Demographic diversity is not represented in the HIV/AIDS workforce. Engagement of underrepresented trainees as early as high school may address this disparity.
We established the Penn Center for AIDS ...Research (CFAR) Scholars Program, a mentored research experience for underrepresented minority (URM) trainees spanning educational stages from high school to medical school. The program provides participants with tailored educational programming, professional skill building, and mentored research experiences. We conducted qualitative interviews with scholar, mentor, and leadership groups to evaluate the program's impact.
Eleven participants were selected to partake in 1 of 5 existing mentored research programs as CFAR scholars. Scholars attended an 8-week HIV Seminar Series that covered concepts in the basic, clinical, behavioral, and community-based HIV/AIDS research. Program evaluation revealed that scholars' knowledge of HIV pathophysiology and community impact increased because of these seminars. In addition, they developed tangible skills in literature review, bench techniques, qualitative assessment, data analysis, and professional network building. Scholars reported improved academic self-efficacy and achieved greater career goal clarity. Areas for improvement included clarification of mentor-mentee roles, expectations for longitudinal mentorship, and long-term engagement between scholars. Financial stressors, lack of social capital, and structural racism were identified as barriers to success for URM trainees.
The Penn CFAR Scholars Program is a novel mentored research program that successfully engaged URM trainees from early educational stages. Barriers and facilitators to sustained efforts of diversifying the HIV/AIDS workforce were identified and will inform future program planning.
Mature mammalian neurons have a limited ability to extend neurites and make new synaptic connections, but the mechanisms that inhibit such plasticity remain poorly understood. Here, we report that ...OFF-type retinal bipolar cells in mice are an exception to this rule, as they form new anatomical connections within their tiled dendritic fields well after retinal maturity. The Down syndrome cell-adhesion molecule (Dscam) confines these anatomical rearrangements within the normal tiled fields, as conditional deletion of the gene permits extension of dendrite and axon arbors beyond these borders. Dscam deletion in the mature retina results in expanded dendritic fields and increased cone photoreceptor contacts, demonstrating that DSCAM actively inhibits circuit-level plasticity. Electrophysiological recordings from Dscam−/−
OFF bipolar cells showed enlarged visual receptive fields, demonstrating that expanded dendritic territories comprise functional synapses. Our results identify cell-adhesion molecule-mediated inhibition as a regulator of circuit-level neuronal plasticity in the adult retina.
PDF