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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
MeSH Review

Thrombosis

 
 
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Disease relevance of Thrombosis

 

Psychiatry related information on Thrombosis

 

High impact information on Thrombosis

  • It also acts at the onset of adverse clinical vascular events, when activated cells within the plaque secrete matrix proteases that degrade extracellular matrix proteins and weaken the fibrous cap, leading to rupture and thrombus formation [9].
  • Protease-activated receptors (PARs) are a unique class of G protein-coupled receptors that play critical roles in thrombosis, inflammation, and vascular biology [10].
  • We show that NO inhibits exocytosis of Weibel-Palade bodies, endothelial granules that mediate vascular inflammation and thrombosis, by regulating the activity of N-ethylmaleimide-sensitive factor (NSF) [11].
  • BACKGROUND: Impairment of the protein C anticoagulation pathway is critical to the thrombosis associated with sepsis and to the development of purpura fulminans in meningococcemia [5].
  • BACKGROUND: Cerebral sinovenous thrombosis in children is a serious disorder, and information is needed about its prevention and treatment [12].
 

Chemical compound and disease context of Thrombosis

 

Biological context of Thrombosis

 

Anatomical context of Thrombosis

 

Gene context of Thrombosis

  • Our data suggest that the determination of protein S levels will be useful in the evaluation of patients with recurrent thrombosis [33].
  • These findings warrant further evaluation of the possible therapeutic use of Gas6 inhibition for prevention of thrombosis [34].
  • Here we show that ablation of the mouse Sult1e1 gene caused placental thrombosis and spontaneous fetal loss [35].
  • Plasminogen deficiency causes severe thrombosis but is compatible with development and reproduction [36].
  • CONTEXT: New bolus fibrinolytics derived from the human tissue-type plasminogen activator (tPA) have emerged as a means of dissolution of occlusive thrombosis associated with acute myocardial infarction [37].
  • MRNA expression analysis showed an exclusive synthesis of tPA and PAI-1 within the wall, whereas uPA mRNA was also expressed within the thrombus [38].
  • In the tissue factor-mediated pathway, vWF plays a role in platelet accumulation during thrombus formation but is not required for platelet activation in vivo [39].
  • These data suggest that targeting the p38 MAPK pathway may be valuable in designing new therapy modalities for treating thrombosis in patients with APS [40].
  • Inhibition of the NK1 receptor may therefore provide benefit in patients vulnerable to thrombosis and may offer an alternative therapeutic target [41].
  • The ablation of in vitro thrombus formation in Prkca-/- platelets was rescued by the addition of ADP, consistent with the key mechanistic finding that dense-granule biogenesis and secretion depend upon PKCalpha expression [42].
 

Analytical, diagnostic and therapeutic context of Thrombosis

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