Background The effects of drastic curricular changes necessitated by the COVID-19 pandemic on medical students’ education and wellbeing have remained largely unstudied. Out study aimed to characterize how medical students were affected by the pandemic, specifically how limitations introduced by the pandemic may have affected the quality, delivery, and experience of medical education. Methods Three hundred students from 5 U.S. allopathic medical schools were surveyed to determine students’ perceptions about their quality of medical education, professional development, and mental health during the COVID-19 pandemic (October 2020-December 2020). Results A large majority of students report that while lecture-based learning has not been significantly affected by the pandemic, small-group and clinical learning have greatly declined in quality. Students also reported higher levels of depression, anxiety, and uncertainty with regards to their futures as physicians. Conclusions The COVID-19 pandemic has greatly affected the medical student education and wellbeing. Although medical schools have implemented measures to continue to train medical students as effectively as they can, further strategies must be devised to ensure the well-being of students in the present and for future national emergencies.

This study establishes a relevant mouse model of nonalcoholic steatohepatitis-fibrosis-hepatocellular carcinoma that closely recapitulates human disease. With this model, we elucidate multitissue dynamics of nonalcoholic steatohepatitis/hepatocellular carcinoma progression, as well as regression. We define the key signaling and cytokine pathways that are critical for disease development and resolution.BACKGROUND & AIMS: How benign liver steatosis progresses to nonalcoholic steatohepatitis (NASH), fibrosis, and hepatocellular carcinoma (HCC) remains elusive. NASH progression entails diverse pathogenic mechanisms and relies on complex cross-talk between multiple tissues such as the gut, adipose tissues, liver, and the brain. Using a hyperphagic mouse fed with a Western diet (WD), we aimed to elucidate the cross-talk and kinetics of hepatic and extrahepatic alterations during NASH-HCC progression, as well as regression.METHODS: Hyperphagic mice lacking a functional Alms1 gene (Foz/Foz) and wild-type littermates were fed WD or standard chow for 12 weeks for NASH/fibrosis and for 24 weeks for HCC development. NASH regression was modeled by switching back to normal chow after NASH development.RESULTS: FozþWD mice were steatotic within 1 to 2 weeks, developed NASH by 4 weeks, and grade 3 fibrosis by 12 weeks, accompanied by chronic kidney injury. FozþWD mice that continued on WD progressed to cirrhosis and HCC within 24 weeks and had reduced survival as a result of cardiac dysfunction. However, NASH mice that were switched to normal chow showed NASH regression, improved survival, and did not develop HCC. Transcriptomic and histologic analyses of Foz/Foz NASH liver showed strong concordance with human NASH. NASH was preceded by an early disruption of gut barrier, microbial dysbiosis, lipopolysaccharide leakage, and intestinal inflammation. This led to acute-phase liver inflammation in FozþWD mice, characterized by neutrophil infiltration and increased levels of several chemokines/cytokines. The liver cytokine/chemokine profile evolved as NASH progressed, with subsequent predominance by monocyte recruitment. CONCLUSIONS:The FozþWD model closely mimics the pathobiology and gene signature of human NASH with fibrosis and subsequent HCC. FozþWD mice provide a robust and

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