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  • thrombosis
  • Normal platelets can respond to an abnormality on the vessel wall rather than to hemorrhage, resulting in inappropriate platelet adhesion/activation and thrombosis: the formation of a clot within an intact vessel. (wikipedia.org)
  • Since platelets interact with leukocytes at the site of vascular injury, thrombosis and vascular inflammation are closely intertwined and occur consecutively. (pubmedcentralcanada.ca)
  • Recent studies using real-time imaging technology demonstrated that platelet-neutrophil interactions on the activated endothelium are an important determinant of microvascular occlusion during thromboinflammatory disease in which inflammation is coupled to thrombosis. (pubmedcentralcanada.ca)
  • coagulation
  • Alpha chain 2b undergoes post-translational cleavage to yield disulfide-linked light and heavy chains that join with beta 3 to form a fibronectin receptor expressed in platelets that plays a crucial role in coagulation. (abnova.com)
  • Platelets, also called thrombocytes (thromb- + -cyte, "blood clot cell"), are a component of blood whose function (along with the coagulation factors) is to stop bleeding by clumping and clotting blood vessel injuries. (wikipedia.org)
  • The mechanism of coagulation involves activation, adhesion, and aggregation of platelets along with deposition and maturation of fibrin. (wikipedia.org)
  • in all mammals, coagulation involves both a cellular (platelet) and a protein (coagulation factor) component. (wikipedia.org)
  • The hemostatic system consists of platelets, coagulation factors, and the endothelial cells lining the blood vessels. (medscape.com)
  • GPIb
  • The leading role in the elimination of high-stress injury is taken by the GPIb-IX-V complex. (wikipedia.org)
  • GPIbα and GPIbβ are linked by disulfide bridges, while the GPV and GPIX associate non-covalently with the complex. (wikipedia.org)
  • The binding between GPIbα and vWF mediates the capture of platelets to the injured vascular wall. (wikipedia.org)
  • Loss of the platelet GPIb/IX/V complex due to abnormalities in GPIba, GPIbb, or GPIX results in the Bernard-Soulier syndrome, which is characterized by giant platelets and thrombocytopenia. (wordpress.com)
  • thromboxane
  • Aspirin irreversibly inhibits platelet cyclooxygenase 1 preventing the formation of prostaglandin H2, and therefore thromboxane A2. (wikipedia.org)
  • Thromboxane-A synthase, an enzyme found in platelets, converts the arachidonic acid derivative prostaglandin H2 to thromboxane. (wikipedia.org)
  • Thromboxane is a vasoconstrictor and a potent hypertensive agent, and it facilitates platelet aggregation. (wikipedia.org)
  • These "Sticky platelets" secrete several chemicals, including thromboxane A2 that stimulate vasoconstriction, reducing blood flow at the site. (wikipedia.org)
  • Thromboxane synthesis inhibitors, in turn, can be classified regarding which step in the synthesis they inhibit: The widely used drug aspirin acts by inhibiting the ability of the COX enzyme to synthesize the precursors of thromboxane within platelets. (wikipedia.org)
  • The widely used drug aspirin acts by inhibiting the ability of the COX enzyme to synthesize the precursors of thromboxane within platelets. (wikipedia.org)
  • receptor function
  • Platelet-surface sheddases, particularly of the metalloproteinase-disintegrin (ADAM) family, can be regulated by many of the same mechanisms that control receptor function, such as calmodulin association or activation of signaling pathways. (ahajournals.org)
  • GPVI
  • Recent biochemical and cellular studies on shedding pathways 7-10 and surface expression 11-13 of GPVI illustrate some of the key mechanisms underlying platelet receptor proteolysis, and recent preclinical studies 14 show how significant these findings may be in the context of thrombotic risk. (ahajournals.org)
  • vessel
  • If the cap of a vulnerable plaque erodes or ruptures, as in MI, platelets stick to the damaged lining of the vessel and to each other within seconds and form a plug. (wikipedia.org)
  • The process includes the following steps: Following damage to the blood vessel, FVII leaves the circulation and comes into contact with tissue factor (TF) expressed on tissue-factor-bearing cells (stromal fibroblasts and leukocytes), forming an activated complex (TF-FVIIa). (wikipedia.org)
  • A number of agonists, generated at the interface between the vessel wall and circulating blood at the site of vascular injury, have been shown to activate platelets. (aspetjournals.org)
  • vascular
  • On vascular injury, platelets adhere to the site of injury, usually the denuded vascular intimal surface. (mhmedical.com)
  • Because the surface of each platelet has about 50,000 Gp IIb/IIIa-binding sites, numerous activated platelets recruited to the site of vascular injury can rapidly form an occlusive aggregate by means of a dense network of intercellular fibrinogen bridges. (mhmedical.com)
  • A variety of drugs that inhibit platelet function have been shown to decrease morbid events in patients with established cardiovascular atherosclerotic diseases, as evidenced by stroke or transient ischemic attacks, myocardial infarction, unstable angina or the need for vascular bypass or angioplasty. (ac.ir)
  • Recent intravital microscopic studies have provided compelling evidence that activated neutrophils adherent to inflamed ECs can support homotypic and heterotypic cell-cell interactions and that platelet-neutrophil aggregation on activated ECs is the crucial determinant of microvascular occlusion during vascular inflammation ( Fig. 1 ) [ 8 , 9 ]. (pubmedcentralcanada.ca)
  • Heterotypic cell-cell interactions during vascular inflammation. (pubmedcentralcanada.ca)
  • Tissue and vascular injuries activate ECs, resulting in not only the expression of adhesion molecules including P-and E-selectins, ICAMs, and vascular cell adhesion mole-cule-1 (VCAM-1) but also the production and release of vWF, reactive oxygen species (ROS), and inflammatory cytokines [ 3 , 17 - 19 ]. (pubmedcentralcanada.ca)
  • antigen
  • In this study we demonstrated that platelet lysate depleted of the antigen through adsorption by an AAP2-solidified affinity column was bound by MAbs against CD62 and CD42 but not by MAb 5.6E against CD31 or AAP2 on the immunoblot. (ahajournals.org)
  • To analyze directly the role of CD31 in platelet function, we produced a MAb, AAP2, which was found to recognize CD31 antigen. (ahajournals.org)
  • thrombus formation
  • Platelet adhesion/thrombus formation in the endocardium was found in limited sites in which the overlying endothelium was deficient in eNOS and CD34. (onlinejacc.org)
  • When warfarin-treated cases were excluded, there was a significant correlation between the immunohistochemical grade for vWF and the degree of platelet adhesion/thrombus formation in the endocardium. (onlinejacc.org)
  • primarily
  • Abnormalities of platelet function manifest themselves primarily as excessive hemorrhage at mucocutaneous sites, with ecchymoses, petechiae, epistaxis, gingival hemorrhage, and menorrhagia most common. (wordpress.com)
  • myeloid
  • Elevated platelet concentration is thrombocytosis and is either congenital, reactive (to cytokines), or due to unregulated production: one of the myeloproliferative neoplasms or certain other myeloid neoplasms. (wikipedia.org)