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Endothelium Modulates the Prothrombotic Phenotype of Factor V Leiden: Evidence From an Ex Vivo Model.
Arterioscler Thromb Vasc Biol
January 2025
Institute of Experimental Hematology and Transfusion Medicine, University Hospital Bonn, Germany.
Background: Clinical expressivity of the thrombophilic factor V Leiden (FVL) mutation is highly variable. Recently, we demonstrated an increased APC (activated protein C) response in asymptomatic FVL carriers compared with FVL carriers with a history of venous thromboembolism (VTE) after in vivo coagulation activation. Here, we further explored this association using a recently developed ex vivo model based on patient-specific endothelial colony-forming cells (ECFCs).
View Article and Find Full Text PDFEfficacy and safety of anticoagulants on venous thromboembolism: a systematic review and network meta-analysis of randomized controlled trials.
Front Pharmacol
January 2025
Department of Cardiovascular Surgery, Affiliated Hospital of Southwest Jiaotong University, The General Hospital of Western Theater Command, Chengdu, China.
Background: Anticoagulants are the primary means for the treatment and prevention of venous thromboembolism (VTE), but their clinical standardized application still remains controversial. The present study intends to comprehensively compare the efficacy and safety of various anticoagulants in VTE.
Methods: Medline, Embase, and Cochrane Library from their inception up to August 2023 were searched to compare the efficacy and safety of various anticoagulants in VTE.
Functional assessment of genetic variants in thrombomodulin detected in patients with bleeding and thrombosis.
Blood
January 2025
KULeuven, Leuven, Belgium.
Thrombomodulin (TM) expressed on endothelial cells regulates coagulation. Specific nonsense variants in the TM gene, THBD, result in high soluble TM levels causing rare bleeding disorder. In contrast, though THBD variants have been associated with venous thromboembolism, this association remains controversial.
View Article and Find Full Text PDFStructural Conformation and the Binding of Factor VIII R2159C (FVIII-Ise) Mutated in the C1 Domain to Phospholipid.
Thromb Haemost
January 2025
Department of Pediatrics, Nara Medical University, Kashihara, Nara, Japan.
Background: We previously identified a factor (F)VIII molecular defect associated with an R2159C mutation in the C1 domain (named "FVIII-Ise") together with undetectable FVIII antigen (FVIII:Ag) levels measured by two-site sandwich ELISA using an anti-C2 domain alloantibody (alloAb). The patient had clinically mild hemophilia A, and his reduced FVIII:C correlated with FVIII:Ag measured by ELISA using monoclonal antibodies (mAbs) with A2 and A2/B domain epitopes, suggesting that the R2159C mutation modified C2 domain antigenicity.
Aim: To investigate functional and structural characteristics of the FVIII-R2159C mutant.
Disseminated intravascular coagulation: cause, molecular mechanism, diagnosis, and therapy.
MedComm (2020)
February 2025
Department of Emergency Ruijin Hospital, Shanghai Jiao Tong University School of Medicine Shanghai China.
Disseminated intravascular coagulation (DIC) is a complex and serious condition characterized by widespread activation of the coagulation cascade, resulting in both thrombosis and bleeding. This review aims to provide a comprehensive overview of DIC, emphasizing its clinical significance and the need for improved management strategies. We explore the primary causes of DIC, including sepsis, trauma, malignancies, and obstetric complications, which trigger an overactive coagulation response.
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