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Dipak K. Das

Researcher at University of Connecticut

Publications -  329
Citations -  18415

Dipak K. Das is an academic researcher from University of Connecticut. The author has contributed to research in topics: Ischemia & Resveratrol. The author has an hindex of 75, co-authored 327 publications receiving 17708 citations. Previous affiliations of Dipak K. Das include Jawaharlal Nehru University & Baystate Medical Center.

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Resveratrol in cardioprotection: a therapeutic promise of alternative medicine.

TL;DR: It appears that resveratrol-mediated cardioprotection is achieved through the preconditioning effect (the best yet devised method of cardiop rotection), rather than direct protection.
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An essential role of NFκB in tyrosine kinase signaling of p38 MAP kinase regulation of myocardial adaptation to ischemia

TL;DR: It is demonstrated that p38 MAP kinase might be upstream of NFκB which plays a role in ischemic preconditioning of heart, and a synthetic peptide containing a cell membrane‐permeable motif and nuclear sequence, SN 50, significantly inhibited the beneficial effects of adaptation on functional recovery and tissue injury.
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Resveratrol in cardiovascular health and disease.

TL;DR: The successful application of resveratrol in therapy is based upon its hormetic action similar to any toxin: exerting beneficial effects at lower doses and cytotoxic effects at higher doses.
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Transgene overexpression of αB crystallin confers simultaneous protection against cardiomyocyte apoptosis and necrosis during myocardial ischemia and reperfusion

TL;DR: Transgene overexpression of αB crystallin confers simultaneous protection against cardiomyocyte apoptosis and necrosis during myocardial ischemia and reperfusion and was successful in diminishing the independent contributory effects of both necrosis and apoptosis on I/R‐induced cell death.
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Alcohol in Moderation, Cardioprotection, and Neuroprotection : Epidemiological Considerations and Mechanistic Studies

TL;DR: Moderate alcohol exposure appears to trigger analogous mild stress-associated, anti-inflammatory mechanisms in the heart, vasculature, and brain that tend to promote cellular survival pathways, which could underlie cardioprotection.