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Suppressing upregulation of fibrinogen after polytrauma mitigates thrombosis in mice.

J Trauma Acute Care Surg

September 2024

From the Department of Surgery (M.S.S., M.B., A.H., W.G.H., M.d.M., C.J.K.), Division of Trauma, Medical College of Wisconsin; Versiti Blood Research Institute (M.S.S., F.F., M.B., A.H., W.G.H., M.R.D., C.J.K.), Milwaukee, Wisconsin; Michael Smith Laboratories (F.F., C.J.K.), and Department of Biochemistry and Molecular Biology (F.F., C.J.K.), University of British Columbia, Vancouver, British Columbia, Canada; Department of Pathology and Laboratory Medicine (M.J.F.), and Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill (M.J.F.); UNC Blood Research Center (M.J.F.), University of North Carolina at Chapel Hill, Chapel Hill, North Carolina; and Department of Surgery (M.R.D.), Division of Vascular Surgery, and Departments of Biochemistry (C.J.K.), Biomedical Engineering (C.J.K.), and Pharmacology and Toxicology (C.J.K.), Medical College of Wisconsin, Milwaukee, Wisconsin.

Background: Polytrauma results in systemic inflammation and increased circulating fibrinogen, which increases the risk of microvascular and macrovascular thrombosis that contributes to secondary organ damage and venous thromboembolism (VTE). There are no clinically approved agents to prevent hyperfibrinogenemia after polytrauma. We hypothesized that preventing the increase in fibrinogen levels after polytrauma would suppress thrombosis.

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The incidence of endometrial cancer (EC) is increasing worldwide, but the specific mechanism of coagulation dysfunction in EC is not fully understood. The objective of the present study was to explore the relationship between autonomic nervous system function and coagulation function in patients with EC using heart rate variability (HRV) analysis. The study included 100 patients with EC who were treated at the Department of Gynecological Oncology of The First Affiliated Hospital of Bengbu Medical University (Bengbu, China) from December 2021 to March 2023.

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Neoplastic ICAM-1 protects lung carcinoma from apoptosis through ligation of fibrinogen.

Cell Death Dis

August 2024

State Key Laboratory of Multi-Cell Systems, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, Shanghai, China.

Article Synopsis
  • ICAM-1 is often overexpressed in non-small cell lung cancer (NSCLC), which is linked to worse patient outcomes, but the reasons for its harmful effects are not fully understood.
  • Research shows that the survival of NSCLC cells relies on a signal from the interaction between fibrinogen γ chain (FGG) and ICAM-1, which activates survival pathways and prevents cell death.
  • By inhibiting the interaction between ICAM-1 and FGG with a developed monoclonal antibody, researchers were able to decrease NSCLC cell survival and tumor growth in experiments, suggesting a new targeted therapy approach for NSCLC.
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Loss of plasma fibrinogen contributes to platelet hyporeactivity in rats with septic shock.

Thromb Res

September 2024

Graduate Institute of Life Sciences, National Defense Medical Center, Taipei, Taiwan, ROC; Department and Graduate Institute of Pharmacology, National Defense Medical Center, Taipei, Taiwan, ROC. Electronic address:

Article Synopsis
  • Dysregulated host responses to infections, particularly in sepsis, can lead to severe complications like organ dysfunction and impaired platelet function, which can cause bleeding and additional infections.
  • Research in adult male Wistar rats showed that sepsis induced by lipopolysaccharide (LPS) and cecal ligation and puncture (CLP) led to reduced fibrinogen levels and platelet activity.
  • Supplementing fibrinogen significantly improved platelet aggregation, adhesion, and clot retraction in septic rats, suggesting that it may be a valuable therapy for addressing platelet dysfunction in septic patients.
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Polyunsaturated fatty acid-derived lipid mediator Resolvin D1 alleviates sepsis-induced disseminated intravascular coagulation via Caspase-1/Gasdermin D pyroptotic pathway.

Clin Nutr

June 2024

Department of Anesthesia and Critical Care, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 325027, China; Key Laboratory of Pediatric Anesthesiology, Ministry of Education, Wenzhou Medical University, Wenzhou 325027, China; Key Laboratory of Anesthesiology of Zhejiang Province, Wenzhou Medical University, Wenzhou 325027, China. Electronic address:

Background & Aims: Sepsis-induced disseminated intravascular coagulation (DIC) is characterised by abnormal blood clotting resulting from severe infection, contributing to organ dysfunction in sepsis. Resolvin D1 (RvD1) is an endogenous lipid mediator, synthesised from the omega-3 polyunsaturated fatty acid (PUFA) docosahexaenoic acid (DHA) through enzymatic processes involving 15-LOX and 5-LOX. RvD1 is recognised for its protective properties against various inflammatory conditions.

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