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Thromb Haemost 2007; 98(01): 6-7
DOI: 10.1160/TH07-04-0244
Anniversary Issue Contribution
Schattauer GmbH

Thrombosis and haemostasis, where clinical and basic science meet

Jos Vermylen
1   Emeritus Professor of Medicine, Center for Molecular and Vascular Biology, University of Leuven, Leuven, Belgium
,
Erik Mürer
1   Emeritus Professor of Medicine, Center for Molecular and Vascular Biology, University of Leuven, Leuven, Belgium
› Author Affiliations
Further Information

Correspondence to:

Jos Vermylen
Emeritus Professor of Medicine
Center for Molecular and Vascular Biology
University of Leuven, Herenstraat 49, B 3000 Leuven, Belgium
Phone: +32 16 23 31 17   
Fax: +32 16 34 59 90   

Publication History

Received 03 April 2007

Accepted 26 April 2007

Publication Date:
29 November 2017 (online)

 
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  • References

  • 1 Wright IS. The modern treatment of coronary thrombosis with myocardial infarction. Circulation 1950; 2: 927-936.
    PubMedGoogle Scholar
  • 2 Wright IS, Beck DF, Marple CD. Myocardial infarction and its treatment with anticoagulants; summary of findings in 1031 cases. Lancet 1954; 266: 92-95.
    CrossrefPubMedGoogle Scholar
  • 3 Wright IS. Chaos or communication. J Am Med Ass 1957; 163: 358-359.
    CrossrefPubMedGoogle Scholar
  • 4 Amery A, Vermylen J, Maes H. et al. Enchancing the fibrinolytic activity in human blood by occlusion of blood vessels I. The appearance of the phenomenon. Thromb Diath Haemorrh 1962; 7: 70-85.
    PubMedGoogle Scholar
  • 5 Verstraete M, Amery A, Vermylen J. Feasibility of adequate thrombolytic therapy with streptokinase in peripheral arterial occlusions I. Clinical and arterio-graphic results. Br Med J 1963; i: 1499-1504.
    PubMedGoogle Scholar
  • 6 European working party.. Streptokinase in recent myocardial infarction: a controlled multicentre trial. Br Med J 1971; 3: 325-331.
    CrossrefPubMedGoogle Scholar
  • 7 European cooperative study group forstreptokinasetreatment in acute myocardial infarction.. Streptokinase in acute myocardial infarction. N Engl J Med 1979; 301: 797-802.
    CrossrefPubMedGoogle Scholar
  • 8 Dewood MA, Spores J, Notske R. et al. Prevalence of total coronary occlusion during the early hours of transmural myocardial infarction. N Engl J Med 1980; 303: 897-902.
    CrossrefPubMedGoogle Scholar
  • 9 Nurden AT, Caen JP. An abnormal platelet glycoprotein pattern in three cases of Glanzmann’s Thrombasthenia. Br J Haematol 1974; 28: 253-260.
    CrossrefPubMedGoogle Scholar
  • 10 Weiss HJ, Aledort LM. Impaired platelet-connect-ive tissue reaction in man after aspirin ingestion. Lancet 1967; ii: 495-497.
    PubMedGoogle Scholar
  • 11 Elwood PC, Cochrane AL, Burr ML. et al. A randomized controlled trial of acetyl salicylic acid in the secondary prevention of mortality from myocardial infarction. Br Med J 1974; i: 436-440.
    PubMedGoogle Scholar
  • 12 Hamberg M, Svensson J, Samuelsson B. Thromboxanes: a new group of biologically active compounds derived from platelet endoperoxides. Proc Natl Acad Sci USA 1975; 72: 2994-2998.
    CrossrefPubMedGoogle Scholar
  • 13 Dahlback B, Carlsson M, Svensson PJ. Familial thrombophilia due to a previously unrecognized mechanism characterized by poor anticoagulant response to activated protein C: prediction of a cofactor to activated protein C. Proc Natl Acad Sci USA 1993; 90: 1004-1008.
    CrossrefPubMedGoogle Scholar
  • 14 Bertina RM, Koeleman BP, Koster T. et al. Mutation in blood coagulation factor V associated with resistance to activated protein C. Nature 1994; 369: 64-67.
    CrossrefPubMedGoogle Scholar
  • 15 Furlan M, Robles R, Solenthaler M. et al. Deficient activity of von Willebrand factor-cleaving protease in chronic relapsing thrombotic thrombocytopenic purpura. Blood 1997; 89: 3097-3103.
    PubMedGoogle Scholar
  • 16 Zheng X, Chung D, Takayama TK. et al. Structure of von Wlillebrand factor-cleaving protease (ADAMTS 13), a metalloprotease involved in thrombotic thrombocytopenic purpura. J Biol Chem 2001; 276: 41059-41063.
    CrossrefPubMedGoogle Scholar
  • 17 Van Geet C, Jaeken J, Freson K. et al. Congenital disorders of glycosylation type Ia and IIa are associated with different primary haemostatic complications. J Inherit Metab Dis 2001; 24: 477-492.
    CrossrefPubMedGoogle Scholar
  • 18 Freson K, Hoylaerts MF, Jaeken J. et al. Genetic variation of the extra-large stimulatory G protein alpha-subunit leads to Gs hyperfunction in platelets and is a risk factor for bleeding. Thromb Haemost 2001; 86: 733-738.
    Article in Thieme ConnectPubMedGoogle Scholar

Correspondence to:

Jos Vermylen
Emeritus Professor of Medicine
Center for Molecular and Vascular Biology
University of Leuven, Herenstraat 49, B 3000 Leuven, Belgium
Phone: +32 16 23 31 17   
Fax: +32 16 34 59 90   

  • References

  • 1 Wright IS. The modern treatment of coronary thrombosis with myocardial infarction. Circulation 1950; 2: 927-936.
    PubMedGoogle Scholar
  • 2 Wright IS, Beck DF, Marple CD. Myocardial infarction and its treatment with anticoagulants; summary of findings in 1031 cases. Lancet 1954; 266: 92-95.
    CrossrefPubMedGoogle Scholar
  • 3 Wright IS. Chaos or communication. J Am Med Ass 1957; 163: 358-359.
    CrossrefPubMedGoogle Scholar
  • 4 Amery A, Vermylen J, Maes H. et al. Enchancing the fibrinolytic activity in human blood by occlusion of blood vessels I. The appearance of the phenomenon. Thromb Diath Haemorrh 1962; 7: 70-85.
    PubMedGoogle Scholar
  • 5 Verstraete M, Amery A, Vermylen J. Feasibility of adequate thrombolytic therapy with streptokinase in peripheral arterial occlusions I. Clinical and arterio-graphic results. Br Med J 1963; i: 1499-1504.
    PubMedGoogle Scholar
  • 6 European working party.. Streptokinase in recent myocardial infarction: a controlled multicentre trial. Br Med J 1971; 3: 325-331.
    CrossrefPubMedGoogle Scholar
  • 7 European cooperative study group forstreptokinasetreatment in acute myocardial infarction.. Streptokinase in acute myocardial infarction. N Engl J Med 1979; 301: 797-802.
    CrossrefPubMedGoogle Scholar
  • 8 Dewood MA, Spores J, Notske R. et al. Prevalence of total coronary occlusion during the early hours of transmural myocardial infarction. N Engl J Med 1980; 303: 897-902.
    CrossrefPubMedGoogle Scholar
  • 9 Nurden AT, Caen JP. An abnormal platelet glycoprotein pattern in three cases of Glanzmann’s Thrombasthenia. Br J Haematol 1974; 28: 253-260.
    CrossrefPubMedGoogle Scholar
  • 10 Weiss HJ, Aledort LM. Impaired platelet-connect-ive tissue reaction in man after aspirin ingestion. Lancet 1967; ii: 495-497.
    PubMedGoogle Scholar
  • 11 Elwood PC, Cochrane AL, Burr ML. et al. A randomized controlled trial of acetyl salicylic acid in the secondary prevention of mortality from myocardial infarction. Br Med J 1974; i: 436-440.
    PubMedGoogle Scholar
  • 12 Hamberg M, Svensson J, Samuelsson B. Thromboxanes: a new group of biologically active compounds derived from platelet endoperoxides. Proc Natl Acad Sci USA 1975; 72: 2994-2998.
    CrossrefPubMedGoogle Scholar
  • 13 Dahlback B, Carlsson M, Svensson PJ. Familial thrombophilia due to a previously unrecognized mechanism characterized by poor anticoagulant response to activated protein C: prediction of a cofactor to activated protein C. Proc Natl Acad Sci USA 1993; 90: 1004-1008.
    CrossrefPubMedGoogle Scholar
  • 14 Bertina RM, Koeleman BP, Koster T. et al. Mutation in blood coagulation factor V associated with resistance to activated protein C. Nature 1994; 369: 64-67.
    CrossrefPubMedGoogle Scholar
  • 15 Furlan M, Robles R, Solenthaler M. et al. Deficient activity of von Willebrand factor-cleaving protease in chronic relapsing thrombotic thrombocytopenic purpura. Blood 1997; 89: 3097-3103.
    PubMedGoogle Scholar
  • 16 Zheng X, Chung D, Takayama TK. et al. Structure of von Wlillebrand factor-cleaving protease (ADAMTS 13), a metalloprotease involved in thrombotic thrombocytopenic purpura. J Biol Chem 2001; 276: 41059-41063.
    CrossrefPubMedGoogle Scholar
  • 17 Van Geet C, Jaeken J, Freson K. et al. Congenital disorders of glycosylation type Ia and IIa are associated with different primary haemostatic complications. J Inherit Metab Dis 2001; 24: 477-492.
    CrossrefPubMedGoogle Scholar
  • 18 Freson K, Hoylaerts MF, Jaeken J. et al. Genetic variation of the extra-large stimulatory G protein alpha-subunit leads to Gs hyperfunction in platelets and is a risk factor for bleeding. Thromb Haemost 2001; 86: 733-738.
    Article in Thieme ConnectPubMedGoogle Scholar

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