Download 36th Hemophilia Symposium Hamburg 2005: Epidemiology; by Inge Scharrer, Wolfgang Schramm, G. Auerswald, A. Kurth, J. PDF

By Inge Scharrer, Wolfgang Schramm, G. Auerswald, A. Kurth, J. Oldenburg, W. Schramm, B. Zieger

This ebook includes the contribution to the thirty sixth Hemophilia Symposium, Hamburg 2005. the most themes are epidemiolgy, hemophilia remedy, orthopedic remedy in hemophiliacs, hemostaseologic analysis and pediatric hemostaseology. the amount is rounded off through a variety of unfastened papers and posters on hemophilia, inhibitors in hemophilia and diagnostics.

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Read or Download 36th Hemophilia Symposium Hamburg 2005: Epidemiology; Hemophilia Therapy - Management of Bleedings and Inhibitors; Orthopedic Treatment in Hemophiliacs; ... Pediatric Hemostaseology; Free Lectures PDF

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Extra info for 36th Hemophilia Symposium Hamburg 2005: Epidemiology; Hemophilia Therapy - Management of Bleedings and Inhibitors; Orthopedic Treatment in Hemophiliacs; ... Pediatric Hemostaseology; Free Lectures

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Parker ET, Healey JF, Barrow RT, Craddock HN, Lollar P. Reduction of the inhibitory antibody response to human factor VIII in hemophilia A mice by mutagenesis of the A2 domain B-cell epitope. Blood 2004; 104: 704–10. Update of the Inhibitor-Immunology-Study I. Wieland, C. Wermes, B. Eifrig, K. Holstein, H. Pollmann, B. Siegmund, A. Nimtz-Talaska, C. Niekrens, R. Eisert, A. Tiede, K. -W. Sykora Abstract We are presenting an update of our study in which risk factors for the development of inhibitors in patients with hemophilia are to be explored.

Noteworthy, the half-life of infused FVIII in patients with von Willebrand disease can be reverted to the normal level (12–14 hours) by coinfusion of vWF [24]. In vWF-knockout mice, representing an experimental model of vWF disease, clearance of FVIII is faster than in normal mice and can be inhibited by pre-administration of RAP thus confirming that the accelerated clearance of FVIII in the absence of vWF is mediated by LRP [9–11]. 4 h [28]) is observed; patients with shorter FVIII half-life require more clotting factor to prevent joint bleeds and subsequent arthropathy [28].

As judged from the 3D model of intact FVIII [22], both LRPinteractive regions within A2 and A3 domains are positioned at the same flank of 28 E. L. Saenko the FVIII molecule. This implies that when exposed, both regions of FVIII might cooperate in the high-affinity interaction with LRP. Physiological condition leading to dissociation of vWF from FVIII is activation, when the binding sites within LCh become fully exposed and available for interaction with LRP [3, 8]. Interestingly, the recent study demonstrated that activation also increases the affinity of FVIII HCh for LRP as evidenced by SPR and solid-phase binding methods [31].

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