Background: Liver fibrosis is caused by chronic toxic or cholestatic liver injury. Fibrosis results from the recruitment of myeloid cells into the injured liver, the release of inflammatory and fibrogenic cytokines, and the activation of myofibroblasts, which secrete extracellular matrix, mostly collagen type I. Hepatic myofibroblasts originate from liver-resident mesenchymal cells, including HSCs and bone marrow-derived CD45+ collagen type I+ expressing fibrocytes.
View Article and Find Full Text PDFHepatocellular carcinoma (HCC) originates from differentiated hepatocytes undergoing compensatory proliferation in livers damaged by viruses or metabolic-dysfunction-associated steatohepatitis (MASH). While increasing HCC risk, MASH triggers p53-dependent hepatocyte senescence, which we found to parallel hypernutrition-induced DNA breaks. How this tumour-suppressive response is bypassed to license oncogenic mutagenesis and enable HCC evolution was previously unclear.
View Article and Find Full Text PDFBackground & Aims: Metabolic dysfunction-associated steatotic liver disease ranges from metabolic dysfunction-associated steatotic liver (MASL) to metabolic dysfunction-associated steatohepatitis (MASH) with fibrosis. Transdifferentiation of hepatic stellate cells (HSCs) into fibrogenic myofibroblasts plays a critical role in the pathogenesis of MASH liver fibrosis. We compared transcriptome and chromatin accessibility of human HSCs from NORMAL, MASL, and MASH livers at single-cell resolution.
View Article and Find Full Text PDFBackground: Severe hypoglycemia (SH) poses a significant challenge in the management of type 1 diabetes (T1D); however, the factors that offer protection other than diabetes technologies are under-studied. The primary objective of this study was to examine the association between hypoglycemia problem-solving (HPS) abilities and severe hypoglycemic events in adults with T1D using Poisson regression analysis.
Methods: In this cross-sectional study, 287 adults with T1D (mean age: 50.
Materials with enhanced electron and reduced phonon transport properties are preferred for thermoelectric applications. The defect engineering process can optimize the interrelated electron and phonon transport properties to enhance thermoelectric performance. As the influence of various crystalline defects on the functional properties of materials is diverse, it is crucial to scale, optimize, and understand them experimentally.
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