Toward Defining the Foundation of the MD Degree: Core Entrustable Professional Activities for Entering Residency.

Currently, no standard defines the clinical skills that medical students must demonstrate upon graduation. The Liaison Committee on Medical Education bases its standards on required subject matter and student experiences rather than on observable educational outcomes. The absence of such established outcomes for MD graduates contributes to the gap between program directors' expectations and new residents' performance.In response, in 2013, the Association of American Medical Colleges convened a panel of experts from undergraduate and graduate medical education to define the professional activities that every resident should be able to do without direct supervision on day one of residency, regardless of specialty. Using a conceptual framework of entrustable professional activities (EPAs), this Drafting Panel reviewed the literature and sought input from the health professions education community. The result of this process was the publication of 13 core EPAs for entering residency in 2014. Each EPA includes a description, a list of key functions, links to critical competencies and milestones, and narrative descriptions of expected behaviors and clinical vignettes for both novice learners and learners ready for entrustment.The medical education community has already begun to develop the curricula, assessment tools, faculty development resources, and pathways to entrustment for each of the 13 EPAs. Adoption of these core EPAs could significantly narrow the gap between program directors' expectations and new residents' performance, enhancing patient safety and increasing residents', educators', and patients' confidence in the care these learners provide in the first months of their residency training.

Five-step authorship framework to improve transparency in disclosing contributors to industry-sponsored clinical trial publications.

Authorship guidelines have established criteria to guide author selection based on significance of contribution and helped to define associated responsibilities and accountabilities for the published findings. However, low awareness, variable interpretation, and inconsistent application of these guidelines can lead to confusion and a lack of transparency when recognizing those who merit authorship. This article describes a research project led by the Medical Publishing Insights and Practices (MPIP) Initiative to identify current challenges when determining authorship for industry-sponsored clinical trials and develop an improved approach to facilitate decision-making when recognizing authors from related publications. A total of 498 clinical investigators, journal editors, publication professionals and medical writers were surveyed to understand better how they would adjudicate challenging, real-world authorship case scenarios, determine the perceived frequency of each scenario and rate their confidence in the responses provided. Multiple rounds of discussions about these results with journal editors, clinical investigators and industry representatives led to the development of key recommendations intended to enhance transparency when determining authorship. These included forming a representative group to establish authorship criteria early in a trial, having all trial contributors agree to these criteria and documenting trial contributions to objectively determine who warrants an invitation to participate in the manuscript development process. The resulting Five-step Authorship Framework is designed to create a more standardized approach when determining authorship for clinical trial publications. Overall, these recommendations aim to facilitate more transparent authorship decisions and help readers better assess the credibility of results and perspectives of the authors for medical research more broadly. Please see related article: http://www.biomedcentral.com/1741-7015/12/214.

Learner deficits and academic outcomes of medical students, residents, fellows, and attending physicians referred to a remediation program, 2006-2012.

PURPOSE: To identify deficit types and predictors of poor academic outcomes among students, residents, fellows, and physicians referred to the University of Colorado School of Medicine's remediation program. METHOD: During 2006-2012, 151 learners were referred. After a standardized assessment process, program faculty developed individualized learning plans that incorporated deliberate practice, feedback, and reflection, followed by independent reassessment. The authors collected data on training levels, identified deficits, remediation plan details, outcomes, and faculty time invested. They examined relationships between gender, training level, and specific deficits. They analyzed faculty time by deficit and explored predictors of negative outcomes. RESULTS: Most learners had more than one deficit; medical knowledge, clinical reasoning, and professionalism were most common. Medical students were more likely than others to have mental well-being issues (P = .03), whereas the prevalence of professionalism deficits increased steadily as training level increased. Men struggled more than women with communication (P = .01) and mental well-being. Poor professionalism was the only predictor of probationary status (P < .001), and probation was a predictor of other negative outcomes (P < .0001). Remediation of clinical reasoning and mental well-being deficits required significantly more faculty time (P < .001 and P = .03, respectively). Per hour, faculty face time reduced the odds of probation by 3.1% (95% CI, 0.09-0.63) and all negative outcomes by 2.6% (95% CI, 0.96-0.99). CONCLUSIONS: Remediation required substantial resources but was successful for 90% of learners. Future studies should compare remediation strategies and assess how to optimize faculty time.

Atrial natriuretic peptide stability.

OBJECTIVE: Atrial natriuretic peptide (ANP) is a key regulator in the homeostasis of water excretion and has emerged as an important prognostic marker for symptomatic chronic heart failure (CHF). The stability of ANP represents a crucial factor in assessing its use as a cardiac biomarker. Accordingly, we assessed the stability of ANP in blood samples collected from healthy controls and CHF subjects for a 12 month period. METHODS: Blood samples from 10 healthy controls and 12 symptomatic CHF subjects with left ventricular systolic dysfunction were drawn. Determination of plasma ANP was performed by a standardized radioimmunoassay protocol. RESULTS: The ANP levels of healthy subjects were 68.5+/-11.6 pg/mL at baseline and 69.9+/-17.2 pg/mL at 12 months (p=0.71). The ANP concentrations of CHF subjects were 199.25+/-44.8 pg/mL at baseline and 197.83+/-47.4 pg/mL at 12 months (p=0.70) respectively. CONCLUSION: ANP is a stable molecule with no evidence of degradation when stored at -80 degrees C.

Enhanced insulin signaling via Shc in human breast cancer.

Insulin is a mild mitogen and has been shown to potentiate mitogenic influence of other growth factors. Because hyperinsulinemia and/or overexpression of insulin receptors have been linked to development, progression, and outcome of breast cancer, we attempted to evaluate the mechanism of these associations. We have compared the expression of insulin receptors and the magnitude of insulin signaling in breast tumors and adjacent normal mammary tissue samples obtained from 20 patients. We observed that insulin binding more than doubled in the tumors as compared with the normal tissue (P <.01 by paired t test). Insulin signaling to Shc, judged by the magnitude of its phosphorylation, was also significantly enhanced in the tumors. In contrast, the phosphorylation of the insulin-receptor substrate-1 (IRS-1), Akt, and mitogen-activated protein (MAP) kinase were identical in the tumorous and normal mammary tissues. Finally, tumors displayed significantly increased amounts of farnesylated p21 Ras and geranylgeranylated Rho-A (P <.01), consistent with Shc-dependent activation of farnesyl (FTase) and geranylgeranyl transferases (GGTase) in the tumor tissue. We conclude that the mechanism of the mitogenic influence of insulin in breast cancer may include increased expression of insulin receptors, preferential hyperphosphorylation of Shc, and increased amounts of prenylated p21 Ras and Rho-A in tumor tissue as compared with adjacent normal mammary tissue.

Human placental growth hormone causes severe insulin resistance in transgenic mice.

OBJECTIVE: The insulin resistance of pregnancy is considered to be mediated by human placental lactogen, but the metabolic effects of human placental growth hormone have not been well defined. Our aim was to evaluate the effect of placental growth hormone on insulin sensitivity in vivo using transgenic mice that overexpress the human placental growth hormone gene. STUDY DESIGN: Glucose and insulin tolerance tests were performed on 5 transgenic mice that overexpressed the human placental growth hormone variant gene and 6 normal littermate controls. The body composition of the mice was assessed by dual-energy radiograph absorptiometry, and free fatty acid levels were measured as a marker of lipolysis. RESULTS: The human placental growth hormone levels in the transgenic mice were comparable to those attained in the third trimester of pregnancy. These mice were nearly twice as heavy as the control mice, and their body composition differed by a significant increase in bone density and a small decrease in percentage of body fat. Fasting insulin levels in the transgenic mice that overexpressed placental growth hormone were approximately 4-fold higher than the control mice (1.57 +/- 0.22 ng/mL vs 0.38 +/- 0.07 ng/mL; P <.001) and 7 times higher 30 minutes after glucose stimulation (4.17 +/- 0.54 ng/mL vs 0.62 +/- 0.10 ng/mL; P <.0001) with no significant difference in either fasting or postchallenge glucose levels. Insulin sensitivity was markedly decreased in the transgenic mice, as demonstrated by an insignificant decline in glucose levels after insulin injection compared with the control mice, which demonstrated more than a 65% reduction in glucose levels (P <.001). CONCLUSION: Human placental growth hormone causes insulin resistance as manifested by fasting and postprandial hyperinsulinemia and minimal glucose lowering in response to insulin injection. Human placental growth hormone is a highly likely candidate to mediate the insulin resistance of pregnancy.