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\n  \n 2022\n \n \n (2)\n \n \n
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\n \n\n \n \n \n \n \n Effects of the Mindfulness-Based Blood Pressure Reduction (MB-BP) program on depression and neural structural connectivity.\n \n \n \n\n\n \n Polcari, J., J.; Cali, R., J.; Nephew, B., C.; Lu, S.; Rashkovskii, M.; Wu, J.; Saadeh, F.; Loucks, E.; and King, J., A.\n\n\n \n\n\n\n Journal of Affective Disorders, 311: 31-39. 5 2022.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{\n title = {Effects of the Mindfulness-Based Blood Pressure Reduction (MB-BP) program on depression and neural structural connectivity},\n type = {article},\n year = {2022},\n pages = {31-39},\n volume = {311},\n month = {5},\n id = {e6070705-bfe3-38fc-b027-629a42528583},\n created = {2022-05-21T02:53:53.620Z},\n file_attached = {false},\n profile_id = {87c992c1-10d8-3542-a95f-de865d710d61},\n group_id = {2fb46359-0450-327e-9ad8-3208cfcefebc},\n last_modified = {2022-05-21T02:53:53.620Z},\n read = {false},\n starred = {false},\n authored = {false},\n confirmed = {false},\n hidden = {false},\n source_type = {article},\n private_publication = {false},\n abstract = {Hypertension-related illnesses are a leading cause of disability and death in the United States, where hypertension prevalence in adults is 46%, with only half of those afflicted having it under control. Due to the significant challenges in long-term efficacy and adverse effects associated with pharmacological interventions, there is an eminent need for complimentary approaches for treating hypertension. Although initial studies of the Mindfulness-Based Blood Pressure Reduction program (MB-BP) indicate that this novel 8-week intervention is effective at inducing lasting decreases in blood pressure, the neural correlates are unknown.},\n bibtype = {article},\n author = {Polcari, Justin J and Cali, Ryan J and Nephew, Benjamin C and Lu, Senbao and Rashkovskii, Mikhail and Wu, Julianne and Saadeh, Frances and Loucks, Eric and King, Jean A},\n doi = {10.1016/j.jad.2022.05.059},\n journal = {Journal of Affective Disorders}\n}
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\n\n\n
\n Hypertension-related illnesses are a leading cause of disability and death in the United States, where hypertension prevalence in adults is 46%, with only half of those afflicted having it under control. Due to the significant challenges in long-term efficacy and adverse effects associated with pharmacological interventions, there is an eminent need for complimentary approaches for treating hypertension. Although initial studies of the Mindfulness-Based Blood Pressure Reduction program (MB-BP) indicate that this novel 8-week intervention is effective at inducing lasting decreases in blood pressure, the neural correlates are unknown.\n
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\n \n\n \n \n \n \n \n Long-Term Effects of Repeated Blast Exposure in United States Special Operations Forces Personnel: A Pilot Study Protocol.\n \n \n \n\n\n \n Edlow, B., L.; Bodien, Y., G.; Baxter, T.; Belanger, H.; Cali, R.; Deary, K.; Fischl, B.; Foulkes, A., S.; Gilmore, N.; Greve, D., N.; Hooker, J., M.; Huang, S., Y.; Kelemen, J., N.; Kimberly, W., T.; Maffei, C.; Masood, M.; Perl, D.; Polimeni, J., R.; Rosen, B., R.; Tromly, S.; Tseng, C., J.; Yao, E., F.; Zurcher, N., R.; Mac Donald, C., L.; and Dams-O'Connor, K.\n\n\n \n\n\n\n Journal of Neurotrauma. 5 2022.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{\n title = {Long-Term Effects of Repeated Blast Exposure in United States Special Operations Forces Personnel: A Pilot Study Protocol},\n type = {article},\n year = {2022},\n month = {5},\n day = {27},\n id = {9506ab8a-9bef-39bf-86d0-d150bf2178c8},\n created = {2022-05-31T01:35:05.452Z},\n file_attached = {false},\n profile_id = {87c992c1-10d8-3542-a95f-de865d710d61},\n group_id = {2fb46359-0450-327e-9ad8-3208cfcefebc},\n last_modified = {2022-05-31T01:35:05.452Z},\n read = {false},\n starred = {false},\n authored = {false},\n confirmed = {false},\n hidden = {false},\n private_publication = {false},\n abstract = {Emerging evidence suggests that repeated blast exposure (RBE) is associated with brain injury in military personnel. United States (U.S.) Special Operations Forces (SOF) personnel experience high rates of blast exposure during training and combat, but the effects of low-level RBE on brain structure and function in SOF have not been comprehensively characterized. Furthermore, the pathophysiological link between RBE-related brain injuries and cognitive, behavioral, and physical symptoms has not been fully elucidated. We present a protocol for an observational pilot study, Long-Term Effects of Repeated Blast Exposure in U.S. SOF Personnel (ReBlast). In this exploratory study, 30 active-duty SOF personnel with RBE will participate in a comprehensive evaluation of: 1) brain network structure and function using Connectome MRI and 7 Tesla MRI; 2) neuroinflammation and tau deposition using positron emission tomography; 3) blood proteomics and metabolomics; 4) behavioral and physical symptoms using self-report measures; and 5) cognition using a battery of conventional and digitized assessments designed to detect subtle deficits in otherwise high-performing individuals. We will identify clinical, neuroimaging, and blood-based phenotypes that are associated with level of RBE, as measured by the Generalized Blast Exposure Value. Candidate biomarkers of RBE-related brain injury will inform the design of a subsequent study that will test a diagnostic assessment battery for detecting RBE-related brain injury. Ultimately, we anticipate that the ReBlast study will facilitate the development of interventions to optimize the brain health, quality of life, and battle readiness of U.S. SOF personnel.},\n bibtype = {article},\n author = {Edlow, Brian L. and Bodien, Yelena G and Baxter, Timothy and Belanger, Heather and Cali, Ryan and Deary, Katryna and Fischl, Bruce and Foulkes, Andrea S and Gilmore, Natalie and Greve, Douglas N and Hooker, Jacob M and Huang, Susie Y and Kelemen, Jessica N and Kimberly, W Taylor and Maffei, Chiara and Masood, Maryam and Perl, Daniel and Polimeni, Jonathan R and Rosen, Bruce R. and Tromly, Samantha and Tseng, Chieh-En J and Yao, Eveline F and Zurcher, Nicole R and Mac Donald, Christine L and Dams-O'Connor, Kristen},\n doi = {10.1089/neu.2022.0030},\n journal = {Journal of Neurotrauma}\n}
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\n Emerging evidence suggests that repeated blast exposure (RBE) is associated with brain injury in military personnel. United States (U.S.) Special Operations Forces (SOF) personnel experience high rates of blast exposure during training and combat, but the effects of low-level RBE on brain structure and function in SOF have not been comprehensively characterized. Furthermore, the pathophysiological link between RBE-related brain injuries and cognitive, behavioral, and physical symptoms has not been fully elucidated. We present a protocol for an observational pilot study, Long-Term Effects of Repeated Blast Exposure in U.S. SOF Personnel (ReBlast). In this exploratory study, 30 active-duty SOF personnel with RBE will participate in a comprehensive evaluation of: 1) brain network structure and function using Connectome MRI and 7 Tesla MRI; 2) neuroinflammation and tau deposition using positron emission tomography; 3) blood proteomics and metabolomics; 4) behavioral and physical symptoms using self-report measures; and 5) cognition using a battery of conventional and digitized assessments designed to detect subtle deficits in otherwise high-performing individuals. We will identify clinical, neuroimaging, and blood-based phenotypes that are associated with level of RBE, as measured by the Generalized Blast Exposure Value. Candidate biomarkers of RBE-related brain injury will inform the design of a subsequent study that will test a diagnostic assessment battery for detecting RBE-related brain injury. Ultimately, we anticipate that the ReBlast study will facilitate the development of interventions to optimize the brain health, quality of life, and battle readiness of U.S. SOF personnel.\n
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\n  \n 2021\n \n \n (4)\n \n \n
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\n \n\n \n \n \n \n \n Altered neural networks and cognition in a hereditary colon cancer.\n \n \n \n\n\n \n Cali, R., J.; Nephew, B., C.; Moore, C., M.; Chumachenko, S.; Sala, A., C.; Cintron, B.; Luciano, C.; King, J., A.; Hooper, S., R.; Giardiello, F., M.; and Cruz-Correa, M.\n\n\n \n\n\n\n IBRO Neuroscience Reports, 11. 2021.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{\n title = {Altered neural networks and cognition in a hereditary colon cancer},\n type = {article},\n year = {2021},\n keywords = {Cancer,Cognition,Familial Adenomatous Polyposis,Neural networks,Resting state functional connectivity,fMRI},\n volume = {11},\n id = {55e582f3-346f-3e3d-86a1-cdf1b1afe9a1},\n created = {2022-05-21T02:53:51.111Z},\n file_attached = {false},\n profile_id = {87c992c1-10d8-3542-a95f-de865d710d61},\n group_id = {2fb46359-0450-327e-9ad8-3208cfcefebc},\n last_modified = {2022-05-21T02:53:51.111Z},\n read = {false},\n starred = {false},\n authored = {false},\n confirmed = {false},\n hidden = {false},\n source_type = {article},\n private_publication = {false},\n abstract = {Familial Adenomatous Polyposis (FAP) is an autosomal dominant disorder caused by mutation of the APC gene presenting with numerous colorectal adenomatous polyps and a near 100% risk of colon cancer. Preliminary research findings from our group indicate that FAP patients experience significant deficits across many cognitive domains. In the current study, fMRI brain metrics in a FAP population and matched controls were used to further the mechanistic understanding of reported cognitive deficits. This research identified and characterized any possible differences in resting brain networks and associations between neural network changes and cognition from 34 participants (18 FAP patients, 16 healthy controls). Functional connectivity analysis was performed using FSL with independent component analysis (ICA) to identify functional networks. Significant differences between cases and controls were observed in 8 well-established resting state networks. With the addition of an aggregate cognitive measure as a covariate, these differences were virtually non-existent, indicating a strong correlation between cognition and brain activity at the network level. The data indicate robust and pervasive effects on functional neural network activity among FAP patients and these effects are likely involved in cognitive deficits associated with this disease.},\n bibtype = {article},\n author = {Cali, R J and Nephew, B C and Moore, C M and Chumachenko, S and Sala, A C and Cintron, B and Luciano, C and King, J A and Hooper, S R and Giardiello, F M and Cruz-Correa, M},\n doi = {10.1016/j.ibneur.2021.09.007},\n journal = {IBRO Neuroscience Reports}\n}
\n
\n\n\n
\n Familial Adenomatous Polyposis (FAP) is an autosomal dominant disorder caused by mutation of the APC gene presenting with numerous colorectal adenomatous polyps and a near 100% risk of colon cancer. Preliminary research findings from our group indicate that FAP patients experience significant deficits across many cognitive domains. In the current study, fMRI brain metrics in a FAP population and matched controls were used to further the mechanistic understanding of reported cognitive deficits. This research identified and characterized any possible differences in resting brain networks and associations between neural network changes and cognition from 34 participants (18 FAP patients, 16 healthy controls). Functional connectivity analysis was performed using FSL with independent component analysis (ICA) to identify functional networks. Significant differences between cases and controls were observed in 8 well-established resting state networks. With the addition of an aggregate cognitive measure as a covariate, these differences were virtually non-existent, indicating a strong correlation between cognition and brain activity at the network level. The data indicate robust and pervasive effects on functional neural network activity among FAP patients and these effects are likely involved in cognitive deficits associated with this disease.\n
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\n \n\n \n \n \n \n \n Biopsychosocial correlates of psychological distress in Latina mothers.\n \n \n \n\n\n \n Santos, H., P.; Adynski, H.; Harris, R.; Bhattacharya, A.; Rodriguez, A., C., I.; Cali, R.; Yabar, A., T.; Nephew, B., C.; and Murgatroyd, C.\n\n\n \n\n\n\n Journal of Affective Disorders, 282. 2021.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
\n
@article{\n title = {Biopsychosocial correlates of psychological distress in Latina mothers},\n type = {article},\n year = {2021},\n keywords = {Biomarkers,DNA methylation,Latinas,Postpartum,Prenatal,Psychological distress},\n volume = {282},\n id = {ec6df6c6-1d42-360a-a2ba-5d970e60e681},\n created = {2022-05-21T02:53:51.738Z},\n file_attached = {false},\n profile_id = {87c992c1-10d8-3542-a95f-de865d710d61},\n group_id = {2fb46359-0450-327e-9ad8-3208cfcefebc},\n last_modified = {2022-05-21T02:53:51.738Z},\n read = {false},\n starred = {false},\n authored = {false},\n confirmed = {false},\n hidden = {false},\n source_type = {article},\n private_publication = {false},\n abstract = {Background: Few studies have explored the relationship between psychological, psychosocial and biological factors among Latinas. An integrated understanding of how these factors associate with psychological distress is necessary for the development of culturally relevant screening tools and interventions. The study aim was to examine the relationships among (a) psychological distress symptoms, (b) psychosocial factors (discrimination, acculturation, acculturative stress, economic hardship), and (c) biological (DNA methylation of stress-related genes) factors among Latinas during pregnancy and postpartum period. Methods: A sample of 150 pregnant Latinas completed the Inventory of Depression and Anxiety Symptoms II (IDAS-II), psychosocial questionnaires (discrimination, acculturation, acculturative stress, economic hardship) before (24-32 weeks) and after gestation (4-6 weeks postpartum). Blood samples were collected between 24-32 weeks gestation. Correlations were determined between psychosocial and biological measures and psychological distress measures. Multivariable linear regression models were conducted to assess the relationships between IDAS and stressors. Results: Several correlations among psychosocial measures,DNA methylation factors and IDAS-II variables were identified. Among the psychosocial measures, everyday discrimination was the most strongly and consistently associated with IDAS-II. DNA methylation of NR3C1 affects the associations between psychological and psychosocial distress. Limitations: We only assessed DNA methylation during pregnancy and focused on four HPA-related genes. Longitudinal assessment of DNA methylation and genome-wide analysis can provide a better picture of the role of methylation in psychological distress. Conclusions: This work may assist clinicians and policy makers in effectively recognizing and preventing maternal mental health disparities based on discrimination and other psychosocial stressors in at-risk groups.},\n bibtype = {article},\n author = {Santos, H P and Adynski, H and Harris, R and Bhattacharya, A and Rodriguez, A C Incollingo and Cali, R and Yabar, A T and Nephew, B C and Murgatroyd, C},\n doi = {10.1016/j.jad.2020.12.193},\n journal = {Journal of Affective Disorders}\n}
\n
\n\n\n
\n Background: Few studies have explored the relationship between psychological, psychosocial and biological factors among Latinas. An integrated understanding of how these factors associate with psychological distress is necessary for the development of culturally relevant screening tools and interventions. The study aim was to examine the relationships among (a) psychological distress symptoms, (b) psychosocial factors (discrimination, acculturation, acculturative stress, economic hardship), and (c) biological (DNA methylation of stress-related genes) factors among Latinas during pregnancy and postpartum period. Methods: A sample of 150 pregnant Latinas completed the Inventory of Depression and Anxiety Symptoms II (IDAS-II), psychosocial questionnaires (discrimination, acculturation, acculturative stress, economic hardship) before (24-32 weeks) and after gestation (4-6 weeks postpartum). Blood samples were collected between 24-32 weeks gestation. Correlations were determined between psychosocial and biological measures and psychological distress measures. Multivariable linear regression models were conducted to assess the relationships between IDAS and stressors. Results: Several correlations among psychosocial measures,DNA methylation factors and IDAS-II variables were identified. Among the psychosocial measures, everyday discrimination was the most strongly and consistently associated with IDAS-II. DNA methylation of NR3C1 affects the associations between psychological and psychosocial distress. Limitations: We only assessed DNA methylation during pregnancy and focused on four HPA-related genes. Longitudinal assessment of DNA methylation and genome-wide analysis can provide a better picture of the role of methylation in psychological distress. Conclusions: This work may assist clinicians and policy makers in effectively recognizing and preventing maternal mental health disparities based on discrimination and other psychosocial stressors in at-risk groups.\n
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\n \n\n \n \n \n \n \n The impact of ultrafine particles on mental health.\n \n \n \n\n\n \n Nephew, B., C.; Nephew, G., J.; Cali, R.; Lu, S.; Howell-Munson, A.; and Yabar, A., T.\n\n\n \n\n\n\n 2021.\n \n\n\n\n
\n\n\n\n \n\n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n
@book{\n title = {The impact of ultrafine particles on mental health},\n type = {book},\n year = {2021},\n source = {Ambient Combustion Ultrafine Particles and Health},\n id = {ac6ea628-d619-30f5-becc-5fd045367c0e},\n created = {2022-05-21T02:53:52.329Z},\n file_attached = {false},\n profile_id = {87c992c1-10d8-3542-a95f-de865d710d61},\n group_id = {2fb46359-0450-327e-9ad8-3208cfcefebc},\n last_modified = {2022-05-21T02:53:52.329Z},\n read = {false},\n starred = {false},\n authored = {false},\n confirmed = {false},\n hidden = {false},\n source_type = {book},\n private_publication = {false},\n abstract = {While there is robust evidence of the critical role of PM2.5 in mental health and psychiatric disorders, much less is known about the specific role of ultrafine particle exposure. Lack of assessment of ultrafine particles (UFP) makes it difficult to attribute adverse effects specifically to this size range of particulate matter. This is despite a wealth of predominantly short term epidemiological studies indicating that some of the adverse effects of particulate matter on health are strongly mediated by UFP. The objective of this review is to summarize evidence of the role of UFP in cognitive and mental health from studies of humans and related animal models. Strategies to enhance both human and animal studies through increased collaborative interaction are also discussed. Human studies of UFP clearly indicate the potential for adverse effects on mental health. In areas where PM2.5 concentration exceeds government standards, there are increased risks of impaired cognitive development, autism, Alzheimer’s/dementia, depression, and ADHD. Air pollution and UFP specifically may cause cognitive deficits in both early and late life. Compared to other research areas where there are often differences between the findings of clinical and animal studies, work in animal models of the effects of UFP on mental health have been consistent with, and supportive of, the epidemiological and clinical findings. The further minimization of lab related experimental studies through the expansion of naturalistic paradigms and increased direct collaboration between basic researchers and clinicians will enhance the collection of translationally relevant data. Taken together, these human and animal studies indicate that elevated concentrations of UFP air pollution have a considerable adverse impact on the brain and mental health, both in early and late life.},\n bibtype = {book},\n author = {Nephew, B C and Nephew, G J and Cali, R and Lu, S and Howell-Munson, A and Yabar, A T}\n}
\n
\n\n\n
\n While there is robust evidence of the critical role of PM2.5 in mental health and psychiatric disorders, much less is known about the specific role of ultrafine particle exposure. Lack of assessment of ultrafine particles (UFP) makes it difficult to attribute adverse effects specifically to this size range of particulate matter. This is despite a wealth of predominantly short term epidemiological studies indicating that some of the adverse effects of particulate matter on health are strongly mediated by UFP. The objective of this review is to summarize evidence of the role of UFP in cognitive and mental health from studies of humans and related animal models. Strategies to enhance both human and animal studies through increased collaborative interaction are also discussed. Human studies of UFP clearly indicate the potential for adverse effects on mental health. In areas where PM2.5 concentration exceeds government standards, there are increased risks of impaired cognitive development, autism, Alzheimer’s/dementia, depression, and ADHD. Air pollution and UFP specifically may cause cognitive deficits in both early and late life. Compared to other research areas where there are often differences between the findings of clinical and animal studies, work in animal models of the effects of UFP on mental health have been consistent with, and supportive of, the epidemiological and clinical findings. The further minimization of lab related experimental studies through the expansion of naturalistic paradigms and increased direct collaboration between basic researchers and clinicians will enhance the collection of translationally relevant data. Taken together, these human and animal studies indicate that elevated concentrations of UFP air pollution have a considerable adverse impact on the brain and mental health, both in early and late life.\n
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\n \n\n \n \n \n \n \n Keeping weight off: Mindfulness-Based Stress Reduction alters amygdala functional connectivity during weight loss maintenance in a randomized control trial.\n \n \n \n\n\n \n Chumachenko, S., Y.; Cali, R., J.; Rosal, M., C.; Allison, J., J.; Person, S., J.; Ziedonis, D.; Nephew, B., C.; Moore, C., M.; Zhang, N.; King, J., A.; and Fulwiler, C.\n\n\n \n\n\n\n PLoS ONE, 16(1 January). 2021.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
\n
@article{\n title = {Keeping weight off: Mindfulness-Based Stress Reduction alters amygdala functional connectivity during weight loss maintenance in a randomized control trial},\n type = {article},\n year = {2021},\n volume = {16},\n id = {c4a01034-70eb-34be-9778-c6c1473f7b73},\n created = {2022-05-21T02:53:52.750Z},\n file_attached = {false},\n profile_id = {87c992c1-10d8-3542-a95f-de865d710d61},\n group_id = {2fb46359-0450-327e-9ad8-3208cfcefebc},\n last_modified = {2022-05-21T02:53:52.750Z},\n read = {false},\n starred = {false},\n authored = {false},\n confirmed = {false},\n hidden = {false},\n source_type = {article},\n private_publication = {false},\n abstract = {Obesity is associated with significant comorbidities and financial costs. While behavioral interventions produce clinically meaningful weight loss, weight loss maintenance is challenging. The objective was to improve understanding of the neural and psychological mechanisms modified by mindfulness that may predict clinical outcomes. Individuals who intentionally recently lost weight were randomized to Mindfulness-Based Stress Reduction (MBSR) or a control healthy living course. Anthropometric and psychological factors were measured at baseline, 8 weeks and 6 months. Functional connectivity (FC) analysis was performed at baseline and 8 weeks to examine FC changes between regions of interest selected a priori, and independent components identified by independent component analysis. The association of pre-post FC changes with 6-month weight and psychometric outcomes was then analyzed. Significant group x time interaction was found for FC between the amygdala and ventromedial prefrontal cortex, such that FC increased in the MBSR group and decreased in controls. Non-significant changes in weight were observed at 6 months, where the mindfulness group maintained their weight while the controls showed a weight increase of 3.4% in BMI. Change in FC at 8-weeks between ventromedial prefrontal cortex and several ROIs was associated with change in depression symptoms but not weight at 6 months. This pilot study provides preliminary evidence of neural mechanisms that may be involved in MBSR’s impact on weight loss maintenance that may be useful for designing future clinical trials and mechanistic studies.},\n bibtype = {article},\n author = {Chumachenko, S Y and Cali, R J and Rosal, M C and Allison, J J and Person, S J and Ziedonis, D and Nephew, B C and Moore, C M and Zhang, N and King, J A and Fulwiler, C},\n doi = {10.1371/journal.pone.0244847},\n journal = {PLoS ONE},\n number = {1 January}\n}
\n
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\n Obesity is associated with significant comorbidities and financial costs. While behavioral interventions produce clinically meaningful weight loss, weight loss maintenance is challenging. The objective was to improve understanding of the neural and psychological mechanisms modified by mindfulness that may predict clinical outcomes. Individuals who intentionally recently lost weight were randomized to Mindfulness-Based Stress Reduction (MBSR) or a control healthy living course. Anthropometric and psychological factors were measured at baseline, 8 weeks and 6 months. Functional connectivity (FC) analysis was performed at baseline and 8 weeks to examine FC changes between regions of interest selected a priori, and independent components identified by independent component analysis. The association of pre-post FC changes with 6-month weight and psychometric outcomes was then analyzed. Significant group x time interaction was found for FC between the amygdala and ventromedial prefrontal cortex, such that FC increased in the MBSR group and decreased in controls. Non-significant changes in weight were observed at 6 months, where the mindfulness group maintained their weight while the controls showed a weight increase of 3.4% in BMI. Change in FC at 8-weeks between ventromedial prefrontal cortex and several ROIs was associated with change in depression symptoms but not weight at 6 months. This pilot study provides preliminary evidence of neural mechanisms that may be involved in MBSR’s impact on weight loss maintenance that may be useful for designing future clinical trials and mechanistic studies.\n
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\n  \n 2020\n \n \n (2)\n \n \n
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\n \n\n \n \n \n \n \n Traffic-related particulate matter affects behavior, inflammation, and neural integrity in a developmental rodent model.\n \n \n \n\n\n \n Nephew, B., C.; Nemeth, A.; Hudda, N.; Beamer, G.; Mann, P.; Petitto, J.; Cali, R.; Febo, M.; Kulkarni, P.; Poirier, G.; King, J.; Durant, J., L.; and Brugge, D.\n\n\n \n\n\n\n Environmental Research, 183. 2020.\n \n\n\n\n
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@article{\n title = {Traffic-related particulate matter affects behavior, inflammation, and neural integrity in a developmental rodent model},\n type = {article},\n year = {2020},\n keywords = {Behavior,Development,Inflammation,Particulate matter,Rodent},\n volume = {183},\n id = {be7bb452-12ef-3afb-85cc-fdff8ce8dae0},\n created = {2022-05-21T02:53:53.165Z},\n file_attached = {false},\n profile_id = {87c992c1-10d8-3542-a95f-de865d710d61},\n group_id = {2fb46359-0450-327e-9ad8-3208cfcefebc},\n last_modified = {2022-05-21T02:53:53.165Z},\n read = {false},\n starred = {false},\n authored = {false},\n confirmed = {false},\n hidden = {false},\n source_type = {article},\n private_publication = {false},\n abstract = {Recent studies indicate that exposure to airborne particulate matter (PM) is associated with cognitive delay, depression, anxiety, autism, and neurodegenerative diseases; however, the role of PM in the etiology of these outcomes is not well-understood. Therefore, there is a need for controlled animal studies to better elucidate the causes and mechanisms by which PM impacts these health outcomes. We assessed the effects of gestational and early life exposure to traffic-related PM on social- and anxiety-related behaviors, cognition, inflammatory markers, and neural integrity in juvenile male rats. Gestating and lactating rats were exposed to PM from a Boston (MA, USA) traffic tunnel for 5 h/day, 5 days/week for 6 weeks (3 weeks gestation, 3 weeks lactation). The target exposure concentration for the fine fraction of nebulized PM, measured as PM2.5, was 200 μg/m3. To assess anxiety and cognitive function, F1 male juveniles underwent elevated platform, cricket predation, nest building, social behavior and marble burying tests at 32–60 days of age. Upon completion of behavioral testing, multiple cytokines and growth factors were measured in these animals and their brains were analyzed with diffusion tensor MRI to assess neural integrity. PM exposure had no effect on litter size or weight, or offspring growth; however, F1 litters developmentally exposed to PM exhibited significantly increased anxiety (p = 0.04), decreased cognition reflected in poorer nest-organization (p = 0.04), and decreased social play and allogrooming (p = 0.003). MRI analysis of ex vivo brains revealed decreased structural integrity of neural tissues in the anterior cingulate and hippocampus in F1 juveniles exposed to PM (p < 0.01, p = 0.03, respectively). F1 juvenile males exposed to PM also exhibited significantly decreased plasma levels of both IL-18 (p = 0.03) and VEGF (p = 0.04), and these changes were inversely correlated with anxiety-related behavior. Chronic exposure of rat dams and their offspring to traffic-related PM during gestation and lactation decreases social behavior, increases anxiety, impairs cognition, decreases levels of inflammatory and growth factors (which are correlated with behavioral changes), and disrupts neural integrity in the juvenile male offspring. Our findings add evidence that exposure to traffic-related air pollution during gestation and lactation is involved in the etiology of autism spectrum disorder and other disorders which include social and cognitive deficits and/or increased anxiety.},\n bibtype = {article},\n author = {Nephew, B C and Nemeth, A and Hudda, N and Beamer, G and Mann, P and Petitto, J and Cali, R and Febo, M and Kulkarni, P and Poirier, G and King, J and Durant, J L and Brugge, D},\n doi = {10.1016/j.envres.2020.109242},\n journal = {Environmental Research}\n}
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\n Recent studies indicate that exposure to airborne particulate matter (PM) is associated with cognitive delay, depression, anxiety, autism, and neurodegenerative diseases; however, the role of PM in the etiology of these outcomes is not well-understood. Therefore, there is a need for controlled animal studies to better elucidate the causes and mechanisms by which PM impacts these health outcomes. We assessed the effects of gestational and early life exposure to traffic-related PM on social- and anxiety-related behaviors, cognition, inflammatory markers, and neural integrity in juvenile male rats. Gestating and lactating rats were exposed to PM from a Boston (MA, USA) traffic tunnel for 5 h/day, 5 days/week for 6 weeks (3 weeks gestation, 3 weeks lactation). The target exposure concentration for the fine fraction of nebulized PM, measured as PM2.5, was 200 μg/m3. To assess anxiety and cognitive function, F1 male juveniles underwent elevated platform, cricket predation, nest building, social behavior and marble burying tests at 32–60 days of age. Upon completion of behavioral testing, multiple cytokines and growth factors were measured in these animals and their brains were analyzed with diffusion tensor MRI to assess neural integrity. PM exposure had no effect on litter size or weight, or offspring growth; however, F1 litters developmentally exposed to PM exhibited significantly increased anxiety (p = 0.04), decreased cognition reflected in poorer nest-organization (p = 0.04), and decreased social play and allogrooming (p = 0.003). MRI analysis of ex vivo brains revealed decreased structural integrity of neural tissues in the anterior cingulate and hippocampus in F1 juveniles exposed to PM (p < 0.01, p = 0.03, respectively). F1 juvenile males exposed to PM also exhibited significantly decreased plasma levels of both IL-18 (p = 0.03) and VEGF (p = 0.04), and these changes were inversely correlated with anxiety-related behavior. Chronic exposure of rat dams and their offspring to traffic-related PM during gestation and lactation decreases social behavior, increases anxiety, impairs cognition, decreases levels of inflammatory and growth factors (which are correlated with behavioral changes), and disrupts neural integrity in the juvenile male offspring. Our findings add evidence that exposure to traffic-related air pollution during gestation and lactation is involved in the etiology of autism spectrum disorder and other disorders which include social and cognitive deficits and/or increased anxiety.\n
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\n \n\n \n \n \n \n \n Pregnancy associated epigenetic markers of inflammation predict depression and anxiety symptoms in response to discrimination.\n \n \n \n\n\n \n Sluiter, F.; Rodriguez, A., C., I.; Nephew, B., C.; Cali, R.; Murgatroyd, C.; and Santos, H., P.\n\n\n \n\n\n\n Neurobiology of Stress, 13. 2020.\n \n\n\n\n
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@article{\n title = {Pregnancy associated epigenetic markers of inflammation predict depression and anxiety symptoms in response to discrimination},\n type = {article},\n year = {2020},\n keywords = {Discrimination,Epigenetic,Inflammation,Latina,Maternal stress,TNFα,Treg cells},\n volume = {13},\n id = {4b9b3df4-5a8a-34be-87ca-d169fbda55dc},\n created = {2022-05-21T02:53:54.072Z},\n file_attached = {false},\n profile_id = {87c992c1-10d8-3542-a95f-de865d710d61},\n group_id = {2fb46359-0450-327e-9ad8-3208cfcefebc},\n last_modified = {2022-05-21T02:53:54.072Z},\n read = {false},\n starred = {false},\n authored = {false},\n confirmed = {false},\n hidden = {false},\n source_type = {article},\n private_publication = {false},\n abstract = {Latina mothers, who have one of the highest fertility rates among ethnic groups in the United States (US), often experience discrimination. Psychosocial influences during pregnancy, such as discrimination stress, promotes inflammation. However, the role of epigenetic markers of inflammation as a mediator between, and predictor of, maternal discrimination stress and neuropsychiatric outcomes has not been extensively studied. The current study investigates the role of DNA methylation at FOXP3 Treg-cell-specific demethylated region (TSDR), as a marker of regulatory T (Treg) cells that are important negative regulators of inflammation, and the promoter of tumour necrosis factor-alpha (TNF-α) gene, an important pro-inflammatory cytokine, in relation to discrimination stress during pregnancy and depression and anxiety symptomatology. A sample of 148 Latina women residing in the US (mean age 27.6 years) were assessed prenatally at 24–32 weeks’ gestation and 4–6 weeks postnatally for perceived discrimination exposure (Everyday Discrimination Scale, EDS), emotional distress (depression, anxiety, perinatal-specific depression), acculturation, and acculturative stress. DNA methylation levels at the FOXP3 and TNFα promoter regions from blood samples collected at the prenatal stage were assessed by bisulphite pyrosequencing. Regression analyses showed that prenatal EDS associated with postnatal emotional distress, depression and anxiety symptoms only in those individuals with higher than mean levels of FOXP3 TSDR and TNFα promoter methylation; no such significant associations were found in those with lower than mean levels of methylation for either. We further found that these relationships were mediated by TNFα only in those with high FOXP3 TSDR methylation, implying that immunosuppression via TNFα promoter methylation buffers the impact of discrimination stress on postpartum symptomatology. These results indicate that epigenetic markers of immunosuppression and inflammation play an important role in resilience or sensitivity, respectively, to prenatal stress.},\n bibtype = {article},\n author = {Sluiter, F and Rodriguez, A C Incollingo and Nephew, B C and Cali, R and Murgatroyd, C and Santos, H P},\n doi = {10.1016/j.ynstr.2020.100273},\n journal = {Neurobiology of Stress}\n}
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\n Latina mothers, who have one of the highest fertility rates among ethnic groups in the United States (US), often experience discrimination. Psychosocial influences during pregnancy, such as discrimination stress, promotes inflammation. However, the role of epigenetic markers of inflammation as a mediator between, and predictor of, maternal discrimination stress and neuropsychiatric outcomes has not been extensively studied. The current study investigates the role of DNA methylation at FOXP3 Treg-cell-specific demethylated region (TSDR), as a marker of regulatory T (Treg) cells that are important negative regulators of inflammation, and the promoter of tumour necrosis factor-alpha (TNF-α) gene, an important pro-inflammatory cytokine, in relation to discrimination stress during pregnancy and depression and anxiety symptomatology. A sample of 148 Latina women residing in the US (mean age 27.6 years) were assessed prenatally at 24–32 weeks’ gestation and 4–6 weeks postnatally for perceived discrimination exposure (Everyday Discrimination Scale, EDS), emotional distress (depression, anxiety, perinatal-specific depression), acculturation, and acculturative stress. DNA methylation levels at the FOXP3 and TNFα promoter regions from blood samples collected at the prenatal stage were assessed by bisulphite pyrosequencing. Regression analyses showed that prenatal EDS associated with postnatal emotional distress, depression and anxiety symptoms only in those individuals with higher than mean levels of FOXP3 TSDR and TNFα promoter methylation; no such significant associations were found in those with lower than mean levels of methylation for either. We further found that these relationships were mediated by TNFα only in those with high FOXP3 TSDR methylation, implying that immunosuppression via TNFα promoter methylation buffers the impact of discrimination stress on postpartum symptomatology. These results indicate that epigenetic markers of immunosuppression and inflammation play an important role in resilience or sensitivity, respectively, to prenatal stress.\n
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