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dc.typeArtigo de periódicopt_BR
dc.titleCorticosteroids Reduce Glial Fibrillary Acidic Protein Expression In Response To Spinal Cord Injury In A Fetal Rat Model Of Dysraphism.pt_BR
dc.contributor.authorMelo-Filho, Antônio Aldopt_BR
dc.contributor.authorWeber Guimarães Barreto, Mariapt_BR
dc.contributor.authorCapelli Nassr, Azize Cristinapt_BR
dc.contributor.authorRogério, Fábiopt_BR
dc.contributor.authorLangone, Francescopt_BR
dc.contributor.authorPereira, Luis Antonio Violinpt_BR
dc.contributor.authorSbragia, Lourençopt_BR
unicamp.authorAntônio Aldo Melo-Filho, Division of Pediatric Surgery, Department of Surgery, Faculty of Medical Sciences, University of Campinas, UNICAMP, Campinas, Brazil.pt_BR Weber Guimarães Barreto,pt Cristina Capelli Nassr,ptábio Rogério,pt Langone,pt Antonio Violin Pereira,ptço Sbragia,pt
dc.subjectAdrenal Cortex Hormonespt_BR
dc.subjectBiological Markerspt_BR
dc.subjectDisease Models, Animalpt_BR
dc.subjectGlial Fibrillary Acidic Proteinpt_BR
dc.subjectRats, Sprague-dawleypt_BR
dc.subjectSpinal Cordpt_BR
dc.subjectSpinal Cord Injuriespt_BR
dc.subjectSpinal Dysraphismpt_BR
dc.description.abstractExposure 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. 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. 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. 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.en
dc.relation.ispartofPediatric Neurosurgerypt_BR
dc.relation.ispartofabbreviationPediatr Neurosurgpt_BR
dc.identifier.citationPediatric Neurosurgery. v. 45, n. 3, p. 198-204, 2009.pt_BR
dc.rights.holderCopyright 2009 S. Karger AG, Basel.pt_BR
dc.description.provenanceMade available in DSpace on 2015-11-27T13:15:17Z (GMT). No. of bitstreams: 1 pmed_19494564.pdf: 654499 bytes, checksum: 7af4325f689dfcfc13489265ff36e763 (MD5) Previous issue date: 2009en
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