Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033036 (APC)
 10,214 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anti-phospholipid syndrome (APS) is defined based on both clinical findings (recurrent arterial and/or venous thrombosis and recurrent fetal loss) and laboratory evidence of persistent anti-phospholipid antibodies (anti-cardiolipin antibodies, anti-beta2 glycoprotein I antibodies, or LA activity). However, the precise mechanism responsible for arterial and/or venous thromboembolic complications in APS patients remains unclear. To clarify the association between the various types of anti phospholipid antibodies (aPLs) and thrombotic complications, we examined the prevalence of seven types of aPLs [anti-cardiolipin/beta2-glycoprotein I antibodies(anti-CL/beta2-GPI), anti-phosphatidylserine/prothrombin antibodies(anti-PS/PT), anti-beta2-glycoprotein I antibodies (anti-beta2-GPI), anti prothrombin antibodies (anti-PT), anti-protein C antibodies (anti-PC), anti-protein S antibodies(anti-PS), and annexin V antibodies(anti-AN)] in 168 patients with systemic lupus erythematosus (SLE). We confirmed that the presence of anti-CL/beta2-GPI, anti-PS/PT, and anti-beta2-GPI is closely related to arterial thrombosis, and that the presence of anti-protein S is closely related to venous thromboembolism. Furthermore, our in-vitro experiment suggests that anti-CL/beta2-GPI and anti-PS/PT may cooperate to promote platelet activation, and may be involved in the pathogenesis of arterial thrombosis. On the other hand, anti-protein S led to APC resistance, which may represent an important mechanism responsible for the development of venous thrombosis. Furthermore, our study showed that anti-CL/beta2-GPI causes a persistently high-level expression of tissue factor on monocytes, and this may increase the risk of atherosclerosis.
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PMID:[Advanced clinical laboratory studies in the graduate school of medicine--studies on pathogenic mechanisms of anti-phospholipid syndrome]. 1976 14

We have adapted the corn-trypsin inhibitor whole-blood model to include EA.hy926 as an endothelium surrogate to evaluate the vascular modulation of blood coagulation initiated by relipidated recombinant tissue factor (rTf) and a cellular Tf surrogate, lipopolysaccharide (LPS)-stimulated THP1 cells (LPS-THP-1). Compared with bare tubes, EA.hy926 with rTf decreased the rate of thrombin formation, ITS accumulation, and the production of fibrinopeptide A. These phenomena occurred with increased rates of factor Va (fVa) inactivation by cleavages at R(506) and R(306). Thus, EA.hy926 provides thrombin-dependent protein C activation and APC fVa inactivation. Comparisons of rTf with LPS-THP-1 showed that the latter gave reduced rates for TAT formation but equivalent fibrinopeptide A, and fV activation/inactivation. In the presence of EA.hy926, the reverse was obtained; with the surrogate endothelium and LPS-THP-1 the rates of TAT generation, fibrinopeptide release, and fV activation were almost doubled, whereas cleavage at R(306) was equivalent. These observations suggest cooperativity between the 2 cell surrogates. These data suggest that the use of these 2 cell lines provides a reproducible quasi-endothelial quasi-inflammatory cytokine-stimulated monocyte system that provides a method to evaluate the variations in blood phenotype against the background of stable inflammatory cell activator and a stable vascular endothelial surrogate.
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PMID:Cellular regulation of blood coagulation: a model for venous stasis. 2086 79


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