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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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dc.affiliation.dptoUC3M. Departamento de Bioingenieríaes
dc.affiliation.grupoinvUC3M. Grupo de Investigación: Biomedical Imaging and Instrumentation Groupes
dc.affiliation.grupoinvUC3M. Grupo de Investigación: BSEL - Laboratorio de Ciencia e Ingeniería Biomédicaes
dc.contributor.authorZingone, A.
dc.contributor.authorSeidel, J.
dc.contributor.authorAloj, L.
dc.contributor.authorCaraco, C.
dc.contributor.authorVaquero López, Juan José
dc.contributor.authorJagoda, E. M.
dc.contributor.authorChou, J. Y.
dc.contributor.authorGreen, M. V.
dc.contributor.authorEckelman, William C.
dc.date.accessioned2010-10-05T08:38:06Z
dc.date.available2010-10-05T08:38:06Z
dc.date.issued2002-08-02
dc.description.abstractMonitoring 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
dc.description.statusPublicado
dc.format.mimetypeapplication/pdf
dc.identifier.bibliographicCitationLife Sciences, 2002, vol. 71, n. 11, p. 1293-1301
dc.identifier.doi10.1016/S0024-3205(02)01831-3
dc.identifier.issn0024-3205
dc.identifier.publicationfirstpage1293
dc.identifier.publicationissue11
dc.identifier.publicationlastpage1301
dc.identifier.publicationtitleLife Sciences
dc.identifier.publicationvolume71
dc.identifier.urihttps://hdl.handle.net/10016/9344
dc.language.isoeng
dc.publisherElsevier
dc.relation.publisherversionhttp://dx.doi.org/10.1016/S0024-3205(02)01831-3
dc.rights© Elsevier
dc.rights.accessRightsopen access
dc.subject.ecienciaBiología y Biomedicina
dc.subject.otherGlycogen storage disease type 1a
dc.subject.otherMouse
dc.subject.other[18F]FDG
dc.subject.otherG6Pase
dc.titleMonitoring the correction of glycogen storage disease type 1a in a mouse model using [18F]FDG and a dedicated animal scanner
dc.typeresearch article*
dc.type.reviewPeerReviewed
dspace.entity.typePublication
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