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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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Pharmacological preconditioning with resveratrol: role of nitric oxide

TL;DR: It is demonstrated that resveratrol can pharmacologically precondition the heart in a NO-dependent manner and provided cardioprotection as evidenced by improved postischemic ventricular functional recovery and reduced myocardial infarct size and cardiomyocyte apoptosis.
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Alpha 1-adrenoceptor-mediated phosphoinositide breakdown and inotropic response in rat left ventricular papillary muscles.

TL;DR: The results suggest that cardiac α1-adrenoceptor stimulation occur through the phosphodiesteratic cleavage of PI-4,5-PI, such that IP, may produce transient inotropic effects by mobilizing intracellular Ca2+, whil e diacylglycerol, along with cofactors that are also generated on a, adreno receptor stimulation, may provoke a sustained positive inotropic effect by potentiating slow Ca2+ channels through activation of protein kin
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Grape seed proanthocyanidins improved cardiac recovery during reperfusion after ischemia in isolated rat hearts

TL;DR: Grape seed proanthocyanidins have cardioprotective effects against reperfusion-induced injury via their ability to reduce or remove, directly or indirectly, free radicals in myocardium that is reperfused after ischemia.
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Grape seed proanthocyanidin reduces cardiomyocyte apoptosis by inhibiting ischemia/reperfusion-induced activation of JNK-1 and C-JUN.

TL;DR: GSPE functioned as an in vivo antioxidant, and its cardioprotective properties may be at least partially attributed to its ability to block antideath signal through the inhibition of proapoptotic transcription factor and gene, JNK-1 and c-Jun.
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Oxidative stress developed during the reperfusion of ischemic myocardium induces apoptosis.

TL;DR: It is shown that oxidative stress developed in the ischemic reperfused myocardium induces apoptosis, a genetically controlled response for cells to commit suicide and is associated with DNA fragmentation or laddering.