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Marsha P. Cole

Researcher at University of Louisville

Publications -  47
Citations -  3402

Marsha P. Cole is an academic researcher from University of Louisville. The author has contributed to research in topics: Nitric oxide & Mitochondrion. The author has an hindex of 30, co-authored 46 publications receiving 3109 citations. Previous affiliations of Marsha P. Cole include University of Kentucky & University of Pittsburgh.

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Cyclooxygenase-2 generates anti-inflammatory mediators from omega-3 fatty acids

TL;DR: The data support the idea that EFOX are signaling mediators that transduce the beneficial clinical effects of omega-3 fatty acids, COX-2 and aspirin, and confirm the anti-inflammatory nature of DHA- and DPA-derived EFOX.
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Adriamycin-induced, TNF-α-mediated central nervous system toxicity

TL;DR: It is demonstrated that ADR autofluorescence was detected only in areas of the brain located outside the blood–brain barrier, but a strong tumor necrosis factor alpha immunoreactivity was detected in the cortex and hippocampus of ADR-treated mice, consistent with the notion that TNF is an important mediator by which ADR induces central nervous system (CNS) injury.
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Oxidative and nitrative stress in neurodegeneration

TL;DR: A significant role is proposed for OS/NS and more specifically, lipid peroxidation (LPO) and other lipid modifications, by triggering microglial activation to elicit a neuroinflammatory state potentiated by diabetes or abnormal dopamine metabolism.
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Endogenous generation and protective effects of nitro-fatty acids in a murine model of focal cardiac ischaemia and reperfusion.

TL;DR: This study reveals the de novo generation of fatty acid nitration products in vivo and reveals the anti-inflammatory and potential therapeutic actions of OA-NO(2) in myocardial I/R injury.
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Adriamycin-mediated nitration of manganese superoxide dismutase in the central nervous system: insight into the mechanism of chemobrain.

TL;DR: It is demonstrated that treatment with ADR led to an increased circulating level of tumor necrosis factor‐alpha in wild‐type mice and in mice deficient in the inducible form of nitric oxide (iNOSKO), and it is suggested that NO is an important mediator, coupling the effect of ADR with cytokine production and subsequent activation of iNOS expression.