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http://dx.doi.org/10.34172/aim.33531DOI Listing

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Post-traumatic stress disorder (PTSD) remains a significant clinical challenge with limited treatment options. Although electroencephalogram (EEG) neurofeedback has garnered attention as a prospective treatment modality for PTSD, no comprehensive meta-analysis has been conducted to assess its efficacy and compare different treatment protocols. This study aims to provide a multi-variable meta-regression analysis of EEG neurofeedback's impact on PTSD symptoms, while also assessing variables that may influence treatment outcomes.

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Introduction: Little is known about the effects of parental mental health burdens during pregnancy on infant health among military families, who are subject to various stressors unique to military life. The present study leveraged infant data from the DoD Birth and Infant Health Research (BIHR) program and self-reported parental survey data from the Millennium Cohort Study (MCS) to examine associations of parental mental health conditions with adverse infant health outcomes.

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Purpose Of Review: Traumatic childbirth can lead to childbirth-related post-traumatic stress disorder (CB-PTSD) or retraumatize those with prior trauma, contributing to long-term maternal and neonatal morbidity and mortality. This condition affects approximately 4-7% of postpartum patients. Given the concerningly high maternal morbidity and mortality rates in the USA, it is crucial to further analyze the risk factors and clinical management recommendations for the prevention of CB-PTSD.

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Background: Predator stress (PS) is used to model trauma leading to post-traumatic stress disorder, and it increases ethanol drinking in a proportion of male and female rodents. The goals of the present studies were to identify male and female mice with prior binge drinking experience that exhibited sensitivity and resilience to PS-enhanced drinking and then to test two target molecules (corticotropin releasing factor receptor 1 [CRF-R1] antagonist NBI-27914 [NBI] and G-protein coupled receptor 39 [GPR39] agonist TC-G 1008 [TC-G]) for their ability to selectively reduce PS-enhanced drinking.

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