Monitoring the correction of glycogen storage disease type 1a in a mouse model using [18F]FDG and a dedicated animal scanner (358 views)
Life Sci (ISSN: 0024-3205), 2002; 71(11): 1293-1301.
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Paper type: Journal Article,
Impact factor: 1.824, 5-year impact factor: 2.538
Url: http://www.scopus.com/inward/record.url?eid=2-s2.0-0037008385&partnerID=40&md5=5f780c4dcacc443be87547db8448afce
Keywords: [18f]fdg, G6pase, Glycogen Storage Disease Type 1a, Mouse, Fluorine 18, Glucose 6 Phosphatase, Recombinant Dna, Adenovirus, Animal Experiment, Animal Model, Article, Blood, Controlled Study, Drug Monitoring, Drug Retention, Drug Transport, Gene Therapy, Heart, Knockout Mouse, Liver, Liver Function, Mouse Strain, Nonhuman, Strain Difference, Virus Recombinant, Wild Type, Disease Models, Fluorodeoxyglucose F18, Glucose-6-Phosphatase, Mice, Inbred Balb C, Radiopharmaceuticals, Tomography, Emission-Computed, Adenoviridae, Murinae, [18f] Fdg,
Affiliations:
*** IBB - CNR ***
National Institute of Child Health and Development, Bethesda, MD 20892, United States
Department of Nuclear Medicine, National Institutes of Health, Bethesda, MD 20892, United States
PET Department, National Institutes of Health, Bethesda, MD 20892, United States
PET Department, Warren Grant Magnuson Clinical Center, Bld. 10, 10 Center Drive, Bethesda, MD 20892, United States
References:
Not available.
Life Sci (ISSN: 0024-3205), 2002; 71(11): 1293-1301.
Export to BibTeX Export to EndNote
Paper type: Journal Article,
Impact factor: 1.824, 5-year impact factor: 2.538
Url: http://www.scopus.com/inward/record.url?eid=2-s2.0-0037008385&partnerID=40&md5=5f780c4dcacc443be87547db8448afce
Keywords: [18f]fdg, G6pase, Glycogen Storage Disease Type 1a, Mouse, Fluorine 18, Glucose 6 Phosphatase, Recombinant Dna, Adenovirus, Animal Experiment, Animal Model, Article, Blood, Controlled Study, Drug Monitoring, Drug Retention, Drug Transport, Gene Therapy, Heart, Knockout Mouse, Liver, Liver Function, Mouse Strain, Nonhuman, Strain Difference, Virus Recombinant, Wild Type, Disease Models, Fluorodeoxyglucose F18, Glucose-6-Phosphatase, Mice, Inbred Balb C, Radiopharmaceuticals, Tomography, Emission-Computed, Adenoviridae, Murinae, [18f] Fdg,
Affiliations:
*** IBB - CNR ***
National Institute of Child Health and Development, Bethesda, MD 20892, United States
Department of Nuclear Medicine, National Institutes of Health, Bethesda, MD 20892, United States
PET Department, National Institutes of Health, Bethesda, MD 20892, United States
PET Department, Warren Grant Magnuson Clinical Center, Bld. 10, 10 Center Drive, Bethesda, MD 20892, United States
References:
Not available.
Monitoring the correction of glycogen storage disease type 1a in a mouse model using [18F]FDG and a dedicated animal scanner
Monitoring gene therapy of glycogen storage disease type 1a in a mouse model was achieved using [18F]FDG and a dedicated animal scanner. The G6Pase knockout (KO) mice were compared to the same mice after infusion with a recombinant adenovirus containing the murine G6Pase gene (Ad-mG6Pase). Serial images of the same mouse before and after therapy were obtained and compared with wild-type (WT) mice of the same strain to determine the uptake and retention of [18F]FDG in the liver. Image data were acquired from heart, blood pool and liver for twenty minutes after injection of [18F]FDG. The retention of [18F]FDG was lower for the WT mice compared to the KO mice. The mice treated with adenovirus-mediated gene therapy had retention similar to that found in age-matched WT mice. These studies show that FDG can be used to monitor the G6Pase concentration in liver of WT mice as compared to G6Pase KO mice. In these mice, gene therapy returned the liver function to that found in age matched WT controls as measured by the FDG kinetics in the liver compared to that found in age matched wild type controls.
Monitoring gene therapy of glycogen storage disease type 1a in a mouse model was achieved using [18F]FDG and a dedicated animal scanner. The G6Pase knockout (KO) mice were compared to the same mice after infusion with a recombinant adenovirus containing the murine G6Pase gene (Ad-mG6Pase). Serial images of the same mouse before and after therapy were obtained and compared with wild-type (WT) mice of the same strain to determine the uptake and retention of [18F]FDG in the liver. Image data were acquired from heart, blood pool and liver for twenty minutes after injection of [18F]FDG. The retention of [18F]FDG was lower for the WT mice compared to the KO mice. The mice treated with adenovirus-mediated gene therapy had retention similar to that found in age-matched WT mice. These studies show that FDG can be used to monitor the G6Pase concentration in liver of WT mice as compared to G6Pase KO mice. In these mice, gene therapy returned the liver function to that found in age matched WT controls as measured by the FDG kinetics in the liver compared to that found in age matched wild type controls.
Monitoring the correction of glycogen storage disease type 1a in a mouse model using [18F]FDG and a dedicated animal scanner
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Monitoring the correction of glycogen storage disease type 1a in a mouse model using [18F]FDG and a dedicated animal scanner
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20 Records (18 excluding Abstracts).
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Total impact factor: 98.969 (92.21 excluding Abstracts).
Total 5 year impact factor: 99.41 (92.569 excluding Abstracts).
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