RESUMO
Objectives: Despite decades of literature recognizing racial disparities (RDs) in emergency medicine (EM), published curricula dedicated to addressing them are sparse. We present details of our novel RD curriculum for EM clerkships and its educational outcomes. Methods: We created a 30-min interactive didactic module on the topic designed for third- and fourth-year medical students enrolled in our EM clerkships. Through a modified Delphi process, education faculty and content experts in RD developed a 10-question multiple-choice test of knowledge on RD that the students completed immediately prior to and 2 weeks following the activity. Students also completed a Likert-style learner satisfaction survey. Median pre- and posttest scores were compared using a paired Wilcoxon signed-rank test and presented using medians and 95% confidence intervals (CIs). Satisfaction survey responses were dichotomized into favorable and neutral/not favorable. Results: For the 36 students who completed the module, the median pretest score was 40% (95% CI 36%-50%) and the posttest score was 70% (95% CI 60%-70%) with a p-value of <0.001. Thirty-five of the 36 students improved on the posttest with a mean increase of 24.2% (95% CI 20.2-28.2). The satisfaction survey also showed a positive response, with at least 83% of participants responding favorably to all statements (overall mean favorable response 93%, 95% CI 90%-96%).ConclusionsThis EM-based module on RD led to improvement in students' knowledge on the topic and positive reception by participants. This is a feasible option for educating students in EM on the topic of RD.
RESUMO
Normal aging is characterized by declines in processing speed, learning, memory, and executive function even in the absence of neurodegenerative diseases such as Alzheimer's Disease (AD). In normal aging monkeys and humans, neuronal loss does not account for cognitive impairment. Instead, loss of white matter volume and an accumulation of myelin sheath pathology begins in middle age and is associated with cognitive decline. It is unknown what causes this myelin pathology, but it likely involves increased neuroinflammation in white matter and failures in oligodendrocyte function (maturation and repair). In frontal white matter tracts vulnerable to myelin damage, microglia become chronically reactive and secrete harmful pro-inflammatory cytokines. Despite being in a phagocytic state, these microglia are ineffective at phagocytosing accruing myelin debris, which directly inhibits myelin sheath repair. Here, we asked whether reported age-related increases in pro-inflammatory markers were accompanied by an adaptive immune response involving T cells. We quantified T cells with immunohistochemistry in the brains of 34 cognitively characterized monkeys and found an age-related increase in perivascular T cells that surround CNS vasculature. We found a surprising age-related increase in T cells that infiltrate the white matter parenchyma. In the cingulum bundle the percentage of these parenchymal T cells increased with age relative to those in the perivascular space. In contrast, infiltrating T cells were rarely found in surrounding gray matter regions. We assessed whether T cell infiltration correlated with fibrinogen extravasation from the vasculature as a measure of BBB leakiness and found no correlation, suggesting that T cell infiltration is not a result of passive extravasation. Importantly, the density of T cells in the cingulum bundle correlated with microglial reactivity and with cognitive impairment. This is the first demonstration that T cell infiltration of white matter is associated with cognitive decline in the normal aging monkey.