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Objective The authors conducted a systematic review of the published literature to identify interventions to prevent and/or reduce burnout among medical students and residents. Methods The authors searched 10 databases (from the start of each through September 21, 2016) using keywords related to burnout, medical education, and prevention. Teams of two authors independently reviewed the search results to select peer-reviewed, English language articles describing educational interventions to prevent and/or reduce burnout among medical students and/or residents that were evaluated using validated burnout measures. They assessed study quality using the Medical Education Research Study Quality Instrument and the Cochrane Risk of Bias Tool. Results Fourteen studies met inclusion criteria and all used the Maslach Burnout Inventory as at least one measure of burnout. Four were single group pre-post studies, 6 non-randomized two-group studies, and 4 randomized controlled trials. None of the studies were designed specifically to target burnout prevention. In 12 studies, residents were the targeted learners. Six of the 14 studies reported statistically significant changes in burnout scores: 5 reported improvement and 1 reported worsening of burnout. Of the 5 studies that reported statistically significant benefit, 1 studied a complementary and alternative medicine elective, 1 studied the Respiratory One Meditation method, and 3 studied duty hour changes. Conclusions This review highlights the need for rigorously designed studies in burnout prevention and reduction among residents and especially medical students.

The implementation of interprofessional education (IPE) activities into health care education is a challenge for many training programs owing to time and location constraints of both faculty and learners. The integration of social media into these IPE activities may provide a solution to these problems. This review of the published literature aims to identify health care IPE activities using social media. The authors searched 5 databases (from the beginning coverage date to May 27, 2017) using keywords related to IPE and social media. Teams of 2 authors independently reviewed the search results to identify peer-reviewed, English language papers reporting on IPE activities using social media. They assessed the study quality of identified papers using the Medical Education Research Study Quality Instrument. A total of 8 studies met the review's inclusion criteria. Of these 8 papers, 3 had single-group, posttest-only study design; 4 had single-group, pre- and posttest design; and 1 had nonrandomized 3-group design. Qualitative and quantitative outcome measures showed mixed results with the majority of student feedback being positive. Despite a need for additional research, this review suggests that the use of social media may aid the implementation of health care IPE.

Early vascular aging plays a central role in chronic kidney disease (CKD), but its molecular causes remain unclear. Somatic mutations accumulate in various cells with age, yet their functional contribution to aging tissues is not well understood. Here we found progerin, the protein responsible for the premature aging disease Hutchinson–Gilford progeria syndrome, steadily recurring in vascular smooth muscle cells of patients with CKD. Notably, the most common progeria-causing mutation, LMNA c.1824C>T, was identified as a somatic mutation in CKD arteries. Clusters of proliferative progerin-expressing cells in CKD arteries and in vivo lineage-tracing in mice revealed clonal expansion capacity of mutant cells. Mosaic progerin expression contributed to genomic damage, endoplasmic reticulum stress and senescence in CKD arteries and resulted in vascular aging phenotypes in vivo. These findings suggest that certain somatic mutations may be clonally expanded in the arterial wall, contributing to the disease-related functional decline of the tissue. Progerin, a truncated version of lamin A, causes Hutchinson–Gilford progeria syndrome characterized by premature aging and cardiovascular complications. Here the authors show that the most common progeria-causing mutation, LMNA c.1824C>T, is a somatic mutation in arteries from patients with chronic kidney disease, and that clonal propagation of the mutation in the vascular wall results in vascular aging phenotypes in mice.

Peripheral blood-derived endothelial cells (pBD-ECs) are an attractive tool for cell therapies and tissue engineering, but have been limited by their low isolation yield. We increase pBD-EC yield via administration of the chemokine receptor type 4 antagonist AMD3100, as well as via a diluted whole blood incubation (DWBI). Porcine pBD-ECs were isolated using AMD3100 and DWBI and tested for EC markers, acetylated LDL uptake, growth kinetics, metabolic activity, flow-mediated nitric oxide production and seeded onto titanium tubes implanted into vessels of pigs. DWBI increased the yield of porcine pBD-ECs 6.6-fold, and AMD3100 increased the yield 4.5-fold. AMD3100-mobilized ECs were phenotypically indistinguishable from nonmobilized ECs. In porcine implants, the cells expressed endothelial nitric oxide synthase, reduced thrombin-antithrombin complex systemically and prevented thrombosis. Administration of AMD3100 and the DWBI method both increase pBD-EC yield.