Affiliation: University of Michigan
- Macrovascular thrombosis is driven by tissue factor derived primarily from the blood vessel wallSharlene M Day
Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109, USA
Blood 105:192-8. 2005..Therefore, our results suggest that thrombus formation in the arterial and venous macrovasculature is driven primarily by TF derived from the blood vessel wall as opposed to leukocytes...
- Exercise in hypertrophic cardiomyopathySharlene M Day
Division of Cardiovascular Medicine, University of Michigan Health System, Ann Arbor, MI, 48109, USA
J Cardiovasc Transl Res 2:407-14. 2009....
- The ubiquitin proteasome system in human cardiomyopathies and heart failureSharlene M Day
Division of Cardiovascular Medicine, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, MI, USA
Am J Physiol Heart Circ Physiol 304:H1283-93. 2013..Accordingly, this review will focus on UPS dysfunction in human dilated and hypertrophic cardiomyopathies and highlight areas rich for further study in this expanding field...
- Tuning cardiac performance in ischemic heart disease and failure by modulating myofilament functionSharlene M Day
Department of Internal Medicine, University of Michigan, 1150 W Medical Center Drive, 7301 MSRB III, Ann Arbor, MI 48109 0644, USA
J Mol Med (Berl) 85:911-21. 2007....
- Chronic iron administration increases vascular oxidative stress and accelerates arterial thrombosisSharlene M Day
University of Michigan Medical School, Division of Cardiology, Ann Arbor, USA
Circulation 107:2601-6. 2003..Iron overload has been implicated in the pathogenesis of ischemic cardiovascular events. However, the effects of iron excess on vascular function and the thrombotic response to vascular injury are not well understood...
- Ca2+-independent positive molecular inotropy for failing rabbit and human cardiac muscle by alpha-myosin motor gene transferTodd J Herron
Department of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, Michigan, USA
FASEB J 24:415-24. 2010..Our data provide evidence for a novel form of calcium-independent positive inotropy in failing cardiac myocytes by fast alpha-myosin motor protein gene transfer...
- Murine thrombosis modelsSharlene M Day
Department of Internal Medicine, University of Michigan Medical Center, 7301 MSRB III, 1150 W Medical Center Drive, Ann Arbor, Michigan 48109 0644, USA
Thromb Haemost 92:486-94. 2004..The advantages and limitations of different models are examined. Related topics of mouse anesthesia, phlebotomy, and in vitro hemostasis testing are also reviewed...
- Histidine button engineered into cardiac troponin I protects the ischemic and failing heartSharlene M Day
Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan 48109, USA
Nat Med 12:181-9. 2006..Myofilament-based inotropy may represent a therapeutic avenue to improve myocardial performance in the ischemic and failing heart...
- Genetic engineering and therapy for inherited and acquired cardiomyopathiesSharlene Day
Department of Internal Medicine, University of Michigan, 1301 E Catherine Street, Ann Arbor MI 48109 0622, USA
Ann N Y Acad Sci 1080:437-50. 2006..Nonetheless, studies focusing on the principles of acute genetic engineering of the sarcomere hold value as they lay the essential foundation on which to build potential gene-based therapies for heart disease...
- Rad GTPase deficiency leads to cardiac hypertrophyLin Chang
Cardiovascular Center, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, MI 48109, USA
Circulation 116:2976-83. 2007..Rad (Ras associated with diabetes) GTPase is the prototypic member of a subfamily of Ras-related small G proteins. The aim of the present study was to define whether Rad plays an important role in mediating cardiac hypertrophy...
- Single histidine-substituted cardiac troponin I confers protection from age-related systolic and diastolic dysfunctionNathan J Palpant
Department of Molecular and Integrative Physiology, University of Michigan Medical School, 1301 E Catherine Street, 7727 Medical Science II, Ann Arbor, MI 48109 0622, USA
Cardiovasc Res 80:209-18. 2008..Strategies to protect the aged heart from ischaemia-mediated pump failure are needed. We hypothesized that troponin I-mediated augmentation of myofilament calcium sensitivity would protect cardiac function in aged mice...
- Dystrophic heart failure blocked by membrane sealant poloxamerSoichiro Yasuda
Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, Michigan 48109 0622, USA
Nature 436:1025-9. 2005....
- Ubiquitin proteasome dysfunction in human hypertrophic and dilated cardiomyopathiesJaime M Predmore
1150 W Medical Center Dr, 7301 MSRB III, Ann Arbor, MI 48109 0644, USA
Circulation 121:997-1004. 2010..The present study evaluated ubiquitin proteasome system function in human heart failure and hypertrophic cardiomyopathy (HCM)...
- Parvalbumin corrects slowed relaxation in adult cardiac myocytes expressing hypertrophic cardiomyopathy-linked alpha-tropomyosin mutationsPierre Coutu
Department of Biomedical Engineering, University of Michigan, Ann Arbor, Mich 48109 0622, USA
Circ Res 94:1235-41. 2004..Collectively, these findings show that slow relaxation caused by alpha-Tm mutants can be corrected by modifying calcium handling with Parv...
- Cardiac-directed parvalbumin transgene expression in mice shows marked heart rate dependence of delayed Ca2+ buffering actionSharlene M Day
Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, Michigan 48109 0644, USA
Physiol Genomics 33:312-22. 2008....
- Regulation of Proteasome Function in CardiomyopathiesSharlene M Day; Fiscal Year: 2010....