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Levente Kiss

Researcher at Semmelweis University

Publications -  37
Citations -  2284

Levente Kiss is an academic researcher from Semmelweis University. The author has contributed to research in topics: Mesenchymal stem cell & Nitric oxide. The author has an hindex of 18, co-authored 34 publications receiving 2083 citations. Previous affiliations of Levente Kiss include University of Medicine and Dentistry of New Jersey & Rutgers University.

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Hydrogen sulfide attenuates myocardial ischemia-reperfusion injury by preservation of mitochondrial function

TL;DR: It is demonstrated that the delivery of H2S at the time of reperfusion limits infarct size and preserves left ventricular (LV) function in an in vivo model of myocardial ischemia-reperfusion (MI-R) and that either administration of H 2S or the modulation of endogenous production may be of clinical benefit in ischemic disorders.
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Mesenchymal stem cells rescue cardiomyoblasts from cell death in an in vitro ischemia model via direct cell-to-cell connections.

TL;DR: It is hypothesize that mesenchymal stem cells may reduce the number of dead cardiomyoblasts after ischemic damage via direct cell-to-cell interactions and intercellular tubular connections may play an important role in these processes.
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Mitochondrial NO and reactive nitrogen species production: does mtNOS exist?

TL;DR: The present review aims to summarize the most recent developments in mitochondrial NO production, highlights a few unsolved questions, and proposes new directions for future work in this research area.
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Protective effect of hydrogen sulfide in a murine model of acute lung injury induced by combined burn and smoke inhalation

TL;DR: It is suggested that H2S exerts protective effects in acute lung injury, at least in part through the activation of anti-inflammatory and antioxidant pathways.
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Hydrogen sulfide decreases adenosine triphosphate levels in aortic rings and leads to vasorelaxation via metabolic inhibition

TL;DR: H(2)S, a new gasotransmitter of emerging importance, leads to relaxation via Cl(-)/HCO(3)(-) channels and metabolic inhibition and the interactions of these two factors depend on the oxygen levels of the tissue.