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Purnima Narasimhan

Researcher at Stanford University

Publications -  39
Citations -  3902

Purnima Narasimhan is an academic researcher from Stanford University. The author has contributed to research in topics: Oxidative stress & Neuroprotection. The author has an hindex of 29, co-authored 38 publications receiving 3495 citations. Previous affiliations of Purnima Narasimhan include University of California, San Francisco.

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Oxidative Stress in Ischemic Brain Damage: Mechanisms of Cell Death and Potential Molecular Targets for Neuroprotection

TL;DR: It is proposed that superoxide dismutase and NOX activity in the brain is a major determinant for ischemic damage/repair and that these major anti- and pro-oxidant enzymes are potential endogenous molecular targets for stroke therapy.
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NADPH oxidase is the primary source of superoxide induced by NMDA receptor activation

TL;DR: NADPH oxidase is identified as the primary source of NMDA-induced superoxide production and neuronal death, and is blocked by the NADPH oxid enzyme inhibitor apocynin and in neurons lacking the p47phox subunit, which is required for NADPH oxidation.
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Neuronal death/survival signaling pathways in cerebral ischemia.

TL;DR: Cumulative evidence suggests that apoptosis plays a pivotal role in cell death in vitro after hypoxia and in in vivo ischemia models, and genetic manipulation of intrinsic antioxidants and factors in the signaling pathways has provided substantial understanding of the mechanisms involved.
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Reperfusion and Neurovascular Dysfunction in Stroke: from Basic Mechanisms to Potential Strategies for Neuroprotection

TL;DR: This study has developed a focal stroke model using mice deficient in mitochondrial manganese-superoxide dismutase (SOD2−/+) to investigate neurovascular endothelial damage that occurs during reperfusion and identified the signal transducer and activator of transcription 3 (STAT3) as a transcription factor of the mouse SOD2 gene.
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Oxidative stress and neuronal death/survival signaling in cerebral ischemia

TL;DR: Genetic manipulation of intrinsic antioxidants and factors in the signaling pathways has provided substantial understanding of the mechanisms involved in cell death/survival signaling pathways and the role of oxygen radicals in ischemic cerebral injury.