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David R. Janero
Researcher at Novartis
Publications - 31
Citations - 4184
David R. Janero is an academic researcher from Novartis. The author has contributed to research in topics: Oxidative stress & Nitric oxide. The author has an hindex of 19, co-authored 31 publications receiving 3943 citations. Previous affiliations of David R. Janero include Northeastern University & Ciba Specialty Chemicals.
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Malondialdehyde and thiobarbituric acid-reactivity as diagnostic indices of lipid peroxidation and peroxidative tissue injury.
TL;DR: The conclusion is reached that MDA determination and the TBA test can offer, at best, a narrow and somewhat empirical window on the complex process of lipid peroxidation.
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Eicosanoids in inflammation: biosynthesis, pharmacology, and therapeutic frontiers.
TL;DR: Mechanisms for the production of pro-inflammatory eicosanoid mediators contributing to inflammation are described and promising options for the prevention of inflammatory mediator formation and the therapeutic inhibition of pain and inflammation are summarized.
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Tissue processing of nitrite in hypoxia: an intricate interplay of nitric oxide-generating and -scavenging systems.
Martin Feelisch,Martin Feelisch,Bernadette O. Fernandez,Bernadette O. Fernandez,Nathan S. Bryan,Maria F. Garcia-Saura,Selena Bauer,David R. Whitlock,Peter C. Ford,David R. Janero,David R. Janero,Juan Rodriguez,Houman Ashrafian +12 more
TL;DR: Most tissues (except erythrocytes) produce free NO at rates that are maximal under hypoxia and that correlate robustly with each tissue's capacity for mitochondrial oxygen consumption, as well as comparing the kinetics of NO release before and after ferricyanide addition in tissue homogenates to mathematical models of \batchmode.
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Therapeutic potential of vitamin E in the pathogenesis of spontaneous atherosclerosis.
TL;DR: Pharmacologic investigation of vitamin E (and synthetic, vitamin E-like antioxidants) in nutritional and hyperlipidemic animal models of spontaneous atherosclerosis is required to establish whether any atherosclerotic impact is associated with vitamin E and, if so, what the mechanistic basis of the therapeutic benefit is.
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Hydroperoxide-induced oxidative stress impairs heart muscle cell carbohydrate metabolism
TL;DR: The biochemical pathology of H2O2 overload on cardiomyocyte carbohydrate metabolism has implications for post-ischemic cardiac bioenergetics and function and establishes that specific aspects of heart muscle hexose catabolism are H 2O2-sensitive injury targets.