Medical Humanities Coursework Is Associated with Greater Measured Empathy in Medical Students.

PURPOSE: The primary focus of the study was to determine whether coursework in the medical humanities would ameliorate students' loss of and failure to develop empathy, a problem known to be common during medical education. METHODS: Students were offered an elective course in the Medical Humanities for academic credit. The Jefferson Scale of Empathy Student Version (JSE-S) was administered at the beginning and end of an academic year in which humanities courses were offered. Changes in JSE-S scores among students who studied Medical Humanities were compared with changes in student who did not take any humanities coursework. RESULTS: Medical humanities coursework correlated with superior empathy outcomes among the medical students. Of students not enrolled in humanities courses, 71% declined or failed to increase in JSE-S score over the academic year. Of those who took humanities coursework, 46% declined or failed to increase in JSE-S scores. The difference was statistically significant (P = .03). The medical humanities curriculum correlated with favorable empathy outcomes as measured by the JSE-S. CONCLUSIONS: Elective medical humanities coursework correlated with improved empathy score outcomes in a group of US medical students. This may reflect a direct effect of the humanities coursework. Alternately, students' elective choice to take medical humanities coursework may be a marker for students with a propensity to favorable empathy outcomes.

A selective small molecule agonist of the melanocortin-1 receptor inhibits lipopolysaccharide-induced cytokine accumulation and leukocyte infiltration in mice.

It is well established that melanocortins are peptides that have potent anti-inflammatory activity. Recent research has focused on understanding which of the known melanocortin receptors mediates the anti-inflammatory actions of the melanocortins. The aim of this study was to assess the anti-inflammatory activity of a synthetic MC-1R agonist. BMS-470539 is a potent, selective, full agonist of human and murine MC-1R with EC(50) values in a cAMP accumulation assay of 16.8 and 11.6 nM, respectively. BMS-470539 dose-dependently inhibited TNF-alpha-induced activation of a NF-kappaB transcriptional reporter in human melanoma cells, which endogenously express MC-1R. In vivo studies with BMS-470539 demonstrated that subcutaneous administration of BMS-470539 resulted in a dose-dependent inhibition of LPS-induced TNF-alpha production in BALB/c mice. In this model, the compound had an ED(50) of approximately 10 micromol/kg and a pharmacodynamic half-life of approximately 8 h. Pharmacokinetic analysis of the compound indicated that the compound had a t(1/2) of 1.7 h. In a model of lung inflammation, administration of 15 micromol/kg BMS-470539 resulted in a 45% reduction in LPS-induced leukocyte infiltration (an infiltrate comprised primarily of neutrophils). The compound was also effective in a model of delayed-type hypersensitivity, reducing paw swelling by 59%, comparable with that seen with 5 mg/kg dexamethasone. These studies demonstrate that a selective small molecule agonist of the melanocortin-1 receptor is a potent anti-inflammatory agent in vivo and provides compelling evidence for the involvement of this receptor in the modulation of inflammation.