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John Ross

Researcher at University of California, San Diego

Publications -  260
Citations -  28923

John Ross is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Myocardial infarction & Heart failure. The author has an hindex of 91, co-authored 258 publications receiving 28177 citations. Previous affiliations of John Ross include Scripps Health & University of Vienna.

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Factors Influencing Infarct Size Following Experimental Coronary Artery Occlusions

TL;DR: It is concluded that the hemodynamic status and neurohumoral background at the time of occlusion and for up to 3 hr thereafter can alter the extent and severity of myocardial ischemic injury andMyocardial necrosis.
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Cardiac Muscle Cell Hypertrophy and Apoptosis Induced by Distinct Members of the p38 Mitogen-activated Protein Kinase Family

TL;DR: The direct involvement of p38 pathways in cardiac hypertrophy and apoptosis suggests a significant role for p38 signaling in the pathophysiology of heart failure.
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MLP-Deficient Mice Exhibit a Disruption of Cardiac Cytoarchitectural Organization, Dilated Cardiomyopathy, and Heart Failure

TL;DR: In vivo analysis revealed that MLP-deficient mice reproduce the morphological and clinical picture of dilated cardiomyopathy and heart failure in humans, providing the first model for this condition in a genetically manipulatable organism.
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Segregation of atrial-specific and inducible expression of an atrial natriuretic factor transgene in an in vivo murine model of cardiac hypertrophy

TL;DR: Evidence is provided that atrial-specific and inducible expression of the atrial natriuretic factor gene can be segregated, suggesting that a distinct set of regulatory cis sequences may mediate the up-regulation of the ANF gene during in vivo pressure overload hypertrophy.
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Regional Myocardial Function during Acute Coronary Artery Occlusion and Its Modification by Pharmacologic Agents in the Dog

TL;DR: The results indicate the power of this approach, which provides continuous quantification of regional wall function in myocardial ischemia and during therapeutic interventions, and suggests a protective effect of this drug.