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Jung H. Kim

Researcher at Yale University

Publications -  103
Citations -  9067

Jung H. Kim is an academic researcher from Yale University. The author has contributed to research in topics: Hippocampal formation & Temporal lobe. The author has an hindex of 51, co-authored 102 publications receiving 8749 citations. Previous affiliations of Jung H. Kim include Veterans Health Administration.

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Hippocampal interneuron loss and plasticity in human temporal lobe epilepsy

TL;DR: This paper provides the first evidence of such reorganization of a hippocampal seizure focus in human temporal lobe epilepsy (TLE), which involves the selective loss of somatostatin and neuropeptide Y immunoreactive interneurons, and axonal sprouting of other neuropePTide Y neurons and dynorphin-A immunore active granule cells.
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Characteristics of medial temporal lobe epilepsy: II. Interictal and ictal scalp electroencephalography, neuropsychological testing, neuroimaging, surgical results, and pathology

TL;DR: Sixty‐seven patients with temporal lobe epilepsy without circumscribed, potentially epileptogenic lesions, who were studied with intracranial electrodes and who became seizure free following temporal lobectomy were retrospectively evaluated with regard to preoperative scalp electroencephalographic (EEG) findings, neuropsychological test results, neuroimaging findings, results of surgery, and pathology of resected tissue.
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Quantitative magnetic resonance imaging in temporal lobe epilepsy: Relationship to neuropathology and neuropsychological function

TL;DR: MRI hippocampal measurements were compared to hippocampal neuronal densities obtained postoperatively and significant correlations existed between MRI measurements of the left hippocampus and the Wechsler logical memory percent retention scores and between the left temporal lobe measurements and the verbal Selective Reminding Test scores for patients with seizure foci in theleft temporal lobe.
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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.