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The release of endotoxin is the mechanism by which Gram-negative sepsis provokes DIC.
In acute promyelocytic leukemia, treatment causes the destruction of leukemic granulocyte precursors, resulting in the release of large amounts of proteolytic enzymes from their storage granules, causing microvascular damage.
Other malignancies may enhance the expression of various oncogenes that result in the release of TF and plasminogen activator inhibitor-1 ( PAI-1 ), which prevents fibrinolysis.

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