Search Results - (Author, Cooperation:M. Laffan)

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  1. 1
    L. Chen ; M. Kostadima ; J. H. Martens ; G. Canu ; S. P. Garcia ; E. Turro ; K. Downes ; I. C. Macaulay ; E. Bielczyk-Maczynska ; S. Coe ; S. Farrow ; P. Poudel ; F. Burden ; S. B. Jansen ; W. J. Astle ; A. Attwood ; T. Bariana ; B. de Bono ; A. Breschi ; J. C. Chambers ; F. A. Choudry ; L. Clarke ; P. Coupland ; M. van der Ent ; W. N. Erber ; J. H. Jansen ; R. Favier ; M. E. Fenech ; N. Foad ; K. Freson ; C. van Geet ; K. Gomez ; R. Guigo ; D. Hampshire ; A. M. Kelly ; H. H. Kerstens ; J. S. Kooner ; M. Laffan ; C. Lentaigne ; C. Labalette ; T. Martin ; S. Meacham ; A. Mumford ; S. Nurnberg ; E. Palumbo ; B. A. van der Reijden ; D. Richardson ; S. J. Sammut ; G. Slodkowicz ; A. U. Tamuri ; L. Vasquez ; K. Voss ; S. Watt ; S. Westbury ; P. Flicek ; R. Loos ; N. Goldman ; P. Bertone ; R. J. Read ; S. Richardson ; A. Cvejic ; N. Soranzo ; W. H. Ouwehand ; H. G. Stunnenberg ; M. Frontini ; A. Rendon
    American Association for the Advancement of Science (AAAS)
    Published 2014
    Staff View
    Publication Date:
    2014-09-27
    Publisher:
    American Association for the Advancement of Science (AAAS)
    Print ISSN:
    0036-8075
    Electronic ISSN:
    1095-9203
    Topics:
    Biology
    Chemistry and Pharmacology
    Computer Science
    Medicine
    Natural Sciences in General
    Physics
    Keywords:
    *Alternative Splicing ; Cell Lineage/*genetics ; Genetic Variation ; Hematopoiesis/*genetics ; Hematopoietic Stem Cells/*cytology/metabolism ; Humans ; NFI Transcription Factors/genetics/metabolism ; RNA-Binding Proteins/metabolism ; Thrombopoiesis/genetics ; Transcriptome
    Published by:
    http://www.aaas.org/

    Latest Papers from Table of Contents or Articles in Press
  2. 2
    Beltrán-Miranda, C. P. ; Khan, A. ; Jaloma-Cruz, A. R. ; Laffan, M. A.

    Oxford, UK : Blackwell Science Ltd
    Published 2005
    Staff View
    ISSN:
    1365-2516
    Source:
    Blackwell Publishing Journal Backfiles 1879-2005
    Topics:
    Medicine
    Notes:
    Summary.  The clinical phenotype of patients with haemophilia A (HA) often differs between individuals with the same factor VIII (FVIII) gene defect (e.g. within the same family) or the same coagulant activity of FVIII (FVIII:C). We proposed that because the thrombin generation assay in platelet-poor plasma of HA patients provides more information [peak thrombin concentration, endogenous thrombin potential (ETP), rate of thrombin generation and lag-time] than a clot-based FVIII assay it might provide insight into these differences. We therefore investigated the relation between the results of the thrombin generation assay and the clinical severity in nine families with HA (23 patients with different phenotypes). We also examined the contribution of prothrombotic risk factors: (FV Leiden G1691A and prothrombin G20210A), the coagulant activity of FVIII and tissue factor (5′UTR) polymorphisms. Our data detect marked differences between individuals but these did not correlate with the reported clinical phenotype. These differences were also reflected in a marked difference in response to the therapeutic amounts of FVIII. This might account for differences in amounts of treatment consumption. Reduced peak and possibly rate of thrombin generation, rather than FVIII:C or ETP appear to represent the critical defects in FVIII-deficient plasma. We suggest that the analysis of parameters in thrombin generation is a useful tool to detect bleeding tendency in HA but not to predict the modulation of the haemorrhagic tendency in patients within families. However the presence of the other factors such as vessel wall components, protein C and platelets might need to be incorporated into this system.
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1111/j.1365-2516.2005.01107.x

    Articles: DFG German National Licenses
  3. 3
    Laffan, M. ; Brown, S. A. ; Collins, P. W. ; Cumming, A. M. ; Hill, F. G. H. ; Keeling, D. ; Peake, I. R. ; Pasi, K. J.

    Oxford, UK : Blackwell Science Ltd
    Published 2004
    Staff View
    ISSN:
    1365-2516
    Source:
    Blackwell Publishing Journal Backfiles 1879-2005
    Topics:
    Medicine
    Notes:
    Summary.  von Willebrand disease (VWD) is the commonest inherited bleeding disorder. However, despite an increasing understanding of the pathophysiology of VWD, the diagnosis of VWD is frequently difficult because of uncertainty regarding the relationship between laboratory assays and function in vivo. The objective of this guideline is to provide contemporary advice on a rational approach to the diagnosis of VWD. This is the second edition of this UK Haemophilia Centre Doctors’ Organisation (UKHCDO) guideline and supersedes the previous edition which was published in 1997.
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1111/j.1365-2516.2004.00894.x

    Articles: DFG German National Licenses
  4. 4
    Staff View
    ISSN:
    1365-2516
    Source:
    Blackwell Publishing Journal Backfiles 1879-2005
    Topics:
    Medicine
    Notes:
    Summary.  von Willebrand disease (VWD) is the commonest inherited bleeding disorder. The aim of therapy for VWD is to correct the two defects of haemostasis in this disorder, impaired primary haemostasis because of defective platelet adhesion and aggregation and impaired coagulation as a result of low levels of factor VIII. The objective of this guideline is to inform individuals making choices about the treatment and management of VWD including the use of therapeutic products. This is the second edition of this UK Haemophilia Centre Doctors' Organization (UKHCDO) guideline and supersedes the previous edition which was published in 1994.
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1111/j.1365-2516.2004.00886.x

    Articles: DFG German National Licenses