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The pre-clinical medical school curriculum provides students with extraordinary experiences in preparation to become physicians. However, it was not originally designed to be delivered remotely. The COVID-19 pandemic promptly threw the medical education process into unforeseen circumstances. A model of student-faculty collaboration created to address new challenges and implement practical solutions rapidly is presented. This model was used effectively to respond to pre-clinical educational interruptions that were imposed by the COVID-19 pandemic and maintain high-quality training. Our experience provides valuable insights and lessons learned that can be applied to the ongoing pandemic response and to future educational challenges., Competing Interests: Conflict of InterestThe authors declare no competing interests., (© The Author(s) under exclusive licence to International Association of Medical Science Educators 2022, Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.)

As future physicians, nearly all medical students will be required to provide face-to-face feedback. Moreover, receiving high quality feedback from multiple perspectives is particularly valuable during the pre-clerkship training period. To address these needs, we developed a straightforward, easy to implement exercise that affords students the opportunity to practice giving and receiving feedback with peers. We describe how this exercise has been tailored to fit within the case-based learning small groups of our first-year curriculum and how to enhance the activity by weaving the basic principles of quality feedback into preparation sessions. This exercise has been valued greatly by students., Competing Interests: Conflict of Interest Statement On behalf of all authors, the corresponding author states that there is no conflict of interest.

Competency-based assessment seeks to align measures of performance directly with desired learning outcomes based upon the needs of patients and the healthcare system. Recognizing that assessment methods profoundly influence student motivation and effort, it is critical to measure all desired aspects of performance throughout an individual's medical training. The Accreditation Council for Graduate Medical Education (ACGME) defined domains of competency for residency; the subsequent Milestones Project seeks to describe each learner's progress toward competence within each domain. Because the various clinical disciplines defined unique competencies and milestones within each domain, it is difficult for undergraduate medical education to adopt existing GME milestones language. This paper outlines the process undertaken by one medical school to design, implement and improve competency milestones for medical students. A team of assessment experts developed milestones for a set of focus competencies; these have now been monitored in medical students over two years. A unique digital dashboard enables individual, aggregate and longitudinal views of student progress by domain. Validation and continuous quality improvement cycles are based upon expert review, user feedback, and analysis of variation between students and between assessors. Experience to date indicates that milestone-based assessment has significant potential to guide the development of medical students.

Physicians-in-training require skills and attitudes beyond medical knowledge in order to mature into successful clinicians. However, because assessments in pre-clerkship curricula historically have focused almost exclusively on medical knowledge, faculty contributions to early student development often have been limited. To address this challenge and enhance student progress, we re-designed our pre-clerkship curriculum to include settings in which diverse facets of student performance could be observed and fostered. Concurrently, we transitioned to an assessment strategy focused on competency-based milestones. The implementation of this strategy has allowed pre-clerkship science faculty to provide early-stage students with rich holistic feedback designed to stimulate their professional growth.

Background: Little is known regarding the impact of lecture recordings on medical education., Aim: This study was designed to assess the impact of lecture recordings on the educational experience of first-year medical students., Methods: Students were provided with digital lecture recordings in Molecular Foundations of Medicine, an integrated preclinical science block. Students could access recordings as audio/visual rich media, in which lectures were linked to slide presentations, and as audio-only podcasts. Student reactions were assessed by a mandatory questionnaire on the use of recordings and by a voluntary follow-up questionnaire on the effects of recordings on learning, stress and anxiety., Results: Student response to lecture recordings was universally positive. A high proportion of the class accessed recordings, with rich media being the preferred format. Students felt that the lecture recordings helped them learn course material and reduced stress and anxiety. Finally, the availability of lecture recordings had no apparent adverse effect on classroom attendance., Conclusions: The availability of lecture recordings aided medical students in their studies and reduced stress and anxiety. Student response to the recordings was universally positive, and no negative outcomes were noted by students or faculty.

We cloned and characterized an 83-kb fragment of mouse genomic DNA containing the entire glucokinase (GK) gene. The 11 exons of the gene span a total distance of 49 kb, with exons 1 beta and 1L being separated by 35 kb. A total of 25,266 bp of DNA sequence information was determined: from approximately -9.2 to approximately +15 kb (24,195 bp), relative to the hepatocyte transcription start site, and from -335 to +736 bp (1071 bp), relative to the transcription start site in beta cells. These sequences revealed that mouse GK is > 94% identical to rat and human GK. Mouse hepatic GK mRNA is regulated by fasting and refeeding, as also occurs in the rat. Alignment of the upstream and downstream promoter regions of the mouse, rat, and human genes revealed several evolutionarily conserved regions that may contribute to transcriptional regulation. However, fusion gene studies in transgenic mice indicate that the conserved regions near the transcription start site in hepatocytes are themselves not sufficient for position-independent expression in liver. Analysis of the chromatin structure of a 48-kb region of the mouse gene using DNase I revealed eight liver-specific hypersensitive sites whose locations ranged from 0.1 to 36 kb upstream of the liver transcription start site. The availability of a single, contiguous DNA fragment containing the entire mouse GK gene should allow further studies of cell-specific expression of GK to be performed.

A transgene consisting of an upstream glucokinase (GK) promoter fragment linked to coding sequences of the human growth hormone gene was expressed in certain neuroendocrine cells of the pancreas, pituitary, brain, gut, thyroid, and lungs of mice. In pancreas, the transgene was expressed in a nonuniform manner among beta cells and in a variable but substantial fraction of the other islet cell types. In pituitary, it was expressed in corticotropes, and in brain, it was expressed in cells of the medial hypothalamus. Within the gut transgene expression was detected in a subset of enteroendocrine cells of the stomach and duodenal epithelium, some of which also exhibited glucagon-like polypeptide-1 immunoreactivity. In thyroid, transgene expression was observed in C cells of neonatal animals, whereas in the lung, it was expressed among rare endocrine cells of the bronchopulmonary mucosa. RNA polymerase chain reaction analysis of human growth hormone mRNA corroborated the tissue-specific transgene expression pattern. Prompted by the finding of transgene expression in specific neuroendocrine cells, we sought to determine whether GK mRNA and GK itself was also expressed in the brain and gut, tissues not previously associated with the expression of this enzyme. Using rat tissues, GK mRNA was detected by RNA polymerase chain reaction in both the brain and intestine and was localized to specific cells in the hypothalamus and enteric mucosa by in situ hybridization. A high Km glucose phosphorylating activity was detected from isolated rat jejunal enterocytes that displayed a chromatographic elution profile identical to hepatic GK. GK immunoreactivity was detected in cells of the medial hypothalamus with many of the same cells also displaying GLUT2 immunoreactivity. Together, these studies provide evidence for upstream GK promoter activity, GK mRNA, and GK itself in certain neuroendocrine cells outside the pancreatic islet and lead us to suggest that GK may play a broader role in glucose sensing by neuroendocrine cells than was thought previously.

Studies were initiated to investigate whether mechanisms exist within mitochondria to repair damage incurred by mitochondrial DNA after exposure to alkylating toxins. A clonal isolate from a rat insulinoma cell line was utilized to measure the formation and repair of alkali-labile sites within the mitochondrial genome after exposure to the alkylating antibiotic streptozotocin. Alkali-labile sites were formed in mitochondrial DNA in a dose-dependent fashion. Eight hours after exposure to the toxin, 55% of the lesions were removed. The level of repair increased to 70% after 24 h. In comparison, only 46% of N7-methylguanines were removed across the entire cellular genome. These studies demonstrate that streptozotocin causes appreciable mitochondrial DNA damage in a dose-dependent manner and provide the first evidence that a repair mechanism for alkali-labile sites is present within the mitochondrion.