Introduction: Given the unique experiences of military service members and their families, military-dependent young adults (18-25 years old) with autism spectrum disorder (ASD) and their military or veteran families experience unique barriers to accessing quality mental health care during the transition to adulthood. In fact, developing services to address ASD challenges for military families is a burgeoning area of interest for the department of defense. However, there is a limited knowledge on the specific needs of military families as the young adult's transition outside of high school and lose supports.
View Article and Find Full Text PDFPurpose: As the understanding of autism spectrum disorder (ASD) across the lifespan has increased, so has the number of individuals being identified with ASD for the first time in adulthood. Understanding co-occurring psychiatric conditions in this subset of the ASD population is a growing focus of research; however, little is known about the rate at which psychiatric medications are prescribed to adults with a first-time diagnosis of ASD. The purpose of this study was to examine self-reported medication use in persons diagnosed with ASD in adulthood in a clinic sample (2012-2022) in the United States.
View Article and Find Full Text PDFStudy Question: Does the chemokine/chemokine receptor axis, involved in immune cell trafficking, contribute to the pathology of testicular inflammation and how does activin A modulate this network?
Summary Answer: Testicular chemokines and their receptors (especially those essential for trafficking of monocytes) are elevated in orchitis, and activin A modulates the expression of the chemokine/chemokine receptor network to promote monocyte/macrophage and T cell infiltration into the testes, causing extensive tissue damage.
What Is Known Already: The levels of CC motif chemokine receptor (CCR)2 and its ligand CC motif chemokine ligand (CCL)2 are increased in experimental autoimmune orchitis (EAO) compared with healthy testes, and mice deficient in CCR2 are protected from EAO-induced tissue damage. Activin A induces CCR2 expression in macrophages, promoting their migration.