Yabing Chen

Summary

Affiliation: University of Vermont
Country: USA

Publications

  1. ncbi request reprint Paradoxical inhibition of fibrinogen binding and potentiation of alpha-granule release by specific types of inhibitors of glycoprotein IIb-IIIa
    D J Schneider
    Department of Medicine, University of Vermont, Burlington, Colchester 05446, USA
    Cardiovasc Res 45:437-46. 2000
  2. ncbi request reprint Increased concentrations of tirofiban in blood and their correlation with inhibition of platelet aggregation after greater bolus doses of tirofiban
    David J Schneider
    University of Vermont, Burlington, Vermont 05446, USA
    Am J Cardiol 91:334-6. 2003
  3. ncbi request reprint Increased reactivity of platelets induced by fibrinogen independent of its binding to the IIb-IIIa surface glycoprotein: a potential contributor to cardiovascular risk
    D J Schneider
    Department of Medicine, The University of Vermont College of Medicine, Burlington 05446, USA
    J Am Coll Cardiol 33:261-6. 1999
  4. ncbi request reprint Enhanced early inhibition of platelet aggregation with an increased bolus of tirofiban
    David J Schneider
    University of Vermont, Burlington, Vermont, USA
    Am J Cardiol 90:1421-3. 2002
  5. ncbi request reprint Changes in arterial expression of fibrinolytic system proteins in atherogenesis
    D J Schneider
    Department of Medicine, University of Vermont, Burlington
    Arterioscler Thromb Vasc Biol 17:3294-301. 1997
  6. ncbi request reprint Differential effects of anticoagulants on the activation of platelets ex vivo
    D J Schneider
    Department of Medicine, University of Vermont College of Medicine, Burlington 05405, USA
    Circulation 96:2877-83. 1997
  7. ncbi request reprint Dependence of augmentation of arterial endothelial cell expression of plasminogen activator inhibitor type 1 by insulin on soluble factors released from vascular smooth muscle cells
    D J Schneider
    Department of Medicine, The University of Vermont, Burlington 05405, USA
    Circulation 96:2868-76. 1997
  8. ncbi request reprint Time and dose dependent augmentation of inhibitory effects of abciximab by aspirin
    D J Schneider
    Department of Medicine, University of Vermont, Burlington 05446, USA
    Thromb Haemost 85:309-13. 2001
  9. ncbi request reprint Influence of preparative procedures on assay of platelet function and apparent effects of antiplatelet agents
    Nathaniel J Madsen
    Cardiology Unit, Department of Medicine, University of Vermont, Burlington, Vermont, USA
    Am J Cardiol 100:722-7. 2007
  10. ncbi request reprint Differences between activation thresholds for platelet P-selectin glycoprotein IIb-IIIa expression and their clinical implications
    M B Holmes
    Department of Medicine, University of Vermont College of Medicine, Burlington 05401, USA
    Thromb Res 95:75-82. 1999

Detail Information

Publications85

  1. ncbi request reprint Paradoxical inhibition of fibrinogen binding and potentiation of alpha-granule release by specific types of inhibitors of glycoprotein IIb-IIIa
    D J Schneider
    Department of Medicine, University of Vermont, Burlington, Colchester 05446, USA
    Cardiovasc Res 45:437-46. 2000
    ....
  2. ncbi request reprint Increased concentrations of tirofiban in blood and their correlation with inhibition of platelet aggregation after greater bolus doses of tirofiban
    David J Schneider
    University of Vermont, Burlington, Vermont 05446, USA
    Am J Cardiol 91:334-6. 2003
  3. ncbi request reprint Increased reactivity of platelets induced by fibrinogen independent of its binding to the IIb-IIIa surface glycoprotein: a potential contributor to cardiovascular risk
    D J Schneider
    Department of Medicine, The University of Vermont College of Medicine, Burlington 05446, USA
    J Am Coll Cardiol 33:261-6. 1999
    ....
  4. ncbi request reprint Enhanced early inhibition of platelet aggregation with an increased bolus of tirofiban
    David J Schneider
    University of Vermont, Burlington, Vermont, USA
    Am J Cardiol 90:1421-3. 2002
  5. ncbi request reprint Changes in arterial expression of fibrinolytic system proteins in atherogenesis
    D J Schneider
    Department of Medicine, University of Vermont, Burlington
    Arterioscler Thromb Vasc Biol 17:3294-301. 1997
    ..Decreased mural proteolysis in early atherogenesis may exacerbate matrix accumulation. Increased mural proteolysis later is associated with, and may potentiate, smooth muscle cell migration and proliferation...
  6. ncbi request reprint Differential effects of anticoagulants on the activation of platelets ex vivo
    D J Schneider
    Department of Medicine, University of Vermont College of Medicine, Burlington 05405, USA
    Circulation 96:2877-83. 1997
    ....
  7. ncbi request reprint Dependence of augmentation of arterial endothelial cell expression of plasminogen activator inhibitor type 1 by insulin on soluble factors released from vascular smooth muscle cells
    D J Schneider
    Department of Medicine, The University of Vermont, Burlington 05405, USA
    Circulation 96:2868-76. 1997
    ....
  8. ncbi request reprint Time and dose dependent augmentation of inhibitory effects of abciximab by aspirin
    D J Schneider
    Department of Medicine, University of Vermont, Burlington 05446, USA
    Thromb Haemost 85:309-13. 2001
    ..Acetylation of glycoprotein IIb-IIIa by aspirin augments inhibitory effects of abciximab in a dose- and time-dependent manner by increasing binding of abciximab to platelets...
  9. ncbi request reprint Influence of preparative procedures on assay of platelet function and apparent effects of antiplatelet agents
    Nathaniel J Madsen
    Cardiology Unit, Department of Medicine, University of Vermont, Burlington, Vermont, USA
    Am J Cardiol 100:722-7. 2007
    ..The accuracy of platelet function testing may be improved by performance in whole blood...
  10. ncbi request reprint Differences between activation thresholds for platelet P-selectin glycoprotein IIb-IIIa expression and their clinical implications
    M B Holmes
    Department of Medicine, University of Vermont College of Medicine, Burlington 05401, USA
    Thromb Res 95:75-82. 1999
    ..Analysis of platelet reactivity with flow cytometry characterizes activation with respect to specific components of the process and should facilitate development and optimal titration of antiplatelet therapy...
  11. ncbi request reprint Decreased platelet reactivity in blood anticoagulated with bivalirudin or enoxaparin compared with unfractionated heparin: implications for coronary intervention
    Atul Aggarwal
    Department of Medicine, The University of Vermont College of Medicine, Burlington, VT, USA
    J Thromb Thrombolysis 13:161-5. 2002
    ..This study was designed to determine the effects of therapeutic concentrations of unfractionated heparin (UFH), bivalirudin, or enoxaparin alone or in combination with tirofiban on platelet reactivity...
  12. ncbi request reprint Quantification by flow cytometry of the efficacy of and interindividual variation of platelet inhibition induced by treatment with tirofiban and abciximab
    M B Holmes
    Department of Medicine, The University of Vermont College of Medicine, USA
    Coron Artery Dis 12:245-53. 2001
    ..After exposure of platelets to abciximab and tirofiban in vitro, we have observed variable inhibition of fibrinogen binding and a lack of inhibition of alpha-granule degranulation...
  13. ncbi request reprint Increased expression of platelet P-selectin and formation of platelet-leukocyte aggregates in blood from patients treated with unfractionated heparin plus eptifibatide compared with bivalirudin
    Friederike K Keating
    Cardiology Unit, Department of Medicine, University of Vermont Fletcher Allen Health Care, 111 Colchester Avenue, Burlington, VT 05401, USA
    Thromb Res 118:361-9. 2006
    ....
  14. ncbi request reprint Biphasic effects of hemodialysis on platelet reactivity in patients with end-stage renal disease: a potential contributor to cardiovascular risk
    Atul Aggarwal
    Department of Medicine, The University of Vermont College of Medicine, Burlington, VT 05401, USA
    Am J Kidney Dis 40:315-22. 2002
    ..This study is designed to determine effects of hemodialysis in patients with ESRD on platelet reactivity per se...
  15. ncbi request reprint Increased platelet reactivity in patients given orbofiban after an acute coronary syndrome: an OPUS-TIMI 16 substudy. Orbofiban in Patients with Unstable coronary syndromes. Thrombolysis In Myocardial Infarction
    M B Holmes
    Department of Medicine, The University of Vermont College of Medicine, Burlington 05401, USA
    Am J Cardiol 85:491-3, A10. 2000
    ..Thus, sensitive assays of platelet reactivity may be helpful in the design of further clinical studies and implementation of antiplatelet therapy in patients...
  16. ncbi request reprint The effects of bivalirudin compared with those of unfractionated heparin plus eptifibatide on inflammation and thrombin generation and activity during coronary intervention
    Friederike K Keating
    Cardiology Unit, Department of Medicine, University of Vermont Burlington, Colchester, Vermont 05446, USA
    Coron Artery Dis 16:401-5. 2005
    ..To characterize effects of bivalirudin compared with unfractionated heparin plus eptifibatide on inflammation, and thrombin generation and activity after percutaneous coronary intervention...
  17. ncbi request reprint Platelet reactivity characterized prospectively: a determinant of outcome 90 days after percutaneous coronary intervention
    S S Kabbani
    Department of Medicine, The University of Vermont College of Medicine, Burlington, VT, USA
    Circulation 104:181-6. 2001
    ..9% versus with 3.6%, P=0.029). CONCLUSIONS: Prospective assessment of platelet GP IIb/IIIa activation permits stratification of patients into low- and high-risk groups with respect to adverse events after PCI...
  18. ncbi request reprint Variable responses to inhibition of fibrinogen binding induced by tirofiban and eptifibatide in blood from healthy subjects
    M B Holmes
    Department of Medicine, The University of Vermont College of Medicine, Burlington 05401, USA
    Am J Cardiol 84:203-7. 1999
    ..Thus, the approach developed should facilitate definition of optimal platelet inhibition and individualized tailoring of therapy to induce optimal effects...
  19. ncbi request reprint Augmentation of proliferation of vascular smooth muscle cells by plasminogen activator inhibitor type 1
    Yabing Chen
    Department of Medicine and Cardiovascular Research Institute, University of Vermont, Burlington, USA
    Arterioscler Thromb Vasc Biol 26:1777-83. 2006
    ..Because apoptosis and proliferation appear to be linked, we sought to determine whether increased PAI-1 would affect VSMC proliferation...
  20. ncbi request reprint The retardation of vasculopathy induced by attenuation of insulin resistance in the corpulent JCR:LA-cp rat is reflected by decreased vascular smooth muscle cell proliferation in vivo
    P M Absher
    University of Vermont College of Medicine, Department of Medicine, Burlington 05405, USA
    Atherosclerosis 143:245-51. 1999
    ....
  21. ncbi request reprint Increased plasminogen activator inhibitor type 1 in coronary artery atherectomy specimens from type 2 diabetic compared with nondiabetic patients: a potential factor predisposing to thrombosis and its persistence
    B E Sobel
    Department of Medicine, The University of Vermont College of Medicine, Burlington 05401, USA
    Circulation 97:2213-21. 1998
    ....
  22. ncbi request reprint Augmentation of inhibitory effects of glycoprotein IIb-IIIa antagonists in patients with diabetes
    F K Keating
    Cardiology Unit, Department of Medicine, Fletcher Allen Health Care, McClure 1, University of Vermont, 111 Colchester Avenue, Burlington, VT 05401, USA
    Thromb Res 113:27-34. 2004
    ..To determine mechanisms potentially responsible we characterized the binding of fibrinogen to platelets from patients with and without diabetes in the presence and absence of GP IIb-IIIa antagonists...
  23. ncbi request reprint Platelet protagonist/antagonist: understanding the distinguishing characteristics of anticoagulants
    David J Schneider
    Cardiology Unit, Department of Medicine, Cardiovascular Research Institute, University of Vermont, Burlington, Vermont, USA
    Rev Cardiovasc Med 7:S3-11. 2006
    ..Pharmacologic concentrations of a direct thrombin inhibitor, bivalirudin, inhibit thrombin-induced activation of platelets to a greater extent than pharmacologic concentrations of unfractionated heparin...
  24. ncbi request reprint Attenuation of platelet reactivity by enoxaparin compared with unfractionated heparin in patients undergoing haemodialysis
    Atul Aggarwal
    Department of Medicine, University of Vermont College of Medicine, Burlington, VT, USA
    Nephrol Dial Transplant 19:1559-63. 2004
    ..Because both haemodialysis and unfractionated heparin (UFH) can increase platelet reactivity, we compared platelet reactivity during haemodialysis when patients were anticoagulated with UFH or enoxaparin...
  25. doi request reprint The influence of platelet activating factor on the effects of platelet agonists and antiplatelet agents in vitro
    Friederike K Keating
    Department of Medicine, University of Vermont Fletcher Allen Health Care, Burlington, VT 05401, USA
    J Thromb Thrombolysis 28:38-45. 2009
    ..Accordingly, PAF synergistically augments platelet activation in response to ADP and thrombin, and the extent of inhibition exerted by P2Y receptor antagonists is decreased in the presence of PAF...
  26. ncbi request reprint Suboptimal early inhibition of platelets by treatment with tirofiban and implications for coronary interventions
    Samer S Kabbani
    University of Vermont, Burlington, Vermont 05446, USA
    Am J Cardiol 89:647-50. 2002
  27. ncbi request reprint Attenuation of accumulation of neointimal lipid by pioglitazone in mice genetically deficient in insulin receptor substrate-2 and apolipoprotein E
    Maria H Clough
    Department of Pathology, 89 Beaumont Avenue, College of Medicine, University of Vermont, Burlington, VT 05405, USA
    J Histochem Cytochem 53:603-10. 2005
    ..018. Accordingly, genetically induced intensification of insulin resistance increases atheroma formation. Furthermore, attenuation of insulin resistance by treatment with pioglitazone decreases accumulation of lipid in the neointima...
  28. ncbi request reprint The effect of plasminogen activator inhibitor type 1 on apoptosis
    David J Schneider
    Department of Medicine, University of Vermont, 208 South Park Drive, Suite 2, Colchester, VT 05446, USA
    Thromb Haemost 100:1037-40. 2008
    ..Inhibition of caspase 3 by PAI-1 may divert intracellular signalling from induction of apoptosis to induction of proliferation...
  29. ncbi request reprint Improved quantitative characterization of atherosclerotic plaque composition with immunohistochemistry, confocal fluorescence microscopy, and computer-assisted image analysis
    D J Taatjes
    Department of Pathology, College of Medicine, University of Vermont, Burlington 05405, USA
    Histochem Cell Biol 113:161-73. 2000
    ....
  30. ncbi request reprint Delineation of the evolution of compositional changes in atheroma
    Marilyn P Wadsworth
    Department of Pathology, College of Medicine, HSRF 208, 89 Beaumont Avenue, University of Vermont, Burlington, VT 05405, USA
    Histochem Cell Biol 118:59-68. 2002
    ..However, the percentage composition of plaque attributable to collagen increased 2.5-fold in 20-week-old female animals compared with that in males or females of 10 weeks of age and males of 20 weeks of age...
  31. ncbi request reprint Increased plasminogen activator inhibitor type-1 (PAI-1) in the heart as a function of age
    Burton E Sobel
    University of Vermont, Cardiovascular Research Institute, Colchester Research Facility, 208 South Park Drive, Colchester, VT 05446, USA
    Life Sci 79:1600-5. 2006
    ....
  32. ncbi request reprint Insulin resistance increases PAI-1 in the heart
    Burton E Sobel
    University of Vermont, Cardiovascular Research Institute Burlington, VT, USA
    Biochem Biophys Res Commun 346:102-7. 2006
    ..Such increases may contribute to fibrosis and diastolic dysfunction typical late after infarction in patients with insulin resistance...
  33. ncbi request reprint Effects of insulin sensitizers on plaque vulnerability associated with elevated lipid content in atheroma in ApoE-knockout mice
    W T Cefalu
    University of Vermont College of Medicine, UHC Campus, Arnold 3433, One South Prospect Street, 05401, Burlington, VT, USA
    Acta Diabetol 41:25-31. 2004
    ..Thus, improvement in insulin resistance induced by a high-fat diet in this animal model of vasculopathy did not alter plaque composition...
  34. ncbi request reprint Immunoelectron microscopic localization of plasminogen activator inhibitor type 1 (PAI-1) in smooth muscle cells from morphologically normal and atherosclerotic human arteries
    D J Taatjes
    Department of Pathology, College of Medicine, University of Vermont, Burlington 05405, USA
    Ultrastruct Pathol 21:527-36. 1997
    ..Because PAI-1 is associated predominantly with contractile filaments in smooth muscle cells, the net amount of immunodetectable PAI-1 appears to be greater in contractile compared with synthetic phenotype cells...
  35. ncbi request reprint Platelet function, coagulopathy, and impaired fibrinolysis in diabetes
    Burton E Sobel
    Department of Medicine, University of Vermont, Colchester Research Facility, 208 South Park Drive, Colchester, VT 05446, USA
    Cardiol Clin 22:511-26. 2004
    ..In aggregate,these derangements contribute to accelerated atherosclerosis, premature coronary artery dis-ease, and a profound toll from both...
  36. ncbi request reprint Intramural plasminogen activator inhibitor type-1 and coronary atherosclerosis
    Burton E Sobel
    Department of Medicine, University of Vermont, Burlington, USA
    Arterioscler Thromb Vasc Biol 23:1979-89. 2003
    ....
  37. ncbi request reprint Effects of increased concentrations of glucose on platelet reactivity in healthy subjects and in patients with and without diabetes mellitus
    Friederike K Keating
    Department of Medicine, University of Vermont, Burlington, Vermont 05446, USA
    Am J Cardiol 92:1362-5. 2003
    ....
  38. ncbi request reprint Induction of hyperinsulinemia combined with hyperglycemia and hypertriglyceridemia increases plasminogen activator inhibitor 1 in blood in normal human subjects
    J Calles-Escandon
    Department of Medicine, The University of Vermont College of Medicine, Burlington 05405, USA
    Diabetes 47:290-3. 1998
    ..Moreover, these results underscore the potential importance of modifying insulin resistance as well as achieving glycemic and lipidemic control in individuals with type 2 diabetes...
  39. ncbi request reprint Platelet reactivity in coronary ostial blood: a reflection of the thrombotic state accompanying plaque rupture and of the adequacy of anti-thrombotic therapy
    S S Kabbani
    The University of Vermont, Burlington, VT, USA
    J Thromb Thrombolysis 12:171-6. 2001
    ....
  40. doi request reprint The influence of obesity and consequent insulin resistance on coronary risk factors in medically treated patients with coronary disease
    P A Ades
    Division of Cardiology, University of Vermont College of Medicine, Burlington, VT 05403, USA
    Int J Obes (Lond) 32:967-74. 2008
    ..We assessed whether these relationships persist in patients with established CHD treated with evidence-based preventive pharmacologic therapies...
  41. ncbi request reprint Plasminogen activator inhibitor type 1 in adults with Down syndrome and protection against macrovascular disease
    W E Hopkins
    Department of Medicine, University of Vermont College of Medicine, Burlington, 05401, USA
    Am J Cardiol 85:784-6, A9. 2000
    ....
  42. ncbi request reprint Conundrums in the combined use of anticoagulants and antiplatelet drugs
    David J Schneider
    Cardiology Division and Cardiovascular Research Institute, University of Vermont, Burlington, USA
    Circulation 116:305-15. 2007
  43. ncbi request reprint Contributions of young platelets and of previously activated platelets to platelet reactivity in patients with coronary artery disease
    David J Schneider
    Cardiology Unit, Department of Medicine, University of Vermont, Burlington, Vermont, USA
    Thromb Res 121:455-62. 2008
    ....
  44. ncbi request reprint Greater inhibitory effects of bivalirudin compared with unfractionated heparin plus eptifibitide on thrombin-induced platelet activation
    David J Schneider
    Department of Medicine, Cardiology Unit and Cardiovascular Research Institute, University of Vermont, Burlington, Vermont, USA
    Coron Artery Dis 17:471-6. 2006
    ..The effects of antithrombotic agents on the activation of platelets by thrombin were determined in blood from patients (n=12) with symptomatic coronary artery disease...
  45. ncbi request reprint Effect of combination glipizide GITS/metformin on fibrinolytic and metabolic parameters in poorly controlled type 2 diabetic subjects
    William T Cefalu
    Department of Medicine, University of Vermont College of Medicine, Burlington 05401, USA
    Diabetes Care 25:2123-8. 2002
    ..We sought to determine whether metabolic control, independent of its oral mode of implementation, affects PAI-1 in patients with marked hyperglycemia...
  46. ncbi request reprint A novel dual staining method for identification of apoptotic cells reveals a modest apoptotic response in infarcted mouse myocardium
    Douglas J Taatjes
    Department of Pathology, College of Medicine, University of Vermont, 89 Beaumont Avenue, Burlington, VT 05405, USA
    Histochem Cell Biol 128:275-83. 2007
    ..Again, only scattered cells were found displaying both markers in the zones of infarction, suggesting that 3 days of persistent ischemia results in a robust necrotic response, but only a very minor apoptotic response in this mouse model...
  47. ncbi request reprint Coronary intervention in patients with diabetes, chronic renal disease, and the elderly: therapeutic implications
    David J Schneider
    Cardiology Division, Department of Medicine, University of Vermont, Burlington, Vermont, USA
    Rev Cardiovasc Med 8:S35-41. 2007
    ..This article reviews the clinical implications of these conditions and discusses the therapeutic options currently available for these patient groups...
  48. doi request reprint Augmentation of megakaryocyte expression of FcgammaRIIa by interferon gamma
    David J Schneider
    Cardiology Unit, and Cardiovascular Research Institute, Department of Medicine, University of Vermont, Burlington, USA
    Arterioscler Thromb Vasc Biol 29:1138-43. 2009
    ..The purpose of this study was to identify factors that alter expression of FcgammaRIIa by megakaryocytes...
  49. doi request reprint Lack of early augmentation of platelet reactivity after coronary intervention in patients treated with bivalirudin
    David J Schneider
    Cardiovascular Research Institute, Department of Medicine, University of Vermont, Burlington, VT 05446, USA
    J Thromb Thrombolysis 28:6-9. 2009
    ....
  50. doi request reprint Adenosine diphosphate-induced platelet aggregation correlates with platelet activation identified with the use of flow cytometry
    Milagros Garcia
    Department of Medicine, University of Vermont College of Medicine, Colchester, VT 05446, USA
    Pathophysiol Haemost Thromb 36:75-9. 2008
    ..We have developed a method to assess individual components of platelet activation with the use of flow cytometry that is performed in minimally altered whole blood...
  51. doi request reprint Attenuation of apoptosis and the eye of the beholder
    Burton E Sobel
    Cardiovascular Research Institute, University of Vermont College of Medicine, Burlington, Vermont, USA
    Coron Artery Dis 19:55-8. 2008
    ....
  52. doi request reprint A profibrotic effect of plasminogen activator inhibitor type-1 (PAI-1) in the heart
    A K M Tarikuz Zaman
    University of Vermont, Colchester Research Facility, 208 South Park Drive, Colchester, VT 05446, USA
    Exp Biol Med (Maywood) 234:246-54. 2009
    ..05). Thus, PAI-1 is profibrotic in the heart subjected to infarction. Accordingly, overexpression of PAI-1 is a promising target for attenuation of heart failure after MI that may be exacerbated by fibrosis...
  53. doi request reprint Streamlining the design of promising clinical trials: in-vitro testing of antithrombotic regimens and multiple agonists of platelet activation
    David J Schneider
    Department of Medicine, Cardiology Unit and Cardiovascular Research Institute, University of Vermont, Burlington, Vermont 05446, USA
    Coron Artery Dis 20:175-8. 2009
    ..These results and this approach to selection of promising interventions should be helpful in streamlining the design of clinical trials...
  54. pmc Association between increased platelet P-selectin expression and obesity in patients with type 2 diabetes: a BARI 2D (Bypass Angioplasty Revascularization Investigation 2 Diabetes) substudy
    David J Schneider
    Cardiology Division and Cardiovascular Research Institute, University of Vermont, Burlington, Vermont, USA
    Diabetes Care 32:944-9. 2009
    ..To determine whether obesity increases platelet reactivity and thrombin activity in patients with type 2 diabetes plus stable coronary artery disease...
  55. ncbi request reprint wnt3a but not wnt11 supports self-renewal of embryonic stem cells
    Dinender K Singla
    Cardiovascular Research Institute, Department of Medicine, University of Vermont, Colchester, VT 05446, USA
    Biochem Biophys Res Commun 345:789-95. 2006
    ..Thus, our results show that conditioned medium from wnt3a but not wnt11 expressing cells can maintain ES cells in self-renewal and in a pluripotent state...
  56. ncbi request reprint Increased ability of tirofiban to maintain its inhibitory effects on the binding of fibrinogen to platelets in blood from patients with and without diabetes mellitus
    David J Schneider
    Cardiology Unit, Department of Medicine, University of Vermont, Burlington, Vermont 05446, USA
    Coron Artery Dis 17:57-61. 2006
    ..To determine the influence of affinity on inhibitory effects in blood from patients with (n=20) and without (n=20) diabetes mellitus, we characterized the extent of inhibition as a function of time...
  57. ncbi request reprint Attenuation of neointimal vascular smooth muscle cellularity in atheroma by plasminogen activator inhibitor type 1 (PAI-1)
    David J Schneider
    University of Vermont, Colchester Research Facility, 208 S Park Drive, Colchester, VT 05446, USA
    J Histochem Cytochem 52:1091-9. 2004
    ..03). Accordingly, increased expression of PAI-1 protein by VSMCs reduces their migration in vitro and their contribution to neointimal cellularity in vivo...
  58. ncbi request reprint Efficiency in clinical research: assessment in vitro of potential anti-thrombotic drug interactions
    David J Schneider
    Department of Medicine, University of Vermont, Burlington, Vermont, USA
    Coron Artery Dis 15:177-81. 2004
    ....
  59. ncbi request reprint Variation in the ability of glycoprotein IIb-IIIa antagonists to exert and maintain their inhibitory effects on the binding of fibrinogen
    David J Schneider
    Cardiology Unit, Department of Medicine, University of Vermont, Burlington, Vermont 05446, USA
    J Cardiovasc Pharmacol 46:41-5. 2005
    ..01). The differences are consistent with the biphasic binding of fibrinogen to GP IIb-IIIa. The clinical implications of this observation merit evaluation to potentially improve care of patients and to guide future drug development...
  60. ncbi request reprint Abnormalities of coagulation, platelet function, and fibrinolysis associated with syndromes of insulin resistance
    David J Schneider
    University of Vermont, Burlington, Vermont 05446, USA
    Coron Artery Dis 16:473-6. 2005
    ..Therapies that improve insulin sensitivity and thereby decrease insulin resistance, hyperinsulinemia, and metabolic abnormalities decrease the prothrombotic state...
  61. ncbi request reprint Development of glycoprotein IIb-IIIa antagonists: translation of pharmacodynamic effects into clinical benefit
    David J Schneider
    University of Vermont, 208 South Park Drive, Suite 2, Colchester, VT 05446, USA
    Expert Rev Cardiovasc Ther 2:903-13. 2004
    ....
  62. ncbi request reprint Inhibition of apoptosis and caspase-3 in vascular smooth muscle cells by plasminogen activator inhibitor type-1
    Yabing Chen
    Department of Medicine, The University of Vermont, Burlington, Vermont 05405, USA
    J Cell Biochem 92:178-88. 2004
    ..Accordingly, attenuated apoptosis resulting from elevated expression of PAI-1 by VSMC may be attributable, at least in part, to reversible inhibition of caspase-3 by active PAI-1...
  63. ncbi request reprint Relation of augmented platelet reactivity to the magnitude of distribution of atherosclerosis
    Friederike K Keating
    Cardiology Unit, University of Vermont College of Medicine, 111 Colchester Avenue, Burlington, VT 05401 USA
    Am J Cardiol 94:725-8. 2004
    ..Accordingly, patients who have more widely distributed vascular disease are likely to derive particular benefit from antiplatelet regimens that suppress platelet function to a greater extent...
  64. ncbi request reprint On rendering continuous glucose monitoring ready for prime time in the cardiac care unit
    Michaelanne Rowen
    Cardiovascular Research Institute, University of Vermont College of Medicine, Burlington, Vermont 05446, USA
    Coron Artery Dis 18:405-9. 2007
    ..We therefore explored the potential value of use of a continuous glucose monitoring system to enhance glycemic control in the CCU and sought to identify pitfalls that could be overcome to increase its utility...
  65. ncbi request reprint Effect of fatty acid chain length and thioesterification on the augmentation of expression of plasminogen activator inhibitor-1
    Y Chen
    Department of Medicine, University of Vermont, 208A South Park Drive, Suite 2, Colchester, VT 05446, USA
    Nutr Metab Cardiovasc Dis 12:325-30. 2002
    ..This study was designed to determine whether FFA chain length, saturation, or both affect agonist properties and whether agonist properties are mediated by activated, thioesterified FFA (fatty acyl-CoA)...
  66. ncbi request reprint Quantitative analysis of atherosclerotic lesion composition in mice
    Marilyn P Wadsworth
    Department of Pathology, University of Vermont, Burlington, USA
    Methods Mol Biol 319:137-52. 2006
    ..This method can be expanded to employ a rich variety of histochemical and immunohistochemical staining protocols...
  67. ncbi request reprint Comparison of inflammatory markers in patients with diabetes mellitus versus those without before and after coronary arterial stenting
    Atul Aggarwal
    Cardiology Unit, University of Vermont, Burlington, Vermont 05401, USA
    Am J Cardiol 92:924-9. 2003
    ..Thus, patients with and without diabetes exhibit different inflammatory responses to stenting, reflecting the lower preprocedural inflammation in those without diabetes versus those with diabetes...
  68. pmc High-calorie-expenditure exercise: a new approach to cardiac rehabilitation for overweight coronary patients
    Philip A Ades
    Division of Cardiology, University of Vermont College of Medicine, Burlington, VT, USA
    Circulation 119:2671-8. 2009
    ..Current CR exercise protocols result in little weight loss and minimal changes in cardiac risk factors. We sought to design an exercise protocol that would lead to greater weight loss and risk factor change...
  69. ncbi request reprint Comparison of effects of abciximab versus eptifibatide on C-reactive protein, interleukin-6, and interleukin-1 receptor antagonist after coronary arterial stenting
    Atul Aggarwal
    Cardiac Unit, University of Vermont College of Medicine, 111 Colchester Avenue, Burlington, VT 05401, USA
    Am J Cardiol 91:1346-9. 2003
  70. ncbi request reprint Deleterious effects of lack of cardiac PAI-1 after coronary occlusion in mice and their pathophysiologic determinants
    A K M Tarikuz Zaman
    Cardiovascular Research Institute, University of Vermont, Colchester Research Facility, 208 South Park Drive, Colchester, VT 05446, USA
    Histochem Cell Biol 128:135-45. 2007
    ..006 vs. 0.022 microg hydroxyproline/mg dry weight). Thus, lack of PAI-1 in the heart exerted deleterious effects mediated, at least in part by increased inflammation and hemorrhage and attenuating of fibrosis...
  71. pmc The independence of signaling pathways mediating increased expression of plasminogen activator inhibitor type 1 in HepG2 cells exposed to free fatty acids or triglycerides
    Yabing Chen
    Department of Medicine, The University of Vermont, Burlington 05405, USA
    Int J Exp Diabetes Res 3:109-18. 2002
    ..Inhibition of protein kinase C inhibited the response to FFA but not TG. Accordingly, increased FFA and TG contribute to increased PAI-1 through independent mechanisms...
  72. ncbi request reprint Survivin promoter-based conditionally replicative adenoviruses target cholangiocarcinoma
    Zeng Bian Zhu
    Division of Human Gene Therapy, Department of Medicine, Gene Therapy Center, University of Alabama at Birmingham, Birmingham, AL 35291, USA
    Int J Oncol 29:1319-29. 2006
    ..Such results should provide important insights into the identification of novel therapeutic strategies for cholangiocarcinoma...
  73. ncbi request reprint Relation of leukocytosis to C-reactive protein and interleukin-6 among patients undergoing percutaneous coronary intervention
    Prospero B Gogo
    Division of Cardiology, University of Vermont College of Medicine, Burlington, Vermont, USA
    Am J Cardiol 96:538-42. 2005
    ..78, 95% confidence interval 1.07 to 13.3, p = 0.04). In conclusion, in patients with troponin I negative coronary syndromes, a pre-PCI elevation in the WBC count reflected cytokine-mediated inflammation...
  74. ncbi request reprint Cardiovascular complications in diabetes mellitus
    Burton E Sobel
    University of Vermont, Colchester, VT 05446, USA
    Curr Opin Pharmacol 5:143-8. 2005
    ....
  75. ncbi request reprint Usefulness of platelet reactivity before percutaneous coronary intervention in determining cardiac risk one year later
    Samer S Kabbani
    University of Vermont College of Medicine, Burlington, USA
    Am J Cardiol 91:876-8. 2003
  76. doi request reprint Induction of platelet white blood cell (WBC) aggregate formation by platelets and WBCs in red blood cell units
    Friederike K Keating
    Department of Medicine and Pathology and Laboratory Medicine, University of Vermont, Burlington, VT 05401, USA
    Transfusion 48:1099-105. 2008
    ..Transfusion of red blood cell (RBC) preparations is independently associated with adverse clinical outcomes in patients with acute cardiovascular disease. This study was designed to define mechanisms potentially contributing...
  77. ncbi request reprint Consistent door-to-balloon times of less than 90 minutes for STEMI patients transferred for primary PCI
    Bina Ahmed
    Department of Cardiology, University of Vermont, 111 Colchester Avenue, Burlington, VT 05401, USA
    J Invasive Cardiol 21:429-33. 2009
    ..We established a streamlined STEMI protocol to allow rapid transfer of STEMI patients for primary PCI to meet the ACC D2B goal of < or = 90 minutes in at least 75% of the patients...
  78. ncbi request reprint Increased coronary arterial release of interleukin-1 receptor antagonist and soluble CD40 ligand indicative of inflammation associated with culprit coronary plaques
    Atul Aggarwal
    Cardiac Unit, University of Vermont College of Medicine, Burlington, Vermont 05401, USA
    Am J Cardiol 93:6-9. 2004
    ....
  79. ncbi request reprint Increase in interleukin-6 in the first hour after coronary stenting: an early marker of the inflammatory response
    Atul Aggarwal
    Cardiology Unit, University of Vermont College of Medicine, Burlington, VT 05401, USA
    J Thromb Thrombolysis 15:25-31. 2003
    ..This study was designed to determine if a systemic inflammatory response could be measured within the first hour after stenting...
  80. doi request reprint Gender-dependent differences in echocardiographic characteristics of murine hearts
    Patricia Q Baumann
    Cardiovascular Research Institute, University of Vermont, Burlington, Vermont 05446, USA
    Echocardiography 25:739-48. 2008
    ..Furthermore, the results suggest that gender-dependent differences are likely to be present in other species, including humans, and accordingly, that normal values should be established separately for males and females...
  81. ncbi request reprint Systemic inflammation after drug-eluting stent placement
    Prospero B Gogo
    Division of Cardiology, University of Vermont College of Medicine, 111 Colchester Avenue, Burlington, Vermont 05401, USA
    J Thromb Thrombolysis 19:87-92. 2005
    ..Thus, we sought to determine whether attenuation of the systemic inflammatory response was contributing to the improved outcomes...
  82. ncbi request reprint Soluble CD40 ligand is an early initiator of inflammation after coronary intervention
    Atul Aggarwal
    Nebraska Heart Institute, Hastings, Nebraska 68901, USA
    Coron Artery Dis 15:471-5. 2004
    ..The role of soluble CD40 ligand (sCD40L) as a potential initiator of inflammation after stenting has not been described...
  83. ncbi request reprint Determining the efficacy of antiplatelet therapies for the individual: lessons from clinical trials
    Steven R Steinhubl
    Division of Cardiology, University of Kentucky, 900 S Limestone Ave, 326 Charles T Wethington Bldg, Lexington, KY 40536, USA
    J Thromb Thrombolysis 26:8-13. 2008
    ....
  84. ncbi request reprint Endothelial dysfunction and inflammation after percutaneous coronary intervention
    Arnon Blum
    Department of Internal Medicine A, Poria Medical Center, Lower Galilee, Israel
    Am J Cardiol 94:1420-3. 2004
    ..Thus, endothelium-dependent dilation abnormalities were related to the systemic inflammatory state, whereas endothelium-independent dilation abnormalities were not related to the inflammatory status of the patient...
  85. ncbi request reprint On defining aspirin resistance
    David J Schneider
    J Am Coll Cardiol 46:1710-1. 2005