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Claude A. Piantadosi

Researcher at Duke University

Publications -  382
Citations -  21857

Claude A. Piantadosi is an academic researcher from Duke University. The author has contributed to research in topics: Mitochondrion & Lung injury. The author has an hindex of 78, co-authored 381 publications receiving 20412 citations. Previous affiliations of Claude A. Piantadosi include University of Pittsburgh & Johns Hopkins University.

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Blood flow regulation by S-nitrosohemoglobin in the physiological oxygen gradient

TL;DR: By sensing the physiological oxygen gradient in tissues, hemoglobin exploits conformation-associated changes in the position of cysteinebeta93 SNO to bring local blood flow into line with oxygen requirements.
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Heme Oxygenase-1 Regulates Cardiac Mitochondrial Biogenesis via Nrf2-Mediated Transcriptional Control of Nuclear Respiratory Factor-1

TL;DR: Findings consign HO-1/CO signaling through Nrf2 and Akt to the myocardial transcriptional program for mitochondrial biogenesis, provide a rationale for targeted mitochondrial CO therapy, and connect cardiac mitochondrial volume expansion with the inducible network of xenobiotic and antioxidant cellular defenses.
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Nitric oxide in the human respiratory cycle.

TL;DR: In this paper, it was shown that in in vitro and ex vivo systems as well as healthy adults alternately exposed to hypoxia or hyperoxia (to dilate or constrict pulmonary and systemic arteries in vivo), binding of NO to hemes (FeNO) and thiols (SNO) of hemoglobin (Hb) varies as a function of oxygen tension (pO2) saturation (FeO(2) over a wide range.
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Mitochondrial Generation of Reactive Oxygen Species After Brain Ischemia in the Rat

TL;DR: The data indicate that reactive oxygen species generated by mitochondrial electron transport escape cellular antioxidant defenses and promote highly damaging hydroxyl radical activity after transient brain ischemia in the rat.
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Survival in critical illness is associated with early activation of mitochondrial biogenesis.

TL;DR: Eventual survivors responded early to critical illness with mitochondrial biogenesis and antioxidant defense responses, which may partially counteract mitochondrial protein depletion, helping to maintain functionality and energetic status.