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David E. Kuhl

Researcher at University of California, Los Angeles

Publications -  134
Citations -  18917

David E. Kuhl is an academic researcher from University of California, Los Angeles. The author has contributed to research in topics: Emission computed tomography & Ictal. The author has an hindex of 65, co-authored 134 publications receiving 18635 citations. Previous affiliations of David E. Kuhl include National Institutes of Health.

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Tomographic measurement of local cerebral glucose metabolic rate in humans with (F-18)2-fluoro-2-deoxy-D-glucose: validation of method.

TL;DR: The data indicate that cerebral FDG‐6‐PO4 in humans increases for about 90 minutes, plateaus, and then slowly decreases, and that cerebral blood FDG activity levels were found to be a minor fraction of tissue activity.
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The [18F]fluorodeoxyglucose method for the measurement of local cerebral glucose utilization in man.

TL;DR: A mathematical model and derived operational equation are used which enable local cerebral glucose consumption to be calculated in terms of the following measurable variables: gray matter, white matter, and whole brain metabolic rates, calculated as a weighted average based on the approximate volume of each structure.
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Noninvasive determination of local cerebral metabolic rate of glucose in man

TL;DR: The rate constants of FDG in man were found to be comparable to those of deoxyglucose in rat and in rhesus monkey and the subject-to-subject variation of LCMRGlc as measured by the present method was comparable to that of other methods that measure whole-brain CMRglc.
Journal ArticleDOI

Tomographic measurement of local cerebral glucose metabolic rate in humans with (f-18)2-fluoro-2-deoxy-d-glucose: validation of method

TL;DR: The data indicate that cerebral FDG-6-PO4 in humans increases for about 90 minutes, plateaus, and then slowly decreases, and that cerebral blood FDG activity levels were found to be a minor fraction of tissue activity.
Journal ArticleDOI

Cerebral metabolism and atrophy in huntington's disease determined by 18FDG and computed tomographic scan

TL;DR: The results suggest the possibility that the caudate may be hypometabolic in some asymptomatic subjects who are potential carriers of the autosomal dominant gene for HD.