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James O. McNamara

Researcher at Duke University

Publications -  300
Citations -  24071

James O. McNamara is an academic researcher from Duke University. The author has contributed to research in topics: Epilepsy & Hippocampal formation. The author has an hindex of 79, co-authored 296 publications receiving 23061 citations. Previous affiliations of James O. McNamara include United States Department of Veterans Affairs & Louisiana Tech University.

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Comparison of carbamazepine, phenobarbital, phenytoin, and primidone in partial and secondarily generalized tonic-clonic seizures

TL;DR: Overall, carbamazepine and phenytoin are recommended drugs of first choice for single-drug therapy of adults with partial or generalized tonic-clonic seizures or with both.
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Cell type-specific delivery of siRNAs with aptamer-siRNA chimeras.

TL;DR: A aptamer-siRNA chimeric RNAs capable of cell type–specific binding and delivery of functional siRNAs into cells and specifically inhibit tumor growth and mediate tumor regression in a xenograft model of prostate cancer.
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Remote control of neuronal activity in transgenic mice expressing evolved G protein-coupled receptors.

TL;DR: Transgenic mice expressing an evolved G protein-coupled receptor (hM3Dq) selectively activated by the pharmacologically inert, orally bioavailable drug clozapine-N-oxide are created and demonstrated a powerful chemical-genetic tool for remotely controlling the activity of discrete populations of neurons in vivo.
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Autoantibodies to glutamate receptor GluR3 in Rasmussen's encephalitis

TL;DR: Repeated plasma exchanges in one seriously ill child transiently reduced serum titers of GluR3 antibodies, decreased seizure frequency, and improved neurologic function, suggesting an autoimmune process may underlie Rasmussen's encephalitis.
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Cellular and molecular basis of epilepsy

TL;DR: A special effort to show how investigations of the epilepsies with methods from diverse disciplines can be complementary and mutually reinforcing and explain how electrophysiologic insights into the mechanisms of seizures induced by high K+ provide a plausible connection between the genotype and phenotype in a familial epilepsy.