Professional Development of Medical Students Transitioning from Preclinical to Clinical Training ​

Background: Personal and professional development (PPD) is a competency domain for graduated U.S. medical students. Current research shows that PPD is lowest at transitional periods, such as the transition from preclinical to clinical training. Methods: To assess professional development at a large, allopathic medical school, a survey with seven statements regarding professional development was formed. The statements encompassed domains of mentorship, communication skills, professionalism, team work, and innovation and asked students to rank each statement from 1-5 (1 - highly deficient, 5 - highly proficient). The online, anonymous survey was emailed to all second year medical students at Wayne State University School of Medicine (WSUSOM) (n=303) over a 2-month time period after completion of a Service Learning course that fostered professional development and taught about the social determinants of health. Results: 114 (37.6%) students responded to the survey. Overall, students reported feeling most proficient in working with people from different backgrounds (average = 3.91) and least proficient in seeking advice from advisors and mentors (3.27). On average, students felt proficient or highly proficient in all categories. Conclusion: Overall, students felt their professional skills improved after the Service Learning course, and in general felt most proficient in team-based competencies. These preliminary results indicate a need for empowering students to seek advice from mentors. Guidance is especially crucial when students are facing transition periods. There is also room for improvement in teaching students to navigate difficult conversations with empathy and courage. It is also important to continue monitoring professional development over the course of clinical rotations to prevent declines in competencies

Longitudinal Professional Identity Development Amongst Medical Students

Abstract Title: Longitudinal Professional Identity Development Amongst Medical Students Background: Professional development is a core competency for medical student education. A standardized model for assessment of student longitudinal professional identity development will allow medical schools to better implement interventions. Methods: To assess professional development at a large, Midwest, allopathic medical school, a survey with seven statements regarding professional development was created. The statements encompassed domains of mentorship, communication skills, professionalism, and innovation and asked students to rank each statement from 1-5 (1 - highly deficient, 5 - highly proficient). The online, anonymous survey was emailed to all students (n = 1154) over a 2 month time period. Results: 319 (27.6%) surveys were completed. Responses between year 1-2 and year 3-4 showed a unanimous increase in average proficiency across all 7 statements. Year 3-4 had a significant increase in overall proficiency (p Conclusion: Although professional identity development follows an overall upward trend, year 3 is a vulnerable period for professional identity development. While increased accessibility to advising is needed in all four years, it is even more necessary in year 3. The power of the study is limited by the number of responses

The Signal Transducer and Activator of Transcription 1 (STAT1) Inhibits Mitochondrial Biogenesis in Liver and Fatty Acid Oxidation in Adipocytes

The transcription factor STAT1 plays a central role in orchestrating responses to various pathogens by activating the transcription of nuclear-encoded genes that mediate the antiviral, the antigrowth, and immune surveillance effects of interferons and other cytokines. In addition to regulating gene expression, we report that STAT1-/- mice display increased energy expenditure and paradoxically decreased release of triglycerides from white adipose tissue (WAT). Liver mitochondria from STAT1-/- mice show both defects in coupling of the electron transport chain (ETC) and increased numbers of mitochondria. Consistent with elevated numbers of mitochondria, STAT1-/- mice expressed increased amounts of PGC1α, a master regulator of mitochondrial biogenesis. STAT1 binds to the PGC1α promoter in fed mice but not in fasted animals, suggesting that STAT1 inhibited transcription of PGC1α. Since STAT1-/-mice utilized more lipids we examined white adipose tissue (WAT) stores. Contrary to expectations, fasted STAT1-/- mice did not lose lipid from WAT. β-adrenergic stimulation of glycerol release from isolated STAT1-/- WAT was decreased, while activation of hormone sensitive lipase was not changed. These findings suggest that STAT1-/- adipose tissue does not release glycerol and that free fatty acids (FFA) re-esterify back to triglycerides, thus maintaining fat mass in fasted STAT1-/- mice

Deep short-read sequencing of chromosome 17 from the mouse strains A/J and CAST/Ei identifies significant germline variation and candidate genes that regulate liver triglyceride levels

Methods for accurate identification of nucleotide and structural variation using de novo short read sequencing of mouse chromosomes are described

The Artificial Sweetener Splenda Promotes Gut Proteobacteria, Dysbiosis, and Myeloperoxidase Reactivity in Crohn’s Disease–Like Ileitis

We thank John D. Ward and Lindsey N. Kaydo for their technical support and Dr. Wei Xin for the histological scoring of ileitis severity. ARP is an Assistant Professor of Medicine at CWRU School of Medicine. Metagenomic sequencing was conducted in the laboratory of Dr. Skip Virgin at Washington University, School of Medicine, St. Louis, MO. Raw sequencing data files will be available upon request.Peer reviewedPostprin

A p300 and SIRT1 Regulated Acetylation Switch of C/EBPα Controls Mitochondrial Function

Summary: Cellular metabolism is a tightly controlled process in which the cell adapts fluxes through metabolic pathways in response to changes in nutrient supply. Among the transcription factors that regulate gene expression and thereby cause changes in cellular metabolism is the basic leucine-zipper (bZIP) transcription factor CCAAT/enhancer-binding protein alpha (C/EBPα). Protein lysine acetylation is a key post-translational modification (PTM) that integrates cellular metabolic cues with other physiological processes. Here, we show that C/EBPα is acetylated by the lysine acetyl transferase (KAT) p300 and deacetylated by the lysine deacetylase (KDAC) sirtuin1 (SIRT1). SIRT1 is activated in times of energy demand by high levels of nicotinamide adenine dinucleotide (NAD+) and controls mitochondrial biogenesis and function. A hypoacetylated mutant of C/EBPα induces the transcription of mitochondrial genes and results in increased mitochondrial respiration. Our study identifies C/EBPα as a key mediator of SIRT1-controlled adaption of energy homeostasis to changes in nutrient supply. : Zaini et al. show that the transcription factor C/EBPα is acetylated by p300 and deacetylated by the lysine deacetylase SIRT1. Hypoacetylated C/EBPα induces the transcription of mitochondrial genes and results in increased mitochondrial respiration. C/EBPα is a key mediator of SIRT1-controlled adaption of energy homeostasis to changes in nutrient supply. Keywords: C/EBPα, SIRT1, p300, lysine acetylation, mitochondrial function, cellular metabolism, NAD+, gene regulatio

Complement component 3 (C3) expression in the hippocampus after excitotoxic injury: role of C/EBPβ

[Background] The CCAAT/enhancer-binding protein β (C/EBPβ) is a transcription factor implicated in the control of proliferation, differentiation, and inflammatory processes mainly in adipose tissue and liver; although more recent results have revealed an important role for this transcription factor in the brain. Previous studies from our laboratory indicated that CCAAT/enhancer-binding protein β is implicated in inflammatory process and brain injury, since mice lacking this gene were less susceptible to kainic acid-induced injury. More recently, we have shown that the complement component 3 gene (C3) is a downstream target of CCAAT/enhancer-binding protein β and it could be a mediator of the proinflammatory effects of this transcription factor in neural cells.[Methods] Adult male Wistar rats (8–12 weeks old) were used throughout the study. C/EBPβ+/+ and C/EBPβ–/– mice were generated from heterozygous breeding pairs. Animals were injected or not with kainic acid, brains removed, and brain slices containing the hippocampus analyzed for the expression of both CCAAT/enhancer-binding protein β and C3.[Results] In the present work, we have further extended these studies and show that CCAAT/enhancer-binding protein β and C3 co-express in the CA1 and CA3 regions of the hippocampus after an excitotoxic injury. Studies using CCAAT/enhancer-binding protein β knockout mice demonstrate a marked reduction in C3 expression after kainic acid injection in these animals, suggesting that indeed this protein is regulated by C/EBPβ in the hippocampus in vivo.[Conclusions] Altogether these results suggest that CCAAT/enhancer-binding protein β could regulate brain disorders, in which excitotoxic and inflammatory processes are involved, at least in part through the direct regulation of C3.This work was supported by MINECO, Grant SAF2014-52940-R and partially financed with FEDER funds. CIBERNED is funded by the Instituto de Salud Carlos III. JAM-G was supported by CIBERNED. We acknowledge support of the publication fee by the CSIC Open Access Publication Support Initiative through its Unit of Information Resources for Research (URICI).Peer reviewe