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Jack T. Saari

Researcher at United States Department of Agriculture

Publications -  92
Citations -  2631

Jack T. Saari is an academic researcher from United States Department of Agriculture. The author has contributed to research in topics: Copper deficiency & Histamine. The author has an hindex of 27, co-authored 92 publications receiving 2513 citations. Previous affiliations of Jack T. Saari include Agricultural Research Service & University of Louisville.

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Cardiac Metallothionein Induction Plays the Major Role in the Prevention of Diabetic Cardiomyopathy by Zinc Supplementation

TL;DR: The results suggest that the prevention of diabetic cardiomyopathy by zinc supplementation is predominantly mediated by an increase in cardiac MT.
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Zinc Supplementation Prevents Alcoholic Liver Injury in Mice through Attenuation of Oxidative Stress

TL;DR: Zinc supplementation prevents alcoholic liver injury in an metallothionein-independent manner by inhibiting the generation of reactive oxygen species (P450 2E1) and enhancing the activity of antioxidant pathways.
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High-fat diet-induced juvenile obesity leads to cardiomyocyte dysfunction and upregulation of Foxo3a transcription factor independent of lipotoxicity and apoptosis.

TL;DR: The data show that high-fat diet-induced obesity resulted in impaired cardiomyocyte function, upregulated Foxo3a transcription factor and mitochondrial damage without overt lipotoxicity or apoptosis.
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Dietary copper supplementation reverses hypertrophic cardiomyopathy induced by chronic pressure overload in mice

TL;DR: Dietary supplementation with physiologically relevant levels of copper reverses preestablished hypertrophic cardiomyopathy caused by pressure overload induced by ascending aortic constriction in a mouse model and improves the condition of hypertrophic heart failure at least in part through CCS-mediated HIF-1α activation of VEGF expression and angiogenesis.
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Catalase-overexpressing transgenic mouse heart is resistant to ischemia-reperfusion injury

TL;DR: Findings support the view that hydrogen peroxide is an important cause of ischemia-reperfusion damage and suggest that protection may be provided by elevation of catalase activity.