Zobrazeno 1 - 10
of 315
pro vyhledávání: '"Ka, Bauer"'
Publikováno v:
Blood. 84:2214-2220
We analyzed the mutations in patients from 10 Polish kindreds with a bleeding diathesis due to factor VII deficiency. Patients from eight families had plasma levels of factor VII coagulant activity (VII:C) and factor VII antigen (VII:Ag) that were le
Publikováno v:
Blood. 84:1314-1319
Virally inactivated, high-purity factor XI concentrates are available for treatment of patients with factor XI deficiency. However, preliminary experience indicates that some preparations may be thrombogenic. We evaluated whether a highly purified co
Publikováno v:
Blood. 78:1744-1752
Fibrinogen Ledyard was discovered in a 10-year-old boy with a mild bleeding history. His father had the same defect and a bleeding history after surgery. Both patients were heterozygous. The plasma fibrinogen concentration was normal immunologically
Publikováno v:
Blood. 76:2540-2545
Prothrombin complex concentrates (PCC), licensed for the treatment of hemophilia B, are known to carry a significant risk of thromboembolic complications. Although the reasons for thrombogenicity are not completely understood, several manufacturers h
Publikováno v:
Blood. 76:2284-2289
Several investigators have reported that tumor necrosis factor (TNF) can alter the production of plasminogen activator type-1 (PAI-1) and plasminogen activators (PAs) by endothelial cells in vitro. We have examined the in vivo effects of recombinant
Publikováno v:
Europe PubMed Central
We investigated the mechanisms responsible for severe factor VII (FVII) deficiency in homozygous Italian patients with either Gly97Cys or Gln100Arg mutations in the second epidermal growth factor domain of FVII. Transient expression of complementary
Autor:
mathilde hunault, Marsh-Scott C, Jou C, Marshall R, Scheffel C, Ld, Fiore, Ka, Bauer, Mj, Mitchell
Publikováno v:
Europe PubMed Central
The factor V Leiden mutation, a G--A transition at position 1691 in exon 10 of the gene that codes for factor V, produces an Arg506Gln substitution and is the most common genetic risk factor for venous thrombosis. We have developed a rapid, sensitive
Autor:
Da, Lane, Pm, Mannucci, Ka, Bauer, Rm, Bertina, Np, Bochkov, Boulyjenkov V, Chandy M, Bjorn Dahlback, Ek, Ginter, Jp, Miletich, Fr, Rosendaal, Seligsohn U
Publikováno v:
Europe PubMed Central
Publikováno v:
Blood. 76(4)
Despite significant progress in elucidating the biochemistry of the hemostatic mechanism, the process of blood coagulation in vivo remains poorly understood. Factor IX is a vitamin K-dependent glycoprotein that can be activated by factor XIa or the f
Publikováno v:
Blood. 74:165-172
Several investigators have reported that tumor necrosis factor (TNF) can alter the hemostatic properties of vascular endothelial cells in vitro. We have examined the in vivo effects on the hemostatic mechanism of recombinant human TNF administered as