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School-based mental health professionals are in an ideal position to intervene and prevent problematic substance use among adolescents (Lasser & Schmidt, 2010). Although specialized graduate training in addictions is commonplace for clinical, counseling, and social work, it has not been as readily available in preservice programs for school psychologists. Consequently, offering a graduate level preservice specialization in addictions to school psychology students was seen as an ideal way to increase the mental health workforce who can address these issues and strengthen outcomes for adolescents with substance abuse and addiction problems. The concept of "It takes a village" was at the forefront of a new collaborative effort to create a specialization in substance abuse and addictions that could be taken by graduate students in school psychology and school counseling. In support of the interprofessional mission of the Morgridge College of Education at the University of Denver, a new addictions specialization was created as a collaboration between the Counseling Psychology Department and the Child, Family & School Psychology Program. This specialization in adolescent addictions was focused on work best conducted within schools by trained mental health support professionals, such as school counselors, school social workers, and school psychologists. The new program was developed cooperatively with input from current faculty, administrators, and practitioners in the field of addictions. The major purpose of the new program was to provide high-quality preparation for students within these fields to work interprofessionally within the school environment. A brief overview will be provided of the critical components and benefits of this new specialization currently in its second year of implementation, highlighting what has been learned and what is needed to guarantee its continuation in the future.

Abstract: Background and purpose: Prostaglandin ethanolamides or prostamides are naturally occurring neutral lipid derivatives of prostaglandins that have been shown to be synthesised in vivo following COX-facilitated oxygenation of arachidonoyl ethanolamine (anandamide). Although the actions of prostaglandins have been extensively studied, little is known about the physiological or pathophysiological effects of prostamides. Since prostaglandin E2 has potent immunosuppressive/immunomodulating actions, the aim of the present study was to determine whether the derivative, prostaglandin E2 ethanolamide (PGE2-EA), could modulate the production of the pro-inflammatory cytokine tumour necrosis factor-α in human blood and human monocytic cells and indicate whether this action involved the same receptor systems/signals as PGE2. Experimental approach: Whole human blood, monocytes isolated from the blood or the human monocytic cell line THP-1 was incubated with LPS and the level of TNF-α produced was measured by ELISA assay. The actions of PGE2-EA were assessed on the LPS-induced TNF-α release. In addition, in order to ascertain the receptors involved, the levels of cyclic AMP in cells were measured in monocytes and THP-1 cells in response to PGE2-EA and directly compared to those of PGE2. The effect of PGE2-EA on the binding of radiolabelled PGE2 to cells was also measured. Cells were incubated with radiolabelled arachidonic acid and ethanolamine to estimate the production of PGE2-EA. Key results: PGE2-EA potently suppressed TNF-α production in blood, monocytes and the cell line THP-1 in a concentration-dependent manner. This occurred via cyclic AMP pathways as indicated by agents which interfere with these pathways and also direct ligand binding experiments. It was also shown that the cells were able to endogenously produce PGE2-EA. Conclusions and implications: This study reports that PGE2-EA can downregulate the production of TNF-α by human mononuclear cells in response to an immune stimulus, i.e. LPS-activated TLR4, and that this appears to occur via a cAMP-dependent mechanism that most likely involves binding to the EP2 receptor. [Copyright &y& Elsevier]