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Laura L. Dugan

Researcher at University of California, San Diego

Publications -  73
Citations -  9755

Laura L. Dugan is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Superoxide & Neuroprotection. The author has an hindex of 47, co-authored 72 publications receiving 9229 citations. Previous affiliations of Laura L. Dugan include Vanderbilt University Medical Center & Washington University in St. Louis.

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Mitochondrial production of reactive oxygen species in cortical neurons following exposure to N-methyl-D-aspartate

TL;DR: Data support the possibility that NMDA receptor-mediated, Ca(2+)-dependent uncoupling of neuronal mitochondrial electron transport may contribute to the oxidative stress initiated by glutamate exposure.
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Carboxyfullerenes as neuroprotective agents

TL;DR: Data suggest that polar carboxylic acid C60 derivatives may have attractive therapeutic properties in several acute or chronic neurodegenerative diseases.
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Mediation of neuronal apoptosis by enhancement of outward potassium current.

TL;DR: Attenuating outward K+ current with tetraethylammonium or elevated extracellular K+, but not blockers of Ca2+, Cl-, or other K+ channels, reduced apoptosis, even if associated increases in intracellular Ca2+ concentration were prevented.
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Ketamine-induced loss of phenotype of fast-spiking interneurons is mediated by NADPH-oxidase

TL;DR: It is shown that exposure of mice to ketamine induced a persistent increase in brain superoxide due to activation in neurons of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, which suggests that NADPH oxidase may represent a novel target for the treatment of ketamine-induced psychosis.
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Early elevation of cochlear reactive oxygen species following noise exposure.

TL;DR: These ROS measures extend previous results indicating that noise-induced PTS is associated with elevated cochlear ROS production and ROS-mediated injury, and suggests a sustained process of oxidative stress which might be amenable to intervention with chronic antioxidant therapy.