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William T Rivers

Showing results (1-10 of 14) with videos related to

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Cardiology Clinics|October 9, 2018
Cardiopulmonary Resuscitation Quality IssuesEssie Reed-Schrader, William T Rivers, Lynn J White, et al.
American Journal of Physiology. Heart and Circulatory Physiology|October 12, 2010
Heterogeneity in MT1-MMP activity with ischemia-reperfusion and previous myocardial infarction: relation to regional myocardial functionJennifer A Dixon, William F Gaillard, William T Rivers, et al.
American Journal of Physiology. Heart and Circulatory Physiology|September 8, 2009
Calpain inhibition preserves myocardial structure and function following myocardial infarctionSanthosh K Mani, Sundaravadivel Balasubramanian, Juozas A Zavadzkas, et al.
The Journal of Thoracic and Cardiovascular Surgery|March 15, 2011
Hemodynamics and myocardial blood flow patterns after placement of a cardiac passive restraint device in a model of dilated cardiomyopathyJennifer A Dixon, Amy M Goodman, William F Gaillard, et al.
American Journal of Physiology. Heart and Circulatory Physiology|August 12, 2008
Cardiac-restricted overexpression of extracellular matrix metalloproteinase inducer causes myocardial remodeling and dysfunction in aging miceJuozas A Zavadzkas, Rebecca A Plyler, Shenikqua Bouges, et al.
American Journal of Physiology. Heart and Circulatory Physiology|May 18, 2010
Short-term disruption in regional left ventricular electrical conduction patterns increases interstitial matrix metalloproteinase activityRupak Mukherjee, Juozas A Zavadzkas, William T Rivers, et al.
American Journal of Physiology. Heart and Circulatory Physiology|June 14, 2011
Direct regulation of membrane type 1 matrix metalloproteinase following myocardial infarction causes changes in survival, cardiac function, and remodelingJuozas A Zavadzkas, Rupak Mukherjee, William T Rivers, et al.
American Journal of Physiology. Heart and Circulatory Physiology|March 22, 2015
Inhibition of class I histone deacetylase activity represses matrix metalloproteinase-2 and -9 expression and preserves LV function postmyocardial infarctionSanthosh K Mani, Christine B Kern, Denise Kimbrough, et al.
The Journal of Thoracic and Cardiovascular Surgery|November 8, 2011
Progressive induction of left ventricular pressure overload in a large animal model elicits myocardial remodeling and a unique matrix signatureWilliam M Yarbrough, Rupak Mukherjee, Robert E Stroud, et al.
Journal of Cardiovascular Pharmacology|October 9, 2008
Aprotinin exacerbates left ventricular dysfunction after ischemia/reperfusion in mice lacking tumor necrosis factor receptor IMichel J Sabbagh, J Michael Looper, Juozas A Zavadzkas, et al.
Pageof 2

Showing results (1-10 of 14) with videos related to

Sort By:
Pageof 2
Cardiology Clinics|October 9, 2018
Cardiopulmonary Resuscitation Quality IssuesEssie Reed-Schrader, William T Rivers, Lynn J White, et al.
American Journal of Physiology. Heart and Circulatory Physiology|October 12, 2010
Heterogeneity in MT1-MMP activity with ischemia-reperfusion and previous myocardial infarction: relation to regional myocardial functionJennifer A Dixon, William F Gaillard, William T Rivers, et al.
American Journal of Physiology. Heart and Circulatory Physiology|September 8, 2009
Calpain inhibition preserves myocardial structure and function following myocardial infarctionSanthosh K Mani, Sundaravadivel Balasubramanian, Juozas A Zavadzkas, et al.
The Journal of Thoracic and Cardiovascular Surgery|March 15, 2011
Hemodynamics and myocardial blood flow patterns after placement of a cardiac passive restraint device in a model of dilated cardiomyopathyJennifer A Dixon, Amy M Goodman, William F Gaillard, et al.
American Journal of Physiology. Heart and Circulatory Physiology|August 12, 2008
Cardiac-restricted overexpression of extracellular matrix metalloproteinase inducer causes myocardial remodeling and dysfunction in aging miceJuozas A Zavadzkas, Rebecca A Plyler, Shenikqua Bouges, et al.
American Journal of Physiology. Heart and Circulatory Physiology|May 18, 2010
Short-term disruption in regional left ventricular electrical conduction patterns increases interstitial matrix metalloproteinase activityRupak Mukherjee, Juozas A Zavadzkas, William T Rivers, et al.
American Journal of Physiology. Heart and Circulatory Physiology|June 14, 2011
Direct regulation of membrane type 1 matrix metalloproteinase following myocardial infarction causes changes in survival, cardiac function, and remodelingJuozas A Zavadzkas, Rupak Mukherjee, William T Rivers, et al.
American Journal of Physiology. Heart and Circulatory Physiology|March 22, 2015
Inhibition of class I histone deacetylase activity represses matrix metalloproteinase-2 and -9 expression and preserves LV function postmyocardial infarctionSanthosh K Mani, Christine B Kern, Denise Kimbrough, et al.
The Journal of Thoracic and Cardiovascular Surgery|November 8, 2011
Progressive induction of left ventricular pressure overload in a large animal model elicits myocardial remodeling and a unique matrix signatureWilliam M Yarbrough, Rupak Mukherjee, Robert E Stroud, et al.
Journal of Cardiovascular Pharmacology|October 9, 2008
Aprotinin exacerbates left ventricular dysfunction after ischemia/reperfusion in mice lacking tumor necrosis factor receptor IMichel J Sabbagh, J Michael Looper, Juozas A Zavadzkas, et al.
Pageof 2