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OTUB1 mediates PARP1 deubiquitination to alleviate NAFLD by regulating HMGB1.

Exp Cell Res

January 2025

Department of Gastroenterology, The Second Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang City, 421001, Hunan province, China; Department of Gastroenterology, Ningyuan County People's Hospital, Yongzhou City, 425600, Hunan province, China. Electronic address:

Nonalcoholic fatty liver disease (NAFLD) is a common chronic disease characterized by hepatocyte steatosis, which excludes alcohol, drugs and other definite liver damage-related factors. It has been reported that OTUB1 serves a significant role in the regulation of glucose and lipid metabolism. The present study aimed to investigate the molecular mechanism underlying the effect of OTUB1 on regulating NAFLD.

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Background: Cholangiocarcinoma (CCA) is a rare neoplasm, with high mortality, originating in the bile ducts. Its incidence is higher in Eastern countries due to the endemic prevalence of liver parasites. Factors such as metabolic syndrome, smoking, and pro-inflammatory conditions are also linked to the disease.

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Introduction: Bone turnover markers reflected the bone remodeling process and bone health in clinical studies. Studies on variation of bone remodeling markers in different stage CKD were scant, and this study investigated the role of bedside intradialytic cycling in altering concentrations of bone-remodeling markers in patients with end-stage renal disease (ESRD).

Materials And Methods: Participants were segmented into four groups: a group with eGFR >60 ml/min/1.

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Introduction: The objective of this study was to improve the economic value of the processed by-products of farmed miiuy croaker () by evaluating the nutrient composition and osteogenic activity of its bones. We prepared bone peptides (MMBP) and analyzed their osteogenic potential.

Methods: We assessed the osteogenic activity of MMBP by molecular docking, MC3T3-E1 cell proliferation assay and zebrafish growth model, and evaluated its effect on osteoporosis (OP) using a retinoic acid-induced osteoporosis rat model.

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