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dc.contributor.authorEtus, V
dc.contributor.authorBelce, A
dc.date.accessioned2021-03-03T07:57:54Z
dc.date.available2021-03-03T07:57:54Z
dc.date.issued2003
dc.identifier.citationEtus V., Belce A., "Total sialic acid levels decrease in the periventricular area of infantile rats with hydrocephalus", CHILDS NERVOUS SYSTEM, cilt.19, sa.12, ss.825-828, 2003
dc.identifier.issn0256-7040
dc.identifier.otherav_14dee314-dfe6-4636-80f9-d43cfbeafb05
dc.identifier.othervv_1032021
dc.identifier.urihttp://hdl.handle.net/20.500.12627/19409
dc.identifier.urihttps://doi.org/10.1007/s00381-003-0832-z
dc.description.abstractObject. Besides mechanical damage done by the enlarging ventricles, biochemical impairment in the periventricular tissue represents an important factor resulting from or contributing to the pathogenesis of hydrocephalus. In this study the changes in periventricular region total sialic acid levels in the early stage of experimentally induced hydrocephalus were evaluated. Methods. Hydrocephalus was induced in 3-week-old rat pups by kaolin injection into the cisterna magna. Ten days after hydrocephalus induction rats were sacrificed and total sialic acid levels in the periventricular area were determined by the thiobarbituric acid method. Conclusion. Sialic acid, a vital component of brain gangliosides, which play an essential role in the transmission and storage of information in the brain, was found to be significantly decreased in the periventricular area of hydrocephalic infantile rats.
dc.language.isoeng
dc.subjectKlinik Tıp
dc.subjectPEDİATRİ
dc.subjectKLİNİK NEUROLOJİ
dc.subjectCERRAHİ
dc.subjectTıp
dc.subjectSağlık Bilimleri
dc.subjectDahili Tıp Bilimleri
dc.subjectÇocuk Sağlığı ve Hastalıkları
dc.subjectNöroloji
dc.subjectCerrahi Tıp Bilimleri
dc.subjectKlinik Tıp (MED)
dc.titleTotal sialic acid levels decrease in the periventricular area of infantile rats with hydrocephalus
dc.typeMakale
dc.relation.journalCHILDS NERVOUS SYSTEM
dc.contributor.department, ,
dc.identifier.volume19
dc.identifier.issue12
dc.identifier.startpage825
dc.identifier.endpage828
dc.contributor.firstauthorID170021


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