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Ulinastatin treatment mitigates glycocalyx degradation and associated with lower postoperative delirium risk in patients undergoing cardiac surgery: a multicentre observational study.
Crit Care
January 2025
Department of Anesthesiology, Hubei Key Laboratory of Geriatric Anesthesia and Perioperative Brain Health, Wuhan Clinical Research Center for Geriatric Anesthesia, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095# Jiefang Ave, Wuhan, 430030, China.
Background: Ulinastatin (UTI), recognized for its anti-inflammatory properties, holds promise for patients undergoing cardiac surgery. This study aimed to investigate the relationship between intraoperative UTI administration and the incidence of delirium following cardiac surgery.
Methods: A retrospective analysis was performed on a retrospective cohort of 6,522 adult cardiac surgery patients to evaluate the relationship between UTI treatment and the incident of postoperative delirium (POD) in patients ongoing cardiac surgery.
Epidermal stem cell derived exosomes-induced dedifferentiation of myofibroblasts inhibits scarring via the miR-203a-3p/PIK3CA axis.
J Nanobiotechnology
January 2025
Department of Burns, Wound Repair and Reconstruction, First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong, 510080, China.
Hypertrophic scar (HS) is a common fibroproliferative disorders with no fully effective treatments. The conversion of fibroblasts to myofibroblasts is known to play a critical role in HS formation, making it essential to identify molecules that promote myofibroblast dedifferentiation and to elucidate their underlying mechanisms. In this study, we used comparative transcriptomics and single-cell sequencing to identify key molecules and pathways that mediate fibrosis and myofibroblast transdifferentiation.
View Article and Find Full Text PDFAssociations between systemic inflammatory biomarkers and metabolic dysfunction associated steatotic liver disease: a cross-sectional study of NHANES 2017-2020.
BMC Gastroenterol
January 2025
Department of Gastroenterology, The First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a primary cause of chronic liver disease, with potential progression to cirrhosis and hepatocellular carcinoma (HCC). Although systemic inflammatory biomarkers are associated with liver diseases, their specific role in MASLD remains unclear. This study examines the association between systemic inflammatory biomarkers and MASLD.
View Article and Find Full Text PDFAltered mitochondrial unfolded protein response and FGF21 secretion in MASLD progression and the effect of exercise intervention.
Sci Rep
January 2025
School of Sports and Health, Nanjing Sport Institute, Nanjing, China.
A high-calorie diet and lack of exercise are the most important risk factors contributing to metabolic dysfunction-associated steatotic liver disease (MASLD) initiation and progression. The precise molecular mechanisms of mitochondrial function alteration during MASLD development remain to be fully elucidated. In this study, a total of 60 male C57BL/6J mice were maintained on a normal or amylin liver NASH (AMLN) diet for 6 or 10 weeks.
View Article and Find Full Text PDFHsa_circ_0001304 promotes vascular neointimal hyperplasia accompanied by autophagy activation.
Commun Biol
January 2025
Department of Biochemistry and Molecular Biology, Key Laboratory of Neural and Vascular Biology, Ministry of Education, Hebei Key Laboratory of Forensic Medicine, Hebei Medical University, Shijiazhuang, 050017, China.
Aberrant autophagy in vascular smooth muscle cells (VSMCs) is associated with the progression of vascular remodeling diseases caused by neointimal hyperplasia. Platelet-derived growth factor-BB (PDGF-BB)-induced vascular remodeling is accompanied by autophagy activation, however, the involvement of circular RNAs (circRNAs) remains unclear. Here, we show the role of PDGF-BB-regulated hsa_circ_0001304 (circ-1304) in neointimal hyperplasia and its potential involvement in VSMC autophagy, while also elucidating the potential mechanisms.
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