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FxIII-A, the activated form of the coagulation factor XIII (FXIII-A2B2), is a hemostatic enzyme that inhibits fibrin dissolution by irreversibly cross-linking fibrillin and anti-fibre-soluble protein.
Although FXIII-A is very important, there is no way to adjust FXIII-A.
Given the observed phenomenon in patients with FXIII-B defects: FXIII-A is reduced, but no severe bleeding, Strilchuk and others speculate that targeting liver FXIII-B with suitable small interfering RNA (siRNA) may safely reduce FXIII-A.
experimentally proven, Strilchuk and others have confirmed that the removal of FXIII-B with siRNA can lead to a sustained and controlled reduction of FXIII-A.
after a single injection, the plasma FXIII-A concentration was reduced by 90% for several weeks and repeated injections lasted for more than 5 months, but the FXIII-A concentration in platelets remained the same.
in vitro, the cross-linking of alpha2-anti-fisolysozyme and fibrin is impaired and the fiscota is enhanced.
in the body, the cervical artery thrombosis is closed and the perfusion is enhanced. The
increased after stimulation, but blood loss did not increase significantly.
, the method simulates congenital FXIII-B deficiency and provides a potential pharmacological and experimental method to regulate the activity of FXIII-A2B2.
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