Research Topics
| Edwin G BovillSummaryAffiliation: University of Vermont Country: USA Publications
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Detail Information
Publications
Venous valvular stasis-associated hypoxia and thrombosis: what is the link?Edwin G Bovill
Department of Pathology, University of Vermont College of Medicine, Burlington, 05405, USA
Annu Rev Physiol 73:527-45. 2011..Thus, the effects of blood flow stasis, hypercoagulability of blood, and the characteristics of the vessel wall within the venous valvular sinus are assessed in turn...
Effect of tamoxifen on venous thrombosis risk factors in women without cancer: the Breast Cancer Prevention TrialMary Cushman
Department of Medicine, University of Vermont, Burlington, VT, USA
Br J Haematol 120:109-16. 2003..Reductions of antithrombin and protein S, but not protein C or APC resistance, might relate to the increased risk of venous thrombosis associated with tamoxifen treatment...
Imaging aspects of cardiovascular disease at the cell and molecular levelDouglas J Taatjes
Department of Pathology, College of Medicine, University of Vermont, 89 Beaumont Avenue, Burlington, VT 05405, USA
Histochem Cell Biol 130:235-45. 2008....
Evaluating chronic venous disease with a new venous severity scoring systemMichael A Ricci
Department of Surgery, Vermont College of Medicine, Burlington, 05405 0068, USA
J Vasc Surg 38:909-15. 2003..However, validation of the VCSS against an objective test is lacking. The purpose of this study was to test the VCSS against abnormalities found on venous ultrasound (US) scans...
SELDI-TOF plasma profiles distinguish individuals in a protein C-deficient family with thrombotic episodes occurring before age 40Annika M Svensson
Department of Pathology, University of Vermont College of Medicine, Burlington, Vermont, USA
Thromb Haemost 96:725-30. 2006..This is the first study to apply SELDI-TOF technology in conjunction with a bioinformatics tool to analyze low-molecular-weight proteomic patterns in patients with venous thrombosis...
Normal retinal vasculature despite familial protein C deficiencyCarla Y Vossen
Department of Pathology, University of Vermont, 199 Main Street, Burlington, VT 05401, USA
Am J Ophthalmol 139:944-5. 2005..CONCLUSIONS: This study showed no evidence of involvement of the retinal vascular bed in a family with an increased risk of nonocular venous thrombosis attributable to the deficiency of protein C...
No effect of the prothrombin G20210A mutation on protein C activation in a large kindred with type I protein C deficiencyCarla Y Vossen
Department of Pathology, University of Vermont, Burlington, Vermont 05405, USA
Blood Coagul Fibrinolysis 15:573-6. 2004..Thus, carriers of the prothrombin G20210A mutation do not have increased protein C activation despite the increased thrombin generation resulting from the higher prothrombin concentrations associated with the G20210A mutation...
A review of the technical, diagnostic, and epidemiologic considerations for protein S assaysAndrew J Goodwin
Department of Pathology, University of Vermont, Burlington 05405, USA
Arch Pathol Lab Med 126:1349-66. 2002..These 2 problems point out the need for better standardized assays and rigorous studies of the diagnostic utility of these assays...
Sensitivity of a questionnaire for data collection on venous thrombosisCarla Y Vossen
Department of Pathology, University of Vermont, Given Building #E208, 89 Beaumont Avenue, Burlington, VT 05405, USA
Thromb Res 114:259-63. 2004
The protein C system in placental massive perivillous fibrin depositionAnnika M Svensson
Department of Pathology, University of Vermont, Burlington, Vermont 05401, USA
Blood Coagul Fibrinolysis 15:491-5. 2004..This could imply an underlying defect of trophoblastic protein C activation. Alternatively, it may represent a degenerative change secondary to impedence of oxygen and nutrient supply to the trophoblastic epithelium...
Lipoprotein-associated phospholipase A2 and risk of venous thrombosis in older adultsNels Olson
Department of Pathology, University of Vermont College of Medicine, Burlington, Vermont, USA
Am J Hematol 83:524-7. 2008..Results were robust to several definitions of low or high Lp-PLA2. While the association of Lp-PLA(2) levels with arterial disease events implies a role for this enzyme in atherogenesis, our findings suggest that it is not prothrombotic...
Human monoclonal antiphospholipid antibodies disrupt the annexin A5 anticoagulant crystal shield on phospholipid bilayers: evidence from atomic force microscopy and functional assayJacob H Rand
Department of Pathology, Montefiore Medical Center, Albert Einstein College of Medicine, Moses Division Campus, Core Laboratory Office, North 8, 110 East 210th Street, Bronx, NY 10467, USA
Am J Pathol 163:1193-200. 2003..The aPL antibody-mediated disruption of the annexin A5 anticoagulant shield may be an important prothrombotic mechanism in the aPL syndrome...
Valves of the deep venous system: an overlooked risk factorErin G Brooks
Department of Pathology, University of Vermont, Burlington, VT 05482, USA
Blood 114:1276-9. 2009..001; for VWF, P = .01). These data support our hypothesis and suggest that variation in valvular sinus thromboresistance may be an important factor in venous thrombogenesis...
