and treatment of various diseases through the reestablishment of physiological homeostasis. Electrical vagus nerve stimulation has recently been proposed as a revolutionary therapeutic option for rheumatoid arthritis (RA) in combination with or even as a replacement for conventional and biological drugs. In the past few years, disruption of the autonomic system has been linked to RA onset and activity. Novel research on the link between the autonomic nervous system and the immune system (immune-autonomics) has paved the way for the development of innovative RA management strategies. Clinical evidence supports this approach. Cardiovascular involvement, in terms of reduced baroreflex sensitivity and heart rate variability-derived indices, and mood disorders, common comorbidities in patients with RA, have been linked to autonomic nervous system dysfunction, which in turn is influenced by increased levels of circulating pro-inflammatory cytokines. This narrative review provides an overview of the autonomic nervous system and RA connection, discussing most of the common cardiac and mental health-related RA comorbidities and their potential relationships to systemic and joint inflammation.

@article{shukla_integrative_2020,
	title = {Integrative {Omics} for {Informed} {Drug} {Repurposing}: {Targeting} {CNS} {Disorders}},
	copyright = {© 2020, Posted by Cold Spring Harbor Laboratory. The copyright holder for this pre-print is the author. All rights reserved. The material may not be redistributed, re-used or adapted without the author's permission.},
	shorttitle = {Integrative {Omics} for {Informed} {Drug} {Repurposing}},
	url = {https://www.biorxiv.org/content/10.1101/2020.04.24.060392v1},
	doi = {10.1101/2020.04.24.060392},
	abstract = {{\textless}h3{\textgreater}Abstract{\textless}/h3{\textgreater} {\textless}p{\textgreater}The treatment of CNS disorders, and in particular psychiatric illnesses, lacks disease-altering therapeutics for many conditions. This is likely due to regulatory challenges involving the high cost and slow-pace of drug development for CNS disorders as well as due to limited understanding of disease causality. Repurposing drugs for new indications have lower cost and shorter development timeline compared to that of de novo drug development. Historically, empirical drug-repurposing is a standard practice in psychiatry; however, recent advances in characterizing molecules with their structural and transcriptomic signatures along with ensemble of data analysis approaches, provides informed and cost-effective repurposing strategies that ameliorate the regulatory challenges. In addition, the potential to incorporate ontological approaches along with signature-based repurposing techniques addresses the various knowledge-based challenges associated with CNS drug development. In this review we primarily discuss signature-based \textit{in silico} approaches to drug repurposing, and its integration with data science platforms for evidence-based drug repurposing. We contrast various \textit{in silico} and empirical approaches and discuss possible avenues to improve the clinical relevance. These concepts provide a promising new translational avenue for developing new therapies for difficult to treat disorders, and offer the possibility of connecting drug discovery platforms and big data analytics with personalized disease signatures.{\textless}/p{\textgreater}},
	language = {en},
	urldate = {2021-03-21},
	journal = {bioRxiv},
	author = {Shukla, Rammohan and Henkel, Nicholas D. and Alganem, Khaled and Hamoud, Abdul-rizaq and Reigle, James and Alnafisah, Rawan S. and Eby, Hunter M. and Imami, Ali S. and Creeden, Justin and Miruzzi, Scott A. and Meller, Jaroslaw and Mccullumsmith, Robert E.},
	month = apr,
	year = {2020},
	note = {ZSCC: NoCitationData[s0] 
Publisher: Cold Spring Harbor Laboratory
Section: New Results},
	pages = {2020.04.24.060392},
}

\textlessh3\textgreaterAbstract\textless/h3\textgreater \textlessp\textgreaterThe treatment of CNS disorders, and in particular psychiatric illnesses, lacks disease-altering therapeutics for many conditions. This is likely due to regulatory challenges involving the high cost and slow-pace of drug development for CNS disorders as well as due to limited understanding of disease causality. Repurposing drugs for new indications have lower cost and shorter development timeline compared to that of de novo drug development. Historically, empirical drug-repurposing is a standard practice in psychiatry; however, recent advances in characterizing molecules with their structural and transcriptomic signatures along with ensemble of data analysis approaches, provides informed and cost-effective repurposing strategies that ameliorate the regulatory challenges. In addition, the potential to incorporate ontological approaches along with signature-based repurposing techniques addresses the various knowledge-based challenges associated with CNS drug development. In this review we primarily discuss signature-based in silico approaches to drug repurposing, and its integration with data science platforms for evidence-based drug repurposing. We contrast various in silico and empirical approaches and discuss possible avenues to improve the clinical relevance. These concepts provide a promising new translational avenue for developing new therapies for difficult to treat disorders, and offer the possibility of connecting drug discovery platforms and big data analytics with personalized disease signatures.\textless/p\textgreater

@misc{noauthor_sciencebeam_2020,
	title = {{ScienceBeam}: {Using} open technology to extract knowledge from research {PDFs}},
	copyright = {© 2020 eLife Sciences Publications Limited. This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.},
	shorttitle = {{ScienceBeam}},
	url = {https://elifesciences.org/labs/743da0fc/sciencebeam-using-open-technology-to-extract-knowledge-from-research-pdfs},
	abstract = {We report on our progress towards an open-source machine learning solution for the automatic extraction of semantically structured data from research PDFs.},
	language = {en},
	urldate = {2021-03-13},
	journal = {eLife},
	month = dec,
	year = {2020},
	note = {Publisher: eLife Sciences Publications Limited},
}

We report on our progress towards an open-source machine learning solution for the automatic extraction of semantically structured data from research PDFs.

@article{light_neurophysiological_2020,
	title = {Neurophysiological biomarkers for schizophrenia therapeutics},
	volume = {2},
	issn = {26661446},
	url = {https://linkinghub.elsevier.com/retrieve/pii/S2666144620300022},
	doi = {10.1016/j.bionps.2020.100012},
	language = {en},
	urldate = {2020-10-06},
	journal = {Biomarkers in Neuropsychiatry},
	author = {Light, Gregory A. and Joshi, Yash B. and Molina, Juan L. and Bhakta, Savita G. and Nungaray, John A. and Cardoso, Lauren and Kotz, Juliana E. and Thomas, Michael L. and Swerdlow, Neal R.},
	month = jun,
	year = {2020},
	note = {ZSCC: 0000002},
	pages = {100012},
}

@article{pei_brainkilter_2020,
	title = {{BrainKilter}: {A} {Real}-{Time} {EEG} {Analysis} {Platform} for {Neurofeedback} {Design} and {Training}},
	volume = {8},
	issn = {2169-3536},
	shorttitle = {{BrainKilter}},
	doi = {10.1109/ACCESS.2020.2967903},
	abstract = {Neurofeedback targets self-regularized brain activity to normalized brain function based on brain-computer interface (BCI) technology. Although BCI software or platforms have continued to mature in other fields, little effort has been expended on neurofeedback applications. Hence, we present BrainKilter, a real-time electroencephalogram (EEG) analysis platform based on a “4-tier layered model”. The purposes of BrainKilter are to improve portability and accessibility, allowing different users to choose various options to perform EEG processing, target stimulation-induction through a pipeline, and analyze data online, essentially, to design a protocol paradigm and applicable BCI technology for neurofeedback experiments. The data processing effectiveness and application value of BrainKilter were tested using multiple-parameter neurofeedback training, in which BrainKilter regulated the amplitude of mismatch negative (MMN) signals for healthy individuals. The proposed platform consists of a set of software modules for online protocol design and signal decoding that can be conveniently and efficiently integrated for neurofeedback design and training. The BrainKilter platform provides a truly easy-to-use environment for customizing the experimental paradigm and for optimizing the parameters of neurofeedback experiments for research and clinical neurofeedback applications using BCI technology.},
	journal = {IEEE Access},
	author = {Pei, Guangying and Guo, Guoxin and Chen, Duanduan and Yang, Ruoshui and Shi, Zhongyan and Wang, Shujie and Zhang, Jinpu and Wu, Jinglong and Yan, Tianyi},
	year = {2020},
	note = {ZSCC: 0000002 
Conference Name: IEEE Access},
	keywords = {4-tier layered model, BCI, BCI software, BCI technology, BrainKilter, BrainKilter platform, Data processing, EEG processing, Electroencephalography, MMN, Neurofeedback, Protocols, Real-time systems, Software, Training, brain-computer interface technology, brain-computer interfaces, clinical neurofeedback applications, data processing effectiveness, electroencephalography, medical signal processing, mismatch negative signals, multiple-parameter neurofeedback training, neurofeedback, neurofeedback design, neurofeedback experiments, neurophysiology, normalized brain function, online protocol design, platform, real-time, real-time EEG analysis platform, real-time electroencephalogram analysis platform, self-regularized brain activity, signal decoding, software modules, target stimulation-induction},
	pages = {57661--57673},
}

Neurofeedback targets self-regularized brain activity to normalized brain function based on brain-computer interface (BCI) technology. Although BCI software or platforms have continued to mature in other fields, little effort has been expended on neurofeedback applications. Hence, we present BrainKilter, a real-time electroencephalogram (EEG) analysis platform based on a “4-tier layered model”. The purposes of BrainKilter are to improve portability and accessibility, allowing different users to choose various options to perform EEG processing, target stimulation-induction through a pipeline, and analyze data online, essentially, to design a protocol paradigm and applicable BCI technology for neurofeedback experiments. The data processing effectiveness and application value of BrainKilter were tested using multiple-parameter neurofeedback training, in which BrainKilter regulated the amplitude of mismatch negative (MMN) signals for healthy individuals. The proposed platform consists of a set of software modules for online protocol design and signal decoding that can be conveniently and efficiently integrated for neurofeedback design and training. The BrainKilter platform provides a truly easy-to-use environment for customizing the experimental paradigm and for optimizing the parameters of neurofeedback experiments for research and clinical neurofeedback applications using BCI technology.

@article{ros_consensus_2020,
	title = {Consensus on the reporting and experimental design of clinical and cognitive-behavioural neurofeedback studies ({CRED}-nf checklist)},
	volume = {143},
	issn = {0006-8950, 1460-2156},
	url = {https://academic.oup.com/brain/article/143/6/1674/5807912},
	doi = {10.1093/brain/awaa009},
	abstract = {Abstract
            Neurofeedback has begun to attract the attention and scrutiny of the scientific and medical mainstream. Here, neurofeedback researchers present a consensus-derived checklist that aims to improve the reporting and experimental design standards in the field.},
	language = {en},
	number = {6},
	urldate = {2020-10-06},
	journal = {Brain},
	author = {Ros, Tomas and Enriquez-Geppert, Stefanie and Zotev, Vadim and Young, Kymberly D and Wood, Guilherme and Whitfield-Gabrieli, Susan and Wan, Feng and Vuilleumier, Patrik and Vialatte, François and Van De Ville, Dimitri and Todder, Doron and Surmeli, Tanju and Sulzer, James S and Strehl, Ute and Sterman, Maurice Barry and Steiner, Naomi J and Sorger, Bettina and Soekadar, Surjo R and Sitaram, Ranganatha and Sherlin, Leslie H and Schönenberg, Michael and Scharnowski, Frank and Schabus, Manuel and Rubia, Katya and Rosa, Agostinho and Reiner, Miriam and Pineda, Jaime A and Paret, Christian and Ossadtchi, Alexei and Nicholson, Andrew A and Nan, Wenya and Minguez, Javier and Micoulaud-Franchi, Jean-Arthur and Mehler, David M A and Lührs, Michael and Lubar, Joel and Lotte, Fabien and Linden, David E J and Lewis-Peacock, Jarrod A and Lebedev, Mikhail A and Lanius, Ruth A and Kübler, Andrea and Kranczioch, Cornelia and Koush, Yury and Konicar, Lilian and Kohl, Simon H and Kober, Silivia E and Klados, Manousos A and Jeunet, Camille and Janssen, T W P and Huster, Rene J and Hoedlmoser, Kerstin and Hirshberg, Laurence M and Heunis, Stephan and Hendler, Talma and Hampson, Michelle and Guggisberg, Adrian G and Guggenberger, Robert and Gruzelier, John H and Göbel, Rainer W and Gninenko, Nicolas and Gharabaghi, Alireza and Frewen, Paul and Fovet, Thomas and Fernández, Thalía and Escolano, Carlos and Ehlis, Ann-Christine and Drechsler, Renate and Christopher deCharms, R and Debener, Stefan and De Ridder, Dirk and Davelaar, Eddy J and Congedo, Marco and Cavazza, Marc and Breteler, Marinus H M and Brandeis, Daniel and Bodurka, Jerzy and Birbaumer, Niels and Bazanova, Olga M and Barth, Beatrix and Bamidis, Panagiotis D and Auer, Tibor and Arns, Martijn and Thibault, Robert T},
	month = jun,
	year = {2020},
	note = {ZSCC: NoCitationData[s0]},
	pages = {1674--1685},
}

Abstract Neurofeedback has begun to attract the attention and scrutiny of the scientific and medical mainstream. Here, neurofeedback researchers present a consensus-derived checklist that aims to improve the reporting and experimental design standards in the field.

@article{tong_transcranial_2020,
	title = {Transcranial direct current stimulation influences bilingual language control mechanism: evidence from cross-frequency coupling},
	volume = {14},
	issn = {1871-4099},
	shorttitle = {Transcranial direct current stimulation influences bilingual language control mechanism},
	url = {https://doi.org/10.1007/s11571-019-09561-w},
	doi = {10.1007/s11571-019-09561-w},
	abstract = {How to better suppress the interference from the non-target language when switching from one language to the other in bilingual production? The current study applied transcranial direct current stimulation over the right dorsolateral prefrontal cortex to modulate language control measured by cross-frequency coupling. We found that switching to L2 was more modulated by F4–F3 alpha–beta phase-amplitude compared to switching to L1 after receiving the anodal stimulation at the language task schema phase. These findings suggest that anodal stimulation affects the selection of the target language task schema by enhancing the activation of frontal areas and facilitating the coordination between the left and the right frontal hemispheres.},
	language = {en},
	number = {2},
	urldate = {2020-10-06},
	journal = {Cognitive Neurodynamics},
	author = {Tong, Jing and Kong, Chao and Wang, Xin and Liu, Huanhuan and Li, Baike and He, Yuying},
	month = apr,
	year = {2020},
	note = {ZSCC: 0000002},
	pages = {203--214},
}

How to better suppress the interference from the non-target language when switching from one language to the other in bilingual production? The current study applied transcranial direct current stimulation over the right dorsolateral prefrontal cortex to modulate language control measured by cross-frequency coupling. We found that switching to L2 was more modulated by F4–F3 alpha–beta phase-amplitude compared to switching to L1 after receiving the anodal stimulation at the language task schema phase. These findings suggest that anodal stimulation affects the selection of the target language task schema by enhancing the activation of frontal areas and facilitating the coordination between the left and the right frontal hemispheres.

@article{swyer_voluntary_2020,
	title = {Voluntary control of auditory hallucinations: phenomenology to therapeutic implications},
	volume = {6},
	copyright = {2020 The Author(s)},
	issn = {2334-265X},
	shorttitle = {Voluntary control of auditory hallucinations},
	url = {https://www.nature.com/articles/s41537-020-0106-8},
	doi = {10.1038/s41537-020-0106-8},
	abstract = {Auditory verbal hallucinations (AVH) have traditionally been thought to be outside the influence of conscious control. However, recent work with voice hearers makes clear that both treatment-seeking and non-treatment-seeking voice hearers may exert varying degrees of control over their voices. Evidence suggests that this ability may be a key factor in determining health status, but little systematic examination of control in AVH has been carried out. This review provides an overview of the research examining control over AVH in both treatment-seeking and non-treatment-seeking populations. We first examine the relationship between control over AVH and health status as well as the psychosocial factors that may influence control and functioning. We then link control to various cognitive constructs that appear to be important for voice hearing. Finally, we reconcile the possibility of control with the field’s current understanding of the proposed cognitive, computational, and neural underpinnings of hallucinations and perception more broadly. Established relationships between control, health status, and functioning suggest that the development of control over AVH could increase functioning and reduce distress. A more detailed understanding of the discrete types of control, their development, and their neural underpinnings is essential for translating this knowledge into new therapeutic approaches.},
	language = {en},
	number = {1},
	urldate = {2020-10-06},
	journal = {npj Schizophrenia},
	author = {Swyer, Ariel and Powers, Albert R.},
	month = aug,
	year = {2020},
	note = {ZSCC: 0000000 
Number: 1
Publisher: Nature Publishing Group},
	pages = {1--9},
}

Auditory verbal hallucinations (AVH) have traditionally been thought to be outside the influence of conscious control. However, recent work with voice hearers makes clear that both treatment-seeking and non-treatment-seeking voice hearers may exert varying degrees of control over their voices. Evidence suggests that this ability may be a key factor in determining health status, but little systematic examination of control in AVH has been carried out. This review provides an overview of the research examining control over AVH in both treatment-seeking and non-treatment-seeking populations. We first examine the relationship between control over AVH and health status as well as the psychosocial factors that may influence control and functioning. We then link control to various cognitive constructs that appear to be important for voice hearing. Finally, we reconcile the possibility of control with the field’s current understanding of the proposed cognitive, computational, and neural underpinnings of hallucinations and perception more broadly. Established relationships between control, health status, and functioning suggest that the development of control over AVH could increase functioning and reduce distress. A more detailed understanding of the discrete types of control, their development, and their neural underpinnings is essential for translating this knowledge into new therapeutic approaches.

@article{myers_sensorimotor_2020,
	title = {Sensorimotor {Integration} {Can} {Enhance} {Auditory} {Perception}},
	volume = {10},
	copyright = {2020 The Author(s)},
	issn = {2045-2322},
	url = {https://www.nature.com/articles/s41598-020-58447-z},
	doi = {10.1038/s41598-020-58447-z},
	abstract = {Whenever we move, speak, or play musical instruments, our actions generate auditory sensory input. The sensory consequences of our actions are thought to be predicted via sensorimotor integration, which involves anatomical and functional links between auditory and motor brain regions. The physiological connections are relatively well established, but less is known about how sensorimotor integration affects auditory perception. The sensory attenuation hypothesis suggests that the perceived loudness of self-generated sounds is attenuated to help distinguish self-generated sounds from ambient sounds. Sensory attenuation would work for louder ambient sounds, but could lead to less accurate perception if the ambient sounds were quieter. We hypothesize that a key function of sensorimotor integration is the facilitated processing of self-generated sounds, leading to more accurate perception under most conditions. The sensory attenuation hypothesis predicts better performance for higher but not lower intensity comparisons, whereas sensory facilitation predicts improved perception regardless of comparison sound intensity. A series of experiments tested these hypotheses, with results supporting the enhancement hypothesis. Overall, people were more accurate at comparing the loudness of two sounds when making one of the sounds themselves. We propose that the brain selectively modulates the perception of self-generated sounds to enhance representations of action consequences.},
	language = {en},
	number = {1},
	urldate = {2020-10-06},
	journal = {Scientific Reports},
	author = {Myers, John C. and Mock, Jeffrey R. and Golob, Edward J.},
	month = jan,
	year = {2020},
	note = {ZSCC: 0000000 
Number: 1
Publisher: Nature Publishing Group},
	pages = {1496},
}

Whenever we move, speak, or play musical instruments, our actions generate auditory sensory input. The sensory consequences of our actions are thought to be predicted via sensorimotor integration, which involves anatomical and functional links between auditory and motor brain regions. The physiological connections are relatively well established, but less is known about how sensorimotor integration affects auditory perception. The sensory attenuation hypothesis suggests that the perceived loudness of self-generated sounds is attenuated to help distinguish self-generated sounds from ambient sounds. Sensory attenuation would work for louder ambient sounds, but could lead to less accurate perception if the ambient sounds were quieter. We hypothesize that a key function of sensorimotor integration is the facilitated processing of self-generated sounds, leading to more accurate perception under most conditions. The sensory attenuation hypothesis predicts better performance for higher but not lower intensity comparisons, whereas sensory facilitation predicts improved perception regardless of comparison sound intensity. A series of experiments tested these hypotheses, with results supporting the enhancement hypothesis. Overall, people were more accurate at comparing the loudness of two sounds when making one of the sounds themselves. We propose that the brain selectively modulates the perception of self-generated sounds to enhance representations of action consequences.

@article{kiverstein_free_2020,
	title = {Free {Energy} and the {Self}: {An} {Ecological}–{Enactive} {Interpretation}},
	volume = {39},
	issn = {1572-8749},
	shorttitle = {Free {Energy} and the {Self}},
	url = {https://doi.org/10.1007/s11245-018-9561-5},
	doi = {10.1007/s11245-018-9561-5},
	abstract = {According to the free energy principle all living systems aim to minimise free energy in their sensory exchanges with the environment. Processes of free energy minimisation are thus ubiquitous in the biological world. Indeed it has been argued that even plants engage in free energy minimisation. Not all living things however feel alive. How then did the feeling of being alive get started? In line with the arguments of the phenomenologists, I will claim that every feeling must be felt by someone. It must have mineness built into it if it is to feel a particular way. The question I take up in this paper asks how mineness might have arisen out of processes of free energy minimisation, given that many systems that keep themselves alive lack mineness. The hypothesis I develop in this paper is that the life of an organism can be seen as an inferential process. Every living system embodies a probability distribution conditioned on a model of the sensory, physiological, and morphological states that are highly probably given the life it leads and the niche it inhabits. I argue for an ecological and enactive interpretation of free energy. I show how once the life of an organism reaches a certain level of complexity mineness emerges as an intrinsic part of the process of life itself.},
	language = {en},
	number = {3},
	urldate = {2020-10-06},
	journal = {Topoi},
	author = {Kiverstein, Julian},
	month = jul,
	year = {2020},
	note = {ZSCC: 0000014},
	pages = {559--574},
}

According to the free energy principle all living systems aim to minimise free energy in their sensory exchanges with the environment. Processes of free energy minimisation are thus ubiquitous in the biological world. Indeed it has been argued that even plants engage in free energy minimisation. Not all living things however feel alive. How then did the feeling of being alive get started? In line with the arguments of the phenomenologists, I will claim that every feeling must be felt by someone. It must have mineness built into it if it is to feel a particular way. The question I take up in this paper asks how mineness might have arisen out of processes of free energy minimisation, given that many systems that keep themselves alive lack mineness. The hypothesis I develop in this paper is that the life of an organism can be seen as an inferential process. Every living system embodies a probability distribution conditioned on a model of the sensory, physiological, and morphological states that are highly probably given the life it leads and the niche it inhabits. I argue for an ecological and enactive interpretation of free energy. I show how once the life of an organism reaches a certain level of complexity mineness emerges as an intrinsic part of the process of life itself.

@article{gellner_direct_2020,
	title = {Direct current stimulation-induced synaptic plasticity in the sensorimotor cortex: structure follows function},
	volume = {13},
	issn = {1935-861X},
	shorttitle = {Direct current stimulation-induced synaptic plasticity in the sensorimotor cortex},
	url = {http://www.sciencedirect.com/science/article/pii/S1935861X19303419},
	doi = {10.1016/j.brs.2019.07.026},
	abstract = {Background
Non-invasive direct current stimulation (DCS) of the brain induces functional plasticity in vitro and facilitates motor learning across species. The effect of DCS on structural synaptic plasticity is currently unknown.
Objective
This study addresses the effects and the underlying mechanisms of anodal DCS on structural plasticity and morphology of dendritic spines in the sensorimotor cortex (M1/S1).
Methods
A DCS electrode setup was combined with a chronic cranial window over M1/S1 in transgenic Thy1-GFP mice, to allow for in vivo 2-photon microscopy and simultaneous DCS. Contralateral electrical forepaw stimulation (eFS) was used to mimic the second synapse specific input, a previously shown requirement to induce functional plasticity by DCS. Changes in spine density and spine morphology were compared between DCS/eFS and sham, as well as two control conditions (sham-DCS/eFS, DCS/sham-eFS). Furthermore, the role of BDNF for stimulation-induced changes in spine density was assessed in heterozygous Thy1-GFP x BDNF+/- mice.
Results
Combined DCS/eFS rapidly increased spine density during stimulation and changes outlasted the intervention for 24 h. This effect was due to increased survival of original spines and a preferential formation of new spines after intervention. The latter were morphologically characterized by larger head sizes. The DCS-induced spine density increase was absent in mice with reduced BDNF expression.
Conclusion
Previous findings of DCS-induced functional synaptic plasticity can be extended to structural plasticity in M1/S1 that similarly depends on a second synaptic input (eFS) and requires physiological BDNF expression. These findings show considerable parallels to motor learning-induced M1 spine dynamics.},
	language = {en},
	number = {1},
	urldate = {2020-10-04},
	journal = {Brain Stimulation},
	author = {Gellner, Anne-Kathrin and Reis, Janine and Holtick, Carsten and Schubert, Charlotte and Fritsch, Brita},
	month = jan,
	year = {2020},
	note = {ZSCC: 0000006},
	keywords = {Dendritic spine, Noninvasive brain stimulation, Spine morphology, Structural plasticity},
	pages = {80--88},
}

Background Non-invasive direct current stimulation (DCS) of the brain induces functional plasticity in vitro and facilitates motor learning across species. The effect of DCS on structural synaptic plasticity is currently unknown. Objective This study addresses the effects and the underlying mechanisms of anodal DCS on structural plasticity and morphology of dendritic spines in the sensorimotor cortex (M1/S1). Methods A DCS electrode setup was combined with a chronic cranial window over M1/S1 in transgenic Thy1-GFP mice, to allow for in vivo 2-photon microscopy and simultaneous DCS. Contralateral electrical forepaw stimulation (eFS) was used to mimic the second synapse specific input, a previously shown requirement to induce functional plasticity by DCS. Changes in spine density and spine morphology were compared between DCS/eFS and sham, as well as two control conditions (sham-DCS/eFS, DCS/sham-eFS). Furthermore, the role of BDNF for stimulation-induced changes in spine density was assessed in heterozygous Thy1-GFP x BDNF+/- mice. Results Combined DCS/eFS rapidly increased spine density during stimulation and changes outlasted the intervention for 24 h. This effect was due to increased survival of original spines and a preferential formation of new spines after intervention. The latter were morphologically characterized by larger head sizes. The DCS-induced spine density increase was absent in mice with reduced BDNF expression. Conclusion Previous findings of DCS-induced functional synaptic plasticity can be extended to structural plasticity in M1/S1 that similarly depends on a second synaptic input (eFS) and requires physiological BDNF expression. These findings show considerable parallels to motor learning-induced M1 spine dynamics.

@article{hoffmann-vold_need_2020,
	title = {The need for a holistic approach for {SSc}-{ILD} – achievements and ambiguity in a devastating disease},
	volume = {21},
	issn = {1465-993X},
	url = {https://doi.org/10.1186/s12931-020-01459-0},
	doi = {10.1186/s12931-020-01459-0},
	abstract = {Systemic sclerosis (SSc) is a multi-organ autoimmune disease with complex interactions between immune-mediated inflammatory processes and vascular pathology leading to small vessel obliteration, promoting uncontrolled fibrosis of skin and internal organs. Interstitial lung disease (ILD) is a common but highly variable manifestation of SSc and is associated with high morbidity and mortality. Treatment approaches have focused on immunosuppressive therapies, which have shown some efficacy on lung function. Recently, a large phase 3 trial showed that treatment with nintedanib was associated with a reduction in lung function decline. None of the conducted randomized clinical trials have so far shown convincing efficacy on other outcome measures including quality of life determined by patient reported outcomes. Little evidence is available for non-pharmacological treatment and supportive care specifically for SSc-ILD patients, including pulmonary rehabilitation, supplemental oxygen, symptom relief and adequate information. Improved management of SSc-ILD patients based on a holistic approach is necessary to support patients in maintaining as much quality of life as possible throughout the disease course and to improve long-term outcomes.},
	number = {1},
	urldate = {2020-10-03},
	journal = {Respiratory Research},
	author = {Hoffmann-Vold, Anna-Maria and Allanore, Yannick and Bendstrup, Elisabeth and Bruni, Cosimo and Distler, Oliver and Maher, Toby M. and Wijsenbeek, Marlies and Kreuter, Michael},
	month = jul,
	year = {2020},
	note = {ZSCC: 0000000},
	pages = {197},
}

Systemic sclerosis (SSc) is a multi-organ autoimmune disease with complex interactions between immune-mediated inflammatory processes and vascular pathology leading to small vessel obliteration, promoting uncontrolled fibrosis of skin and internal organs. Interstitial lung disease (ILD) is a common but highly variable manifestation of SSc and is associated with high morbidity and mortality. Treatment approaches have focused on immunosuppressive therapies, which have shown some efficacy on lung function. Recently, a large phase 3 trial showed that treatment with nintedanib was associated with a reduction in lung function decline. None of the conducted randomized clinical trials have so far shown convincing efficacy on other outcome measures including quality of life determined by patient reported outcomes. Little evidence is available for non-pharmacological treatment and supportive care specifically for SSc-ILD patients, including pulmonary rehabilitation, supplemental oxygen, symptom relief and adequate information. Improved management of SSc-ILD patients based on a holistic approach is necessary to support patients in maintaining as much quality of life as possible throughout the disease course and to improve long-term outcomes.

@article{okano_real-time_2020,
	title = {Real-time {fMRI} feedback impacts brain activation, results in auditory hallucinations reduction: {Part} 1: {Superior} temporal gyrus -{Preliminary} evidence},
	volume = {286},
	issn = {1872-7123},
	shorttitle = {Real-time {fMRI} feedback impacts brain activation, results in auditory hallucinations reduction},
	doi = {10.1016/j.psychres.2020.112862},
	abstract = {Auditory hallucinations (AH) are one of the core symptoms of schizophrenia (SZ) and constitute a significant source of suffering and disability. One third of SZ patients experience pharmacology-resistant AH, so an alternative/complementary treatment strategy is needed to alleviate this debilitating condition. In this study, real-time functional Magnetic Resonance Imaging neurofeedback (rt-fMRI NFB), a non-invasive technique, was used to teach 10 SZ patients with pharmacology-resistant AH to modulate their brain activity in the superior temporal gyrus (STG), a key area in the neurophysiology of AH. A functional task was designed in order to provide patients with a specific strategy to help them modify their brain activity in the desired direction. Specifically, they received neurofeedback from their own STG and were trained to upregulate it while listening to their own voice recording and downregulate it while ignoring a stranger's voice recording. This guided performance neurofeedback training resulted in a) a significant reduction in STG activation while ignoring a stranger's voice, and b) reductions in AH scores after the neurofeedback session. A single, 21-minute session of rt-fMRI NFB was enough to produce these effects, suggesting that this approach may be an efficient and clinically viable alternative for the treatment of pharmacology-resistant AH.},
	language = {eng},
	journal = {Psychiatry Research},
	author = {Okano, Kana and Bauer, Clemens C. C. and Ghosh, Satrajit S. and Lee, Yoon Ji and Melero, Helena and de Los Angeles, Carlo and Nestor, Paul G. and Del Re, Elisabetta C. and Northoff, Georg and Whitfield-Gabrieli, Susan and Niznikiewicz, Margaret A.},
	month = feb,
	year = {2020},
	pmid = {32113035},
	note = {ZSCC: NoCitationData[s0] },
	pages = {112862},
}

Auditory hallucinations (AH) are one of the core symptoms of schizophrenia (SZ) and constitute a significant source of suffering and disability. One third of SZ patients experience pharmacology-resistant AH, so an alternative/complementary treatment strategy is needed to alleviate this debilitating condition. In this study, real-time functional Magnetic Resonance Imaging neurofeedback (rt-fMRI NFB), a non-invasive technique, was used to teach 10 SZ patients with pharmacology-resistant AH to modulate their brain activity in the superior temporal gyrus (STG), a key area in the neurophysiology of AH. A functional task was designed in order to provide patients with a specific strategy to help them modify their brain activity in the desired direction. Specifically, they received neurofeedback from their own STG and were trained to upregulate it while listening to their own voice recording and downregulate it while ignoring a stranger's voice recording. This guided performance neurofeedback training resulted in a) a significant reduction in STG activation while ignoring a stranger's voice, and b) reductions in AH scores after the neurofeedback session. A single, 21-minute session of rt-fMRI NFB was enough to produce these effects, suggesting that this approach may be an efficient and clinically viable alternative for the treatment of pharmacology-resistant AH.

@article{zelmann_closes_2020,
	title = {{CLoSES}: {A} platform for closed-loop intracranial stimulation in humans},
	volume = {223},
	issn = {1053-8119},
	shorttitle = {{CLoSES}},
	url = {http://www.sciencedirect.com/science/article/pii/S1053811920308004},
	doi = {10.1016/j.neuroimage.2020.117314},
	abstract = {Targeted interrogation of brain networks through invasive brain stimulation has become an increasingly important research tool as well as therapeutic modality. The majority of work with this emerging capability has been focused on open-loop approaches. Closed-loop techniques, however, could improve neuromodulatory therapies and research investigations by optimizing stimulation approaches using neurally informed, personalized targets. Implementing closed-loop systems is challenging particularly with regard to applying consistent strategies considering inter-individual variability. In particular, during intracranial epilepsy monitoring, where much of this research is currently progressing, electrodes are implanted exclusively for clinical reasons. Thus, detection and stimulation sites must be participant- and task-specific. The system must run in parallel with clinical systems, integrate seamlessly with existing setups, and ensure safety features are in place. In other words, a robust, yet flexible platform is required to perform different tests with a single participant and to comply with clinical requirements. In order to investigate closed-loop stimulation for research and therapeutic use, we developed a Closed-Loop System for Electrical Stimulation (CLoSES) that computes neural features which are then used in a decision algorithm to trigger stimulation in near real-time. To summarize CLoSES, intracranial electroencephalography (iEEG) signals are acquired, band-pass filtered, and local and network features are continuously computed. If target features are detected (e.g. above a preset threshold for a certain duration), stimulation is triggered. Not only could the system trigger stimulation while detecting real-time neural features, but we incorporated a pipeline wherein we used an encoder/decoder model to estimate a hidden cognitive state from the neural features. CLoSES provides a flexible platform to implement a variety of closed-loop experimental paradigms in humans. CLoSES has been successfully used with twelve patients implanted with depth electrodes in the epilepsy monitoring unit. During cognitive tasks (N=5), stimulation in closed loop modified a cognitive hidden state on a trial by trial basis. Sleep spindle oscillations (N=6) and sharp transient epileptic activity (N=9) were detected in near real-time, and stimulation was applied during the event or at specified delays (N=3). In addition, we measured the capabilities of the CLoSES system. Total latency was related to the characteristics of the event being detected, with tens of milliseconds for epileptic activity and hundreds of milliseconds for spindle detection. Stepwise latency, the actual duration of each continuous step, was within the specified fixed-step duration and increased linearly with the number of channels and features. We anticipate that probing neural dynamics and interaction between brain states and stimulation responses with CLoSES will lead to novel insights into the mechanism of normal and pathological brain activity, the discovery and evaluation of potential electrographic biomarkers of neurological and psychiatric disorders, and the development and testing of patient-specific stimulation targets and control signals before implanting a therapeutic device.},
	language = {en},
	urldate = {2020-09-28},
	journal = {NeuroImage},
	author = {Zelmann, Rina and Paulk, Angelique C. and Basu, Ishita and Sarma, Anish and Yousefi, Ali and Crocker, Britni and Eskandar, Emad and Williams, Ziv and Cosgrove, G. Rees and Weisholtz, Daniel S. and Dougherty, Darin D. and Truccolo, Wilson and Widge, Alik S. and Cash, Sydney S.},
	month = dec,
	year = {2020},
	note = {ZSCC: NoCitationData[s0]},
	keywords = {Closed-loop, Direct electrical stimulation, Neuromodulation, intracranial EEG},
	pages = {117314},
}

Targeted interrogation of brain networks through invasive brain stimulation has become an increasingly important research tool as well as therapeutic modality. The majority of work with this emerging capability has been focused on open-loop approaches. Closed-loop techniques, however, could improve neuromodulatory therapies and research investigations by optimizing stimulation approaches using neurally informed, personalized targets. Implementing closed-loop systems is challenging particularly with regard to applying consistent strategies considering inter-individual variability. In particular, during intracranial epilepsy monitoring, where much of this research is currently progressing, electrodes are implanted exclusively for clinical reasons. Thus, detection and stimulation sites must be participant- and task-specific. The system must run in parallel with clinical systems, integrate seamlessly with existing setups, and ensure safety features are in place. In other words, a robust, yet flexible platform is required to perform different tests with a single participant and to comply with clinical requirements. In order to investigate closed-loop stimulation for research and therapeutic use, we developed a Closed-Loop System for Electrical Stimulation (CLoSES) that computes neural features which are then used in a decision algorithm to trigger stimulation in near real-time. To summarize CLoSES, intracranial electroencephalography (iEEG) signals are acquired, band-pass filtered, and local and network features are continuously computed. If target features are detected (e.g. above a preset threshold for a certain duration), stimulation is triggered. Not only could the system trigger stimulation while detecting real-time neural features, but we incorporated a pipeline wherein we used an encoder/decoder model to estimate a hidden cognitive state from the neural features. CLoSES provides a flexible platform to implement a variety of closed-loop experimental paradigms in humans. CLoSES has been successfully used with twelve patients implanted with depth electrodes in the epilepsy monitoring unit. During cognitive tasks (N=5), stimulation in closed loop modified a cognitive hidden state on a trial by trial basis. Sleep spindle oscillations (N=6) and sharp transient epileptic activity (N=9) were detected in near real-time, and stimulation was applied during the event or at specified delays (N=3). In addition, we measured the capabilities of the CLoSES system. Total latency was related to the characteristics of the event being detected, with tens of milliseconds for epileptic activity and hundreds of milliseconds for spindle detection. Stepwise latency, the actual duration of each continuous step, was within the specified fixed-step duration and increased linearly with the number of channels and features. We anticipate that probing neural dynamics and interaction between brain states and stimulation responses with CLoSES will lead to novel insights into the mechanism of normal and pathological brain activity, the discovery and evaluation of potential electrographic biomarkers of neurological and psychiatric disorders, and the development and testing of patient-specific stimulation targets and control signals before implanting a therapeutic device.

@article{di_paolo_enactive_2020,
	title = {Enactive becoming},
	issn = {1572-8676},
	url = {https://doi.org/10.1007/s11097-019-09654-1},
	doi = {10.1007/s11097-019-09654-1},
	abstract = {The enactive approach provides a perspective on human bodies in their organic, sensorimotor, social, and linguistic dimensions, but many fundamental issues still remain unaddressed. A crucial desideratum for a theory of human bodies is that it be able to account for concrete human becoming. In this article I show that enactive theory possesses resources to achieve this goal. Being an existential structure, human becoming is best approached by a series of progressive formal indications. I discuss three standpoints on human becoming as open, indeterminate, and therefore historical using the voices of Pico della Mirandola, Gordon W. Allport, and Paulo Freire. Drawing on Gilbert Simondon’s philosophy of individuation we move from an existential to an ontological register in looking at modes of embodied becoming. His scheme of interpretation of the relation between modes of individuation allows us to understand human becoming in terms of a tendency to neotenization. I compare this ontology with an enactive theoretical account of the dimensions of embodiment, finding several compatibilities and complementarities. Various forms of bodily unfinishedness in enaction fit the Simondonian ontology and the existential analysis, where transindividuality corresponds to participatory sense-making and Freire’s joint becoming of individuals and communities correlates with the open tensions in linguistic bodies between incorporation and incarnation of linguistic acts. I test some of this ideas by considering the plausibility of artificial bodies and personal becoming from an enactive perspective, using the case of replicants in the film Blade Runner. The conclusion is that any kind of personhood, replicants included, requires living through an actual history of concrete becoming.},
	language = {en},
	urldate = {2020-08-24},
	journal = {Phenomenology and the Cognitive Sciences},
	author = {Di Paolo, Ezequiel A.},
	month = jan,
	year = {2020},
	keywords = {Communities, Enaction, Gilbert Simondon, Human becoming, Individuality, Replicants},
}

The enactive approach provides a perspective on human bodies in their organic, sensorimotor, social, and linguistic dimensions, but many fundamental issues still remain unaddressed. A crucial desideratum for a theory of human bodies is that it be able to account for concrete human becoming. In this article I show that enactive theory possesses resources to achieve this goal. Being an existential structure, human becoming is best approached by a series of progressive formal indications. I discuss three standpoints on human becoming as open, indeterminate, and therefore historical using the voices of Pico della Mirandola, Gordon W. Allport, and Paulo Freire. Drawing on Gilbert Simondon’s philosophy of individuation we move from an existential to an ontological register in looking at modes of embodied becoming. His scheme of interpretation of the relation between modes of individuation allows us to understand human becoming in terms of a tendency to neotenization. I compare this ontology with an enactive theoretical account of the dimensions of embodiment, finding several compatibilities and complementarities. Various forms of bodily unfinishedness in enaction fit the Simondonian ontology and the existential analysis, where transindividuality corresponds to participatory sense-making and Freire’s joint becoming of individuals and communities correlates with the open tensions in linguistic bodies between incorporation and incarnation of linguistic acts. I test some of this ideas by considering the plausibility of artificial bodies and personal becoming from an enactive perspective, using the case of replicants in the film Blade Runner. The conclusion is that any kind of personhood, replicants included, requires living through an actual history of concrete becoming.

@inproceedings{wang_causal_2020,
	title = {Causal inference in degenerate systems: {An} impossibility result},
	shorttitle = {Causal inference in degenerate systems},
	url = {http://proceedings.mlr.press/v108/wang20i.html},
	abstract = {Causal relationships among variables are commonly represented via directed acyclic graphs. There are many methods in the literature to quantify the strength of arrows in a causal acyclic graph. The...},
	language = {en},
	urldate = {2020-08-20},
	booktitle = {International {Conference} on {Artificial} {Intelligence} and {Statistics}},
	publisher = {PMLR},
	author = {Wang, Yue and Wang, Linbo},
	month = jun,
	year = {2020},
	note = {ZSCC: 0000000 
ISSN: 2640-3498},
	pages = {3383--3392},
}

Causal relationships among variables are commonly represented via directed acyclic graphs. There are many methods in the literature to quantify the strength of arrows in a causal acyclic graph. The...

@article{guleken_investigation_2020,
	title = {Investigation of the effects of transcranial direct current stimulation and neurofeedback by continuous performance test},
	volume = {716},
	issn = {0304-3940},
	url = {http://www.sciencedirect.com/science/article/pii/S0304394019307517},
	doi = {10.1016/j.neulet.2019.134648},
	abstract = {Transcranial direct current stimulation (tDCS) is a noninvasive neuromodulation technique based on weak direct current stimulation through the scalp. Neurofeedback (NFB) is a learning strategy that may help alter to brain wave parameters, by monitoring electroencephalography (EEG) feedback via special programs. We aimed to investigate the supportive effects of tDCS in addition to NFB training. 16 healthy volunteers were divided equally into two groups. One of the groups was trained by NFB with the sensorimotor rhythm (SMR) protocol; 2 days per week, 10 sessions of 30 min, the other group received 10 min of tDCS before each NFB sessions. Continuous Performance Test (CPT) was used to measure, response time and suppression and to determine selective attention condition. Also, Beck Depression and Anxiety Inventories were used to exclude people with depression and anxiety. Depression scores of NFB + tDCS group were decreased significantly. CPT scores were better at last sessions for both groups compared to the first sessions. Sessions were analyzed by comparing 1st, 2nd, 5th and 10th sessions. While the NFB + tDCS group had statistically significant changes at theta/beta ratios with SMR and alpha band amplitudes, NFB group statistics had changed at theta/SMR ratios. NFB training shows its effects at the end of 10 sessions. Despite an increase in the latencies of correct and commission responses on the task of CPT, additional use of tDCS improves cognitive performance. Also, tDCS has a supportive effect on the healthy participants who have mild anxiety and depression; also inhibition deficits of subjects were clear.},
	language = {en},
	urldate = {2020-08-18},
	journal = {Neuroscience Letters},
	author = {Guleken, Zozan and Eskikurt, Gökçer and Karamürsel, Sacit},
	month = jan,
	year = {2020},
	note = {ZSCC: 0000000},
	keywords = {Continuous performance test, Inhibition, Neurofeedback, Neuromodulation, Sensorimotor rhythm, Transcranial direct current stimulation},
	pages = {134648},
}

Transcranial direct current stimulation (tDCS) is a noninvasive neuromodulation technique based on weak direct current stimulation through the scalp. Neurofeedback (NFB) is a learning strategy that may help alter to brain wave parameters, by monitoring electroencephalography (EEG) feedback via special programs. We aimed to investigate the supportive effects of tDCS in addition to NFB training. 16 healthy volunteers were divided equally into two groups. One of the groups was trained by NFB with the sensorimotor rhythm (SMR) protocol; 2 days per week, 10 sessions of 30 min, the other group received 10 min of tDCS before each NFB sessions. Continuous Performance Test (CPT) was used to measure, response time and suppression and to determine selective attention condition. Also, Beck Depression and Anxiety Inventories were used to exclude people with depression and anxiety. Depression scores of NFB + tDCS group were decreased significantly. CPT scores were better at last sessions for both groups compared to the first sessions. Sessions were analyzed by comparing 1st, 2nd, 5th and 10th sessions. While the NFB + tDCS group had statistically significant changes at theta/beta ratios with SMR and alpha band amplitudes, NFB group statistics had changed at theta/SMR ratios. NFB training shows its effects at the end of 10 sessions. Despite an increase in the latencies of correct and commission responses on the task of CPT, additional use of tDCS improves cognitive performance. Also, tDCS has a supportive effect on the healthy participants who have mild anxiety and depression; also inhibition deficits of subjects were clear.

@article{brodrick_free_2020,
	title = {Free to {Choose}: {A} {Moral} {Defense} of the {Right}-to-{Try} {Movement}},
	volume = {45},
	issn = {0360-5310},
	shorttitle = {Free to {Choose}},
	url = {https://academic.oup.com/jmp/article/45/1/61/5700356},
	doi = {10.1093/jmp/jhz028},
	abstract = {Abstract.  The claim that individuals legitimately differ with respect to their values seems to be uncontroversial among bioethicists, yet many bioethicists nev},
	language = {en},
	number = {1},
	urldate = {2020-08-12},
	journal = {The Journal of Medicine and Philosophy: A Forum for Bioethics and Philosophy of Medicine},
	author = {Brodrick, Michael},
	month = jan,
	year = {2020},
	note = {ZSCC: 0000001 
Publisher: Oxford Academic},
	pages = {61--85},
}

Abstract. The claim that individuals legitimately differ with respect to their values seems to be uncontroversial among bioethicists, yet many bioethicists nev

@article{ojeda_simbsi_2020,
	title = {{SimBSI}: {An} open-source {Simulink} library for developing closed-loop brain signal interfaces in animals and humans},
	volume = {6},
	issn = {2057-1976},
	shorttitle = {{SimBSI}},
	url = {https://iopscience.iop.org/article/10.1088/2057-1976/ab6e20},
	doi = {10.1088/2057-1976/ab6e20},
	number = {3},
	urldate = {2020-07-17},
	journal = {Biomedical Physics \& Engineering Express},
	author = {Ojeda, Alejandro and Buscher, Nathalie and Balasubramani, Pragathi and Maric, Vojislav and Ramanathan, Dhakshin and Mishra, Jyoti},
	month = apr,
	year = {2020},
	note = {ZSCC: 0000001},
	pages = {035023},
}

@article{maric_respiratory_2020,
	title = {Respiratory regulation \& interactions with neuro-cognitive circuitry},
	volume = {112},
	issn = {01497634},
	url = {https://linkinghub.elsevier.com/retrieve/pii/S0149763419301599},
	doi = {10.1016/j.neubiorev.2020.02.001},
	language = {en},
	urldate = {2020-07-17},
	journal = {Neuroscience \& Biobehavioral Reviews},
	author = {Maric, Vojislav and Ramanathan, Dhakshin and Mishra, Jyoti},
	month = may,
	year = {2020},
	note = {ZSCC: 0000001},
	pages = {95--106},
}

@article{judge_identifying_2020,
	title = {Identifying {Polyhedra} {Enabling} {Memorable} {Strategic} {Mapping}},
	url = {https://www.laetusinpraesens.org/docs10s/polypoly.php},
	language = {en},
	urldate = {2020-06-24},
	author = {Judge, Anthony},
	month = jun,
	year = {2020},
	note = {ZSCC: NoCitationData[s0]},
}

@article{holub_philosopher_2020,
	title = {The {Philosopher} as the {Therapist}: {A} {Lesson} from the {Past}},
	volume = {68},
	issn = {0035-7685, 2450-002X},
	shorttitle = {The {Philosopher} as the {Therapist}},
	url = {https://ojs.tnkul.pl/index.php/rf/article/view/10333},
	doi = {10.18290/rf20681-2},
	abstract = {Filozof jako terapeuta — lekcja z przeszłości 
Artykuł dotyczy filozofa, który może pełnić funkcję terapeuty. W pierwszej części ukazane są tendencje do postaw terapeutycznych dostrzegane w środowisku filozofów współczesnych zaangażowanych w tzw. ulepszanie człowieka. Wykorzystując najnowsze osiągnięcia genetyki, inżynierii genetycznej i farmakologii, filozofowie ci oferują terapie ukierunkowane na „ulepszenie” ludzkiej kondycji. W drugiej części artykułu ukazane są wybrane idee dotyczące terapii filozoficznej w postaci, jaką praktykowali niektórzy filozofowie starożytni. Ich propozycje opierały się zasadniczo na kontakcie osobowym, rozmowie i radach o charakterze mądrościowym. W kolejnej części artykułu te dwa podejścia są skontrastowane i porównane. Stanowiska współczesne podkreślają wagę nowych, technicznych metod ingerencji w życie człowieka, ale są ślepe, jeśli chodzi o ujęcie istotnych celów i dóbr ludzkich. Pomimo wielu poważnych różnic kulturowych współczesna terapia może się wiele nauczyć od tej rozwijanej w starożytności. Jeśli istota ludzka ma być poddana terapii praktykowanej przez filozofa, konieczne jest wzięcie pod uwagę jej integralnego obrazu. Oznacza to, że tak jej wnętrze, również jej zewnętrzność powinny stać się przedmiotem ewentualnego oddziaływania terapeutycznego.},
	language = {en},
	number = {1},
	urldate = {2020-06-24},
	journal = {Roczniki Filozoficzne},
	author = {Hołub, Grzegorz},
	month = mar,
	year = {2020},
	note = {ZSCC: 0000000},
	pages = {33--48},
}

Filozof jako terapeuta — lekcja z przeszłości Artykuł dotyczy filozofa, który może pełnić funkcję terapeuty. W pierwszej części ukazane są tendencje do postaw terapeutycznych dostrzegane w środowisku filozofów współczesnych zaangażowanych w tzw. ulepszanie człowieka. Wykorzystując najnowsze osiągnięcia genetyki, inżynierii genetycznej i farmakologii, filozofowie ci oferują terapie ukierunkowane na „ulepszenie” ludzkiej kondycji. W drugiej części artykułu ukazane są wybrane idee dotyczące terapii filozoficznej w postaci, jaką praktykowali niektórzy filozofowie starożytni. Ich propozycje opierały się zasadniczo na kontakcie osobowym, rozmowie i radach o charakterze mądrościowym. W kolejnej części artykułu te dwa podejścia są skontrastowane i porównane. Stanowiska współczesne podkreślają wagę nowych, technicznych metod ingerencji w życie człowieka, ale są ślepe, jeśli chodzi o ujęcie istotnych celów i dóbr ludzkich. Pomimo wielu poważnych różnic kulturowych współczesna terapia może się wiele nauczyć od tej rozwijanej w starożytności. Jeśli istota ludzka ma być poddana terapii praktykowanej przez filozofa, konieczne jest wzięcie pod uwagę jej integralnego obrazu. Oznacza to, że tak jej wnętrze, również jej zewnętrzność powinny stać się przedmiotem ewentualnego oddziaływania terapeutycznego.

@article{panaro_emerging_2020,
	title = {The {Emerging} {Role} of {Curcumin} in the {Modulation} of {TLR}-4 {Signaling} {Pathway}: {Focus} on {Neuroprotective} and {Anti}-{Rheumatic} {Properties}},
	volume = {21},
	issn = {1422-0067},
	shorttitle = {The {Emerging} {Role} of {Curcumin} in the {Modulation} of {TLR}-4 {Signaling} {Pathway}},
	url = {https://www.mdpi.com/1422-0067/21/7/2299},
	doi = {10.3390/ijms21072299},
	abstract = {Natural products have been used in medicine for thousands of years. Given their potential health benefits, they have gained significant popularity in recent times. The administration of phytochemicals existed shown to regulate differential gene expression and modulate various cellular pathways implicated in cell protection. Curcumin is a natural dietary polyphenol extracted from Curcuma Longa Linn with different biological and pharmacological effects. One of the important targets of curcumin is Toll-like receptor-4 (TLR-4), the receptor which plays a key role in the modulation of the immune responses and the stimulation of inflammatory chemokines and cytokines production. Different studies have demonstrated that curcumin attenuates inflammatory response via TLR-4 acting directly on receptor, or by its downstream pathway. Curcumin bioavailability is low, so the use of exosomes, as nano drug delivery, could improve the efficacy of curcumin in inflammatory diseases. The focus of this review is to explore the therapeutic effect of curcumin interacting with TLR-4 receptor and how this modulation could improve the prognosis of neuroinflammatory and rheumatic diseases.},
	language = {en},
	number = {7},
	urldate = {2020-05-22},
	journal = {International Journal of Molecular Sciences},
	author = {Panaro, Maria Antonietta and Corrado, Addolorata and Benameur, Tarek and Paolo, Cantatore Francesco and Cici, Daniela and Porro, Chiara},
	month = mar,
	year = {2020},
	note = {ZSCC: 0000000},
	pages = {2299},
}

Natural products have been used in medicine for thousands of years. Given their potential health benefits, they have gained significant popularity in recent times. The administration of phytochemicals existed shown to regulate differential gene expression and modulate various cellular pathways implicated in cell protection. Curcumin is a natural dietary polyphenol extracted from Curcuma Longa Linn with different biological and pharmacological effects. One of the important targets of curcumin is Toll-like receptor-4 (TLR-4), the receptor which plays a key role in the modulation of the immune responses and the stimulation of inflammatory chemokines and cytokines production. Different studies have demonstrated that curcumin attenuates inflammatory response via TLR-4 acting directly on receptor, or by its downstream pathway. Curcumin bioavailability is low, so the use of exosomes, as nano drug delivery, could improve the efficacy of curcumin in inflammatory diseases. The focus of this review is to explore the therapeutic effect of curcumin interacting with TLR-4 receptor and how this modulation could improve the prognosis of neuroinflammatory and rheumatic diseases.

@article{zager_modulating_2020,
	title = {Modulating the immune response with the wake-promoting drug modafinil: {A} potential therapeutic approach for inflammatory disorders},
	issn = {0889-1591},
	shorttitle = {Modulating the immune response with the wake-promoting drug modafinil},
	url = {http://www.sciencedirect.com/science/article/pii/S0889159119314953},
	doi = {10.1016/j.bbi.2020.04.038},
	abstract = {Modafinil is a psychostimulant drug approved by the FDA primarily for the treatment of sleep disorders such as narcolepsy, excessive daytime sleepiness and sleep apnea. Several documented but not yet approved uses for modafinil have been described over the last 30 years, including alleviating fatigue in neurological and neurodegenerative disorders. Recent evidence has suggested that modafinil may have an immunomodulatory effect. Here, we review the different effects of modafinil treatment in animal models of brain inflammation and peripheral immune function. We conclude that there is unequivocal evidence of an anti-inflammatory effect of modafinil in experimental animal models of brain inflammation and neurodegenerative disorders, including systemic inflammation and methamphetamine-induced neuroinflammation, Parkinson’s disease, brain ischemia, and multiple sclerosis. Modafinil acts on resident glial cells and infiltrating immune cells, negatively affecting both innate and adaptive immune responses in the brain. We also review the outcomes of modafinil treatment on peripheral immune function. The results of studies on this subject are still controversial and far from conclusive, but point to a new avenue of research in relation to peripheral inflammation. The data reviewed here raise the possibility of modafinil being used as adjuvant treatment for neurological disorders in which inflammation plays an important role.},
	language = {en},
	urldate = {2020-05-22},
	journal = {Brain, Behavior, and Immunity},
	author = {Zager, Adriano},
	month = apr,
	year = {2020},
	keywords = {Dopamine, Immunity, Inflammation, Macrophages, Microglia, Modafinil, T cells},
}

Modafinil is a psychostimulant drug approved by the FDA primarily for the treatment of sleep disorders such as narcolepsy, excessive daytime sleepiness and sleep apnea. Several documented but not yet approved uses for modafinil have been described over the last 30 years, including alleviating fatigue in neurological and neurodegenerative disorders. Recent evidence has suggested that modafinil may have an immunomodulatory effect. Here, we review the different effects of modafinil treatment in animal models of brain inflammation and peripheral immune function. We conclude that there is unequivocal evidence of an anti-inflammatory effect of modafinil in experimental animal models of brain inflammation and neurodegenerative disorders, including systemic inflammation and methamphetamine-induced neuroinflammation, Parkinson’s disease, brain ischemia, and multiple sclerosis. Modafinil acts on resident glial cells and infiltrating immune cells, negatively affecting both innate and adaptive immune responses in the brain. We also review the outcomes of modafinil treatment on peripheral immune function. The results of studies on this subject are still controversial and far from conclusive, but point to a new avenue of research in relation to peripheral inflammation. The data reviewed here raise the possibility of modafinil being used as adjuvant treatment for neurological disorders in which inflammation plays an important role.

@article{nikpour_metformin_2020,
	title = {Metformin in {SLE}: metabolism as a therapeutic target in autoimmune disease},
	volume = {2},
	issn = {2665-9913},
	shorttitle = {Metformin in {SLE}},
	url = {https://www.thelancet.com/journals/lanrhe/article/PIIS2665-9913(20)30040-0/abstract},
	doi = {10.1016/S2665-9913(20)30040-0},
	abstract = {The central role of metabolism in the modulation of immune responses is increasingly
recognised in the pathogenesis of autoimmune diseases such as systemic lupus erythematosus
(SLE).1 Accordingly, it is not implausible that metformin, an anti-diabetic drug that
regulates systemic and cellular metabolism, might have a disease-modifying effect
in SLE. Indeed, metformin has been shown to have metabolic effects in many lineages
of immune cell, including T-helper and regulatory T cells, neutrophils, and dendritic
cells, which are all key mediators of the autoimmunity and inflammation that are characteristic
of SLE.},
	language = {English},
	number = {4},
	urldate = {2020-05-22},
	journal = {The Lancet Rheumatology},
	author = {Nikpour, Mandana},
	month = apr,
	year = {2020},
	note = {Publisher: Elsevier},
	pages = {e196--e197},
}

The central role of metabolism in the modulation of immune responses is increasingly recognised in the pathogenesis of autoimmune diseases such as systemic lupus erythematosus (SLE).1 Accordingly, it is not implausible that metformin, an anti-diabetic drug that regulates systemic and cellular metabolism, might have a disease-modifying effect in SLE. Indeed, metformin has been shown to have metabolic effects in many lineages of immune cell, including T-helper and regulatory T cells, neutrophils, and dendritic cells, which are all key mediators of the autoimmunity and inflammation that are characteristic of SLE.

@article{fava_decline_2020,
	title = {The {Decline} of {Pluralism} in {Medicine}: {Dissent} {Is} {Welcome}},
	volume = {89},
	issn = {0033-3190, 1423-0348},
	shorttitle = {The {Decline} of {Pluralism} in {Medicine}},
	url = {https://www.karger.com/Article/FullText/505085},
	doi = {10.1159/000505085},
	language = {en},
	number = {1},
	urldate = {2020-04-24},
	journal = {Psychotherapy and Psychosomatics},
	author = {Fava, Giovanni A.},
	year = {2020},
	note = {ZSCC: 0000001},
	pages = {1--5},
}

@article{krumrei-mancuso_links_2020,
	title = {Links between intellectual humility and acquiring knowledge},
	volume = {15},
	issn = {1743-9760, 1743-9779},
	url = {https://www.tandfonline.com/doi/full/10.1080/17439760.2019.1579359},
	doi = {10.1080/17439760.2019.1579359},
	abstract = {Five studies (N = 1,189) examined how intellectual humility (IH) relates to acquiring knowledge (learning). IH was associated with more general knowledge, but was unrelated to cognitive ability, and associated with slightly lower GPA. Findings were also mixed for meta-cognition. IH was associated with less claiming of knowledge one doesn’t have, indicating a more accurate assessment of one’s knowledge. However, IH was also associated with underestimating one’s cognitive ability. The differences may have resulted from using multiple measures of IH, each tapping unique aspects of the construct. Finally, IH was associated with a variety of characteristics associated with knowledge acquisition, including reflective thinking, need for cognition, intellectual engagement, curiosity, intellectual openness, and open-minded thinking. IH was also associated with less social vigilantism, which may promote collaborative learning. Finally, IH was associated with an intrinsic motivation to learn. These links may help explain the observed relationship between IH and possessing more knowledge.},
	language = {en},
	number = {2},
	urldate = {2020-04-05},
	journal = {The Journal of Positive Psychology},
	author = {Krumrei-Mancuso, Elizabeth J. and Haggard, Megan C. and LaBouff, Jordan P. and Rowatt, Wade C.},
	month = mar,
	year = {2020},
	note = {ZSCC: NoCitationData[s0]},
	pages = {155--170},
}

Five studies (N = 1,189) examined how intellectual humility (IH) relates to acquiring knowledge (learning). IH was associated with more general knowledge, but was unrelated to cognitive ability, and associated with slightly lower GPA. Findings were also mixed for meta-cognition. IH was associated with less claiming of knowledge one doesn’t have, indicating a more accurate assessment of one’s knowledge. However, IH was also associated with underestimating one’s cognitive ability. The differences may have resulted from using multiple measures of IH, each tapping unique aspects of the construct. Finally, IH was associated with a variety of characteristics associated with knowledge acquisition, including reflective thinking, need for cognition, intellectual engagement, curiosity, intellectual openness, and open-minded thinking. IH was also associated with less social vigilantism, which may promote collaborative learning. Finally, IH was associated with an intrinsic motivation to learn. These links may help explain the observed relationship between IH and possessing more knowledge.

@article{aftab_conceptual_2020,
	title = {Conceptual {Competence} in {Psychiatry}: {Recommendations} for {Education} and {Training}},
	issn = {1545-7230},
	shorttitle = {Conceptual {Competence} in {Psychiatry}},
	url = {https://doi.org/10.1007/s40596-020-01183-3},
	doi = {10.1007/s40596-020-01183-3},
	language = {en},
	urldate = {2020-03-23},
	journal = {Academic Psychiatry},
	author = {Aftab, Awais and Waterman, G. Scott},
	month = jan,
	year = {2020},
}

@article{horien_complexity_2020,
	title = {Complexity, {Intellectual} {Humility}, and the {Psychiatric} {Trainee}},
	issn = {1042-9670, 1545-7230},
	url = {http://link.springer.com/10.1007/s40596-020-01217-w},
	doi = {10.1007/s40596-020-01217-w},
	language = {en},
	urldate = {2020-03-20},
	journal = {Academic Psychiatry},
	author = {Horien, Corey and Bommersbach, Tanner},
	month = mar,
	year = {2020},
	pages = {s40596--020--01217--w},
}

@article{marder_schizophrenia_2019,
	title = {Schizophrenia},
	volume = {381},
	issn = {0028-4793, 1533-4406},
	url = {http://www.nejm.org/doi/10.1056/NEJMra1808803},
	doi = {10.1056/NEJMra1808803},
	language = {en},
	number = {18},
	urldate = {2022-05-29},
	journal = {New England Journal of Medicine},
	author = {Marder, Stephen R. and Cannon, Tyrone D.},
	editor = {Ropper, Allan H.},
	month = oct,
	year = {2019},
	note = {Number: 18},
	pages = {1753--1761},
}

@article{corlett_hallucinations_2019,
	title = {Hallucinations and {Strong} {Priors}},
	volume = {23},
	issn = {1879-307X},
	doi = {10.1016/j.tics.2018.12.001},
	abstract = {Hallucinations, perceptions in the absence of objectively identifiable stimuli, illustrate the constructive nature of perception. Here, we highlight the role of prior beliefs as a critical elicitor of hallucinations. Recent empirical work from independent laboratories shows strong, overly precise priors can engender hallucinations in healthy subjects and that individuals who hallucinate in the real world are more susceptible to these laboratory phenomena. We consider these observations in light of work demonstrating apparently weak, or imprecise, priors in psychosis. Appreciating the interactions within and between hierarchies of inference can reconcile this apparent disconnect. Data from neural networks, human behavior, and neuroimaging support this contention. This work underlines the continuum from normal to aberrant perception, encouraging a more empathic approach to clinical hallucinations.},
	language = {eng},
	number = {2},
	journal = {Trends in Cognitive Sciences},
	author = {Corlett, Philip R. and Horga, Guillermo and Fletcher, Paul C. and Alderson-Day, Ben and Schmack, Katharina and Powers, Albert R.},
	month = feb,
	year = {2019},
	pmid = {30583945},
	pmcid = {PMC6368358},
	note = {Number: 2},
	keywords = {Hallucinations, Humans, Illusions, Nerve Net, Speech Perception, auditory verbal hallucinations, hallucinations, predictive coding, prior beliefs, psychosis},
	pages = {114--127},
}

Hallucinations, perceptions in the absence of objectively identifiable stimuli, illustrate the constructive nature of perception. Here, we highlight the role of prior beliefs as a critical elicitor of hallucinations. Recent empirical work from independent laboratories shows strong, overly precise priors can engender hallucinations in healthy subjects and that individuals who hallucinate in the real world are more susceptible to these laboratory phenomena. We consider these observations in light of work demonstrating apparently weak, or imprecise, priors in psychosis. Appreciating the interactions within and between hierarchies of inference can reconcile this apparent disconnect. Data from neural networks, human behavior, and neuroimaging support this contention. This work underlines the continuum from normal to aberrant perception, encouraging a more empathic approach to clinical hallucinations.

@article{cinel_neurotechnologies_2019,
	title = {Neurotechnologies for {Human} {Cognitive} {Augmentation}: {Current} {State} of the {Art} and {Future} {Prospects}},
	volume = {13},
	issn = {1662-5161},
	shorttitle = {Neurotechnologies for {Human} {Cognitive} {Augmentation}},
	url = {https://www.frontiersin.org/articles/10.3389/fnhum.2019.00013},
	abstract = {Recent advances in neuroscience have paved the way to innovative applications that cognitively augment and enhance humans in a variety of contexts. This paper aims at providing a snapshot of the current state of the art and a motivated forecast of the most likely developments in the next two decades. Firstly, we survey the main neuroscience technologies for both observing and influencing brain activity, which are necessary ingredients for human cognitive augmentation. We also compare and contrast such technologies, as their individual characteristics (e.g., spatio-temporal resolution, invasiveness, portability, energy requirements, and cost) influence their current and future role in human cognitive augmentation. Secondly, we chart the state of the art on neurotechnologies for human cognitive augmentation, keeping an eye both on the applications that already exist and those that are emerging or are likely to emerge in the next two decades. Particularly, we consider applications in the areas of communication, cognitive enhancement, memory, attention monitoring/enhancement, situation awareness and complex problem solving, and we look at what fraction of the population might benefit from such technologies and at the demands they impose in terms of user training. Thirdly, we briefly review the ethical issues associated with current neuroscience technologies. These are important because they may differentially influence both present and future research on (and adoption of) neurotechnologies for human cognitive augmentation: an inferior technology with no significant ethical issues may thrive while a superior technology causing widespread ethical concerns may end up being outlawed. Finally, based on the lessons learned in our analysis, using past trends and considering other related forecasts, we attempt to forecast the most likely future developments of neuroscience technology for human cognitive augmentation and provide informed recommendations for promising future research and exploitation avenues.},
	urldate = {2022-10-31},
	journal = {Frontiers in Human Neuroscience},
	author = {Cinel, Caterina and Valeriani, Davide and Poli, Riccardo},
	year = {2019},
}

Recent advances in neuroscience have paved the way to innovative applications that cognitively augment and enhance humans in a variety of contexts. This paper aims at providing a snapshot of the current state of the art and a motivated forecast of the most likely developments in the next two decades. Firstly, we survey the main neuroscience technologies for both observing and influencing brain activity, which are necessary ingredients for human cognitive augmentation. We also compare and contrast such technologies, as their individual characteristics (e.g., spatio-temporal resolution, invasiveness, portability, energy requirements, and cost) influence their current and future role in human cognitive augmentation. Secondly, we chart the state of the art on neurotechnologies for human cognitive augmentation, keeping an eye both on the applications that already exist and those that are emerging or are likely to emerge in the next two decades. Particularly, we consider applications in the areas of communication, cognitive enhancement, memory, attention monitoring/enhancement, situation awareness and complex problem solving, and we look at what fraction of the population might benefit from such technologies and at the demands they impose in terms of user training. Thirdly, we briefly review the ethical issues associated with current neuroscience technologies. These are important because they may differentially influence both present and future research on (and adoption of) neurotechnologies for human cognitive augmentation: an inferior technology with no significant ethical issues may thrive while a superior technology causing widespread ethical concerns may end up being outlawed. Finally, based on the lessons learned in our analysis, using past trends and considering other related forecasts, we attempt to forecast the most likely future developments of neuroscience technology for human cognitive augmentation and provide informed recommendations for promising future research and exploitation avenues.

@article{corlett_hallucinations_2019,
	title = {Hallucinations and {Strong} {Priors}},
	volume = {23},
	issn = {1879-307X},
	doi = {10.1016/j.tics.2018.12.001},
	abstract = {Hallucinations, perceptions in the absence of objectively identifiable stimuli, illustrate the constructive nature of perception. Here, we highlight the role of prior beliefs as a critical elicitor of hallucinations. Recent empirical work from independent laboratories shows strong, overly precise priors can engender hallucinations in healthy subjects and that individuals who hallucinate in the real world are more susceptible to these laboratory phenomena. We consider these observations in light of work demonstrating apparently weak, or imprecise, priors in psychosis. Appreciating the interactions within and between hierarchies of inference can reconcile this apparent disconnect. Data from neural networks, human behavior, and neuroimaging support this contention. This work underlines the continuum from normal to aberrant perception, encouraging a more empathic approach to clinical hallucinations.},
	language = {eng},
	number = {2},
	journal = {Trends in Cognitive Sciences},
	author = {Corlett, Philip R. and Horga, Guillermo and Fletcher, Paul C. and Alderson-Day, Ben and Schmack, Katharina and Powers, Albert R.},
	month = feb,
	year = {2019},
	pmid = {30583945},
	pmcid = {PMC6368358},
	keywords = {Hallucinations, Humans, Illusions, Nerve Net, Speech Perception, auditory verbal hallucinations, hallucinations, predictive coding, prior beliefs, psychosis},
	pages = {114--127},
}

Hallucinations, perceptions in the absence of objectively identifiable stimuli, illustrate the constructive nature of perception. Here, we highlight the role of prior beliefs as a critical elicitor of hallucinations. Recent empirical work from independent laboratories shows strong, overly precise priors can engender hallucinations in healthy subjects and that individuals who hallucinate in the real world are more susceptible to these laboratory phenomena. We consider these observations in light of work demonstrating apparently weak, or imprecise, priors in psychosis. Appreciating the interactions within and between hierarchies of inference can reconcile this apparent disconnect. Data from neural networks, human behavior, and neuroimaging support this contention. This work underlines the continuum from normal to aberrant perception, encouraging a more empathic approach to clinical hallucinations.

@article{ropper_schizophrenia_2019,
	title = {Schizophrenia},
	volume = {381},
	issn = {0028-4793, 1533-4406},
	url = {http://www.nejm.org/doi/10.1056/NEJMra1808803},
	doi = {10.1056/NEJMra1808803},
	language = {en},
	number = {18},
	urldate = {2022-05-29},
	journal = {New England Journal of Medicine},
	author = {Marder, Stephen R. and Cannon, Tyrone D.},
	editor = {Ropper, Allan H.},
	month = oct,
	year = {2019},
	pages = {1753--1761},
}

@misc{whackthewheeze_bupropion_2019,
	type = {Reddit {Post}},
	title = {Bupropion ({Wellbutrin}) and impact on sexual drive/arousal?},
	url = {www.reddit.com/r/sexover30/comments/acpxnf/bupropion_wellbutrin_and_impact_on_sexual/},
	urldate = {2021-12-28},
	journal = {r/sexover30},
	author = {whackthewheeze},
	month = jan,
	year = {2019},
}

@article{murray_beginners_2019,
	title = {A {Beginner}'s and {Expert}'s {Developmental} {Guide}},
	volume = {15},
	language = {en},
	number = {1},
	author = {Murray, Tom},
	year = {2019},
	pages = {139},
}

@article{greenhalgh_frameworks_2019,
	title = {Frameworks for supporting patient and public involvement in research: {Systematic} review and co-design pilot},
	volume = {22},
	issn = {1369-7625},
	shorttitle = {Frameworks for supporting patient and public involvement in research},
	url = {https://onlinelibrary.wiley.com/doi/abs/10.1111/hex.12888},
	doi = {10.1111/hex.12888},
	abstract = {Background Numerous frameworks for supporting, evaluating and reporting patient and public involvement in research exist. The literature is diverse and theoretically heterogeneous. Objectives To identify and synthesize published frameworks, consider whether and how these have been used, and apply design principles to improve usability. Search strategy Keyword search of six databases; hand search of eight journals; ancestry and snowball search; requests to experts. Inclusion criteria Published, systematic approaches (frameworks) designed to support, evaluate or report on patient or public involvement in health-related research. Data extraction and synthesis Data were extracted on provenance; collaborators and sponsors; theoretical basis; lay input; intended user(s) and use(s); topics covered; examples of use; critiques; and updates. We used the Canadian Centre for Excellence on Partnerships with Patients and Public (CEPPP) evaluation tool and hermeneutic methodology to grade and synthesize the frameworks. In five co-design workshops, we tested evidence-based resources based on the review findings. Results Our final data set consisted of 65 frameworks, most of which scored highly on the CEPPP tool. They had different provenances, intended purposes, strengths and limitations. We grouped them into five categories: power-focused; priority-setting; study-focused; report-focused; and partnership-focused. Frameworks were used mainly by the groups who developed them. The empirical component of our study generated a structured format and evidence-based facilitator notes for a “build your own framework” co-design workshop. Conclusion The plethora of frameworks combined with evidence of limited transferability suggests that a single, off-the-shelf framework may be less useful than a menu of evidence-based resources which stakeholders can use to co-design their own frameworks.},
	language = {en},
	number = {4},
	urldate = {2021-07-12},
	journal = {Health Expectations},
	author = {Greenhalgh, Trisha and Hinton, Lisa and Finlay, Teresa and Macfarlane, Alastair and Fahy, Nick and Clyde, Ben and Chant, Alan},
	year = {2019},
	note = {\_eprint: https://onlinelibrary.wiley.com/doi/pdf/10.1111/hex.12888},
	keywords = {codesign, framework, hermeneutic review, patient and public involvement, systematic review},
	pages = {785--801},
}

Background Numerous frameworks for supporting, evaluating and reporting patient and public involvement in research exist. The literature is diverse and theoretically heterogeneous. Objectives To identify and synthesize published frameworks, consider whether and how these have been used, and apply design principles to improve usability. Search strategy Keyword search of six databases; hand search of eight journals; ancestry and snowball search; requests to experts. Inclusion criteria Published, systematic approaches (frameworks) designed to support, evaluate or report on patient or public involvement in health-related research. Data extraction and synthesis Data were extracted on provenance; collaborators and sponsors; theoretical basis; lay input; intended user(s) and use(s); topics covered; examples of use; critiques; and updates. We used the Canadian Centre for Excellence on Partnerships with Patients and Public (CEPPP) evaluation tool and hermeneutic methodology to grade and synthesize the frameworks. In five co-design workshops, we tested evidence-based resources based on the review findings. Results Our final data set consisted of 65 frameworks, most of which scored highly on the CEPPP tool. They had different provenances, intended purposes, strengths and limitations. We grouped them into five categories: power-focused; priority-setting; study-focused; report-focused; and partnership-focused. Frameworks were used mainly by the groups who developed them. The empirical component of our study generated a structured format and evidence-based facilitator notes for a “build your own framework” co-design workshop. Conclusion The plethora of frameworks combined with evidence of limited transferability suggests that a single, off-the-shelf framework may be less useful than a menu of evidence-based resources which stakeholders can use to co-design their own frameworks.

@article{stanley_why_2019,
	title = {Why {Open}-{Endedness} {Matters}},
	volume = {25},
	issn = {1530-9185},
	doi = {10.1162/artl_a_00294},
	abstract = {Rather than acting as a review or analysis of the field, this essay focuses squarely on the motivations for investigating open-endedness and the opportunities it opens up. It begins by contemplating the awesome accomplishments of evolution in nature and the profound implications if such a process could be ignited on a computer. Some of the milestones in our understanding so far are then discussed, finally closing by highlighting the grand challenge of formalizing open-endedness as a computational process that can be encoded as an algorithm. The main contribution is to articulate why open-endedness deserves a place alongside artificial intelligence as one of the great computational challenges, and opportunities, of our time.},
	language = {eng},
	number = {3},
	journal = {Artificial Life},
	author = {Stanley, Kenneth O.},
	year = {2019},
	pmid = {31397603},
	note = {ZSCC: 0000011 },
	keywords = {Algorithms, Artificial Intelligence, Biological Evolution, Computational Biology, Models, Theoretical, Open-endedness, artificial intelligence, machine learning, novelty search, open-ended algorithms, open-ended evolution, quality diversity},
	pages = {232--235},
}

Rather than acting as a review or analysis of the field, this essay focuses squarely on the motivations for investigating open-endedness and the opportunities it opens up. It begins by contemplating the awesome accomplishments of evolution in nature and the profound implications if such a process could be ignited on a computer. Some of the milestones in our understanding so far are then discussed, finally closing by highlighting the grand challenge of formalizing open-endedness as a computational process that can be encoded as an algorithm. The main contribution is to articulate why open-endedness deserves a place alongside artificial intelligence as one of the great computational challenges, and opportunities, of our time.

@article{corlett_hallucinations_2019,
	title = {Hallucinations and {Strong} {Priors}},
	volume = {23},
	issn = {1364-6613},
	url = {https://www.sciencedirect.com/science/article/pii/S1364661318302821},
	doi = {10.1016/j.tics.2018.12.001},
	abstract = {Hallucinations, perceptions in the absence of objectively identifiable stimuli, illustrate the constructive nature of perception. Here, we highlight the role of prior beliefs as a critical elicitor of hallucinations. Recent empirical work from independent laboratories shows strong, overly precise priors can engender hallucinations in healthy subjects and that individuals who hallucinate in the real world are more susceptible to these laboratory phenomena. We consider these observations in light of work demonstrating apparently weak, or imprecise, priors in psychosis. Appreciating the interactions within and between hierarchies of inference can reconcile this apparent disconnect. Data from neural networks, human behavior, and neuroimaging support this contention. This work underlines the continuum from normal to aberrant perception, encouraging a more empathic approach to clinical hallucinations.},
	language = {en},
	number = {2},
	urldate = {2021-06-05},
	journal = {Trends in Cognitive Sciences},
	author = {Corlett, Philip R. and Horga, Guillermo and Fletcher, Paul C. and Alderson-Day, Ben and Schmack, Katharina and Powers, Albert R.},
	month = feb,
	year = {2019},
	note = {ZSCC: 0000202},
	keywords = {auditory verbal hallucinations, hallucinations, predictive coding, prior beliefs, psychosis},
	pages = {114--127},
}

Hallucinations, perceptions in the absence of objectively identifiable stimuli, illustrate the constructive nature of perception. Here, we highlight the role of prior beliefs as a critical elicitor of hallucinations. Recent empirical work from independent laboratories shows strong, overly precise priors can engender hallucinations in healthy subjects and that individuals who hallucinate in the real world are more susceptible to these laboratory phenomena. We consider these observations in light of work demonstrating apparently weak, or imprecise, priors in psychosis. Appreciating the interactions within and between hierarchies of inference can reconcile this apparent disconnect. Data from neural networks, human behavior, and neuroimaging support this contention. This work underlines the continuum from normal to aberrant perception, encouraging a more empathic approach to clinical hallucinations.

@article{corlett_hallucinations_2019-1,
	title = {Hallucinations and {Strong} {Priors}},
	volume = {23},
	issn = {1364-6613},
	url = {https://www.sciencedirect.com/science/article/pii/S1364661318302821},
	doi = {10.1016/j.tics.2018.12.001},
	abstract = {Hallucinations, perceptions in the absence of objectively identifiable stimuli, illustrate the constructive nature of perception. Here, we highlight the role of prior beliefs as a critical elicitor of hallucinations. Recent empirical work from independent laboratories shows strong, overly precise priors can engender hallucinations in healthy subjects and that individuals who hallucinate in the real world are more susceptible to these laboratory phenomena. We consider these observations in light of work demonstrating apparently weak, or imprecise, priors in psychosis. Appreciating the interactions within and between hierarchies of inference can reconcile this apparent disconnect. Data from neural networks, human behavior, and neuroimaging support this contention. This work underlines the continuum from normal to aberrant perception, encouraging a more empathic approach to clinical hallucinations.},
	language = {en},
	number = {2},
	urldate = {2021-06-06},
	journal = {Trends in Cognitive Sciences},
	author = {Corlett, Philip R. and Horga, Guillermo and Fletcher, Paul C. and Alderson-Day, Ben and Schmack, Katharina and Powers, Albert R.},
	month = feb,
	year = {2019},
	note = {ZSCC: 0000202},
	keywords = {auditory verbal hallucinations, hallucinations, predictive coding, prior beliefs, psychosis},
	pages = {114--127},
}

Hallucinations, perceptions in the absence of objectively identifiable stimuli, illustrate the constructive nature of perception. Here, we highlight the role of prior beliefs as a critical elicitor of hallucinations. Recent empirical work from independent laboratories shows strong, overly precise priors can engender hallucinations in healthy subjects and that individuals who hallucinate in the real world are more susceptible to these laboratory phenomena. We consider these observations in light of work demonstrating apparently weak, or imprecise, priors in psychosis. Appreciating the interactions within and between hierarchies of inference can reconcile this apparent disconnect. Data from neural networks, human behavior, and neuroimaging support this contention. This work underlines the continuum from normal to aberrant perception, encouraging a more empathic approach to clinical hallucinations.

@article{milham_be_2019,
	title = {Be the change you seek in science},
	volume = {17},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6436210/},
	doi = {10.1186/s12915-019-0647-3},
	abstract = {Few would argue that science is better done in silos, with no transparency or sharing of methods and resources. Yet scientists and scientific stakeholders (e.g., academic institutions, funding agencies, journals) alike continue to find themselves at a ...},
	language = {en},
	urldate = {2021-04-22},
	journal = {BMC Biology},
	author = {Milham, Michael P. and Klein, Arno},
	year = {2019},
	pmid = {30914050},
	note = {Publisher: BioMed Central},
}

Few would argue that science is better done in silos, with no transparency or sharing of methods and resources. Yet scientists and scientific stakeholders (e.g., academic institutions, funding agencies, journals) alike continue to find themselves at a ...

@article{han_tolerating_2019,
	title = {Tolerating uncertainty about conceptual models of uncertainty in health care},
	volume = {25},
	issn = {1365-2753},
	url = {https://onlinelibrary.wiley.com/doi/abs/10.1111/jep.13110},
	doi = {10.1111/jep.13110},
	language = {en},
	number = {2},
	urldate = {2020-10-24},
	journal = {Journal of Evaluation in Clinical Practice},
	author = {Han, Paul K. J. and Djulbegovic, Benjamin},
	year = {2019},
	note = {ZSCC: 0000006},
	pages = {183--185},
}

@article{holliman_visual_2019,
	title = {Visual {Entropy} and the {Visualization} of {Uncertainty}},
	url = {http://arxiv.org/abs/1907.12879},
	abstract = {Background: It is possible to find many different visual representations of data values in visualizations, it is less common to see visual representations that include uncertainty, especially in visualizations intended for non-technical audiences. Objective: our aim is to rigorously define and evaluate the novel use of visual entropy as a measure of shape that allows us to construct an ordered scale of glyphs for use in representing both uncertainty and value in 2D and 3D environments. Method: We use sample entropy as a numerical measure of visual entropy to construct a set of glyphs using R and Blender which vary in their complexity. Results: A Bradley-Terry analysis of a pairwise comparison of the glyphs shows participants (n=19) ordered the glyphs as predicted by the visual entropy score (linear regression R2 {\textbackslash}textgreater0.97, p{\textbackslash}textless0.001). We also evaluate whether the glyphs can effectively represent uncertainty using a signal detection method, participants (n=15) were able to search for glyphs representing uncertainty with high sensitivity and low error rates. Conclusion: visual entropy is a novel cue for representing ordered data and provides a channel that allows the uncertainty of a measure to be presented alongside its mean value.},
	urldate = {2020-10-14},
	journal = {arXiv:1907.12879 [cs, math]},
	author = {Holliman, Nicolas S. and Coltekin, Arzu and Fernstad, Sara J. and Simpson, Michael D. and Wilson, Kevin J. and Woods, Andrew J.},
	month = jul,
	year = {2019},
	note = {ZSCC: 0000003},
	keywords = {Computer Science - Graphics, Computer Science - Human-Computer Interaction, Computer Science - Information Theory},
}

Background: It is possible to find many different visual representations of data values in visualizations, it is less common to see visual representations that include uncertainty, especially in visualizations intended for non-technical audiences. Objective: our aim is to rigorously define and evaluate the novel use of visual entropy as a measure of shape that allows us to construct an ordered scale of glyphs for use in representing both uncertainty and value in 2D and 3D environments. Method: We use sample entropy as a numerical measure of visual entropy to construct a set of glyphs using R and Blender which vary in their complexity. Results: A Bradley-Terry analysis of a pairwise comparison of the glyphs shows participants (n=19) ordered the glyphs as predicted by the visual entropy score (linear regression R2 \textgreater0.97, p\textless0.001). We also evaluate whether the glyphs can effectively represent uncertainty using a signal detection method, participants (n=15) were able to search for glyphs representing uncertainty with high sensitivity and low error rates. Conclusion: visual entropy is a novel cue for representing ordered data and provides a channel that allows the uncertainty of a measure to be presented alongside its mean value.

@article{elsner_beyond_2019,
	title = {Beyond {Medical} {Paternalism}: {Undoing} the {Doctor}-{Patient} {Relationship} in {Simone} de {Beauvoir}'s {A} {Very} {Easy} {Death}},
	volume = {37},
	issn = {1080-6571},
	shorttitle = {Beyond {Medical} {Paternalism}},
	url = {https://muse.jhu.edu/article/745344},
	doi = {10.1353/lm.2019.0019},
	abstract = {In A Very Easy Death Simone de Beauvoir documents the illness, hospitalization, and death of her mother Françoise. Critics in the fields of bioethics and the medical humanities have concentrated on the text’s paternalistic doctor-patient encounter, which culminates in the withholding of the cancer diagnosis from Beauvoir’s mother and entails an unnecessary medical intervention to which the patient never consents. Reviewing the text’s reception, this article argues that a focus on the ways in which it depicts breaches of several tenets of medical ethics have decontextualized A Very Easy Death and occluded the key role Beauvoir plays in the doctor-patient relationship. By situating the text within Beauvoir’s œuvre and debates in French philosophy of medicine at the time of publication, this article proposes that Beauvoir’s part in the withholding of the cancer diagnosis emerges less as a submission to medical paternalism than as a form of maternal caregiving.},
	language = {en},
	number = {2},
	urldate = {2020-03-25},
	journal = {Literature and Medicine},
	author = {Elsner, Anna Magdalena},
	month = dec,
	year = {2019},
	note = {ZSCC: 0000000},
	pages = {420--441},
}

In A Very Easy Death Simone de Beauvoir documents the illness, hospitalization, and death of her mother Françoise. Critics in the fields of bioethics and the medical humanities have concentrated on the text’s paternalistic doctor-patient encounter, which culminates in the withholding of the cancer diagnosis from Beauvoir’s mother and entails an unnecessary medical intervention to which the patient never consents. Reviewing the text’s reception, this article argues that a focus on the ways in which it depicts breaches of several tenets of medical ethics have decontextualized A Very Easy Death and occluded the key role Beauvoir plays in the doctor-patient relationship. By situating the text within Beauvoir’s œuvre and debates in French philosophy of medicine at the time of publication, this article proposes that Beauvoir’s part in the withholding of the cancer diagnosis emerges less as a submission to medical paternalism than as a form of maternal caregiving.

@article{dellazizzo_comprehensive_2019,
	title = {Comprehensive review on virtual reality for the treatment of violence: implications for youth with schizophrenia},
	volume = {5},
	copyright = {2019 The Author(s)},
	issn = {2334-265X},
	shorttitle = {Comprehensive review on virtual reality for the treatment of violence},
	url = {https://www.nature.com/articles/s41537-019-0079-7},
	doi = {10.1038/s41537-019-0079-7},
	abstract = {Youth violence is a complex and multifactorial issue that has severe health and social consequences. While treatment options exist to treat/reduce violence in at-risk populations such as schizophrenia, there remains limitations in the efficacy of current interventions. Virtual reality (VR) appears to be a unique possibility to expose offenders and to train coping skills in virtual situations that are capable of eliciting aggression‐relevant behavior without threatening others. The focus of this paper is to provide a comprehensive review of studies using VR to manage violence across several at-risk populations, with a particular emphasis on youth with schizophrenia. Despite the encouraging success of VR applications for the treatment of different mental health problems, no studies have explored the usability of VR to specifically treat violence in patients with schizophrenia. A limited number of studies have focused on violence risk factors in other mental health problems (i.e., emotion regulation in individual suffering from post-traumatic disorders) that may be targeted in treatments to reduce the risk of violence. The preliminary studies using VR as a therapeutic element have shown reductions in anger, improvements in conflict-resolution skills as well as in empathy levels, and decreases in aggression. Possible applications of these interventions in youth with schizophrenia will be discussed.},
	language = {en},
	number = {1},
	urldate = {2021-04-10},
	journal = {npj Schizophrenia},
	author = {Dellazizzo, Laura and Potvin, Stéphane and Bahig, Sami and Dumais, Alexandre},
	month = jul,
	year = {2019},
	note = {ZSCC: 0000007 
Number: 1
Publisher: Nature Publishing Group},
	pages = {1--12},
}

Youth violence is a complex and multifactorial issue that has severe health and social consequences. While treatment options exist to treat/reduce violence in at-risk populations such as schizophrenia, there remains limitations in the efficacy of current interventions. Virtual reality (VR) appears to be a unique possibility to expose offenders and to train coping skills in virtual situations that are capable of eliciting aggression‐relevant behavior without threatening others. The focus of this paper is to provide a comprehensive review of studies using VR to manage violence across several at-risk populations, with a particular emphasis on youth with schizophrenia. Despite the encouraging success of VR applications for the treatment of different mental health problems, no studies have explored the usability of VR to specifically treat violence in patients with schizophrenia. A limited number of studies have focused on violence risk factors in other mental health problems (i.e., emotion regulation in individual suffering from post-traumatic disorders) that may be targeted in treatments to reduce the risk of violence. The preliminary studies using VR as a therapeutic element have shown reductions in anger, improvements in conflict-resolution skills as well as in empathy levels, and decreases in aggression. Possible applications of these interventions in youth with schizophrenia will be discussed.

@article{kim_statins_2019,
	title = {Statins and {Inflammation}: {New} {Therapeutic} {Opportunities} in {Psychiatry}},
	volume = {10},
	issn = {1664-0640},
	shorttitle = {Statins and {Inflammation}},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6413672/},
	doi = {10.3389/fpsyt.2019.00103},
	abstract = {Statins, which are widely used to treat hypercholesterolemia, have anti-inflammatory and anti-oxidant effects. These are thought to be responsible for the potential effects of statins on various psychiatric disorders. In this study, we comprehensively review the literature to investigate the effects of statins on various psychiatric disorders including depression, schizophrenia, and dementia. In addition, we review adverse effects and drug interactions of statins to give clinically useful information guiding statin use in the psychiatric field. Statins seem useful in reducing depression, particularly in patients with physical disorders such as cardiovascular disease. In patients with schizophrenia, negative symptoms may be reduced by adjuvant statin therapy. Studies on cohorts at risk for dementia have generally shown protective effects of statins, while those on treatment for dementia show inconsistent results. In conclusion, statins used in combination with conventional psychotropic medications may be effective for various psychiatric disorders including depression, schizophrenia, and dementia. Further study is required to determine optimal doses and duration of statin use for the treatment of psychiatric disorders.},
	urldate = {2021-04-10},
	journal = {Frontiers in Psychiatry},
	author = {Kim, Sung-Wan and Kang, Hee-Ju and Jhon, Min and Kim, Ju-Wan and Lee, Ju-Yeon and Walker, Adam J. and Agustini, Bruno and Kim, Jae-Min and Berk, Michael},
	month = mar,
	year = {2019},
	pmid = {30890971},
	pmcid = {PMC6413672},
	note = {ZSCC: 0000020 },
}

Statins, which are widely used to treat hypercholesterolemia, have anti-inflammatory and anti-oxidant effects. These are thought to be responsible for the potential effects of statins on various psychiatric disorders. In this study, we comprehensively review the literature to investigate the effects of statins on various psychiatric disorders including depression, schizophrenia, and dementia. In addition, we review adverse effects and drug interactions of statins to give clinically useful information guiding statin use in the psychiatric field. Statins seem useful in reducing depression, particularly in patients with physical disorders such as cardiovascular disease. In patients with schizophrenia, negative symptoms may be reduced by adjuvant statin therapy. Studies on cohorts at risk for dementia have generally shown protective effects of statins, while those on treatment for dementia show inconsistent results. In conclusion, statins used in combination with conventional psychotropic medications may be effective for various psychiatric disorders including depression, schizophrenia, and dementia. Further study is required to determine optimal doses and duration of statin use for the treatment of psychiatric disorders.

@misc{articlespsychologyjanuary_9_statins_2019,
	title = {Statins {May} {Help} {Treat} {Serious} {Mental} {Illness}},
	url = {https://neurosciencenews.com/statins-mental-health-10473/},
	abstract = {A new study reveals statins, biguanides and other drugs that help treat physical conditions may have significant benefits for the treatment of bipolar disorder and schizophrenia.},
	language = {en-US},
	urldate = {2021-04-10},
	journal = {Neuroscience News},
	author = {ArticlesPsychology·January 9, FeaturedNeuroscienceOpen Neuroscience and {2019}},
	month = jan,
	year = {2019},
	note = {ZSCC: NoCitationData[s0]},
}

A new study reveals statins, biguanides and other drugs that help treat physical conditions may have significant benefits for the treatment of bipolar disorder and schizophrenia.

@article{palacios_emergence_2019,
	title = {The emergence of synchrony in networks of mutually inferring neurons},
	volume = {9},
	issn = {2045-2322},
	url = {http://www.nature.com/articles/s41598-019-42821-7},
	doi = {10.1038/s41598-019-42821-7},
	language = {en},
	number = {1},
	urldate = {2021-04-09},
	journal = {Scientific Reports},
	author = {Palacios, Ensor Rafael and Isomura, Takuya and Parr, Thomas and Friston, Karl},
	month = dec,
	year = {2019},
	note = {ZSCC: 0000046},
	pages = {6412},
}

@article{davidson_cognitive_2019,
	title = {Cognitive impairment as a diagnostic criterion and treatment target in schizophrenia},
	volume = {18},
	issn = {1723-8617},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6502436/},
	doi = {10.1002/wps.20651},
	number = {2},
	urldate = {2021-04-08},
	journal = {World Psychiatry},
	author = {Davidson, Michael},
	month = jun,
	year = {2019},
	pmid = {31059612},
	pmcid = {PMC6502436},
	note = {ZSCC: 0000002 },
	pages = {171--172},
}

@article{pape_immunoneuropsychiatry_2019,
	title = {Immunoneuropsychiatry — novel perspectives on brain disorders},
	volume = {15},
	copyright = {2019 Springer Nature Limited},
	issn = {1759-4766},
	url = {https://www.nature.com/articles/s41582-019-0174-4},
	doi = {10.1038/s41582-019-0174-4},
	abstract = {Immune processes have a vital role in CNS homeostasis, resilience and brain reserve. Our cognitive and social abilities rely on a highly sensitive and fine-tuned equilibrium of immune responses that involve both innate and adaptive immunity. Autoimmunity, chronic inflammation, infection and psychosocial stress can tip the scales towards disruption of higher-order networks. However, not only classical neuroinflammatory diseases, such as multiple sclerosis and autoimmune encephalitis, are caused by immune dysregulation that affects CNS function. Recent insight indicates that similar processes are involved in psychiatric diseases such as schizophrenia, autism spectrum disorder, bipolar disorder and depression. Pathways that are common to these disorders include microglial activation, pro-inflammatory cytokines, molecular mimicry, anti-neuronal autoantibodies, self-reactive T cells and disturbance of the blood–brain barrier. These discoveries challenge our traditional classification of neurological and psychiatric diseases. New clinical paths are required to identify subgroups of neuropsychiatric disorders that are phenotypically distinct but pathogenically related and to pave the way for mechanism-based immune treatments. Combined expertise from neurologists and psychiatrists will foster translation of these paths into clinical practice. The aim of this Review is to highlight outstanding findings that have transformed our understanding of neuropsychiatric diseases and to suggest new diagnostic and therapeutic criteria for the emerging field of immunoneuropsychiatry.},
	language = {en},
	number = {6},
	urldate = {2021-04-08},
	journal = {Nature Reviews Neurology},
	author = {Pape, Katrin and Tamouza, Ryad and Leboyer, Marion and Zipp, Frauke},
	month = jun,
	year = {2019},
	note = {ZSCC: 0000105 
Number: 6
Publisher: Nature Publishing Group},
	pages = {317--328},
}

Immune processes have a vital role in CNS homeostasis, resilience and brain reserve. Our cognitive and social abilities rely on a highly sensitive and fine-tuned equilibrium of immune responses that involve both innate and adaptive immunity. Autoimmunity, chronic inflammation, infection and psychosocial stress can tip the scales towards disruption of higher-order networks. However, not only classical neuroinflammatory diseases, such as multiple sclerosis and autoimmune encephalitis, are caused by immune dysregulation that affects CNS function. Recent insight indicates that similar processes are involved in psychiatric diseases such as schizophrenia, autism spectrum disorder, bipolar disorder and depression. Pathways that are common to these disorders include microglial activation, pro-inflammatory cytokines, molecular mimicry, anti-neuronal autoantibodies, self-reactive T cells and disturbance of the blood–brain barrier. These discoveries challenge our traditional classification of neurological and psychiatric diseases. New clinical paths are required to identify subgroups of neuropsychiatric disorders that are phenotypically distinct but pathogenically related and to pave the way for mechanism-based immune treatments. Combined expertise from neurologists and psychiatrists will foster translation of these paths into clinical practice. The aim of this Review is to highlight outstanding findings that have transformed our understanding of neuropsychiatric diseases and to suggest new diagnostic and therapeutic criteria for the emerging field of immunoneuropsychiatry.

@article{tenenbaum_translational_2019,
	title = {Translational bioinformatics in mental health: open access data sources and computational biomarker discovery},
	volume = {20},
	issn = {1477-4054},
	shorttitle = {Translational bioinformatics in mental health},
	url = {https://academic.oup.com/bib/article/20/3/842/4662948},
	doi = {10.1093/bib/bbx157},
	language = {en},
	number = {3},
	urldate = {2021-03-21},
	journal = {Briefings in Bioinformatics},
	author = {Tenenbaum, Jessica D and Bhuvaneshwar, Krithika and Gagliardi, Jane P and Fultz Hollis, Kate and Jia, Peilin and Ma, Liang and Nagarajan, Radhakrishnan and Rakesh, Gopalkumar and Subbian, Vignesh and Visweswaran, Shyam and Zhao, Zhongming and Rozenblit, Leon},
	month = may,
	year = {2019},
	note = {ZSCC: NoCitationData[s0]},
	pages = {842--856},
}

@article{karunakaran_potentially_2019,
	title = {Potentially repurposable drugs for schizophrenia identified from its interactome},
	volume = {9},
	copyright = {2019 The Author(s)},
	issn = {2045-2322},
	url = {https://www.nature.com/articles/s41598-019-48307-w},
	doi = {10.1038/s41598-019-48307-w},
	abstract = {We previously presented the protein-protein interaction network of schizophrenia associated genes, and from it, the drug-protein interactome which showed the drugs that target any of the proteins in the interactome. Here, we studied these drugs further to identify whether any of them may potentially be repurposable for schizophrenia. In schizophrenia, gene expression has been described as a measurable aspect of the disease reflecting the action of risk genes. We studied each of the drugs from the interactome using the BaseSpace Correlation Engine, and shortlisted those that had a negative correlation with differential gene expression of schizophrenia. This analysis resulted in 12 drugs whose differential gene expression (drug versus normal) had an anti-correlation with differential expression for schizophrenia (disorder versus normal). Some of these drugs were already being tested for their clinical activity in schizophrenia and other neuropsychiatric disorders. Several proteins in the protein interactome of the targets of several of these drugs were associated with various neuropsychiatric disorders. The network of genes with opposite drug-induced versus schizophrenia-associated expression profiles were significantly enriched in pathways relevant to schizophrenia etiology and GWAS genes associated with traits or diseases that had a pathophysiological overlap with schizophrenia. Drugs that targeted the same genes as the shortlisted drugs, have also demonstrated clinical activity in schizophrenia and other related disorders. This integrated computational analysis will help translate insights from the schizophrenia drug-protein interactome to clinical research - an important step, especially in the field of psychiatric drug development which faces a high failure rate.},
	language = {en},
	number = {1},
	urldate = {2021-03-19},
	journal = {Scientific Reports},
	author = {Karunakaran, Kalyani B. and Chaparala, Srilakshmi and Ganapathiraju, Madhavi K.},
	month = sep,
	year = {2019},
	note = {ZSCC: 0000004 
Number: 1
Publisher: Nature Publishing Group},
	pages = {12682},
}

We previously presented the protein-protein interaction network of schizophrenia associated genes, and from it, the drug-protein interactome which showed the drugs that target any of the proteins in the interactome. Here, we studied these drugs further to identify whether any of them may potentially be repurposable for schizophrenia. In schizophrenia, gene expression has been described as a measurable aspect of the disease reflecting the action of risk genes. We studied each of the drugs from the interactome using the BaseSpace Correlation Engine, and shortlisted those that had a negative correlation with differential gene expression of schizophrenia. This analysis resulted in 12 drugs whose differential gene expression (drug versus normal) had an anti-correlation with differential expression for schizophrenia (disorder versus normal). Some of these drugs were already being tested for their clinical activity in schizophrenia and other neuropsychiatric disorders. Several proteins in the protein interactome of the targets of several of these drugs were associated with various neuropsychiatric disorders. The network of genes with opposite drug-induced versus schizophrenia-associated expression profiles were significantly enriched in pathways relevant to schizophrenia etiology and GWAS genes associated with traits or diseases that had a pathophysiological overlap with schizophrenia. Drugs that targeted the same genes as the shortlisted drugs, have also demonstrated clinical activity in schizophrenia and other related disorders. This integrated computational analysis will help translate insights from the schizophrenia drug-protein interactome to clinical research - an important step, especially in the field of psychiatric drug development which faces a high failure rate.

@article{kinon_group_2019,
	title = {The {Group} of {Treatment} {Resistant} {Schizophrenias}. {Heterogeneity} in {Treatment} {Resistant} {Schizophrenia} ({TRS})},
	volume = {9},
	issn = {1664-0640},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6363683/},
	doi = {10.3389/fpsyt.2018.00757},
	abstract = {Schizophrenia is composed of a heterogeneous group of patient segments. Our current notion of the heterogeneity in schizophrenia is based on patients presenting with diverse disease symptom phenotypes, risk factors, structural and functional neuropathology, and a mixed range of expressed response to treatment. It is important for clinicians to recognize the various clinical presentations of resistance to treatment in schizophrenia and to understand how heterogeneity across treatment resistant patient segments may potentially inform new strategies for the development of effective treatments for Treatment Resistant Schizophrenia (TRS). The heterogeneity of schizophrenia may be reduced by parsing patient segments based on whether patients demonstrate an adequate or inadequate response to treatment. In our current concept of TRS, TRS is defined as non-response to at least two adequate trials of antipsychotic medication and is estimated to affect about 30\% of all patients with schizophrenia. In this narrative review, the author discusses that the demonstration of inadequate response to antipsychotic drugs (APDs) may infer that some TRS patients may be suffering from a non-dopamine pathophysiology since D2 receptor antagonist-based treatment is ineffective. Preliminary neurobiological findings may further support the pathophysiologic distinction of TRS from that of general schizophrenia. Investigation of the basis for heterogeneity in TRS through the systematic investigation of relevant “clusters” of similarly at risk individuals may hopefully bring us closer to realize a precision medicine approach for developing effective therapies for TRS patient segments.},
	urldate = {2021-03-18},
	journal = {Frontiers in Psychiatry},
	author = {Kinon, Bruce J.},
	month = jan,
	year = {2019},
	pmid = {30761026},
	pmcid = {PMC6363683},
	note = {ZSCC: 0000015 },
}

Schizophrenia is composed of a heterogeneous group of patient segments. Our current notion of the heterogeneity in schizophrenia is based on patients presenting with diverse disease symptom phenotypes, risk factors, structural and functional neuropathology, and a mixed range of expressed response to treatment. It is important for clinicians to recognize the various clinical presentations of resistance to treatment in schizophrenia and to understand how heterogeneity across treatment resistant patient segments may potentially inform new strategies for the development of effective treatments for Treatment Resistant Schizophrenia (TRS). The heterogeneity of schizophrenia may be reduced by parsing patient segments based on whether patients demonstrate an adequate or inadequate response to treatment. In our current concept of TRS, TRS is defined as non-response to at least two adequate trials of antipsychotic medication and is estimated to affect about 30% of all patients with schizophrenia. In this narrative review, the author discusses that the demonstration of inadequate response to antipsychotic drugs (APDs) may infer that some TRS patients may be suffering from a non-dopamine pathophysiology since D2 receptor antagonist-based treatment is ineffective. Preliminary neurobiological findings may further support the pathophysiologic distinction of TRS from that of general schizophrenia. Investigation of the basis for heterogeneity in TRS through the systematic investigation of relevant “clusters” of similarly at risk individuals may hopefully bring us closer to realize a precision medicine approach for developing effective therapies for TRS patient segments.

@article{karunakaran_potentially_2019-1,
	title = {Potentially repurposable drugs for schizophrenia identified from its interactome},
	volume = {9},
	copyright = {2019 The Author(s)},
	issn = {2045-2322},
	url = {https://www.nature.com/articles/s41598-019-48307-w},
	doi = {10.1038/s41598-019-48307-w},
	abstract = {We previously presented the protein-protein interaction network of schizophrenia associated genes, and from it, the drug-protein interactome which showed the drugs that target any of the proteins in the interactome. Here, we studied these drugs further to identify whether any of them may potentially be repurposable for schizophrenia. In schizophrenia, gene expression has been described as a measurable aspect of the disease reflecting the action of risk genes. We studied each of the drugs from the interactome using the BaseSpace Correlation Engine, and shortlisted those that had a negative correlation with differential gene expression of schizophrenia. This analysis resulted in 12 drugs whose differential gene expression (drug versus normal) had an anti-correlation with differential expression for schizophrenia (disorder versus normal). Some of these drugs were already being tested for their clinical activity in schizophrenia and other neuropsychiatric disorders. Several proteins in the protein interactome of the targets of several of these drugs were associated with various neuropsychiatric disorders. The network of genes with opposite drug-induced versus schizophrenia-associated expression profiles were significantly enriched in pathways relevant to schizophrenia etiology and GWAS genes associated with traits or diseases that had a pathophysiological overlap with schizophrenia. Drugs that targeted the same genes as the shortlisted drugs, have also demonstrated clinical activity in schizophrenia and other related disorders. This integrated computational analysis will help translate insights from the schizophrenia drug-protein interactome to clinical research - an important step, especially in the field of psychiatric drug development which faces a high failure rate.},
	language = {en},
	number = {1},
	urldate = {2021-03-19},
	journal = {Scientific Reports},
	author = {Karunakaran, Kalyani B. and Chaparala, Srilakshmi and Ganapathiraju, Madhavi K.},
	month = sep,
	year = {2019},
	note = {ZSCC: 0000004},
	pages = {12682},
}

We previously presented the protein-protein interaction network of schizophrenia associated genes, and from it, the drug-protein interactome which showed the drugs that target any of the proteins in the interactome. Here, we studied these drugs further to identify whether any of them may potentially be repurposable for schizophrenia. In schizophrenia, gene expression has been described as a measurable aspect of the disease reflecting the action of risk genes. We studied each of the drugs from the interactome using the BaseSpace Correlation Engine, and shortlisted those that had a negative correlation with differential gene expression of schizophrenia. This analysis resulted in 12 drugs whose differential gene expression (drug versus normal) had an anti-correlation with differential expression for schizophrenia (disorder versus normal). Some of these drugs were already being tested for their clinical activity in schizophrenia and other neuropsychiatric disorders. Several proteins in the protein interactome of the targets of several of these drugs were associated with various neuropsychiatric disorders. The network of genes with opposite drug-induced versus schizophrenia-associated expression profiles were significantly enriched in pathways relevant to schizophrenia etiology and GWAS genes associated with traits or diseases that had a pathophysiological overlap with schizophrenia. Drugs that targeted the same genes as the shortlisted drugs, have also demonstrated clinical activity in schizophrenia and other related disorders. This integrated computational analysis will help translate insights from the schizophrenia drug-protein interactome to clinical research - an important step, especially in the field of psychiatric drug development which faces a high failure rate.

@article{han_tolerating_2019,
	title = {Tolerating uncertainty about conceptual models of uncertainty in health care},
	volume = {25},
	issn = {1365-2753},
	url = {https://onlinelibrary.wiley.com/doi/abs/10.1111/jep.13110},
	doi = {10.1111/jep.13110},
	language = {en},
	number = {2},
	urldate = {2020-10-24},
	journal = {Journal of Evaluation in Clinical Practice},
	author = {Han, Paul K. J. and Djulbegovic, Benjamin},
	year = {2019},
	note = {ZSCC: 0000004 
\_eprint: https://onlinelibrary.wiley.com/doi/pdf/10.1111/jep.13110},
	pages = {183--185},
}

@article{holliman_visual_2019,
	title = {Visual {Entropy} and the {Visualization} of {Uncertainty}},
	url = {http://arxiv.org/abs/1907.12879},
	abstract = {Background: It is possible to find many different visual representations of data values in visualizations, it is less common to see visual representations that include uncertainty, especially in visualizations intended for non-technical audiences. Objective: our aim is to rigorously define and evaluate the novel use of visual entropy as a measure of shape that allows us to construct an ordered scale of glyphs for use in representing both uncertainty and value in 2D and 3D environments. Method: We use sample entropy as a numerical measure of visual entropy to construct a set of glyphs using R and Blender which vary in their complexity. Results: A Bradley-Terry analysis of a pairwise comparison of the glyphs shows participants (n=19) ordered the glyphs as predicted by the visual entropy score (linear regression R2 {\textgreater}0.97, p{\textless}0.001). We also evaluate whether the glyphs can effectively represent uncertainty using a signal detection method, participants (n=15) were able to search for glyphs representing uncertainty with high sensitivity and low error rates. Conclusion: visual entropy is a novel cue for representing ordered data and provides a channel that allows the uncertainty of a measure to be presented alongside its mean value.},
	urldate = {2020-10-14},
	journal = {arXiv:1907.12879 [cs, math]},
	author = {Holliman, Nicolas S. and Coltekin, Arzu and Fernstad, Sara J. and Simpson, Michael D. and Wilson, Kevin J. and Woods, Andrew J.},
	month = jul,
	year = {2019},
	note = {ZSCC: 0000002 
arXiv: 1907.12879},
	keywords = {Computer Science - Graphics, Computer Science - Human-Computer Interaction, Computer Science - Information Theory},
}

Background: It is possible to find many different visual representations of data values in visualizations, it is less common to see visual representations that include uncertainty, especially in visualizations intended for non-technical audiences. Objective: our aim is to rigorously define and evaluate the novel use of visual entropy as a measure of shape that allows us to construct an ordered scale of glyphs for use in representing both uncertainty and value in 2D and 3D environments. Method: We use sample entropy as a numerical measure of visual entropy to construct a set of glyphs using R and Blender which vary in their complexity. Results: A Bradley-Terry analysis of a pairwise comparison of the glyphs shows participants (n=19) ordered the glyphs as predicted by the visual entropy score (linear regression R2 \textgreater0.97, p\textless0.001). We also evaluate whether the glyphs can effectively represent uncertainty using a signal detection method, participants (n=15) were able to search for glyphs representing uncertainty with high sensitivity and low error rates. Conclusion: visual entropy is a novel cue for representing ordered data and provides a channel that allows the uncertainty of a measure to be presented alongside its mean value.

@article{van_der_bles_communicating_2019,
	title = {Communicating uncertainty about facts, numbers and science},
	volume = {6},
	issn = {2054-5703, 2054-5703},
	url = {https://royalsocietypublishing.org/doi/10.1098/rsos.181870},
	doi = {10.1098/rsos.181870},
	abstract = {Uncertainty is an inherent part of knowledge, and yet in an era of contested expertise, many shy away from openly communicating their uncertainty about what they know, fearful of their audience's reaction. But what effect does communication of such epistemic uncertainty have? Empirical research is widely scattered across many disciplines. This interdisciplinary review structures and summarizes current practice and research across domains, combining a statistical and psychological perspective. This informs a framework for uncertainty communication in which we identify three objects of uncertainty—facts, numbers and science—and two levels of uncertainty: direct and indirect. An examination of current practices provides a scale of nine expressions of direct uncertainty. We discuss attempts to codify indirect uncertainty in terms of quality of the underlying evidence. We review the limited literature about the effects of communicating epistemic uncertainty on cognition, affect, trust and decision-making. While there is some evidence that communicating epistemic uncertainty does not necessarily affect audiences negatively, impact can vary between individuals and communication formats. Case studies in economic statistics and climate change illustrate our framework in action. We conclude with advice to guide both communicators and future researchers in this important but so far rather neglected field.},
	language = {en},
	number = {5},
	urldate = {2020-10-14},
	journal = {Royal Society Open Science},
	author = {van der Bles, Anne Marthe and van der Linden, Sander and Freeman, Alexandra L. J. and Mitchell, James and Galvao, Ana B. and Zaval, Lisa and Spiegelhalter, David J.},
	month = may,
	year = {2019},
	pages = {181870},
}

Uncertainty is an inherent part of knowledge, and yet in an era of contested expertise, many shy away from openly communicating their uncertainty about what they know, fearful of their audience's reaction. But what effect does communication of such epistemic uncertainty have? Empirical research is widely scattered across many disciplines. This interdisciplinary review structures and summarizes current practice and research across domains, combining a statistical and psychological perspective. This informs a framework for uncertainty communication in which we identify three objects of uncertainty—facts, numbers and science—and two levels of uncertainty: direct and indirect. An examination of current practices provides a scale of nine expressions of direct uncertainty. We discuss attempts to codify indirect uncertainty in terms of quality of the underlying evidence. We review the limited literature about the effects of communicating epistemic uncertainty on cognition, affect, trust and decision-making. While there is some evidence that communicating epistemic uncertainty does not necessarily affect audiences negatively, impact can vary between individuals and communication formats. Case studies in economic statistics and climate change illustrate our framework in action. We conclude with advice to guide both communicators and future researchers in this important but so far rather neglected field.

@article{haberl_contributions_2019,
	title = {Contributions of sociometabolic research to sustainability science},
	volume = {2},
	issn = {2398-9629},
	url = {http://www.nature.com/articles/s41893-019-0225-2},
	doi = {10.1038/s41893-019-0225-2},
	language = {en},
	number = {3},
	urldate = {2020-10-06},
	journal = {Nature Sustainability},
	author = {Haberl, Helmut and Wiedenhofer, Dominik and Pauliuk, Stefan and Krausmann, Fridolin and Müller, Daniel B. and Fischer-Kowalski, Marina},
	month = mar,
	year = {2019},
	note = {ZSCC: 0000048},
	pages = {173--184},
}

@incollection{lysen_interface_2019,
	address = {Cham},
	title = {The {Interface} {Is} the ({Art}){Work}: {EEG}-{Feedback}, {Circuited} {Selves} and the {Rise} of {Real}-{Time} {Brainmedia} (1964–1977)},
	isbn = {978-3-030-14323-7},
	shorttitle = {The {Interface} {Is} the ({Art}){Work}},
	url = {https://doi.org/10.1007/978-3-030-14323-7_2},
	abstract = {This chapter examines the rise of EEG-feedback research in the period between 1964 and 1977, the time between the first EEG-feedback setup that gained public attention and the subsequent waning of the explosive enthusiasm for EEG-feedback in the late 1970s. Studying both artistic and scientific experiments of EEG-feedback during this period, the chapter traces the emergence of a new direction within this subdomain of EEG-research—beyond an interest in the meaning of measured brain wave states, towards the significance of the design of brain-feedback situations that perform and emphasize the relationality and mutability of brain activity. By examining research cultures and practices of EEG-feedback, the chapter traces conditions of possibility for a shifting epistemological commitment, revolving around the idea that ‘the interface is the work.’ Research cultures of EEG feedback were impacted by both artistic and scientific experiments with media environments and the idea of a ‘circuited self’. In turn, artists and researchers were actively engaged with the public manifestation of EEG-feedback in popular news reports and television broadcasts, which created a particular sphere of resonance for the emphasis on playful and spectacular demonstrations of circuits. When computing was introduced in EEG-feedback after 1970, it brought notions of ‘on-line’ and ‘real-time’ into the circuit. These developments were not only understood as technological advancement through faster feedback, but they also brought an emphasis on the social potential of computing: self-insight, augmenting the self and connecting with others. The chapter ends with a reflection on the resonance of histories of performance and design-oriented approaches in neuroscientific research today.},
	language = {en},
	urldate = {2020-10-06},
	booktitle = {Brain {Art}: {Brain}-{Computer} {Interfaces} for {Artistic} {Expression}},
	publisher = {Springer International Publishing},
	author = {Lysen, Flora},
	editor = {Nijholt, Anton},
	year = {2019},
	doi = {10.1007/978-3-030-14323-7_2},
	note = {ZSCC: NoCitationData[s0] },
	keywords = {Art-science interaction, Brainmedia, EEG-feedback, Interface, Real-time},
	pages = {33--63},
}

This chapter examines the rise of EEG-feedback research in the period between 1964 and 1977, the time between the first EEG-feedback setup that gained public attention and the subsequent waning of the explosive enthusiasm for EEG-feedback in the late 1970s. Studying both artistic and scientific experiments of EEG-feedback during this period, the chapter traces the emergence of a new direction within this subdomain of EEG-research—beyond an interest in the meaning of measured brain wave states, towards the significance of the design of brain-feedback situations that perform and emphasize the relationality and mutability of brain activity. By examining research cultures and practices of EEG-feedback, the chapter traces conditions of possibility for a shifting epistemological commitment, revolving around the idea that ‘the interface is the work.’ Research cultures of EEG feedback were impacted by both artistic and scientific experiments with media environments and the idea of a ‘circuited self’. In turn, artists and researchers were actively engaged with the public manifestation of EEG-feedback in popular news reports and television broadcasts, which created a particular sphere of resonance for the emphasis on playful and spectacular demonstrations of circuits. When computing was introduced in EEG-feedback after 1970, it brought notions of ‘on-line’ and ‘real-time’ into the circuit. These developments were not only understood as technological advancement through faster feedback, but they also brought an emphasis on the social potential of computing: self-insight, augmenting the self and connecting with others. The chapter ends with a reflection on the resonance of histories of performance and design-oriented approaches in neuroscientific research today.

@article{coben_19_2019,
	title = {19 {Channel} {Z}-{Score} and {LORETA} {Neurofeedback}: {Does} the {Evidence} {Support} the {Hype}?},
	volume = {44},
	issn = {1573-3270},
	shorttitle = {19 {Channel} {Z}-{Score} and {LORETA} {Neurofeedback}},
	url = {https://doi.org/10.1007/s10484-018-9420-6},
	doi = {10.1007/s10484-018-9420-6},
	abstract = {Neurofeedback is a well-investigated treatment for ADHD and epilepsy, especially when restricted to standard protocols such as theta/beta, slow cortical potentials and sensori-motor rhythm neurofeedback. Advances in any field are welcome and other techniques are being pursued. Manufacturers and clinicians are marketing ‘superior’ neurofeedback approaches including 19 channel Z-score neurofeedback (ZNFB) and 3-D LORETA neurofeedback (with or without Z-scores; LNFB). We conducted a review of the empirical literature to determine if such claims were warranted. This review included the above search terms in Pubmed, Google scholar and any references that met our criteria from the ZNFB publication list and was restricted to group based studies examining improvement in a clinical population that underwent peer review (book chapters, magazine articles or conference presentations are not included since these are not peer reviewed). Fifteen relevant studies emerged with only six meeting our criterion. Based on review of these studies it was concluded that empirical validation of these approaches is sorely lacking. There is no empirical data that supports the notion that 19-channel z-score neurofeedback is effective or superior. The quality of studies for LNFB was better compared to ZNFB and some suggestion for efficacy was demonstrated for ADHD and Tinnitus distress. However, these findings need to be replicated, extended to other populations and have yet to show any “superiority.” Our conclusions continue to emphasize the pervasive lack of evidence supporting these approaches to neurofeedback and the implications of this are discussed.},
	language = {en},
	number = {1},
	urldate = {2020-10-06},
	journal = {Applied Psychophysiology and Biofeedback},
	author = {Coben, Robert and Hammond, D. Corydon and Arns, Martijn},
	month = mar,
	year = {2019},
	note = {ZSCC: 0000010},
	pages = {1--8},
}

Neurofeedback is a well-investigated treatment for ADHD and epilepsy, especially when restricted to standard protocols such as theta/beta, slow cortical potentials and sensori-motor rhythm neurofeedback. Advances in any field are welcome and other techniques are being pursued. Manufacturers and clinicians are marketing ‘superior’ neurofeedback approaches including 19 channel Z-score neurofeedback (ZNFB) and 3-D LORETA neurofeedback (with or without Z-scores; LNFB). We conducted a review of the empirical literature to determine if such claims were warranted. This review included the above search terms in Pubmed, Google scholar and any references that met our criteria from the ZNFB publication list and was restricted to group based studies examining improvement in a clinical population that underwent peer review (book chapters, magazine articles or conference presentations are not included since these are not peer reviewed). Fifteen relevant studies emerged with only six meeting our criterion. Based on review of these studies it was concluded that empirical validation of these approaches is sorely lacking. There is no empirical data that supports the notion that 19-channel z-score neurofeedback is effective or superior. The quality of studies for LNFB was better compared to ZNFB and some suggestion for efficacy was demonstrated for ADHD and Tinnitus distress. However, these findings need to be replicated, extended to other populations and have yet to show any “superiority.” Our conclusions continue to emphasize the pervasive lack of evidence supporting these approaches to neurofeedback and the implications of this are discussed.

@article{khambhati_functional_2019,
	title = {Functional control of electrophysiological network architecture using direct neurostimulation in humans},
	volume = {3},
	url = {https://doi.org/10.1162/netn_a_00089},
	doi = {10.1162/netn_a_00089},
	abstract = {Chronically implantable neurostimulation devices are becoming a clinically viable option for treating patients with neurological disease and psychiatric disorders. Neurostimulation offers the ability to probe and manipulate distributed networks of interacting brain areas in dysfunctional circuits. Here, we use tools from network control theory to examine the dynamic reconfiguration of functionally interacting neuronal ensembles during targeted neurostimulation of cortical and subcortical brain structures. By integrating multimodal intracranial recordings and diffusion-weighted imaging from patients with drug-resistant epilepsy, we test hypothesized structural and functional rules that predict altered patterns of synchronized local field potentials. We demonstrate the ability to predictably reconfigure functional interactions depending on stimulation strength and location. Stimulation of areas with structurally weak connections largely modulates the functional hubness of downstream areas and concurrently propels the brain towards more difficult-to-reach dynamical states. By using focal perturbations to bridge large-scale structure, function, and markers of behavior, our findings suggest that stimulation may be tuned to influence different scales of network interactions driving cognition.},
	number = {3},
	urldate = {2020-10-06},
	journal = {Network Neuroscience},
	author = {Khambhati, Ankit N. and Kahn, Ari E. and Costantini, Julia and Ezzyat, Youssef and Solomon, Ethan A. and Gross, Robert E. and Jobst, Barbara C. and Sheth, Sameer A. and Zaghloul, Kareem A. and Worrell, Gregory and Seger, Sarah and Lega, Bradley C. and Weiss, Shennan and Sperling, Michael R. and Gorniak, Richard and Das, Sandhitsu R. and Stein, Joel M. and Rizzuto, Daniel S. and Kahana, Michael J. and Lucas, Timothy H. and Davis, Kathryn A. and Tracy, Joseph I. and Bassett, Danielle S.},
	month = jan,
	year = {2019},
	note = {ZSCC: NoCitationData[s0] 
Publisher: MIT Press},
	pages = {848--877},
}

Chronically implantable neurostimulation devices are becoming a clinically viable option for treating patients with neurological disease and psychiatric disorders. Neurostimulation offers the ability to probe and manipulate distributed networks of interacting brain areas in dysfunctional circuits. Here, we use tools from network control theory to examine the dynamic reconfiguration of functionally interacting neuronal ensembles during targeted neurostimulation of cortical and subcortical brain structures. By integrating multimodal intracranial recordings and diffusion-weighted imaging from patients with drug-resistant epilepsy, we test hypothesized structural and functional rules that predict altered patterns of synchronized local field potentials. We demonstrate the ability to predictably reconfigure functional interactions depending on stimulation strength and location. Stimulation of areas with structurally weak connections largely modulates the functional hubness of downstream areas and concurrently propels the brain towards more difficult-to-reach dynamical states. By using focal perturbations to bridge large-scale structure, function, and markers of behavior, our findings suggest that stimulation may be tuned to influence different scales of network interactions driving cognition.

@article{widge_targeting_2019,
	title = {Targeting {Cognition} and {Networks} {Through} {Neural} {Oscillations}: {Next}-{Generation} {Clinical} {Brain} {Stimulation}},
	volume = {76},
	issn = {2168-622X},
	shorttitle = {Targeting {Cognition} and {Networks} {Through} {Neural} {Oscillations}},
	url = {http://archpsyc.jamanetwork.com/article.aspx?doi=10.1001/jamapsychiatry.2019.0740},
	doi = {10.1001/jamapsychiatry.2019.0740},
	language = {en},
	number = {7},
	urldate = {2020-09-24},
	journal = {JAMA Psychiatry},
	author = {Widge, Alik S. and Miller, Earl K.},
	month = jul,
	year = {2019},
	note = {ZSCC: 0000006},
	pages = {671},
}

@article{di_rosa_reward_2019,
	title = {Reward motivation and neurostimulation interact to improve working memory performance in healthy older adults: {A} simultaneous {tDCS}-{fNIRS} study},
	volume = {202},
	issn = {10538119},
	shorttitle = {Reward motivation and neurostimulation interact to improve working memory performance in healthy older adults},
	url = {https://linkinghub.elsevier.com/retrieve/pii/S1053811919306445},
	doi = {10.1016/j.neuroimage.2019.116062},
	language = {en},
	urldate = {2020-08-18},
	journal = {NeuroImage},
	author = {Di Rosa, Elisa and Brigadoi, Sabrina and Cutini, Simone and Tarantino, Vincenza and Dell’Acqua, Roberto and Mapelli, Daniela and Braver, Todd S. and Vallesi, Antonino},
	month = nov,
	year = {2019},
	pages = {116062},
}

@article{kantrowitz_significant_2019,
	title = {Significant improvement in treatment resistant auditory verbal hallucinations after 5 days of double-blind, randomized, sham controlled, fronto-temporal, transcranial direct current stimulation ({tDCS}): {A} replication/extension study},
	volume = {12},
	issn = {1935-861X},
	shorttitle = {Significant improvement in treatment resistant auditory verbal hallucinations after 5 days of double-blind, randomized, sham controlled, fronto-temporal, transcranial direct current stimulation ({tDCS})},
	url = {http://www.sciencedirect.com/science/article/pii/S1935861X19300828},
	doi = {10.1016/j.brs.2019.03.003},
	abstract = {Background
Transcranial direct current stimulation (tDCS) is a potentially novel treatment for antipsychotic-resistant auditory verbal hallucinations (AVH) in schizophrenia. Nevertheless, results have been mixed across studies.
Methods
89 schizophrenia/schizoaffective subjects (active: 47; Sham: 42) were randomized to five days of twice-daily 20-min active tDCS vs. sham treatments across two recruitment sites. AVH severity was assessed using the Auditory Hallucination Rating Scale (AHRS) total score. To assess target engagement, MRI was obtained in a sub sample.
Results
We observed a statistically significant, moderate effect-size change in AHRS total score across one-week and one-month favoring active treatment following covariation for baseline symptoms and antipsychotic dose (p = 0.036; d = 0.48). Greatest change was observed on the AHRS loudness item (p = 0.003; d = 0.69). In exploratory analyses, greatest effects on AHRS were observed in patients with lower cognitive symptoms (d = 0.61). In target engagement analysis, suprathreshold mean field-strength ({\textgreater}0.2 V/m) was seen within language-sensitive regions. However, off-target field-strength, which correlated significantly with less robust clinical response, was observed in anterior regions.
Conclusions
This is the largest study of tDCS for persistent AVH conducted to date. We replicate previous reports of significant therapeutic benefit, but only if medication dosage is considered, with patients receiving lowest medication dosage showing greatest effect. Response was also greatest in patients with lowest levels of cognitive symptoms. Overall, these findings support continued development of tDCS for persistent AVH, but also suggest that response may be influenced by specific patient and treatment characteristics.
ClinicalTrials.gov
NCT01898299.},
	language = {en},
	number = {4},
	urldate = {2020-08-13},
	journal = {Brain Stimulation},
	author = {Kantrowitz, Joshua T. and Sehatpour, Pejman and Avissar, Michael and Horga, Guillermo and Gwak, Anna and Hoptman, Mathew J. and Beggel, Odeta and Girgis, Ragy R. and Vail, Blair and Silipo, Gail and Carlson, Marlene and Javitt, Daniel C.},
	month = jul,
	year = {2019},
	note = {ZSCC: NoCitationData[s0]},
	keywords = {Auditory hallucinations, Clinical trial, Schizophrenia, Target engagement, tDCS},
	pages = {981--991},
}

Background Transcranial direct current stimulation (tDCS) is a potentially novel treatment for antipsychotic-resistant auditory verbal hallucinations (AVH) in schizophrenia. Nevertheless, results have been mixed across studies. Methods 89 schizophrenia/schizoaffective subjects (active: 47; Sham: 42) were randomized to five days of twice-daily 20-min active tDCS vs. sham treatments across two recruitment sites. AVH severity was assessed using the Auditory Hallucination Rating Scale (AHRS) total score. To assess target engagement, MRI was obtained in a sub sample. Results We observed a statistically significant, moderate effect-size change in AHRS total score across one-week and one-month favoring active treatment following covariation for baseline symptoms and antipsychotic dose (p = 0.036; d = 0.48). Greatest change was observed on the AHRS loudness item (p = 0.003; d = 0.69). In exploratory analyses, greatest effects on AHRS were observed in patients with lower cognitive symptoms (d = 0.61). In target engagement analysis, suprathreshold mean field-strength (\textgreater0.2 V/m) was seen within language-sensitive regions. However, off-target field-strength, which correlated significantly with less robust clinical response, was observed in anterior regions. Conclusions This is the largest study of tDCS for persistent AVH conducted to date. We replicate previous reports of significant therapeutic benefit, but only if medication dosage is considered, with patients receiving lowest medication dosage showing greatest effect. Response was also greatest in patients with lowest levels of cognitive symptoms. Overall, these findings support continued development of tDCS for persistent AVH, but also suggest that response may be influenced by specific patient and treatment characteristics. ClinicalTrials.gov NCT01898299.

@misc{articlespsychologyjanuary_9_statins_2019,
	title = {Statins {May} {Help} {Treat} {Serious} {Mental} {Illness}},
	url = {https://neurosciencenews.com/statins-mental-health-10473/},
	abstract = {A new study reveals statins, biguanides and other drugs that help treat physical conditions may have significant benefits for the treatment of bipolar disorder and schizophrenia.},
	language = {en-US},
	urldate = {2020-08-13},
	journal = {Neuroscience News},
	author = {ArticlesPsychology·January 9, FeaturedNeuroscienceOpen Neuroscience and {2019}},
	month = jan,
	year = {2019},
	note = {ZSCC: NoCitationData[s0]},
}

A new study reveals statins, biguanides and other drugs that help treat physical conditions may have significant benefits for the treatment of bipolar disorder and schizophrenia.

@article{gaspar_unconventional_2019,
	title = {Unconventional settings and uses of human enhancement technologies: {A} non-systematic review of public and experts' views on self-enhancement and {DIY} biology/biohacking risks},
	volume = {1},
	issn = {2578-1863},
	shorttitle = {Unconventional settings and uses of human enhancement technologies},
	url = {https://onlinelibrary.wiley.com/doi/abs/10.1002/hbe2.175},
	doi = {10.1002/hbe2.175},
	abstract = {Human enhancement aims at improving individual human performance through science-based or technology-based interventions in the human body. For various decades, associated research and applications/interventions were performed in conventional settings (e.g., research institutes) through conventional regulated and controlled procedures (e.g., clinical trials). In the last decade there has been an emergence of science activities grounded on emerging technologies used in unconventional settings (e.g., households; community labs), often through unconventional unregulated and uncontrolled procedures (e.g., self-administration of substances). The Do-It-Yourself Biology or Biohacking movement is an example of communities supportive of such activities, which use emerging technologies such as the CRISPR technique. Among others, these can have other or self-enhancement goals. Because such activities are anticipated to increase in the future, and due to the methods novelty, lack of regulation, quality, and safety control, there is uncertainty regarding personal and social consequences. Thus, these can be considered to present an emerging risk to human health and the environment. A first step in risk regulation is considering ethical aspects of emerging technologies use, which has been implemented. A second step to sustain subsequent evidence-based risk management and risk communication to citizen scientists, is necessary. It should involve risk assessment by experts and an understanding of public views on human enhancement technologies. Due to the scarce literature, gathering information to support this step was the goal of a non-systematic literature review. This focused on internal enhancements through substances intake and human body manipulations, specifically DIY biology/biohacking activities with this goal.},
	language = {en},
	number = {4},
	urldate = {2020-06-23},
	journal = {Human Behavior and Emerging Technologies},
	author = {Gaspar, Rui and Rohde, Paul and Giger, Jean-Christophe},
	year = {2019},
	note = {ZSCC: 0000000 
\_eprint: https://onlinelibrary.wiley.com/doi/pdf/10.1002/hbe2.175},
	keywords = {DIY biology, biohacking, emerging risks, emerging technologies, human enhancement, transhumanism},
	pages = {295--305},
}

Human enhancement aims at improving individual human performance through science-based or technology-based interventions in the human body. For various decades, associated research and applications/interventions were performed in conventional settings (e.g., research institutes) through conventional regulated and controlled procedures (e.g., clinical trials). In the last decade there has been an emergence of science activities grounded on emerging technologies used in unconventional settings (e.g., households; community labs), often through unconventional unregulated and uncontrolled procedures (e.g., self-administration of substances). The Do-It-Yourself Biology or Biohacking movement is an example of communities supportive of such activities, which use emerging technologies such as the CRISPR technique. Among others, these can have other or self-enhancement goals. Because such activities are anticipated to increase in the future, and due to the methods novelty, lack of regulation, quality, and safety control, there is uncertainty regarding personal and social consequences. Thus, these can be considered to present an emerging risk to human health and the environment. A first step in risk regulation is considering ethical aspects of emerging technologies use, which has been implemented. A second step to sustain subsequent evidence-based risk management and risk communication to citizen scientists, is necessary. It should involve risk assessment by experts and an understanding of public views on human enhancement technologies. Due to the scarce literature, gathering information to support this step was the goal of a non-systematic literature review. This focused on internal enhancements through substances intake and human body manipulations, specifically DIY biology/biohacking activities with this goal.

@article{orkibi_linking_2019,
	title = {Linking trauma to posttraumatic growth and mental health through emotional and cognitive creativity},
	volume = {13},
	issn = {1931-390X(Electronic),1931-3896(Print)},
	doi = {10.1037/aca0000193},
	abstract = {The association between adverse life events and creativity has almost exclusively been investigated qualitatively and with eminent creators. Also, the mediating roles of emotional creativity (the ability to experience novel and appropriate emotions), divergent thinking (the cognitive ability to think of multiple ideas), and creative self-efficacy (CSE; one’s confidence in their ability to be creative) have not been explored simultaneously or in this context. The goal of the present study was to test a multiple mediation model which theorized that exposure to traumatic events would be associated with posttraumatic growth (PTG) and mental health symptoms through emotional creativity, divergent thinking, and CSE in the general population. Findings from a sample of 252 Israeli adults (73\% females, aged 19–58), of whom 64\% had been exposed to war as civilians, showed that exposure to a greater number of traumatic events was related to higher CSE scores, emotional creativity, and overall divergent thinking. A path analysis to test indirect effects indicated that emotional creativity (but not divergent thinking) followed by CSE mediated the positive association between exposure and PTG as well as the negative association between exposure and mental health symptoms. CSE mediated the association between emotional creativity and divergent thinking to both PTG and mental health symptoms. The results may provide a better understanding of possible paths through which exposure to traumatic events relates to psychological outcomes, highlighting the role of CSE as a mediator that may account for how emotional and cognitive creative abilities are associated with PTG and mental health. (PsycINFO Database Record (c) 2020 APA, all rights reserved)},
	number = {4},
	journal = {Psychology of Aesthetics, Creativity, and the Arts},
	author = {Orkibi, Hod and Ram-Vlasov, Neta},
	year = {2019},
	note = {Place: US
Publisher: Educational Publishing Foundation},
	keywords = {Creativity, Divergent Thinking, Emotions, Illness Attribution/Appraisal, Posttraumatic Growth, Self-Efficacy, Trauma},
	pages = {416--430},
}

The association between adverse life events and creativity has almost exclusively been investigated qualitatively and with eminent creators. Also, the mediating roles of emotional creativity (the ability to experience novel and appropriate emotions), divergent thinking (the cognitive ability to think of multiple ideas), and creative self-efficacy (CSE; one’s confidence in their ability to be creative) have not been explored simultaneously or in this context. The goal of the present study was to test a multiple mediation model which theorized that exposure to traumatic events would be associated with posttraumatic growth (PTG) and mental health symptoms through emotional creativity, divergent thinking, and CSE in the general population. Findings from a sample of 252 Israeli adults (73% females, aged 19–58), of whom 64% had been exposed to war as civilians, showed that exposure to a greater number of traumatic events was related to higher CSE scores, emotional creativity, and overall divergent thinking. A path analysis to test indirect effects indicated that emotional creativity (but not divergent thinking) followed by CSE mediated the positive association between exposure and PTG as well as the negative association between exposure and mental health symptoms. CSE mediated the association between emotional creativity and divergent thinking to both PTG and mental health symptoms. The results may provide a better understanding of possible paths through which exposure to traumatic events relates to psychological outcomes, highlighting the role of CSE as a mediator that may account for how emotional and cognitive creative abilities are associated with PTG and mental health. (PsycINFO Database Record (c) 2020 APA, all rights reserved)

@article{ceccaroni_opportunities_2019,
	title = {Opportunities and {Risks} for {Citizen} {Science} in the {Age} of {Artificial} {Intelligence}},
	volume = {4},
	copyright = {Authors who publish with this journal agree to the following terms:    Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a  Creative Commons Attribution License  that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.  Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgement of its initial publication in this journal.  Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) prior to and during the submission process, as it can lead to productive exchanges, as well as earlier and greater citation of published work (See  The Effect of Open Access ).  All third-party images reproduced on this journal are shared under Educational Fair Use. For more information on  Educational Fair Use , please see  this useful checklist prepared by Columbia University Libraries .   All copyright  of third-party content posted here for research purposes belongs to its original owners.  Unless otherwise stated all references to characters and comic art presented on this journal are ©, ® or ™ of their respective owners. No challenge to any owner’s rights is intended or should be inferred.},
	issn = {2057-4991},
	url = {http://theoryandpractice.citizenscienceassociation.org/articles/10.5334/cstp.241/},
	doi = {10.5334/cstp.241},
	abstract = {Members of the public are making substantial contributions to science as citizen scientists, and advances in technologies have enabled citizens to make even more substantial contributions. Technologies that allow computers and machines to function in an intelligent manner, often referred to as artificial intelligence (AI), are now being applied in citizen science. Discussions about guidelines, responsibilities, and ethics of AI usage are already happening outside the field of citizen science. We suggest such considerations should also be explored carefully in the context of citizen science applications. To start the conversation, we offer the citizen science community an essay to introduce the state-of-play for AI in citizen science and its potential uses in the future. We begin by presenting a systematic overview of AI technologies currently being applied, highlighting exemplary projects for each technology type described. We then discuss how AI is likely to be increasingly utilised in citizen science into the future, and, through scenarios, we explore both future opportunities and potential risks. Lastly, we conclude by providing recommendations that warrant consideration by the citizen science community, such as developing a data stewardship plan to inform citizens in advance of plans and expected outcomes of using data for AI training, or adopting good practice around anonymity. Our intent is for this essay to lead to further critical discussions among citizen science practitioners, which is needed for responsible, ethical, and useful use of AI in citizen science.},
	language = {en},
	number = {1},
	urldate = {2020-06-05},
	journal = {Citizen Science: Theory and Practice},
	author = {Ceccaroni, Luigi and Bibby, James and Roger, Erin and Flemons, Paul and Michael, Katina and Fagan, Laura and Oliver, Jessica L.},
	month = nov,
	year = {2019},
	note = {ZSCC: 0000003 
Number: 1
Publisher: Ubiquity Press},
	pages = {29},
}

Members of the public are making substantial contributions to science as citizen scientists, and advances in technologies have enabled citizens to make even more substantial contributions. Technologies that allow computers and machines to function in an intelligent manner, often referred to as artificial intelligence (AI), are now being applied in citizen science. Discussions about guidelines, responsibilities, and ethics of AI usage are already happening outside the field of citizen science. We suggest such considerations should also be explored carefully in the context of citizen science applications. To start the conversation, we offer the citizen science community an essay to introduce the state-of-play for AI in citizen science and its potential uses in the future. We begin by presenting a systematic overview of AI technologies currently being applied, highlighting exemplary projects for each technology type described. We then discuss how AI is likely to be increasingly utilised in citizen science into the future, and, through scenarios, we explore both future opportunities and potential risks. Lastly, we conclude by providing recommendations that warrant consideration by the citizen science community, such as developing a data stewardship plan to inform citizens in advance of plans and expected outcomes of using data for AI training, or adopting good practice around anonymity. Our intent is for this essay to lead to further critical discussions among citizen science practitioners, which is needed for responsible, ethical, and useful use of AI in citizen science.

@article{teunisse_human_2019,
	title = {Human enhancement through the lens of experimental and speculative neurotechnologies},
	volume = {1},
	issn = {2578-1863},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6919332/},
	doi = {10.1002/hbe2.179},
	abstract = {Human enhancement deals with improving on and overcoming limitations of the human body and mind. Pharmaceutical compounds that alter consciousness and cognitive performance have been used and discussed for a long time. The prospect of neurotechnological applications such as brain‐steered devices or using invasive and noninvasive electromagnetic stimulations of the human brain, however, has received less attention—especially outside of therapeutic practices—and remains relatively unexplored. Reflection and debates about neurotechnology for human enhancement are limited and remain predominantly with neurotech engineers, science‐fiction enthusiasts and a small circle of academics in the field of neuroethics. It is well known, and described as the Collingridge dilemma, that at an early stage of development, changes can easily be enacted, but the need for changes can hardly be foreseen. Once the technology is entrenched, opportunities and risks start to materialize, and the need to adapt and change is clearly visible. However, carrying out these changes at such a late stage, in turn, becomes very difficult, tremendously expensive, and sometimes practically impossible. In this manuscript, we compile and categorize an overview of existing experimental and speculative applications of neurotechnologies, with the aim to find out, if these real or diegetic prototypes could be used to better understand the paths these applications are forging. In particular, we will investigate what kind of tools, motivations, and normative goals underpin experimental implementations by neurohackers, speculative designers and artists.},
	number = {4},
	urldate = {2020-06-01},
	journal = {Human Behavior and Emerging Technologies},
	author = {Teunisse, Wessel and Youssef, Sandra and Schmidt, Markus},
	month = oct,
	year = {2019},
	pmid = {31894206},
	pmcid = {PMC6919332},
	pages = {361--372},
}

Human enhancement deals with improving on and overcoming limitations of the human body and mind. Pharmaceutical compounds that alter consciousness and cognitive performance have been used and discussed for a long time. The prospect of neurotechnological applications such as brain‐steered devices or using invasive and noninvasive electromagnetic stimulations of the human brain, however, has received less attention—especially outside of therapeutic practices—and remains relatively unexplored. Reflection and debates about neurotechnology for human enhancement are limited and remain predominantly with neurotech engineers, science‐fiction enthusiasts and a small circle of academics in the field of neuroethics. It is well known, and described as the Collingridge dilemma, that at an early stage of development, changes can easily be enacted, but the need for changes can hardly be foreseen. Once the technology is entrenched, opportunities and risks start to materialize, and the need to adapt and change is clearly visible. However, carrying out these changes at such a late stage, in turn, becomes very difficult, tremendously expensive, and sometimes practically impossible. In this manuscript, we compile and categorize an overview of existing experimental and speculative applications of neurotechnologies, with the aim to find out, if these real or diegetic prototypes could be used to better understand the paths these applications are forging. In particular, we will investigate what kind of tools, motivations, and normative goals underpin experimental implementations by neurohackers, speculative designers and artists.

@article{venkatasubramanian_transcranial_2019,
	title = {Transcranial direct current stimulation in psychiatry: {Clinical} neurobiology \& translational implications},
	volume = {5},
	issn = {2455-8559},
	shorttitle = {Transcranial direct current stimulation in psychiatry},
	url = {https://www.innovativepublication.com/journal-article-details/TJP/article/10175/volume/271/issue/793},
	doi = {10.18231/j.tjp.2019.020},
	language = {en},
	number = {2},
	urldate = {2020-06-01},
	journal = {Telangana Journal of Psychiatry},
	author = {Venkatasubramanian, Ganesan and {Psychiatry}},
	month = dec,
	year = {2019},
	pages = {90--91},
}

@article{morya_beyond_2019,
	title = {Beyond the target area: an integrative view of {tDCS}-induced motor cortex modulation in patients and athletes},
	volume = {16},
	issn = {1743-0003},
	shorttitle = {Beyond the target area},
	url = {https://jneuroengrehab.biomedcentral.com/articles/10.1186/s12984-019-0581-1},
	doi = {10.1186/s12984-019-0581-1},
	abstract = {Transcranial Direct Current Stimulation (tDCS) is a non-invasive technique used to modulate neural tissue. Neuromodulation apparently improves cognitive functions in several neurologic diseases treatment and sports performance. In this study, we present a comprehensive, integrative review of tDCS for motor rehabilitation and motor learning in healthy individuals, athletes and multiple neurologic and neuropsychiatric conditions. We also report on neuromodulation mechanisms, main applications, current knowledge including areas such as language, embodied cognition, functional and social aspects, and future directions. We present the use and perspectives of new developments in tDCS technology, namely high-definition tDCS (HD-tDCS) which promises to overcome one of the main tDCS limitation (i.e., low focality) and its application for neurological disease, pain relief, and motor learning/rehabilitation. Finally, we provided information regarding the Transcutaneous Spinal Direct Current Stimulation (tsDCS) in clinical applications, Cerebellar tDCS (ctDCS) and its influence on motor learning, and TMS combined with electroencephalography (EEG) as a tool to evaluate tDCS effects on brain function.},
	language = {en},
	number = {1},
	urldate = {2020-06-01},
	journal = {Journal of NeuroEngineering and Rehabilitation},
	author = {Morya, Edgard and Monte-Silva, Kátia and Bikson, Marom and Esmaeilpour, Zeinab and Biazoli, Claudinei Eduardo and Fonseca, Andre and Bocci, Tommaso and Farzan, Faranak and Chatterjee, Raaj and Hausdorff, Jeffrey M. and da Silva Machado, Daniel Gomes and Brunoni, André Russowsky and Mezger, Eva and Moscaleski, Luciane Aparecida and Pegado, Rodrigo and Sato, João Ricardo and Caetano, Marcelo Salvador and Sá, Kátia Nunes and Tanaka, Clarice and Li, Li Min and Baptista, Abrahão Fontes and Okano, Alexandre Hideki},
	month = dec,
	year = {2019},
	pages = {141},
}

Transcranial Direct Current Stimulation (tDCS) is a non-invasive technique used to modulate neural tissue. Neuromodulation apparently improves cognitive functions in several neurologic diseases treatment and sports performance. In this study, we present a comprehensive, integrative review of tDCS for motor rehabilitation and motor learning in healthy individuals, athletes and multiple neurologic and neuropsychiatric conditions. We also report on neuromodulation mechanisms, main applications, current knowledge including areas such as language, embodied cognition, functional and social aspects, and future directions. We present the use and perspectives of new developments in tDCS technology, namely high-definition tDCS (HD-tDCS) which promises to overcome one of the main tDCS limitation (i.e., low focality) and its application for neurological disease, pain relief, and motor learning/rehabilitation. Finally, we provided information regarding the Transcutaneous Spinal Direct Current Stimulation (tsDCS) in clinical applications, Cerebellar tDCS (ctDCS) and its influence on motor learning, and TMS combined with electroencephalography (EEG) as a tool to evaluate tDCS effects on brain function.

@article{garcia-larrea_at-home_2019,
	title = {At-{Home} {Cortical} {Stimulation} for {Neuropathic} {Pain}: a {Feasibility} {Study} with {Initial} {Clinical} {Results}},
	volume = {16},
	issn = {1878-7479},
	shorttitle = {At-{Home} {Cortical} {Stimulation} for {Neuropathic} {Pain}},
	url = {https://doi.org/10.1007/s13311-019-00734-3},
	doi = {10.1007/s13311-019-00734-3},
	abstract = {The clinical use of noninvasive cortical stimulation procedures is hampered by the limited duration of the analgesic effects and the need to perform stimulation in hospital settings. Here, we tested the feasibility and pilot efficacy of an internet-based system for at-home, long-duration, medically controlled transcranial motor cortex stimulation (H-tDCS), via a double-blinded, sham-controlled trial in patients with neuropathic pain refractory to standard-of-care drug therapy. Each patient was first trained at hospital, received a stimulation kit, allotted a password-protected Web space, and completed daily tDCS sessions during 5 weeks, via a Bluetooth connection between stimulator and a minilaptop. Each session was validated and internet-controlled by hospital personnel. Daily pain ratings were obtained during 11 consecutive weeks, and afterwards via iterative visits/phone contacts. Twenty full procedures were completed in 12 consecutive patients (500 daily tDCS sessions, including 20\% sham). No serious adverse effects were recorded. Superficial burning at electrode position occurred in 2 patients, and nausea/headache in two others, all of whom wished to pursue stimulation. Six out of the 12 patients achieved satisfactory relief on a scale combining pain scores, drug intake, and quality of life. Daily pain reports correlated with such combined assessment, and differentiated responders from nonresponders without overlap. Clinical improvement in responders could last up to 6 months. Five patients asked to repeat the whole procedure when pain resumed again, with comparable results. At-home, long-duration tDCS proved safe and technically feasible, and provided long-lasting relief in 50\% of a small sample of patients with drug-resistant neuropathic pain.},
	language = {en},
	number = {4},
	urldate = {2020-05-22},
	journal = {Neurotherapeutics},
	author = {Garcia-Larrea, Luis and Perchet, Caroline and Hagiwara, Koichi and André-Obadia, Nathalie},
	month = oct,
	year = {2019},
	note = {ZSCC: 0000002},
	pages = {1198--1209},
}

The clinical use of noninvasive cortical stimulation procedures is hampered by the limited duration of the analgesic effects and the need to perform stimulation in hospital settings. Here, we tested the feasibility and pilot efficacy of an internet-based system for at-home, long-duration, medically controlled transcranial motor cortex stimulation (H-tDCS), via a double-blinded, sham-controlled trial in patients with neuropathic pain refractory to standard-of-care drug therapy. Each patient was first trained at hospital, received a stimulation kit, allotted a password-protected Web space, and completed daily tDCS sessions during 5 weeks, via a Bluetooth connection between stimulator and a minilaptop. Each session was validated and internet-controlled by hospital personnel. Daily pain ratings were obtained during 11 consecutive weeks, and afterwards via iterative visits/phone contacts. Twenty full procedures were completed in 12 consecutive patients (500 daily tDCS sessions, including 20% sham). No serious adverse effects were recorded. Superficial burning at electrode position occurred in 2 patients, and nausea/headache in two others, all of whom wished to pursue stimulation. Six out of the 12 patients achieved satisfactory relief on a scale combining pain scores, drug intake, and quality of life. Daily pain reports correlated with such combined assessment, and differentiated responders from nonresponders without overlap. Clinical improvement in responders could last up to 6 months. Five patients asked to repeat the whole procedure when pain resumed again, with comparable results. At-home, long-duration tDCS proved safe and technically feasible, and provided long-lasting relief in 50% of a small sample of patients with drug-resistant neuropathic pain.

@article{brietzke_large_2019,
	title = {Large {Treatment} {Effect} {With} {Extended} {Home}-{Based} {Transcranial} {Direct} {Current} {Stimulation} {Over} {Dorsolateral} {Prefrontal} {Cortex} in {Fibromyalgia}: {A} {Proof} of {Concept} {Sham}-{Randomized} {Clinical} {Study}},
	issn = {1526-5900},
	shorttitle = {Large {Treatment} {Effect} {With} {Extended} {Home}-{Based} {Transcranial} {Direct} {Current} {Stimulation} {Over} {Dorsolateral} {Prefrontal} {Cortex} in {Fibromyalgia}},
	url = {http://www.sciencedirect.com/science/article/pii/S1526590019307709},
	doi = {10.1016/j.jpain.2019.06.013},
	abstract = {This randomized, double-blind controlled trial tested the hypothesis that 60 sessions of home-based anodal (a)-transcranial direct current stimulation (tDCS) over dorsolateral prefrontal cortex (DLPFC) would be better than home-based sham-tDCS to improve the widespread pain and the disability-related to pain. The anodal-tDCS (2 mA for 30 minutes) over the left DLPFC was self-administered with a specially developed device following in-person training. Twenty women, 18 to 65 years old were randomized into 2 groups [active-(a)-tDCS (n = 10) or sham-(s)-tDCS (n = 10)]. Post hoc analysis revealed that after the first 20 sessions of a-tDCS, the cumulative pain scores reduced by 45.65\% [7.25 (1.43) vs 3.94 (1.14), active vs sham tDCS, respectively]. After 60 sessions, during the 12-week assessment, pain scores reduced by 62.06\% in the actively group [visual analogue scale reduction, 7.25 (1.43) to 2.75 (.85)] compared to 24.92\% in the s-tDCS group, [mean (SD) 7.10 (1.81) vs 5.33 (.90)], respectively. It reduced the risk for analgesic use in 55\%. Higher serum levels of the brain-derived neurotrophic factor predicted higher decreases on the pain scores across of treatment.
Perspective
These findings bring 3 important insights: 1) show that an extended period of treatment (60 sessions, to date the largest number of tDCS sessions tested) for fibromyalgia induces large pain decreases (a large effect size of 1.59) and 2) support the feasibility of home-based tDCS as a method of intervention; 3) provide additional data on DLPFC target for the treatment of fibromyalgia. Finally, our findings also highlight that brain-derived neurotrophic factor to index neuroplasticity may be a valuable predictor of the tDCS effect on pain scores decreases across the treatment.},
	language = {en},
	urldate = {2020-05-22},
	journal = {The Journal of Pain},
	author = {Brietzke, Aline P. and Zortea, Maxciel and Carvalho, Fabiana and Sanches, Paulo R. S. and Silva, Danton P. Jr. and Torres, Iraci Lucena da Silva and Fregni, Felipe and Caumo, Wolnei},
	month = jul,
	year = {2019},
	note = {ZSCC: 0000001},
	keywords = {BDNF, Fibromyalgia, depression, disability, pain, tDCS},
}

This randomized, double-blind controlled trial tested the hypothesis that 60 sessions of home-based anodal (a)-transcranial direct current stimulation (tDCS) over dorsolateral prefrontal cortex (DLPFC) would be better than home-based sham-tDCS to improve the widespread pain and the disability-related to pain. The anodal-tDCS (2 mA for 30 minutes) over the left DLPFC was self-administered with a specially developed device following in-person training. Twenty women, 18 to 65 years old were randomized into 2 groups [active-(a)-tDCS (n = 10) or sham-(s)-tDCS (n = 10)]. Post hoc analysis revealed that after the first 20 sessions of a-tDCS, the cumulative pain scores reduced by 45.65% [7.25 (1.43) vs 3.94 (1.14), active vs sham tDCS, respectively]. After 60 sessions, during the 12-week assessment, pain scores reduced by 62.06% in the actively group [visual analogue scale reduction, 7.25 (1.43) to 2.75 (.85)] compared to 24.92% in the s-tDCS group, [mean (SD) 7.10 (1.81) vs 5.33 (.90)], respectively. It reduced the risk for analgesic use in 55%. Higher serum levels of the brain-derived neurotrophic factor predicted higher decreases on the pain scores across of treatment. Perspective These findings bring 3 important insights: 1) show that an extended period of treatment (60 sessions, to date the largest number of tDCS sessions tested) for fibromyalgia induces large pain decreases (a large effect size of 1.59) and 2) support the feasibility of home-based tDCS as a method of intervention; 3) provide additional data on DLPFC target for the treatment of fibromyalgia. Finally, our findings also highlight that brain-derived neurotrophic factor to index neuroplasticity may be a valuable predictor of the tDCS effect on pain scores decreases across the treatment.

@article{wang_metformin_2019,
	title = {Metformin attenuates bleomycin-induced scleroderma by regulating the balance of {Treg}/{Teff} cells and reducing spleen germinal center formation},
	volume = {114},
	issn = {01615890},
	url = {https://linkinghub.elsevier.com/retrieve/pii/S0161589019300100},
	doi = {10.1016/j.molimm.2019.07.002},
	abstract = {Scleroderma is an inflammatory autoimmune disease characterized by extensive tissue fibrosis. The imbalance of effector T (Teff) and regulatory T (Treg) cells and the production of autoantibodies contribute to the pathogenesis of this disease. Metformin (MET) has anti-inflammatory and anti-fibrotic effects, but its effect on the in vivo pathogenesis of scleroderma remains unknown. Therefore, we investigated the potential therapeutic effects of MET treatment of mice with bleomycin (BLM)-induced scleroderma. Scleroderma was induced in female C57BL mice by daily subcutaneous injections of BLM for 28 days. After each 2 h BLM injection, mice received MET (200, 100 or 50 mg/kg) or saline (control) by intraperitoneal injection. At the end of the fourth week, spleen mononuclear cells were collected for flow cytometry analysis. Skin samples were harvested for immunohistochemistry and quantification of other biological parameters.Our results showed that BLM increased dermal thickness, collagen deposition, and hydroxyproline level, and MET markedly mitigated these effects. MET also restored the Treg/Teff cell balance. Accordingly, the level of IL-17A and RORγt (related to Th17 cells) decreased, but Foxp3 (related to Treg function) increased in a dose-dependent manner. In addition, MET treatment inhibited spleen germinal center formation. These results indicate that the immunomodulatory and anti-fibrosis effects of MET on BLM-induced scleroderma are mediated by the upregulation of Treg cell differentiation, inhibition of Teff cell differentiation, and suppression of spleen germinal center formation. These results suggest that MET may be a potential therapeutic for scleroderma.},
	language = {en},
	urldate = {2020-05-22},
	journal = {Molecular Immunology},
	author = {Wang, Yanlin and Zhang, Shulan and Liang, Zhaojun and Feng, Min and Zhao, Xiangcong and Qin, Kaili and Gao, Chong and Li, Xiaofeng and Guo, Hui and Luo, Jing},
	month = oct,
	year = {2019},
	pages = {72--80},
}

Scleroderma is an inflammatory autoimmune disease characterized by extensive tissue fibrosis. The imbalance of effector T (Teff) and regulatory T (Treg) cells and the production of autoantibodies contribute to the pathogenesis of this disease. Metformin (MET) has anti-inflammatory and anti-fibrotic effects, but its effect on the in vivo pathogenesis of scleroderma remains unknown. Therefore, we investigated the potential therapeutic effects of MET treatment of mice with bleomycin (BLM)-induced scleroderma. Scleroderma was induced in female C57BL mice by daily subcutaneous injections of BLM for 28 days. After each 2 h BLM injection, mice received MET (200, 100 or 50 mg/kg) or saline (control) by intraperitoneal injection. At the end of the fourth week, spleen mononuclear cells were collected for flow cytometry analysis. Skin samples were harvested for immunohistochemistry and quantification of other biological parameters.Our results showed that BLM increased dermal thickness, collagen deposition, and hydroxyproline level, and MET markedly mitigated these effects. MET also restored the Treg/Teff cell balance. Accordingly, the level of IL-17A and RORγt (related to Th17 cells) decreased, but Foxp3 (related to Treg function) increased in a dose-dependent manner. In addition, MET treatment inhibited spleen germinal center formation. These results indicate that the immunomodulatory and anti-fibrosis effects of MET on BLM-induced scleroderma are mediated by the upregulation of Treg cell differentiation, inhibition of Teff cell differentiation, and suppression of spleen germinal center formation. These results suggest that MET may be a potential therapeutic for scleroderma.

@article{ryff_entrepreneurship_2019,
	title = {Entrepreneurship and eudaimonic well-being: {Five} venues for new science},
	volume = {34},
	issn = {08839026},
	shorttitle = {Entrepreneurship and eudaimonic well-being},
	url = {https://linkinghub.elsevier.com/retrieve/pii/S0883902617307899},
	doi = {10.1016/j.jbusvent.2018.09.003},
	abstract = {Researchers in entrepreneurial studies are increasingly interested in the psychological well-being of entrepreneurs. Approaches to well-being tend to be partitioned into hedonic and eudaimonic formulations. Most entrepreneurial studies have focused on hedonic indicators (life satisfaction, happiness, positive affect). The central objective of this essay is to examine the relevance of eudaimonic well-being for understanding entrepreneurial experience. The theoretical background and key dimensions of eudaimonic well-being are described and their relevance for entrepreneurial studies is considered. Illustrative findings from prior well-being studies are examined, also with emphasis on possible extensions to entrepreneurship. Five key venues for the entrepreneurial field are then considered: (1) entrepreneurship and autonomy, viewed both as a motive (self-determination theory) and as an aspect of well-being (eudaimonic well-being theory); (2) varieties of entrepreneurship (opportunity versus necessity) and eudaimonic wellbeing; (3) eudaimonia in the entrepreneurial journey (beginning, middle, end); (4) entrepreneurship, well-being and health; and (5) entrepreneurs and the eudaimonia of others –contrasting virtuous and vicious types. In each topic, extant findings from entrepreneurial studies are considered and new research directions proposed. The overall aim is to be generative regarding the interplay between entrepreneurial experience and eudaimonic well-being.},
	language = {en},
	number = {4},
	urldate = {2020-04-02},
	journal = {Journal of Business Venturing},
	author = {Ryff, Carol D.},
	month = jul,
	year = {2019},
	note = {ZSCC: 0000013},
	pages = {646--663},
}

Researchers in entrepreneurial studies are increasingly interested in the psychological well-being of entrepreneurs. Approaches to well-being tend to be partitioned into hedonic and eudaimonic formulations. Most entrepreneurial studies have focused on hedonic indicators (life satisfaction, happiness, positive affect). The central objective of this essay is to examine the relevance of eudaimonic well-being for understanding entrepreneurial experience. The theoretical background and key dimensions of eudaimonic well-being are described and their relevance for entrepreneurial studies is considered. Illustrative findings from prior well-being studies are examined, also with emphasis on possible extensions to entrepreneurship. Five key venues for the entrepreneurial field are then considered: (1) entrepreneurship and autonomy, viewed both as a motive (self-determination theory) and as an aspect of well-being (eudaimonic well-being theory); (2) varieties of entrepreneurship (opportunity versus necessity) and eudaimonic wellbeing; (3) eudaimonia in the entrepreneurial journey (beginning, middle, end); (4) entrepreneurship, well-being and health; and (5) entrepreneurs and the eudaimonia of others –contrasting virtuous and vicious types. In each topic, extant findings from entrepreneurial studies are considered and new research directions proposed. The overall aim is to be generative regarding the interplay between entrepreneurial experience and eudaimonic well-being.

@article{thomas_potential_2019,
	title = {Potential {Applications} of {Digital} {Technology} in {Assessment}, {Treatment}, and {Self}-help for {Hallucinations}},
	volume = {45},
	issn = {0586-7614, 1745-1701},
	url = {https://academic.oup.com/schizophreniabulletin/article/45/Supplement_1/S32/5305655},
	doi = {10.1093/schbul/sby103},
	language = {en},
	number = {Supplement\_1},
	urldate = {2020-04-02},
	journal = {Schizophrenia Bulletin},
	author = {Thomas, Neil and Bless, Josef J and Alderson-Day, Ben and Bell, Imogen H and Cella, Matteo and Craig, Tom and Delespaul, Philippe and Hugdahl, Kenneth and Laloyaux, Julien and Larøi, Frank and Lincoln, Tania M and Schlier, Björn and Urwyler, Prabitha and van den Berg, David and Jardri, Renaud},
	month = feb,
	year = {2019},
	note = {ZSCC: NoCitationData[s0]},
	pages = {S32--S42},
}

@article{goldberg_ketogenic_2019,
	title = {Ketogenic diet activates protective γδ {T} cell responses against influenza virus infection},
	volume = {4},
	copyright = {Copyright © 2019 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. http://www.sciencemag.org/about/science-licenses-journal-article-reuseThis is an article distributed under the terms of the Science Journals Default License.},
	issn = {2470-9468},
	url = {https://immunology.sciencemag.org/content/4/41/eaav2026},
	doi = {10.1126/sciimmunol.aav2026},
	abstract = {Putting mice on a keto diet
Our immune responses to infections are influenced by several extrinsic factors, including weather, social interactions, and diet. Here, Goldberg et al. report that feeding mice a high-fat, low-carbohydrate ketogenic diet confers protection in the context of lethal influenza infection. By characterizing the immune response in the lungs, the authors identified that ketogenic diet promoted the expansion of γδ T cells in the lung. Using mice lacking γδ T cells, the authors have established the functional importance of these cells in conferring protection. Their findings suggest that γδ T cells improve barrier function in the lungs by modifying differentiation and function of the airway epithelial cells.
Influenza A virus (IAV) infection–associated morbidity and mortality are a key global health care concern, necessitating the identification of new therapies capable of reducing the severity of IAV infections. In this study, we show that the consumption of a low-carbohydrate, high-fat ketogenic diet (KD) protects mice from lethal IAV infection and disease. KD feeding resulted in an expansion of γδ T cells in the lung that improved barrier functions, thereby enhancing antiviral resistance. Expansion of these protective γδ T cells required metabolic adaptation to a ketogenic diet because neither feeding mice a high-fat, high-carbohydrate diet nor providing chemical ketone body substrate that bypasses hepatic ketogenesis protected against infection. Therefore, KD-mediated immune-metabolic integration represents a viable avenue toward preventing or alleviating influenza disease.
Ketogenic diet protects mice against influenza virus infection through γδ T cell expansion and metabolic adaptation.
Ketogenic diet protects mice against influenza virus infection through γδ T cell expansion and metabolic adaptation.},
	language = {en},
	number = {41},
	urldate = {2020-04-01},
	journal = {Science Immunology},
	author = {Goldberg, Emily L. and Molony, Ryan D. and Kudo, Eriko and Sidorov, Sviatoslav and Kong, Yong and Dixit, Vishwa Deep and Iwasaki, Akiko},
	month = nov,
	year = {2019},
	pmid = {31732517},
	note = {ZSCC: 0000004 
Publisher: Science Immunology
Section: Reports},
}

Putting mice on a keto diet Our immune responses to infections are influenced by several extrinsic factors, including weather, social interactions, and diet. Here, Goldberg et al. report that feeding mice a high-fat, low-carbohydrate ketogenic diet confers protection in the context of lethal influenza infection. By characterizing the immune response in the lungs, the authors identified that ketogenic diet promoted the expansion of γδ T cells in the lung. Using mice lacking γδ T cells, the authors have established the functional importance of these cells in conferring protection. Their findings suggest that γδ T cells improve barrier function in the lungs by modifying differentiation and function of the airway epithelial cells. Influenza A virus (IAV) infection–associated morbidity and mortality are a key global health care concern, necessitating the identification of new therapies capable of reducing the severity of IAV infections. In this study, we show that the consumption of a low-carbohydrate, high-fat ketogenic diet (KD) protects mice from lethal IAV infection and disease. KD feeding resulted in an expansion of γδ T cells in the lung that improved barrier functions, thereby enhancing antiviral resistance. Expansion of these protective γδ T cells required metabolic adaptation to a ketogenic diet because neither feeding mice a high-fat, high-carbohydrate diet nor providing chemical ketone body substrate that bypasses hepatic ketogenesis protected against infection. Therefore, KD-mediated immune-metabolic integration represents a viable avenue toward preventing or alleviating influenza disease. Ketogenic diet protects mice against influenza virus infection through γδ T cell expansion and metabolic adaptation. Ketogenic diet protects mice against influenza virus infection through γδ T cell expansion and metabolic adaptation.

@article{elsner_beyond_2019,
	title = {Beyond {Medical} {Paternalism}: {Undoing} the {Doctor}-{Patient} {Relationship} in {Simone} de {Beauvoir}'s {A} {Very} {Easy} {Death}},
	volume = {37},
	issn = {1080-6571},
	shorttitle = {Beyond {Medical} {Paternalism}},
	url = {https://muse.jhu.edu/article/745344},
	doi = {10.1353/lm.2019.0019},
	abstract = {In A Very Easy Death Simone de Beauvoir documents the illness, hospitalization, and death of her mother Françoise. Critics in the fields of bioethics and the medical humanities have concentrated on the text’s paternalistic doctor-patient encounter, which culminates in the withholding of the cancer diagnosis from Beauvoir’s mother and entails an unnecessary medical intervention to which the patient never consents. Reviewing the text’s reception, this article argues that a focus on the ways in which it depicts breaches of several tenets of medical ethics have decontextualized A Very Easy Death and occluded the key role Beauvoir plays in the doctor-patient relationship. By situating the text within Beauvoir’s œuvre and debates in French philosophy of medicine at the time of publication, this article proposes that Beauvoir’s part in the withholding of the cancer diagnosis emerges less as a submission to medical paternalism than as a form of maternal caregiving.},
	language = {en},
	number = {2},
	urldate = {2020-03-25},
	journal = {Literature and Medicine},
	author = {Elsner, Anna Magdalena},
	month = dec,
	year = {2019},
	note = {ZSCC: 0000000 
Publisher: Johns Hopkins University Press},
	pages = {420--441},
}

In A Very Easy Death Simone de Beauvoir documents the illness, hospitalization, and death of her mother Françoise. Critics in the fields of bioethics and the medical humanities have concentrated on the text’s paternalistic doctor-patient encounter, which culminates in the withholding of the cancer diagnosis from Beauvoir’s mother and entails an unnecessary medical intervention to which the patient never consents. Reviewing the text’s reception, this article argues that a focus on the ways in which it depicts breaches of several tenets of medical ethics have decontextualized A Very Easy Death and occluded the key role Beauvoir plays in the doctor-patient relationship. By situating the text within Beauvoir’s œuvre and debates in French philosophy of medicine at the time of publication, this article proposes that Beauvoir’s part in the withholding of the cancer diagnosis emerges less as a submission to medical paternalism than as a form of maternal caregiving.

@article{schwartz_psychiatric_2019,
	title = {Psychiatric {Skepticism} in {Medical} {Education}: {Why} {We} {Need} {Philosophy}},
	volume = {43},
	issn = {1545-7230},
	shorttitle = {Psychiatric {Skepticism} in {Medical} {Education}},
	url = {https://doi.org/10.1007/s40596-019-01049-3},
	doi = {10.1007/s40596-019-01049-3},
	language = {en},
	number = {4},
	urldate = {2020-03-23},
	journal = {Academic Psychiatry},
	author = {Schwartz, Zachary H.},
	month = aug,
	year = {2019},
	pages = {461--463},
}

@article{banker_hypo-egoic_2019,
	title = {Hypo-{Egoic} {Nonentitlement} as a {Feature} of {Humility}},
	issn = {0146-1672},
	url = {https://doi.org/10.1177/0146167219875144},
	doi = {10.1177/0146167219875144},
	abstract = {Two studies tested the hypothesis that humility is characterized by the belief that, no matter how extraordinary one’s accomplishments or characteristics may be, one is not entitled to be treated special because of them (hypo-egoic nonentitlement). Participants identified either one (Study 1) or five (Study 2) positive accomplishments or characteristics, rated those accomplishments/characteristics, indicated how they believed they should be treated because of them, and completed measures of humility and related constructs. As predicted, humility was inversely associated with the belief that other people should treat one special because of one’s accomplishments and positive characteristics. However, humility was not related to participants’ ratings of the positivity of their accomplishments or characteristics or of themselves. Ancillary analyses examined the relationships between hypo-egoic nonentitlement, humility, and measures of self-esteem, narcissism, self- and other-interest, psychological entitlement, individualism-collectivism, and identification with humanity.},
	language = {en},
	urldate = {2020-03-20},
	journal = {Personality and Social Psychology Bulletin},
	author = {Banker, Chloe C. and Leary, Mark R.},
	month = sep,
	year = {2019},
	note = {Publisher: SAGE Publications Inc},
	pages = {0146167219875144},
}

Two studies tested the hypothesis that humility is characterized by the belief that, no matter how extraordinary one’s accomplishments or characteristics may be, one is not entitled to be treated special because of them (hypo-egoic nonentitlement). Participants identified either one (Study 1) or five (Study 2) positive accomplishments or characteristics, rated those accomplishments/characteristics, indicated how they believed they should be treated because of them, and completed measures of humility and related constructs. As predicted, humility was inversely associated with the belief that other people should treat one special because of one’s accomplishments and positive characteristics. However, humility was not related to participants’ ratings of the positivity of their accomplishments or characteristics or of themselves. Ancillary analyses examined the relationships between hypo-egoic nonentitlement, humility, and measures of self-esteem, narcissism, self- and other-interest, psychological entitlement, individualism-collectivism, and identification with humanity.

@article{walker_falling_2019,
	title = {Falling {UP} to {Recovery}: co-created, artistic practice for holistic mental health care in {Scotland}},
	volume = {22},
	issn = {1460-6925, 1756-3062},
	shorttitle = {Falling {UP} to {Recovery}},
	url = {https://www.tandfonline.com/doi/full/10.1080/14606925.2019.1595443},
	doi = {10.1080/14606925.2019.1595443},
	abstract = {This paper focuses on Gugging’s model of therapeutic care for mental illness. It introduces the constantly evolving concept of Gugging and its holistic methodology as a sustainable, humane, creative alternative to the predominant model currently adopted in Scotland. Primary research fieldwork is carried out through participation, residency and collaborative processes, in Austria. Gugging advocates an empathetic, person-centred model of healthcare connecting to principles of on-going design for mental health. The theme and concept of Gugging’s process underpins the exploratory nature and creative processes of Falling UP, which itself is a unique, holistic creative intervention, constantly evolving, adapted and honed through practice-based doctoral research; offering a radical rethink of how mental healthcare can be conceptualized and considered in Scotland. In this paper, both Gugging and Falling UP are presented as integral to the lead author’s ongoing recovery from mental illness and his ever-developing relationship to it.},
	language = {en},
	number = {sup1},
	urldate = {2020-03-20},
	journal = {The Design Journal},
	author = {Walker, Drew Max and Valentine, Louise and Mackenna, Tracy},
	month = apr,
	year = {2019},
	pages = {627--640},
}

This paper focuses on Gugging’s model of therapeutic care for mental illness. It introduces the constantly evolving concept of Gugging and its holistic methodology as a sustainable, humane, creative alternative to the predominant model currently adopted in Scotland. Primary research fieldwork is carried out through participation, residency and collaborative processes, in Austria. Gugging advocates an empathetic, person-centred model of healthcare connecting to principles of on-going design for mental health. The theme and concept of Gugging’s process underpins the exploratory nature and creative processes of Falling UP, which itself is a unique, holistic creative intervention, constantly evolving, adapted and honed through practice-based doctoral research; offering a radical rethink of how mental healthcare can be conceptualized and considered in Scotland. In this paper, both Gugging and Falling UP are presented as integral to the lead author’s ongoing recovery from mental illness and his ever-developing relationship to it.

@article{calo_exploring_2019,
	title = {Exploring the contribution of social enterprise to health and social care: {A} realist evaluation},
	volume = {222},
	issn = {02779536},
	shorttitle = {Exploring the contribution of social enterprise to health and social care},
	url = {https://linkinghub.elsevier.com/retrieve/pii/S0277953619300073},
	doi = {10.1016/j.socscimed.2019.01.007},
	abstract = {Since the late 1990s social enterprises have been increasingly utilised as a means of delivering of health and social care services. However, there is little evidence on if, and how, provision by social enterprise might achieve positive health outcomes, particularly in comparison to other modes of delivery. In this paper, we draw upon the multiple perspectives offered by stakeholders involved in a rural social enterprise initiative based in Scotland, UK, and in a nearby comparator public sector organisation. Both types of organisation aim to increase the physical activity levels of people with chronic health conditions. In order to gain perspectives on the range of mechanisms and outcomes involved in different types of organisation providing similar interventions, realist evaluation of data gathered from in-depth semi-structured interviews (n = 68) was undertaken. Interviews were carried out with beneficiaries, service providers and external stakeholders and Context-Mechanism-Outcome (CMO) configurations developed to support our explanations for how, and in what ways, social enterprise might impact differently on health. Our findings highlight that the social enterprise is differentiated from the publiclyrun service in two distinct ways: firstly, the social enterprise was better able to flexibly deliver a bespoke programme designed around the needs of service users; and secondly, their role as a community ‘boundary spanner’ helped facilitate strong ties and feelings of connectedness between beneficiaries, organisational staff and community stakeholders. However, these advantages were significantly compromised when funding was constrained. Our findings serve as an important basis for future research to better understand the means by which social enterprises might deliver health outcomes, particularly in comparison with public sector providers.},
	language = {en},
	urldate = {2020-03-19},
	journal = {Social Science \& Medicine},
	author = {Caló, Francesca and Roy, Michael James and Donaldson, Cam and Teasdale, Simon and Baglioni, Simone},
	month = feb,
	year = {2019},
	pages = {154--161},
}

Since the late 1990s social enterprises have been increasingly utilised as a means of delivering of health and social care services. However, there is little evidence on if, and how, provision by social enterprise might achieve positive health outcomes, particularly in comparison to other modes of delivery. In this paper, we draw upon the multiple perspectives offered by stakeholders involved in a rural social enterprise initiative based in Scotland, UK, and in a nearby comparator public sector organisation. Both types of organisation aim to increase the physical activity levels of people with chronic health conditions. In order to gain perspectives on the range of mechanisms and outcomes involved in different types of organisation providing similar interventions, realist evaluation of data gathered from in-depth semi-structured interviews (n = 68) was undertaken. Interviews were carried out with beneficiaries, service providers and external stakeholders and Context-Mechanism-Outcome (CMO) configurations developed to support our explanations for how, and in what ways, social enterprise might impact differently on health. Our findings highlight that the social enterprise is differentiated from the publiclyrun service in two distinct ways: firstly, the social enterprise was better able to flexibly deliver a bespoke programme designed around the needs of service users; and secondly, their role as a community ‘boundary spanner’ helped facilitate strong ties and feelings of connectedness between beneficiaries, organisational staff and community stakeholders. However, these advantages were significantly compromised when funding was constrained. Our findings serve as an important basis for future research to better understand the means by which social enterprises might deliver health outcomes, particularly in comparison with public sector providers.

@incollection{steingard_toward_2019,
	address = {Cham},
	title = {Toward {Conceptual} {Competence} in {Psychiatric} {Diagnosis}: {An} {Ecological} {Model} for {Critiques} of the {DSM}},
	isbn = {978-3-030-02731-5 978-3-030-02732-2},
	shorttitle = {Toward {Conceptual} {Competence} in {Psychiatric} {Diagnosis}},
	url = {http://link.springer.com/10.1007/978-3-030-02732-2_2},
	language = {en},
	urldate = {2020-03-18},
	booktitle = {Critical {Psychiatry}},
	publisher = {Springer International Publishing},
	author = {Karter, Justin M. and Kamens, Sarah R.},
	editor = {Steingard, Sandra},
	year = {2019},
	doi = {10.1007/978-3-030-02732-2_2},
	pages = {17--69},
}

@article{lane_expanding_2019,
	title = {Expanding boundaries in psychiatry: uncertainty in the context of diagnosis-seeking and negotiation},
	shorttitle = {Expanding boundaries in psychiatry},
	journal = {Sociology of Health \& Illness},
	author = {Lane, Rhiannon},
	year = {2019},
	note = {Publisher: Wiley Online Library},
	keywords = {ethno, ethnography, identity, medicalisation, mental health services, professional–patient interaction, uncertainty},
}

@article{tong_concurrent_2019,
	title = {Concurrent and {Temporal} {Relationships} {Between} {Humility} and {Emotional} and {Psychological} {Well}-{Being}},
	volume = {20},
	issn = {1389-4978, 1573-7780},
	url = {http://link.springer.com/10.1007/s10902-018-0002-3},
	doi = {10.1007/s10902-018-0002-3},
	abstract = {The present research is a preliminary investigation of the concurrent and temporal relationships between humility and two forms of well-being: emotional and psychological wellbeing. Humility, emotional well-being and psychological well-being were measured twice 6 weeks apart. Humility correlated positively with psychological well-being at both timepoints, but was positively related to emotional well-being at only one time-point. In addition, we used structural equation modeling to perform cross-lagged panel analyses, and found that psychological well-being predicted an increase in humility over time, but humility did not predict changes in psychological well-being over time. In addition, there were no cross-lagged associations between emotional well-being and humility. The results suggest that humility does not necessarily lead to more pleasant or fulfilling experiences, but psychological well-being is conducive to cultivating humility.},
	language = {en},
	number = {5},
	urldate = {2020-03-13},
	journal = {Journal of Happiness Studies},
	author = {Tong, Eddie M. W. and Lum, Darren J. K. and Sasaki, Eri and Yu, Zhaoliang},
	month = jun,
	year = {2019},
	pages = {1343--1358},
}

The present research is a preliminary investigation of the concurrent and temporal relationships between humility and two forms of well-being: emotional and psychological wellbeing. Humility, emotional well-being and psychological well-being were measured twice 6 weeks apart. Humility correlated positively with psychological well-being at both timepoints, but was positively related to emotional well-being at only one time-point. In addition, we used structural equation modeling to perform cross-lagged panel analyses, and found that psychological well-being predicted an increase in humility over time, but humility did not predict changes in psychological well-being over time. In addition, there were no cross-lagged associations between emotional well-being and humility. The results suggest that humility does not necessarily lead to more pleasant or fulfilling experiences, but psychological well-being is conducive to cultivating humility.

@article{szilagyi_drug_2018,
	title = {Drug discovery strategies and the preclinical development of {D}-amino-acid oxidase inhibitors as antipsychotic therapies},
	volume = {13},
	issn = {1746-0441},
	url = {https://doi.org/10.1080/17460441.2018.1524459},
	doi = {10.1080/17460441.2018.1524459},
	abstract = {Introduction: D-amino-acid oxidase (DAAO) degrades D-serine, a co-agonist of the NMDA receptor whose dysfunction is involved in the positive, negative, and cognitive symptoms of schizophrenia. The inhibition of DAAO appears to be a viable strategy to increase D-serine level and to have therapeutic potential in schizophrenia.Areas covered: This review describes the efforts to develop DAAO inhibitors and to optimize their in vitro and in vivo effects in preclinical settings. The structural evolution of DAAO inhibitors is presented from simple carboxylic acid derivatives via small, planar compounds with carboxylic acid mimetics to extended compounds whose binding is possible owing to DAAO flexibility. Inhibitory potency and pharmacokinetic properties are discussed in the context of compounds’ ability to increase D-serine level and to show efficacy in animal models of schizophrenia.Expert opinion: The accumulated knowledge on the structural requirements of DAAO inhibitors and on their in vitro and in vivo effects provides appropriate basis to develop inhibitors with optimized potency, selectivity and pharmacokinetic profile including blood-brain penetration. In addition, the validation of DAAO inhibition therapy in alleviating the symptoms of schizophrenia requires further studies on the efficacy of DAAO inhibitors in behavioral assays of animals and on the species differences in D-serine metabolism.},
	number = {10},
	urldate = {2021-12-21},
	journal = {Expert Opinion on Drug Discovery},
	author = {Szilágyi, Bence and Ferenczy, György G. and Keserű, György M.},
	month = oct,
	year = {2018},
	pmid = {30220232},
	note = {Publisher: Taylor \& Francis
\_eprint: https://doi.org/10.1080/17460441.2018.1524459},
	keywords = {D-amino-acid oxidase, D-serine, schizophrenia},
	pages = {973--982},
}

Introduction: D-amino-acid oxidase (DAAO) degrades D-serine, a co-agonist of the NMDA receptor whose dysfunction is involved in the positive, negative, and cognitive symptoms of schizophrenia. The inhibition of DAAO appears to be a viable strategy to increase D-serine level and to have therapeutic potential in schizophrenia.Areas covered: This review describes the efforts to develop DAAO inhibitors and to optimize their in vitro and in vivo effects in preclinical settings. The structural evolution of DAAO inhibitors is presented from simple carboxylic acid derivatives via small, planar compounds with carboxylic acid mimetics to extended compounds whose binding is possible owing to DAAO flexibility. Inhibitory potency and pharmacokinetic properties are discussed in the context of compounds’ ability to increase D-serine level and to show efficacy in animal models of schizophrenia.Expert opinion: The accumulated knowledge on the structural requirements of DAAO inhibitors and on their in vitro and in vivo effects provides appropriate basis to develop inhibitors with optimized potency, selectivity and pharmacokinetic profile including blood-brain penetration. In addition, the validation of DAAO inhibition therapy in alleviating the symptoms of schizophrenia requires further studies on the efficacy of DAAO inhibitors in behavioral assays of animals and on the species differences in D-serine metabolism.

@article{bellmund_navigating_2018,
	title = {Navigating cognition: {Spatial} codes for human thinking},
	volume = {362},
	copyright = {Copyright © 2018 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. http://www.sciencemag.org/about/science-licenses-journal-article-reuseThis is an article distributed under the terms of the Science Journals Default License.},
	issn = {0036-8075, 1095-9203},
	shorttitle = {Navigating cognition},
	url = {https://science.sciencemag.org/content/362/6415/eaat6766},
	doi = {10.1126/science.aat6766},
	abstract = {A framework for cognitive spaces
Ever since Tolman's proposal of cognitive maps in the 1940s, the question of how spatial representations support flexible behavior has been a contentious topic. Bellmund et al. review and combine concepts from cognitive science and philosophy with findings from neurophysiology of spatial navigation in rodents to propose a framework for cognitive neuroscience. They argue that spatial-processing principles in the hippocampalentorhinal region provide a geometric code to map information domains of cognitive spaces for high-level cognition and discuss recent evidence for this proposal.
Science, this issue p. eaat6766
Structured Abstract
BACKGROUNDEver since Edward Tolman’s proposal that comprehensive cognitive maps underlie spatial navigation and, more generally, psychological functions, the question of how past experience guides behavior has been contentious. The discovery of place cells in rodents, signaling the animal’s position in space, suggested that such cognitive maps reside in the hippocampus, a core brain region for human memory. Building on the description of place cells, several other functionally defined cell types were discovered in the hippocampal-entorhinal region. Among them are grid cells in the entorhinal cortex, whose characteristic periodic, six-fold symmetric firing patterns are thought to provide a spatial metric. These findings were complemented by insights into key coding principles of the hippocampal-entorhinal region: Spatial representations vary in scale along the hippocampal long axis, place cells remap to map different environments, and sequential hippocampal activity represents nonlocal trajectories through space. In humans, the existence of spatially tuned cells has been demonstrated in presurgical patients, and functional magnetic resonance imaging provides proxy measures for the noninvasive investigation of these processing mechanisms in human cognition. Intriguingly, recent advances indicate that place and grid cells can encode positions along dimensions of experience beyond Euclidean space for navigation, suggesting a more general role of hippocampal-entorhinal processing mechanisms in cognition.
ADVANCESWe combine hippocampal-entorhinal processing mechanisms identified in spatial navigation research with ideas from cognitive science describing a spatial representational format for cognition. Cognitive spaces are spanned by dimensions satisfying geometric constraints such as betweenness and equidistance, enabling the representation of properties and concepts as convex regions of cognitive space. We propose that the continuous population code of place and grid cells in the hippocampal-entorhinal region maps the dimensions of cognitive spaces. In these, each stimulus is located according to its feature values along the relevant dimensions, resulting in nearby positions for similar stimuli and larger distances between dissimilar stimuli. The low-dimensional, rigid firing properties of the entorhinal grid system make it a candidate to provide a metric or distance code for cognitive spaces, whereas hippocampal place cells flexibly represent positions in a given space. This mapping of cognitive spaces is complemented by the additional coding principles outlined above: Along the hippocampal long axis, cognitive spaces are mapped with varying spatial scale, supporting memory and knowledge representations at different levels of granularity. Via hippocampal remapping, spaces spanned by different dimensions can be flexibly mapped and established maps can be reinstated via attractor dynamics. The geometric definition of cognitive spaces allows flexible generalization and inference, and sequential hippocampal activity can simulate trajectories through cognitive spaces for adaptive decision-making and behavior.
OUTLOOKCognitive spaces provide a domain-general format for processing in the hippocampal-entorhinal region, in line with its involvement beyond navigation and memory. Spatial navigation serves as a model system to identify key coding principles governing cognitive spaces. An important question concerns the extent to which firing properties of spatially tuned cells are preserved in cognitive spaces. Technological advances such as calcium imaging will clarify coding principles on the population level and facilitate the translation to human cognitive neuroscience. Spatial navigation is mostly investigated in two dimensions and naturally limited to three dimensions; however, the processing of complex, multidimensional concepts is vital to high-level human cognition, and the representation of such high-dimensional spaces is an intriguing question for future research. Further, the role of brain networks acting in concert with the hippocampus, in navigation specifically and cognitive function in general, will provide insight into whether and how cognitive spaces are supported beyond the hippocampal-entorhinal region. Finally, the precise way in which cognitive spaces and trajectories through them are read out for behavior remains to be elucidated. {\textless}img class="fragment-image" aria-describedby="F1-caption" src="https://science.sciencemag.org/content/sci/362/6415/eaat6766/F1.medium.gif"/{\textgreater} Download high-res image Open in new tab Download Powerpoint Place and grid cells map cognitive spaces.Cognitive spaces are defined by dimensions satisfying geometric constraints. The example space (left) is spanned by the dimensions of engine power and car weight. Black dots show different vehicles whose positions reflect their feature combinations. Place cells (center; colored circles represent firing fields of different cells) and grid cells (right; circles illustrate firing pattern of one cell) provide a continuous code for cognitive spaces.
The hippocampal formation has long been suggested to underlie both memory formation and spatial navigation. We discuss how neural mechanisms identified in spatial navigation research operate across information domains to support a wide spectrum of cognitive functions. In our framework, place and grid cell population codes provide a representational format to map variable dimensions of cognitive spaces. This highly dynamic mapping system enables rapid reorganization of codes through remapping between orthogonal representations across behavioral contexts, yielding a multitude of stable cognitive spaces at different resolutions and hierarchical levels. Action sequences result in trajectories through cognitive space, which can be simulated via sequential coding in the hippocampus. In this way, the spatial representational format of the hippocampal formation has the capacity to support flexible cognition and behavior.},
	language = {en},
	number = {6415},
	urldate = {2021-07-28},
	journal = {Science},
	author = {Bellmund, Jacob L. S. and Gärdenfors, Peter and Moser, Edvard I. and Doeller, Christian F.},
	month = nov,
	year = {2018},
	pmid = {30409861},
	note = {Publisher: American Association for the Advancement of Science
Section: Review},
}

A framework for cognitive spaces Ever since Tolman's proposal of cognitive maps in the 1940s, the question of how spatial representations support flexible behavior has been a contentious topic. Bellmund et al. review and combine concepts from cognitive science and philosophy with findings from neurophysiology of spatial navigation in rodents to propose a framework for cognitive neuroscience. They argue that spatial-processing principles in the hippocampalentorhinal region provide a geometric code to map information domains of cognitive spaces for high-level cognition and discuss recent evidence for this proposal. Science, this issue p. eaat6766 Structured Abstract BACKGROUNDEver since Edward Tolman’s proposal that comprehensive cognitive maps underlie spatial navigation and, more generally, psychological functions, the question of how past experience guides behavior has been contentious. The discovery of place cells in rodents, signaling the animal’s position in space, suggested that such cognitive maps reside in the hippocampus, a core brain region for human memory. Building on the description of place cells, several other functionally defined cell types were discovered in the hippocampal-entorhinal region. Among them are grid cells in the entorhinal cortex, whose characteristic periodic, six-fold symmetric firing patterns are thought to provide a spatial metric. These findings were complemented by insights into key coding principles of the hippocampal-entorhinal region: Spatial representations vary in scale along the hippocampal long axis, place cells remap to map different environments, and sequential hippocampal activity represents nonlocal trajectories through space. In humans, the existence of spatially tuned cells has been demonstrated in presurgical patients, and functional magnetic resonance imaging provides proxy measures for the noninvasive investigation of these processing mechanisms in human cognition. Intriguingly, recent advances indicate that place and grid cells can encode positions along dimensions of experience beyond Euclidean space for navigation, suggesting a more general role of hippocampal-entorhinal processing mechanisms in cognition. ADVANCESWe combine hippocampal-entorhinal processing mechanisms identified in spatial navigation research with ideas from cognitive science describing a spatial representational format for cognition. Cognitive spaces are spanned by dimensions satisfying geometric constraints such as betweenness and equidistance, enabling the representation of properties and concepts as convex regions of cognitive space. We propose that the continuous population code of place and grid cells in the hippocampal-entorhinal region maps the dimensions of cognitive spaces. In these, each stimulus is located according to its feature values along the relevant dimensions, resulting in nearby positions for similar stimuli and larger distances between dissimilar stimuli. The low-dimensional, rigid firing properties of the entorhinal grid system make it a candidate to provide a metric or distance code for cognitive spaces, whereas hippocampal place cells flexibly represent positions in a given space. This mapping of cognitive spaces is complemented by the additional coding principles outlined above: Along the hippocampal long axis, cognitive spaces are mapped with varying spatial scale, supporting memory and knowledge representations at different levels of granularity. Via hippocampal remapping, spaces spanned by different dimensions can be flexibly mapped and established maps can be reinstated via attractor dynamics. The geometric definition of cognitive spaces allows flexible generalization and inference, and sequential hippocampal activity can simulate trajectories through cognitive spaces for adaptive decision-making and behavior. OUTLOOKCognitive spaces provide a domain-general format for processing in the hippocampal-entorhinal region, in line with its involvement beyond navigation and memory. Spatial navigation serves as a model system to identify key coding principles governing cognitive spaces. An important question concerns the extent to which firing properties of spatially tuned cells are preserved in cognitive spaces. Technological advances such as calcium imaging will clarify coding principles on the population level and facilitate the translation to human cognitive neuroscience. Spatial navigation is mostly investigated in two dimensions and naturally limited to three dimensions; however, the processing of complex, multidimensional concepts is vital to high-level human cognition, and the representation of such high-dimensional spaces is an intriguing question for future research. Further, the role of brain networks acting in concert with the hippocampus, in navigation specifically and cognitive function in general, will provide insight into whether and how cognitive spaces are supported beyond the hippocampal-entorhinal region. Finally, the precise way in which cognitive spaces and trajectories through them are read out for behavior remains to be elucidated. \textlessimg class="fragment-image" aria-describedby="F1-caption" src="https://science.sciencemag.org/content/sci/362/6415/eaat6766/F1.medium.gif"/\textgreater Download high-res image Open in new tab Download Powerpoint Place and grid cells map cognitive spaces.Cognitive spaces are defined by dimensions satisfying geometric constraints. The example space (left) is spanned by the dimensions of engine power and car weight. Black dots show different vehicles whose positions reflect their feature combinations. Place cells (center; colored circles represent firing fields of different cells) and grid cells (right; circles illustrate firing pattern of one cell) provide a continuous code for cognitive spaces. The hippocampal formation has long been suggested to underlie both memory formation and spatial navigation. We discuss how neural mechanisms identified in spatial navigation research operate across information domains to support a wide spectrum of cognitive functions. In our framework, place and grid cell population codes provide a representational format to map variable dimensions of cognitive spaces. This highly dynamic mapping system enables rapid reorganization of codes through remapping between orthogonal representations across behavioral contexts, yielding a multitude of stable cognitive spaces at different resolutions and hierarchical levels. Action sequences result in trajectories through cognitive space, which can be simulated via sequential coding in the hippocampus. In this way, the spatial representational format of the hippocampal formation has the capacity to support flexible cognition and behavior.

@article{jordan_positive_2018,
	title = {Positive {Changes} {Experienced} {After} a {First} {Episode} of {Psychosis}: {A} {Systematic} {Review}},
	volume = {69},
	issn = {1075-2730, 1557-9700},
	shorttitle = {Positive {Changes} {Experienced} {After} a {First} {Episode} of {Psychosis}},
	url = {http://psychiatryonline.org/doi/10.1176/appi.ps.201600586},
	doi = {10.1176/appi.ps.201600586},
	language = {en},
	number = {1},
	urldate = {2020-04-02},
	journal = {Psychiatric Services},
	author = {Jordan, Gerald and MacDonald, Kathleen and Pope, Megan A. and Schorr, Emily and Malla, Ashok K. and Iyer, Srividya N.},
	month = jan,
	year = {2018},
	note = {ZSCC: 0000012},
	keywords = {Illness Attribution/Appraisal},
	pages = {84--99},
}

@article{borsboom_brain_2018,
	title = {Brain disorders? {Not} really… {Why} network structures block reductionism in psychopathology research},
	issn = {1469-1825},
	shorttitle = {Brain disorders?},
	doi = {10.1017/S0140525X17002266},
	abstract = {In the past decades, reductionism has dominated both research directions and funding policies in clinical psychology and psychiatry. However, the intense search for the biological basis of mental disorders has not resulted in conclusive reductionist explanations of psychopathology. Recently, network models have been proposed as an alternative framework for the analysis of mental disorders, in which mental disorders arise from the causal interplay between symptoms. In this paper, we show that this conceptualization can help understand why reductionist approaches in psychiatry and clinical psychology are on the wrong track. First, symptom networks preclude the identification of a common cause of symptomatology with a neurobiological condition, because in symptom networks there is no such common cause. Second, symptom network relations depend on the content of mental states and as such feature intentionality. Third, the strength of network relations is highly likely to partially depend on cultural and historical contexts as well as external mechanisms in the environment. Taken together, these properties suggest that, if mental disorders are indeed networks of causally related symptoms, reductionist accounts cannot achieve the level of success associated with reductionist disease models in modern medicine. As an alternative strategy, we propose to interpret network structures in terms of D. C. Dennett's (1987) notion of real patterns, and suggest that, instead of being reducible to a biological basis, mental disorders feature biological and psychological factors that are deeply intertwined in feedback loops. This suggests that neither psychological nor biological levels can claim causal or explanatory priority, and that a holistic research strategy is necessary for progress in the study of mental disorders.},
	language = {eng},
	journal = {The Behavioral and Brain Sciences},
	author = {Borsboom, Denny and Cramer, Angélique and Kalis, Annemarie},
	month = jan,
	year = {2018},
	pmid = {29361992},
	note = {ZSCC: NoCitationData[s0] },
	pages = {1--54},
}

In the past decades, reductionism has dominated both research directions and funding policies in clinical psychology and psychiatry. However, the intense search for the biological basis of mental disorders has not resulted in conclusive reductionist explanations of psychopathology. Recently, network models have been proposed as an alternative framework for the analysis of mental disorders, in which mental disorders arise from the causal interplay between symptoms. In this paper, we show that this conceptualization can help understand why reductionist approaches in psychiatry and clinical psychology are on the wrong track. First, symptom networks preclude the identification of a common cause of symptomatology with a neurobiological condition, because in symptom networks there is no such common cause. Second, symptom network relations depend on the content of mental states and as such feature intentionality. Third, the strength of network relations is highly likely to partially depend on cultural and historical contexts as well as external mechanisms in the environment. Taken together, these properties suggest that, if mental disorders are indeed networks of causally related symptoms, reductionist accounts cannot achieve the level of success associated with reductionist disease models in modern medicine. As an alternative strategy, we propose to interpret network structures in terms of D. C. Dennett's (1987) notion of real patterns, and suggest that, instead of being reducible to a biological basis, mental disorders feature biological and psychological factors that are deeply intertwined in feedback loops. This suggests that neither psychological nor biological levels can claim causal or explanatory priority, and that a holistic research strategy is necessary for progress in the study of mental disorders.

@article{sterzer_predictive_2018,
	title = {The {Predictive} {Coding} {Account} of {Psychosis}},
	volume = {84},
	issn = {0006-3223, 1873-2402},
	url = {https://www.biologicalpsychiatryjournal.com/article/S0006-3223(18)31532-4/abstract},
	doi = {10.1016/j.biopsych.2018.05.015},
	abstract = {{\textless}h2{\textgreater}Abstract{\textless}/h2{\textgreater}{\textless}p{\textgreater}Fueled by developments in computational neuroscience, there has been increasing interest in the underlying neurocomputational mechanisms of psychosis. One successful approach involves predictive coding and Bayesian inference. Here, inferences regarding the current state of the world are made by combining prior beliefs with incoming sensory signals. Mismatches between prior beliefs and incoming signals constitute prediction errors that drive new learning. Psychosis has been suggested to result from a decreased precision in the encoding of prior beliefs relative to the sensory data, thereby garnering maladaptive inferences. Here, we review the current evidence for aberrant predictive coding and discuss challenges for this canonical predictive coding account of psychosis. For example, hallucinations and delusions may relate to distinct alterations in predictive coding, despite their common co-occurrence. More broadly, some studies implicate weakened prior beliefs in psychosis, and others find stronger priors. These challenges might be answered with a more nuanced view of predictive coding. Different priors may be specified for different sensory modalities and their integration, and deficits in each modality need not be uniform. Furthermore, hierarchical organization may be critical. Altered processes at lower levels of a hierarchy need not be linearly related to processes at higher levels (and vice versa). Finally, canonical theories do not highlight active inference—the process through which the effects of our actions on our sensations are anticipated and minimized. It is possible that conflicting findings might be reconciled by considering these complexities, portending a framework for psychosis more equipped to deal with its many manifestations.{\textless}/p{\textgreater}},
	language = {English},
	number = {9},
	urldate = {2021-06-23},
	journal = {Biological Psychiatry},
	author = {Sterzer, Philipp and Adams, Rick A. and Fletcher, Paul and Frith, Chris and Lawrie, Stephen M. and Muckli, Lars and Petrovic, Predrag and Uhlhaas, Peter and Voss, Martin and Corlett, Philip R.},
	month = nov,
	year = {2018},
	pmid = {30007575},
	note = {ZSCC: 0000269 
Publisher: Elsevier},
	pages = {634--643},
}

\textlessh2\textgreaterAbstract\textless/h2\textgreater\textlessp\textgreaterFueled by developments in computational neuroscience, there has been increasing interest in the underlying neurocomputational mechanisms of psychosis. One successful approach involves predictive coding and Bayesian inference. Here, inferences regarding the current state of the world are made by combining prior beliefs with incoming sensory signals. Mismatches between prior beliefs and incoming signals constitute prediction errors that drive new learning. Psychosis has been suggested to result from a decreased precision in the encoding of prior beliefs relative to the sensory data, thereby garnering maladaptive inferences. Here, we review the current evidence for aberrant predictive coding and discuss challenges for this canonical predictive coding account of psychosis. For example, hallucinations and delusions may relate to distinct alterations in predictive coding, despite their common co-occurrence. More broadly, some studies implicate weakened prior beliefs in psychosis, and others find stronger priors. These challenges might be answered with a more nuanced view of predictive coding. Different priors may be specified for different sensory modalities and their integration, and deficits in each modality need not be uniform. Furthermore, hierarchical organization may be critical. Altered processes at lower levels of a hierarchy need not be linearly related to processes at higher levels (and vice versa). Finally, canonical theories do not highlight active inference—the process through which the effects of our actions on our sensations are anticipated and minimized. It is possible that conflicting findings might be reconciled by considering these complexities, portending a framework for psychosis more equipped to deal with its many manifestations.\textless/p\textgreater

@article{mackay_multidimensional_2018,
	title = {Multidimensional {Connectomics} and {Treatment}-{Resistant} {Schizophrenia}: {Linking} {Phenotypic} {Circuits} to {Targeted} {Therapeutics}},
	volume = {9},
	issn = {1664-0640},
	shorttitle = {Multidimensional {Connectomics} and {Treatment}-{Resistant} {Schizophrenia}},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6218602/},
	doi = {10.3389/fpsyt.2018.00537},
	abstract = {Schizophrenia is a very complex syndrome that involves widespread brain multi-dysconnectivity. Neural circuits within specific brain regions and their links to corresponding regions are abnormal in the illness. Theoretical models of dysconnectivity and the investigation of connectomics and brain network organization have been examined in schizophrenia since the early nineteenth century. In more recent years, advancements have been achieved with the development of neuroimaging tools that have provided further clues to the structural and functional organization of the brain and global neural networks in the illness. Neural circuitry that extends across prefrontal, temporal and parietal areas of the cortex as well as limbic and other subcortical brain regions is disrupted in schizophrenia. As a result, many patients have a poor response to antipsychotic treatment and treatment failure is common. Treatment resistance that is specific to positive, negative, and cognitive domains of the illness may be related to distinct circuit phenotypes unique to treatment-refractory disease. Currently, there are no customized neural circuit-specific and targeted therapies that address this neural dysconnectivity. Investigation of targeted therapeutics that addresses particular areas of substantial regional dysconnectivity is an intriguing approach to precision medicine in schizophrenia. This review examines current findings of system and circuit-level brain dysconnectivity in treatment-resistant schizophrenia based on neuroimaging studies. Within a connectome context, on-off circuit connectivity synonymous with excitatory and inhibitory neuronal pathways is discussed. Mechanistic cellular, neurochemical and molecular studies are included with specific emphasis given to cell pathology and synaptic communication in glutamatergic and GABAergic systems. In this review we attempt to deconstruct how augmenting treatments may be applied within a circuit context to improve circuit integration and treatment response. Clinical studies that have used a variety of glutamate receptor and GABA interneuron modulators, nitric oxide-based therapies and a variety of other strategies as augmenting treatments with antipsychotic drugs are included. This review supports the idea that the methodical mapping of system-level networks to both on (excitatory) and off (inhibitory) cellular circuits specific to treatment-resistant disease may be a logical and productive approach in directing future research toward the advancement of targeted pharmacotherapeutics in schizophrenia.},
	urldate = {2021-06-16},
	journal = {Frontiers in Psychiatry},
	author = {MacKay, Mary-Anne B. and Paylor, John W. and Wong, James T. F. and Winship, Ian R. and Baker, Glen B. and Dursun, Serdar M.},
	month = oct,
	year = {2018},
	pmid = {30425662},
	pmcid = {PMC6218602},
	note = {ZSCC: 0000006 },
}

Schizophrenia is a very complex syndrome that involves widespread brain multi-dysconnectivity. Neural circuits within specific brain regions and their links to corresponding regions are abnormal in the illness. Theoretical models of dysconnectivity and the investigation of connectomics and brain network organization have been examined in schizophrenia since the early nineteenth century. In more recent years, advancements have been achieved with the development of neuroimaging tools that have provided further clues to the structural and functional organization of the brain and global neural networks in the illness. Neural circuitry that extends across prefrontal, temporal and parietal areas of the cortex as well as limbic and other subcortical brain regions is disrupted in schizophrenia. As a result, many patients have a poor response to antipsychotic treatment and treatment failure is common. Treatment resistance that is specific to positive, negative, and cognitive domains of the illness may be related to distinct circuit phenotypes unique to treatment-refractory disease. Currently, there are no customized neural circuit-specific and targeted therapies that address this neural dysconnectivity. Investigation of targeted therapeutics that addresses particular areas of substantial regional dysconnectivity is an intriguing approach to precision medicine in schizophrenia. This review examines current findings of system and circuit-level brain dysconnectivity in treatment-resistant schizophrenia based on neuroimaging studies. Within a connectome context, on-off circuit connectivity synonymous with excitatory and inhibitory neuronal pathways is discussed. Mechanistic cellular, neurochemical and molecular studies are included with specific emphasis given to cell pathology and synaptic communication in glutamatergic and GABAergic systems. In this review we attempt to deconstruct how augmenting treatments may be applied within a circuit context to improve circuit integration and treatment response. Clinical studies that have used a variety of glutamate receptor and GABA interneuron modulators, nitric oxide-based therapies and a variety of other strategies as augmenting treatments with antipsychotic drugs are included. This review supports the idea that the methodical mapping of system-level networks to both on (excitatory) and off (inhibitory) cellular circuits specific to treatment-resistant disease may be a logical and productive approach in directing future research toward the advancement of targeted pharmacotherapeutics in schizophrenia.

@article{roulston_qualitative_2018,
	title = {Qualitative interviewing and epistemics},
	volume = {18},
	issn = {1468-7941, 1741-3109},
	url = {http://journals.sagepub.com/doi/10.1177/1468794117721738},
	doi = {10.1177/1468794117721738},
	abstract = {Work on epistemics in conversation analysis (CA) has demonstrated how speakers attend closely to the knowledge claims they and others make and how this shapes interaction. This paper uses work on epistemics in CA to explore how interviewers and interviewees orient to knowledge claims involving the asking and answering of questions. Since research participants are recruited to represent a category identified by the researcher, interviewees are assumed to have greater knowledge relative to the research topic as compared to interviewers, who typically work to demonstrate that they are eager learners about others’ experiences, perceptions and beliefs and so forth. This paper examines sequences from research interviews to focus on the fine-grained work involved in asking questions and making knowledge claims within interviews. Epistemics provides a powerful tool to examine how speakers’ orientations to others’ knowledge claims is central to the interactional work of conducting interviews.},
	language = {en},
	number = {3},
	urldate = {2020-03-12},
	journal = {Qualitative Research},
	author = {Roulston, Kathryn},
	month = jun,
	year = {2018},
	note = {ZSCC: 0000038},
	pages = {322--341},
}

Work on epistemics in conversation analysis (CA) has demonstrated how speakers attend closely to the knowledge claims they and others make and how this shapes interaction. This paper uses work on epistemics in CA to explore how interviewers and interviewees orient to knowledge claims involving the asking and answering of questions. Since research participants are recruited to represent a category identified by the researcher, interviewees are assumed to have greater knowledge relative to the research topic as compared to interviewers, who typically work to demonstrate that they are eager learners about others’ experiences, perceptions and beliefs and so forth. This paper examines sequences from research interviews to focus on the fine-grained work involved in asking questions and making knowledge claims within interviews. Epistemics provides a powerful tool to examine how speakers’ orientations to others’ knowledge claims is central to the interactional work of conducting interviews.

@article{li_erythropoietin_2018,
	title = {Erythropoietin for {Cognitive} {Deficits} {Associated} with {Schizophrenia}, {Bipolar} {Disorder}, and {Major} {Depression}: {A} {Systematic} {Review}},
	volume = {51},
	issn = {0176-3679 DOI  - 10.1055/s-0043-114670},
	language = {EN},
	number = {03},
	journal = {Pharmacopsychiatry},
	author = {Li, Xian-Bin and Zheng, Wei and Ning, Yu-Ping and Cai, Dong-Bin and Yang, Xin-Hu and Ungvari, Gabor S. and Ng, Chee H. and Wang, Chuan-Yue and Xiang, Yu-Tao},
	month = sep,
	year = {2018},
	note = {ZSCC: 0000013 
Edition: 17.07.2017
100},
	pages = {100--104},
}

@article{chang_effects_2018,
	title = {The {Effects} of {Add}-on {Fronto}-{Temporal} {Transcranial} {Direct} {Current} {Stimulation} ({tDCS}) on {Auditory} {Verbal} {Hallucinations}, {Other} {Psychopathological} {Symptoms}, and {Insight} in {Schizophrenia}: {A} {Randomized}, {Double}-{Blind}, {Sham}-{Controlled} {Trial}},
	volume = {21},
	issn = {1461-1457},
	shorttitle = {The {Effects} of {Add}-on {Fronto}-{Temporal} {Transcranial} {Direct} {Current} {Stimulation} ({tDCS}) on {Auditory} {Verbal} {Hallucinations}, {Other} {Psychopathological} {Symptoms}, and {Insight} in {Schizophrenia}},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6209860/},
	doi = {10.1093/ijnp/pyy074},
	abstract = {Background
The efficacy of fronto-temporal transcranial direct current stimulation in treating auditory verbal hallucinations and other psychopathological symptoms of schizophrenia patients has been examined in a small number of clinical trials with limited sample sizes, but the results are mixed. Fronto-temporal transcranial direct current stimulation has also been demonstrated to enhance patients’ insight into their mental illness in an open-label pilot study. The current investigation aimed to investigate the therapeutic effects of fronto-temporal transcranial direct current stimulation on the severity of auditory verbal hallucinations, other schizophrenia symptoms, and insight in a large double blind, randomized, sham-controlled trial.

Methods
Sixty patients with medication-refractory auditory verbal hallucinations were randomized over 2 conditions: transcranial direct current stimulation with 2-mA, twice-daily sessions for 5 consecutive days, with anodal stimulation to the left prefrontal cortex and cathodal stimulation to the left temporo-parietal junction, and sham treatment.

Results
Fronto-temporal transcranial direct current stimulation failed to cause significant changes in the severity of auditory verbal hallucinations and other schizophrenia symptoms. The levels of insight into illness (effect size=0.511, P{\textless}.001) and positive symptoms (effect size=0.781, P{\textless}.001) were largely promoted by 5 days of transcranial direct current stimulation relative to sham treatment. The beneficial effects on the 2 insight dimensions remained 1 month after transcranial direct current stimulation.

Conclusions
Fronto-temporal transcranial direct current stimulation is not more effective for auditory verbal hallucinations and other schizophrenia symptoms than sham treatment. But the results of transcranial direct current stimulation-associated improvement in awareness of illness and positive symptoms show promise and provide a new direction for future research into insight promotion interventions in schizophrenia.},
	number = {11},
	urldate = {2021-04-10},
	journal = {International Journal of Neuropsychopharmacology},
	author = {Chang, Chuan-Chia and Tzeng, Nian-Sheng and Chao, Che-Yi and Yeh, Chin-Bin and Chang, Hsin-An},
	month = aug,
	year = {2018},
	pmid = {30107404},
	pmcid = {PMC6209860},
	note = {ZSCC: NoCitationData[s0] },
	pages = {979--987},
}

Background The efficacy of fronto-temporal transcranial direct current stimulation in treating auditory verbal hallucinations and other psychopathological symptoms of schizophrenia patients has been examined in a small number of clinical trials with limited sample sizes, but the results are mixed. Fronto-temporal transcranial direct current stimulation has also been demonstrated to enhance patients’ insight into their mental illness in an open-label pilot study. The current investigation aimed to investigate the therapeutic effects of fronto-temporal transcranial direct current stimulation on the severity of auditory verbal hallucinations, other schizophrenia symptoms, and insight in a large double blind, randomized, sham-controlled trial. Methods Sixty patients with medication-refractory auditory verbal hallucinations were randomized over 2 conditions: transcranial direct current stimulation with 2-mA, twice-daily sessions for 5 consecutive days, with anodal stimulation to the left prefrontal cortex and cathodal stimulation to the left temporo-parietal junction, and sham treatment. Results Fronto-temporal transcranial direct current stimulation failed to cause significant changes in the severity of auditory verbal hallucinations and other schizophrenia symptoms. The levels of insight into illness (effect size=0.511, P\textless.001) and positive symptoms (effect size=0.781, P\textless.001) were largely promoted by 5 days of transcranial direct current stimulation relative to sham treatment. The beneficial effects on the 2 insight dimensions remained 1 month after transcranial direct current stimulation. Conclusions Fronto-temporal transcranial direct current stimulation is not more effective for auditory verbal hallucinations and other schizophrenia symptoms than sham treatment. But the results of transcranial direct current stimulation-associated improvement in awareness of illness and positive symptoms show promise and provide a new direction for future research into insight promotion interventions in schizophrenia.

@article{rohde_effectiveness_2018,
	title = {Effectiveness of {Prescription}-{Based} {CNS} {Stimulants} on {Hospitalization} in {Patients} {With} {Schizophrenia}: {A} {Nation}-{Wide} {Register} {Study}},
	volume = {44},
	issn = {0586-7614},
	shorttitle = {Effectiveness of {Prescription}-{Based} {CNS} {Stimulants} on {Hospitalization} in {Patients} {With} {Schizophrenia}},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5768038/},
	doi = {10.1093/schbul/sbx043},
	abstract = {Objective: Negative symptoms and cognitive deficits are main features of schizophrenia but with limited treatment options. Earlier studies have suggested that central nervous system (CNS) stimulants have a small effect on these domains, but with inconclusive results. As the first study to date, we aimed to investigate whether CNS stimulants improve naturalistic outcomes (psychiatric admissions and antipsychotic use) in patients with schizophrenia. Methods: By using extensive health registers all patients with schizophrenia and their use of CNS stimulants in Denmark were identified. Two models were used to investigate the effectiveness of CNS stimulants in patients with schizophrenia between 1995 and 2014; a mirror-image model with 605 individuals, using paired t tests and Wilcoxon signed rank tests, and a follow-up study with 789 individuals, using a conditional risk-set model. Results: CNS stimulants use was associated with a reduction in number of psychiatric admissions from 3.43 (95\% CI = 2.86 to 4.01) to 2.62 (95\% CI = 1.99 to 3.25) (P = .009), with a more pronounced reduction for women (mean difference: −1.37, 95\% CI = −2.34 to −0.40, P = .006). Psychiatric bed-days were reduced by 40 (95\% CI = 24.5 to 55.6, P {\textless} .001) for individuals with at least 1 admission before CNS stimulant use. In addition, the total amount of antipsychotic use (Defined Daily Dose [DDD]) was reduced (P = .001). The Hazard rate ratio in psychiatric admissions between women taking CNS stimulants compared to women not taking CNS stimulants was 0.77 (95\% CI = 0.67 to 0.88). Conclusion: CNS stimulants may have clinical potentials for improving functional outcomes in patients with schizophrenia and randomized clinical studies evaluating this topic are warranted.},
	number = {1},
	urldate = {2021-04-10},
	journal = {Schizophrenia Bulletin},
	author = {Rohde, Christopher and Polcwiartek, Christoffer and Asztalos, Marton and Nielsen, Jimmi},
	month = jan,
	year = {2018},
	pmid = {28379483},
	pmcid = {PMC5768038},
	note = {ZSCC: 0000010 },
	pages = {93--100},
}

Objective: Negative symptoms and cognitive deficits are main features of schizophrenia but with limited treatment options. Earlier studies have suggested that central nervous system (CNS) stimulants have a small effect on these domains, but with inconclusive results. As the first study to date, we aimed to investigate whether CNS stimulants improve naturalistic outcomes (psychiatric admissions and antipsychotic use) in patients with schizophrenia. Methods: By using extensive health registers all patients with schizophrenia and their use of CNS stimulants in Denmark were identified. Two models were used to investigate the effectiveness of CNS stimulants in patients with schizophrenia between 1995 and 2014; a mirror-image model with 605 individuals, using paired t tests and Wilcoxon signed rank tests, and a follow-up study with 789 individuals, using a conditional risk-set model. Results: CNS stimulants use was associated with a reduction in number of psychiatric admissions from 3.43 (95% CI = 2.86 to 4.01) to 2.62 (95% CI = 1.99 to 3.25) (P = .009), with a more pronounced reduction for women (mean difference: −1.37, 95% CI = −2.34 to −0.40, P = .006). Psychiatric bed-days were reduced by 40 (95% CI = 24.5 to 55.6, P \textless .001) for individuals with at least 1 admission before CNS stimulant use. In addition, the total amount of antipsychotic use (Defined Daily Dose [DDD]) was reduced (P = .001). The Hazard rate ratio in psychiatric admissions between women taking CNS stimulants compared to women not taking CNS stimulants was 0.77 (95% CI = 0.67 to 0.88). Conclusion: CNS stimulants may have clinical potentials for improving functional outcomes in patients with schizophrenia and randomized clinical studies evaluating this topic are warranted.

@article{kauppi_revisiting_2018,
	title = {Revisiting antipsychotic drug actions through gene networks associated with schizophrenia},
	volume = {175},
	issn = {0002-953X},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6028303/},
	doi = {10.1176/appi.ajp.2017.17040410},
	abstract = {Antipsychotic drugs were incidentally discovered in the 1950s, but their mechanisms of action are still not understood. Better understanding of schizophrenia pathogenesis could shed light on actions of current drugs and reveal novel druggable pathways for unmet therapeutic needs. Recent genome-wide association studies offer unprecedented opportunities to characterize disease gene networks and uncover drug-disease relationships. Polygenic overlap between schizophrenia risk genes and antipsychotic drug targets has been demonstrated. However, the specific genes and pathways constituting this overlap are undetermined. Risk genes of polygenic disorders do not operate in isolation, but in combination with other genes. Thus, we utilized protein-protein interaction networks (interactome) to map antipsychotic drug targets (n=88) to networks of schizophrenia risk genes (n=328). Our results showed that schizophrenia risk genes were significantly localized in the interactome (p=0.0015), forming a distinct disease module. Core genes of the module were enriched for genes involved in developmental biology and cognition, which may have a central role in schizophrenia etiology. Intriguingly, antipsychotic drug targets overlapped with the core disease module and comprised multiple pathways beyond dopamine. Some important risk genes like CHRN, PCDH and HCN families were not connected to existing antipsychotics, but may be suitable targets for novel drugs or drug repurposing opportunities to treat other aspects of schizophrenia such as cognitive dysfunction and negative symptoms. This network medicine approach provides a platform to collate information of disease genetics and drug-gene interactions to shift focus from development of antipsychotics to multi-target anti-schizophrenia drugs. This approach is transferable to other diseases.},
	number = {7},
	urldate = {2021-03-19},
	journal = {The American journal of psychiatry},
	author = {Kauppi, Karolina and Rosenthal, Sara Brin and Lo, Min-Tzu and Sanyal, Nilotpal and Jiang, Mian and Abagyan, Ruben and McEvoy, Linda K and Andreassen, Ole A and Chen, Chi-Hua},
	month = jul,
	year = {2018},
	pmid = {29495895},
	pmcid = {PMC6028303},
	note = {ZSCC: 0000010 },
	pages = {674--682},
}

Antipsychotic drugs were incidentally discovered in the 1950s, but their mechanisms of action are still not understood. Better understanding of schizophrenia pathogenesis could shed light on actions of current drugs and reveal novel druggable pathways for unmet therapeutic needs. Recent genome-wide association studies offer unprecedented opportunities to characterize disease gene networks and uncover drug-disease relationships. Polygenic overlap between schizophrenia risk genes and antipsychotic drug targets has been demonstrated. However, the specific genes and pathways constituting this overlap are undetermined. Risk genes of polygenic disorders do not operate in isolation, but in combination with other genes. Thus, we utilized protein-protein interaction networks (interactome) to map antipsychotic drug targets (n=88) to networks of schizophrenia risk genes (n=328). Our results showed that schizophrenia risk genes were significantly localized in the interactome (p=0.0015), forming a distinct disease module. Core genes of the module were enriched for genes involved in developmental biology and cognition, which may have a central role in schizophrenia etiology. Intriguingly, antipsychotic drug targets overlapped with the core disease module and comprised multiple pathways beyond dopamine. Some important risk genes like CHRN, PCDH and HCN families were not connected to existing antipsychotics, but may be suitable targets for novel drugs or drug repurposing opportunities to treat other aspects of schizophrenia such as cognitive dysfunction and negative symptoms. This network medicine approach provides a platform to collate information of disease genetics and drug-gene interactions to shift focus from development of antipsychotics to multi-target anti-schizophrenia drugs. This approach is transferable to other diseases.

@article{kauppi_revisiting_2018-1,
	title = {Revisiting antipsychotic drug actions through gene networks associated with schizophrenia},
	volume = {175},
	issn = {0002-953X},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6028303/},
	doi = {10.1176/appi.ajp.2017.17040410},
	abstract = {Antipsychotic drugs were incidentally discovered in the 1950s, but their mechanisms of action are still not understood. Better understanding of schizophrenia pathogenesis could shed light on actions of current drugs and reveal novel druggable pathways for unmet therapeutic needs. Recent genome-wide association studies offer unprecedented opportunities to characterize disease gene networks and uncover drug-disease relationships. Polygenic overlap between schizophrenia risk genes and antipsychotic drug targets has been demonstrated. However, the specific genes and pathways constituting this overlap are undetermined. Risk genes of polygenic disorders do not operate in isolation, but in combination with other genes. Thus, we utilized protein-protein interaction networks (interactome) to map antipsychotic drug targets (n=88) to networks of schizophrenia risk genes (n=328). Our results showed that schizophrenia risk genes were significantly localized in the interactome (p=0.0015), forming a distinct disease module. Core genes of the module were enriched for genes involved in developmental biology and cognition, which may have a central role in schizophrenia etiology. Intriguingly, antipsychotic drug targets overlapped with the core disease module and comprised multiple pathways beyond dopamine. Some important risk genes like CHRN, PCDH and HCN families were not connected to existing antipsychotics, but may be suitable targets for novel drugs or drug repurposing opportunities to treat other aspects of schizophrenia such as cognitive dysfunction and negative symptoms. This network medicine approach provides a platform to collate information of disease genetics and drug-gene interactions to shift focus from development of antipsychotics to multi-target anti-schizophrenia drugs. This approach is transferable to other diseases.},
	number = {7},
	urldate = {2021-03-19},
	journal = {The American journal of psychiatry},
	author = {Kauppi, Karolina and Rosenthal, Sara Brin and Lo, Min-Tzu and Sanyal, Nilotpal and Jiang, Mian and Abagyan, Ruben and McEvoy, Linda K and Andreassen, Ole A and Chen, Chi-Hua},
	month = jul,
	year = {2018},
	pmid = {29495895},
	pmcid = {PMC6028303},
	note = {ZSCC: 0000010 },
	pages = {674--682},
}

Antipsychotic drugs were incidentally discovered in the 1950s, but their mechanisms of action are still not understood. Better understanding of schizophrenia pathogenesis could shed light on actions of current drugs and reveal novel druggable pathways for unmet therapeutic needs. Recent genome-wide association studies offer unprecedented opportunities to characterize disease gene networks and uncover drug-disease relationships. Polygenic overlap between schizophrenia risk genes and antipsychotic drug targets has been demonstrated. However, the specific genes and pathways constituting this overlap are undetermined. Risk genes of polygenic disorders do not operate in isolation, but in combination with other genes. Thus, we utilized protein-protein interaction networks (interactome) to map antipsychotic drug targets (n=88) to networks of schizophrenia risk genes (n=328). Our results showed that schizophrenia risk genes were significantly localized in the interactome (p=0.0015), forming a distinct disease module. Core genes of the module were enriched for genes involved in developmental biology and cognition, which may have a central role in schizophrenia etiology. Intriguingly, antipsychotic drug targets overlapped with the core disease module and comprised multiple pathways beyond dopamine. Some important risk genes like CHRN, PCDH and HCN families were not connected to existing antipsychotics, but may be suitable targets for novel drugs or drug repurposing opportunities to treat other aspects of schizophrenia such as cognitive dysfunction and negative symptoms. This network medicine approach provides a platform to collate information of disease genetics and drug-gene interactions to shift focus from development of antipsychotics to multi-target anti-schizophrenia drugs. This approach is transferable to other diseases.

@article{buckley_rheumatoid_2018,
	title = {Rheumatoid {Arthritis} {Drugs} for {Schizophrenia}?},
	volume = {48},
	issn = {0048-5713, 1938-2456},
	url = {https://www.healio.com/psychiatry/journals/psycann/2018-5-48-5/{4a1c3326-1508-4ca0-9577-146258e785bb}/rheumatoid-arthritis-drugs-for-schizophrenia},
	doi = {10.3928/00485713-20180405-01},
	abstract = {Psychiatric Annals {\textbar} Any relationship between treatment of rheumatoid arthritis and the current treatment of schizophrenia seems, at first glance, far-fetched. And yet, in a relatively short period of intensive research work, the field of schizophrenia research has come to appreciate that there are fundamental immunological associations with schizophrenia. Several groups have conducted studies of antirheumatic},
	language = {en},
	number = {5},
	urldate = {2020-08-13},
	journal = {Psychiatric Annals},
	author = {Buckley, Peter F. and Miller, Brian J.},
	month = may,
	year = {2018},
	note = {ZSCC: 0000001 
Publisher: SLACK Incorporated},
	pages = {232--236},
}

Psychiatric Annals \textbar Any relationship between treatment of rheumatoid arthritis and the current treatment of schizophrenia seems, at first glance, far-fetched. And yet, in a relatively short period of intensive research work, the field of schizophrenia research has come to appreciate that there are fundamental immunological associations with schizophrenia. Several groups have conducted studies of antirheumatic

@article{shippey_hydroxychloroquine_2018,
	title = {Hydroxychloroquine: {An} old drug with new relevance},
	volume = {85},
	issn = {0891-1150, 1939-2869},
	shorttitle = {Hydroxychloroquine},
	url = {https://www.ccjm.org//lookup/doi/10.3949/ccjm.85a.17034},
	doi = {10.3949/ccjm.85a.17034},
	abstract = {Hydroxychloroquine is an immunomodulatory drug that has been used for 60 years to treat malaria and autoimmune diseases such as systemic lupus erythematosus and inflammatory arthritis, and potential new uses and benefits continue to emerge. Toxicity concerns have been addressed with updated prescribing recommendations.},
	language = {en},
	number = {6},
	urldate = {2020-06-26},
	journal = {Cleveland Clinic Journal of Medicine},
	author = {Shippey, Eugen Alexander and Wagler, Vanya D. and Collamer, Angelique N.},
	month = jun,
	year = {2018},
	note = {ZSCC: 0000030},
	pages = {459--467},
}

Hydroxychloroquine is an immunomodulatory drug that has been used for 60 years to treat malaria and autoimmune diseases such as systemic lupus erythematosus and inflammatory arthritis, and potential new uses and benefits continue to emerge. Toxicity concerns have been addressed with updated prescribing recommendations.

@article{heather_challenging_2018,
	title = {Challenging the brain disease model of addiction: {European} launch of the addiction theory network},
	volume = {26},
	issn = {1606-6359},
	shorttitle = {Challenging the brain disease model of addiction},
	url = {https://doi.org/10.1080/16066359.2017.1399659},
	doi = {10.1080/16066359.2017.1399659},
	number = {4},
	urldate = {2020-06-19},
	journal = {Addiction Research \& Theory},
	author = {Heather, Nick and Best, David and Kawalek, Anna and Field, Matt and Lewis, Marc and Rotgers, Frederick and Wiers, Reinout W. and Heim, Derek},
	month = jul,
	year = {2018},
	note = {ZSCC: 0000069 
Publisher: Taylor \& Francis
\_eprint: https://doi.org/10.1080/16066359.2017.1399659},
	pages = {249--255},
}

@article{longo_brain_2018,
	title = {Brain {Change} in {Addiction} as {Learning}, {Not} {Disease}},
	volume = {379},
	issn = {0028-4793, 1533-4406},
	url = {http://www.nejm.org/doi/10.1056/NEJMra1602872},
	doi = {10.1056/NEJMra1602872},
	language = {en},
	number = {16},
	urldate = {2020-06-19},
	journal = {New England Journal of Medicine},
	author = {Lewis, Marc},
	editor = {Longo, Dan L.},
	month = oct,
	year = {2018},
	note = {ZSCC: NoCitationData[s0]},
	keywords = {Review Article},
	pages = {1551--1560},
}

@article{kirchhoff_markov_2018,
	title = {The {Markov} blankets of life: autonomy, active inference and the free energy principle},
	volume = {15},
	issn = {1742-5689, 1742-5662},
	shorttitle = {The {Markov} blankets of life},
	url = {https://royalsocietypublishing.org/doi/10.1098/rsif.2017.0792},
	doi = {10.1098/rsif.2017.0792},
	language = {en},
	number = {138},
	urldate = {2020-06-18},
	journal = {Journal of The Royal Society Interface},
	author = {Kirchhoff, Michael and Parr, Thomas and Palacios, Ensor and Friston, Karl and Kiverstein, Julian},
	month = jan,
	year = {2018},
	note = {ZSCC: 0000103},
	pages = {20170792},
}

@article{hofmann_how_2018,
	title = {How medical technologies shape the experience of illness},
	volume = {14},
	issn = {2195-7819},
	url = {https://doi.org/10.1186/s40504-018-0069-y},
	doi = {10.1186/s40504-018-0069-y},
	abstract = {In this article we explore how diagnostic and therapeutic technologies shape the lived experiences of illness for patients. By analysing a wide range of examples, we identify six ways that technology can (trans)form the experience of illness (and health). First, technology may create awareness of disease by revealing asymptomatic signs or markers (imaging techniques, blood tests). Second, the technology can reveal risk factors for developing diseases (e.g., high blood pressure or genetic tests that reveal risks of falling ill in the future). Third, the technology can affect and change an already present illness experience (e.g., the way blood sugar measurement affects the perceived symptoms of diabetes). Fourth, therapeutic technologies may redefine our experiences of a certain condition as diseased rather than unfortunate (e.g. assisted reproductive technologies or symptom based diagnoses in psychiatry). Fifth, technology influences illness experiences through altering social-cultural norms and values regarding various diagnoses. Sixth, technology influences and changes our experiences of being healthy in contrast and relation to being diseased and ill. This typology of how technology forms illness and related conditions calls for reflection regarding the phenomenology of technology and health. How are medical technologies and their outcomes perceived and understood by patients? The phenomenological way of approaching illness as a lived, bodily being-in-the-world is an important approach for better understanding and evaluating the effects that medical technologies may have on our health, not only in defining, diagnosing, or treating diseases, but also in making us feel more vulnerable and less healthy in different regards.},
	number = {1},
	urldate = {2020-03-20},
	journal = {Life Sciences, Society and Policy},
	author = {Hofmann, Bjørn and Svenaeus, Fredrik},
	month = feb,
	year = {2018},
	keywords = {Illness Attribution/Appraisal},
	pages = {3},
}

In this article we explore how diagnostic and therapeutic technologies shape the lived experiences of illness for patients. By analysing a wide range of examples, we identify six ways that technology can (trans)form the experience of illness (and health). First, technology may create awareness of disease by revealing asymptomatic signs or markers (imaging techniques, blood tests). Second, the technology can reveal risk factors for developing diseases (e.g., high blood pressure or genetic tests that reveal risks of falling ill in the future). Third, the technology can affect and change an already present illness experience (e.g., the way blood sugar measurement affects the perceived symptoms of diabetes). Fourth, therapeutic technologies may redefine our experiences of a certain condition as diseased rather than unfortunate (e.g. assisted reproductive technologies or symptom based diagnoses in psychiatry). Fifth, technology influences illness experiences through altering social-cultural norms and values regarding various diagnoses. Sixth, technology influences and changes our experiences of being healthy in contrast and relation to being diseased and ill. This typology of how technology forms illness and related conditions calls for reflection regarding the phenomenology of technology and health. How are medical technologies and their outcomes perceived and understood by patients? The phenomenological way of approaching illness as a lived, bodily being-in-the-world is an important approach for better understanding and evaluating the effects that medical technologies may have on our health, not only in defining, diagnosing, or treating diseases, but also in making us feel more vulnerable and less healthy in different regards.

@article{ursini_metformin_2018,
	title = {Metformin and {Autoimmunity}: {A} “{New} {Deal}” of an {Old} {Drug}},
	volume = {9},
	issn = {1664-3224},
	shorttitle = {Metformin and {Autoimmunity}},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5994909/},
	doi = {10.3389/fimmu.2018.01236},
	abstract = {Metformin (dimethyl biguanide) is a synthetic derivative of guanidine, isolated from the extracts of Galega officinalis, a plant with a prominent antidiabetic effect. Since its discovery more than 50 years ago, metformin represents a worldwide milestone in treatment of patients with type 2 diabetes (T2D). Recent evidence in humans indicates novel pleiotropic actions of metformin which span from its consolidated role in T2D management up to various regulatory properties, including cardio- and nephro-protection, as well as antiproliferative, antifibrotic, and antioxidant effects. These findings, together with ground-breaking studies demonstrating its ability to prolong healthspan and lifespan in mice, provided the basis for defining metformin as a potential antiaging molecule. Moreover, emerging in vivo and in vitro evidence support the novel hypothesis that metformin can exhibit immune-modulatory features. Studies suggest that metformin interferes with key immunopathological mechanisms involved in systemic autoimmune diseases, such as the T helper 17/regulatory T cell balance, germinal centers formation, autoantibodies production, macrophage polarization, cytokine synthesis, neutrophil extracellular traps release, and bone or extracellular matrix remodeling. These effects may represent a powerful contributor to antiaging and anticancer properties exerted by metformin and, from another standpoint, may open the way to assess whether metformin can be a candidate molecule for clinical trials involving patients with immune-mediated diseases. In this article, we will review the available preclinical and clinical evidence regarding the effect of metformin on individual cells of the immune system, with emphasis on immunological mechanisms related to the development and maintenance of autoimmunity and its potential relevance in treatment of autoimmune diseases.},
	urldate = {2020-05-22},
	journal = {Frontiers in Immunology},
	author = {Ursini, Francesco and Russo, Emilio and Pellino, Gianluca and D’Angelo, Salvatore and Chiaravalloti, Agostino and De Sarro, Giovambattista and Manfredini, Roberto and De Giorgio, Roberto},
	month = jun,
	year = {2018},
	pmid = {29915588},
	pmcid = {PMC5994909},
}

Metformin (dimethyl biguanide) is a synthetic derivative of guanidine, isolated from the extracts of Galega officinalis, a plant with a prominent antidiabetic effect. Since its discovery more than 50 years ago, metformin represents a worldwide milestone in treatment of patients with type 2 diabetes (T2D). Recent evidence in humans indicates novel pleiotropic actions of metformin which span from its consolidated role in T2D management up to various regulatory properties, including cardio- and nephro-protection, as well as antiproliferative, antifibrotic, and antioxidant effects. These findings, together with ground-breaking studies demonstrating its ability to prolong healthspan and lifespan in mice, provided the basis for defining metformin as a potential antiaging molecule. Moreover, emerging in vivo and in vitro evidence support the novel hypothesis that metformin can exhibit immune-modulatory features. Studies suggest that metformin interferes with key immunopathological mechanisms involved in systemic autoimmune diseases, such as the T helper 17/regulatory T cell balance, germinal centers formation, autoantibodies production, macrophage polarization, cytokine synthesis, neutrophil extracellular traps release, and bone or extracellular matrix remodeling. These effects may represent a powerful contributor to antiaging and anticancer properties exerted by metformin and, from another standpoint, may open the way to assess whether metformin can be a candidate molecule for clinical trials involving patients with immune-mediated diseases. In this article, we will review the available preclinical and clinical evidence regarding the effect of metformin on individual cells of the immune system, with emphasis on immunological mechanisms related to the development and maintenance of autoimmunity and its potential relevance in treatment of autoimmune diseases.

@article{bergstrom_family-oriented_2018,
	title = {The family-oriented open dialogue approach in the treatment of first-episode psychosis: {Nineteen}–year outcomes},
	volume = {270},
	issn = {01651781},
	shorttitle = {The family-oriented open dialogue approach in the treatment of first-episode psychosis},
	url = {https://linkinghub.elsevier.com/retrieve/pii/S0165178117323338},
	doi = {10.1016/j.psychres.2018.09.039},
	abstract = {Open Dialogue (OD) is a family-oriented early intervention approach which has demonstrated good outcomes in the treatment of first-episode psychosis (FEP). Nevertheless, more evidence is needed. In this register-based cohort study the long-term outcomes of OD were evaluated through a comparison with a control group over a period of approximately 19 years. We examined the mortality, the need for psychiatric treatment, and the granting of disability allowances. Data were obtained from Finnish national registers regarding all OD patients whose treatment for FEP commenced within the time of the original interventions (total N = 108). The control group consisted of all Finnish FEP patients who had a follow-up of 19–20 years and who were guided to other Finnish specialized mental healthcare facilities (N = 1763). No difference between the samples was found regarding the annual incidence of FEP, the diagnosis, and suicide rates. Over the entire follow-up, the figures for durations of hospital treatment, disability allowances, and the need for neuroleptics remained significantly lower with OD group. Findings indicated that many positive outcomes of OD are sustained over a long time period. Due to the observational nature of the study, randomized trials are still needed to provide more information on effectiveness of approach.},
	language = {en},
	urldate = {2020-04-02},
	journal = {Psychiatry Research},
	author = {Bergström, Tomi and Seikkula, Jaakko and Alakare, Birgitta and Mäki, Pirjo and Köngäs-Saviaro, Päivi and Taskila, Jyri J. and Tolvanen, Asko and Aaltonen, Jukka},
	month = dec,
	year = {2018},
	note = {ZSCC: 0000025},
	pages = {168--175},
}

Open Dialogue (OD) is a family-oriented early intervention approach which has demonstrated good outcomes in the treatment of first-episode psychosis (FEP). Nevertheless, more evidence is needed. In this register-based cohort study the long-term outcomes of OD were evaluated through a comparison with a control group over a period of approximately 19 years. We examined the mortality, the need for psychiatric treatment, and the granting of disability allowances. Data were obtained from Finnish national registers regarding all OD patients whose treatment for FEP commenced within the time of the original interventions (total N = 108). The control group consisted of all Finnish FEP patients who had a follow-up of 19–20 years and who were guided to other Finnish specialized mental healthcare facilities (N = 1763). No difference between the samples was found regarding the annual incidence of FEP, the diagnosis, and suicide rates. Over the entire follow-up, the figures for durations of hospital treatment, disability allowances, and the need for neuroleptics remained significantly lower with OD group. Findings indicated that many positive outcomes of OD are sustained over a long time period. Due to the observational nature of the study, randomized trials are still needed to provide more information on effectiveness of approach.

@article{longden_assessing_2018,
	title = {Assessing the {Impact} and {Effectiveness} of {Hearing} {Voices} {Network} {Self}-{Help} {Groups}},
	volume = {54},
	issn = {0010-3853, 1573-2789},
	url = {http://link.springer.com/10.1007/s10597-017-0148-1},
	doi = {10.1007/s10597-017-0148-1},
	abstract = {The Hearing Voices Network (HVN) is an influential service-user led organisation that promotes selfhelp as an important aspect of recovery. This study presents the first systematic assessment of the impact and effectiveness of HVN self-help groups. A customized 45-item questionnaire, the Hearing Voices Groups Survey, was sent to 62 groups affiliated with the English HVN. 101 responses were received. Group attendance was credited with a range of positive emotional, social and clinical outcomes. Aspects that were particularly valued included: opportunities to meet other voice hearers, provision of support that was unavailable elsewhere, and the group being a safe and confidential place to discuss difficult issues. Participants perceived HVN groups to facilitate recovery processes and to be an important resource for helping them cope with their experiences. Mental health professionals can use their expertise to support the successful running of these groups.},
	language = {en},
	number = {2},
	urldate = {2020-04-02},
	journal = {Community Mental Health Journal},
	author = {Longden, Eleanor and Read, John and Dillon, Jacqui},
	month = feb,
	year = {2018},
	note = {ZSCC: 0000020},
	pages = {184--188},
}

The Hearing Voices Network (HVN) is an influential service-user led organisation that promotes selfhelp as an important aspect of recovery. This study presents the first systematic assessment of the impact and effectiveness of HVN self-help groups. A customized 45-item questionnaire, the Hearing Voices Groups Survey, was sent to 62 groups affiliated with the English HVN. 101 responses were received. Group attendance was credited with a range of positive emotional, social and clinical outcomes. Aspects that were particularly valued included: opportunities to meet other voice hearers, provision of support that was unavailable elsewhere, and the group being a safe and confidential place to discuss difficult issues. Participants perceived HVN groups to facilitate recovery processes and to be an important resource for helping them cope with their experiences. Mental health professionals can use their expertise to support the successful running of these groups.

@article{wright_be_2018,
	title = {Be it ever so humble: {Proposing} a dual-dimension account and measurement of humility},
	volume = {17},
	issn = {1529-8868, 1529-8876},
	shorttitle = {Be it ever so humble},
	url = {https://www.tandfonline.com/doi/full/10.1080/15298868.2017.1327454},
	doi = {10.1080/15298868.2017.1327454},
	abstract = {What does it mean to be humble? We argue that humility is an epistemically and ethically aligned state of awareness – the experience of ourselves as a small part of a larger universe and as one among a host of other morally relevant beings. So conceived, humility can be operationalized and measured along the dual dimensions of low self-focus and high other-focus and is distinct from other related constructs (e.g., modesty and open-mindedness). We discuss our newly developed scale (Study 1 and 2), and provide preliminary validation using self-report (Study 3) and behavioral measures (Study 4), showing that humility is related to people’s general ethical orientation (e.g., empathy, universalism/benevolence, and civic responsibility), their well-being (e.g., sense of autonomy, lifepurpose, and secure attachment), mature religious beliefs/practices, and reactions to disagreement – specifically, people high in humility sat closer and less angled away from their conversation partner with whom they disagreed. Together, this provides support for our new Dual-Dimension Humility Scale.},
	language = {en},
	number = {1},
	urldate = {2020-04-02},
	journal = {Self and Identity},
	author = {Wright, Jennifer Cole and Nadelhoffer, Thomas and Thomson Ross, Lisa and Sinnott-Armstrong, Walter},
	month = jan,
	year = {2018},
	pages = {92--125},
}

What does it mean to be humble? We argue that humility is an epistemically and ethically aligned state of awareness – the experience of ourselves as a small part of a larger universe and as one among a host of other morally relevant beings. So conceived, humility can be operationalized and measured along the dual dimensions of low self-focus and high other-focus and is distinct from other related constructs (e.g., modesty and open-mindedness). We discuss our newly developed scale (Study 1 and 2), and provide preliminary validation using self-report (Study 3) and behavioral measures (Study 4), showing that humility is related to people’s general ethical orientation (e.g., empathy, universalism/benevolence, and civic responsibility), their well-being (e.g., sense of autonomy, lifepurpose, and secure attachment), mature religious beliefs/practices, and reactions to disagreement – specifically, people high in humility sat closer and less angled away from their conversation partner with whom they disagreed. Together, this provides support for our new Dual-Dimension Humility Scale.

@article{porter_intellectual_2018,
	title = {Intellectual humility and openness to the opposing view},
	volume = {17},
	issn = {1529-8868, 1529-8876},
	url = {https://www.tandfonline.com/doi/full/10.1080/15298868.2017.1361861},
	doi = {10.1080/15298868.2017.1361861},
	abstract = {Strong disagreements have stymied today’s political discourse. We investigate intellectual humility – recognizing the limits of one’s knowledge and appreciating others’ intellectual strengths – as one factor that can make disagreements more constructive. In Studies 1 and 2, participants with higher intellectual humility were more open to learning about the opposition’s views during imagined disagreements. In Study 3, those with higher intellectual humility exposed themselves to a greater proportion of opposing political perspectives. In Study 4, making salient a growth mindset of intelligence boosted intellectual humility, and, in turn, openness to opposing views. Results suggest that intellectual humility is associated with openness during disagreement, and that a growth mindset of intelligence may increase intellectual humility. Implications for current political polarization are discussed.},
	language = {en},
	number = {2},
	urldate = {2020-04-02},
	journal = {Self and Identity},
	author = {Porter, Tenelle and Schumann, Karina},
	month = mar,
	year = {2018},
	note = {ZSCC: 0000026},
	pages = {139--162},
}

Strong disagreements have stymied today’s political discourse. We investigate intellectual humility – recognizing the limits of one’s knowledge and appreciating others’ intellectual strengths – as one factor that can make disagreements more constructive. In Studies 1 and 2, participants with higher intellectual humility were more open to learning about the opposition’s views during imagined disagreements. In Study 3, those with higher intellectual humility exposed themselves to a greater proportion of opposing political perspectives. In Study 4, making salient a growth mindset of intelligence boosted intellectual humility, and, in turn, openness to opposing views. Results suggest that intellectual humility is associated with openness during disagreement, and that a growth mindset of intelligence may increase intellectual humility. Implications for current political polarization are discussed.

@article{aftab_didactic_2018,
	title = {A {Didactic} {Course} on “{Philosophy} of {Psychiatry}” for {Psychiatry} {Residents}},
	volume = {42},
	issn = {1545-7230},
	url = {https://doi.org/10.1007/s40596-017-0853-7},
	doi = {10.1007/s40596-017-0853-7},
	language = {en},
	number = {4},
	urldate = {2020-03-23},
	journal = {Academic Psychiatry},
	author = {Aftab, Awais and Nassir Ghaemi, S. and Stagno, Susan},
	month = aug,
	year = {2018},
	pages = {559--563},
}

@article{rayner_existential_2018,
	title = {Existential {Experimentation}: {Structure} and {Principles} for a {Short}-{Term} {Psychological} {Therapy}},
	volume = {58},
	issn = {0022-1678, 1552-650X},
	shorttitle = {Existential {Experimentation}},
	url = {http://journals.sagepub.com/doi/10.1177/0022167816655925},
	doi = {10.1177/0022167816655925},
	abstract = {This article follows and expands upon the description of an intervention that attained promising results with depressed and anxious patients in a feasibility study run in a U.K. primary care setting. This protocol for shortterm existential therapy will also represent the primary reference for training and supervision of an ongoing pilot. The therapeutic approach described here aims to address in a constructive way the issues raised by the topical criticism around the application of the medical model in psychology. At the same time, this article will address the theoretical issues emerging, while trying to describe in a pragmatic way, how to apply an existential and phenomenological approach to low-intensity short-term psychological therapy. This short-term intervention aims to promote a proactive and creative engagement with clients with their personal difficulties and to attain recovery as a result of a greater sense of empowered resilience.},
	language = {en},
	number = {2},
	urldate = {2020-03-13},
	journal = {Journal of Humanistic Psychology},
	author = {Rayner, Mark and Vitali, Diego},
	month = mar,
	year = {2018},
	pages = {194--213},
}

This article follows and expands upon the description of an intervention that attained promising results with depressed and anxious patients in a feasibility study run in a U.K. primary care setting. This protocol for shortterm existential therapy will also represent the primary reference for training and supervision of an ongoing pilot. The therapeutic approach described here aims to address in a constructive way the issues raised by the topical criticism around the application of the medical model in psychology. At the same time, this article will address the theoretical issues emerging, while trying to describe in a pragmatic way, how to apply an existential and phenomenological approach to low-intensity short-term psychological therapy. This short-term intervention aims to promote a proactive and creative engagement with clients with their personal difficulties and to attain recovery as a result of a greater sense of empowered resilience.

@article{dunne_embracing_2018,
	title = {Embracing {Uncertainty} to {Enable} {Transformation}: {The} {Process} of {Engaging} in {Trialogue} for {Mental} {Health} {Communities} in {Ireland}},
	volume = {18},
	issn = {1568-4156},
	shorttitle = {Embracing {Uncertainty} to {Enable} {Transformation}},
	url = {http://www.ijic.org/articles/10.5334/ijic.3085/},
	doi = {10.5334/ijic.3085},
	abstract = {Introduction: Community-based participatory approaches are valuable methods for improving outcomes and effectively integrating care among mental health communities. Trialogue is one such approach which uses Open Dialogue methods with groups of three or more people from different backgrounds who deal with mental health systems. Theory and Method: The current study employed a participatory action research design, which prospectively documented the processes and challenges of participating in Trialogue Meetings. Individuals from participating communities took part in interviews, focus groups or Open Dialogue discussions across three cycles of research.
Results: Three prospective themes were identified from participants’ dialogue across the three cycles of research relating to the experience of participating in Trialogue, the development of Open Dialogue skills and the growth of individual Trialogue communities.
Conclusions and Discussion: The findings demonstrate that, where desirable conditions are present, T­ rialogue Meetings are worthwhile and sustainable community-based participatory approaches which encourage disclosure and dialogue surrounding mental health, and may assist in improved integration of care between mental health stakeholders. In particular, Trialogue Meetings stimulate the development of Open Dialogue skills, provide a platform for “vital” and “transformative” self-expression with the ­potential for positive mental health outcomes and may facilitate the growth of communities surrounding mental health.},
	language = {en},
	number = {2},
	urldate = {2020-03-19},
	journal = {International Journal of Integrated Care},
	author = {Dunne, Simon and MacGabhann, Liam and McGowan, Paddy and Amering, Michaela},
	month = apr,
	year = {2018},
	keywords = {Open Dialogue, community-based participatory approach, mental health, trialogue},
	pages = {3},
}

Introduction: Community-based participatory approaches are valuable methods for improving outcomes and effectively integrating care among mental health communities. Trialogue is one such approach which uses Open Dialogue methods with groups of three or more people from different backgrounds who deal with mental health systems. Theory and Method: The current study employed a participatory action research design, which prospectively documented the processes and challenges of participating in Trialogue Meetings. Individuals from participating communities took part in interviews, focus groups or Open Dialogue discussions across three cycles of research. Results: Three prospective themes were identified from participants’ dialogue across the three cycles of research relating to the experience of participating in Trialogue, the development of Open Dialogue skills and the growth of individual Trialogue communities. Conclusions and Discussion: The findings demonstrate that, where desirable conditions are present, T­ rialogue Meetings are worthwhile and sustainable community-based participatory approaches which encourage disclosure and dialogue surrounding mental health, and may assist in improved integration of care between mental health stakeholders. In particular, Trialogue Meetings stimulate the development of Open Dialogue skills, provide a platform for “vital” and “transformative” self-expression with the ­potential for positive mental health outcomes and may facilitate the growth of communities surrounding mental health.

@article{russo-netzer_positive_2018,
	title = {Positive growth from adversity and beyond: {Insights} gained from cross-examination of clinical and nonclinical samples.},
	volume = {88},
	issn = {1939-0025, 0002-9432},
	shorttitle = {Positive growth from adversity and beyond},
	url = {http://doi.apa.org/getdoi.cfm?doi=10.1037/ort0000224},
	doi = {10.1037/ort0000224},
	language = {en},
	number = {1},
	urldate = {2020-03-19},
	journal = {American Journal of Orthopsychiatry},
	author = {Russo-Netzer, Pninit and Moran, Galia},
	year = {2018},
	pages = {59--68},
}

@article{rohde_effectiveness_2018,
	title = {Effectiveness of {Prescription}-{Based} {CNS} {Stimulants} on {Hospitalization} in {Patients} {With} {Schizophrenia}: {A} {Nation}-{Wide} {Register} {Study}},
	volume = {44},
	issn = {0586-7614, 1745-1701},
	shorttitle = {Effectiveness of {Prescription}-{Based} {CNS} {Stimulants} on {Hospitalization} in {Patients} {With} {Schizophrenia}},
	url = {http://academic.oup.com/schizophreniabulletin/article/44/1/93/3098163},
	doi = {10.1093/schbul/sbx043},
	language = {en},
	number = {1},
	urldate = {2020-03-19},
	journal = {Schizophrenia Bulletin},
	author = {Rohde, Christopher and Polcwiartek, Christoffer and Asztalos, Marton and Nielsen, Jimmi},
	month = jan,
	year = {2018},
	pages = {93--100},
}

@article{rubin_classification_2018,
	title = {The {Classification} and {Statistical} {Manual} of {Mental} {Health} {Concerns}: {A} {Proposed} {Practical} {Scientific} {Alternative} to the \textit{{DSM}} and \textit{{ICD}}},
	volume = {58},
	issn = {0022-1678, 1552-650X},
	shorttitle = {The {Classification} and {Statistical} {Manual} of {Mental} {Health} {Concerns}},
	url = {http://journals.sagepub.com/doi/10.1177/0022167817718079},
	doi = {10.1177/0022167817718079},
	language = {en},
	number = {1},
	urldate = {2020-03-18},
	journal = {Journal of Humanistic Psychology},
	author = {Rubin, Jeffrey},
	month = jan,
	year = {2018},
	pages = {93--114},
}

@article{johnstone_psychological_2018,
	title = {Psychological {Formulation} as an {Alternative} to {Psychiatric} {Diagnosis}},
	volume = {58},
	issn = {0022-1678, 1552-650X},
	url = {http://journals.sagepub.com/doi/10.1177/0022167817722230},
	doi = {10.1177/0022167817722230},
	abstract = {The article gives an overview of psychological formulation, a rapidly expanding practice in the United Kingdom that is supported by the British Psychological Society. It is argued that formulation can provide a credible alternative to psychiatric diagnosis in the context of public admissions about lack of reliability and validity of current diagnostic systems. However, vigilance and best-practice principles are essential to ensure that this approach is not assimilated back into the status quo.},
	language = {en},
	number = {1},
	urldate = {2020-03-18},
	journal = {Journal of Humanistic Psychology},
	author = {Johnstone, Lucy},
	month = jan,
	year = {2018},
	pages = {30--46},
}

The article gives an overview of psychological formulation, a rapidly expanding practice in the United Kingdom that is supported by the British Psychological Society. It is argued that formulation can provide a credible alternative to psychiatric diagnosis in the context of public admissions about lack of reliability and validity of current diagnostic systems. However, vigilance and best-practice principles are essential to ensure that this approach is not assimilated back into the status quo.

@article{duncan_beyond_2018,
	title = {Beyond {Critique}: {The} {Partners} for {Change} {Outcome} {Management} {System} as an {Alternative} {Paradigm} to {Psychiatric} {Diagnosis}},
	volume = {58},
	issn = {0022-1678, 1552-650X},
	shorttitle = {Beyond {Critique}},
	url = {http://journals.sagepub.com/doi/10.1177/0022167817719975},
	doi = {10.1177/0022167817719975},
	abstract = {Critics claim that current psychiatric diagnostic systems lack reliability, validity, and clinical utility; are incompatible with known evidence of how change occurs in psychotherapy; are compromised by bias; and risk harmful effects for clients. This article argues that the Partners for Change Outcome Management System (PCOMS), a transparent, egalitarian process that collects and utilizes client feedback at each session, convincingly addresses these concerns. Furthermore, it suggests that PCOMS offers a viable alternative to the reimbursement and administrative functions of the Diagnostic and Statistical Manual of Mental Disorders and the International Classification of Diseases. The authors propose that PCOMS represents a radical realignment of the practitioner/client relationship via full, dialogical partnership at every level of psychotherapy practice and thus constitutes a step toward a new paradigm that reconnects psychotherapy and humanistic psychology with its core relational values.},
	language = {en},
	number = {1},
	urldate = {2020-03-18},
	journal = {Journal of Humanistic Psychology},
	author = {Duncan, Barry L. and Sparks, Jacqueline A. and Timimi, Sami},
	month = jan,
	year = {2018},
	pages = {7--29},
}

Critics claim that current psychiatric diagnostic systems lack reliability, validity, and clinical utility; are incompatible with known evidence of how change occurs in psychotherapy; are compromised by bias; and risk harmful effects for clients. This article argues that the Partners for Change Outcome Management System (PCOMS), a transparent, egalitarian process that collects and utilizes client feedback at each session, convincingly addresses these concerns. Furthermore, it suggests that PCOMS offers a viable alternative to the reimbursement and administrative functions of the Diagnostic and Statistical Manual of Mental Disorders and the International Classification of Diseases. The authors propose that PCOMS represents a radical realignment of the practitioner/client relationship via full, dialogical partnership at every level of psychotherapy practice and thus constitutes a step toward a new paradigm that reconnects psychotherapy and humanistic psychology with its core relational values.

@article{cooke_but_2018,
	title = {“{But} {What} {About} {Real} {Mental} {Illnesses}?” {Alternatives} to the {Disease} {Model} {Approach} to “{Schizophrenia}”},
	volume = {58},
	issn = {0022-1678, 1552-650X},
	shorttitle = {“{But} {What} {About} {Real} {Mental} {Illnesses}?},
	url = {http://journals.sagepub.com/doi/10.1177/0022167817745621},
	doi = {10.1177/0022167817745621},
	language = {en},
	number = {1},
	urldate = {2020-03-18},
	journal = {Journal of Humanistic Psychology},
	author = {Cooke, Anne and Kinderman, Peter},
	month = jan,
	year = {2018},
	pages = {47--71},
}

@article{kim_understanding_2018,
	title = {Understanding uncertainty in medicine: concepts and implications in medical education},
	volume = {30},
	issn = {2005-727X},
	shorttitle = {Understanding uncertainty in medicine},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6127608/},
	doi = {10.3946/kjme.2018.92},
	abstract = {In an era of high technology and low trust, acknowledging and coping with uncertainty is more crucial than ever. Medical uncertainty has been considered an innate feature of medicine and medical practice. An intolerance to uncertainty increases physicians’ stress and the effects of burnout and may be a potential threat to patient safety. Understanding medical uncertainty and acquiring proper coping strategies has been regarded to be a core clinical competency for medical graduates and trainees. Integrating intuition and logic and creating a culture that acknowledges medical uncertainty could be suggested ways to teach medical uncertainty. In this article, the authors describe the concepts of medical uncertainty, its influences on physicians and on medical students toward medical decision making, the role of tolerance/intolerance to uncertainty, and proposed strategies to improve coping with medical uncertainty.},
	number = {3},
	urldate = {2020-03-12},
	journal = {Korean Journal of Medical Education},
	author = {Kim, Kangmoon and Lee, Young-Mee},
	month = sep,
	year = {2018},
	pmid = {30180505},
	pmcid = {PMC6127608},
	keywords = {Heuristics, competenecy-based education, decision making, medical education, uncertainty},
	pages = {181--188},
}

In an era of high technology and low trust, acknowledging and coping with uncertainty is more crucial than ever. Medical uncertainty has been considered an innate feature of medicine and medical practice. An intolerance to uncertainty increases physicians’ stress and the effects of burnout and may be a potential threat to patient safety. Understanding medical uncertainty and acquiring proper coping strategies has been regarded to be a core clinical competency for medical graduates and trainees. Integrating intuition and logic and creating a culture that acknowledges medical uncertainty could be suggested ways to teach medical uncertainty. In this article, the authors describe the concepts of medical uncertainty, its influences on physicians and on medical students toward medical decision making, the role of tolerance/intolerance to uncertainty, and proposed strategies to improve coping with medical uncertainty.

@article{haggard_finding_2018,
	title = {Finding middle ground between intellectual arrogance and intellectual servility: {Development} and assessment of the limitations-owning intellectual humility scale},
	volume = {124},
	issn = {01918869},
	shorttitle = {Finding middle ground between intellectual arrogance and intellectual servility},
	url = {https://linkinghub.elsevier.com/retrieve/pii/S0191886917307286},
	doi = {10.1016/j.paid.2017.12.014},
	abstract = {Recent scholarship in intellectual humility (IH) has attempted to provide deeper understanding of the virtue as personality trait and its impact on an individual's thoughts, beliefs, and actions. A limitations-owning perspective of IH focuses on a proper recognition of the impact of intellectual limitations and a motivation to overcome them, placing it as the mean between intellectual arrogance and intellectual servility. We developed the Limitations-Owning Intellectual Humility Scale to assess this conception of IH with related personality constructs. In Studies 1 (n = 386) and 2 (n = 296), principal factor and confirmatory factor analyses revealed a three-factor model – owning one's intellectual limitations, appropriate discomfort with intellectual limitations, and love of learning. Study 3 (n = 322) demonstrated strong test-retest reliability of the measure over 5 months, while Study 4 (n = 612) revealed limitations-owning IH correlated negatively with dogmatism, closed-mindedness, and hubristic pride and positively with openness, assertiveness, authentic pride. It also predicted openness and closed-mindedness over and above education, social desirability, and other measures of IH. The limitations-owning understanding of IH and scale allow for a more nuanced, spectrum interpretation and measurement of the virtue, which directs future study inside and outside of psychology.},
	language = {en},
	urldate = {2020-03-13},
	journal = {Personality and Individual Differences},
	author = {Haggard, Megan and Rowatt, Wade C. and Leman, Joseph C. and Meagher, Benjamin and Moore, Courtney and Fergus, Thomas and Whitcomb, Dennis and Battaly, Heather and Baehr, Jason and Howard-Snyder, Dan},
	month = apr,
	year = {2018},
	pages = {184--193},
}

Recent scholarship in intellectual humility (IH) has attempted to provide deeper understanding of the virtue as personality trait and its impact on an individual's thoughts, beliefs, and actions. A limitations-owning perspective of IH focuses on a proper recognition of the impact of intellectual limitations and a motivation to overcome them, placing it as the mean between intellectual arrogance and intellectual servility. We developed the Limitations-Owning Intellectual Humility Scale to assess this conception of IH with related personality constructs. In Studies 1 (n = 386) and 2 (n = 296), principal factor and confirmatory factor analyses revealed a three-factor model – owning one's intellectual limitations, appropriate discomfort with intellectual limitations, and love of learning. Study 3 (n = 322) demonstrated strong test-retest reliability of the measure over 5 months, while Study 4 (n = 612) revealed limitations-owning IH correlated negatively with dogmatism, closed-mindedness, and hubristic pride and positively with openness, assertiveness, authentic pride. It also predicted openness and closed-mindedness over and above education, social desirability, and other measures of IH. The limitations-owning understanding of IH and scale allow for a more nuanced, spectrum interpretation and measurement of the virtue, which directs future study inside and outside of psychology.

@article{roulston_qualitative_2018,
	title = {Qualitative interviewing and epistemics},
	volume = {18},
	issn = {1468-7941, 1741-3109},
	url = {http://journals.sagepub.com/doi/10.1177/1468794117721738},
	doi = {10.1177/1468794117721738},
	abstract = {Work on epistemics in conversation analysis (CA) has demonstrated how speakers attend closely to the knowledge claims they and others make and how this shapes interaction. This paper uses work on epistemics in CA to explore how interviewers and interviewees orient to knowledge claims involving the asking and answering of questions. Since research participants are recruited to represent a category identified by the researcher, interviewees are assumed to have greater knowledge relative to the research topic as compared to interviewers, who typically work to demonstrate that they are eager learners about others’ experiences, perceptions and beliefs and so forth. This paper examines sequences from research interviews to focus on the fine-grained work involved in asking questions and making knowledge claims within interviews. Epistemics provides a powerful tool to examine how speakers’ orientations to others’ knowledge claims is central to the interactional work of conducting interviews.},
	language = {en},
	number = {3},
	urldate = {2020-03-12},
	journal = {Qualitative Research},
	author = {Roulston, Kathryn},
	month = jun,
	year = {2018},
	pages = {322--341},
}

Work on epistemics in conversation analysis (CA) has demonstrated how speakers attend closely to the knowledge claims they and others make and how this shapes interaction. This paper uses work on epistemics in CA to explore how interviewers and interviewees orient to knowledge claims involving the asking and answering of questions. Since research participants are recruited to represent a category identified by the researcher, interviewees are assumed to have greater knowledge relative to the research topic as compared to interviewers, who typically work to demonstrate that they are eager learners about others’ experiences, perceptions and beliefs and so forth. This paper examines sequences from research interviews to focus on the fine-grained work involved in asking questions and making knowledge claims within interviews. Epistemics provides a powerful tool to examine how speakers’ orientations to others’ knowledge claims is central to the interactional work of conducting interviews.

@article{mittal_what_2017,
	title = {What {Can} {Different} {Motor} {Circuits} {Tell} {Us} {About} {Psychosis}? {An} {RDoC} {Perspective}},
	volume = {43},
	issn = {0586-7614},
	shorttitle = {What {Can} {Different} {Motor} {Circuits} {Tell} {Us} {About} {Psychosis}?},
	url = {https://doi.org/10.1093/schbul/sbx087},
	doi = {10.1093/schbul/sbx087},
	abstract = {Signs of motor dysfunction are evidenced across a range of psychiatric disorders including schizophrenia. Historically, these features have been neglected but emerging theoretical and methodological advancements have shed new light on the utility of considering movement abnormalities. Indeed, the National Institute of Mental Health Research Domain Criteria initiative has recently met to develop a Motor Systems Domain. This reflects a growing appreciation for the enhanced reliability and validity that can come along with evaluating disturbances relevant to psychiatric illnesses from multiple levels of analysis, and conceptualizing these domains with respect to the complexity of their role in a broader integrated system (ie, weighing contributions and interactions between the cognitive, affective, and motor domains). This article discusses motor behaviors and seeks to explain how research into basal ganglia, cerebellar, and cortico-motor circuit function/dysfunction, grounded in brain circuit-motor behavior relationships, can elucidate our understanding of pathophysiology, provide vital links to other key systems of interest, significantly improve identification and classification, and drive development of targeted individualized treatments.},
	number = {5},
	urldate = {2022-07-24},
	journal = {Schizophrenia Bulletin},
	author = {Mittal, Vijay A and Bernard, Jessica A and Northoff, Georg},
	month = sep,
	year = {2017},
	note = {Number: 5},
	pages = {949--955},
}

Signs of motor dysfunction are evidenced across a range of psychiatric disorders including schizophrenia. Historically, these features have been neglected but emerging theoretical and methodological advancements have shed new light on the utility of considering movement abnormalities. Indeed, the National Institute of Mental Health Research Domain Criteria initiative has recently met to develop a Motor Systems Domain. This reflects a growing appreciation for the enhanced reliability and validity that can come along with evaluating disturbances relevant to psychiatric illnesses from multiple levels of analysis, and conceptualizing these domains with respect to the complexity of their role in a broader integrated system (ie, weighing contributions and interactions between the cognitive, affective, and motor domains). This article discusses motor behaviors and seeks to explain how research into basal ganglia, cerebellar, and cortico-motor circuit function/dysfunction, grounded in brain circuit-motor behavior relationships, can elucidate our understanding of pathophysiology, provide vital links to other key systems of interest, significantly improve identification and classification, and drive development of targeted individualized treatments.

@article{mittal_what_2017,
	title = {What {Can} {Different} {Motor} {Circuits} {Tell} {Us} {About} {Psychosis}? {An} {RDoC} {Perspective}},
	volume = {43},
	issn = {0586-7614},
	shorttitle = {What {Can} {Different} {Motor} {Circuits} {Tell} {Us} {About} {Psychosis}?},
	url = {https://doi.org/10.1093/schbul/sbx087},
	doi = {10.1093/schbul/sbx087},
	abstract = {Signs of motor dysfunction are evidenced across a range of psychiatric disorders including schizophrenia. Historically, these features have been neglected but emerging theoretical and methodological advancements have shed new light on the utility of considering movement abnormalities. Indeed, the National Institute of Mental Health Research Domain Criteria initiative has recently met to develop a Motor Systems Domain. This reflects a growing appreciation for the enhanced reliability and validity that can come along with evaluating disturbances relevant to psychiatric illnesses from multiple levels of analysis, and conceptualizing these domains with respect to the complexity of their role in a broader integrated system (ie, weighing contributions and interactions between the cognitive, affective, and motor domains). This article discusses motor behaviors and seeks to explain how research into basal ganglia, cerebellar, and cortico-motor circuit function/dysfunction, grounded in brain circuit-motor behavior relationships, can elucidate our understanding of pathophysiology, provide vital links to other key systems of interest, significantly improve identification and classification, and drive development of targeted individualized treatments.},
	number = {5},
	urldate = {2022-07-24},
	journal = {Schizophrenia Bulletin},
	author = {Mittal, Vijay A and Bernard, Jessica A and Northoff, Georg},
	month = sep,
	year = {2017},
	pages = {949--955},
}

Signs of motor dysfunction are evidenced across a range of psychiatric disorders including schizophrenia. Historically, these features have been neglected but emerging theoretical and methodological advancements have shed new light on the utility of considering movement abnormalities. Indeed, the National Institute of Mental Health Research Domain Criteria initiative has recently met to develop a Motor Systems Domain. This reflects a growing appreciation for the enhanced reliability and validity that can come along with evaluating disturbances relevant to psychiatric illnesses from multiple levels of analysis, and conceptualizing these domains with respect to the complexity of their role in a broader integrated system (ie, weighing contributions and interactions between the cognitive, affective, and motor domains). This article discusses motor behaviors and seeks to explain how research into basal ganglia, cerebellar, and cortico-motor circuit function/dysfunction, grounded in brain circuit-motor behavior relationships, can elucidate our understanding of pathophysiology, provide vital links to other key systems of interest, significantly improve identification and classification, and drive development of targeted individualized treatments.

@article{goldstein_hypoactive_2017,
	title = {Hypoactive {Sexual} {Desire} {Disorder}},
	volume = {92},
	issn = {00256196},
	url = {https://linkinghub.elsevier.com/retrieve/pii/S0025619616305961},
	doi = {10.1016/j.mayocp.2016.09.018},
	abstract = {The objective of the International Society for the Study of Women’s Sexual Health expert consensus panel was to develop a concise, clinically relevant, evidence-based review of the epidemiology, physiology, pathogenesis, diagnosis, and treatment of hypoactive sexual desire disorder (HSDD), a sexual dysfunction affecting approximately 10\% of adult women. Etiologic factors include conditions or drugs that decrease brain dopamine, melanocortin, oxytocin, and norepinephrine levels and augment brain serotonin, endocannabinoid, prolactin, and opioid levels. Symptoms include lack or loss of motivation to participate in sexual activity due to absent or decreased spontaneous desire, sexual desire in response to erotic cues or stimulation, or ability to maintain desire or interest through sexual activity for at least 6 months, with accompanying distress. Treatment follows a biopsychosocial model and is guided by history and assessment of symptoms. Sex therapy has been the standard treatment, although there is a paucity of studies assessing efficacy, except for mindfulness-based cognitive behavior therapy. Bupropion and buspirone may be considered off-label treatments for HSDD, despite limited safety and efficacy data. Menopausal women with HSDD may benefit from off-label testosterone treatment, as evidenced by multiple clinical trials reporting some efficacy and short-term safety. Currently, flibanserin is the only Food and Drug Administrationeapproved medication to treat premenopausal women with generalized acquired HSDD. Based on existing data, we hypothesize that all these therapies alter central inhibitory and excitatory pathways. In conclusion, HSDD significantly affects quality of life in women and can effectively be managed by health care providers with appropriate assessments and individualized treatments.},
	language = {en},
	number = {1},
	urldate = {2021-12-28},
	journal = {Mayo Clinic Proceedings},
	author = {Goldstein, Irwin and Kim, Noel N. and Clayton, Anita H. and DeRogatis, Leonard R. and Giraldi, Annamaria and Parish, Sharon J. and Pfaus, James and Simon, James A. and Kingsberg, Sheryl A. and Meston, Cindy and Stahl, Stephen M. and Wallen, Kim and Worsley, Roisin},
	month = jan,
	year = {2017},
	pages = {114--128},
}

The objective of the International Society for the Study of Women’s Sexual Health expert consensus panel was to develop a concise, clinically relevant, evidence-based review of the epidemiology, physiology, pathogenesis, diagnosis, and treatment of hypoactive sexual desire disorder (HSDD), a sexual dysfunction affecting approximately 10% of adult women. Etiologic factors include conditions or drugs that decrease brain dopamine, melanocortin, oxytocin, and norepinephrine levels and augment brain serotonin, endocannabinoid, prolactin, and opioid levels. Symptoms include lack or loss of motivation to participate in sexual activity due to absent or decreased spontaneous desire, sexual desire in response to erotic cues or stimulation, or ability to maintain desire or interest through sexual activity for at least 6 months, with accompanying distress. Treatment follows a biopsychosocial model and is guided by history and assessment of symptoms. Sex therapy has been the standard treatment, although there is a paucity of studies assessing efficacy, except for mindfulness-based cognitive behavior therapy. Bupropion and buspirone may be considered off-label treatments for HSDD, despite limited safety and efficacy data. Menopausal women with HSDD may benefit from off-label testosterone treatment, as evidenced by multiple clinical trials reporting some efficacy and short-term safety. Currently, flibanserin is the only Food and Drug Administrationeapproved medication to treat premenopausal women with generalized acquired HSDD. Based on existing data, we hypothesize that all these therapies alter central inhibitory and excitatory pathways. In conclusion, HSDD significantly affects quality of life in women and can effectively be managed by health care providers with appropriate assessments and individualized treatments.

@article{krystal_computational_2017,
	title = {Computational {Psychiatry} and the {Challenge} of {Schizophrenia}},
	volume = {43},
	issn = {1745-1701},
	doi = {10.1093/schbul/sbx025},
	abstract = {Schizophrenia research is plagued by enormous challenges in integrating and analyzing large datasets and difficulties developing formal theories related to the etiology, pathophysiology, and treatment of this disorder. Computational psychiatry provides a path to enhance analyses of these large and complex datasets and to promote the development and refinement of formal models for features of this disorder. This presentation introduces the reader to the notion of computational psychiatry and describes discovery-oriented and theory-driven applications to schizophrenia involving machine learning, reinforcement learning theory, and biophysically-informed neural circuit models.},
	language = {eng},
	number = {3},
	journal = {Schizophrenia Bulletin},
	author = {Krystal, John H. and Murray, John D. and Chekroud, Adam M. and Corlett, Philip R. and Yang, Genevieve and Wang, Xiao-Jing and Anticevic, Alan},
	month = may,
	year = {2017},
	pmid = {28338845},
	pmcid = {PMC5464204},
	keywords = {Computational Biology, Humans, Neurosciences, Psychiatry, Schizophrenia, computational neuroscience, computational psychiatry, delusions, machine learning, medication selection, schizophrenia, working memory},
	pages = {473--475},
}

Schizophrenia research is plagued by enormous challenges in integrating and analyzing large datasets and difficulties developing formal theories related to the etiology, pathophysiology, and treatment of this disorder. Computational psychiatry provides a path to enhance analyses of these large and complex datasets and to promote the development and refinement of formal models for features of this disorder. This presentation introduces the reader to the notion of computational psychiatry and describes discovery-oriented and theory-driven applications to schizophrenia involving machine learning, reinforcement learning theory, and biophysically-informed neural circuit models.

@article{sitaram_closed-loop_2017,
	title = {Closed-loop brain training: the science of neurofeedback},
	volume = {18},
	issn = {1471-003X, 1471-0048},
	shorttitle = {Closed-loop brain training},
	url = {http://www.nature.com/articles/nrn.2016.164},
	doi = {10.1038/nrn.2016.164},
	abstract = {Neurofeedback is a psychophysiological procedure in which online feedback of neural activation is provided to the participant for the purpose of self-regulation. Learning control over specific neural substrates has been shown to change specific behaviours. As a progenitor of brain–machine interfaces, neurofeedback has provided a novel way to investigate brain function and neuroplasticity. In this Review, we examine the mechanisms underlying neurofeedback, which have started to be uncovered. We also discuss how neurofeedback is being used in novel experimental and clinical paradigms from a multidisciplinary perspective, encompassing neuroscientific, neuroengineering and learning-science viewpoints.},
	language = {en},
	number = {2},
	urldate = {2020-10-06},
	journal = {Nature Reviews Neuroscience},
	author = {Sitaram, Ranganatha and Ros, Tomas and Stoeckel, Luke and Haller, Sven and Scharnowski, Frank and Lewis-Peacock, Jarrod and Weiskopf, Nikolaus and Blefari, Maria Laura and Rana, Mohit and Oblak, Ethan and Birbaumer, Niels and Sulzer, James},
	month = feb,
	year = {2017},
	note = {ZSCC: 0000400},
	pages = {86--100},
}

Neurofeedback is a psychophysiological procedure in which online feedback of neural activation is provided to the participant for the purpose of self-regulation. Learning control over specific neural substrates has been shown to change specific behaviours. As a progenitor of brain–machine interfaces, neurofeedback has provided a novel way to investigate brain function and neuroplasticity. In this Review, we examine the mechanisms underlying neurofeedback, which have started to be uncovered. We also discuss how neurofeedback is being used in novel experimental and clinical paradigms from a multidisciplinary perspective, encompassing neuroscientific, neuroengineering and learning-science viewpoints.

@article{matzke_failures_2017,
	title = {Failures of cognitive control or attention? {The} case of stop-signal deficits in schizophrenia},
	volume = {79},
	issn = {1943-393X},
	shorttitle = {Failures of cognitive control or attention?},
	url = {https://doi.org/10.3758/s13414-017-1287-8},
	doi = {10.3758/s13414-017-1287-8},
	abstract = {We used Bayesian cognitive modelling to identify the underlying causes of apparent inhibitory deficits in the stop-signal paradigm. The analysis was applied to stop-signal data reported by Badcock et al. (Psychological Medicine 32: 87-297, 2002) and Hughes et al. (Biological Psychology 89: 220-231, 2012), where schizophrenia patients and control participants made rapid choice responses, but on some trials were signalled to stop their ongoing response. Previous research has assumed an inhibitory deficit in schizophrenia, because estimates of the mean time taken to react to the stop signal are longer in patients than controls. We showed that these longer estimates are partly due to failing to react to the stop signal (“trigger failures”) and partly due to a slower initiation of inhibition, implicating a failure of attention rather than a deficit in the inhibitory process itself. Correlations between the probability of trigger failures and event-related potentials reported by Hughes et al. are interpreted as supporting the attentional account of inhibitory deficits. Our results, and those of Matzke et al. (2016), who report that controls also display a substantial although lower trigger-failure rate, indicate that attentional factors need to be taken into account when interpreting results from the stop-signal paradigm.},
	language = {en},
	number = {4},
	urldate = {2021-06-24},
	journal = {Attention, Perception, \& Psychophysics},
	author = {Matzke, Dora and Hughes, Matthew and Badcock, Johanna C. and Michie, Patricia and Heathcote, Andrew},
	month = may,
	year = {2017},
	note = {ZSCC: 0000061},
	pages = {1078--1086},
}

We used Bayesian cognitive modelling to identify the underlying causes of apparent inhibitory deficits in the stop-signal paradigm. The analysis was applied to stop-signal data reported by Badcock et al. (Psychological Medicine 32: 87-297, 2002) and Hughes et al. (Biological Psychology 89: 220-231, 2012), where schizophrenia patients and control participants made rapid choice responses, but on some trials were signalled to stop their ongoing response. Previous research has assumed an inhibitory deficit in schizophrenia, because estimates of the mean time taken to react to the stop signal are longer in patients than controls. We showed that these longer estimates are partly due to failing to react to the stop signal (“trigger failures”) and partly due to a slower initiation of inhibition, implicating a failure of attention rather than a deficit in the inhibitory process itself. Correlations between the probability of trigger failures and event-related potentials reported by Hughes et al. are interpreted as supporting the attentional account of inhibitory deficits. Our results, and those of Matzke et al. (2016), who report that controls also display a substantial although lower trigger-failure rate, indicate that attentional factors need to be taken into account when interpreting results from the stop-signal paradigm.

@article{payne_open_2017,
	title = {{OPEN} {DATA} {FOR} {DISCOVERY} {SCIENCE}},
	volume = {22},
	issn = {2335-6936},
	doi = {10.1142/9789813207813_0061},
	abstract = {The modern healthcare and life sciences ecosystem is moving towards an increasingly open and data-centric approach to discovery science. This evolving paradigm is predicated on a complex set of information needs related to our collective ability to share, discover, reuse, integrate, and analyze open biological, clinical, and population level data resources of varying composition, granularity, and syntactic or semantic consistency. Such an evolution is further impacted by a concomitant growth in the size of data sets that can and should be employed for both hypothesis discovery and testing. When such open data can be accessed and employed for discovery purposes, a broad spectrum of high impact end-points is made possible. These span the spectrum from identification of de novo biomarker complexes that can inform precision medicine, to the repositioning or repurposing of extant agents for new and cost-effective therapies, to the assessment of population level influences on disease and wellness. Of note, these types of uses of open data can be either primary, wherein open data is the substantive basis for inquiry, or secondary, wherein open data is used to augment or enrich project-specific or proprietary data that is not open in and of itself. This workshop is concerned with the key challenges, opportunities, and methodological best practices whereby open data can be used to drive the advancement of discovery science in all of the aforementioned capacities.},
	language = {eng},
	journal = {Pacific Symposium on Biocomputing. Pacific Symposium on Biocomputing},
	author = {Payne, Philip R. O. and Huang, Kun and Shah, Nigam H. and Tenenbaum, Jessica},
	year = {2017},
	pmid = {27897016},
	note = {ZSCC: 0000001 },
	keywords = {Computational Biology, Humans},
	pages = {649--652},
}

The modern healthcare and life sciences ecosystem is moving towards an increasingly open and data-centric approach to discovery science. This evolving paradigm is predicated on a complex set of information needs related to our collective ability to share, discover, reuse, integrate, and analyze open biological, clinical, and population level data resources of varying composition, granularity, and syntactic or semantic consistency. Such an evolution is further impacted by a concomitant growth in the size of data sets that can and should be employed for both hypothesis discovery and testing. When such open data can be accessed and employed for discovery purposes, a broad spectrum of high impact end-points is made possible. These span the spectrum from identification of de novo biomarker complexes that can inform precision medicine, to the repositioning or repurposing of extant agents for new and cost-effective therapies, to the assessment of population level influences on disease and wellness. Of note, these types of uses of open data can be either primary, wherein open data is the substantive basis for inquiry, or secondary, wherein open data is used to augment or enrich project-specific or proprietary data that is not open in and of itself. This workshop is concerned with the key challenges, opportunities, and methodological best practices whereby open data can be used to drive the advancement of discovery science in all of the aforementioned capacities.

@article{gubin_systems_2017,
	title = {A {Systems} {Approach} to {Healthcare} {Innovation} {Using} the {MIT} {Hacking} {Medicine} {Model}},
	volume = {5},
	issn = {2405-4712},
	doi = {10.1016/j.cels.2017.02.012},
	abstract = {MIT Hacking Medicine is a student, academic, and community-led organization that uses systems-oriented "healthcare hacking" to address challenges around innovation in healthcare. The group has organized more than 80 events around the world that attract participants with diverse backgrounds. These participants are trained to address clinical needs from the perspective of multiple stakeholders and emphasize utility and implementation viability of proposed solutions. We describe the MIT Hacking Medicine model as a potential method to integrate collaboration and training in rapid innovation techniques into academic medical centers. Built upon a systems approach to healthcare innovation, the time-compressed but expertly guided nature of the events could enable more widely accessible preliminary training in systems-level innovation methodology, as well as creating a structured opportunity for interdisciplinary congregation and collaboration.},
	language = {eng},
	number = {1},
	journal = {Cell Systems},
	author = {Gubin, Tatyana A. and Iyer, Hari P. and Liew, Shirlene N. and Sarma, Aartik and Revelos, Alex and Ribas, João and Movassaghi, Babak and Chu, Zen M. and Khalid, Ayesha N. and Majmudar, Maulik D. and Lee, Christopher Xiang},
	month = jul,
	year = {2017},
	pmid = {28750199},
	note = {ZSCC: 0000023 },
	keywords = {Academic Medical Centers, Delivery of Health Care, Diffusion of Innovation, Humans, Interdisciplinary Studies, Massachusetts, Models, Organizational, Systems Analysis},
	pages = {6--10},
}

MIT Hacking Medicine is a student, academic, and community-led organization that uses systems-oriented "healthcare hacking" to address challenges around innovation in healthcare. The group has organized more than 80 events around the world that attract participants with diverse backgrounds. These participants are trained to address clinical needs from the perspective of multiple stakeholders and emphasize utility and implementation viability of proposed solutions. We describe the MIT Hacking Medicine model as a potential method to integrate collaboration and training in rapid innovation techniques into academic medical centers. Built upon a systems approach to healthcare innovation, the time-compressed but expertly guided nature of the events could enable more widely accessible preliminary training in systems-level innovation methodology, as well as creating a structured opportunity for interdisciplinary congregation and collaboration.

@article{friston_active_2017,
	title = {Active {Inference}, {Curiosity} and {Insight}},
	volume = {29},
	issn = {0899-7667},
	url = {https://doi.org/10.1162/neco_a_00999},
	doi = {10.1162/neco_a_00999},
	abstract = {This article offers a formal account of curiosity and insight in terms of active (Bayesian) inference. It deals with the dual problem of inferring states of the world and learning its statistical structure. In contrast to current trends in machine learning (e.g., deep learning), we focus on how people attain insight and understanding using just a handful of observations, which are solicited through curious behavior. We use simulations of abstract rule learning and approximate Bayesian inference to show that minimizing (expected) variational free energy leads to active sampling of novel contingencies. This epistemic behavior closes explanatory gaps in generative models of the world, thereby reducing uncertainty and satisfying curiosity. We then move from epistemic learning to model selection or structure learning to show how abductive processes emerge when agents test plausible hypotheses about symmetries (i.e., invariances or rules) in their generative models. The ensuing Bayesian model reduction evinces mechanisms associated with sleep and has all the hallmarks of “aha” moments. This formulation moves toward a computational account of consciousness in the pre-Cartesian sense of sharable knowledge (i.e., con: “together”; scire: “to know”).},
	number = {10},
	urldate = {2021-06-05},
	journal = {Neural Computation},
	author = {Friston, Karl J. and Lin, Marco and Frith, Christopher D. and Pezzulo, Giovanni and Hobson, J. Allan and Ondobaka, Sasha},
	month = oct,
	year = {2017},
	note = {ZSCC: 0000226},
	pages = {2633--2683},
}

This article offers a formal account of curiosity and insight in terms of active (Bayesian) inference. It deals with the dual problem of inferring states of the world and learning its statistical structure. In contrast to current trends in machine learning (e.g., deep learning), we focus on how people attain insight and understanding using just a handful of observations, which are solicited through curious behavior. We use simulations of abstract rule learning and approximate Bayesian inference to show that minimizing (expected) variational free energy leads to active sampling of novel contingencies. This epistemic behavior closes explanatory gaps in generative models of the world, thereby reducing uncertainty and satisfying curiosity. We then move from epistemic learning to model selection or structure learning to show how abductive processes emerge when agents test plausible hypotheses about symmetries (i.e., invariances or rules) in their generative models. The ensuing Bayesian model reduction evinces mechanisms associated with sleep and has all the hallmarks of “aha” moments. This formulation moves toward a computational account of consciousness in the pre-Cartesian sense of sharable knowledge (i.e., con: “together”; scire: “to know”).

@article{demkow_genetic_2017,
	title = {Genetic tests in major psychiatric disorders—integrating molecular medicine with clinical psychiatry—why is it so difficult?},
	volume = {7},
	copyright = {2017 The Author(s)},
	issn = {2158-3188},
	url = {https://www.nature.com/articles/tp2017106},
	doi = {10.1038/tp.2017.106},
	abstract = {With the advent of post-genomic era, new technologies create extraordinary possibilities for diagnostics and personalized therapy, transforming todays’ medicine. Rooted in both medical genetics and clinical psychiatry, the paper is designed as an integrated source of information of the current and potential future application of emerging genomic technologies as diagnostic tools in psychiatry, moving beyond the classical concept of patient approach. Selected approaches are presented, starting from currently used technologies (next-generation sequencing (NGS) and microarrays), followed by newer options (reverse phenotyping). Next, we describe an old concept in a new light (endophenotypes), subsequently coming up with a sophisticated and complex approach (gene networks) ending by a nascent field (computational psychiatry). The challenges and barriers that exist to translate genomic research to real-world patient assessment are further discussed. We emphasize the view that only a paradigm shift can bring a fundamental change in psychiatric practice, allowing to disentangle the intricacies of mental diseases. All the diagnostic methods, as described, are directed at uncovering the integrity of the system including many types of relations within a complex structure. The integrative system approach offers new opportunity to connect genetic background with specific diseases entities, or concurrently, with symptoms regardless of a diagnosis. To advance the field, we propose concerted cross-disciplinary effort to provide a diagnostic platform operating at the general level of genetic pathogenesis of complex-trait psychiatric disorders rather than at the individual level of a specific disease.},
	language = {en},
	number = {6},
	urldate = {2021-04-21},
	journal = {Translational Psychiatry},
	author = {Demkow, U. and Wolańczyk, T.},
	month = jun,
	year = {2017},
	note = {ZSCC: 0000037 
Number: 6
Publisher: Nature Publishing Group},
	pages = {e1151--e1151},
}

With the advent of post-genomic era, new technologies create extraordinary possibilities for diagnostics and personalized therapy, transforming todays’ medicine. Rooted in both medical genetics and clinical psychiatry, the paper is designed as an integrated source of information of the current and potential future application of emerging genomic technologies as diagnostic tools in psychiatry, moving beyond the classical concept of patient approach. Selected approaches are presented, starting from currently used technologies (next-generation sequencing (NGS) and microarrays), followed by newer options (reverse phenotyping). Next, we describe an old concept in a new light (endophenotypes), subsequently coming up with a sophisticated and complex approach (gene networks) ending by a nascent field (computational psychiatry). The challenges and barriers that exist to translate genomic research to real-world patient assessment are further discussed. We emphasize the view that only a paradigm shift can bring a fundamental change in psychiatric practice, allowing to disentangle the intricacies of mental diseases. All the diagnostic methods, as described, are directed at uncovering the integrity of the system including many types of relations within a complex structure. The integrative system approach offers new opportunity to connect genetic background with specific diseases entities, or concurrently, with symptoms regardless of a diagnosis. To advance the field, we propose concerted cross-disciplinary effort to provide a diagnostic platform operating at the general level of genetic pathogenesis of complex-trait psychiatric disorders rather than at the individual level of a specific disease.

@article{leal-soto_three-factor_2017,
	title = {Three-factor structure for {Epistemic} {Belief} {Inventory}: {A} cross-validation study},
	volume = {12},
	issn = {1932-6203},
	shorttitle = {Three-factor structure for {Epistemic} {Belief} {Inventory}},
	url = {https://dx.plos.org/10.1371/journal.pone.0173295},
	doi = {10.1371/journal.pone.0173295},
	abstract = {Research on epistemic beliefs has been hampered by lack of validated models and measurement instruments. The most widely used instrument is the Epistemological Questionnaire, which has been criticized for validity, and it has been proposed a new instrument based in the Epistemological Questionnaire: the Epistemic Belief Inventory. The Spanishlanguage version of Epistemic Belief Inventory was applied to 1,785 Chilean high school students. Exploratory and confirmatory factor analyses in independent subsamples were performed. A three factor structure emerged and was confirmed. Reliability was comparable to other studies, and the factor structure was invariant among randomized subsamples. The structure that was found does not replicate the one proposed originally, but results are interpreted in light of embedded systemic model of epistemological beliefs.},
	language = {en},
	number = {3},
	urldate = {2020-03-12},
	journal = {PLOS ONE},
	author = {Leal-Soto, Francisco and Ferrer-Urbina, Rodrigo},
	editor = {Lozano, Sergi},
	month = mar,
	year = {2017},
	note = {ZSCC: NoCitationData[s0]},
	pages = {e0173295},
}

Research on epistemic beliefs has been hampered by lack of validated models and measurement instruments. The most widely used instrument is the Epistemological Questionnaire, which has been criticized for validity, and it has been proposed a new instrument based in the Epistemological Questionnaire: the Epistemic Belief Inventory. The Spanishlanguage version of Epistemic Belief Inventory was applied to 1,785 Chilean high school students. Exploratory and confirmatory factor analyses in independent subsamples were performed. A three factor structure emerged and was confirmed. Reliability was comparable to other studies, and the factor structure was invariant among randomized subsamples. The structure that was found does not replicate the one proposed originally, but results are interpreted in light of embedded systemic model of epistemological beliefs.

@article{pekrun_measuring_2017,
	title = {Measuring emotions during epistemic activities: the {Epistemically}-{Related} {Emotion} {Scales}},
	volume = {31},
	issn = {0269-9931, 1464-0600},
	shorttitle = {Measuring emotions during epistemic activities},
	url = {https://www.tandfonline.com/doi/full/10.1080/02699931.2016.1204989},
	doi = {10.1080/02699931.2016.1204989},
	abstract = {Measurement instruments assessing multiple emotions during epistemic activities are largely lacking. We describe the construction and validation of the EpistemicallyRelated Emotion Scales, which measure surprise, curiosity, enjoyment, confusion, anxiety, frustration, and boredom occurring during epistemic cognitive activities. The instrument was tested in a multinational study of emotions during learning from conflicting texts (N = 438 university students from the United States, Canada, and Germany). The findings document the reliability, internal validity, and external validity of the instrument. A seven-factor model best fit the data, suggesting that epistemically-related emotions should be conceptualised in terms of discrete emotion categories, and the scales showed metric invariance across the North American and German samples. Furthermore, emotion scores changed over time as a function of conflicting task information and related significantly to perceived task value and use of cognitive and metacognitive learning strategies.},
	language = {en},
	number = {6},
	urldate = {2020-04-02},
	journal = {Cognition and Emotion},
	author = {Pekrun, Reinhard and Vogl, Elisabeth and Muis, Krista R. and Sinatra, Gale M.},
	month = aug,
	year = {2017},
	note = {ZSCC: 0000135},
	pages = {1268--1276},
}

Measurement instruments assessing multiple emotions during epistemic activities are largely lacking. We describe the construction and validation of the EpistemicallyRelated Emotion Scales, which measure surprise, curiosity, enjoyment, confusion, anxiety, frustration, and boredom occurring during epistemic cognitive activities. The instrument was tested in a multinational study of emotions during learning from conflicting texts (N = 438 university students from the United States, Canada, and Germany). The findings document the reliability, internal validity, and external validity of the instrument. A seven-factor model best fit the data, suggesting that epistemically-related emotions should be conceptualised in terms of discrete emotion categories, and the scales showed metric invariance across the North American and German samples. Furthermore, emotion scores changed over time as a function of conflicting task information and related significantly to perceived task value and use of cognitive and metacognitive learning strategies.

@misc{julapalli_tenet_2017,
	title = {Tenet 6 ({Continued}): {Health} 3.0 is {Antifragile} — {Hormesis} in {Health} {Care}},
	shorttitle = {Tenet 6 ({Continued})},
	url = {https://medium.com/@vrjula/tenet-6-5-health-3-0-is-antifragile-hormesis-in-health-care-85b8c9e02d70},
	abstract = {There is nothing more Finnish than a sauna.},
	language = {en},
	urldate = {2021-04-09},
	journal = {Medium},
	author = {Julapalli, Venu},
	month = sep,
	year = {2017},
	note = {ZSCC: NoCitationData[s0]},
}

There is nothing more Finnish than a sauna.

@article{donegan_stem_2017,
	title = {Stem cell derived interneuron transplants as a treatment for schizophrenia: preclinical validation in a rodent model},
	volume = {22},
	issn = {1359-4184},
	shorttitle = {Stem cell derived interneuron transplants as a treatment for schizophrenia},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5290293/},
	doi = {10.1038/mp.2016.121},
	abstract = {An increasing literature suggests that schizophrenia is associated with a reduction in hippocampal interneuron function. Thus, we posit that stem cell-derived interneuron transplants may be an effective therapeutic strategy to reduce hippocampal hyperactivity and attenuate behavioral deficits in schizophrenia. Here we used a dual-reporter embryonic stem cell line to generate enriched populations of parvalbumin (PV)- or somatostatin (SST)-positive interneurons, which were transplanted into the ventral hippocampus of the methylazoxymethanol (MAM) rodent model of schizophrenia. These interneuron transplants integrate within the existing circuitry, reduce hippocampal hyperactivity, and normalize aberrant dopamine neuron activity. Further, interneuron transplants alleviate behaviors that model negative and cognitive symptoms, including deficits in social interaction and cognitive inflexibility. Interestingly, PV- and SST-enriched transplants produced differential effects on behavior, with PV-enriched populations effectively normalizing all the behaviors examined. These data suggest that stem cell-derived interneuron transplants may represent a novel therapeutic strategy for schizophrenia.},
	number = {10},
	urldate = {2021-04-09},
	journal = {Molecular psychiatry},
	author = {Donegan, Jennifer J. and Tyson, Jennifer A. and Branch, Sarah Y. and Beckstead, Michael J. and Anderson, Stewart A. and Lodge, Daniel J.},
	month = oct,
	year = {2017},
	pmid = {27480492},
	pmcid = {PMC5290293},
	note = {ZSCC: 0000032 },
	pages = {1492--1501},
}

An increasing literature suggests that schizophrenia is associated with a reduction in hippocampal interneuron function. Thus, we posit that stem cell-derived interneuron transplants may be an effective therapeutic strategy to reduce hippocampal hyperactivity and attenuate behavioral deficits in schizophrenia. Here we used a dual-reporter embryonic stem cell line to generate enriched populations of parvalbumin (PV)- or somatostatin (SST)-positive interneurons, which were transplanted into the ventral hippocampus of the methylazoxymethanol (MAM) rodent model of schizophrenia. These interneuron transplants integrate within the existing circuitry, reduce hippocampal hyperactivity, and normalize aberrant dopamine neuron activity. Further, interneuron transplants alleviate behaviors that model negative and cognitive symptoms, including deficits in social interaction and cognitive inflexibility. Interestingly, PV- and SST-enriched transplants produced differential effects on behavior, with PV-enriched populations effectively normalizing all the behaviors examined. These data suggest that stem cell-derived interneuron transplants may represent a novel therapeutic strategy for schizophrenia.

@misc{staff_patient-driven_2017,
	title = {Patient-{Driven} {Medical} {Innovations}: {Building} a {Precision} {Medicine} {Supply} {Chain} for {All}},
	shorttitle = {Patient-{Driven} {Medical} {Innovations}},
	url = {https://blog.petrieflom.law.harvard.edu/2017/03/06/patient-driven-medical-innovations-building-a-precision-medicine-supply-chain-for-all/},
	abstract = {Kingshuk K. Sinha, PhD (Department Chair and Mosaic Company-Jim Prokopanko Professor of Corporate Responsibility Supply Chain and Operations Department, Carlson School of Management, University of Minnesota) This post is part of a series on how patients are creating the future of medicine.  The introduction to the series is available here, and all posts in the […]},
	language = {en-US},
	urldate = {2021-03-17},
	journal = {Bill of Health},
	author = {Staff, The Petrie-Flom Center},
	month = mar,
	year = {2017},
	note = {ZSCC: NoCitationData[s0]},
}

Kingshuk K. Sinha, PhD (Department Chair and Mosaic Company-Jim Prokopanko Professor of Corporate Responsibility Supply Chain and Operations Department, Carlson School of Management, University of Minnesota) This post is part of a series on how patients are creating the future of medicine.  The introduction to the series is available here, and all posts in the […]

@article{borsboom_network_2017,
	title = {A network theory of mental disorders},
	volume = {16},
	issn = {2051-5545},
	url = {https://onlinelibrary.wiley.com/doi/abs/10.1002/wps.20375},
	doi = {10.1002/wps.20375},
	abstract = {In recent years, the network approach to psychopathology has been advanced as an alternative way of conceptualizing mental disorders. In this approach, mental disorders arise from direct interactions between symptoms. Although the network approach has led to many novel methodologies and substantive applications, it has not yet been fully articulated as a scientific theory of mental disorders. The present paper aims to develop such a theory, by postulating a limited set of theoretical principles regarding the structure and dynamics of symptom networks. At the heart of the theory lies the notion that symptoms of psychopathology are causally connected through myriads of biological, psychological and societal mechanisms. If these causal relations are sufficiently strong, symptoms can generate a level of feedback that renders them self-sustaining. In this case, the network can get stuck in a disorder state. The network theory holds that this is a general feature of mental disorders, which can therefore be understood as alternative stable states of strongly connected symptom networks. This idea naturally leads to a comprehensive model of psychopathology, encompassing a common explanatory model for mental disorders, as well as novel definitions of associated concepts such as mental health, resilience, vulnerability and liability. In addition, the network theory has direct implications for how to understand diagnosis and treatment, and suggests a clear agenda for future research in psychiatry and associated disciplines.},
	language = {en},
	number = {1},
	urldate = {2020-10-13},
	journal = {World Psychiatry},
	author = {Borsboom, Denny},
	year = {2017},
	note = {ZSCC: 0000706 
\_eprint: https://onlinelibrary.wiley.com/doi/pdf/10.1002/wps.20375},
	keywords = {Psychopathology, diagnosis, mental disorders, mental health, network approach, resilience, symptom networks, treatment, vulnerability},
	pages = {5--13},
}

In recent years, the network approach to psychopathology has been advanced as an alternative way of conceptualizing mental disorders. In this approach, mental disorders arise from direct interactions between symptoms. Although the network approach has led to many novel methodologies and substantive applications, it has not yet been fully articulated as a scientific theory of mental disorders. The present paper aims to develop such a theory, by postulating a limited set of theoretical principles regarding the structure and dynamics of symptom networks. At the heart of the theory lies the notion that symptoms of psychopathology are causally connected through myriads of biological, psychological and societal mechanisms. If these causal relations are sufficiently strong, symptoms can generate a level of feedback that renders them self-sustaining. In this case, the network can get stuck in a disorder state. The network theory holds that this is a general feature of mental disorders, which can therefore be understood as alternative stable states of strongly connected symptom networks. This idea naturally leads to a comprehensive model of psychopathology, encompassing a common explanatory model for mental disorders, as well as novel definitions of associated concepts such as mental health, resilience, vulnerability and liability. In addition, the network theory has direct implications for how to understand diagnosis and treatment, and suggests a clear agenda for future research in psychiatry and associated disciplines.

@article{zhang_transcranial_2017,
	title = {Transcranial {Direct} {Current} {Stimulation} in {Patients} with {Prolonged} {Disorders} of {Consciousness}: {Combined} {Behavioral} and {Event}-{Related} {Potential} {Evidence}},
	volume = {8},
	issn = {1664-2295},
	shorttitle = {Transcranial {Direct} {Current} {Stimulation} in {Patients} with {Prolonged} {Disorders} of {Consciousness}},
	url = {https://www.frontiersin.org/articles/10.3389/fneur.2017.00620/full},
	doi = {10.3389/fneur.2017.00620},
	abstract = {Background: The electrophysiological evidence supporting the therapeutic efficacy of multiple transcranial direct current stimulation (tDCS) sessions on consciousness improvement in patients with prolonged disorders of consciousness (DOCs) has not been firmly established. Objectives: To assess the effects of repeated tDCS in patients with prolonged DOCs by Coma Recovery Scale-Revised (CRS-R) score and event-related potential (ERP). Method: Using a sham-controlled randomized double-blind design, twenty-six patients were randomly assigned to either a real (five vegetative state (VS) and eight minimally conscious state (MCS) patients) or sham (six VS and seven MCS patients) stimulation group. The patients in the real stimulation group underwent 20 anodal tDCS sessions of the left dorsolateral prefrontal cortex (DLPFC) over 10 consecutive working days. The CRS-R score and P300 amplitude and latency in a hierarchical cognitive assessment were recorded to evaluate the consciousness level before tDCS and immediately after the 20 sessions. Results: The intra-group CRS-R analysis revealed a clinically significant improvement in the MCS patients in the real stimulation group. The inter-group CRS-R analysis showed a significant difference in CRS-R between VS and MCS patients at baseline in both the real and sham stimulation groups. The intra-group ERP analysis revealed a significant increase in P300 amplitude after tDCS in the MCS patients in the real stimulation group, but no significant differences in P300 latency. For the inter-group ERP analysis, we observed significant differences regarding the presence of P300 at baseline between the VS and MCS patients in both groups. Conclusion: The repeated anodal tDCS of the left DLPFC could produce clinically significant improvements in MCS patients. The observed tDCS-related consciousness improvements might be related to improvements in attention resource allocation (reflected by the P300 amplitude). The findings support the use of tDCS in clinical practice and ERP might serve as an efficient electrophysiological assessment tool in patients with DOCs.},
	language = {English},
	urldate = {2020-08-18},
	journal = {Frontiers in Neurology},
	author = {Zhang, Ye and Song, Weiqun and Du, Jubao and Huo, Su and Shan, Guixiang and Li, Ran},
	year = {2017},
	note = {ZSCC: 0000017 
Publisher: Frontiers},
	keywords = {Coma Recovery Scale-Revised, Event-related potentials, P300, disorders of consciousness, transcranial direct current stimulation},
}

Background: The electrophysiological evidence supporting the therapeutic efficacy of multiple transcranial direct current stimulation (tDCS) sessions on consciousness improvement in patients with prolonged disorders of consciousness (DOCs) has not been firmly established. Objectives: To assess the effects of repeated tDCS in patients with prolonged DOCs by Coma Recovery Scale-Revised (CRS-R) score and event-related potential (ERP). Method: Using a sham-controlled randomized double-blind design, twenty-six patients were randomly assigned to either a real (five vegetative state (VS) and eight minimally conscious state (MCS) patients) or sham (six VS and seven MCS patients) stimulation group. The patients in the real stimulation group underwent 20 anodal tDCS sessions of the left dorsolateral prefrontal cortex (DLPFC) over 10 consecutive working days. The CRS-R score and P300 amplitude and latency in a hierarchical cognitive assessment were recorded to evaluate the consciousness level before tDCS and immediately after the 20 sessions. Results: The intra-group CRS-R analysis revealed a clinically significant improvement in the MCS patients in the real stimulation group. The inter-group CRS-R analysis showed a significant difference in CRS-R between VS and MCS patients at baseline in both the real and sham stimulation groups. The intra-group ERP analysis revealed a significant increase in P300 amplitude after tDCS in the MCS patients in the real stimulation group, but no significant differences in P300 latency. For the inter-group ERP analysis, we observed significant differences regarding the presence of P300 at baseline between the VS and MCS patients in both groups. Conclusion: The repeated anodal tDCS of the left DLPFC could produce clinically significant improvements in MCS patients. The observed tDCS-related consciousness improvements might be related to improvements in attention resource allocation (reflected by the P300 amplitude). The findings support the use of tDCS in clinical practice and ERP might serve as an efficient electrophysiological assessment tool in patients with DOCs.

@article{giordano_mechanisms_2017,
	title = {Mechanisms and {Effects} of {Transcranial} {Direct} {Current} {Stimulation}},
	volume = {15},
	issn = {1559-3258},
	url = {https://doi.org/10.1177/1559325816685467},
	doi = {10.1177/1559325816685467},
	abstract = {The US Air Force Office of Scientific Research convened a meeting of researchers in the fields of neuroscience, psychology, engineering, and medicine to discuss most pressing issues facing ongoing research in the field of transcranial direct current stimulation (tDCS) and related techniques. In this study, we present opinions prepared by participants of the meeting, focusing on the most promising areas of research, immediate and future goals for the field, and the potential for hormesis theory to inform tDCS research. Scientific, medical, and ethical considerations support the ongoing testing of tDCS in healthy and clinical populations, provided best protocols are used to maximize safety. Notwithstanding the need for ongoing research, promising applications include enhancing vigilance/attention in healthy volunteers, which can accelerate training and support learning. Commonly, tDCS is used as an adjunct to training/rehabilitation tasks with the goal of leftward shift in the learning/treatment effect curves. Although trials are encouraging, elucidating the basic mechanisms of tDCS will accelerate validation and adoption. To this end, biomarkers (eg, clinical neuroimaging and findings from animal models) can support hypotheses linking neurobiological mechanisms and behavioral effects. Dosage can be optimized using computational models of current flow and understanding dose?response. Both biomarkers and dosimetry should guide individualized interventions with the goal of reducing variability. Insights from other applied energy domains, including ionizing radiation, transcranial magnetic stimulation, and low-level laser (light) therapy, can be prudently leveraged.},
	number = {1},
	urldate = {2020-08-11},
	journal = {Dose-Response},
	author = {Giordano, James and Bikson, Marom and Kappenman, Emily S. and Clark, Vincent P. and Coslett, H. Branch and Hamblin, Michael R. and Hamilton, Roy and Jankord, Ryan and Kozumbo, Walter J. and McKinley, R. Andrew and Nitsche, Michael A. and Reilly, J. Patrick and Richardson, Jessica and Wurzman, Rachel and Calabrese, Edward},
	month = mar,
	year = {2017},
	note = {ZSCC: NoCitationData[s0] 
Publisher: SAGE Publications Inc},
	pages = {1559325816685467},
}

The US Air Force Office of Scientific Research convened a meeting of researchers in the fields of neuroscience, psychology, engineering, and medicine to discuss most pressing issues facing ongoing research in the field of transcranial direct current stimulation (tDCS) and related techniques. In this study, we present opinions prepared by participants of the meeting, focusing on the most promising areas of research, immediate and future goals for the field, and the potential for hormesis theory to inform tDCS research. Scientific, medical, and ethical considerations support the ongoing testing of tDCS in healthy and clinical populations, provided best protocols are used to maximize safety. Notwithstanding the need for ongoing research, promising applications include enhancing vigilance/attention in healthy volunteers, which can accelerate training and support learning. Commonly, tDCS is used as an adjunct to training/rehabilitation tasks with the goal of leftward shift in the learning/treatment effect curves. Although trials are encouraging, elucidating the basic mechanisms of tDCS will accelerate validation and adoption. To this end, biomarkers (eg, clinical neuroimaging and findings from animal models) can support hypotheses linking neurobiological mechanisms and behavioral effects. Dosage can be optimized using computational models of current flow and understanding dose?response. Both biomarkers and dosimetry should guide individualized interventions with the goal of reducing variability. Insights from other applied energy domains, including ionizing radiation, transcranial magnetic stimulation, and low-level laser (light) therapy, can be prudently leveraged.

@article{clark_three_2017,
	title = {Three {Approaches} to {Understanding} and {Classifying} {Mental} {Disorder}: {ICD}-11, {DSM}-5, and the {National} {Institute} of {Mental} {Health}’s {Research} {Domain} {Criteria} ({RDoC})},
	volume = {18},
	issn = {1529-1006},
	shorttitle = {Three {Approaches} to {Understanding} and {Classifying} {Mental} {Disorder}},
	url = {https://doi.org/10.1177/1529100617727266},
	doi = {10.1177/1529100617727266},
	abstract = {The diagnosis of mental disorder initially appears relatively straightforward: Patients present with symptoms or visible signs of illness; health professionals make diagnoses based primarily on these symptoms and signs; and they prescribe medication, psychotherapy, or both, accordingly. However, despite a dramatic expansion of knowledge about mental disorders during the past half century, understanding of their components and processes remains rudimentary. We provide histories and descriptions of three systems with different purposes relevant to understanding and classifying mental disorder. Two major diagnostic manuals?the International Classification of Diseases and the Diagnostic and Statistical Manual of Mental Disorders?provide classification systems relevant to public health, clinical diagnosis, service provision, and specific research applications, the former internationally and the latter primarily for the United States. In contrast, the National Institute of Mental Health?s Research Domain Criteria provides a framework that emphasizes integration of basic behavioral and neuroscience research to deepen the understanding of mental disorder. We identify four key issues that present challenges to understanding and classifying mental disorder: etiology, including the multiple causality of mental disorder; whether the relevant phenomena are discrete categories or dimensions; thresholds, which set the boundaries between disorder and nondisorder; and comorbidity, the fact that individuals with mental illness often meet diagnostic requirements for multiple conditions. We discuss how the three systems? approaches to these key issues correspond or diverge as a result of their different histories, purposes, and constituencies. Although the systems have varying degrees of overlap and distinguishing features, they share the goal of reducing the burden of suffering due to mental disorder.},
	number = {2},
	urldate = {2020-07-16},
	journal = {Psychological Science in the Public Interest},
	author = {Clark, Lee Anna and Cuthbert, Bruce and Lewis-Fernández, Roberto and Narrow, William E. and Reed, Geoffrey M.},
	month = nov,
	year = {2017},
	note = {ZSCC: NoCitationData[s0] 
Publisher: SAGE Publications Inc},
	pages = {72--145},
}

The diagnosis of mental disorder initially appears relatively straightforward: Patients present with symptoms or visible signs of illness; health professionals make diagnoses based primarily on these symptoms and signs; and they prescribe medication, psychotherapy, or both, accordingly. However, despite a dramatic expansion of knowledge about mental disorders during the past half century, understanding of their components and processes remains rudimentary. We provide histories and descriptions of three systems with different purposes relevant to understanding and classifying mental disorder. Two major diagnostic manuals?the International Classification of Diseases and the Diagnostic and Statistical Manual of Mental Disorders?provide classification systems relevant to public health, clinical diagnosis, service provision, and specific research applications, the former internationally and the latter primarily for the United States. In contrast, the National Institute of Mental Health?s Research Domain Criteria provides a framework that emphasizes integration of basic behavioral and neuroscience research to deepen the understanding of mental disorder. We identify four key issues that present challenges to understanding and classifying mental disorder: etiology, including the multiple causality of mental disorder; whether the relevant phenomena are discrete categories or dimensions; thresholds, which set the boundaries between disorder and nondisorder; and comorbidity, the fact that individuals with mental illness often meet diagnostic requirements for multiple conditions. We discuss how the three systems? approaches to these key issues correspond or diverge as a result of their different histories, purposes, and constituencies. Although the systems have varying degrees of overlap and distinguishing features, they share the goal of reducing the burden of suffering due to mental disorder.

@article{wildschut_need_2017,
	series = {Post-{Normal} science in practice},
	title = {The need for citizen science in the transition to a sustainable peer-to-peer-society},
	volume = {91},
	issn = {0016-3287},
	url = {http://www.sciencedirect.com/science/article/pii/S0016328717300435},
	doi = {10.1016/j.futures.2016.11.010},
	abstract = {Society is changing towards a peer-to-peer society that is characterised by a new way to produce things, ranging from software to food, to cities, to scientific knowledge. This requires a new role for science. Instead of focusing on knowledge production for NGO's, governments and business, scientists should become aware that the citizen will be the new decision-maker in a future peer-to-peer (p2p) society, and produce suitable and accessible knowledge, and work together with citizen scientists.},
	language = {en},
	urldate = {2020-06-05},
	journal = {Futures},
	author = {Wildschut, Diana},
	month = aug,
	year = {2017},
	note = {ZSCC: 0000031},
	pages = {46--52},
}

Society is changing towards a peer-to-peer society that is characterised by a new way to produce things, ranging from software to food, to cities, to scientific knowledge. This requires a new role for science. Instead of focusing on knowledge production for NGO's, governments and business, scientists should become aware that the citizen will be the new decision-maker in a future peer-to-peer (p2p) society, and produce suitable and accessible knowledge, and work together with citizen scientists.

@article{ciovacco_sanity_2017,
	title = {Sanity of {Addiction}: {Contemplative} and {Humanistic} {Reflections} on the \textit{{Surgeon} {General}’s {Report} on {Drugs}}},
	issn = {0022-1678, 1552-650X},
	shorttitle = {Sanity of {Addiction}},
	url = {http://journals.sagepub.com/doi/10.1177/0022167817740464},
	doi = {10.1177/0022167817740464},
	language = {en},
	urldate = {2020-03-19},
	journal = {Journal of Humanistic Psychology},
	author = {Ciovacco, Lauren A. and Hughes, Shannon},
	month = nov,
	year = {2017},
	keywords = {Eastern philosophy, addictions counseling, contemplative, humanistic, neurobiology of addiction},
	pages = {002216781774046},
}

@article{wildschut_need_2017-1,
	series = {Post-{Normal} science in practice},
	title = {The need for citizen science in the transition to a sustainable peer-to-peer-society},
	volume = {91},
	issn = {0016-3287},
	url = {http://www.sciencedirect.com/science/article/pii/S0016328717300435},
	doi = {10.1016/j.futures.2016.11.010},
	abstract = {Society is changing towards a peer-to-peer society that is characterised by a new way to produce things, ranging from software to food, to cities, to scientific knowledge. This requires a new role for science. Instead of focusing on knowledge production for NGO's, governments and business, scientists should become aware that the citizen will be the new decision-maker in a future peer-to-peer (p2p) society, and produce suitable and accessible knowledge, and work together with citizen scientists.},
	language = {en},
	urldate = {2020-06-05},
	journal = {Futures},
	author = {Wildschut, Diana},
	month = aug,
	year = {2017},
	note = {ZSCC: 0000031},
	pages = {46--52},
}

Society is changing towards a peer-to-peer society that is characterised by a new way to produce things, ranging from software to food, to cities, to scientific knowledge. This requires a new role for science. Instead of focusing on knowledge production for NGO's, governments and business, scientists should become aware that the citizen will be the new decision-maker in a future peer-to-peer (p2p) society, and produce suitable and accessible knowledge, and work together with citizen scientists.

@article{macduffie_understanding_2017,
	title = {Understanding {Our} {Own} {Biology}: {The} {Relevance} of {Auto}-{Biological} {Attributions} for {Mental} {Health}},
	volume = {24},
	issn = {09695893},
	shorttitle = {Understanding {Our} {Own} {Biology}},
	url = {http://doi.wiley.com/10.1111/cpsp.12188},
	doi = {10.1111/cpsp.12188},
	abstract = {As knowledge of the neurobiological basis of psychopathology has advanced, public perceptions have shifted toward conceptualizing mental disorders as disorders of biology. However, little is known about how patients respond to biological information about their own disorders. We refer to such information as autobiological—describing our own biological systems as a component of our identity. Drawing on research from attribution theory, we explore the potential for autobiological information to shape how patients view themselves in relation to their disorders. We propose an attributional framework for presenting auto-biological information in a way that encourages agency, rather than destiny. We argue that this framework has the potential to change expectations and improve outcomes in the treatment of psychiatric disorders.},
	language = {en},
	number = {1},
	urldate = {2020-03-13},
	journal = {Clinical Psychology: Science and Practice},
	author = {MacDuffie, Katherine E. and Strauman, Timothy J.},
	month = mar,
	year = {2017},
	keywords = {Illness Attribution/Appraisal, attributions, beliefs, biology, depression, intervention, psychopathology},
	pages = {50--68},
}

As knowledge of the neurobiological basis of psychopathology has advanced, public perceptions have shifted toward conceptualizing mental disorders as disorders of biology. However, little is known about how patients respond to biological information about their own disorders. We refer to such information as autobiological—describing our own biological systems as a component of our identity. Drawing on research from attribution theory, we explore the potential for autobiological information to shape how patients view themselves in relation to their disorders. We propose an attributional framework for presenting auto-biological information in a way that encourages agency, rather than destiny. We argue that this framework has the potential to change expectations and improve outcomes in the treatment of psychiatric disorders.

@article{kendall-taylor_reframing_2017,
	title = {Reframing {Biology}: {The} {Power} of {Explanation} in {Improving} {Individual} and {Social} {Outcomes}},
	volume = {24},
	issn = {09695893},
	shorttitle = {Reframing {Biology}},
	url = {http://doi.wiley.com/10.1111/cpsp.12187},
	doi = {10.1111/cpsp.12187},
	language = {en},
	number = {1},
	urldate = {2020-03-13},
	journal = {Clinical Psychology: Science and Practice},
	author = {Kendall-Taylor, Nathaniel},
	month = mar,
	year = {2017},
	keywords = {Illness Attribution/Appraisal, culture and communication},
	pages = {69--73},
}

@article{peters_clinical_2017,
	title = {Clinical relevance of appraisals of persistent psychotic experiences in people with and without a need for care: an experimental study},
	volume = {4},
	issn = {22150366},
	shorttitle = {Clinical relevance of appraisals of persistent psychotic experiences in people with and without a need for care},
	url = {https://linkinghub.elsevier.com/retrieve/pii/S2215036617304091},
	doi = {10.1016/S2215-0366(17)30409-1},
	abstract = {Background Cognitive models of psychosis propose that appraisals (ie, the interpretation and meaning attributed to experiences) are central to the transition from anomalous experiences to psychotic symptoms. In the Unusual Experiences Enquiry (UNIQUE) study, we investigated the role of appraisals by comparing individuals with persistent psychotic experiences without a need for care with patients and people without psychotic experiences.},
	language = {en},
	number = {12},
	urldate = {2020-04-02},
	journal = {The Lancet Psychiatry},
	author = {Peters, Emmanuelle and Ward, Thomas and Jackson, Mike and Woodruff, Peter and Morgan, Craig and McGuire, Philip and Garety, Philippa A},
	month = dec,
	year = {2017},
	note = {ZSCC: 0000017},
	keywords = {Illness Attribution/Appraisal},
	pages = {927--936},
}

Background Cognitive models of psychosis propose that appraisals (ie, the interpretation and meaning attributed to experiences) are central to the transition from anomalous experiences to psychotic symptoms. In the Unusual Experiences Enquiry (UNIQUE) study, we investigated the role of appraisals by comparing individuals with persistent psychotic experiences without a need for care with patients and people without psychotic experiences.

@article{zhao_anti-aging_2017,
	title = {Anti-aging pharmacology in cutaneous wound healing: effects of metformin, resveratrol, and rapamycin by local application},
	volume = {16},
	issn = {1474-9726},
	shorttitle = {Anti-aging pharmacology in cutaneous wound healing},
	url = {https://onlinelibrary.wiley.com/doi/abs/10.1111/acel.12635},
	doi = {10.1111/acel.12635},
	abstract = {Cutaneous wounds are among the most common soft tissue injuries and are particularly hard to heal in aging. Caloric restriction (CR) is well documented to extend longevity; pharmacologically, profound rejuvenative effects of CR mimetics have been uncovered, especially metformin (MET), resveratrol (RSV), and rapamycin (RAPA). However, locally applied impacts and functional differences of these agents on wound healing remain to be established. Here, we discovered that chronic topical administration of MET and RSV, but not RAPA, accelerated wound healing with improved epidermis, hair follicles, and collagen deposition in young rodents, and MET exerted more profound effects. Furthermore, locally applied MET and RSV improved vascularization of the wound beds, which were attributed to stimulation of adenosine monophosphate-activated protein kinase (AMPK) pathway, the key mediator of wound healing. Notably, in aged skin, AMPK pathway was inhibited, correlated with impaired vasculature and reduced healing ability. As therapeutic approaches, local treatments of MET and RSV prevented age-related AMPK suppression and angiogenic inhibition in wound beds. Moreover, in aged rats, rejuvenative effects of topically applied MET and RSV on cell viability of wound beds were confirmed, of which MET showed more prominent anti-aging effects. We further verified that only MET promoted wound healing and cutaneous integrity in aged skin. These findings clarified differential effects of CR-based anti-aging pharmacology in wound healing, identified critical angiogenic and rejuvenative mechanisms through AMPK pathway in both young and aged skin, and unraveled chronic local application of MET as the optimal and promising regenerative agent in treating cutaneous wound defects.},
	language = {en},
	number = {5},
	urldate = {2020-05-22},
	journal = {Aging Cell},
	author = {Zhao, Pan and Sui, Bing-Dong and Liu, Nu and Lv, Ya-Jie and Zheng, Chen-Xi and Lu, Yong-Bo and Huang, Wen-Tao and Zhou, Cui-Hong and Chen, Ji and Pang, Dan-Lin and Fei, Dong-Dong and Xuan, Kun and Hu, Cheng-Hu and Jin, Yan},
	year = {2017},
	note = {\_eprint: https://onlinelibrary.wiley.com/doi/pdf/10.1111/acel.12635},
	keywords = {AMPK pathway, anti-aging pharmacology, metformin, vascularization, wound healing},
	pages = {1083--1093},
}

Cutaneous wounds are among the most common soft tissue injuries and are particularly hard to heal in aging. Caloric restriction (CR) is well documented to extend longevity; pharmacologically, profound rejuvenative effects of CR mimetics have been uncovered, especially metformin (MET), resveratrol (RSV), and rapamycin (RAPA). However, locally applied impacts and functional differences of these agents on wound healing remain to be established. Here, we discovered that chronic topical administration of MET and RSV, but not RAPA, accelerated wound healing with improved epidermis, hair follicles, and collagen deposition in young rodents, and MET exerted more profound effects. Furthermore, locally applied MET and RSV improved vascularization of the wound beds, which were attributed to stimulation of adenosine monophosphate-activated protein kinase (AMPK) pathway, the key mediator of wound healing. Notably, in aged skin, AMPK pathway was inhibited, correlated with impaired vasculature and reduced healing ability. As therapeutic approaches, local treatments of MET and RSV prevented age-related AMPK suppression and angiogenic inhibition in wound beds. Moreover, in aged rats, rejuvenative effects of topically applied MET and RSV on cell viability of wound beds were confirmed, of which MET showed more prominent anti-aging effects. We further verified that only MET promoted wound healing and cutaneous integrity in aged skin. These findings clarified differential effects of CR-based anti-aging pharmacology in wound healing, identified critical angiogenic and rejuvenative mechanisms through AMPK pathway in both young and aged skin, and unraveled chronic local application of MET as the optimal and promising regenerative agent in treating cutaneous wound defects.

@article{goulart_psychiatrization_2017,
	title = {The psychiatrization of human practices worldwide: discussing new chains and cages},
	volume = {25},
	issn = {1468-1366, 1747-5104},
	shorttitle = {The psychiatrization of human practices worldwide},
	url = {https://www.tandfonline.com/doi/full/10.1080/14681366.2016.1160673},
	doi = {10.1080/14681366.2016.1160673},
	language = {en},
	number = {1},
	urldate = {2020-04-02},
	journal = {Pedagogy, Culture \& Society},
	author = {Goulart, Daniel Magalhães},
	month = jan,
	year = {2017},
	note = {ZSCC: 0000010},
	pages = {151--156},
}

@article{pekrun_measuring_2017,
	title = {Measuring emotions during epistemic activities: the {Epistemically}-{Related} {Emotion} {Scales}},
	volume = {31},
	issn = {0269-9931, 1464-0600},
	shorttitle = {Measuring emotions during epistemic activities},
	url = {https://www.tandfonline.com/doi/full/10.1080/02699931.2016.1204989},
	doi = {10.1080/02699931.2016.1204989},
	abstract = {Measurement instruments assessing multiple emotions during epistemic activities are largely lacking. We describe the construction and validation of the EpistemicallyRelated Emotion Scales, which measure surprise, curiosity, enjoyment, confusion, anxiety, frustration, and boredom occurring during epistemic cognitive activities. The instrument was tested in a multinational study of emotions during learning from conflicting texts (N = 438 university students from the United States, Canada, and Germany). The findings document the reliability, internal validity, and external validity of the instrument. A seven-factor model best fit the data, suggesting that epistemically-related emotions should be conceptualised in terms of discrete emotion categories, and the scales showed metric invariance across the North American and German samples. Furthermore, emotion scores changed over time as a function of conflicting task information and related significantly to perceived task value and use of cognitive and metacognitive learning strategies.},
	language = {en},
	number = {6},
	urldate = {2020-04-02},
	journal = {Cognition and Emotion},
	author = {Pekrun, Reinhard and Vogl, Elisabeth and Muis, Krista R. and Sinatra, Gale M.},
	month = aug,
	year = {2017},
	note = {ZSCC: 0000077},
	pages = {1268--1276},
}

Measurement instruments assessing multiple emotions during epistemic activities are largely lacking. We describe the construction and validation of the EpistemicallyRelated Emotion Scales, which measure surprise, curiosity, enjoyment, confusion, anxiety, frustration, and boredom occurring during epistemic cognitive activities. The instrument was tested in a multinational study of emotions during learning from conflicting texts (N = 438 university students from the United States, Canada, and Germany). The findings document the reliability, internal validity, and external validity of the instrument. A seven-factor model best fit the data, suggesting that epistemically-related emotions should be conceptualised in terms of discrete emotion categories, and the scales showed metric invariance across the North American and German samples. Furthermore, emotion scores changed over time as a function of conflicting task information and related significantly to perceived task value and use of cognitive and metacognitive learning strategies.

@article{haskins_relational-cultural_2017,
	title = {Relational-{Cultural} {Theory} and {Reality} {Therapy}: {A} {Culturally} {Responsive} {Integrative} {Framework}},
	volume = {95},
	issn = {07489633},
	shorttitle = {Relational-{Cultural} {Theory} and {Reality} {Therapy}},
	url = {http://doi.wiley.com/10.1002/jcad.12120},
	doi = {10.1002/jcad.12120},
	abstract = {The authors propose an integration of relational-cultural theory and reality therapy. The authors contend that the traditional assumptions of reality therapy are consistent with the relational aspects of relational-cultural theory and together provide a culturally responsive approach for diverse clients. The authors also include an overview of the 2 theories as well as highlight the convergences and divergences. In addition, the authors present a case illustration depicting the integration method in practice.},
	language = {en},
	number = {1},
	urldate = {2020-04-02},
	journal = {Journal of Counseling \& Development},
	author = {Haskins, Natoya Hill and Appling, Brandee},
	month = jan,
	year = {2017},
	note = {ZSCC: 0000017},
	pages = {87--99},
}

The authors propose an integration of relational-cultural theory and reality therapy. The authors contend that the traditional assumptions of reality therapy are consistent with the relational aspects of relational-cultural theory and together provide a culturally responsive approach for diverse clients. The authors also include an overview of the 2 theories as well as highlight the convergences and divergences. In addition, the authors present a case illustration depicting the integration method in practice.

@article{watson_teaching_2017,
	title = {Teaching {Not}-{Knowing}: {Strategies} for {Cultural} {Competence} in {Psychotherapy} {Supervision}},
	volume = {41},
	issn = {1042-9670, 1545-7230},
	shorttitle = {Teaching {Not}-{Knowing}},
	url = {http://link.springer.com/10.1007/s40596-016-0552-9},
	doi = {10.1007/s40596-016-0552-9},
	language = {en},
	number = {1},
	urldate = {2020-04-02},
	journal = {Academic Psychiatry},
	author = {Watson, Priya and Raju, Priya and Soklaridis, Sophie},
	month = feb,
	year = {2017},
	note = {ZSCC: 0000010},
	pages = {55--61},
}

@article{stone_cultivating_2017,
	title = {Cultivating {Humility} and {Diagnostic} {Openness} in {Clinical} {Judgment}},
	volume = {19},
	issn = {2376-6980},
	url = {https://journalofethics.ama-assn.org/article/cultivating-humility-and-diagnostic-openness-clinical-judgment/2017-10},
	doi = {10.1001/journalofethics.2017.19.10.ecas1-1710.},
	abstract = {In this case},
	number = {10},
	urldate = {2020-03-20},
	journal = {AMA Journal of Ethics},
	author = {Stone, John R.},
	month = oct,
	year = {2017},
	note = {Publisher: American Medical Association},
	pages = {970--977},
}

In this case

@inproceedings{meissner_-it-yourself_2017,
	address = {Edinburgh, United Kingdom},
	title = {Do-{It}-{Yourself} {Empowerment} as {Experienced} by {Novice} {Makers} with {Disabilities}},
	isbn = {978-1-4503-4922-2},
	url = {http://dl.acm.org/citation.cfm?doid=3064663.3064674},
	doi = {10.1145/3064663.3064674},
	abstract = {Recent HCI research has highlighted the potential afforded by maker technologies for supporting new forms of DIY Assistive Technology (DIY-AT) for people with disabilities. Furthermore, the popular discourse surrounding both the maker movement and disability is one of democratisation and empowerment. Despite this, critics argue that maker movement membership lacks diversity and that within DIY-AT, it is seldom the people with disabilities who are creating such designs. We conducted a qualitative study that explored how people with disabilities experience the empowering potential of making. We analysed online videos by makers with disabilities and conducted fieldwork at two makerspaces. These informed the design of DIY-Abilities, a series of workshops for people with disabilities in which participants could learn different maker technologies and complete their own maker project. Through analysis of participants’ narratives we contribute a new perspective on the specific social and material capacities of accessible maker initiatives.},
	language = {en},
	urldate = {2020-03-19},
	booktitle = {Proceedings of the 2017 {Conference} on {Designing} {Interactive} {Systems} - {DIS} '17},
	publisher = {ACM Press},
	author = {Meissner, Janis Lena and Vines, John and McLaughlin, Janice and Nappey, Thomas and Maksimova, Jekaterina and Wright, Peter},
	year = {2017},
	pages = {1053--1065},
}

Recent HCI research has highlighted the potential afforded by maker technologies for supporting new forms of DIY Assistive Technology (DIY-AT) for people with disabilities. Furthermore, the popular discourse surrounding both the maker movement and disability is one of democratisation and empowerment. Despite this, critics argue that maker movement membership lacks diversity and that within DIY-AT, it is seldom the people with disabilities who are creating such designs. We conducted a qualitative study that explored how people with disabilities experience the empowering potential of making. We analysed online videos by makers with disabilities and conducted fieldwork at two makerspaces. These informed the design of DIY-Abilities, a series of workshops for people with disabilities in which participants could learn different maker technologies and complete their own maker project. Through analysis of participants’ narratives we contribute a new perspective on the specific social and material capacities of accessible maker initiatives.

@article{macaulay_conceptualizing_2017,
	title = {Conceptualizing the health and well-being impacts of social enterprise: a {UK}-based study},
	issn = {0957-4824, 1460-2245},
	shorttitle = {Conceptualizing the health and well-being impacts of social enterprise},
	url = {https://academic.oup.com/heapro/article-lookup/doi/10.1093/heapro/dax009},
	doi = {10.1093/heapro/dax009},
	abstract = {Social enterprises–businesses that work for social benefit rather than for the maximization of financial returns to shareholders or owners–could potentially prove to be an innovative and sustainable way of tackling ‘upstream’ social determinants of health. However, empirical work focusing upon how, and to what extent, social enterprise-led activity may impact upon health and well-being is still relatively scarce. This study examines how social enterprises portray their impact, and how such impacts may be considered in health and well-being terms. Through analysing evaluative reports of the work of social enterprises in Scotland (n ¼ 17) utilizing a ‘process coding’ method, we investigate both the selfreported impacts of the work of social enterprises and the mechanisms by which these are said to be derived. Revisiting previous conceptualizations in the extant literature, this work allows us to present an ‘empirically-informed’ conceptual model of the health and well-being impacts of social enterpriseled activity, and thus presents a significant advance on previous hypothetical, theoretically-based conceptualizations. It is considered that these findings further improve our overall knowledge of ways in which social enterprise and other parts of the third sector could be considered as potentially valuable ‘non-obvious’ public health actors.},
	language = {en},
	urldate = {2020-03-19},
	journal = {Health Promotion International},
	author = {Macaulay, Bobby and Roy, Michael J. and Donaldson, Cam and Teasdale, Simon and Kay, Alan},
	month = mar,
	year = {2017},
}

Social enterprises–businesses that work for social benefit rather than for the maximization of financial returns to shareholders or owners–could potentially prove to be an innovative and sustainable way of tackling ‘upstream’ social determinants of health. However, empirical work focusing upon how, and to what extent, social enterprise-led activity may impact upon health and well-being is still relatively scarce. This study examines how social enterprises portray their impact, and how such impacts may be considered in health and well-being terms. Through analysing evaluative reports of the work of social enterprises in Scotland (n ¼ 17) utilizing a ‘process coding’ method, we investigate both the selfreported impacts of the work of social enterprises and the mechanisms by which these are said to be derived. Revisiting previous conceptualizations in the extant literature, this work allows us to present an ‘empirically-informed’ conceptual model of the health and well-being impacts of social enterpriseled activity, and thus presents a significant advance on previous hypothetical, theoretically-based conceptualizations. It is considered that these findings further improve our overall knowledge of ways in which social enterprise and other parts of the third sector could be considered as potentially valuable ‘non-obvious’ public health actors.

@article{gomory_solving_2017,
	title = {The {Solving} {Problems} in {Everyday} {Living} {Model}: {Toward} a {Demedicalized}, {Education}-{Based} {Approach} to “{Mental} {Health}”},
	issn = {0022-1678, 1552-650X},
	shorttitle = {The {Solving} {Problems} in {Everyday} {Living} {Model}},
	url = {http://journals.sagepub.com/doi/10.1177/0022167817722430},
	doi = {10.1177/0022167817722430},
	abstract = {We argue that human existential pain and threat may usefully be helped by a noncoercive educational approach that also resonates with many interpersonally focused psychological approaches, rather than by the widely touted current medical model of “mental health” treatment (using psychoactive drugs and supportive psychotherapy). First, the “progress” leading to the latest Diagnostic and Statistical Manual of Mental Disorders is briefly reviewed, highlighting the scientific limitations of the medical model. Next, an educational model of self-understanding and change, based on Popper’s fallibilism, Freire’s critical pedagogy, and Miller’s feedback-informed treatment is explicated. Finally, some options for funding and testing the model are discussed. We hope this offers mental health clinicians another important alternative to conceptualize the helping encounter to ameliorate personal problems in living.},
	language = {en},
	urldate = {2020-03-18},
	journal = {Journal of Humanistic Psychology},
	author = {Gomory, Tomi and Dunleavy, Daniel J. and Lieber, Angela S.},
	month = jul,
	year = {2017},
	pages = {002216781772243},
}

We argue that human existential pain and threat may usefully be helped by a noncoercive educational approach that also resonates with many interpersonally focused psychological approaches, rather than by the widely touted current medical model of “mental health” treatment (using psychoactive drugs and supportive psychotherapy). First, the “progress” leading to the latest Diagnostic and Statistical Manual of Mental Disorders is briefly reviewed, highlighting the scientific limitations of the medical model. Next, an educational model of self-understanding and change, based on Popper’s fallibilism, Freire’s critical pedagogy, and Miller’s feedback-informed treatment is explicated. Finally, some options for funding and testing the model are discussed. We hope this offers mental health clinicians another important alternative to conceptualize the helping encounter to ameliorate personal problems in living.

@article{davis_development_2017,
	title = {Development of the {Experiences} of {Humility} {Scale}},
	volume = {45},
	issn = {0091-6471, 2328-1162},
	url = {http://journals.sagepub.com/doi/10.1177/009164711704500101},
	doi = {10.1177/009164711704500101},
	language = {en},
	number = {1},
	urldate = {2020-03-13},
	journal = {Journal of Psychology and Theology},
	author = {Davis, Don E. and McElroy, Stacey and Choe, Elise and Westbrook, Charles J. and DeBlaere, Cirleen and Van Tongeren, Daryl R. and Hook, Joshua and Sandage, Steven J. and Placeres, Vanessa},
	month = mar,
	year = {2017},
	pages = {3--16},
}

@article{alfano_development_2017,
	title = {Development and validation of a multi-dimensional measure of intellectual humility},
	volume = {12},
	issn = {1932-6203},
	url = {https://dx.plos.org/10.1371/journal.pone.0182950},
	doi = {10.1371/journal.pone.0182950},
	language = {en},
	number = {8},
	urldate = {2020-03-13},
	journal = {PLOS ONE},
	author = {Alfano, Mark and Iurino, Kathryn and Stey, Paul and Robinson, Brian and Christen, Markus and Yu, Feng and Lapsley, Daniel},
	editor = {Tractenberg, Rochelle E.},
	month = aug,
	year = {2017},
	pages = {e0182950},
}

@article{leary_cognitive_2017,
	title = {Cognitive and {Interpersonal} {Features} of {Intellectual} {Humility}},
	volume = {43},
	issn = {0146-1672, 1552-7433},
	url = {http://journals.sagepub.com/doi/10.1177/0146167217697695},
	doi = {10.1177/0146167217697695},
	abstract = {Four studies examined intellectual humility—the degree to which people recognize that their beliefs might be wrong. Using a new Intellectual Humility (IH) Scale, Study 1 showed that intellectual humility was associated with variables related to openness, curiosity, tolerance of ambiguity, and low dogmatism. Study 2 revealed that participants high in intellectual humility were less certain that their beliefs about religion were correct and judged people less on the basis of their religious opinions. In Study 3, participants high in intellectual humility were less inclined to think that politicians who changed their attitudes were “flip-flopping,” and Study 4 showed that people high in intellectual humility were more attuned to the strength of persuasive arguments than those who were low. In addition to extending our understanding of intellectual humility, this research demonstrates that the IH Scale is a valid measure of the degree to which people recognize that their beliefs are fallible.},
	language = {en},
	number = {6},
	urldate = {2020-03-13},
	journal = {Personality and Social Psychology Bulletin},
	author = {Leary, Mark R. and Diebels, Kate J. and Davisson, Erin K. and Jongman-Sereno, Katrina P. and Isherwood, Jennifer C. and Raimi, Kaitlin T. and Deffler, Samantha A. and Hoyle, Rick H.},
	month = jun,
	year = {2017},
	pages = {793--813},
}

Four studies examined intellectual humility—the degree to which people recognize that their beliefs might be wrong. Using a new Intellectual Humility (IH) Scale, Study 1 showed that intellectual humility was associated with variables related to openness, curiosity, tolerance of ambiguity, and low dogmatism. Study 2 revealed that participants high in intellectual humility were less certain that their beliefs about religion were correct and judged people less on the basis of their religious opinions. In Study 3, participants high in intellectual humility were less inclined to think that politicians who changed their attitudes were “flip-flopping,” and Study 4 showed that people high in intellectual humility were more attuned to the strength of persuasive arguments than those who were low. In addition to extending our understanding of intellectual humility, this research demonstrates that the IH Scale is a valid measure of the degree to which people recognize that their beliefs are fallible.

@article{leal-soto_three-factor_2017,
	title = {Three-factor structure for {Epistemic} {Belief} {Inventory}: {A} cross-validation study},
	volume = {12},
	issn = {1932-6203},
	shorttitle = {Three-factor structure for {Epistemic} {Belief} {Inventory}},
	url = {https://dx.plos.org/10.1371/journal.pone.0173295},
	doi = {10.1371/journal.pone.0173295},
	abstract = {Research on epistemic beliefs has been hampered by lack of validated models and measurement instruments. The most widely used instrument is the Epistemological Questionnaire, which has been criticized for validity, and it has been proposed a new instrument based in the Epistemological Questionnaire: the Epistemic Belief Inventory. The Spanishlanguage version of Epistemic Belief Inventory was applied to 1,785 Chilean high school students. Exploratory and confirmatory factor analyses in independent subsamples were performed. A three factor structure emerged and was confirmed. Reliability was comparable to other studies, and the factor structure was invariant among randomized subsamples. The structure that was found does not replicate the one proposed originally, but results are interpreted in light of embedded systemic model of epistemological beliefs.},
	language = {en},
	number = {3},
	urldate = {2020-03-12},
	journal = {PLOS ONE},
	author = {Leal-Soto, Francisco and Ferrer-Urbina, Rodrigo},
	editor = {Lozano, Sergi},
	month = mar,
	year = {2017},
	pages = {e0173295},
}

Research on epistemic beliefs has been hampered by lack of validated models and measurement instruments. The most widely used instrument is the Epistemological Questionnaire, which has been criticized for validity, and it has been proposed a new instrument based in the Epistemological Questionnaire: the Epistemic Belief Inventory. The Spanishlanguage version of Epistemic Belief Inventory was applied to 1,785 Chilean high school students. Exploratory and confirmatory factor analyses in independent subsamples were performed. A three factor structure emerged and was confirmed. Reliability was comparable to other studies, and the factor structure was invariant among randomized subsamples. The structure that was found does not replicate the one proposed originally, but results are interpreted in light of embedded systemic model of epistemological beliefs.

@article{wise_embracing_2017,
	title = {Embracing {Not}-{Knowing}: {Toward} {Narration} and {Humanism} in {Medicine}},
	volume = {80},
	issn = {0033-2747, 1943-281X},
	shorttitle = {Embracing {Not}-{Knowing}},
	url = {https://www.tandfonline.com/doi/full/10.1080/00332747.2017.1397459},
	doi = {10.1080/00332747.2017.1397459},
	language = {en},
	number = {4},
	urldate = {2020-03-12},
	journal = {Psychiatry},
	author = {Wise, Joseph E.},
	month = oct,
	year = {2017},
	pages = {331--334},
}

@article{strauss_uncertainty_2017,
	title = {Uncertainty {Theory}: {A} {Powerful} {Approach} to {Understanding} {Psychiatric} {Disorder}},
	volume = {80},
	issn = {0033-2747, 1943-281X},
	shorttitle = {Uncertainty {Theory}},
	url = {https://www.tandfonline.com/doi/full/10.1080/00332747.2016.1247623},
	doi = {10.1080/00332747.2016.1247623},
	language = {en},
	number = {4},
	urldate = {2020-03-12},
	journal = {Psychiatry},
	author = {Strauss, John S.},
	month = oct,
	year = {2017},
	pages = {301--308},
}

@article{estes_maternal_2016,
	title = {Maternal immune activation: {Implications} for neuropsychiatric disorders},
	volume = {353},
	issn = {0036-8075, 1095-9203},
	shorttitle = {Maternal immune activation},
	url = {https://www.science.org/doi/10.1126/science.aag3194},
	doi = {10.1126/science.aag3194},
	abstract = {Epidemiological evidence implicates maternal infection as a risk factor for autism spectrum disorder and schizophrenia. Animal models corroborate this link and demonstrate that maternal immune activation (MIA) alone is sufficient to impart lifelong neuropathology and altered behaviors in offspring. This Review describes common principles revealed by these models, highlighting recent findings that strengthen their relevance for schizophrenia and autism and are starting to reveal the molecular mechanisms underlying the effects of MIA on offspring. The role of MIA as a primer for a much wider range of psychiatric and neurologic disorders is also discussed. Finally, the need for more research in this nascent field and the implications for identifying and developing new treatments for individuals at heightened risk for neuroimmune disorders are considered.},
	language = {en},
	number = {6301},
	urldate = {2022-05-29},
	journal = {Science},
	author = {Estes, Myka L. and McAllister, A. Kimberley},
	month = aug,
	year = {2016},
	note = {Number: 6301},
	pages = {772--777},
}

Epidemiological evidence implicates maternal infection as a risk factor for autism spectrum disorder and schizophrenia. Animal models corroborate this link and demonstrate that maternal immune activation (MIA) alone is sufficient to impart lifelong neuropathology and altered behaviors in offspring. This Review describes common principles revealed by these models, highlighting recent findings that strengthen their relevance for schizophrenia and autism and are starting to reveal the molecular mechanisms underlying the effects of MIA on offspring. The role of MIA as a primer for a much wider range of psychiatric and neurologic disorders is also discussed. Finally, the need for more research in this nascent field and the implications for identifying and developing new treatments for individuals at heightened risk for neuroimmune disorders are considered.

@article{gilson_bindingdb_2016,
	title = {{BindingDB} in 2015: {A} public database for medicinal chemistry, computational chemistry and systems pharmacology},
	volume = {44},
	issn = {1362-4962},
	shorttitle = {{BindingDB} in 2015},
	doi = {10.1093/nar/gkv1072},
	abstract = {BindingDB, www.bindingdb.org, is a publicly accessible database of experimental protein-small molecule interaction data. Its collection of over a million data entries derives primarily from scientific articles and, increasingly, US patents. BindingDB provides many ways to browse and search for data of interest, including an advanced search tool, which can cross searches of multiple query types, including text, chemical structure, protein sequence and numerical affinities. The PDB and PubMed provide links to data in BindingDB, and vice versa; and BindingDB provides links to pathway information, the ZINC catalog of available compounds, and other resources. The BindingDB website offers specialized tools that take advantage of its large data collection, including ones to generate hypotheses for the protein targets bound by a bioactive compound, and for the compounds bound by a new protein of known sequence; and virtual compound screening by maximal chemical similarity, binary kernel discrimination, and support vector machine methods. Specialized data sets are also available, such as binding data for hundreds of congeneric series of ligands, drawn from BindingDB and organized for use in validating drug design methods. BindingDB offers several forms of programmatic access, and comes with extensive background material and documentation. Here, we provide the first update of BindingDB since 2007, focusing on new and unique features and highlighting directions of importance to the field as a whole.},
	language = {eng},
	number = {D1},
	journal = {Nucleic Acids Research},
	author = {Gilson, Michael K. and Liu, Tiqing and Baitaluk, Michael and Nicola, George and Hwang, Linda and Chong, Jenny},
	month = jan,
	year = {2016},
	pmid = {26481362},
	pmcid = {PMC4702793},
	note = {Number: D1},
	keywords = {Databases, Pharmaceutical, Drug Design, Internet, Ligands, Patents as Topic, Pharmaceutical Preparations, Protein Binding, Protein Folding, Proteins, Software, Systems Biology},
	pages = {D1045--1053},
}

BindingDB, www.bindingdb.org, is a publicly accessible database of experimental protein-small molecule interaction data. Its collection of over a million data entries derives primarily from scientific articles and, increasingly, US patents. BindingDB provides many ways to browse and search for data of interest, including an advanced search tool, which can cross searches of multiple query types, including text, chemical structure, protein sequence and numerical affinities. The PDB and PubMed provide links to data in BindingDB, and vice versa; and BindingDB provides links to pathway information, the ZINC catalog of available compounds, and other resources. The BindingDB website offers specialized tools that take advantage of its large data collection, including ones to generate hypotheses for the protein targets bound by a bioactive compound, and for the compounds bound by a new protein of known sequence; and virtual compound screening by maximal chemical similarity, binary kernel discrimination, and support vector machine methods. Specialized data sets are also available, such as binding data for hundreds of congeneric series of ligands, drawn from BindingDB and organized for use in validating drug design methods. BindingDB offers several forms of programmatic access, and comes with extensive background material and documentation. Here, we provide the first update of BindingDB since 2007, focusing on new and unique features and highlighting directions of importance to the field as a whole.

@article{gilson_bindingdb_2016,
	title = {{BindingDB} in 2015: {A} public database for medicinal chemistry, computational chemistry and systems pharmacology},
	volume = {44},
	issn = {1362-4962},
	shorttitle = {{BindingDB} in 2015},
	doi = {10.1093/nar/gkv1072},
	abstract = {BindingDB, www.bindingdb.org, is a publicly accessible database of experimental protein-small molecule interaction data. Its collection of over a million data entries derives primarily from scientific articles and, increasingly, US patents. BindingDB provides many ways to browse and search for data of interest, including an advanced search tool, which can cross searches of multiple query types, including text, chemical structure, protein sequence and numerical affinities. The PDB and PubMed provide links to data in BindingDB, and vice versa; and BindingDB provides links to pathway information, the ZINC catalog of available compounds, and other resources. The BindingDB website offers specialized tools that take advantage of its large data collection, including ones to generate hypotheses for the protein targets bound by a bioactive compound, and for the compounds bound by a new protein of known sequence; and virtual compound screening by maximal chemical similarity, binary kernel discrimination, and support vector machine methods. Specialized data sets are also available, such as binding data for hundreds of congeneric series of ligands, drawn from BindingDB and organized for use in validating drug design methods. BindingDB offers several forms of programmatic access, and comes with extensive background material and documentation. Here, we provide the first update of BindingDB since 2007, focusing on new and unique features and highlighting directions of importance to the field as a whole.},
	language = {eng},
	number = {D1},
	journal = {Nucleic Acids Research},
	author = {Gilson, Michael K. and Liu, Tiqing and Baitaluk, Michael and Nicola, George and Hwang, Linda and Chong, Jenny},
	month = jan,
	year = {2016},
	pmid = {26481362},
	pmcid = {PMC4702793},
	keywords = {Databases, Pharmaceutical, Drug Design, Internet, Ligands, Patents as Topic, Pharmaceutical Preparations, Protein Binding, Protein Folding, Proteins, Software, Systems Biology},
	pages = {D1045--1053},
}

BindingDB, www.bindingdb.org, is a publicly accessible database of experimental protein-small molecule interaction data. Its collection of over a million data entries derives primarily from scientific articles and, increasingly, US patents. BindingDB provides many ways to browse and search for data of interest, including an advanced search tool, which can cross searches of multiple query types, including text, chemical structure, protein sequence and numerical affinities. The PDB and PubMed provide links to data in BindingDB, and vice versa; and BindingDB provides links to pathway information, the ZINC catalog of available compounds, and other resources. The BindingDB website offers specialized tools that take advantage of its large data collection, including ones to generate hypotheses for the protein targets bound by a bioactive compound, and for the compounds bound by a new protein of known sequence; and virtual compound screening by maximal chemical similarity, binary kernel discrimination, and support vector machine methods. Specialized data sets are also available, such as binding data for hundreds of congeneric series of ligands, drawn from BindingDB and organized for use in validating drug design methods. BindingDB offers several forms of programmatic access, and comes with extensive background material and documentation. Here, we provide the first update of BindingDB since 2007, focusing on new and unique features and highlighting directions of importance to the field as a whole.

@article{estes_maternal_2016,
	title = {Maternal immune activation: {Implications} for neuropsychiatric disorders},
	volume = {353},
	issn = {0036-8075, 1095-9203},
	shorttitle = {Maternal immune activation},
	url = {https://www.science.org/doi/10.1126/science.aag3194},
	doi = {10.1126/science.aag3194},
	abstract = {Epidemiological evidence implicates maternal infection as a risk factor for autism spectrum disorder and schizophrenia. Animal models corroborate this link and demonstrate that maternal immune activation (MIA) alone is sufficient to impart lifelong neuropathology and altered behaviors in offspring. This Review describes common principles revealed by these models, highlighting recent findings that strengthen their relevance for schizophrenia and autism and are starting to reveal the molecular mechanisms underlying the effects of MIA on offspring. The role of MIA as a primer for a much wider range of psychiatric and neurologic disorders is also discussed. Finally, the need for more research in this nascent field and the implications for identifying and developing new treatments for individuals at heightened risk for neuroimmune disorders are considered.},
	language = {en},
	number = {6301},
	urldate = {2022-05-29},
	journal = {Science},
	author = {Estes, Myka L. and McAllister, A. Kimberley},
	month = aug,
	year = {2016},
	pages = {772--777},
}

Epidemiological evidence implicates maternal infection as a risk factor for autism spectrum disorder and schizophrenia. Animal models corroborate this link and demonstrate that maternal immune activation (MIA) alone is sufficient to impart lifelong neuropathology and altered behaviors in offspring. This Review describes common principles revealed by these models, highlighting recent findings that strengthen their relevance for schizophrenia and autism and are starting to reveal the molecular mechanisms underlying the effects of MIA on offspring. The role of MIA as a primer for a much wider range of psychiatric and neurologic disorders is also discussed. Finally, the need for more research in this nascent field and the implications for identifying and developing new treatments for individuals at heightened risk for neuroimmune disorders are considered.

@article{baehr_is_2016,
	title = {Is intellectual character growth a realistic educational aim?},
	volume = {45},
	issn = {0305-7240, 1465-3877},
	url = {http://www.tandfonline.com/doi/full/10.1080/03057240.2016.1174676},
	doi = {10.1080/03057240.2016.1174676},
	language = {en},
	number = {2},
	urldate = {2021-11-27},
	journal = {Journal of Moral Education},
	author = {Baehr, Jason},
	month = apr,
	year = {2016},
	pages = {117--131},
}

@article{friston_dysconnection_2016,
	title = {The dysconnection hypothesis (2016)},
	volume = {176},
	issn = {0920-9964},
	doi = {10.1016/j.schres.2016.07.014},
	abstract = {Twenty years have passed since the dysconnection hypothesis was first proposed (Friston and Frith, 1995; Weinberger, 1993). In that time, neuroscience has witnessed tremendous advances: we now live in a world of non-invasive neuroanatomy, computational neuroimaging and the Bayesian brain. The genomics era has come and gone. Connectomics and large-scale neuroinformatics initiatives are emerging everywhere. So where is the dysconnection hypothesis now? This article considers how the notion of schizophrenia as a dysconnection syndrome has developed – and how it has been enriched by recent advances in clinical neuroscience. In particular, we examine the dysconnection hypothesis in the context of (i) theoretical neurobiology and computational psychiatry; (ii) the empirical insights afforded by neuroimaging and associated connectomics – and (iii) how bottom-up (molecular biology and genetics) and top-down (systems biology) perspectives are converging on the mechanisms and nature of dysconnections in schizophrenia.},
	number = {2-3},
	journal = {Schizophrenia Research},
	author = {Friston, Karl and Brown, Harriet R. and Siemerkus, Jakob and Stephan, Klaas E.},
	year = {2016},
	pmid = {27450778},
	pages = {83--94},
}

Twenty years have passed since the dysconnection hypothesis was first proposed (Friston and Frith, 1995; Weinberger, 1993). In that time, neuroscience has witnessed tremendous advances: we now live in a world of non-invasive neuroanatomy, computational neuroimaging and the Bayesian brain. The genomics era has come and gone. Connectomics and large-scale neuroinformatics initiatives are emerging everywhere. So where is the dysconnection hypothesis now? This article considers how the notion of schizophrenia as a dysconnection syndrome has developed – and how it has been enriched by recent advances in clinical neuroscience. In particular, we examine the dysconnection hypothesis in the context of (i) theoretical neurobiology and computational psychiatry; (ii) the empirical insights afforded by neuroimaging and associated connectomics – and (iii) how bottom-up (molecular biology and genetics) and top-down (systems biology) perspectives are converging on the mechanisms and nature of dysconnections in schizophrenia.

@article{friston_dysconnection_2016-1,
	title = {The dysconnection hypothesis (2016)},
	volume = {176},
	issn = {0920-9964},
	url = {https://www.sciencedirect.com/science/article/pii/S0920996416303310},
	doi = {10.1016/j.schres.2016.07.014},
	abstract = {Twenty years have passed since the dysconnection hypothesis was first proposed (Friston and Frith, 1995; Weinberger, 1993). In that time, neuroscience has witnessed tremendous advances: we now live in a world of non-invasive neuroanatomy, computational neuroimaging and the Bayesian brain. The genomics era has come and gone. Connectomics and large-scale neuroinformatics initiatives are emerging everywhere. So where is the dysconnection hypothesis now? This article considers how the notion of schizophrenia as a dysconnection syndrome has developed – and how it has been enriched by recent advances in clinical neuroscience. In particular, we examine the dysconnection hypothesis in the context of (i) theoretical neurobiology and computational psychiatry; (ii) the empirical insights afforded by neuroimaging and associated connectomics – and (iii) how bottom-up (molecular biology and genetics) and top-down (systems biology) perspectives are converging on the mechanisms and nature of dysconnections in schizophrenia.},
	language = {en},
	number = {2},
	urldate = {2021-06-24},
	journal = {Schizophrenia Research},
	author = {Friston, Karl and Brown, Harriet R. and Siemerkus, Jakob and Stephan, Klaas E.},
	month = oct,
	year = {2016},
	keywords = {Bayesian, Dysconnection, Neurogenetics, Neuromodulation, Predictive coding, Schizophrenia},
	pages = {83--94},
}

Twenty years have passed since the dysconnection hypothesis was first proposed (Friston and Frith, 1995; Weinberger, 1993). In that time, neuroscience has witnessed tremendous advances: we now live in a world of non-invasive neuroanatomy, computational neuroimaging and the Bayesian brain. The genomics era has come and gone. Connectomics and large-scale neuroinformatics initiatives are emerging everywhere. So where is the dysconnection hypothesis now? This article considers how the notion of schizophrenia as a dysconnection syndrome has developed – and how it has been enriched by recent advances in clinical neuroscience. In particular, we examine the dysconnection hypothesis in the context of (i) theoretical neurobiology and computational psychiatry; (ii) the empirical insights afforded by neuroimaging and associated connectomics – and (iii) how bottom-up (molecular biology and genetics) and top-down (systems biology) perspectives are converging on the mechanisms and nature of dysconnections in schizophrenia.

@article{sandoval_understanding_2016,
	title = {Understanding and {Promoting} {Thinking} {About} {Knowledge}: {Origins}, {Issues}, and {Future} {Directions} of {Research} on {Epistemic} {Cognition}},
	volume = {40},
	issn = {0091-732X, 1935-1038},
	shorttitle = {Understanding and {Promoting} {Thinking} {About} {Knowledge}},
	url = {http://journals.sagepub.com/doi/10.3102/0091732X16669319},
	doi = {10.3102/0091732X16669319},
	language = {en},
	number = {1},
	urldate = {2020-03-12},
	journal = {Review of Research in Education},
	author = {Sandoval, William A. and Greene, Jeffrey A. and Bråten, Ivar},
	month = mar,
	year = {2016},
	note = {ZSCC: 0000085},
	pages = {457--496},
}

@article{leblanc_toward_2016,
	title = {Toward {Epistemic} {Justice}: {A} {Critically} {Reflexive} {Examination} of ‘{Sanism}’ and {Implications} for {Knowledge} {Generation}},
	volume = {10},
	issn = {1911-4788},
	shorttitle = {Toward {Epistemic} {Justice}},
	url = {https://journals.library.brocku.ca/index.php/SSJ/article/view/1324},
	doi = {10.26522/ssj.v10i1.1324},
	abstract = {The dominance of medicalized “psy” discourses in the West has marginalized alternative perspectives and analyses of madness, resulting in the underinclusion (or exclusion) from mainstream discourse of the firsthand experiences and perspectives of those who identify as Mad. We argue that this marginalization of firsthand knowledge(s) demands closer critical scrutiny, particularly through the use of critical reflexivity. This paper draws on Fricker’s concept of epistemic injustice, whereby a person is wronged in his or her capacity as a knower, as a useful framework for interrogating the subjugation of Mad knowledge(s). Also examined is the problem of sanism, a deeply embedded system of discrimination and oppression, as an underlying component of epistemic injustice. Sanism assumes a pathological view of madness, which can be attributed to what Rimke has termed psychocentrism: the notion that pathologies are rooted in the mind and/or body of the individual, rather than the product of social structures, relations, and problems. The paper examines how sanism marginalizes the knowledge(s) of Mad persons and contributes to epistemic injustice, and considers possibilities for advancing social justice using Mad epistemological perspectives.},
	language = {en},
	number = {1},
	urldate = {2020-04-02},
	journal = {Studies in Social Justice},
	author = {LeBlanc, Stephanie and Kinsella, Elizabeth Anne},
	month = aug,
	year = {2016},
	note = {ZSCC: 0000062},
	pages = {59--78},
}

The dominance of medicalized “psy” discourses in the West has marginalized alternative perspectives and analyses of madness, resulting in the underinclusion (or exclusion) from mainstream discourse of the firsthand experiences and perspectives of those who identify as Mad. We argue that this marginalization of firsthand knowledge(s) demands closer critical scrutiny, particularly through the use of critical reflexivity. This paper draws on Fricker’s concept of epistemic injustice, whereby a person is wronged in his or her capacity as a knower, as a useful framework for interrogating the subjugation of Mad knowledge(s). Also examined is the problem of sanism, a deeply embedded system of discrimination and oppression, as an underlying component of epistemic injustice. Sanism assumes a pathological view of madness, which can be attributed to what Rimke has termed psychocentrism: the notion that pathologies are rooted in the mind and/or body of the individual, rather than the product of social structures, relations, and problems. The paper examines how sanism marginalizes the knowledge(s) of Mad persons and contributes to epistemic injustice, and considers possibilities for advancing social justice using Mad epistemological perspectives.

@article{birrell_ethics_2016,
	title = {Ethics and {Relationship}: {From} {Risk} {Management} to {Relational} {Engagement}},
	volume = {94},
	issn = {07489633},
	shorttitle = {Ethics and {Relationship}},
	url = {http://doi.wiley.com/10.1002/jcad.12097},
	doi = {10.1002/jcad.12097},
	language = {en},
	number = {4},
	urldate = {2020-04-02},
	journal = {Journal of Counseling \& Development},
	author = {Birrell, Pamela J. and Bruns, Cindy M.},
	month = oct,
	year = {2016},
	note = {ZSCC: 0000014},
	pages = {391--397},
}

@article{birrell_ethics_2016-1,
	title = {Ethics and {Relationship}: {From} {Risk} {Management} to {Relational} {Engagement}},
	volume = {94},
	issn = {07489633},
	shorttitle = {Ethics and {Relationship}},
	url = {http://doi.wiley.com/10.1002/jcad.12097},
	doi = {10.1002/jcad.12097},
	language = {en},
	number = {4},
	urldate = {2020-04-02},
	journal = {Journal of Counseling \& Development},
	author = {Birrell, Pamela J. and Bruns, Cindy M.},
	month = oct,
	year = {2016},
	note = {ZSCC: 0000014},
	pages = {391--397},
}

@article{domen_ethics_2016,
	title = {The {Ethics} of {Ambiguity}: {Rethinking} the {Role} and {Importance} of {Uncertainty} in {Medical} {Education} and {Practice}},
	volume = {3},
	issn = {2374-2895, 2374-2895},
	shorttitle = {The {Ethics} of {Ambiguity}},
	url = {http://journals.sagepub.com/doi/10.1177/2374289516654712},
	doi = {10.1177/2374289516654712},
	abstract = {Understanding and embracing uncertainty are critical for effective teacher–learner relationships as well as for shared decisionmaking in the physician–patient relationship. However, ambiguity has not been given serious consideration in either the undergraduate or graduate medical curricula or in the role it plays in patient-centered care. In this article, the author examines the ethics of ambiguity and argues for a pedagogy that includes education in the importance of, and tolerance of, ambiguity that is inherent in medical education and practice. Common threads running through the ethics of ambiguity are the virtue of respect, and the development of a culture of respect is required for the successful understanding and implementation of a pedagogy of ambiguity.},
	language = {en},
	urldate = {2020-03-12},
	journal = {Academic Pathology},
	author = {Domen, Ronald E.},
	month = aug,
	year = {2016},
	note = {ZSCC: 0000023},
	keywords = {ambiguity, ethics, medical education, patient-centered care, professionalism, respect, uncertainty},
	pages = {237428951665471},
}

Understanding and embracing uncertainty are critical for effective teacher–learner relationships as well as for shared decisionmaking in the physician–patient relationship. However, ambiguity has not been given serious consideration in either the undergraduate or graduate medical curricula or in the role it plays in patient-centered care. In this article, the author examines the ethics of ambiguity and argues for a pedagogy that includes education in the importance of, and tolerance of, ambiguity that is inherent in medical education and practice. Common threads running through the ethics of ambiguity are the virtue of respect, and the development of a culture of respect is required for the successful understanding and implementation of a pedagogy of ambiguity.

@article{edwards_academic_2016,
	title = {Academic {Research} in the 21st {Century}: {Maintaining} {Scientific} {Integrity} in a {Climate} of {Perverse} {Incentives} and {Hypercompetition}},
	volume = {34},
	shorttitle = {Academic {Research} in the 21st {Century}},
	url = {https://www.liebertpub.com/doi/10.1089/ees.2016.0223},
	doi = {10.1089/ees.2016.0223},
	abstract = {Over the last 50 years, we argue that incentives for academic scientists have become increasingly perverse in terms of competition for research funding, development of quantitative metrics to measure performance, and a changing business model for higher education itself. Furthermore, decreased discretionary funding at the federal and state level is creating a hypercompetitive environment between government agencies (e.g., EPA, NIH, CDC), for scientists in these agencies, and for academics seeking funding from all sources—the combination of perverse incentives and decreased funding increases pressures that can lead to unethical behavior. If a critical mass of scientists become untrustworthy, a tipping point is possible in which the scientific enterprise itself becomes inherently corrupt and public trust is lost, risking a new dark age with devastating consequences to humanity. Academia and federal agencies should better support science as a public good, and incentivize altruistic and ethical outcomes, while de-emphasizing output.},
	number = {1},
	urldate = {2021-04-13},
	journal = {Environmental Engineering Science},
	author = {Edwards, Marc A. and Roy, Siddhartha},
	month = sep,
	year = {2016},
	note = {ZSCC: NoCitationData[s0] 
Publisher: Mary Ann Liebert, Inc., publishers},
	pages = {51--61},
}

Over the last 50 years, we argue that incentives for academic scientists have become increasingly perverse in terms of competition for research funding, development of quantitative metrics to measure performance, and a changing business model for higher education itself. Furthermore, decreased discretionary funding at the federal and state level is creating a hypercompetitive environment between government agencies (e.g., EPA, NIH, CDC), for scientists in these agencies, and for academics seeking funding from all sources—the combination of perverse incentives and decreased funding increases pressures that can lead to unethical behavior. If a critical mass of scientists become untrustworthy, a tipping point is possible in which the scientific enterprise itself becomes inherently corrupt and public trust is lost, risking a new dark age with devastating consequences to humanity. Academia and federal agencies should better support science as a public good, and incentivize altruistic and ethical outcomes, while de-emphasizing output.

@article{shilling_potential_2016,
	title = {Potential of {Oxytocin} in the {Treatment} of {Schizophrenia}},
	volume = {30},
	issn = {1172-7047},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5458113/},
	doi = {10.1007/s40263-016-0315-x},
	abstract = {Schizophrenia is a heterogeneous, debilitating disorder characterized by three distinct sets of clinical features: positive symptoms, negative symptoms and cognitive deficits. Extant antipsychotic drugs have been most successful at treating the positive symptoms of patients that suffer from schizophrenia but have minimal therapeutic effects on negative symptoms and cognitive deficits, which are the symptoms that best predict the poor prognosis of these patients. Therefore, there has been a major effort towards identifying compounds that alleviate these symptoms., Oxytocin (OT) is a nonapeptide that regulates peripheral reproductive-relevant functions, and also acts as a neurotransmitter in the brain. Converging evidence from both preclinical and clinical research suggests that OT may have therapeutic efficacy for the positive symptoms, negative symptoms and cognitive deficits of schizophrenia. In the majority of the small-randomized placebo controlled clinical trials conducted to date, OT has shown particular promise in its potential to treat the intractable negative symptoms and social cognitive deficits exhibited by most of the patients with this debilitating disorder., In this leading article, we summarize the clinical evidence relevant to 1) endogenous OT and schizophrenia, and 2) the putative therapeutic effects of OT on each of the three clinical domains.},
	number = {3},
	urldate = {2021-04-10},
	journal = {CNS drugs},
	author = {Shilling, Paul D. and Feifel, David},
	month = mar,
	year = {2016},
	pmid = {26895254},
	pmcid = {PMC5458113},
	note = {ZSCC: 0000042 },
	pages = {193--208},
}

Schizophrenia is a heterogeneous, debilitating disorder characterized by three distinct sets of clinical features: positive symptoms, negative symptoms and cognitive deficits. Extant antipsychotic drugs have been most successful at treating the positive symptoms of patients that suffer from schizophrenia but have minimal therapeutic effects on negative symptoms and cognitive deficits, which are the symptoms that best predict the poor prognosis of these patients. Therefore, there has been a major effort towards identifying compounds that alleviate these symptoms., Oxytocin (OT) is a nonapeptide that regulates peripheral reproductive-relevant functions, and also acts as a neurotransmitter in the brain. Converging evidence from both preclinical and clinical research suggests that OT may have therapeutic efficacy for the positive symptoms, negative symptoms and cognitive deficits of schizophrenia. In the majority of the small-randomized placebo controlled clinical trials conducted to date, OT has shown particular promise in its potential to treat the intractable negative symptoms and social cognitive deficits exhibited by most of the patients with this debilitating disorder., In this leading article, we summarize the clinical evidence relevant to 1) endogenous OT and schizophrenia, and 2) the putative therapeutic effects of OT on each of the three clinical domains.

@article{gaume_psychoengineering_2016,
	title = {A psychoengineering paradigm for the neurocognitive mechanisms of biofeedback and neurofeedback},
	volume = {68},
	issn = {01497634},
	url = {https://linkinghub.elsevier.com/retrieve/pii/S0149763416300902},
	doi = {10.1016/j.neubiorev.2016.06.012},
	language = {en},
	urldate = {2020-10-06},
	journal = {Neuroscience \& Biobehavioral Reviews},
	author = {Gaume, A. and Vialatte, A. and Mora-Sánchez, A. and Ramdani, C. and Vialatte, F.B.},
	month = sep,
	year = {2016},
	note = {ZSCC: NoCitationData[s0]},
	pages = {891--910},
}

@book{kramer_case_2016,
	address = {Cambridge, Massachusetts},
	series = {Computational neuroscience series},
	title = {Case studies in neural data analysis: a guide for the practicing neuroscientist},
	isbn = {978-0-262-52937-2},
	shorttitle = {Case studies in neural data analysis},
	language = {en},
	publisher = {The MIT Press},
	author = {Kramer, Mark A. and Eden, Uri T.},
	year = {2016},
	note = {ZSCC: NoCitationData[s0]},
	keywords = {Neural analyzers, Neuropsychological tests},
}

@book{kramer_case_2016-1,
	address = {Cambridge, Massachusetts},
	series = {Computational neuroscience series},
	title = {Case studies in neural data analysis: a guide for the practicing neuroscientist},
	isbn = {978-0-262-52937-2},
	shorttitle = {Case studies in neural data analysis},
	language = {en},
	publisher = {The MIT Press},
	author = {Kramer, Mark A. and Eden, Uri T.},
	year = {2016},
	note = {ZSCC: NoCitationData[s0]},
	keywords = {Neural analyzers, Neuropsychological tests},
}

@article{mondino_effects_2016,
	title = {Effects of {Fronto}-{Temporal} {Transcranial} {Direct} {Current} {Stimulation} on {Auditory} {Verbal} {Hallucinations} and {Resting}-{State} {Functional} {Connectivity} of the {Left} {Temporo}-{Parietal} {Junction} in {Patients} {With} {Schizophrenia}},
	volume = {42},
	issn = {0586-7614},
	url = {https://academic.oup.com/schizophreniabulletin/article/42/2/318/2518927},
	doi = {10.1093/schbul/sbv114},
	abstract = {Abstract.  Auditory verbal hallucinations (AVH) in patients with schizophrenia are associated with abnormal hyperactivity in the left temporo-parietal junction},
	language = {en},
	number = {2},
	urldate = {2020-08-11},
	journal = {Schizophrenia Bulletin},
	author = {Mondino, Marine and Jardri, Renaud and Suaud-Chagny, Marie-Françoise and Saoud, Mohamed and Poulet, Emmanuel and Brunelin, Jérôme},
	month = mar,
	year = {2016},
	note = {ZSCC: NoCitationData[s0] 
Publisher: Oxford Academic},
	pages = {318--326},
}

Abstract. Auditory verbal hallucinations (AVH) in patients with schizophrenia are associated with abnormal hyperactivity in the left temporo-parietal junction

@article{de_villers-sidani_neuroplastic_2016,
	title = {Neuroplastic {Mechanisms} {Underlying} {Perceptual} and {Cognitive} {Enhancement}},
	volume = {2016},
	issn = {2090-5904, 1687-5443},
	url = {http://www.hindawi.com/journals/np/2016/6238571/},
	doi = {10.1155/2016/6238571},
	language = {en},
	urldate = {2020-07-17},
	journal = {Neural Plasticity},
	author = {de Villers-Sidani, Etienne and Mishra, Jyoti and Zhou, Xiaoming and Voss, Patrice},
	year = {2016},
	note = {ZSCC: 0000000},
	pages = {1--2},
}

@article{agapov_review_2016,
	title = {Review of analytical instruments for {EEG} analysis},
	url = {http://arxiv.org/abs/1605.01381},
	abstract = {Since it was first used in 1926, EEG has been one of the most useful instruments of neuroscience. In order to start using EEG data we need not only EEG apparatus, but also some analytical tools and skills to understand what our data mean. This article describes several classical analytical tools and also new one which appeared only several years ago. We hope it will be useful for those researchers who have only started working in the field of cognitive EEG.},
	urldate = {2020-06-05},
	journal = {arXiv:1605.01381 [q-bio]},
	author = {Agapov, S. N. and Bulanov, V. A. and Zakharov, A. V. and Sergeeva, M. S.},
	month = mar,
	year = {2016},
	note = {ZSCC: 0000001 
arXiv: 1605.01381},
	keywords = {Quantitative Biology - Neurons and Cognition},
}

Since it was first used in 1926, EEG has been one of the most useful instruments of neuroscience. In order to start using EEG data we need not only EEG apparatus, but also some analytical tools and skills to understand what our data mean. This article describes several classical analytical tools and also new one which appeared only several years ago. We hope it will be useful for those researchers who have only started working in the field of cognitive EEG.

@article{gordon_adapting_2016,
	title = {Adapting {Open} {Dialogue} for {Early}-{Onset} {Psychosis} {Into} the {U}.{S}. {Health} {Care} {Environment}: {A} {Feasibility} {Study}},
	volume = {67},
	issn = {1075-2730, 1557-9700},
	shorttitle = {Adapting {Open} {Dialogue} for {Early}-{Onset} {Psychosis} {Into} the {U}.{S}. {Health} {Care} {Environment}},
	url = {http://psychiatryonline.org/doi/10.1176/appi.ps.201600271},
	doi = {10.1176/appi.ps.201600271},
	language = {en},
	number = {11},
	urldate = {2020-04-02},
	journal = {Psychiatric Services},
	author = {Gordon, Christopher and Gidugu, Vasudha and Rogers, E. Sally and DeRonck, John and Ziedonis, Douglas},
	month = nov,
	year = {2016},
	note = {ZSCC: 0000029},
	pages = {1166--1168},
}

@article{leblanc_toward_2016,
	title = {Toward {Epistemic} {Justice}: {A} {Critically} {Reflexive} {Examination} of ‘{Sanism}’ and {Implications} for {Knowledge} {Generation}},
	volume = {10},
	issn = {1911-4788},
	shorttitle = {Toward {Epistemic} {Justice}},
	url = {https://journals.library.brocku.ca/index.php/SSJ/article/view/1324},
	doi = {10.26522/ssj.v10i1.1324},
	abstract = {The dominance of medicalized “psy” discourses in the West has marginalized alternative perspectives and analyses of madness, resulting in the underinclusion (or exclusion) from mainstream discourse of the firsthand experiences and perspectives of those who identify as Mad. We argue that this marginalization of firsthand knowledge(s) demands closer critical scrutiny, particularly through the use of critical reflexivity. This paper draws on Fricker’s concept of epistemic injustice, whereby a person is wronged in his or her capacity as a knower, as a useful framework for interrogating the subjugation of Mad knowledge(s). Also examined is the problem of sanism, a deeply embedded system of discrimination and oppression, as an underlying component of epistemic injustice. Sanism assumes a pathological view of madness, which can be attributed to what Rimke has termed psychocentrism: the notion that pathologies are rooted in the mind and/or body of the individual, rather than the product of social structures, relations, and problems. The paper examines how sanism marginalizes the knowledge(s) of Mad persons and contributes to epistemic injustice, and considers possibilities for advancing social justice using Mad epistemological perspectives.},
	language = {en},
	number = {1},
	urldate = {2020-04-02},
	journal = {Studies in Social Justice},
	author = {LeBlanc, Stephanie and Kinsella, Elizabeth Anne},
	month = aug,
	year = {2016},
	note = {ZSCC: 0000044},
	pages = {59--78},
}

The dominance of medicalized “psy” discourses in the West has marginalized alternative perspectives and analyses of madness, resulting in the underinclusion (or exclusion) from mainstream discourse of the firsthand experiences and perspectives of those who identify as Mad. We argue that this marginalization of firsthand knowledge(s) demands closer critical scrutiny, particularly through the use of critical reflexivity. This paper draws on Fricker’s concept of epistemic injustice, whereby a person is wronged in his or her capacity as a knower, as a useful framework for interrogating the subjugation of Mad knowledge(s). Also examined is the problem of sanism, a deeply embedded system of discrimination and oppression, as an underlying component of epistemic injustice. Sanism assumes a pathological view of madness, which can be attributed to what Rimke has termed psychocentrism: the notion that pathologies are rooted in the mind and/or body of the individual, rather than the product of social structures, relations, and problems. The paper examines how sanism marginalizes the knowledge(s) of Mad persons and contributes to epistemic injustice, and considers possibilities for advancing social justice using Mad epistemological perspectives.

@article{rosen_finland_2016,
	title = {Finland in {Boston}? {Applying} {Open} {Dialogue} {Ideals} on a {Psychotic} {Disorders} {Inpatient} {Teaching} {Unit}},
	volume = {67},
	issn = {1075-2730, 1557-9700},
	shorttitle = {Finland in {Boston}?},
	url = {http://psychiatryonline.org/doi/10.1176/appi.ps.201600340},
	doi = {10.1176/appi.ps.201600340},
	language = {en},
	number = {12},
	urldate = {2020-04-02},
	journal = {Psychiatric Services},
	author = {Rosen, Kayla and Stoklosa, Joseph},
	month = dec,
	year = {2016},
	note = {ZSCC: 0000013},
	pages = {1283--1285},
}

@article{gordon_adapting_2016,
	title = {Adapting {Open} {Dialogue} for {Early}-{Onset} {Psychosis} {Into} the {U}.{S}. {Health} {Care} {Environment}: {A} {Feasibility} {Study}},
	volume = {67},
	issn = {1075-2730, 1557-9700},
	shorttitle = {Adapting {Open} {Dialogue} for {Early}-{Onset} {Psychosis} {Into} the {U}.{S}. {Health} {Care} {Environment}},
	url = {http://psychiatryonline.org/doi/10.1176/appi.ps.201600271},
	doi = {10.1176/appi.ps.201600271},
	language = {en},
	number = {11},
	urldate = {2020-04-02},
	journal = {Psychiatric Services},
	author = {Gordon, Christopher and Gidugu, Vasudha and Rogers, E. Sally and DeRonck, John and Ziedonis, Douglas},
	month = nov,
	year = {2016},
	note = {ZSCC: 0000029},
	pages = {1166--1168},
}

@article{birrell_ethics_2016,
	title = {Ethics and {Relationship}: {From} {Risk} {Management} to {Relational} {Engagement}},
	volume = {94},
	issn = {07489633},
	shorttitle = {Ethics and {Relationship}},
	url = {http://doi.wiley.com/10.1002/jcad.12097},
	doi = {10.1002/jcad.12097},
	language = {en},
	number = {4},
	urldate = {2020-04-02},
	journal = {Journal of Counseling \& Development},
	author = {Birrell, Pamela J. and Bruns, Cindy M.},
	month = oct,
	year = {2016},
	note = {ZSCC: 0000005},
	pages = {391--397},
}

@article{birrell_ethics_2016-1,
	title = {Ethics and {Relationship}: {From} {Risk} {Management} to {Relational} {Engagement}},
	volume = {94},
	issn = {07489633},
	shorttitle = {Ethics and {Relationship}},
	url = {http://doi.wiley.com/10.1002/jcad.12097},
	doi = {10.1002/jcad.12097},
	language = {en},
	number = {4},
	urldate = {2020-04-02},
	journal = {Journal of Counseling \& Development},
	author = {Birrell, Pamela J. and Bruns, Cindy M.},
	month = oct,
	year = {2016},
	note = {ZSCC: 0000005},
	pages = {391--397},
}

@article{domen_ethics_2016,
	title = {The {Ethics} of {Ambiguity}: {Rethinking} the {Role} and {Importance} of {Uncertainty} in {Medical} {Education} and {Practice}},
	volume = {3},
	issn = {2374-2895, 2374-2895},
	shorttitle = {The {Ethics} of {Ambiguity}},
	url = {http://journals.sagepub.com/doi/10.1177/2374289516654712},
	doi = {10.1177/2374289516654712},
	abstract = {Understanding and embracing uncertainty are critical for effective teacher–learner relationships as well as for shared decisionmaking in the physician–patient relationship. However, ambiguity has not been given serious consideration in either the undergraduate or graduate medical curricula or in the role it plays in patient-centered care. In this article, the author examines the ethics of ambiguity and argues for a pedagogy that includes education in the importance of, and tolerance of, ambiguity that is inherent in medical education and practice. Common threads running through the ethics of ambiguity are the virtue of respect, and the development of a culture of respect is required for the successful understanding and implementation of a pedagogy of ambiguity.},
	language = {en},
	urldate = {2020-03-12},
	journal = {Academic Pathology},
	author = {Domen, Ronald E.},
	month = aug,
	year = {2016},
	keywords = {ambiguity, ethics, medical education, patient-centered care,, professionalism, respect, uncertainty},
	pages = {237428951665471},
}

Understanding and embracing uncertainty are critical for effective teacher–learner relationships as well as for shared decisionmaking in the physician–patient relationship. However, ambiguity has not been given serious consideration in either the undergraduate or graduate medical curricula or in the role it plays in patient-centered care. In this article, the author examines the ethics of ambiguity and argues for a pedagogy that includes education in the importance of, and tolerance of, ambiguity that is inherent in medical education and practice. Common threads running through the ethics of ambiguity are the virtue of respect, and the development of a culture of respect is required for the successful understanding and implementation of a pedagogy of ambiguity.

@article{gordon_adapting_2016,
	title = {Adapting {Open} {Dialogue} for {Early}-{Onset} {Psychosis} {Into} the {U}.{S}. {Health} {Care} {Environment}: {A} {Feasibility} {Study}},
	volume = {67},
	issn = {1075-2730, 1557-9700},
	shorttitle = {Adapting {Open} {Dialogue} for {Early}-{Onset} {Psychosis} {Into} the {U}.{S}. {Health} {Care} {Environment}},
	url = {http://psychiatryonline.org/doi/10.1176/appi.ps.201600271},
	doi = {10.1176/appi.ps.201600271},
	language = {en},
	number = {11},
	urldate = {2020-03-19},
	journal = {Psychiatric Services},
	author = {Gordon, Christopher and Gidugu, Vasudha and Rogers, E. Sally and DeRonck, John and Ziedonis, Douglas},
	month = nov,
	year = {2016},
	pages = {1166--1168},
}

@article{moran_understanding_2016,
	title = {Understanding {Universal} {Elements} in {Mental} {Health} {Recovery}: {A} {Cross}-{Examination} of {Peer} {Providers} and a {Non}-{Clinical} {Sample}},
	volume = {26},
	issn = {1049-7323, 1552-7557},
	shorttitle = {Understanding {Universal} {Elements} in {Mental} {Health} {Recovery}},
	url = {http://journals.sagepub.com/doi/10.1177/1049732315570124},
	doi = {10.1177/1049732315570124},
	abstract = {In our study, we examined underlying human elements embedded in mental health recovery, by exploring shared positive change among peer providers with serious mental illnesses in recovery and a normative sample in spiritual growth following adversity. We conducted secondary analysis based on two independent qualitative study samples consisting of 31 American peer providers and 27 Israeli adults. We identified three shared and two distinct enablers of positive change: peer groups, significant mentor, self-transcendent experiences. Distinct enablers were having meaningful task/role (clinical sample) and deliberate choice to commit to change in face of uncertainty (non-clinical sample). Enablers facilitated positive processes of meaning making and enhancement of agency. Enablers provided opportunities to which the person responded and made use of—thus, enacting a positive reinforcement of change processes. The findings highlight the value of examining mental health recovery in a broad holistic perspective and have implications for practice.},
	language = {en},
	number = {2},
	urldate = {2020-03-19},
	journal = {Qualitative Health Research},
	author = {Moran, Galia and Russo-Netzer, Pninit},
	month = jan,
	year = {2016},
	pages = {273--287},
}

In our study, we examined underlying human elements embedded in mental health recovery, by exploring shared positive change among peer providers with serious mental illnesses in recovery and a normative sample in spiritual growth following adversity. We conducted secondary analysis based on two independent qualitative study samples consisting of 31 American peer providers and 27 Israeli adults. We identified three shared and two distinct enablers of positive change: peer groups, significant mentor, self-transcendent experiences. Distinct enablers were having meaningful task/role (clinical sample) and deliberate choice to commit to change in face of uncertainty (non-clinical sample). Enablers facilitated positive processes of meaning making and enhancement of agency. Enablers provided opportunities to which the person responded and made use of—thus, enacting a positive reinforcement of change processes. The findings highlight the value of examining mental health recovery in a broad holistic perspective and have implications for practice.

@article{taylor_moving_2016,
	title = {Moving beyond the other: {A} critique of the reductionist drugs discourse},
	volume = {6},
	issn = {2211-9507},
	shorttitle = {Moving beyond the other},
	url = {http://tijdschriften.boomcriminologie.nl/tijdschrift/tcc/2016/1/TCC_2211-9507_2016_006_001_007},
	doi = {10.5553/TCC/221195072016006001007},
	abstract = {This paper uses the UK as a vehicle through which to argue that a dominant reductionist drugs discourse exists which simplifies understandings of drug use and drug users leading to socio-cultural misrepresentations of harm, risk and dangerousness. It contends that at the centre of this discourse lies the process of othering - the identification of specific substances and substance users as a threat to UK society. Interestingly, within the wider context of global drug policy reform this othering process appears to be expanding to target a wider variety of factors and actors - those policies, research findings and individuals which contest normative notions, resulting in the marginalisation of alte ati e oi es which question the entrenched assumptions associated with drug prohibition. The paper concludes that there is a need for collective action by critical scholars to move beyond the other, calling for academics to be innovative in their research agendas, creative in their dissemination of knowledge and resolute despite the threat of being othered themselves.},
	language = {en},
	number = {1},
	urldate = {2020-03-19},
	journal = {Tijdschrift over Cultuur \& Criminaliteit},
	author = {Taylor, Stuart},
	month = mar,
	year = {2016},
	pages = {100--118},
}

This paper uses the UK as a vehicle through which to argue that a dominant reductionist drugs discourse exists which simplifies understandings of drug use and drug users leading to socio-cultural misrepresentations of harm, risk and dangerousness. It contends that at the centre of this discourse lies the process of othering - the identification of specific substances and substance users as a threat to UK society. Interestingly, within the wider context of global drug policy reform this othering process appears to be expanding to target a wider variety of factors and actors - those policies, research findings and individuals which contest normative notions, resulting in the marginalisation of alte ati e oi es which question the entrenched assumptions associated with drug prohibition. The paper concludes that there is a need for collective action by critical scholars to move beyond the other, calling for academics to be innovative in their research agendas, creative in their dissemination of knowledge and resolute despite the threat of being othered themselves.

@article{krause_humility_2016,
	title = {Humility, stressful life events, and psychological well-being: {Findings} from the landmark spirituality and health survey},
	volume = {11},
	issn = {1743-9760, 1743-9779},
	shorttitle = {Humility, stressful life events, and psychological well-being},
	url = {http://www.tandfonline.com/doi/full/10.1080/17439760.2015.1127991},
	doi = {10.1080/17439760.2015.1127991},
	language = {en},
	number = {5},
	urldate = {2020-03-13},
	journal = {The Journal of Positive Psychology},
	author = {Krause, Neal and Pargament, Kenneth I. and Hill, Peter C. and Ironson, Gail},
	month = sep,
	year = {2016},
	pages = {499--510},
}

@misc{krumrei-mancuso_comprehensive_2016,
	title = {Comprehensive {Intellectual} {Humility} {Scale}},
	url = {http://doi.apa.org/getdoi.cfm?doi=10.1037/t47726-000},
	doi = {10.1037/t47726-000},
	language = {en},
	urldate = {2020-03-13},
	publisher = {American Psychological Association},
	author = {Krumrei-Mancuso, Elizabeth J. and Rouse, Steven V.},
	month = apr,
	year = {2016},
}

@article{sandoval_understanding_2016,
	title = {Understanding and {Promoting} {Thinking} {About} {Knowledge}: {Origins}, {Issues}, and {Future} {Directions} of {Research} on {Epistemic} {Cognition}},
	volume = {40},
	issn = {0091-732X, 1935-1038},
	shorttitle = {Understanding and {Promoting} {Thinking} {About} {Knowledge}},
	url = {http://journals.sagepub.com/doi/10.3102/0091732X16669319},
	doi = {10.3102/0091732X16669319},
	language = {en},
	number = {1},
	urldate = {2020-03-12},
	journal = {Review of Research in Education},
	author = {Sandoval, William A. and Greene, Jeffrey A. and Bråten, Ivar},
	month = mar,
	year = {2016},
	pages = {457--496},
}

@article{brockman_this_2015,
	title = {This {Idea} {Must} {Die}: {Scientific} {Theories} {That} {Are} {Blocking} {Progress} ({Edge} {Question} {Series})},
	shorttitle = {This {Idea} {Must} {Die}},
	url = {https://philpapers.org/rec/BROTIM-11},
	urldate = {2023-10-01},
	author = {Brockman, John},
	year = {2015},
}

@article{kingsberg_female_2015,
	title = {The {Female} {Sexual} {Response}: {Current} {Models}, {Neurobiological} {Underpinnings} and {Agents} {Currently} {Approved} or {Under} {Investigation} for the {Treatment} of {Hypoactive} {Sexual} {Desire} {Disorder}},
	volume = {29},
	issn = {1179-1934},
	shorttitle = {The {Female} {Sexual} {Response}},
	doi = {10.1007/s40263-015-0288-1},
	abstract = {How a woman responds to sexual cues is highly dependent on a number of distinct, yet related, factors. Researchers have attempted to explain the female sexual response for decades, but no single model reigns supreme. Proper female sexual function relies on the interplay of somatic, psychosocial and neurobiological factors; misregulation of any of these components could result in sexual dysfunction. The most common sexual dysfunction disorder is hypoactive sexual desire disorder (HSDD). HSDD is a disorder affecting women across the world; a recent in-person diagnostic interview study conducted in the USA found that an estimated 7.4\% of US women suffer from HSDD. Despite the disorder's prevalence, it is often overlooked as a formal diagnosis. In a survey of primary care physicians and obstetrics/gynaecology specialists, the number one reason for not assigning an HSDD diagnosis was the lack of a safe and effective therapy approved by the US Food and Drug Administration (FDA). This changed with the recent FDA approval of flibanserin (Addyi™) for the treatment of premenopausal women with acquired, generalized HSDD; there are still, however, no treatments approved outside the USA. HSDD is characterized by a marked decrease in sexual desire, an absence of motivation (also known as avolition) to engage in sexual activity, and the condition's hallmark symptom, marked patient distress. Research suggests that HSDD may arise from an imbalance of the excitatory and inhibitory neurobiological pathways that regulate the mammalian sexual response; top-down inhibition from the prefrontal cortex may be hyperactive, and/or bottom-up excitation to the limbic system may be hypoactive. Key neuromodulators for the excitatory pathways include norepinephrine, oxytocin, dopamine and melanocortins. Serotonin, opioids and endocannabinoids serve as key neuromodulators for the inhibitory pathways. Evolving treatment strategies have relied heavily on these crucial research findings, as many of the agents currently being investigated as treatment options for HSDD target and influence key players within these excitatory and inhibitory pathways, including various hormone therapies and centrally acting drugs, such as buspirone, bupropion and bremelanotide.},
	language = {eng},
	number = {11},
	journal = {CNS drugs},
	author = {Kingsberg, Sheryl A. and Clayton, Anita H. and Pfaus, James G.},
	month = nov,
	year = {2015},
	pmid = {26519340},
	keywords = {Animals, Brain, Female, Humans, Models, Neurological, Sexual Dysfunctions, Psychological},
	pages = {915--933},
}

How a woman responds to sexual cues is highly dependent on a number of distinct, yet related, factors. Researchers have attempted to explain the female sexual response for decades, but no single model reigns supreme. Proper female sexual function relies on the interplay of somatic, psychosocial and neurobiological factors; misregulation of any of these components could result in sexual dysfunction. The most common sexual dysfunction disorder is hypoactive sexual desire disorder (HSDD). HSDD is a disorder affecting women across the world; a recent in-person diagnostic interview study conducted in the USA found that an estimated 7.4% of US women suffer from HSDD. Despite the disorder's prevalence, it is often overlooked as a formal diagnosis. In a survey of primary care physicians and obstetrics/gynaecology specialists, the number one reason for not assigning an HSDD diagnosis was the lack of a safe and effective therapy approved by the US Food and Drug Administration (FDA). This changed with the recent FDA approval of flibanserin (Addyi™) for the treatment of premenopausal women with acquired, generalized HSDD; there are still, however, no treatments approved outside the USA. HSDD is characterized by a marked decrease in sexual desire, an absence of motivation (also known as avolition) to engage in sexual activity, and the condition's hallmark symptom, marked patient distress. Research suggests that HSDD may arise from an imbalance of the excitatory and inhibitory neurobiological pathways that regulate the mammalian sexual response; top-down inhibition from the prefrontal cortex may be hyperactive, and/or bottom-up excitation to the limbic system may be hypoactive. Key neuromodulators for the excitatory pathways include norepinephrine, oxytocin, dopamine and melanocortins. Serotonin, opioids and endocannabinoids serve as key neuromodulators for the inhibitory pathways. Evolving treatment strategies have relied heavily on these crucial research findings, as many of the agents currently being investigated as treatment options for HSDD target and influence key players within these excitatory and inhibitory pathways, including various hormone therapies and centrally acting drugs, such as buspirone, bupropion and bremelanotide.

@article{oliveira_innovation_2015,
	title = {Innovation by patients with rare diseases and chronic needs},
	volume = {10},
	issn = {1750-1172},
	url = {http://www.ojrd.com/content/10/1/41},
	doi = {10.1186/s13023-015-0257-2},
	abstract = {Methods: We administered a questionnaire via telephone interviewing to a sample of 500 rare disease patients and caregivers. The solutions reported were pre-screened by the authors for their fit with the self-developed innovation aim of the study. All the reported solutions were then validated for their novelty by two medical professionals. Logistic regression models were used to test the relationships between our key variables, patient innovation and solution sharing.
Results: 263 (53\%) of our survey respondents reported developing and using a solution to improve management of their diseases. An initial screening removed 81 (16\%) solutions for being an obvious misfit to the self-developed innovation aim of the study. This lowered the sample of potentially innovative solutions to 182 (36\%). Assessment of novelty and usefulness of the solutions, conducted by two medical evaluators, confirmed that 40 solutions (8\%) were indeed novel, while the remaining 142 (28\%) were already known to medicine. The likelihood of patient innovation increased as the education level increased (OR 2, p {\textless} 0.05), and as their perception of limitations imposed by their disease increased (OR 1.3, p {\textless} 0.05). 55 individuals diffused their solutions to some degree, with 50 of these sharing via direct diffusion to other patients. There is a positive relationship between the impact of a solution on the respondents’ overall quality of life and likelihood of solution sharing.
Conclusions: Given that hundreds of millions of people worldwide are afflicted by rare diseases, patient and their caregivers can be a tremendous source of innovation for many who are similarly afflicted. Our findings suggest that many patients could be greatly assisted by improved diffusion of known solutions and best practices to and among patients and their caregivers.},
	language = {en},
	number = {1},
	urldate = {2021-06-21},
	journal = {Orphanet Journal of Rare Diseases},
	author = {Oliveira, Pedro and Zejnilovic, Leid and Canhão, Helena and von Hippel, Eric},
	month = dec,
	year = {2015},
	note = {ZSCC: 0000069},
	pages = {41},
}

Methods: We administered a questionnaire via telephone interviewing to a sample of 500 rare disease patients and caregivers. The solutions reported were pre-screened by the authors for their fit with the self-developed innovation aim of the study. All the reported solutions were then validated for their novelty by two medical professionals. Logistic regression models were used to test the relationships between our key variables, patient innovation and solution sharing. Results: 263 (53%) of our survey respondents reported developing and using a solution to improve management of their diseases. An initial screening removed 81 (16%) solutions for being an obvious misfit to the self-developed innovation aim of the study. This lowered the sample of potentially innovative solutions to 182 (36%). Assessment of novelty and usefulness of the solutions, conducted by two medical evaluators, confirmed that 40 solutions (8%) were indeed novel, while the remaining 142 (28%) were already known to medicine. The likelihood of patient innovation increased as the education level increased (OR 2, p \textless 0.05), and as their perception of limitations imposed by their disease increased (OR 1.3, p \textless 0.05). 55 individuals diffused their solutions to some degree, with 50 of these sharing via direct diffusion to other patients. There is a positive relationship between the impact of a solution on the respondents’ overall quality of life and likelihood of solution sharing. Conclusions: Given that hundreds of millions of people worldwide are afflicted by rare diseases, patient and their caregivers can be a tremendous source of innovation for many who are similarly afflicted. Our findings suggest that many patients could be greatly assisted by improved diffusion of known solutions and best practices to and among patients and their caregivers.

@article{xu_phenopredict_2015,
	title = {{PhenoPredict}: {A} disease phenome-wide drug repositioning approach towards schizophrenia drug discovery},
	volume = {56},
	issn = {1532-0480},
	shorttitle = {{PhenoPredict}},
	doi = {10.1016/j.jbi.2015.06.027},
	abstract = {Schizophrenia (SCZ) is a common complex disorder with poorly understood mechanisms and no effective drug treatments. Despite the high prevalence and vast unmet medical need represented by the disease, many drug companies have moved away from the development of drugs for SCZ. Therefore, alternative strategies are needed for the discovery of truly innovative drug treatments for SCZ. Here, we present a disease phenome-driven computational drug repositioning approach for SCZ. We developed a novel drug repositioning system, PhenoPredict, by inferring drug treatments for SCZ from diseases that are phenotypically related to SCZ. The key to PhenoPredict is the availability of a comprehensive drug treatment knowledge base that we recently constructed. PhenoPredict retrieved all 18 FDA-approved SCZ drugs and ranked them highly (recall=1.0, and average ranking of 8.49\%). When compared to PREDICT, one of the most comprehensive drug repositioning systems currently available, in novel predictions, PhenoPredict represented clear improvements over PREDICT in Precision-Recall (PR) curves, with a significant 98.8\% improvement in the area under curve (AUC) of the PR curves. In addition, we discovered many drug candidates with mechanisms of action fundamentally different from traditional antipsychotics, some of which had published literature evidence indicating their treatment benefits in SCZ patients. In summary, although the fundamental pathophysiological mechanisms of SCZ remain unknown, integrated systems approaches to studying phenotypic connections among diseases may facilitate the discovery of innovative SCZ drugs.},
	language = {eng},
	journal = {Journal of Biomedical Informatics},
	author = {Xu, Rong and Wang, QuanQiu},
	month = aug,
	year = {2015},
	pmid = {26151312},
	pmcid = {PMC4589865},
	note = {ZSCC: 0000032 },
	keywords = {Algorithms, Antipsychotic Agents, Area Under Curve, Computational Biology, Databases, Factual, Disease phenotype, Drug Delivery Systems, Drug Discovery, Drug Repositioning, Drug discovery, Drug repositioning, Knowledge Bases, Phenotype, Reproducibility of Results, Schizophrenia, Software, Systems biology, United States, United States Food and Drug Administration},
	pages = {348--355},
}

Schizophrenia (SCZ) is a common complex disorder with poorly understood mechanisms and no effective drug treatments. Despite the high prevalence and vast unmet medical need represented by the disease, many drug companies have moved away from the development of drugs for SCZ. Therefore, alternative strategies are needed for the discovery of truly innovative drug treatments for SCZ. Here, we present a disease phenome-driven computational drug repositioning approach for SCZ. We developed a novel drug repositioning system, PhenoPredict, by inferring drug treatments for SCZ from diseases that are phenotypically related to SCZ. The key to PhenoPredict is the availability of a comprehensive drug treatment knowledge base that we recently constructed. PhenoPredict retrieved all 18 FDA-approved SCZ drugs and ranked them highly (recall=1.0, and average ranking of 8.49%). When compared to PREDICT, one of the most comprehensive drug repositioning systems currently available, in novel predictions, PhenoPredict represented clear improvements over PREDICT in Precision-Recall (PR) curves, with a significant 98.8% improvement in the area under curve (AUC) of the PR curves. In addition, we discovered many drug candidates with mechanisms of action fundamentally different from traditional antipsychotics, some of which had published literature evidence indicating their treatment benefits in SCZ patients. In summary, although the fundamental pathophysiological mechanisms of SCZ remain unknown, integrated systems approaches to studying phenotypic connections among diseases may facilitate the discovery of innovative SCZ drugs.

@incollection{probst_epistemological_2015,
	address = {Cham},
	title = {Epistemological {Issues} in {Diagnosis} and {Assessment}},
	isbn = {978-3-319-17773-1 978-3-319-17774-8},
	url = {http://link.springer.com/10.1007/978-3-319-17774-8_2},
	abstract = {This book begins with a thoughtful exploration of two fundamental questions that underlie all clinical decisions. First, what exactly is a “mental disorder,” as opposed to other kinds of suffering or maladaptive behavior that we would call non-mental disorders? What makes a disorder specifically mental? And second, on what do we base these definitions and distinctions? What do we consider reliable (and unreliable) sources of knowledge, and what are some of the pitfalls in our assumptions about what we “know” and how we’ve come to “know” it? Common cognitive errors are explored, along with their consequences. These include circular reasoning, the difficulty of determining threshold or cut-off point, assumptions about causality, and the problems inherent in mental heuristics such as anchoring and availability. The chapter then explores the role of labels and labeling theory, the aims and limitations of classification systems such as the DSM, and the challenge of trying to develop a way to think about mental disorder that is useful for both general purposes (to make predictions based on shared characteristics) and specific aims (to understand and help particular individuals).},
	language = {en},
	urldate = {2020-03-12},
	booktitle = {Critical {Thinking} in {Clinical} {Assessment} and {Diagnosis}},
	publisher = {Springer International Publishing},
	author = {Probst, Barbara},
	editor = {Probst, Barbara},
	year = {2015},
	doi = {10.1007/978-3-319-17774-8_2},
	note = {ZSCC: 0000001 },
	pages = {15--44},
}

This book begins with a thoughtful exploration of two fundamental questions that underlie all clinical decisions. First, what exactly is a “mental disorder,” as opposed to other kinds of suffering or maladaptive behavior that we would call non-mental disorders? What makes a disorder specifically mental? And second, on what do we base these definitions and distinctions? What do we consider reliable (and unreliable) sources of knowledge, and what are some of the pitfalls in our assumptions about what we “know” and how we’ve come to “know” it? Common cognitive errors are explored, along with their consequences. These include circular reasoning, the difficulty of determining threshold or cut-off point, assumptions about causality, and the problems inherent in mental heuristics such as anchoring and availability. The chapter then explores the role of labels and labeling theory, the aims and limitations of classification systems such as the DSM, and the challenge of trying to develop a way to think about mental disorder that is useful for both general purposes (to make predictions based on shared characteristics) and specific aims (to understand and help particular individuals).

@article{cole_efficacy_2015,
	title = {Efficacy of {Transcranial} {Magnetic} {Stimulation} ({TMS}) in the {Treatment} of {Schizophrenia}: {A} {Review} of the {Literature} to {Date}},
	volume = {12},
	issn = {2158-8333},
	shorttitle = {Efficacy of {Transcranial} {Magnetic} {Stimulation} ({TMS}) in the {Treatment} of {Schizophrenia}},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4558786/},
	abstract = {We reviewed the literature on transcranial magnetic stimulation and its uses and efficacy in schizophrenia. Multiple sources were examined on transcranial magnetic stimulation efficacy in relieving positive and negative symptoms of schizophrenia. Literature review was conducted via Ovid Medline and PubMed databases. We found multiple published studies and metaanalyses that give evidence that repetitive transcranial magnetic stimulation can have benefit in relieving positive and negative symptoms of schizophrenia, particularly auditory hallucinations. These findings should encourage the psychiatric community to expand research into other applications for which transcranial magnetic stimulation may be used to treat patients with psychiatric disability.},
	number = {7-8},
	urldate = {2021-04-10},
	journal = {Innovations in Clinical Neuroscience},
	author = {Cole, Jonathan C. and Green Bernacki, Carolyn and Helmer, Amanda and Pinninti, Narsimha and O’reardon, John P.},
	year = {2015},
	pmid = {26351619},
	pmcid = {PMC4558786},
	note = {ZSCC: NoCitationData[s0] },
	pages = {12--19},
}

We reviewed the literature on transcranial magnetic stimulation and its uses and efficacy in schizophrenia. Multiple sources were examined on transcranial magnetic stimulation efficacy in relieving positive and negative symptoms of schizophrenia. Literature review was conducted via Ovid Medline and PubMed databases. We found multiple published studies and metaanalyses that give evidence that repetitive transcranial magnetic stimulation can have benefit in relieving positive and negative symptoms of schizophrenia, particularly auditory hallucinations. These findings should encourage the psychiatric community to expand research into other applications for which transcranial magnetic stimulation may be used to treat patients with psychiatric disability.

@article{cole_efficacy_2015-1,
	title = {Efficacy of {Transcranial} {Magnetic} {Stimulation} ({TMS}) in the {Treatment} of {Schizophrenia}: {A} {Review} of the {Literature} to {Date}},
	volume = {12},
	issn = {2158-8333},
	shorttitle = {Efficacy of {Transcranial} {Magnetic} {Stimulation} ({TMS}) in the {Treatment} of {Schizophrenia}},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4558786/},
	abstract = {We reviewed the literature on transcranial magnetic stimulation and its uses and efficacy in schizophrenia. Multiple sources were examined on transcranial magnetic stimulation efficacy in relieving positive and negative symptoms of schizophrenia. Literature review was conducted via Ovid Medline and PubMed databases. We found multiple published studies and metaanalyses that give evidence that repetitive transcranial magnetic stimulation can have benefit in relieving positive and negative symptoms of schizophrenia, particularly auditory hallucinations. These findings should encourage the psychiatric community to expand research into other applications for which transcranial magnetic stimulation may be used to treat patients with psychiatric disability.},
	number = {7-8},
	urldate = {2021-04-10},
	journal = {Innovations in Clinical Neuroscience},
	author = {Cole, Jonathan C. and Green Bernacki, Carolyn and Helmer, Amanda and Pinninti, Narsimha and O’reardon, John P.},
	year = {2015},
	pmid = {26351619},
	pmcid = {PMC4558786},
	note = {ZSCC: NoCitationData[s0] },
	pages = {12--19},
}

We reviewed the literature on transcranial magnetic stimulation and its uses and efficacy in schizophrenia. Multiple sources were examined on transcranial magnetic stimulation efficacy in relieving positive and negative symptoms of schizophrenia. Literature review was conducted via Ovid Medline and PubMed databases. We found multiple published studies and metaanalyses that give evidence that repetitive transcranial magnetic stimulation can have benefit in relieving positive and negative symptoms of schizophrenia, particularly auditory hallucinations. These findings should encourage the psychiatric community to expand research into other applications for which transcranial magnetic stimulation may be used to treat patients with psychiatric disability.

@article{liedtka_perspective_2015,
	title = {Perspective: {Linking} {Design} {Thinking} with {Innovation} {Outcomes} through {Cognitive} {Bias} {Reduction}},
	volume = {32},
	copyright = {© 2014 Product Development \& Management Association},
	issn = {1540-5885},
	shorttitle = {Perspective},
	url = {https://onlinelibrary.wiley.com/doi/abs/10.1111/jpim.12163},
	doi = {https://doi.org/10.1111/jpim.12163},
	abstract = {“Design thinking” has generated significant attention in the business press and has been heralded as a novel problem-solving methodology well suited to the often-cited challenges business organizations face in encouraging innovation and growth. Yet the specific mechanisms through which the use of design, approached as a thought process, might improve innovation outcomes have not received significant attention from business scholars. In particular, its utility has only rarely been linked to the academic literature on individual cognition and decision-making. This perspective piece advocates addressing this omission by examining “design thinking” as a practice potentially valuable for improving innovation outcomes by helping decision-makers reduce their individual level cognitive biases. In this essay, I first review the assumptions, principles, and key process tools associated with design thinking. I then establish its foundation in the decision-making literature, drawing on an extensive body of research on cognitive biases and their impact. The essay concludes by advancing a set of propositions and research implications, aiming to demonstrate one particular path that future research might take in assessing the utility of design thinking as a method for improving organizational outcomes related to innovation. In doing so, it seeks to address the challenge of conducting academic research on a practice that is obviously popular in management circles but appears resistant to rigorous empirical inquiry because of the multifaceted nature of its “basket” of tools and processes and the complexity of measuring the outcomes it produces.},
	language = {en},
	number = {6},
	urldate = {2021-04-09},
	journal = {Journal of Product Innovation Management},
	author = {Liedtka, Jeanne},
	year = {2015},
	note = {ZSCC: 0000519 
\_eprint: https://onlinelibrary.wiley.com/doi/pdf/10.1111/jpim.12163},
	pages = {925--938},
}

“Design thinking” has generated significant attention in the business press and has been heralded as a novel problem-solving methodology well suited to the often-cited challenges business organizations face in encouraging innovation and growth. Yet the specific mechanisms through which the use of design, approached as a thought process, might improve innovation outcomes have not received significant attention from business scholars. In particular, its utility has only rarely been linked to the academic literature on individual cognition and decision-making. This perspective piece advocates addressing this omission by examining “design thinking” as a practice potentially valuable for improving innovation outcomes by helping decision-makers reduce their individual level cognitive biases. In this essay, I first review the assumptions, principles, and key process tools associated with design thinking. I then establish its foundation in the decision-making literature, drawing on an extensive body of research on cognitive biases and their impact. The essay concludes by advancing a set of propositions and research implications, aiming to demonstrate one particular path that future research might take in assessing the utility of design thinking as a method for improving organizational outcomes related to innovation. In doing so, it seeks to address the challenge of conducting academic research on a practice that is obviously popular in management circles but appears resistant to rigorous empirical inquiry because of the multifaceted nature of its “basket” of tools and processes and the complexity of measuring the outcomes it produces.

@article{martinez_drugnet_2015,
	title = {{DrugNet}: network-based drug-disease prioritization by integrating heterogeneous data},
	volume = {63},
	issn = {1873-2860},
	shorttitle = {{DrugNet}},
	doi = {10.1016/j.artmed.2014.11.003},
	abstract = {OBJECTIVE: Computational drug repositioning can lead to a considerable reduction in cost and time in any drug development process. Recent approaches have addressed the network-based nature of biological information for performing complex prioritization tasks. In this work, we propose a new methodology based on heterogeneous network prioritization that can aid researchers in the drug repositioning process.
METHODS: We have developed DrugNet, a new methodology for drug-disease and disease-drug prioritization. Our approach is based on a network-based prioritization method called ProphNet which has recently been developed by the authors. ProphNet is able to integrate data from complex networks involving a wide range of types of elements and interactions. In this work, we built a network of interconnected drugs, proteins and diseases and applied DrugNet to different types of tests for drug repositioning.
RESULTS: We tested the performance of our approach on different validation tests, including cross validation and tests based on real clinical trials. DrugNet achieved a mean AUC value of 0.9552±0.0015 in 5-fold cross validation tests, and a mean AUC value of 0.8364 for tests based on recent clinical trials (phases 0-4) not present in our data. These results suggest that DrugNet could be very useful for discovering new drug uses. We also studied specific cases of particular interest, proving the benefits of heterogeneous data integration in this problem.
CONCLUSIONS: Our methodology suggests that new drugs can be repositioned by generating ranked lists of drugs based on a given disease query or vice versa. Our study shows that the simultaneous integration of information about diseases, drugs and targets can lead to a significant improvement in drug repositioning tasks. DrugNet is available as a web tool from http://genome2.ugr.es/drugnet/ (accessed 23.09.14). Matlab source code is also available on the website.},
	language = {eng},
	number = {1},
	journal = {Artificial Intelligence in Medicine},
	author = {Martínez, Víctor and Navarro, Carmen and Cano, Carlos and Fajardo, Waldo and Blanco, Armando},
	month = jan,
	year = {2015},
	pmid = {25704113},
	note = {ZSCC: NoCitationData[s0] },
	keywords = {Area Under Curve, Computational Biology, Computer Simulation, Data Mining, Data integration, Databases, Factual, Disease networks, Drug Repositioning, Drug repositioning, Flow propagation, Humans, Models, Theoretical, Network-based prioritization, ROC Curve, Reproducibility of Results, Systems Integration},
	pages = {41--49},
}

OBJECTIVE: Computational drug repositioning can lead to a considerable reduction in cost and time in any drug development process. Recent approaches have addressed the network-based nature of biological information for performing complex prioritization tasks. In this work, we propose a new methodology based on heterogeneous network prioritization that can aid researchers in the drug repositioning process. METHODS: We have developed DrugNet, a new methodology for drug-disease and disease-drug prioritization. Our approach is based on a network-based prioritization method called ProphNet which has recently been developed by the authors. ProphNet is able to integrate data from complex networks involving a wide range of types of elements and interactions. In this work, we built a network of interconnected drugs, proteins and diseases and applied DrugNet to different types of tests for drug repositioning. RESULTS: We tested the performance of our approach on different validation tests, including cross validation and tests based on real clinical trials. DrugNet achieved a mean AUC value of 0.9552±0.0015 in 5-fold cross validation tests, and a mean AUC value of 0.8364 for tests based on recent clinical trials (phases 0-4) not present in our data. These results suggest that DrugNet could be very useful for discovering new drug uses. We also studied specific cases of particular interest, proving the benefits of heterogeneous data integration in this problem. CONCLUSIONS: Our methodology suggests that new drugs can be repositioned by generating ranked lists of drugs based on a given disease query or vice versa. Our study shows that the simultaneous integration of information about diseases, drugs and targets can lead to a significant improvement in drug repositioning tasks. DrugNet is available as a web tool from http://genome2.ugr.es/drugnet/ (accessed 23.09.14). Matlab source code is also available on the website.

@article{oliveira_innovation_2015,
	title = {Innovation by patients with rare diseases and chronic needs},
	volume = {10},
	issn = {1750-1172},
	url = {https://doi.org/10.1186/s13023-015-0257-2},
	doi = {10.1186/s13023-015-0257-2},
	abstract = {We provide the first empirical exploration of disease-related innovation by patients and their caregivers. Our aims were to explore to what degree do patients develop innovative solutions; how many of these are unique developments; and do these solutions have positive perceived impact on the patients’ overall quality of life? In addition, we explored the factors associated with patient innovation development, and sharing of the solutions that the patients developed.},
	number = {1},
	urldate = {2021-03-18},
	journal = {Orphanet Journal of Rare Diseases},
	author = {Oliveira, Pedro and Zejnilovic, Leid and Canhão, Helena and von Hippel, Eric},
	month = apr,
	year = {2015},
	note = {ZSCC: 0000063},
	keywords = {Diffusion of Innovation, Patient Innovation, Rare Diseases, User Innovation in Health},
	pages = {41},
}

We provide the first empirical exploration of disease-related innovation by patients and their caregivers. Our aims were to explore to what degree do patients develop innovative solutions; how many of these are unique developments; and do these solutions have positive perceived impact on the patients’ overall quality of life? In addition, we explored the factors associated with patient innovation development, and sharing of the solutions that the patients developed.

@article{santarnecchi_enhancing_2015,
	title = {Enhancing cognition using transcranial electrical stimulation},
	volume = {4},
	issn = {23521546},
	url = {https://linkinghub.elsevier.com/retrieve/pii/S2352154615000819},
	doi = {10.1016/j.cobeha.2015.06.003},
	language = {en},
	urldate = {2020-11-11},
	journal = {Current Opinion in Behavioral Sciences},
	author = {Santarnecchi, Emiliano and Brem, Anna-Katharine and Levenbaum, Erica and Thompson, Todd and Kadosh, Roi Cohen and Pascual-Leone, Alvaro},
	month = aug,
	year = {2015},
	note = {ZSCC: 0000101},
	pages = {171--178},
}

@article{guastella_single_2015,
	series = {Reproductive hormones and schizophrenia},
	title = {A single dose of oxytocin nasal spray improves higher-order social cognition in schizophrenia},
	volume = {168},
	issn = {0920-9964},
	url = {http://www.sciencedirect.com/science/article/pii/S0920996415003205},
	doi = {10.1016/j.schres.2015.06.005},
	abstract = {Schizophrenia is associated with significant impairments in both higher and lower order social cognitive performance and these impairments contribute to poor social functioning. People with schizophrenia report poor social functioning to be one of their greatest unmet treatment needs. Recent studies have suggested the potential of oxytocin as such a treatment, but mixed results render it uncertain what aspects of social cognition are improved by oxytocin and, subsequently, how oxytocin might best be applied as a therapeutic. The aim of this study was to determine whether a single dose of oxytocin improved higher-order and lower-order social cognition performance for patients with schizophrenia across a well-established battery of social cognition tests. Twenty-one male patients received both a single dose of oxytocin nasal spray (24IU) and a placebo, two weeks apart in a randomized within-subjects placebo controlled design. Following each administration, participants completed the social cognition tasks, as well as a test of general neurocognition. Results revealed that oxytocin particularly enhanced performance on higher order social cognition tasks, with no effects on general neurocognition. Results for individual tasks showed most improvement on tests measuring appreciation of indirect hints and recognition of social faux pas. These results suggest that oxytocin, if combined to enhance social cognition learning, may be beneficial when targeted at higher order social cognition domains. This study also suggests that these higher order tasks, which assess social cognitive processing in a social communication context, may provide useful markers of response to oxytocin in schizophrenia.},
	language = {en},
	number = {3},
	urldate = {2020-10-06},
	journal = {Schizophrenia Research},
	author = {Guastella, Adam J. and Ward, Philip B. and Hickie, Ian B. and Shahrestani, Sara and Hodge, Marie Antoinette Redoblado and Scott, Elizabeth M. and Langdon, Robyn},
	month = nov,
	year = {2015},
	note = {ZSCC: 0000061},
	keywords = {Emotion recognition, Hormone, Neuropeptides, Psychosis, Social behavior},
	pages = {628--633},
}

Schizophrenia is associated with significant impairments in both higher and lower order social cognitive performance and these impairments contribute to poor social functioning. People with schizophrenia report poor social functioning to be one of their greatest unmet treatment needs. Recent studies have suggested the potential of oxytocin as such a treatment, but mixed results render it uncertain what aspects of social cognition are improved by oxytocin and, subsequently, how oxytocin might best be applied as a therapeutic. The aim of this study was to determine whether a single dose of oxytocin improved higher-order and lower-order social cognition performance for patients with schizophrenia across a well-established battery of social cognition tests. Twenty-one male patients received both a single dose of oxytocin nasal spray (24IU) and a placebo, two weeks apart in a randomized within-subjects placebo controlled design. Following each administration, participants completed the social cognition tasks, as well as a test of general neurocognition. Results revealed that oxytocin particularly enhanced performance on higher order social cognition tasks, with no effects on general neurocognition. Results for individual tasks showed most improvement on tests measuring appreciation of indirect hints and recognition of social faux pas. These results suggest that oxytocin, if combined to enhance social cognition learning, may be beneficial when targeted at higher order social cognition domains. This study also suggests that these higher order tasks, which assess social cognitive processing in a social communication context, may provide useful markers of response to oxytocin in schizophrenia.

@incollection{hunsley_controversial_2015,
	address = {New York, NY, US},
	title = {Controversial and questionable assessment techniques},
	isbn = {978-1-4625-1789-3 978-1-4625-1751-0 978-1-4625-1759-6},
	abstract = {The past decade has seen many important developments in the field of clinical assessment. These include (1) statistical approaches for exploring consistency and variability in reliability estimates, (2) theoretical and methodological advances in conceptualizing construct validity, (3) a renewed focus on the utility of assessment data in the clinical enterprise, (4) a compelling, empirically based rationale for routinely monitoring the impact of clinical interventions, and (5) initial attempts to delineate the nature and implications of an evidence-based approach to assessment. Despite this progress, there is widespread use of clinical assessment practices and instruments that lack a strong scientific foundation. In this chapter, we first provide introductory comments on key scientific elements of clinical assessment, and then we examine a subset of commonly used instruments whose use is not justified by scientific evidence. (PsycInfo Database Record (c) 2020 APA, all rights reserved)},
	booktitle = {Science and pseudoscience in clinical psychology, 2nd ed},
	publisher = {The Guilford Press},
	author = {Hunsley, John and Lee, Catherine M. and Wood, James M. and Taylor, Whitney},
	year = {2015},
	note = {ZSCC: 0000145},
	keywords = {Best Practices, Evidence Based Practice, Intervention, Psychological Assessment, Sciences},
	pages = {42--82},
}

The past decade has seen many important developments in the field of clinical assessment. These include (1) statistical approaches for exploring consistency and variability in reliability estimates, (2) theoretical and methodological advances in conceptualizing construct validity, (3) a renewed focus on the utility of assessment data in the clinical enterprise, (4) a compelling, empirically based rationale for routinely monitoring the impact of clinical interventions, and (5) initial attempts to delineate the nature and implications of an evidence-based approach to assessment. Despite this progress, there is widespread use of clinical assessment practices and instruments that lack a strong scientific foundation. In this chapter, we first provide introductory comments on key scientific elements of clinical assessment, and then we examine a subset of commonly used instruments whose use is not justified by scientific evidence. (PsycInfo Database Record (c) 2020 APA, all rights reserved)

@article{lebowitz_emphasizing_2015,
	title = {Emphasizing {Malleability} in the biology of depression: {Durable} effects on perceived agency and prognostic pessimism},
	volume = {71},
	issn = {00057967},
	shorttitle = {Emphasizing {Malleability} in the biology of depression},
	url = {https://linkinghub.elsevier.com/retrieve/pii/S0005796715001047},
	doi = {10.1016/j.brat.2015.06.005},
	abstract = {Biological attributions for depression, which are currently ascendant, can lead to prognostic pessimism—the perception that symptoms are relatively immutable and unlikely to abate (Kvaale, Haslam, \& Gottdiener, 2013; Lebowitz, Ahn, \& Nolen-Hoeksema, 2013). Among symptomatic individuals, this may have important clinical ramifications, as reduced confidence in one’s own ability to overcome depression carries the risk of becoming a self-fulfilling prophecy. Previous research (Lebowitz, Ahn, et al., 2013) has demonstrated that educational interventions teaching symptomatic individuals about how the effects of genetic and neurobiological factors involved in depression are malleable and can be modified by experiences and environmental factors can reduce prognostic pessimism. While previous research demonstrated such effects only in the immediate term, the present research extends these findings by testing whether such benefits persist six weeks after the intervention. Indeed, among individuals who initially considered biological factors to play a major role in influencing their levels of depression, exposure to malleability-focused psychoeducation reduced levels of depression-related prognostic pessimism and stronger belief in their ability to regulate their moods. Critically, this benefit persisted six weeks after the intervention. Clinical implications of the findings are discussed.},
	language = {en},
	urldate = {2020-03-13},
	journal = {Behaviour Research and Therapy},
	author = {Lebowitz, Matthew S. and Ahn, Woo-kyoung},
	month = aug,
	year = {2015},
	keywords = {Illness Attribution/Appraisal, agency, biological explanations, depression, prognostic pessimism, psychoeducation},
	pages = {125--130},
}

Biological attributions for depression, which are currently ascendant, can lead to prognostic pessimism—the perception that symptoms are relatively immutable and unlikely to abate (Kvaale, Haslam, & Gottdiener, 2013; Lebowitz, Ahn, & Nolen-Hoeksema, 2013). Among symptomatic individuals, this may have important clinical ramifications, as reduced confidence in one’s own ability to overcome depression carries the risk of becoming a self-fulfilling prophecy. Previous research (Lebowitz, Ahn, et al., 2013) has demonstrated that educational interventions teaching symptomatic individuals about how the effects of genetic and neurobiological factors involved in depression are malleable and can be modified by experiences and environmental factors can reduce prognostic pessimism. While previous research demonstrated such effects only in the immediate term, the present research extends these findings by testing whether such benefits persist six weeks after the intervention. Indeed, among individuals who initially considered biological factors to play a major role in influencing their levels of depression, exposure to malleability-focused psychoeducation reduced levels of depression-related prognostic pessimism and stronger belief in their ability to regulate their moods. Critically, this benefit persisted six weeks after the intervention. Clinical implications of the findings are discussed.

@article{meddings_recovery_2015,
	title = {Recovery colleges: quality and outcomes},
	volume = {19},
	issn = {2042-8308},
	shorttitle = {Recovery colleges},
	url = {https://www.emerald.com/insight/content/doi/10.1108/MHSI-08-2015-0035/full/html},
	doi = {10.1108/MHSI-08-2015-0035},
	abstract = {Purpose – The purpose of this paper is to explore the process of using a co-production partnership approach in the development of a Recovery College pilot. Design/methodology/approach – This is a case study of the co-production process, using action research to learn from ongoing reflection, mid-project review and feedback questionnaires. Findings – The partnership process is an integral and valued aspect of the Recovery College. Challenges include different organisational cultures and processes and the additional time required. Mutual respect, appreciation of different expertise, communication, a shared vision and development plan have been key to success. The paper focused on governance and fidelity; recruitment and training; curriculum development and evaluation. People are enthusiastic and motivated. Co-production and equal partnership are a valuable approach to developing a Recovery College.},
	language = {en},
	number = {4},
	urldate = {2020-04-02},
	journal = {Mental Health and Social Inclusion},
	author = {Meddings, Sara and McGregor, Jane and Roeg, Waldo and Shepherd, Geoff},
	month = nov,
	year = {2015},
	note = {ZSCC: 0000038},
	pages = {212--221},
}

Purpose – The purpose of this paper is to explore the process of using a co-production partnership approach in the development of a Recovery College pilot. Design/methodology/approach – This is a case study of the co-production process, using action research to learn from ongoing reflection, mid-project review and feedback questionnaires. Findings – The partnership process is an integral and valued aspect of the Recovery College. Challenges include different organisational cultures and processes and the additional time required. Mutual respect, appreciation of different expertise, communication, a shared vision and development plan have been key to success. The paper focused on governance and fidelity; recruitment and training; curriculum development and evaluation. People are enthusiastic and motivated. Co-production and equal partnership are a valuable approach to developing a Recovery College.

@article{micoulaud_neuroenhancement_2015,
	title = {Neuroenhancement in {Healthy} {Adults}, {Part} {I}: {Pharmaceutical} {Cognitive} {Enhancement}: {A} {Systematic} {Review}},
	volume = {06},
	issn = {21559627},
	shorttitle = {Neuroenhancement in {Healthy} {Adults}, {Part} {I}},
	url = {https://www.omicsonline.org/open-access/neuroenhancement-in-healthy-adults-part-i-pharmaceutical-cognitiveenhancement-a-systematic-review-2155-9627-1000213.php?aid=51586},
	doi = {10.4172/2155-9627.1000213},
	abstract = {The term neuroenhancement refers to improvement in the cognitive, emotional and motivational functions of healthy individuals through inter alia, the use of drugs. This popular topic attracts attention both from the general public and the scientific community. Our objective is to summarize in a synthetic review the data of randomized placebo-controlled trials that assessed cognitive effects of administration of neuroenhancers in non-sleep-deprived healthy adults compared to placebo. The major outcomes were attention, memory, learning, executive functions, and vigilance/wakefulness. Details on the pharmacological profile, effectiveness and safety for each drug are provided. We classify them according to their recognized major primary mode of action, namely catecholaminergics (methylphenidate, modafinil, amphetamines, tolcapone, pramipexole, guanfacine, antidepressants), cholinergics (nicotine, varenicline, acetylcholine esterase inhibitors, anticholinergics), glutamatergics (ampakines, memantine, Dcycloserine), histaminergics, and non-specified (caffeine, racetams/phosphodiesterase inhibitors and glucocorticoids).},
	language = {en},
	number = {02},
	urldate = {2020-04-02},
	journal = {Journal of Clinical Research \& Bioethics},
	author = {Micoulaud, Fond G},
	year = {2015},
	note = {ZSCC: 0000019},
}

The term neuroenhancement refers to improvement in the cognitive, emotional and motivational functions of healthy individuals through inter alia, the use of drugs. This popular topic attracts attention both from the general public and the scientific community. Our objective is to summarize in a synthetic review the data of randomized placebo-controlled trials that assessed cognitive effects of administration of neuroenhancers in non-sleep-deprived healthy adults compared to placebo. The major outcomes were attention, memory, learning, executive functions, and vigilance/wakefulness. Details on the pharmacological profile, effectiveness and safety for each drug are provided. We classify them according to their recognized major primary mode of action, namely catecholaminergics (methylphenidate, modafinil, amphetamines, tolcapone, pramipexole, guanfacine, antidepressants), cholinergics (nicotine, varenicline, acetylcholine esterase inhibitors, anticholinergics), glutamatergics (ampakines, memantine, Dcycloserine), histaminergics, and non-specified (caffeine, racetams/phosphodiesterase inhibitors and glucocorticoids).

@article{meyer_view_2015,
	title = {A {View} {Through} the {Lens} of {Practice}},
	volume = {47},
	language = {en},
	number = {4},
	journal = {Design Thinking},
	author = {Meyer, Lisa M},
	year = {2015},
	note = {ZSCC: NoCitationData[s0]},
	pages = {7},
}

@phdthesis{richmond_development_2015,
	title = {Development of an {Instrument} {Measuring} {Existential} {Authenticity}},
	url = {https://etd.ohiolink.edu/pg_10?0::NO:10:P10_ACCESSION_NUM:ucin1439306443},
	language = {en},
	urldate = {2020-03-22},
	school = {University of Cincinnati},
	author = {Richmond, Misty M.},
	year = {2015},
}

@article{mohatt_recovery-oriented_2015,
	title = {From {Recovery}-{Oriented} {Care} to {Public} {Health}: {Case} {Studies} of {Participatory} {Public} {Art} as a {Pathway} to {Wellness} for {Persons} with {Behavioral} {Health} {Challenges}},
	volume = {2},
	issn = {2198-9834, 2198-963X},
	shorttitle = {From {Recovery}-{Oriented} {Care} to {Public} {Health}},
	url = {http://link.springer.com/10.1007/s40737-015-0024-7},
	doi = {10.1007/s40737-015-0024-7},
	abstract = {The objective of this study is to identify individual mechanisms of change that result from engaging in an innovative participatory public art project for persons with significant behavioral health challenges. We present two case studies that examine how participatory public art promotes recovery and wellness. This research is part of a larger, multilevel comparative outcome trial on the impact of participatory public art on the health and well-being of adults in recovery from mental illness and addiction and on the distressed city neighborhoods in which they live. The case studies describe the unique ways in which participatory public art contributed to key recovery domains of growth in friendship, self-discovery, giving back, and hope. The two cases indicate that the development of a strengthsbased sense of self through art was accompanied by a growth in personal social responsibility. The two cases also indicate that participatory public art may have a profound impact on the internalization of stigma. The findings support the value of participatory public art as a strategy for blending recovery and public health perspectives to promote both individual and community wellness.},
	language = {en},
	number = {1},
	urldate = {2020-03-19},
	journal = {Journal of Psychosocial Rehabilitation and Mental Health},
	author = {Mohatt, Nathaniel Vincent and Hunter, Bronwyn A. and Matlin, Samantha L. and Golden, Jane and Evans, Arthur C. and Tebes, Jacob Kraemer},
	month = jun,
	year = {2015},
	pages = {9--18},
}

The objective of this study is to identify individual mechanisms of change that result from engaging in an innovative participatory public art project for persons with significant behavioral health challenges. We present two case studies that examine how participatory public art promotes recovery and wellness. This research is part of a larger, multilevel comparative outcome trial on the impact of participatory public art on the health and well-being of adults in recovery from mental illness and addiction and on the distressed city neighborhoods in which they live. The case studies describe the unique ways in which participatory public art contributed to key recovery domains of growth in friendship, self-discovery, giving back, and hope. The two cases indicate that the development of a strengthsbased sense of self through art was accompanied by a growth in personal social responsibility. The two cases also indicate that participatory public art may have a profound impact on the internalization of stigma. The findings support the value of participatory public art as a strategy for blending recovery and public health perspectives to promote both individual and community wellness.

@article{strong_counselling_2015,
	title = {Counselling the (self?) diagnosed client: generative and reflective conversations},
	volume = {43},
	issn = {0306-9885, 1469-3534},
	shorttitle = {Counselling the (self?},
	url = {http://www.tandfonline.com/doi/full/10.1080/03069885.2014.996736},
	doi = {10.1080/03069885.2014.996736},
	language = {en},
	number = {5},
	urldate = {2020-03-19},
	journal = {British Journal of Guidance \& Counselling},
	author = {Strong, Tom and Ross, Karen H. and Sesma-Vazquez, Monica},
	month = oct,
	year = {2015},
	pages = {598--610},
}

@article{zautra_embodiment_2015,
	title = {Embodiment, {Interaction}, and {Experience}: {Toward} a {Comprehensive} {Model} in {Addiction} {Science}},
	volume = {82},
	issn = {0031-8248, 1539-767X},
	shorttitle = {Embodiment, {Interaction}, and {Experience}},
	url = {https://www.journals.uchicago.edu/doi/10.1086/683437},
	doi = {10.1086/683437},
	language = {en},
	number = {5},
	urldate = {2020-03-19},
	journal = {Philosophy of Science},
	author = {Zautra, Nicholas},
	month = dec,
	year = {2015},
	pages = {1023--1034},
}

@incollection{probst_epistemological_2015,
	address = {Cham},
	title = {Epistemological {Issues} in {Diagnosis} and {Assessment}},
	isbn = {978-3-319-17773-1 978-3-319-17774-8},
	url = {http://link.springer.com/10.1007/978-3-319-17774-8_2},
	abstract = {This book begins with a thoughtful exploration of two fundamental questions that underlie all clinical decisions. First, what exactly is a “mental disorder,” as opposed to other kinds of suffering or maladaptive behavior that we would call non-mental disorders? What makes a disorder specifically mental? And second, on what do we base these definitions and distinctions? What do we consider reliable (and unreliable) sources of knowledge, and what are some of the pitfalls in our assumptions about what we “know” and how we’ve come to “know” it? Common cognitive errors are explored, along with their consequences. These include circular reasoning, the difficulty of determining threshold or cut-off point, assumptions about causality, and the problems inherent in mental heuristics such as anchoring and availability. The chapter then explores the role of labels and labeling theory, the aims and limitations of classification systems such as the DSM, and the challenge of trying to develop a way to think about mental disorder that is useful for both general purposes (to make predictions based on shared characteristics) and specific aims (to understand and help particular individuals).},
	language = {en},
	urldate = {2020-03-12},
	booktitle = {Critical {Thinking} in {Clinical} {Assessment} and {Diagnosis}},
	publisher = {Springer International Publishing},
	author = {Probst, Barbara},
	editor = {Probst, Barbara},
	year = {2015},
	doi = {10.1007/978-3-319-17774-8_2},
	pages = {15--44},
}

This book begins with a thoughtful exploration of two fundamental questions that underlie all clinical decisions. First, what exactly is a “mental disorder,” as opposed to other kinds of suffering or maladaptive behavior that we would call non-mental disorders? What makes a disorder specifically mental? And second, on what do we base these definitions and distinctions? What do we consider reliable (and unreliable) sources of knowledge, and what are some of the pitfalls in our assumptions about what we “know” and how we’ve come to “know” it? Common cognitive errors are explored, along with their consequences. These include circular reasoning, the difficulty of determining threshold or cut-off point, assumptions about causality, and the problems inherent in mental heuristics such as anchoring and availability. The chapter then explores the role of labels and labeling theory, the aims and limitations of classification systems such as the DSM, and the challenge of trying to develop a way to think about mental disorder that is useful for both general purposes (to make predictions based on shared characteristics) and specific aims (to understand and help particular individuals).

@misc{botton_happy_2014,
	title = {The {Happy}, {Sexy}, {Skinny}, {Pill}?},
	url = {https://www.harpersbazaar.com/beauty/health-wellness-articles/the-happy-sexy-skinny-pill},
	abstract = {Wellbutrin, an antidepressant that can spur weight loss and boost libido, is on everyone's lips. Sari Botton reveals why she's on auto-refill.},
	language = {en-US},
	urldate = {2021-12-28},
	journal = {Harper's BAZAAR},
	author = {Botton, Sari},
	month = feb,
	year = {2014},
	note = {Section: Mind \& Body},
}

Wellbutrin, an antidepressant that can spur weight loss and boost libido, is on everyone's lips. Sari Botton reveals why she's on auto-refill.

@article{greenhalgh_evidence_2014,
	title = {Evidence based medicine: a movement in crisis?},
	volume = {348},
	issn = {0959-8138},
	shorttitle = {Evidence based medicine},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4056639/},
	doi = {10.1136/bmj.g3725},
	abstract = {Trisha Greenhalgh and colleagues argue that, although evidence based medicine has had many benefits, it has also had some negative unintended consequences. They offer a preliminary agenda for the movement’s renaissance, refocusing on providing useable evidence that can be combined with context and professional expertise so that individual patients get optimal treatment},
	urldate = {2021-07-12},
	journal = {The BMJ},
	author = {Greenhalgh, Trisha and Howick, Jeremy and Maskrey, Neal},
	month = jun,
	year = {2014},
	pmid = {24927763},
	pmcid = {PMC4056639},
	pages = {g3725},
}

Trisha Greenhalgh and colleagues argue that, although evidence based medicine has had many benefits, it has also had some negative unintended consequences. They offer a preliminary agenda for the movement’s renaissance, refocusing on providing useable evidence that can be combined with context and professional expertise so that individual patients get optimal treatment

@article{gururajan_is_2014,
	title = {Is the {mTOR}-signalling cascade disrupted in {Schizophrenia}?},
	volume = {129},
	issn = {1471-4159},
	url = {https://onlinelibrary.wiley.com/doi/abs/10.1111/jnc.12622},
	doi = {https://doi.org/10.1111/jnc.12622},
	abstract = {The mammalian target of rapamycin (mTOR) signalling cascade is involved in the intracellular regulation of protein synthesis, specifically for proteins involved in controlling neuronal morphology and facilitating synaptic plasticity. Research has revealed that the activity of the mTOR cascade is influenced by several extracellular and environmental factors that have been implicated in schizophrenia. Therefore, there is reason to believe that one of the downstream consequences of dysfunction or hypofunction of these factors in schizophrenia is disrupted mTOR signalling and hence impaired protein synthesis. This results in abnormal neurodevelopment and deficient synaptic plasticity, outcomes which could underlie some of the positive, negative and cognitive symptoms of schizophrenia. This review will discuss the functional roles of the mTOR cascade and present evidence in support of a novel mTOR-based hypothesis of the neuropathology of schizophrenia. During neurodevelopment, genetic and epigenetic factors can disrupt mTOR signalling which affects synthesis of proteins essential for correct neuronal growth and network connectivity. This renders the CNS particularly vulnerable to the effects of secondary factors during adolescence which increases the risk of developing schizophrenia in adulthood. This review discusses the functional roles of the mTOR cascade and presents evidence in support of a novel mTOR-based hypothesis of the neuropathology of schizophrenia. Testing this hypothesis will advance our understanding of the aetiology of this illness and reveal novel therapeutic targets.},
	language = {en},
	number = {3},
	urldate = {2021-04-20},
	journal = {Journal of Neurochemistry},
	author = {Gururajan, Anand and Buuse, Maarten van den},
	year = {2014},
	note = {ZSCC: 0000066 
\_eprint: https://onlinelibrary.wiley.com/doi/pdf/10.1111/jnc.12622},
	keywords = {BDNF, Reelin, glutamate, mammalian target of rapamycin, schizophrenia},
	pages = {377--387},
}

The mammalian target of rapamycin (mTOR) signalling cascade is involved in the intracellular regulation of protein synthesis, specifically for proteins involved in controlling neuronal morphology and facilitating synaptic plasticity. Research has revealed that the activity of the mTOR cascade is influenced by several extracellular and environmental factors that have been implicated in schizophrenia. Therefore, there is reason to believe that one of the downstream consequences of dysfunction or hypofunction of these factors in schizophrenia is disrupted mTOR signalling and hence impaired protein synthesis. This results in abnormal neurodevelopment and deficient synaptic plasticity, outcomes which could underlie some of the positive, negative and cognitive symptoms of schizophrenia. This review will discuss the functional roles of the mTOR cascade and present evidence in support of a novel mTOR-based hypothesis of the neuropathology of schizophrenia. During neurodevelopment, genetic and epigenetic factors can disrupt mTOR signalling which affects synthesis of proteins essential for correct neuronal growth and network connectivity. This renders the CNS particularly vulnerable to the effects of secondary factors during adolescence which increases the risk of developing schizophrenia in adulthood. This review discusses the functional roles of the mTOR cascade and presents evidence in support of a novel mTOR-based hypothesis of the neuropathology of schizophrenia. Testing this hypothesis will advance our understanding of the aetiology of this illness and reveal novel therapeutic targets.

@article{clark_neuroenhancement_2014,
	series = {Neuro-enhancement},
	title = {Neuroenhancement: {Enhancing} brain and mind in health and in disease},
	volume = {85},
	issn = {1053-8119},
	shorttitle = {Neuroenhancement},
	url = {http://www.sciencedirect.com/science/article/pii/S1053811913009385},
	doi = {10.1016/j.neuroimage.2013.08.071},
	abstract = {Humans have long used cognitive enhancement methods to expand the proficiency and range of the various mental activities that they engage in, including writing to store and retrieve information, and computers that allow them to perform myriad activities that are now commonplace in the internet age. Neuroenhancement describes the use of neuroscience-based techniques for enhancing cognitive function by acting directly on the human brain and nervous system, altering its properties to increase performance. Cognitive neuroscience has now reached the point where it may begin to put theory derived from years of experimentation into practice. This special issue includes 16 articles that employ or examine a variety of neuroenhancement methods currently being developed to increase cognition in healthy people and in patients with neurological or psychiatric illness. This includes transcranial electromagnetic stimulation methods, such as transcranial direct current stimulation (tDCS) and transcranial magnetic stimulation (TMS), along with deep brain stimulation, neurofeedback, behavioral training techniques, and these and other techniques in conjunction with neuroimaging. These methods can be used to improve attention, perception, memory and other forms of cognition in healthy individuals, leading to better performance in many aspects of everyday life. They may also reduce the cost, duration and overall impact of brain and mental illness in patients with neurological and psychiatric illness. Potential disadvantages of these techniques are also discussed. Given that the benefits of neuroenhancement outweigh the potential costs, these methods could potentially reduce suffering and improve quality of life for everyone, while further increasing our knowledge about the mechanisms of human cognition.},
	language = {en},
	urldate = {2020-10-24},
	journal = {NeuroImage},
	author = {Clark, Vincent P. and Parasuraman, Raja},
	month = jan,
	year = {2014},
	note = {ZSCC: 0000102},
	pages = {889--894},
}

Humans have long used cognitive enhancement methods to expand the proficiency and range of the various mental activities that they engage in, including writing to store and retrieve information, and computers that allow them to perform myriad activities that are now commonplace in the internet age. Neuroenhancement describes the use of neuroscience-based techniques for enhancing cognitive function by acting directly on the human brain and nervous system, altering its properties to increase performance. Cognitive neuroscience has now reached the point where it may begin to put theory derived from years of experimentation into practice. This special issue includes 16 articles that employ or examine a variety of neuroenhancement methods currently being developed to increase cognition in healthy people and in patients with neurological or psychiatric illness. This includes transcranial electromagnetic stimulation methods, such as transcranial direct current stimulation (tDCS) and transcranial magnetic stimulation (TMS), along with deep brain stimulation, neurofeedback, behavioral training techniques, and these and other techniques in conjunction with neuroimaging. These methods can be used to improve attention, perception, memory and other forms of cognition in healthy individuals, leading to better performance in many aspects of everyday life. They may also reduce the cost, duration and overall impact of brain and mental illness in patients with neurological and psychiatric illness. Potential disadvantages of these techniques are also discussed. Given that the benefits of neuroenhancement outweigh the potential costs, these methods could potentially reduce suffering and improve quality of life for everyone, while further increasing our knowledge about the mechanisms of human cognition.

@article{clark_neuroenhancement_2014-1,
	series = {Neuro-enhancement},
	title = {Neuroenhancement: {Enhancing} brain and mind in health and in disease},
	volume = {85},
	issn = {1053-8119},
	shorttitle = {Neuroenhancement},
	url = {http://www.sciencedirect.com/science/article/pii/S1053811913009385},
	doi = {10.1016/j.neuroimage.2013.08.071},
	abstract = {Humans have long used cognitive enhancement methods to expand the proficiency and range of the various mental activities that they engage in, including writing to store and retrieve information, and computers that allow them to perform myriad activities that are now commonplace in the internet age. Neuroenhancement describes the use of neuroscience-based techniques for enhancing cognitive function by acting directly on the human brain and nervous system, altering its properties to increase performance. Cognitive neuroscience has now reached the point where it may begin to put theory derived from years of experimentation into practice. This special issue includes 16 articles that employ or examine a variety of neuroenhancement methods currently being developed to increase cognition in healthy people and in patients with neurological or psychiatric illness. This includes transcranial electromagnetic stimulation methods, such as transcranial direct current stimulation (tDCS) and transcranial magnetic stimulation (TMS), along with deep brain stimulation, neurofeedback, behavioral training techniques, and these and other techniques in conjunction with neuroimaging. These methods can be used to improve attention, perception, memory and other forms of cognition in healthy individuals, leading to better performance in many aspects of everyday life. They may also reduce the cost, duration and overall impact of brain and mental illness in patients with neurological and psychiatric illness. Potential disadvantages of these techniques are also discussed. Given that the benefits of neuroenhancement outweigh the potential costs, these methods could potentially reduce suffering and improve quality of life for everyone, while further increasing our knowledge about the mechanisms of human cognition.},
	language = {en},
	urldate = {2020-10-14},
	journal = {NeuroImage},
	author = {Clark, Vincent P. and Parasuraman, Raja},
	month = jan,
	year = {2014},
	note = {ZSCC: 0000102},
	pages = {889--894},
}

Humans have long used cognitive enhancement methods to expand the proficiency and range of the various mental activities that they engage in, including writing to store and retrieve information, and computers that allow them to perform myriad activities that are now commonplace in the internet age. Neuroenhancement describes the use of neuroscience-based techniques for enhancing cognitive function by acting directly on the human brain and nervous system, altering its properties to increase performance. Cognitive neuroscience has now reached the point where it may begin to put theory derived from years of experimentation into practice. This special issue includes 16 articles that employ or examine a variety of neuroenhancement methods currently being developed to increase cognition in healthy people and in patients with neurological or psychiatric illness. This includes transcranial electromagnetic stimulation methods, such as transcranial direct current stimulation (tDCS) and transcranial magnetic stimulation (TMS), along with deep brain stimulation, neurofeedback, behavioral training techniques, and these and other techniques in conjunction with neuroimaging. These methods can be used to improve attention, perception, memory and other forms of cognition in healthy individuals, leading to better performance in many aspects of everyday life. They may also reduce the cost, duration and overall impact of brain and mental illness in patients with neurological and psychiatric illness. Potential disadvantages of these techniques are also discussed. Given that the benefits of neuroenhancement outweigh the potential costs, these methods could potentially reduce suffering and improve quality of life for everyone, while further increasing our knowledge about the mechanisms of human cognition.

@article{ahnaou_cortical_2014,
	title = {Cortical {EEG} oscillations and network connectivity as efficacy indices for assessing drugs with cognition enhancing potential},
	volume = {86},
	issn = {0028-3908},
	url = {http://www.sciencedirect.com/science/article/pii/S0028390814002986},
	doi = {10.1016/j.neuropharm.2014.08.015},
	abstract = {Synchronization of electroencephalographic (EEG) oscillations represents a core mechanism for cortical and subcortical networks, and disturbance in neural synchrony underlies cognitive processing deficits in neurological and neuropsychiatric disorders. Here, we investigated the effects of cognition enhancers (donepezil, rivastigmine, tacrine, galantamine and memantine), which are approved for symptomatic treatment of dementia, on EEG oscillations and network connectivity in conscious rats chronically instrumented with epidural electrodes in different cortical areas. Next, EEG network indices of cognitive impairments with the muscarinic receptor antagonist scopolamine were modeled. Lastly, we examined the efficacy of cognition enhancers to normalize those aberrant oscillations. Cognition enhancers elicited systematic (“fingerprint”) enhancement of cortical slow theta (4.5–6 Hz) and gamma (30.5–50 Hz) oscillations correlated with lower activity levels. Principal component analysis (PCA) revealed a compact cluster that corresponds to shared underlying mechanisms as compared to different drug classes. Functional network connectivity revealed consistent elevated coherent slow theta activity in parieto-occipital and between interhemispheric cortical areas. In rats instrumented with depth hippocampal CA1-CA3 electrodes, donepezil elicited similar oscillatory and coherent activities in cortico-hippocampal networks. When combined with scopolamine, the cognition enhancers attenuated the leftward shift in coherent slow delta activity. Such a consistent shift in EEG coherence into slow oscillations associated with altered slow theta and gamma oscillations may underlie cognitive deficits in scopolamine-treated animals, whereas enhanced coherent slow theta and gamma activity may be a relevant mechanism by which cognition enhancers exert their beneficial effect on plasticity and cognitive processes. The findings underscore that PCA and network connectivity are valuable tools to assess efficacy of novel therapeutic drugs with cognition enhancing potential.},
	language = {en},
	urldate = {2020-10-06},
	journal = {Neuropharmacology},
	author = {Ahnaou, A. and Huysmans, H. and Jacobs, T. and Drinkenburg, W. H. I. M.},
	month = nov,
	year = {2014},
	note = {ZSCC: 0000048},
	keywords = {Animal model, Cognition enhancers, Coherent functional network, EEG oscillations, Neurodegenerative disorders, Translational biomarker},
	pages = {362--377},
}

Synchronization of electroencephalographic (EEG) oscillations represents a core mechanism for cortical and subcortical networks, and disturbance in neural synchrony underlies cognitive processing deficits in neurological and neuropsychiatric disorders. Here, we investigated the effects of cognition enhancers (donepezil, rivastigmine, tacrine, galantamine and memantine), which are approved for symptomatic treatment of dementia, on EEG oscillations and network connectivity in conscious rats chronically instrumented with epidural electrodes in different cortical areas. Next, EEG network indices of cognitive impairments with the muscarinic receptor antagonist scopolamine were modeled. Lastly, we examined the efficacy of cognition enhancers to normalize those aberrant oscillations. Cognition enhancers elicited systematic (“fingerprint”) enhancement of cortical slow theta (4.5–6 Hz) and gamma (30.5–50 Hz) oscillations correlated with lower activity levels. Principal component analysis (PCA) revealed a compact cluster that corresponds to shared underlying mechanisms as compared to different drug classes. Functional network connectivity revealed consistent elevated coherent slow theta activity in parieto-occipital and between interhemispheric cortical areas. In rats instrumented with depth hippocampal CA1-CA3 electrodes, donepezil elicited similar oscillatory and coherent activities in cortico-hippocampal networks. When combined with scopolamine, the cognition enhancers attenuated the leftward shift in coherent slow delta activity. Such a consistent shift in EEG coherence into slow oscillations associated with altered slow theta and gamma oscillations may underlie cognitive deficits in scopolamine-treated animals, whereas enhanced coherent slow theta and gamma activity may be a relevant mechanism by which cognition enhancers exert their beneficial effect on plasticity and cognitive processes. The findings underscore that PCA and network connectivity are valuable tools to assess efficacy of novel therapeutic drugs with cognition enhancing potential.

@article{bernini_interdisciplinarity_2014,
	title = {Interdisciplinarity as cognitive integration: auditory verbal hallucinations as a case study},
	volume = {5},
	issn = {1939-5086},
	shorttitle = {Interdisciplinarity as cognitive integration},
	url = {https://onlinelibrary.wiley.com/doi/abs/10.1002/wcs.1305},
	doi = {10.1002/wcs.1305},
	abstract = {In this article, we advocate a bottom-up direction for the methodological modeling of interdisciplinary research based on concrete interactions among individuals within interdisciplinary projects. Drawing on our experience in Hearing the Voice (a cross-disciplinary project on auditory verbal hallucinations running at Durham University), we focus on the dynamic if also problematic integration of cognitive science (neuroscience, cognitive psychology, and of mind), phenomenology, and humanistic disciplines (literature, narratology, history, and theology). We propose a new model for disciplinary integration which brings to the fore an under-investigated dynamic of interdisciplinary projects, namely their being processes of distributed cognition and cognitive integration. WIREs Cogn Sci 2014, 5:603–612. doi: 10.1002/wcs.1305 This article is categorized under: Philosophy {\textgreater} Knowledge and Belief},
	language = {en},
	number = {5},
	urldate = {2020-06-18},
	journal = {WIREs Cognitive Science},
	author = {Bernini, Marco and Woods, Angela},
	year = {2014},
	note = {ZSCC: 0000008 
\_eprint: https://onlinelibrary.wiley.com/doi/pdf/10.1002/wcs.1305},
	keywords = {***},
	pages = {603--612},
}

In this article, we advocate a bottom-up direction for the methodological modeling of interdisciplinary research based on concrete interactions among individuals within interdisciplinary projects. Drawing on our experience in Hearing the Voice (a cross-disciplinary project on auditory verbal hallucinations running at Durham University), we focus on the dynamic if also problematic integration of cognitive science (neuroscience, cognitive psychology, and of mind), phenomenology, and humanistic disciplines (literature, narratology, history, and theology). We propose a new model for disciplinary integration which brings to the fore an under-investigated dynamic of interdisciplinary projects, namely their being processes of distributed cognition and cognitive integration. WIREs Cogn Sci 2014, 5:603–612. doi: 10.1002/wcs.1305 This article is categorized under: Philosophy \textgreater Knowledge and Belief

@article{pahor_effects_2014,
	title = {The effects of theta transcranial alternating current stimulation ({tACS}) on fluid intelligence},
	volume = {93},
	issn = {0167-8760},
	url = {http://www.sciencedirect.com/science/article/pii/S0167876014001664},
	doi = {10.1016/j.ijpsycho.2014.06.015},
	abstract = {The objective of the study was to explore the influence of transcranial alternating current stimulation (tACS) on resting brain activity and on measures of fluid intelligence. Theta tACS was applied to the left parietal and left frontal brain areas of healthy participants after which resting electroencephalogram (EEG) data was recorded. Following sham/active stimulation, the participants solved two tests of fluid intelligence while their EEG was recorded. The results showed that active theta tACS affected spectral power in theta and alpha frequency bands. In addition, active theta tACS improved performance on tests of fluid intelligence. This influence was more pronounced in the group of participants that received stimulation to the left parietal area than in the group of participants that received stimulation to the left frontal area. Left parietal tACS increased performance on the difficult test items of both tests (RAPM and PF\&C) whereas left frontal tACS increased performance only on the easy test items of one test (RAPM). The observed behavioral tACS influences were also accompanied by changes in neuroelectric activity. The behavioral and neuroelectric data tentatively support the P-FIT neurobiological model of intelligence.},
	language = {en},
	number = {3},
	urldate = {2020-10-06},
	journal = {International Journal of Psychophysiology},
	author = {Pahor, Anja and Jaušovec, Norbert},
	month = sep,
	year = {2014},
	note = {ZSCC: 0000063},
	keywords = {EEG, ERD/ERS, Fluid intelligence, Theta frequency, tACS},
	pages = {322--331},
}

The objective of the study was to explore the influence of transcranial alternating current stimulation (tACS) on resting brain activity and on measures of fluid intelligence. Theta tACS was applied to the left parietal and left frontal brain areas of healthy participants after which resting electroencephalogram (EEG) data was recorded. Following sham/active stimulation, the participants solved two tests of fluid intelligence while their EEG was recorded. The results showed that active theta tACS affected spectral power in theta and alpha frequency bands. In addition, active theta tACS improved performance on tests of fluid intelligence. This influence was more pronounced in the group of participants that received stimulation to the left parietal area than in the group of participants that received stimulation to the left frontal area. Left parietal tACS increased performance on the difficult test items of both tests (RAPM and PF&C) whereas left frontal tACS increased performance only on the easy test items of one test (RAPM). The observed behavioral tACS influences were also accompanied by changes in neuroelectric activity. The behavioral and neuroelectric data tentatively support the P-FIT neurobiological model of intelligence.

@article{brem_is_2014,
	title = {Is neuroenhancement by noninvasive brain stimulation a net zero-sum proposition?},
	volume = {85},
	issn = {10538119},
	url = {https://linkinghub.elsevier.com/retrieve/pii/S1053811913007945},
	doi = {10.1016/j.neuroimage.2013.07.038},
	abstract = {In the past several years, the number of studies investigating enhancement of cognitive functions through noninvasive brain stimulation (NBS) has increased considerably. NBS techniques, such as transcranial magnetic stimulation and transcranial current stimulation, seem capable of enhancing cognitive functions in patients and in healthy humans, particularly when combined with other interventions, including pharmacologic, behavioral and cognitive therapies. The “net zero-sum model”, based on the assumption that brain resources are subjected to the physical principle of conservation of energy, is one of the theoretical frameworks proposed to account for such enhancement of function and its potential cost. We argue that to guide future neuroenhancement studies, the net-zero sum concept is helpful, but only if its limits are tightly defined.},
	language = {en},
	urldate = {2020-07-02},
	journal = {NeuroImage},
	author = {Brem, Anna-Katharine and Fried, Peter J. and Horvath, Jared C. and Robertson, Edwin M. and Pascual-Leone, Alvaro},
	month = jan,
	year = {2014},
	pages = {1058--1068},
}

In the past several years, the number of studies investigating enhancement of cognitive functions through noninvasive brain stimulation (NBS) has increased considerably. NBS techniques, such as transcranial magnetic stimulation and transcranial current stimulation, seem capable of enhancing cognitive functions in patients and in healthy humans, particularly when combined with other interventions, including pharmacologic, behavioral and cognitive therapies. The “net zero-sum model”, based on the assumption that brain resources are subjected to the physical principle of conservation of energy, is one of the theoretical frameworks proposed to account for such enhancement of function and its potential cost. We argue that to guide future neuroenhancement studies, the net-zero sum concept is helpful, but only if its limits are tightly defined.

@article{hyman_revitalizing_2014,
	title = {Revitalizing {Psychiatric} {Therapeutics}},
	volume = {39},
	copyright = {2014 American College of Neuropsychopharmacology},
	issn = {1740-634X},
	url = {https://www.nature.com/articles/npp2013181},
	doi = {10.1038/npp.2013.181},
	abstract = {Despite high prevalence and enormous unmet medical need, the pharmaceutical industry has recently de-emphasized neuropsychiatric disorders as ‘too difficult’ a challenge to warrant major investment. Here I describe major obstacles to drug discovery and development including a lack of new molecular targets, shortcomings of current animal models, and the lack of biomarkers for clinical trials. My major focus, however, is on new technologies and scientific approaches to neuropsychiatric disorders that give promise for revitalizing therapeutics and may thus answer industry’s concerns.},
	language = {en},
	number = {1},
	urldate = {2020-06-29},
	journal = {Neuropsychopharmacology},
	author = {Hyman, Steven E.},
	month = jan,
	year = {2014},
	note = {Number: 1
Publisher: Nature Publishing Group},
	pages = {220--229},
}

Despite high prevalence and enormous unmet medical need, the pharmaceutical industry has recently de-emphasized neuropsychiatric disorders as ‘too difficult’ a challenge to warrant major investment. Here I describe major obstacles to drug discovery and development including a lack of new molecular targets, shortcomings of current animal models, and the lack of biomarkers for clinical trials. My major focus, however, is on new technologies and scientific approaches to neuropsychiatric disorders that give promise for revitalizing therapeutics and may thus answer industry’s concerns.

@article{dill_addict_2014,
	title = {The {Addict} in {Us} all},
	volume = {5},
	issn = {1664-0640},
	url = {http://journal.frontiersin.org/article/10.3389/fpsyt.2014.00139/abstract},
	doi = {10.3389/fpsyt.2014.00139},
	abstract = {In this paper, we contend that the psychology of addiction is similar to the psychology of ordinary, non-addictive temptation in important respects, and explore the ways in which these parallels can illuminate both addiction and ordinary action. The incentive salience account of addiction proposed by Robinson and Berridge (1–3) entails that addictive desires are not in their nature different from many of the desires had by non-addicts; what is different is rather the way that addictive desires are acquired, which in turn affects their strength. We examine these “incentive salience” desires, both in addicts and non-addicts, contrasting them with more cognitive desires. On this account, the self-control challenge faced by addicted agents is not different in kind from that faced by non-addicted agents – though the two may, of course, differ greatly in degree of difficulty. We explore a general model of selfcontrol for both the addict and the non-addict, stressing that self-control may be employed at three different stages, and examining the ways in which it might be strengthened. This helps elucidate a general model of intentional action.},
	language = {en},
	urldate = {2020-03-19},
	journal = {Frontiers in Psychiatry},
	author = {Dill, Brendan and Holton, Richard},
	month = oct,
	year = {2014},
	keywords = {addiction, desire, ego depletion, implementation intentions, incentive salience, mental contrasting, mindfulness meditation, self-control},
}

In this paper, we contend that the psychology of addiction is similar to the psychology of ordinary, non-addictive temptation in important respects, and explore the ways in which these parallels can illuminate both addiction and ordinary action. The incentive salience account of addiction proposed by Robinson and Berridge (1–3) entails that addictive desires are not in their nature different from many of the desires had by non-addicts; what is different is rather the way that addictive desires are acquired, which in turn affects their strength. We examine these “incentive salience” desires, both in addicts and non-addicts, contrasting them with more cognitive desires. On this account, the self-control challenge faced by addicted agents is not different in kind from that faced by non-addicted agents – though the two may, of course, differ greatly in degree of difficulty. We explore a general model of selfcontrol for both the addict and the non-addict, stressing that self-control may be employed at three different stages, and examining the ways in which it might be strengthened. This helps elucidate a general model of intentional action.

@article{cohen_five_2014,
	title = {Five methodological challenges in cognitive electrophysiology},
	volume = {85},
	issn = {10538119},
	url = {https://linkinghub.elsevier.com/retrieve/pii/S1053811913008641},
	doi = {10.1016/j.neuroimage.2013.08.010},
	abstract = {Here we discuss five methodological challenges facing the current cognitive electrophysiology literature that address the roles of brain oscillations in cognition. The challenges focus on (1) unambiguous and consistent terminology, (2) neurophysiologically meaningful interpretations of results, (3) evaluation and comparison of different spatial filters often used in M/EEG research, (4) the role of multiscale interactions in brain and cognitive function, and (5) development of biophysically plausible cognitive models. We also suggest research directions that will help address these challenges. We hope that this paper will help foster discussions and debates about important themes in the study of how the brain's rhythmic patterns of spatiotemporal electrophysiological activity support cognition.},
	language = {en},
	urldate = {2020-06-05},
	journal = {NeuroImage},
	author = {Cohen, Michael X and Gulbinaite, Rasa},
	month = jan,
	year = {2014},
	note = {ZSCC: 0000036},
	pages = {702--710},
}

Here we discuss five methodological challenges facing the current cognitive electrophysiology literature that address the roles of brain oscillations in cognition. The challenges focus on (1) unambiguous and consistent terminology, (2) neurophysiologically meaningful interpretations of results, (3) evaluation and comparison of different spatial filters often used in M/EEG research, (4) the role of multiscale interactions in brain and cognitive function, and (5) development of biophysically plausible cognitive models. We also suggest research directions that will help address these challenges. We hope that this paper will help foster discussions and debates about important themes in the study of how the brain's rhythmic patterns of spatiotemporal electrophysiological activity support cognition.

@article{jackson_narrative_2014,
	title = {Narrative and {Open} {Dialogue}: {Strangers} in the {Night} or {Easy} {Bedfellows}?},
	volume = {35},
	issn = {0814723X},
	shorttitle = {Narrative and {Open} {Dialogue}},
	url = {http://doi.wiley.com/10.1002/anzf.1045},
	doi = {10.1002/anzf.1045},
	abstract = {This paper briefly describes narrative and open dialogue approaches before exploring their shared values, ways of working, their differences and the possibilities for integration. Both authors have extensive experience in using a narrative therapy approach, while Val Jackson, a family and systemic psychotherapist, also uses an open dialogue approach in her work in an early intervention in psychosis service in Yorkshire, UK.},
	language = {en},
	number = {1},
	urldate = {2020-04-02},
	journal = {Australian and New Zealand Journal of Family Therapy},
	author = {Jackson, Val and Fox, Hugh},
	month = mar,
	year = {2014},
	note = {ZSCC: 0000004},
	pages = {72--80},
}

This paper briefly describes narrative and open dialogue approaches before exploring their shared values, ways of working, their differences and the possibilities for integration. Both authors have extensive experience in using a narrative therapy approach, while Val Jackson, a family and systemic psychotherapist, also uses an open dialogue approach in her work in an early intervention in psychosis service in Yorkshire, UK.

@article{garland_transdiagnostic_2014,
	title = {A {Transdiagnostic} {Perspective} on {Cognitive}, {Affective}, and {Neurobiological} {Processes} {Underlying} {Human} {Suffering}},
	volume = {24},
	issn = {1049-7315, 1552-7581},
	url = {http://journals.sagepub.com/doi/10.1177/1049731513503909},
	doi = {10.1177/1049731513503909},
	abstract = {The Diagnostic and Statistical Manual of Mental Disorders and International Classification of Diseases classify mental health disorders on the basis of their putatively distinct symptom profiles. Although these nosologies are highly influential, they also have been derided as mere ‘‘field guides’’ because they focus solely on the superficial symptomatic expression of psychiatric syndromes rather than on the commonalities underlying psychiatric disorders. Recently, an alternative transdiagnostic perspective has emerged. This review addresses transdiagnostic processes that underlie a wide range of psychosocial problems commonly addressed by social work practitioners. First, we describe how the transdiagnostic perspective differs from categorical views of psychopathology and accords more closely with scientific evidence. Next, we review current experimental psychopathology and neuroscience research to detail the cognitive, affective, and neurobiological features of five transdiagnostic processes. Finally, we discuss how the transdiagnostic perspective may improve therapeutic outcomes and guide the implementation of targeted social work interventions.},
	language = {en},
	number = {1},
	urldate = {2020-03-19},
	journal = {Research on Social Work Practice},
	author = {Garland, Eric L. and Howard, Matthew O.},
	month = jan,
	year = {2014},
	pages = {142--151},
}

The Diagnostic and Statistical Manual of Mental Disorders and International Classification of Diseases classify mental health disorders on the basis of their putatively distinct symptom profiles. Although these nosologies are highly influential, they also have been derided as mere ‘‘field guides’’ because they focus solely on the superficial symptomatic expression of psychiatric syndromes rather than on the commonalities underlying psychiatric disorders. Recently, an alternative transdiagnostic perspective has emerged. This review addresses transdiagnostic processes that underlie a wide range of psychosocial problems commonly addressed by social work practitioners. First, we describe how the transdiagnostic perspective differs from categorical views of psychopathology and accords more closely with scientific evidence. Next, we review current experimental psychopathology and neuroscience research to detail the cognitive, affective, and neurobiological features of five transdiagnostic processes. Finally, we discuss how the transdiagnostic perspective may improve therapeutic outcomes and guide the implementation of targeted social work interventions.

@article{jackson_narrative_2014,
	title = {Narrative and {Open} {Dialogue}: {Strangers} in the {Night} or {Easy} {Bedfellows}?},
	volume = {35},
	issn = {0814723X},
	shorttitle = {Narrative and {Open} {Dialogue}},
	url = {http://doi.wiley.com/10.1002/anzf.1045},
	doi = {10.1002/anzf.1045},
	abstract = {This paper briefly describes narrative and open dialogue approaches before exploring their shared values, ways of working, their differences and the possibilities for integration. Both authors have extensive experience in using a narrative therapy approach, while Val Jackson, a family and systemic psychotherapist, also uses an open dialogue approach in her work in an early intervention in psychosis service in Yorkshire, UK.},
	language = {en},
	number = {1},
	urldate = {2020-03-19},
	journal = {Australian and New Zealand Journal of Family Therapy},
	author = {Jackson, Val and Fox, Hugh},
	month = mar,
	year = {2014},
	pages = {72--80},
}

This paper briefly describes narrative and open dialogue approaches before exploring their shared values, ways of working, their differences and the possibilities for integration. Both authors have extensive experience in using a narrative therapy approach, while Val Jackson, a family and systemic psychotherapist, also uses an open dialogue approach in her work in an early intervention in psychosis service in Yorkshire, UK.

@article{borchers_need-adapted_2014,
	title = {The {Need}-{Adapted} {Approach} in {Psychosis}: {The} {Impact} of {Psychosis} on the {Treatment} and the {Professionals}},
	volume = {16},
	issn = {1559-4343, 1938-9000},
	shorttitle = {The {Need}-{Adapted} {Approach} in {Psychosis}},
	url = {http://connect.springerpub.com/lookup/doi/10.1891/1559-4343.16.1.5},
	doi = {10.1891/1559-4343.16.1.5},
	abstract = {Psychosis is a challenging phenomenon for professionals. In the need-adapted approach (NAA), therapy meetings constitute a deliberate effort to meet the challenges by bringing all the main parties together within a common discussion. The aims of this study are to analyze and evaluate psychiatrists’ experiences of the treatment processes in psychosis. A qualitative multiple case study approach has been used. Between August 2007 and January 2009, co-research interviews (CR-Is) and stimulated-recall interviews (STR-Is) with 10 psychiatrists from 3 different parts of Finland were videoed and transcribed verbatim. The material was analyzed using qualitative content analysis. The difficult emotions of the professionals and the critical views expressed had a prominent role. It was almost impossible to proceed with the treatment until the memories of coercive acts had been addressed. There were fewer harmful effects in outpatient than in inpatient care. If the client-centered principles of NAA were not followed, the CR-Is functioned primarily as critical evaluations of the treatment processes. The STR-Is helped the psychiatrists to find words for difficult experiences. For the sake of both practice and research, the experiences of staff in the treatment of psychosis should be taken into account. For better prediction of failure, routine measures to obtain feedback could be included in NAA.},
	language = {en},
	number = {1},
	urldate = {2020-03-19},
	journal = {Ethical Human Psychology and Psychiatry},
	author = {Borchers, Pekka and Seikkula, Jaakko and Arnkil, Tom},
	year = {2014},
	pages = {5--19},
}

Psychosis is a challenging phenomenon for professionals. In the need-adapted approach (NAA), therapy meetings constitute a deliberate effort to meet the challenges by bringing all the main parties together within a common discussion. The aims of this study are to analyze and evaluate psychiatrists’ experiences of the treatment processes in psychosis. A qualitative multiple case study approach has been used. Between August 2007 and January 2009, co-research interviews (CR-Is) and stimulated-recall interviews (STR-Is) with 10 psychiatrists from 3 different parts of Finland were videoed and transcribed verbatim. The material was analyzed using qualitative content analysis. The difficult emotions of the professionals and the critical views expressed had a prominent role. It was almost impossible to proceed with the treatment until the memories of coercive acts had been addressed. There were fewer harmful effects in outpatient than in inpatient care. If the client-centered principles of NAA were not followed, the CR-Is functioned primarily as critical evaluations of the treatment processes. The STR-Is helped the psychiatrists to find words for difficult experiences. For the sake of both practice and research, the experiences of staff in the treatment of psychosis should be taken into account. For better prediction of failure, routine measures to obtain feedback could be included in NAA.

@article{olson_key_2014,
	title = {{THE} {KEY} {ELEMENTS} {OF} {DIALOGIC} {PRACTICE} {IN} {OPEN} {DIALOGUE}: {FIDELITY} {CRITERIA}},
	language = {en},
	author = {Olson, Mary and Seikkula, Jaakko and Ziedonis, Douglas},
	year = {2014},
	pages = {33},
}

@article{whooley_nosological_2014,
	title = {Nosological {Reflections}: {The} {Failure} of \textit{{DSM}} -5, the {Emergence} of {RDoC}, and the {Decontextualization} of {Mental} {Distress}},
	volume = {4},
	issn = {2156-8693, 2156-8731},
	shorttitle = {Nosological {Reflections}},
	url = {http://journals.sagepub.com/doi/10.1177/2156869313519114},
	doi = {10.1177/2156869313519114},
	abstract = {Since the establishment of the symptoms-based categories in the Diagnostic and Statistical Manual of Mental Disorders (DSM), Third Edition, sociologists have raised concerns about the DSM’s failure to appreciate social, contextual factors when defining mental disorders. The author describes recent developments in psychiatric nosology—the DSM-5 revision process and the emergence of the Research Domain Criteria (RDoC)—and then considers their implications for decontextualization. Drawing on in-depth interviews with psychiatrists involved in the DSM-5 controversy and a content analysis of key documents, the author first recounts the ambitious DSM-5 revisions, illuminating the DSM-5 Task Force’s embrace of dimensionalization as a solution to the problem of validity and the ultimate rejection of this ‘‘paradigm shift’’ by psychiatrists. The Task Force’s failures prompted the National Institute of Mental Health to promote RDoC as an alternative nosological framework that eschews DSM categories altogether. Next, the author explores the ramifications of these events for decontextualization, which neither DSM-5 nor RDoC explicitly addresses, demonstrating how RDoC is poised to escalate decontextualization through its brain-centric conceptualization of mental disorders. To counteract these developments, sociologists should continue to promote ways of defining mental distress that underscore its social embeddedness.},
	language = {en},
	number = {2},
	urldate = {2020-03-18},
	journal = {Society and Mental Health},
	author = {Whooley, Owen},
	month = jul,
	year = {2014},
	pages = {92--110},
}

Since the establishment of the symptoms-based categories in the Diagnostic and Statistical Manual of Mental Disorders (DSM), Third Edition, sociologists have raised concerns about the DSM’s failure to appreciate social, contextual factors when defining mental disorders. The author describes recent developments in psychiatric nosology—the DSM-5 revision process and the emergence of the Research Domain Criteria (RDoC)—and then considers their implications for decontextualization. Drawing on in-depth interviews with psychiatrists involved in the DSM-5 controversy and a content analysis of key documents, the author first recounts the ambitious DSM-5 revisions, illuminating the DSM-5 Task Force’s embrace of dimensionalization as a solution to the problem of validity and the ultimate rejection of this ‘‘paradigm shift’’ by psychiatrists. The Task Force’s failures prompted the National Institute of Mental Health to promote RDoC as an alternative nosological framework that eschews DSM categories altogether. Next, the author explores the ramifications of these events for decontextualization, which neither DSM-5 nor RDoC explicitly addresses, demonstrating how RDoC is poised to escalate decontextualization through its brain-centric conceptualization of mental disorders. To counteract these developments, sociologists should continue to promote ways of defining mental distress that underscore its social embeddedness.

@article{timimi_no_2014,
	title = {No more psychiatric labels: {Why} formal psychiatric diagnostic systems should be abolished},
	volume = {14},
	issn = {16972600},
	shorttitle = {No more psychiatric labels},
	url = {https://linkinghub.elsevier.com/retrieve/pii/S169726001400009X},
	doi = {10.1016/j.ijchp.2014.03.004},
	abstract = {This article argues that psychiatric diagnoses are not valid or useful. The use of psychiatric diagnosis increases stigma, does not aid treatment decisions, is associated with worsening long-term prognosis for mental health problems, and imposes Western beliefs about mental distress on other cultures. This article reviews the evidence base focusing in particular on empirical findings in relation to the topics of: aetiology, validity, reliability, treatment and outcome, prognosis, colonialism, and cultural and public policy impact. This evidence points toward diagnostic based frameworks for understanding and intervening in mental health difficulties being unable to either improve our scientific knowledge or improve outcomes in clinical practice and suggests that we need to move away from reliance on diagnostic based approaches for organising research and service delivery. Alternative evidence-based models for organising effective mental health care are available. Therefore formal psychiatric diagnostic systems such as the mental health section of the International Classification of Diseases Tenth Edition (ICD-10) and Diagnostic Statistical Manual Fifth Edition (DSM 5) should be abolished.},
	language = {en},
	number = {3},
	urldate = {2020-03-18},
	journal = {International Journal of Clinical and Health Psychology},
	author = {Timimi, Sami},
	month = sep,
	year = {2014},
	pages = {208--215},
}

This article argues that psychiatric diagnoses are not valid or useful. The use of psychiatric diagnosis increases stigma, does not aid treatment decisions, is associated with worsening long-term prognosis for mental health problems, and imposes Western beliefs about mental distress on other cultures. This article reviews the evidence base focusing in particular on empirical findings in relation to the topics of: aetiology, validity, reliability, treatment and outcome, prognosis, colonialism, and cultural and public policy impact. This evidence points toward diagnostic based frameworks for understanding and intervening in mental health difficulties being unable to either improve our scientific knowledge or improve outcomes in clinical practice and suggests that we need to move away from reliance on diagnostic based approaches for organising research and service delivery. Alternative evidence-based models for organising effective mental health care are available. Therefore formal psychiatric diagnostic systems such as the mental health section of the International Classification of Diseases Tenth Edition (ICD-10) and Diagnostic Statistical Manual Fifth Edition (DSM 5) should be abolished.

@article{lakeman_-diagnosing_2014,
	title = {Un-diagnosing mental illness in the process of helping},
	volume = {21},
	language = {en},
	number = {1},
	author = {Lakeman, Richard and Emeleus, Mary},
	year = {2014},
	pages = {9},
}

@article{lakeman_unknowing_2014,
	title = {Unknowing: {A} potential common factor in successful engagement and psychotherapy with people who have complex psychosocial needs: {Unknowing} in {Mental} {Health} {Care}},
	volume = {23},
	issn = {14458330},
	shorttitle = {Unknowing},
	url = {http://doi.wiley.com/10.1111/inm.12067},
	doi = {10.1111/inm.12067},
	abstract = {Mental health nurses have a demonstrated capacity to work with people who have complex mental health and social problems in a respectful and non-coercive way for lengthy periods of time. Despite contributing to positive outcomes, nurses are rarely described as possessing psychotherapeutic skills or having advanced knowledge. More often, they are described as being instrumental to medicine, and nurses are socialized into not overstepping their subordinate position relative to medicine by claiming to know too much. Paradoxically, this position of unknowing, when employed mindfully, could be a critical ingredient in fostering therapeutic relationships with otherwise difficultto-engage people. The concept of unknowing is explored with reference to different schools of psychotherapy. Adopting an unknowing stance, that is, not prematurely assuming to know what the person’s problem is, nor the best way to help, might enable a deeper and more authentic understanding of the person’s experience to emerge over time.},
	language = {en},
	number = {5},
	urldate = {2020-03-12},
	journal = {International Journal of Mental Health Nursing},
	author = {Lakeman, Richard},
	month = oct,
	year = {2014},
	keywords = {humility, mental health nursing, phenomenology, unknowing},
	pages = {383--388},
}

Mental health nurses have a demonstrated capacity to work with people who have complex mental health and social problems in a respectful and non-coercive way for lengthy periods of time. Despite contributing to positive outcomes, nurses are rarely described as possessing psychotherapeutic skills or having advanced knowledge. More often, they are described as being instrumental to medicine, and nurses are socialized into not overstepping their subordinate position relative to medicine by claiming to know too much. Paradoxically, this position of unknowing, when employed mindfully, could be a critical ingredient in fostering therapeutic relationships with otherwise difficultto-engage people. The concept of unknowing is explored with reference to different schools of psychotherapy. Adopting an unknowing stance, that is, not prematurely assuming to know what the person’s problem is, nor the best way to help, might enable a deeper and more authentic understanding of the person’s experience to emerge over time.

@article{mohsen_fatemi_virtual_2014,
	title = {Virtual {Aging} and {Langerian} {Psychology} of {Possibility} ({Revisiting} the {Medical} {Disempowering} {Models} of {Aging})},
	volume = {1},
	issn = {23736445},
	url = {https://medcraveonline.com/JPCPY/virtual-aging-and-langerian-psychology-of-possibility-revisiting-the-medical-disempowering-models-of-aging.html},
	doi = {10.15406/jpcpy.2014.01.00016},
	abstract = {The pervasiveness of the medical model of aging and its focus on physical health may have given rise to the assumption that an increase of age would result not only in the loss of youth and liveliness but also in the dissipation of the overall human competencies. This paper indicates how this assumption and similar propositions are embedded in a mindless understanding of health and aging. Drawing on numerous experimental research and findings, the paper argues that an increase of mindfulness would largely contribute to an enhancement of liveliness, health and vivacity.},
	language = {en},
	number = {3},
	urldate = {2020-03-12},
	journal = {Journal of Psychology \& Clinical Psychiatry},
	author = {Mohsen Fatemi, Sayyed},
	month = jul,
	year = {2014},
	keywords = {Aging, Mindfulness, Mindlessness},
}

The pervasiveness of the medical model of aging and its focus on physical health may have given rise to the assumption that an increase of age would result not only in the loss of youth and liveliness but also in the dissipation of the overall human competencies. This paper indicates how this assumption and similar propositions are embedded in a mindless understanding of health and aging. Drawing on numerous experimental research and findings, the paper argues that an increase of mindfulness would largely contribute to an enhancement of liveliness, health and vivacity.

@article{landrain_-it-yourself_2013,
	title = {Do-it-yourself biology: challenges and promises for an open science and technology movement},
	volume = {7},
	issn = {1872-5325},
	shorttitle = {Do-it-yourself biology},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3740105/},
	doi = {10.1007/s11693-013-9116-4},
	abstract = {The do-it-yourself biology (DIYbio) community is emerging as a movement that fosters open access to resources permitting modern molecular biology, and synthetic biology among others. It promises in particular to be a source of cheaper and simpler solutions for environmental monitoring, personal diagnostic and the use of biomaterials. The successful growth of a global community of DIYbio practitioners will depend largely on enabling safe access to state-of-the-art molecular biology tools and resources. In this paper we analyze the rise of DIYbio, its community, its material resources and its applications. We look at the current projects developed for the international genetically engineered machine competition in order to get a sense of what amateur biologists can potentially create in their community laboratories over the coming years. We also show why and how the DIYbio community, in the context of a global governance development, is putting in place a safety/ethical framework for guarantying the pursuit of its activity. And finally we argue that the global spread of DIY biology potentially reconfigures and opens up access to biological information and laboratory equipment and that, therefore, it can foster new practices and transversal collaborations between professional scientists and amateurs.},
	number = {3},
	urldate = {2022-01-13},
	journal = {Systems and Synthetic Biology},
	author = {Landrain, Thomas and Meyer, Morgan and Perez, Ariel Martin and Sussan, Remi},
	month = sep,
	year = {2013},
	pmid = {24432149},
	pmcid = {PMC3740105},
	pages = {115--126},
}

The do-it-yourself biology (DIYbio) community is emerging as a movement that fosters open access to resources permitting modern molecular biology, and synthetic biology among others. It promises in particular to be a source of cheaper and simpler solutions for environmental monitoring, personal diagnostic and the use of biomaterials. The successful growth of a global community of DIYbio practitioners will depend largely on enabling safe access to state-of-the-art molecular biology tools and resources. In this paper we analyze the rise of DIYbio, its community, its material resources and its applications. We look at the current projects developed for the international genetically engineered machine competition in order to get a sense of what amateur biologists can potentially create in their community laboratories over the coming years. We also show why and how the DIYbio community, in the context of a global governance development, is putting in place a safety/ethical framework for guarantying the pursuit of its activity. And finally we argue that the global spread of DIY biology potentially reconfigures and opens up access to biological information and laboratory equipment and that, therefore, it can foster new practices and transversal collaborations between professional scientists and amateurs.

@article{revel_new_2013,
	title = {A new perspective for schizophrenia: {TAAR1} agonists reveal antipsychotic- and antidepressant-like activity, improve cognition and control body weight},
	volume = {18},
	copyright = {2013 Macmillan Publishers Limited},
	issn = {1476-5578},
	shorttitle = {A new perspective for schizophrenia},
	url = {https://www.nature.com/articles/mp201257},
	doi = {10.1038/mp.2012.57},
	abstract = {Schizophrenia is a chronic, severe and highly complex mental illness. Current treatments manage the positive symptoms, yet have minimal effects on the negative and cognitive symptoms, two prominent features of the disease with critical impact on the long-term morbidity. In addition, antipsychotic treatments trigger serious side effects that precipitate treatment discontinuation. Here, we show that activation of the trace amine-associated receptor 1 (TAAR1), a modulator of monoaminergic neurotransmission, represents a novel therapeutic option. In rodents, activation of TAAR1 by two novel and pharmacologically distinct compounds, the full agonist RO5256390 and the partial agonist RO5263397, blocks psychostimulant-induced hyperactivity and produces a brain activation pattern reminiscent of the antipsychotic drug olanzapine, suggesting antipsychotic-like properties. TAAR1 agonists do not induce catalepsy or weight gain; RO5263397 even reduced haloperidol-induced catalepsy and prevented olanzapine from increasing body weight and fat accumulation. Finally, TAAR1 activation promotes vigilance in rats and shows pro-cognitive and antidepressant-like properties in rodent and primate models. These data suggest that TAAR1 agonists may provide a novel and differentiated treatment of schizophrenia as compared with current medication standards: TAAR1 agonists may improve not only the positive symptoms but also the negative symptoms and cognitive deficits, without causing adverse effects such as motor impairments or weight gain.},
	language = {en},
	number = {5},
	urldate = {2021-12-23},
	journal = {Molecular Psychiatry},
	author = {Revel, F. G. and Moreau, J.-L. and Pouzet, B. and Mory, R. and Bradaia, A. and Buchy, D. and Metzler, V. and Chaboz, S. and Groebke Zbinden, K. and Galley, G. and Norcross, R. D. and Tuerck, D. and Bruns, A. and Morairty, S. R. and Kilduff, T. S. and Wallace, T. L. and Risterucci, C. and Wettstein, J. G. and Hoener, M. C.},
	month = may,
	year = {2013},
	note = {Bandiera\_abtest: a
Cg\_type: Nature Research Journals
Number: 5
Primary\_atype: Research
Publisher: Nature Publishing Group
Subject\_term: Drug therapy;G protein-coupled receptors;Schizophrenia
Subject\_term\_id: drug-therapy;g-protein-coupled-receptors;schizophrenia},
	keywords = {Drug therapy, G protein-coupled receptors, Schizophrenia},
	pages = {543--556},
}

Schizophrenia is a chronic, severe and highly complex mental illness. Current treatments manage the positive symptoms, yet have minimal effects on the negative and cognitive symptoms, two prominent features of the disease with critical impact on the long-term morbidity. In addition, antipsychotic treatments trigger serious side effects that precipitate treatment discontinuation. Here, we show that activation of the trace amine-associated receptor 1 (TAAR1), a modulator of monoaminergic neurotransmission, represents a novel therapeutic option. In rodents, activation of TAAR1 by two novel and pharmacologically distinct compounds, the full agonist RO5256390 and the partial agonist RO5263397, blocks psychostimulant-induced hyperactivity and produces a brain activation pattern reminiscent of the antipsychotic drug olanzapine, suggesting antipsychotic-like properties. TAAR1 agonists do not induce catalepsy or weight gain; RO5263397 even reduced haloperidol-induced catalepsy and prevented olanzapine from increasing body weight and fat accumulation. Finally, TAAR1 activation promotes vigilance in rats and shows pro-cognitive and antidepressant-like properties in rodent and primate models. These data suggest that TAAR1 agonists may provide a novel and differentiated treatment of schizophrenia as compared with current medication standards: TAAR1 agonists may improve not only the positive symptoms but also the negative symptoms and cognitive deficits, without causing adverse effects such as motor impairments or weight gain.

@article{adams_computational_2013,
	title = {The {Computational} {Anatomy} of {Psychosis}},
	volume = {4},
	issn = {1664-0640},
	url = {https://www.frontiersin.org/articles/10.3389/fpsyt.2013.00047/full#h1},
	doi = {10.3389/fpsyt.2013.00047},
	abstract = {This paper considers psychotic symptoms in terms of false inferences or beliefs. It is based on the notion that the brain is an inference machine that actively constructs hypotheses to explain or predict its sensations. This perspective provides a normative (Bayes optimal) account of action and perception that emphasises probabilistic representations; in particular, the confidence or precision of beliefs about the world. We will consider hallucinosis, abnormal eye movements, sensory attenuation deficits, catatonia and delusions as various expressions of the same core pathology: namely, an aberrant encoding of precision. From a cognitive perspective, this represents a pernicious failure of metacognition (beliefs about beliefs) that can confound perceptual inference. In the embodied setting of active (Bayesian) inference, it can lead to behaviours that are paradoxically more accurate than Bayes optimal behaviour. Crucially, this normative account is accompanied by a neuronally plausible process theory based upon hierarchical predictive coding. In predictive coding, precision is thought to be encoded by the postsynaptic gain of neurons reporting prediction error. This suggests that both pervasive trait abnormalities and florid failures of inference in the psychotic state can be linked to factors controlling postsynaptic gain – such as NMDA receptor function and (dopaminergic) neuromodulation. We illustrate these points using biologically plausible simulations of perceptual synthesis, smooth pursuit eye movements and attribution of agency – that all use the same predictive coding scheme and pathology: namely, a reduction in the precision of prior beliefs, relative to sensory evidence.},
	language = {English},
	urldate = {2021-06-22},
	journal = {Frontiers in Psychiatry},
	author = {Adams, Rick A. and Stephan, Klaas Enno and Brown, Harriet R. and Frith, Christopher D. and Friston, Karl J.},
	year = {2013},
	note = {ZSCC: 0000525},
	keywords = {Illusions, Precision, Schizophrenia, Sensory Attenuation, active inference, free energy, psychosis},
}

This paper considers psychotic symptoms in terms of false inferences or beliefs. It is based on the notion that the brain is an inference machine that actively constructs hypotheses to explain or predict its sensations. This perspective provides a normative (Bayes optimal) account of action and perception that emphasises probabilistic representations; in particular, the confidence or precision of beliefs about the world. We will consider hallucinosis, abnormal eye movements, sensory attenuation deficits, catatonia and delusions as various expressions of the same core pathology: namely, an aberrant encoding of precision. From a cognitive perspective, this represents a pernicious failure of metacognition (beliefs about beliefs) that can confound perceptual inference. In the embodied setting of active (Bayesian) inference, it can lead to behaviours that are paradoxically more accurate than Bayes optimal behaviour. Crucially, this normative account is accompanied by a neuronally plausible process theory based upon hierarchical predictive coding. In predictive coding, precision is thought to be encoded by the postsynaptic gain of neurons reporting prediction error. This suggests that both pervasive trait abnormalities and florid failures of inference in the psychotic state can be linked to factors controlling postsynaptic gain – such as NMDA receptor function and (dopaminergic) neuromodulation. We illustrate these points using biologically plausible simulations of perceptual synthesis, smooth pursuit eye movements and attribution of agency – that all use the same predictive coding scheme and pathology: namely, a reduction in the precision of prior beliefs, relative to sensory evidence.

@article{friston_life_2013,
	title = {Life as we know it},
	volume = {10},
	url = {https://royalsocietypublishing.org/doi/full/10.1098/rsif.2013.0475},
	doi = {10.1098/rsif.2013.0475},
	abstract = {This paper presents a heuristic proof (and simulations of a primordial soup) suggesting that life—or biological self-organization—is an inevitable and emergent property of any (ergodic) random dynamical system that possesses a Markov blanket. This conclusion is based on the following arguments: if the coupling among an ensemble of dynamical systems is mediated by short-range forces, then the states of remote systems must be conditionally independent. These independencies induce a Markov blanket that separates internal and external states in a statistical sense. The existence of a Markov blanket means that internal states will appear to minimize a free energy functional of the states of their Markov blanket. Crucially, this is the same quantity that is optimized in Bayesian inference. Therefore, the internal states (and their blanket) will appear to engage in active Bayesian inference. In other words, they will appear to model—and act on—their world to preserve their functional and structural integrity, leading to homoeostasis and a simple form of autopoiesis.},
	number = {86},
	urldate = {2021-06-05},
	journal = {Journal of The Royal Society Interface},
	author = {Friston, Karl},
	month = sep,
	year = {2013},
	note = {ZSCC: 0000519 
Publisher: Royal Society},
	pages = {20130475},
}

This paper presents a heuristic proof (and simulations of a primordial soup) suggesting that life—or biological self-organization—is an inevitable and emergent property of any (ergodic) random dynamical system that possesses a Markov blanket. This conclusion is based on the following arguments: if the coupling among an ensemble of dynamical systems is mediated by short-range forces, then the states of remote systems must be conditionally independent. These independencies induce a Markov blanket that separates internal and external states in a statistical sense. The existence of a Markov blanket means that internal states will appear to minimize a free energy functional of the states of their Markov blanket. Crucially, this is the same quantity that is optimized in Bayesian inference. Therefore, the internal states (and their blanket) will appear to engage in active Bayesian inference. In other words, they will appear to model—and act on—their world to preserve their functional and structural integrity, leading to homoeostasis and a simple form of autopoiesis.

@article{logue_politics_2013,
	title = {The {Politics} of {Unknowing} and the {Virtues} of {Ignorance}: {Toward} a {Pedagogy} of {Epistemic} {Vulnerability}},
	language = {en},
	journal = {PHILOSOPHY OF EDUCATION},
	author = {Logue, Jennifer},
	year = {2013},
	note = {ZSCC: 0000009},
	pages = {10},
}

@article{schraw_conceptual_2013,
	title = {Conceptual {Integration} and {Measurement} of {Epistemological} and {Ontological} {Beliefs} in {Educational} {Research}},
	volume = {2013},
	issn = {2090-8652},
	url = {https://www.hindawi.com/archive/2013/327680/},
	doi = {10.1155/2013/327680},
	abstract = {This paper examines the conceptualization and measurement of epistemological and ontological phenomena and makes recommendations for improving the conceptual framework and methodological assessment of these phenomena. I discuss the ways educational researchers have studied beliefs and how this research can be improved through a comprehensive conceptual framework and better measurement. This paper provides definitions of epistemological and ontological beliefs and world views, discusses six complementary strategies for assessing these beliefs, compares the strengths of these strategies, and provides examples of how they have been used in the research literature. This paper discusses challenges related to the development of a comprehensive theoretical framework for beliefs, as well as ways to improve measurement of these beliefs and summarizes six emergent themes.},
	language = {en},
	urldate = {2020-03-12},
	journal = {ISRN Education},
	author = {Schraw, Gregory},
	year = {2013},
	note = {ZSCC: 0000117},
	pages = {1--19},
}

This paper examines the conceptualization and measurement of epistemological and ontological phenomena and makes recommendations for improving the conceptual framework and methodological assessment of these phenomena. I discuss the ways educational researchers have studied beliefs and how this research can be improved through a comprehensive conceptual framework and better measurement. This paper provides definitions of epistemological and ontological beliefs and world views, discusses six complementary strategies for assessing these beliefs, compares the strengths of these strategies, and provides examples of how they have been used in the research literature. This paper discusses challenges related to the development of a comprehensive theoretical framework for beliefs, as well as ways to improve measurement of these beliefs and summarizes six emergent themes.

@article{boe_change_2013,
	title = {Change is an {Ongoing} {Ethical} {Event}: {Levinas}, {Bakhtin} and the {Dialogical} {Dynamics} of {Becoming}},
	volume = {34},
	issn = {0814723X},
	shorttitle = {Change is an {Ongoing} {Ethical} {Event}},
	url = {http://doi.wiley.com/10.1002/anzf.1003},
	doi = {10.1002/anzf.1003},
	abstract = {In this article, we use the intersubjective ethics of Bakhtin and Levinas and a case illustration to explore change in therapy as an ethical phenomenon. We follow Lakoff and Johnson in their emphasis on the way our conceptions of change seem permeated by metaphors. Bakhtin and Levinas both suggest through a language in which metaphors play a crucial role, that human existence—the consciousness and the subject—emerge within the dialogue of the encounter. They both describe the dynamics of human existence as ethical in their origin. Following this, we argue that change may be seen as an ongoing ethical event and that the dynamics of change are found in the ways we constantly become in this event. We investigate the ethical dynamics of this ongoing event through three themes illuminating the contributions of both Bakhtin and Levinas: (1) we become as responsible, (2) we become in speaking, (3) we become in answering the unknown. We explore these themes through a case illustration. Finally, we briefly point out some possible implications for mental health practice.},
	language = {en},
	number = {1},
	urldate = {2020-04-02},
	journal = {Australian and New Zealand Journal of Family Therapy},
	author = {Bøe, Tore Dag and Kristoffersen, Kjell and Lidbom, Per Arne and Lindvig, Gunnhild Ruud and Seikkula, Jaakko and Ulland, Dagfinn and Zachariassen, Karianne},
	month = mar,
	year = {2013},
	note = {ZSCC: 0000036},
	pages = {18--31},
}

In this article, we use the intersubjective ethics of Bakhtin and Levinas and a case illustration to explore change in therapy as an ethical phenomenon. We follow Lakoff and Johnson in their emphasis on the way our conceptions of change seem permeated by metaphors. Bakhtin and Levinas both suggest through a language in which metaphors play a crucial role, that human existence—the consciousness and the subject—emerge within the dialogue of the encounter. They both describe the dynamics of human existence as ethical in their origin. Following this, we argue that change may be seen as an ongoing ethical event and that the dynamics of change are found in the ways we constantly become in this event. We investigate the ethical dynamics of this ongoing event through three themes illuminating the contributions of both Bakhtin and Levinas: (1) we become as responsible, (2) we become in speaking, (3) we become in answering the unknown. We explore these themes through a case illustration. Finally, we briefly point out some possible implications for mental health practice.

@article{geissler_public_2013,
	title = {Public secrets in public health: {Knowing} not to know while making scientific knowledge},
	volume = {40},
	copyright = {© 2013 The Authors. American Ethnologist published by Wiley Periodicals, Inc. on behalf of the American Anthropological Association. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.},
	issn = {1548-1425},
	shorttitle = {Public secrets in public health},
	url = {https://anthrosource.onlinelibrary.wiley.com/doi/abs/10.1111/amet.12002},
	doi = {10.1111/amet.12002},
	abstract = {Unknown knowns—or “public secrets”—may play an integral part in publicly funded medical science. In one large transnational field research site in Africa, such unknowing pertains to vital material inequalities across the relations of scientific production. These inequalities are open to experience but remain often unacknowledged in public speech and scientific texts. This silence is not usually achieved by suppressing knowledge but through linguistic convention and differentiation between places and moments of knowing and ignorance. Switching between known and unknown according to situation and interlocutor is an important, largely implicit skill that maintains relations necessary to conduct clinical research—linking bodies, lives, institutions, and technologies across differentials of resources, expertise, and power. Unknowing, then, facilitates research; and it shapes the resulting work and perpetuates the political and economic contradictions that pervade the context and the research endeavor itself. Unknowing thus poses a challenge for conventional anthropological modes of critique and engagement.},
	language = {en},
	number = {1},
	urldate = {2020-03-19},
	journal = {American Ethnologist},
	author = {Geissler, P. W.},
	year = {2013},
	note = {ZSCC: 0000169},
	keywords = {Africa, ethics, ignorance, justice, medical research, science},
	pages = {13--34},
}

Unknown knowns—or “public secrets”—may play an integral part in publicly funded medical science. In one large transnational field research site in Africa, such unknowing pertains to vital material inequalities across the relations of scientific production. These inequalities are open to experience but remain often unacknowledged in public speech and scientific texts. This silence is not usually achieved by suppressing knowledge but through linguistic convention and differentiation between places and moments of knowing and ignorance. Switching between known and unknown according to situation and interlocutor is an important, largely implicit skill that maintains relations necessary to conduct clinical research—linking bodies, lives, institutions, and technologies across differentials of resources, expertise, and power. Unknowing, then, facilitates research; and it shapes the resulting work and perpetuates the political and economic contradictions that pervade the context and the research endeavor itself. Unknowing thus poses a challenge for conventional anthropological modes of critique and engagement.

@article{han_conceptual_2013,
	title = {Conceptual, {Methodological}, and {Ethical} {Problems} in {Communicating} {Uncertainty} in {Clinical} {Evidence}},
	volume = {70},
	issn = {1077-5587},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4238424/},
	doi = {10.1177/1077558712459361},
	abstract = {The communication of uncertainty in clinical evidence is an important endeavor that poses difficult conceptual, methodological, and ethical problems. Conceptual problems include logical paradoxes in the meaning of probability and “ambiguity”— second-order uncertainty arising from the lack of reliability, credibility, or adequacy of probability information. Methodological problems include questions about optimal methods for representing fundamental uncertainties and for communicating these uncertainties in clinical practice. Ethical problems include questions about whether communicating uncertainty enhances or diminishes patient autonomy and produces net benefits or harms. This article reviews the limited but growing literature on these problems and efforts to address them and identifies key areas of focus for future research. It is argued that the critical need moving forward is for greater conceptual clarity and consistent representational methods that make the meaning of various uncertainties understandable, and for clinical interventions to support patients in coping with uncertainty in decision making.},
	number = {1 0},
	urldate = {2020-07-01},
	journal = {Medical care research and review : MCRR},
	author = {Han, Paul K. J.},
	month = feb,
	year = {2013},
	pmid = {23132891},
	pmcid = {PMC4238424},
	note = {ZSCC: 0000126 },
	pages = {14S--36S},
}

The communication of uncertainty in clinical evidence is an important endeavor that poses difficult conceptual, methodological, and ethical problems. Conceptual problems include logical paradoxes in the meaning of probability and “ambiguity”— second-order uncertainty arising from the lack of reliability, credibility, or adequacy of probability information. Methodological problems include questions about optimal methods for representing fundamental uncertainties and for communicating these uncertainties in clinical practice. Ethical problems include questions about whether communicating uncertainty enhances or diminishes patient autonomy and produces net benefits or harms. This article reviews the limited but growing literature on these problems and efforts to address them and identifies key areas of focus for future research. It is argued that the critical need moving forward is for greater conceptual clarity and consistent representational methods that make the meaning of various uncertainties understandable, and for clinical interventions to support patients in coping with uncertainty in decision making.

@article{coyle_nitric_2013,
	title = {Nitric {Oxide} and {Symptom} {Reduction} in {Schizophrenia}},
	volume = {70},
	issn = {2168-622X},
	url = {https://doi.org/10.1001/jamapsychiatry.2013.210},
	doi = {10.1001/jamapsychiatry.2013.210},
	abstract = {In this issue of the journal, Hallak et al report results from a placebo-controlled clinical trial showing that infusion of sodium nitroprusside causes a rapid and persistent reduction of symptoms in patients with schizophrenia who have been symptomatically stabilized with antipsychotic medications. The peer reviewers of the manuscript concurred that the study pointed to a potentially new avenue for pharmacologic intervention in schizophrenia, although they recognized that the small number of patients studied was a serious limitation. It is true that the field is littered with small trials with robust outcomes that ultimately are not replicated. However, the rationale for the study was tethered to an increasingly compelling body of evidence from drug challenges, postmortem analysis, and gene association studies that hypofunction of the N-methyl-d-aspartate (NMDA) receptor, a glutamate receptor subtype that mediates neural plasticity, is a core feature of schizophrenia. In particular, NMDA receptor hypofunction appears to be particularly relevant to negative symptoms and cognitive impairments in schizophrenia.},
	number = {7},
	urldate = {2021-04-10},
	journal = {JAMA Psychiatry},
	author = {Coyle, Joseph T.},
	month = jul,
	year = {2013},
	note = {ZSCC: 0000020},
	pages = {664--665},
}

In this issue of the journal, Hallak et al report results from a placebo-controlled clinical trial showing that infusion of sodium nitroprusside causes a rapid and persistent reduction of symptoms in patients with schizophrenia who have been symptomatically stabilized with antipsychotic medications. The peer reviewers of the manuscript concurred that the study pointed to a potentially new avenue for pharmacologic intervention in schizophrenia, although they recognized that the small number of patients studied was a serious limitation. It is true that the field is littered with small trials with robust outcomes that ultimately are not replicated. However, the rationale for the study was tethered to an increasingly compelling body of evidence from drug challenges, postmortem analysis, and gene association studies that hypofunction of the N-methyl-d-aspartate (NMDA) receptor, a glutamate receptor subtype that mediates neural plasticity, is a core feature of schizophrenia. In particular, NMDA receptor hypofunction appears to be particularly relevant to negative symptoms and cognitive impairments in schizophrenia.

@article{han_conceptual_2013,
	title = {Conceptual, {Methodological}, and {Ethical} {Problems} in {Communicating} {Uncertainty} in {Clinical} {Evidence}},
	volume = {70},
	issn = {1077-5587},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4238424/},
	doi = {10.1177/1077558712459361},
	abstract = {The communication of uncertainty in clinical evidence is an important endeavor that poses difficult conceptual, methodological, and ethical problems. Conceptual problems include logical paradoxes in the meaning of probability and “ambiguity”— second-order uncertainty arising from the lack of reliability, credibility, or adequacy of probability information. Methodological problems include questions about optimal methods for representing fundamental uncertainties and for communicating these uncertainties in clinical practice. Ethical problems include questions about whether communicating uncertainty enhances or diminishes patient autonomy and produces net benefits or harms. This article reviews the limited but growing literature on these problems and efforts to address them and identifies key areas of focus for future research. It is argued that the critical need moving forward is for greater conceptual clarity and consistent representational methods that make the meaning of various uncertainties understandable, and for clinical interventions to support patients in coping with uncertainty in decision making.},
	number = {1 0},
	urldate = {2020-10-24},
	journal = {Medical care research and review : MCRR},
	author = {Han, Paul K. J.},
	month = feb,
	year = {2013},
	pmid = {23132891},
	pmcid = {PMC4238424},
	note = {ZSCC: 0000117 },
	pages = {14S--36S},
}

The communication of uncertainty in clinical evidence is an important endeavor that poses difficult conceptual, methodological, and ethical problems. Conceptual problems include logical paradoxes in the meaning of probability and “ambiguity”— second-order uncertainty arising from the lack of reliability, credibility, or adequacy of probability information. Methodological problems include questions about optimal methods for representing fundamental uncertainties and for communicating these uncertainties in clinical practice. Ethical problems include questions about whether communicating uncertainty enhances or diminishes patient autonomy and produces net benefits or harms. This article reviews the limited but growing literature on these problems and efforts to address them and identifies key areas of focus for future research. It is argued that the critical need moving forward is for greater conceptual clarity and consistent representational methods that make the meaning of various uncertainties understandable, and for clinical interventions to support patients in coping with uncertainty in decision making.