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Relative regional glucose metabolism was determined by normalizing (18F FDG data to the whole-brain uptake.
Radiopharmaceuticals most commonly used, such as 18FDG and H 2 15 O, allow imaging of tissue metabolic activity, in terms of regional glucose uptake or blood flow changes, respectively.
Regional glucose uptake (GU), fatty acid uptake (FAU), percentage segment shortening (%SS), and oxygen consumption (MV O2) were determined with normal arterial plasma FFA concentrations (Group 1) or with elevated FFA concentrations (Groups 2 and 3).
This imaging method has conclusively demonstrated that dementing diseases are multifocal, rather than global, brain disorders and has shown that clinically similar dementias may have significantly different patterns of regional glucose metabolism.
Regional glucose uptake into maternal tissues and fetuses was quantified using positron emission tomography (PET).
In addition, regional glucose metabolism in medial prefrontal cortex during rest was observed to correlate with individual differences in neuroticism [30].
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FDG-PET measures regional cerebral glucose metabolism semi-quantitatively and visualizes the distribution of altered glucose metabolism [8, 9].
Aβ: amyloid beta; AD: Alzheimer's disease; C-DED: N-[C-methyl]-L-deuterodeprenyl; C-PIB: Pittsburgh Compound B; CSF: cerebrospinal fluid; F-FDG: 2-[F]-fluoro-2-deoxy-D-glucose; MCI: mild cognitive impairment; PET: positron emission tomography; rCMRglc: regional cerebral glucose metabolism.
Changes in the distribution of regional cerebral glucose metabolism were calculated as a difference image between the corrected postoperative and preoperative FDG-PET images.
Furthermore, overuse of APAP/caffeine/ASA has been shown to affect regional brain glucose metabolism in patients with chronic migraine [85].
Global and normalized regional cerebral glucose metabolic rates (rCMRglu) from the active and sham conditions were compared to baseline and then to each other.
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