نتایج جستجو برای: fviii

تعداد نتایج: 1331  

Journal: :Blood 2013
Henning R Stennicke Marianne Kjalke Ditte M Karpf Kristoffer W Balling Peter B Johansen Torben Elm Kristine Øvlisen Flemming Möller Heidi L Holmberg Charlotte N Gudme Egon Persson Ida Hilden Hermann Pelzer Henrik Rahbek-Nielsen Christina Jespersgaard Are Bogsnes Anette A Pedersen Anne K Kristensen Bernd Peschke Wendy Kappers Frederik Rode Lars Thim Mikael Tranholm Mirella Ezban Eva H N Olsen Søren E Bjørn

Frequent infusions of intravenous factor VIII (FVIII) are required to prevent bleeding associated with hemophilia A. To reduce the treatment burden, recombinant FVIII with a longer half-life was developed without changing the protein structure. FVIII-polyethylene glycol (PEG) conjugates were prepared using an enzymatic process coupling PEG (ranging from 10 to 80 kDa) selectively to a unique O-l...

2013
Stefanie Hausammann Monique Vogel Johanna A. Kremer Hovinga Sebastien Lacroix-Desmazes Beda M. Stadler Michael P. Horn

Inhibitory antibodies directed against coagulation factor VIII (FVIII) can be found in patients with acquired and congenital hemophilia A. Such FVIII-inhibiting antibodies are routinely detected by the functional Bethesda Assay. However, this assay has a low sensitivity and shows a high inter-laboratory variability. Another method to detect antibodies recognizing FVIII is ELISA, but this test d...

Journal: :Blood 1982
M F Fernandez M H Ginsberg Z M Ruggeri F J Batlle T S Zimmerman

The multimeric structure of platelet factor VIII/von Willebrand factor (FVIII/vWF) in cell extracts and in collagen and thrombin releasates has been analyzed by SDS polyacrylamide gel electrophoresis followed by detection with 125I-anti-FVIII/vWF. Platelets contained larger multimers than those normally present in plasma. When secreted FVIII/vWF was analyzed, all platelets. In contrast, in thro...

Journal: :Blood 2005
Mario Berger Manuel Mattheisen Bettina Kulle Henriette Schmidt Johannes Oldenburg Heike Bickeböller Ulrich Walter Tom H Lindner Konstantin Strauch Christian M Schambeck

High factor VIII (FVIII) levels are known to be a risk factor for deep venous thrombosis, but the mechanisms responsible for high FVIII levels remain unclear. Here, a new phenotype "FVIII level residuum" (FVIII-R) was defined in order to eliminate the impact of common determinants on FVIII levels. We studied 13 families of patients with thrombosis and reproducibly high FVIII levels of unknown o...

Journal: :Thrombosis and haemostasis 2004
Christiane Mühle Stefan Schulz-Drost Alexey V Khrenov Evgueni L Saenko Jens Klinge Holm Schneider

Clotting factor VIII (fVIII)-inhibitory antibodies represent a major problem in the treatment of haemophilia A. To understand the inactivation mechanisms and to pave the way towards modifications of recombinant clotting factors that reduce their immunogenicity, the exact localization of immunodominant epitopes is required. Here, a random peptide phage display library was employed to identify ep...

Journal: :Hamostaseologie 2013
A Naumann A K Scherger J Neuwirth A Orlowski J Kahle D Schwabe C Königs

The development of inhibitory anti-FVIII antibodies is currently the most severe complication in the treatment of haemophilia A patients. Inhibitor eradication can be achieved by immune tolerance induction (ITI). Recent findings suggest a correlation between the FVIII-specific IgG subclass distribution and the duration or outcome of ITI. To quantify FVIII-specific IgG subclasses in patients' pl...

2014
Brittany M Gouse Amelia K Boehme Dominique J Monlezun James E Siegler Alex J George Katherine Brag Karen C Albright T Mark Beasley Cindy Leissinger Ramy El Khoury Sheryl Martin-Schild

Background. Heightened levels of Factor VIII (FVIII) have been associated with both arterial and venous thrombosis. While elevated FVIII is common during acute ischemic stroke (AIS), whether elevated FVIII confers an increased risk for recurrent thrombotic events (RTEs) following AIS has not been previously explored. Methods. Consecutive AIS patients who presented to our center between July 200...

1999
Christopher B. Doering Ernest T. Parker Christopher E. Nichols Pete Lollar

Duringhumanfulminanthepatic failure (FHF) circulating levels of most hemostatic proteins fall dramatically. Concurrently, factor VIII (fVIII) procoagulant activity rises despite destruction of the hepatocytes considered responsible for fVIII synthesis. This observation suggests a role for cells other than hepatocytes in fVIII biosynthesis during FHF. We have attempted to identify nonhepatocytic...

Journal: :Blood 1979
M E Switzer S V Pizzo P A McKee

When factor VIII/von Willebrand factor (FVIII/vWF) is chromatographed on 4% agarose in 0.25 M CaCI2. the procoagulant activity partially separates from the void volume protein peak. If FVIII/vWF is reacted with thrombin prior to chromatography, both the magnitude and resolution of the proe.oagulant activity peak are greatly increased. These observations suggest that activated species of FVIII/v...

Journal: :Blood 2014
Scot A Fahs Matthew T Hille Qizhen Shi Hartmut Weiler Robert R Montgomery

The cellular source of coagulation factor VIII (FVIII) remains controversial. Like many coagulation proteins, FVIII is produced in the liver, and FVIII synthesis has long been associated with hepatocytes. But extrahepatic synthesis also occurs, and mounting evidence suggests that hepatocytes are not responsible for FVIII production. To determine the tissue that synthesizes FVIII, we developed a...

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