coagulation

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Related to Extrinsic pathway: Prothrombin time, APTT
  • noun

Synonyms for coagulation

References in periodicals archive ?
Concentration-dependent processing of initiator (caspase-9 and -8) and the executioner (caspase-3) caspases was also observed, indicating that the intrinsic and the extrinsic pathways play an important role in the mechanism of cell death.
The extrinsic pathway is triggered when death ligands bind to their respective cell surface death receptors through recruitment of FAS-associated death domain (FADD) protein, procaspase-8 through the formation of a complex that induces cell death and activation of the caspases (caspase-8 and caspase-10).
In this paper, we describe the extrinsic pathway which are activated by death receptors like the tumour necrosis factor receptor (Fas receptor -APO-1 or CD95) that belongs to TNF receptor super family [8].
An isolated PT prolongation suggests a deficiency or inhibition of the extrinsic pathway (FVII), but mild factor X, V, and II deficiencies are also possible causes.
The extrinsic pathway is an inducible signaling cascade that is triggered by up-regulation of TF upon inflammation or endothelial injury (Chu 2006).
Although the intrinsic pathway involves early activation of caspase-9, and the extrinsic pathway is mediated through caspase-8, both lead to activation of the "executioner" caspase-3 and a variety of proteases and endonucleases.
Activation of the extrinsic pathway occurs as FVII is activated when massive amounts of tissue factor are released during tissue necrosis and organ failure.
The extrinsic pathway is initiated by tissue damage and is primarily responsible for the desired clotting that occurs at the site of injury, limiting blood loss.
The extrinsic pathway induces apoptosis through an active, instructive process mediated by cell surface death receptors that transmit apoptotic signals when bound by their cognate death ligand.
The extrinsic pathway is mediated by stimulation of death receptors and is caspase-dependent.
We assume that membrane phospholipids exposed by the slight erythrocytolysis may compete with the PT reagent (thromboplastin) used for the assay of extrinsic pathway factors, causing prolongation of PT.