Increasing Student Access to Mental Health Services in Virginia Through Staffing and Structures

This dissertation in practice is a response to a request for assistance (RFA) submitted by the Virginia Department of Education (VDOE) Office of Student Services (OoSS). To help school divisions meet Standards of Quality (SOQs) and serve student needs, the VDOE OoSS aims to increase the pipeline of licensed school-based mental health professionals (SMHPs). This Capstone examines staffing and service models that create equitable access to student mental health supports using problem and context analysis, a review of literature, and a three-phased mixed methods data collection. Focus group participants consisted of students and practitioners in the fields of school psychology, counseling, and social work. Document analysis of mental health practice integration was conducted for schools implementing advanced tier models in Virginia Tiered Systems of Support (VTSS) and schools implementing VTSS in conjunction with Recognized ASCA Model Program (RAMP) certification. Additionally, a survey was administered to division-level leadership and SMHPs to examine their understanding of the roles and everyday responsibilities of SMHPs in schools across the state of Virginia

TCDD Inhibition of IgG1 Production in Experimental Autoimmune Encephalomyelitis (EAE) and In Vitro

The environmental contaminant 2,3,7,8-tetrachlorodibenzo-para-dioxin (TCDD) is a ligand for the aryl hydrocarbon receptor (AhR). TCDD is well-characterized to produce immunotoxicity, including suppression of antibody production. Previously we showed that TCDD inhibited myelin oligodendrocyte glycoprotein (MOG) peptide-specific IgG and attenuated disease in experimental autoimmune encephalomyelitis (EAE) model in mice. Thus, the purpose of this study was to characterize the effects of TCDD on IgG subclasses in EAE and in vitro and assess effects in B cells derived from various tissues. TCDD modestly suppressed intracellular IgG expression in splenocytes (SPLC), but not bone marrow (BM) or lymph node (LN) cells. To further understand TCDD’s effects on IgG, we utilized LPS and LPS + IL-4 in vitro to stimulate IgG3 and IgG1 production, respectively. TCDD preferentially suppressed IgG1+ cell surface expression, especially in SPLC. However, TCDD was able to suppress IgG1 and IgG3 secretion from SPLC and B cells, but not BM cells. Lastly, we revisited the EAE model and determined that TCDD suppressed MOG-specific IgG1 production. Together these data show that the IgG1 subclass of IgG is a sensitive target of suppression by TCDD. Part of the pathophysiology of EAE involves production of pathogenic antibodies that can recruit cytolytic cells to destroy MOG-expressing cells that comprise myelin, so inhibition of IgG1 likely contributes to TCDD’s EAE disease attenuation