dc.creatorMelo, AA
dc.creatorBarreto, MWG
dc.creatorNassr, ACC
dc.creatorRogerio, F
dc.creatorLangone, F
dc.creatorPereira, LAV
dc.creatorSbragia, L
dc.date2009
dc.date2014-11-16T00:40:56Z
dc.date2015-11-26T16:31:09Z
dc.date2014-11-16T00:40:56Z
dc.date2015-11-26T16:31:09Z
dc.date.accessioned2018-03-28T23:12:12Z
dc.date.available2018-03-28T23:12:12Z
dc.identifierPediatric Neurosurgery. Karger, v. 45, n. 3, n. 198, n. 204, 2009.
dc.identifier1016-2291
dc.identifierWOS:000267090700007
dc.identifier10.1159/000222670
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/57308
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/57308
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/57308
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1270138
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionBackground: Exposure of the spinal cord in myelomeningocele (MM) throughout gestation increases spinal injury. Astrocyte activation evidenced by glial fibrillary acidic proteins (GFAP) indicates the extent of injury. Corticosteroids modulate GFAP synthesis, but their effect in MM is unclear. The purpose of this study was to evaluate the GFAP expression in a fetal rat model of dysraphism and the effect of corticosteroid treatment on this marker and on clinical neurological disabilities. Methods: Dysraphism was surgically created in 2 groups of 48 rat fetuses; group 1: control, and group 2: treated with corticosteroid. Each group was subdivided into fetuses with surgically created MM, controls and shams on day 18.5 of gestation (term = 22 days). Fetuses were harvested on day 21.5, examined for evidence of neurological deficits, and the following clinical parameters were registered: kyphosis, tail deformities, leg deformities, leg paralysis or paresis and pain perception. The fetuses were fixed for GFAP immunostaining. Results: All fetuses with MM in group 1 presented neurological deficits and glial reactions with GFAP expression, as opposed to controls and shams. In group 2, corticosteroid treatment prevented some neurological deficits (18-25%), reducing glial response and GFAP expression. Conclusions: Experimentally induced dysraphism in the rat fetus is related to glial response and increased GFAP expression in the spinal cord. Corticoid treatment clinically improved nerve injury in some fetuses. It reduced glial reaction and GFAP expression. Copyright (C) 2009 S. Karger AG, Basel
dc.description45
dc.description3
dc.description198
dc.description204
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionCNPq [478539/2007-0]
dc.descriptionFAPESP [00974-3/2003]
dc.languageen
dc.publisherKarger
dc.publisherBasel
dc.publisherSuíça
dc.relationPediatric Neurosurgery
dc.relationPediatr. Neurosurg.
dc.rightsfechado
dc.rightshttp://www.karger.com/Services/RightsPermissions
dc.sourceWeb of Science
dc.subjectMyelomeningocele
dc.subjectNeural tube defect
dc.subjectGlial fibrillary acidic protein
dc.subjectCorticosteroid
dc.subjectDysraphism
dc.subjectNeural-tube Defects
dc.subjectIn-utero
dc.subjectAmniotic-fluid
dc.subjectMyelomeningocele
dc.subjectAstrocytes
dc.subjectSurgery
dc.subjectImmunofluorescence
dc.subjectExposure
dc.subjectSystem
dc.subjectRepair
dc.titleCorticosteroids Reduce Glial Fibrillary Acidic Protein Expression in Response to Spinal Cord Injury in a Fetal Rat Model of Dysraphism
dc.typeArtículos de revistas


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