Problem On March 17, 2020, the Association of American Medical Colleges recommended the suspension of all direct patient contact responsibilities for medical students because of the COVID-19 pandemic. Given this change, medical students nationwide had to grapple with how and where they could fill the evolving needs of their schools’ affiliated clinical sites, physicians, patients, and the community. Approach At Harvard Medical School (HMS), student leaders created a COVID-19 Medical Student Response Team to: (1) develop a student-led organizational structure that would optimize students’ ability to efficiently mobilize interested peers in the COVID-19 response, both clinically and in the community, in a strategic, safe, smart, and resource-conscious way; and (2) serve as a liaison with the administration and hospital leaders to identify evolving needs and rapidly engage students in those efforts. Outcomes Within a week of its inception, the COVID-19 Medical Student Response Team had more than 500 medical student volunteers from HMS and had shared the organizational framework of the response team with multiple medical schools across the country. The HMS student volunteers joined any of the 4 virtual committees to complete this work: Education for the Medical Community, Education for the Broader Community, Activism for Clinical Support, and Community Activism. Next Steps The COVID-19 Medical Student Response Team helped to quickly mobilize hundreds of students and has been integrated into HMS’s daily workflow. It may serve as a useful model for other schools and hospitals seeking medical student assistance during the COVID-19 pandemic. Next steps include expanding the initiative further, working with the leaders of response teams at other medical schools to coordinate efforts, and identifying new areas of need at local hospitals and within nearby communities that might benefit from medical student involvement as the pandemic evolves.
A gene causing autosomal-recessive, nonsyndromic hearing loss, DFNB39, was previously mapped to an 18 Mb interval on chromosome 7q11.22-q21.12. We mapped an additional 40 consanguineous families segregating nonsyndromic hearing loss to the DFNB39 locus and refined the obligate interval to 1.2 Mb. The coding regions of all genes in this interval were sequenced, and no missense, nonsense, or frameshift mutations were found. We sequenced the noncoding sequences of genes, as well as noncoding genes, and found three mutations clustered in intron 4 and exon 5 in the hepatocyte growth factor gene (HGF). Two intron 4 deletions occur in a highly conserved sequence that is part of the 3' untranslated region of a previously undescribed short isoform of HGF. The third mutation is a silent substitution, and we demonstrate that it affects splicing in vitro. HGF is involved in a wide variety of signaling pathways in many different tissues, yet these putative regulatory mutations cause a surprisingly specific phenotype, which is nonsydromic hearing loss. Two mouse models of Hgf dysregulation, one in which an Hgf transgene is ubiquitously overexpressed and the other a conditional knockout that deletes Hgf from a limited number of tissues, including the cochlea, result in deafness. Overexpression of HGF is associated with progressive degeneration of outer hair cells in the cochlea, whereas cochlear deletion of Hgf is associated with more general dysplasia.
As COVID-19 exerts financial strain on clinicians nationwide, its impact on health equity is a pressing concern. In recent surveys, 57% of primary care providers reported their payments were insufficient to cover costs, and 20% reported at least temporarily closing their practice, along with layoffs and furloughs. 1 As providers are forced to cut costs, what services are cut-and whom would be most affected by such cuts-could exacerbate existing disparities. Medical interpretation services for more than 25 million individuals with limited English proficiency (LEP) in the United States is a key example.Adequate interpreter services were limited even before the current pandemic. Currently, less than 70% of all US hospitals offer language concordant care, partly because providers must pay for the services themselves. As a result, patients with LEP often face language-related barriers to care in addition to existing inequities. Cutting medical interpreter services in the face of COVID-19, despite short-term savings, may further hinder the care patients receive.
Beta-catenin is an intracellular signaling molecule that has been shown to be important in activity-dependent dendritic morphogenesis. Here, we investigate the detailed morphological changes elicited in dendritic arbors of cultured hippocampal neurons by overexpression of beta-catenin, and we simulate the electrophysiological consequences of these changes. Compared to control neurons, cells overexpressing beta-catenin have dendritic arbors with significantly greater surface area and more branches, as well as different topological characteristics. To investigate possible effects of beta-catenin expression on the electrophysiological properties of neurons, we converted confocal images of neurons expressing beta-catenin into computational simulator formats using parameters that evenly distributed voltage-dependent channels across the cells' membranes. In simulated current clamp experiments, somata were injected with a normalized current such that the observed electrophysiological differences in the neurons would be due only to morphological differences. We found that the morphology of beta-catenin-expressing neurons contributes to significantly smaller action potential amplitude and greater sensitivity than seen in control neurons. As a consequence, beta-catenin-expressing neurons tended to exhibit higher spike rates and needed less excitation to induce firing. These findings show that beta-catenin, by modifying dendritic arborization, could have profound influences on the electrophysiological behavior of neurons.
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