F
Francis G. Spinale
Researcher at University of South Carolina
Publications - 469
Citations - 24683
Francis G. Spinale is an academic researcher from University of South Carolina. The author has contributed to research in topics: Heart failure & Ventricular remodeling. The author has an hindex of 84, co-authored 451 publications receiving 23239 citations. Previous affiliations of Francis G. Spinale include Biogen Idec & Veterans Health Administration.
Papers
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Journal Article
Abstract 1102: Differential Effect of Wall Tension on Matrix Metalloproteinase Promoter Activation in the Thoracic Aorta
TL;DR: In this article, the authors examined whether MMP promoter activation would occur as a function of wall tension and found that selective MMP induction occurs at wall tension values concordant with hypertension and that a mechanical-molecular set point exists which triggers adverse remodeling within the vascular wall.
Journal ArticleDOI
727-4 Differential Effects of Chronic Angiotensin Converting Enzyme (ACE) Inhibition and Angiotensin II (AT-II) Receptor (AT1AT-II) Blockade on Myocyte Excitation and Contraction in Dilated Cardiomyopathy
Rupak Mukherjee,Rupak Mukherjee,Henry H. Holzgrefe,Henry H. Holzgrefe,James R. Powell,James R. Powell,William H. Koster,William H. Koster,Francis G. Spinale,Francis G. Spinale +9 more
TL;DR: ACEI during the progression of DCM improved MYO function whereas AT-BLOCK had selective effects on MYO electrophysiology, suggesting that ACEI and AT- BLOCK have unique and different mechanisms of action with cardiomyopathic disease.
Journal Article
Abstract 12431: Continuous Localized Monitoring of Plasmin Activity Identifies Differential and Regional Effects of the Serine Protease Inhibitor Aprotinin: Relevance to Antifibrinolytic Therapy
Daryl L. Reust,Jennifer A. Dixon,Richard A McKinney,Risha K Patel,William T Rivers,Rupak Mukherjee,Robert E. Stroud,Scott Reeves,James H. Abernathy,Francis G. Spinale +9 more
TL;DR: Using a large animal model and a continuous method to monitor regional PLact, these unique results demonstrated that an empirical aprotinin dosing protocol causes maximal and rapid suppression in the myocardium and kidney and in turn would likely increase the probability of off-target effects and adverse events.
Journal ArticleDOI
Characterization of myocardial remodeling with diffusion tensor magnetic resonance imaging in chronic porcine model using the toroid-based representation
Patent
Composition for modifying myocardial infarction expansion
TL;DR: A bioscaffolding can be formed within a post-myocardial infarct region sufficient to cause attenuation of a rate of myocardial Infarct expansion.