M I Furman

Summary

Affiliation: University of Massachusetts Medical School
Country: USA

Publications

  1. ncbi request reprint Antithrombotic therapy in the cardiac catheterization laboratory: focus on antiplatelet agents
    M I Furman
    Division of Cardiovascular Medicine, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA
    Curr Cardiol Rep 2:386-94. 2000
  2. ncbi request reprint Leukocyte-platelet aggregation, platelet surface P-selectin, and platelet surface glycoprotein IIIa after percutaneous coronary intervention: Effects of dalteparin or unfractionated heparin in combination with abciximab
    M I Furman
    Center for Platelet Function Studies and the Division of Cardiovascular Medicine, Departments of Medicine, Pediatrics, and Cell Biology, University of Massachusetts Medical School, Worcester, MA 01655, USA
    Am Heart J 142:790-8. 2001
  3. ncbi request reprint GPIIb-IIIa antagonist-induced reduction in platelet surface factor V/Va binding and phosphatidylserine expression in whole blood
    M I Furman
    Center for Platelet Function Studies, University of Massachusetts Medical School, Worcester, PA 01655, USA
    Thromb Haemost 84:492-8. 2000
  4. ncbi request reprint Indices of platelet activation and the stability of coronary artery disease
    M D Linden
    Center for Platelet Function Studies, University of Massachusetts Medical School, Worcester, MA 01655, USA
    J Thromb Haemost 5:761-5. 2007
  5. ncbi request reprint The active metabolite of prasugrel inhibits adenosine diphosphate- and collagen-stimulated platelet procoagulant activities
    A L Frelinger
    Center for Platelet Function Studies, and Department of Pediatrics, University of Massachusetts Medical School, Worcester, MA 01655, USA
    J Thromb Haemost 6:359-65. 2008
  6. ncbi request reprint Evaluation of platelet function by flow cytometry
    A D Michelson
    Center for Platelet Function Studies, University of Massachusetts Medical School, Worcester, Massachusetts, 01655, USA
    Methods 21:259-70. 2000
  7. ncbi request reprint GPIIb-IIIa antagonists reduce thromboinflammatory processes in patients with acute coronary syndromes undergoing percutaneous coronary intervention
    M I Furman
    Cardiac Catheterization Laboratories, UMass Memorial Medical Center, University of Massachusetts Medical School, Worcester, MA 01605, USA
    J Thromb Haemost 3:312-20. 2005
  8. ncbi request reprint Evidence that pre-existent variability in platelet response to ADP accounts for 'clopidogrel resistance'
    A D Michelson
    Center for Platelet Function Studies, University of Massachusetts Medical School, Worcester, MA 01655, USA
    J Thromb Haemost 5:75-81. 2007
  9. ncbi request reprint Circulating monocyte-platelet aggregates are an early marker of acute myocardial infarction
    M I Furman
    Center for Platelet Function Studies, Division of Cardiovascular Medicine, Worcester, Massachusetts 01655, USA
    J Am Coll Cardiol 38:1002-6. 2001
  10. ncbi request reprint Circulating monocyte-platelet aggregates are a more sensitive marker of in vivo platelet activation than platelet surface P-selectin: studies in baboons, human coronary intervention, and human acute myocardial infarction
    A D Michelson
    Center for Platelet Function Studies, Departments of Pediatrics and Medicine, University of Massachusetts Medical School, Worcester, MA 01655, USA
    Circulation 104:1533-7. 2001

Collaborators

Detail Information

Publications18

  1. ncbi request reprint Antithrombotic therapy in the cardiac catheterization laboratory: focus on antiplatelet agents
    M I Furman
    Division of Cardiovascular Medicine, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA
    Curr Cardiol Rep 2:386-94. 2000
    ..Despite the growing use of GP IIb/IIIa antagonists, much information remains unknown as to the proper dosing and the effects these agents have on other elements of the hemostatic and vascular systems...
  2. ncbi request reprint Leukocyte-platelet aggregation, platelet surface P-selectin, and platelet surface glycoprotein IIIa after percutaneous coronary intervention: Effects of dalteparin or unfractionated heparin in combination with abciximab
    M I Furman
    Center for Platelet Function Studies and the Division of Cardiovascular Medicine, Departments of Medicine, Pediatrics, and Cell Biology, University of Massachusetts Medical School, Worcester, MA 01655, USA
    Am Heart J 142:790-8. 2001
    ..Low-molecular-weight heparins have been reported to cause less platelet activation than unfractionated heparin...
  3. ncbi request reprint GPIIb-IIIa antagonist-induced reduction in platelet surface factor V/Va binding and phosphatidylserine expression in whole blood
    M I Furman
    Center for Platelet Function Studies, University of Massachusetts Medical School, Worcester, PA 01655, USA
    Thromb Haemost 84:492-8. 2000
    ..Fibrinogen binding to GPIIb-IIIa is important in the generation of platelet procoagulant activity...
  4. ncbi request reprint Indices of platelet activation and the stability of coronary artery disease
    M D Linden
    Center for Platelet Function Studies, University of Massachusetts Medical School, Worcester, MA 01655, USA
    J Thromb Haemost 5:761-5. 2007
    ..To determine whether indices of platelet activation are associated with the stability of coronary artery disease (CAD)...
  5. ncbi request reprint The active metabolite of prasugrel inhibits adenosine diphosphate- and collagen-stimulated platelet procoagulant activities
    A L Frelinger
    Center for Platelet Function Studies, and Department of Pediatrics, University of Massachusetts Medical School, Worcester, MA 01655, USA
    J Thromb Haemost 6:359-65. 2008
    ..We therefore examined whether R-138727 inhibits ADP- and collagen-triggered platelet procoagulant activities...
  6. ncbi request reprint Evaluation of platelet function by flow cytometry
    A D Michelson
    Center for Platelet Function Studies, University of Massachusetts Medical School, Worcester, Massachusetts, 01655, USA
    Methods 21:259-70. 2000
    ....
  7. ncbi request reprint GPIIb-IIIa antagonists reduce thromboinflammatory processes in patients with acute coronary syndromes undergoing percutaneous coronary intervention
    M I Furman
    Cardiac Catheterization Laboratories, UMass Memorial Medical Center, University of Massachusetts Medical School, Worcester, MA 01605, USA
    J Thromb Haemost 3:312-20. 2005
    ....
  8. ncbi request reprint Evidence that pre-existent variability in platelet response to ADP accounts for 'clopidogrel resistance'
    A D Michelson
    Center for Platelet Function Studies, University of Massachusetts Medical School, Worcester, MA 01655, USA
    J Thromb Haemost 5:75-81. 2007
    ..Clopidogrel is a widely used antithrombotic agent that inhibits the platelet P2Y(12) adenosine diphosphate (ADP) receptor. There is increasing interest in 'clopidogrel resistance'...
  9. ncbi request reprint Circulating monocyte-platelet aggregates are an early marker of acute myocardial infarction
    M I Furman
    Center for Platelet Function Studies, Division of Cardiovascular Medicine, Worcester, Massachusetts 01655, USA
    J Am Coll Cardiol 38:1002-6. 2001
    ..We investigated whether elevated levels of circulating monocyte-platelet aggregates (MPA) can be used to identify patients with acute myocardial infarction (AMI)...
  10. ncbi request reprint Circulating monocyte-platelet aggregates are a more sensitive marker of in vivo platelet activation than platelet surface P-selectin: studies in baboons, human coronary intervention, and human acute myocardial infarction
    A D Michelson
    Center for Platelet Function Studies, Departments of Pediatrics and Medicine, University of Massachusetts Medical School, Worcester, MA 01655, USA
    Circulation 104:1533-7. 2001
    ..Platelet surface P-selectin is considered the "gold standard" marker of platelet activation. Degranulated, P-selectin-positive platelets, however, aggregate with leukocytes in vitro and rapidly lose surface P-selectin in vivo...
  11. ncbi request reprint Dissociation of glycoprotein IIb/IIIa antagonists from platelets does not result in fibrinogen binding or platelet aggregation
    A L Frelinger
    Center for Platelet Function Studies, University of Massachusetts Medical School, Worcester, MA 01655, USA
    Circulation 104:1374-9. 2001
    ..These apparently paradoxical results have been extensively referenced in the cardiology literature...
  12. ncbi request reprint Laser scanning cytometry: a novel method for the detection of platelet--endothelial cell adhesion
    R B Claytor
    Department of Surgery, Division of Vascular Surgery, University of Massachusetts Medical School, Worcester, Massachusetts 01655, USA
    Cytometry 43:308-13. 2001
    ..We report a novel method for in vitro detection of platelet-endothelial cell adhesion that allows endothelial cells to remain as an intact monolayer and for visualization of individual platelets...
  13. ncbi request reprint Effects of platelet binding on whole blood flow cytometry assays of monocyte and neutrophil procoagulant activity
    M R Barnard
    Center for Platelet Function Studies, University of Massachusettes Medical School, Worcester, MA 01655, USA
    J Thromb Haemost 3:2563-70. 2005
    ..The aim of this study was to develop whole blood flow cytometry assays of these procoagulant activities and to investigate the effects of platelet binding to monocytes and neutrophils...
  14. ncbi request reprint Laboratory markers of platelet activation and their clinical significance
    A D Michelson
    Center for Platelet Function Studies, Department of Pediatrics, University of Massachusetts Medical School, Worcester 01655, USA
    Curr Opin Hematol 6:342-8. 1999
    ....
  15. pmc The cleaved peptide of the thrombin receptor is a strong platelet agonist
    M I Furman
    Center for Platelet Function Studies, University of Massachusetts Medical Center, Worcester, MA 01655, USA
    Proc Natl Acad Sci U S A 95:3082-7. 1998
    ..TR1-41-induced platelet activation was synergistic with TR42-55. In summary, the cleaved peptide of the seven-transmembrane domain TR (TR1-41) is a strong platelet agonist...
  16. ncbi request reprint Twenty-two year (1975 to 1997) trends in the incidence, in-hospital and long-term case fatality rates from initial Q-wave and non-Q-wave myocardial infarction: a multi-hospital, community-wide perspective
    M I Furman
    Department of Medicine, University of Massachusetts Medical School, Worcester 01655, USA
    J Am Coll Cardiol 37:1571-80. 2001
    ....
  17. pmc Platelet glycoprotein ibalpha is a counterreceptor for the leukocyte integrin Mac-1 (CD11b/CD18)
    D I Simon
    Cardiovascular Division, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    J Exp Med 192:193-204. 2000
    ..These observations provide a molecular target for disrupting leukocyte-platelet complexes that promote vascular inflammation in thrombosis, atherosclerosis, and angioplasty-related restenosis...
  18. pmc The control of actin nucleotide exchange by thymosin beta 4 and profilin. A potential regulatory mechanism for actin polymerization in cells
    P J Goldschmidt-Clermont
    Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205
    Mol Biol Cell 3:1015-24. 1992
    ..Because ATP-actin subunits polymerize more readily than ADP-actin subunits, this ratio may play a key regulatory role in the assembly of cellular actin structures, particularly under circumstances of rapid filament turnover...