thrombogenesis


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Related to thrombogenesis: fibrinolysis, Extrinsic pathway

thrombogenesis

 [throm″bo-jen´ĕ-sis]
clot formation. adj., adj thrombogen´ic.

thrombogenesis

/throm·bo·gen·e·sis/ (-jen´ĕ-sis) clot formation.thrombogen´ic

thrombogenesis

[-jen′əsis]
formation of a thrombus or blood clot.

throm·bo·gen·e·sis

(thrombō-jenĕ-sis)
Process of formation of a blood clot.

thrombogenesis

clot formation.
References in periodicals archive ?
They cover research in hematopoietic stem cells and blood cell engineering; novel cellular therapeutics and hemapoietic cell transplantation; molecular immunohematology, immunomodulation, and therapeutic apheresis; hemostasis in infection and host defense; platelet-pathogen interactions; organ and vascular bed-specific thrombogenesis and genetic research in thrombophilia; diagnosis and management of bleeding disorders; and challenges in blood donor recruitment and blood supply due to demographic changes.
Toydemir PB, Elhan AH, Tutkun A et al: Effects of factor V gene G1691A, methylenetetrahydrofolate reductase gene C677T, and prothombin gene G20210A mutations on deep venous thrombogenesis in Behcet's disease.
Rheological parameters may promote thrombogenesis and atherosclerosis, and may become important factors in the regulation of cerebral blood flow (Fisher and Meiselman 1991).
52,53) Furthermore, in thrombogenesis n-3 PUFA reduce the platelets aggregation (54,55), and improve the fibrinolysis pathway.
45) MUFA are also related to a lower platelet aggregation 41 and increases of both fibrinolysis and clotting time, which protects against thrombogenesis.
Effects of factor V gene G1 691A, methylenetetrahydrofolate reductase gene C677T, and prothrombin gene G2021 OA mutations on deep venous thrombogenesis in Beh9et's disease.
Periodontal disease may provide a chronic burden of endotoxin and inflammatory cytokines, which serve to initiate and exacerbate atherogenesis and thrombogenesis.
Within the vascular lumen, COX-1 and COX-2 play an important role in the interaction between platelets and endothelial cells and in thrombogenesis.
His clinical research has investigated the effects of lipid-lowering therapies, hypoglycemic therapies and antihypertensive agents on inflammation and thrombogenesis as well as the effects of hypolipidemic and antihypertensive agents on blood viscosity and fibrinogen.
4) This has particular inference given the impact of DM on the vascular endothelium, once thought to be a static, semipermeable monolayer of cells between the blood stream and tissues, which is now recognized to be a dynamic "organ" that plays a fundamental role in the development of atherosclerosis, thrombogenesis and fibrinolysis.
Specifically, elevated levels of homocysteine have been linked to atherosclerosis, endothelial damage, and thrombogenesis.