Hemophilia B

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  Subject Areas on Research

  • A natural choice for hemophilia B. 
  • A past mutation at isoleucine 397 is now a common cause of moderate/mild haemophilia B. 
  • Abnormal joint and bone wound healing in hemophilia mice is improved by extending factor IX activity after hemarthrosis. 
  • An activated factor VII variant with enhanced tissue factor-independent activity speeds wound healing in a mouse hemophilia B model. 
  • Celecoxib does not delay cutaneous wound healing in haemophilia B mice. 
  • Combined deficiency of factors II, VII, IX, and X (Borgschulte-Grigsby deficiency) in pregnancy. 
  • Combined factor IX and XI deficiency discovered at liver biopsy. 
  • Comparison of direct and indirect methods of carrier detection in an X-linked disease. 
  • Consequences of intra-articular bleeding in haemophilia: science to clinical practice and beyond. 
  • Cutaneous wound healing is impaired in hemophilia B. 
  • Direct carrier testing in 14 families with haemophilia B. 
  • Factor IXa as a target for pharmacologic inhibition in acute coronary syndrome. 
  • Functionally important regions of the factor IX gene have a low rate of polymorphism and a high rate of mutation in the dinucleotide CpG. 
  • High dose factor VIIa improves clot structure and stability in a model of haemophilia B. 
  • Hip arthroplasty in hemophilic arthropathy. 
  • Human factor IXLincoln Park: a molecular characterization. 
  • Low intensity laser therapy speeds wound healing in hemophilia by enhancing platelet procoagulant activity. 
  • More on: are randomized clinical trials the only truth? Not always. 
  • Mutations causing hemophilia B: direct estimate of the underlying rates of spontaneous germ-line transitions, transversions, and deletions in a human gene. 
  • Perivascular tissue factor is down-regulated following cutaneous wounding: implications for bleeding in hemophilia. 
  • Progressive improvement in wound healing with increased therapy in haemophilia B mice. 
  • Recurrent nonsense mutations at arginine residues cause severe hemophilia B in unrelated hemophiliacs. 
  • Restoring hemostatic thrombin generation at the time of cutaneous wounding does not normalize healing in hemophilia B. 
  • T296----M, a common mutation causing mild hemophilia B in the Amish and others: founder effect, variability in factor IX activity assays, and rapid carrier detection. 
  • The clotting system - a major player in wound healing. 
  • The optimal mode of delivery for the haemophilia carrier expecting an affected infant is caesarean delivery. 
  • Wound healing in haemophilia--breaking the vicious cycle. 
  • Wound healing in hemophilia B mice and low tissue factor mice. 
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  Keywords of People

  • Hoffman, Maureane, Professor of Pathology, Integrative Immunobiology