Relationships between study habits, burnout, and general surgery resident performance on the American Board of Surgery In-Training Examination.

BACKGROUND: The American Board of Surgery In-Training Examination (ABSITE) is used by programs to evaluate the knowledge and readiness of trainees to sit for the general surgery qualifying examination. It is often used as a tool for resident promotion and may be used by fellowship programs to evaluate candidates. Burnout has been associated with job performance and satisfaction; however, its presence and effects on surgical trainees' performance are not well studied. We sought to understand factors including burnout and study habits that may contribute to performance on the ABSITE examination. METHODS: Anonymous electronic surveys were distributed to all residents at 10 surgical residency programs (n = 326). Questions included demographics as well as study habits, career interests, residency characteristics, and burnout scores using the Oldenburg Burnout Inventory, which assesses burnout because of both exhaustion and disengagement. These surveys were then linked to the individual's 2016 ABSITE and United States Medical Licensing Examination (USMLE) step 1 and 2 scores provided by the programs to determine factors associated with successful ABSITE performance. RESULTS: In total, 48% (n = 157) of the residents completed the survey. Of those completing the survey, 48 (31%) scored in the highest ABSITE quartile (≥75th percentile) and 109 (69%) scored less than the 75th percentile. In univariate analyses, those in the highest ABSITE quartile had significantly higher USMLE step 1 and step 2 scores (P < 0.001), significantly lower burnout scores (disengagement, P < 0.01; exhaustion, P < 0.04), and held opinions that the ABSITE was important for improving their surgical knowledge (P < 0.01). They also read more frequently to prepare for the ABSITE (P < 0.001), had more disciplined study habits (P < 0.001), were more likely to study at the hospital or other public settings (e.g., library, coffee shop compared with at home; P < 0.04), and used active rather than passive study strategies (P < 0.04). Gender, marital status, having children, and debt burden had no correlation with examination success. Backward stepwise multiple regression analysis identified the following independent predictors of ABSITE scores: study location (P < 0.0001), frequency of reading (P = 0.0001), Oldenburg Burnout Inventory exhaustion (P = 0.02), and USMLE step 1 and 2 scores (P = 0.007 and 0.0001, respectively). CONCLUSIONS: Residents who perform higher on the ABSITE have a regular study schedule throughout the year, report less burnout because of exhaustion, study away from home, and have shown success in prior standardized tests. Further study is needed to determine the effects of burnout on clinical duties, career advancement, and satisfaction.

Constitutive cholesterol-dependent endocytosis of melanocortin-4 receptor (MC4R) is essential to maintain receptor responsiveness to α-melanocyte-stimulating hormone (α-MSH).

Melanocortin-4 receptor (MC4R) is a G-protein-coupled receptor expressed in the hypothalamus where it controls feeding behavior. MC4R cycles constitutively and is internalized at the same rate in the presence or absence of stimulation by the agonist, melanocyte-stimulating hormone (α-MSH). This is different from other G-protein-coupled receptors, such as ß(2)-adrenergic receptor (ß(2)AR), which internalizes more rapidly in response to agonist stimulation. Here, it is found that in immortalized neuronal Neuro2A cells expressing exogenous receptors, constitutive endocytosis of MC4R and agonist-dependent internalization of ß(2)AR were equally sensitive to clathrin depletion. Inhibition of MC4R endocytosis by clathrin depletion decreased the number of receptors at the cell surface that were responsive to the agonist, α-MSH, by 75%. Mild membrane cholesterol depletion also inhibited constitutive endocytosis of MC4R by ∼5-fold, while not affecting recycling of MC4R or agonist-dependent internalization of ß(2)AR. Reduced cholesterol did not change the MC4R dose-response curve to α-MSH, but it decreased the amount of cAMP generated per receptor number indicating that a population of MC4R at the cell surface becomes nonfunctional. The loss of MC4R function increased over time (25-50%) and was partially reversed by mutations at putative phosphorylation sites (T312A and S329A). This was reproduced in hypothalamic GT1-7 cells expressing endogenous MC4R. The data indicate that constitutive endocytosis of MC4R is clathrin- and cholesterol-dependent. MC4R endocytosis is required to maintain MC4R responsiveness to α-MSH by constantly eliminating from the plasma membrane a pool of receptors modified at Thr-312 and Ser-329 that have to be cycled to the endosomal compartment to regain function.