Zobrazeno 1 - 10
of 73
pro vyhledávání: '"Alan R. Giles"'
Autor:
Peter Vander Velden, Alan R. Giles
Publikováno v:
British Journal of Haematology. 70:345-355
Publikováno v:
British Journal of Haematology. 69:491-497
A combination of phosphatidylcholine-phosphatidylserine lipid vesicles (PCPS), as a source of coagulant active phospholipid, when infused with factor Xa bypasses factor VIII in vivo. To demonstrate this, a reproducible model of bleeding in haemophili
Autor:
Midori Shima, Saiho Ko, Ichiro Tanaka, Yoshiyuki Nakajima, Hiromichi Kanehiro, Akira Yoshioka, Jun-ichi Ori, Alan R. Giles, Hideki Kanokogi
Publikováno v:
Liver Transplantation. 11:579-584
The cause of hemophilia is deficiency of coagulation factor VIII production in the liver, which can be cured by liver transplantation. Because the hepatic function of hemophilia patients is quite normal except for production of factor VIII, auxiliary
Autor:
Midori Shima, Alan R. Giles, Kazuyoshi Fukuda, Youko Kubota, Akira Yoshioka, Katumi Nishiya, Tomoko Matsumoto, Ichiro Tanaka
Publikováno v:
Thrombosis and Haemostasis. 87:436-441
SummaryThe lower detection limit of the conventional one-stage aPTT based clotting assay for determining FVIII:C levels is generally 1.0-2.0 IU/dl. Consequently, it has been impossible to study the clinical significance of levels of FVIII:C less than
Autor:
Bert Verbruggen, John A. Samis, Kitty Verbeek, Irena Novakova, Alan R. Giles, Ewald J.B.M. Mensink
Publikováno v:
Thrombosis and Haemostasis. 86:1435-1439
SummaryWe have investigated the influence of the type of factor VIII deficient plasma used on the assay results of the Nijmegen modification of the Bethesda method for factor VIII inhibitors. Immuno depleted factor VIII deficient plasmas, lacking bes
Autor:
Marnie DeReske, P. Marlene Absher, Mary Richardson, Alan R. Giles, Yotis A. Senis, Mark W.C. Hatton, John A. Samis, Donald H. Maurice, José C.O Ribau
Publikováno v:
Atherosclerosis. 149:331-342
Endothelial cell injury has been implicated in the increased incidence of vascular disease associated with diabetes mellitus. In diabetic humans, elevated plasma von Willebrand Factor (vWF) has been interpreted as an indication of endothelial damage.
Publikováno v:
Blood. 95:943-951
Previous studies have shown that thrombin generation in vivo caused a 92% decrease in factor IX (F.IX) activity and the appearance of a cleavage product after immunoblotting that comigrated with activated F.IX (F.IXa). Under these conditions, the fib
Publikováno v:
Journal of Thrombosis and Haemostasis. 6:1600-1602
Thrombin activatable fibrinolysis inhibitor (TAFI, proCPU) is a 60kDa plasma zymogen that circulates at a concentration of about 75nM [1]. It is activated by thrombin [2,3], the thrombin/thrombomodulin complex [4], or plasmin [5] by proteolytic cleav
Publikováno v:
Blood. 92:1287-1296
In preliminary studies, the generation of thrombin in vivo was found to induce a 92% loss of functional activity of factor IX (F.IX) despite the detection by Western blotting of a product resembling activated F.IX (F.IXa) and a 25% increase in F.IX a
Human Neutrophil Elastase Activates Human Factor V but Inactivates Thrombin-Activated Human Factor V
Publikováno v:
Blood. 90:1065-1074
The effect of human neutrophil elastase (HNE) on human factor V (F.V) or α-thrombin–activated human factor V (F.Va) was studied in vitro by prothrombinase assays, sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), and NH2 -termi