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Rona G. Giffard

Researcher at Stanford University

Publications -  158
Citations -  12818

Rona G. Giffard is an academic researcher from Stanford University. The author has contributed to research in topics: Astrocyte & Neuroprotection. The author has an hindex of 60, co-authored 158 publications receiving 11550 citations. Previous affiliations of Rona G. Giffard include University of Catania.

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Genomic Analysis of Reactive Astrogliosis

TL;DR: The findings provide transcriptome databases for two subtypes of reactive astrocytes that will be highly useful in generating new and testable hypotheses of their function, as well as for providing new markers to detect different types of reactiveAstrocyte reactive gliosis in human neurological diseases.
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Acidosis reduces NMDA receptor activation, glutamate neurotoxicity, and oxygen-glucose deprivation neuronal injury in cortical cultures.

TL;DR: It is reported that moderate extracellular acidosis markedly reduced the inward whole cell current induced by NMDA on cultured cortical neurons; at pH 6.1, kainate-induced current was additionally reduced and raised the possibility that moderate acidosis may decrease cortical neuronal vulnerability to ischemic damage.
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Microglia Potentiate Damage to Blood–Brain Barrier Constituents Improvement by Minocycline In Vivo and In Vitro

TL;DR: In vivo, minocycline reduced infarct volume and neurological deficits and markedly reduced BBB disruption and hemorrhage in mice after experimental stroke and microglial inhibitors may prove to be an important treatment adjunct to fibrinolysis.
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Antiapoptotic and Anti-inflammatory Mechanisms of Heat-Shock Protein Protection

TL;DR: It is suggested that HSPs are capable of protecting brain cells from lethal insults through a variety of mechanisms and should be explored as a potential therapy against stroke and other neurodegenerative diseases.
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Astrocytes: targets for neuroprotection in stroke.

TL;DR: This review will focus on those functions of astrocytes that can both protect and endanger neurons, and discuss how manipulating these functions provides a novel and important strategy to enhance neuronal survival and improve outcome following cerebral ischemia.