Impact of Varying Active Learning Time on Student Performance on a Standardized Exam in the Psychiatry Clerkship.

OBJECTIVE: As medical schools reform clinical curricula, an increasing amount of time is spent in active learning activities. The authors hypothesized that students who spent more time in active learning educational activities (e.g., team-based learning, small group activities, clinical simulation) would receive higher NBME Subject Exam scores compared to students with less. METHODS: This cohort study included 518 students from 2014 to 2016 who completed at least six contiguous weeks of a psychiatry clerkship. Active learning time percent was calculated by dividing the amount of time in active learning by the total in-classroom time during the clerkship. Analysis was conducted using ANOVA and linear regression. RESULTS: Analysis found that increasing the amount of active learning was not significantly associated with student scores on the NBME Subject Exam in psychiatry (F = 0.91, p = 0.402). However, when controlling for possible confounding variables (including clerkship length and order), clerkship order was a significant predictor of student performance (r = 0.19, ß = 0.18, p < 0.0001); students who took the clerkship later in the academic year-and after the internal medicine rotation-performed significantly better on the exam. CONCLUSIONS: This study found that increasing the amount of active learning did not improve student performance on the NBME Subject Exam in psychiatry. This study provides preliminary, but unexpected, evidence of interest to medical educators and curriculum reformers that increasing the amount of active learning is not significantly associated with improved student test performance.

Pharmacological promotion of inclusion formation: a therapeutic approach for Huntington's and Parkinson's diseases.

Misfolded proteins accumulate in many neurodegenerative diseases, including huntingtin in Huntington's disease and alpha-synuclein in Parkinson's disease. The disease-causing proteins can take various conformations and are prone to aggregate and form larger cytoplasmic or nuclear inclusions. One approach to the development of therapeutic intervention for these diseases has been to identify chemical compounds that reduce the size or number of inclusions. We have, however, identified a compound that promotes inclusion formation in cellular models of both Huntington's disease and Parkinson's disease. Of particular interest, this compound prevents huntingtin-mediated proteasome dysfunction and reduces alpha-synuclein-mediated toxicity. These results demonstrate that compounds that increase inclusion formation may actually lessen cellular pathology in both Huntington's and Parkinson's diseases, suggesting a therapeutic approach for neurodegenerative diseases caused by protein misfolding.