作者: B. M. Mohammed , Q. Cheng , A. Matafonov , D. M. Monroe , J. C. M. Meijers
DOI: 10.1111/JTH.14243
关键词: Tail vein 、 Medicine 、 Deficient mouse 、 Internal medicine 、 Factor IX 、 Hemostasis 、 Endocrinology 、 Coagulation factor XI 、 Vein 、 Plasma levels 、 Phenotype
摘要: Essentials Mice lacking factor IX (FIX) or XI (FXI) were tested in a saphenous vein bleeding model. FIX-deficient mice displayed hemostatic defect and FXI-deficient similar to wild type mice. Infusion of FXI over-expression improved hemostasis. may affect the phenotype FIX-deficiency (hemophilia B). Summary Background In humans, deficiency coagulation be associated with disorder, but, until recently, did not appear have abnormality. A recent study, however, indicated that show moderate (SVB) Objectives To study effect on normal levels substrate FIX (a murine model hemophilia Methods Wild-type either (F9- ) (F11-/- SVB The plasma F11-/- manipulated by infusion its active form FXIa, overexpressing use hydrodynamic tail injection. Results F9- showed significant model, whereas wild-type indistinguishable. Intravenous FXIa into, overexpression in, hemostasis Overexpression variant FIX-binding site also Conclusions Although we unable demonstrate our results support premise supraphysiological improve through FIX-independent pathways.