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James C. K. Lai

Researcher at Idaho State University

Publications -  71
Citations -  2734

James C. K. Lai is an academic researcher from Idaho State University. The author has contributed to research in topics: Oxidative stress & Biochanin A. The author has an hindex of 27, co-authored 69 publications receiving 2509 citations. Previous affiliations of James C. K. Lai include Yale University.

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Loss of glutamine synthetase in the human epileptogenic hippocampus: possible mechanism for raised extracellular glutamate in mesial temporal lobe epilepsy.

TL;DR: Further studies are needed to define the cause of epileptic seizures in mesial temporal lobe epilepsy, but the loss of glutamine synthetase may provide a new focus for therapeutic interventions in MTLE.
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Exposure to titanium dioxide and other metallic oxide nanoparticles induces cytotoxicity on human neural cells and fibroblasts.

TL;DR: It is found that TiO2 micro- and nanoparticles induced cell death on both human cell types in a concentration-related manner and it was noted that zinc oxide (ZnO) nanoparticles were the most effective,TiO2 nanoparticles the secondmost effective, and magnesium oxide (MgO), the least effective in inducing cell death in U87 cells.
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Direct evidence for activity-dependent glucose phosphorylation in neurons with implications for the astrocyte-to-neuron lactate shuttle

TL;DR: It is suggested that neuronal glucose-derived pyruvate is the major oxidative fuel for activated neurons, not lactate-derived from astrocytes, contradicting predictions of the original astroCyte-to-neuron lactate shuttle model under the range of study conditions.
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Recurrent seizures and brain pathology after inhibition of glutamine synthetase in the hippocampus in rats.

TL;DR: The hypothesis that a deficiency in hippocampal glutamine synthetase causes recurrent seizures, even in the absence of classical mesial temporal sclerosis, is supported and restoration of glutamine Synthetase may represent a novel approach to therapeutic intervention in this disease.
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Functional studies in cultured astrocytes.

TL;DR: It is emphasized that some of the conclusions about neuronal-astrocytic interactions reached on the basis of studies in cultured cells and confirmed in intact tissue may not yet have been completely integrated into general neuroscience knowledge.