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This web focus features papers from Laboratory Investigation and Modern Pathology that present new models and techniques, diagnostic advances, mechanistic insights and potential innovative therapies for NAFLD and NASH.Non-alcoholic fatty liver disease (NAFLD) is the most prevalent chronic liver disease worldwide.
This United States and Canadian Academy of Pathology training course will give listeners an introduction to the pathology of COVID-19, with an emphasis on the lung, which is the main target of this disease. This charismatic and evocative review of a multi-institutional collaborative investigation of COVID autopsies will inform and stimulate you.
Ascorbate can act as an oxidant to induce tumor cell death at a pharmacological dose. Here the authors show that this response is associated with increases in GPCR Gi/o activity. This effect promotes rises in intracellular Ca2+ influx through transient receptor potential channel activity in retinoblastoma cells.
Cardiovascular diseases are the leading cause of death worldwide. Myocardial ischaemia/reperfusion (I/R) injury is a major risk for cardiovascular disease. Herein, the authors demonstrate that circPAN3 ameliorates myocardial I/R injury by absorbing miR-421 to regulate Pink1-mediated autophagy, which may provide potential therapeutic targets in I/R injury.
This study demonstrates that NFAT5 promotes oral squamous cell carcinoma progression in the hyperosmotic environment through increased expression of DPAGT1, an essential enzyme for protein glycosylation, and altered EGFR subcellular localization from the cytoplasm to the plasma membrane in tumor cells.
Photoactivatable-Cre (PA-Cre) knock-in mice was established and characterized for the spatial regulation of Cre recombinase activity with blue light exposure. Spot irradiation or long-term irradiation using a wireless LED could induce locus-specific recombination. The PA-Cre knock-in mice promise a useful resource to elucidate gene function in vivo spatiotemporally.
The authors describe a sarcoma with a novel fusion between NUTM1 and MXI1, a member of the MAD gene family. Transcriptome analysis and in vitro studies showed that MXI1-NUTM1 partially phenocopied MYC, providing evidence that MAD family members, normally repressors of MYC activity, can be converted into MYC-like mimics by fusion to NUTM1.
This study describes how miR-221-3p in endothelial cells reduces angiogenesis by inhibiting hypoxia-inducible factor-1α. Because antagonism of miR-221-3p significantly improves the cardiac function of mice with heart failure it may be a new and effective molecular target for progressing and treatment of heart failure.