The inequitable distribution of economic resources and exposure to adversity between racial groups contributes to mental health disparities within the United States. Consideration of the potential neurodevelopmental consequences, however, has been limited particularly for neurocircuitry known to regulate the emotional response to threat. Characterizing the consequences of inequity on threat neurocircuitry is critical for robust and generalizable neurobiological models of psychiatric illness.
View Article and Find Full Text PDFBackground: Prior sexual trauma (ST) is associated with greater risk for posttraumatic stress disorder after a subsequent traumatic event; however, the underlying neurobiological mechanisms remain opaque. We investigated longitudinal posttraumatic dysfunction and amygdala functional dynamics following admission to an emergency department for new primarily nonsexual trauma in participants with and without previous ST.
Methods: Participants ( = 2178) were recruited following acute trauma exposure (primarily motor vehicle collision).
Importance: Differences in neighborhood socioeconomic characteristics are important considerations in understanding differences in risk vs resilience in mental health. Neighborhood disadvantage is associated with alterations in the function and structure of threat neurocircuitry.
Objective: To investigate associations of neighborhood disadvantage with white and gray matter and neural reactivity to positive and negative stimuli in the context of trauma exposure.
Chronic nasal carriage of (SA) has been shown to be significantly higher in GPA patients when compared to healthy subjects, as well as being associated with increased endonasal activity and disease relapse. The aim of this study was to investigate SA involvement in GPA by applying a network-based analysis (NBA) approach to publicly available nasal transcriptomic data. Using these data, our NBA pipeline generated a proteinase 3 (PR3) positive ANCA associated vasculitis (AAV) disease network integrating differentially expressed genes, dysregulated transcription factors (TFs), disease-specific genes derived from GWAS studies, drug-target and protein-protein interactions.
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