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dc.contributor.authorDivani, AA
dc.contributor.authorPhan, J-A
dc.contributor.authorSalazar, P
dc.contributor.authorSantacruz, KS
dc.contributor.authorBachour, O
dc.contributor.authorMahmoudi, J
dc.contributor.authorZhu, X-H
dc.contributor.authorPomper, MG
dc.date.accessioned2018-08-26T08:38:27Z
dc.date.available2018-08-26T08:38:27Z
dc.date.issued2018
dc.identifier.urihttp://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/52930
dc.description.abstractWe present a longitudinal study of cerebral metabolism using [18F]fluorodeoxyglucose (FDG) positron emission tomography (PET) in a rat model of shockwave-induced traumatic brain injury (SW-TBI). Anesthetized rats received 5 or 10 SW pulses to the right anterior lateral or dorsal frontal regions using SW lithotripsy. Animals were scanned for FDG uptake at baseline, 3 h post-injury, and 3 days post-injury, using a small animal PET/computed tomography (CT) scanner. FDG uptake at all time-points was quantified as the ratio of brain activity relative to peripheral activity in the left ventricle (LV) in the heart (Abrain/ALV) for the entire brain, each hemisphere, and four cortices (motor, cingulate, somatosensory, and retrosplenial). The mixed-designed models analysis of variance (ANOVA) for the hemispheric and global FDG uptake ratio showed a significant effect of the time-of-scan (p = 0.038) and measured region (p = 6.12e-09). We also observed a significant effect of the time-of-scan (p = 0.046) and measured region (p = 2.28e-09) for the FDG uptake ratio in four cortical regions. None of the measurements (global or local) showed a significant effect for the number of SW pulses (5 or 10) or SW location (lateral or dorsal frontal regions). Our data suggest that SW-TBI causes hypermetabolism on the impact side of the rat brain at 3 h post-injury compared with the baseline measurements. However, the increase in FDG uptake by day 3 post-injury was not significant. Further studies on post-TBI metabolic changes are needed to understand better the pathophysiology of the injury. é Copyright 2018, Mary Ann Liebert, Inc. 2018.
dc.language.isoEnglish
dc.relation.ispartofJournal of Neurotrauma
dc.subjectamyloid precursor protein
dc.subjectbuprenorphine
dc.subjectfluorodeoxyglucose f 18
dc.subjectglial fibrillary acidic protein
dc.subjectketoprofen
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectArticle
dc.subjectbrain function
dc.subjectbrain metabolism
dc.subjectcingulate gyrus
dc.subjectcontrolled study
dc.subjectelectroencephalogram
dc.subjectexperimental traumatic brain injury
dc.subjectglucose transport
dc.subjectheart left ventricle
dc.subjecthemisphere
dc.subjecthistopathology
dc.subjecthypermetabolism
dc.subjectlithotripsy
dc.subjectlongitudinal study
dc.subjectmale
dc.subjectmotor cortex
dc.subjectnonhuman
dc.subjectpositron emission tomography
dc.subjectrat
dc.subjectretrosplenial cortex
dc.subjectshock wave
dc.subjectsomatosensory cortex
dc.subjectWistar rat
dc.titleChanges in [18F]Fluorodeoxyglucose Activities in a Shockwave-Induced Traumatic Brain Injury Model Using Lithotripsy
dc.typeArticle
dc.citation.volume35
dc.citation.issue1
dc.citation.spage187
dc.citation.epage194
dc.citation.indexScopus
dc.identifier.DOIhttps://doi.org/10.1089/neu.2017.5208


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