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Cited 17 time in webofscience Cited 25 time in scopus
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Role of Ca2+ Homeostasis Disruption in Rotavirus-Associated Seizures

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dc.contributor.authorYeom, Jung Sook-
dc.contributor.authorKim, Young-Soo-
dc.contributor.authorPark, Ji Sook-
dc.contributor.authorSeo, Ji-Hyun-
dc.contributor.authorPark, Eun Sil-
dc.contributor.authorLim, Jae-Young-
dc.contributor.authorPark, Chan-Hoo-
dc.contributor.authorWoo, Hyang-Ok-
dc.contributor.authorYoun, Hee-Shang-
dc.date.accessioned2022-12-26T23:17:44Z-
dc.date.available2022-12-26T23:17:44Z-
dc.date.issued2014-03-
dc.identifier.issn0883-0738-
dc.identifier.issn1708-8283-
dc.identifier.urihttps://scholarworks.gnu.ac.kr/handle/sw.gnu/19125-
dc.description.abstractRotavirus infection disturbs cellular Ca2+ homeostasis by triggering an increase in Ca2+ permeation. A theoretical link between Ca2+ dysregulation and seizures in patients with rotavirus gastroenteritis has been suggested, but no prior studies have investigated this relationship. To test our hypothesis that patients with rotavirus-associated seizures have greater Ca2+ homeostasis disruption than those without seizures, we compared clinical and laboratory dataincluding corrected total serum Ca2+ levelsbetween the 2 groups. Age, gender, maximum body temperature, day of admission, levels of electrolytes except Ca2+, blood pH, and urine ketone levels were not related to seizure occurrence. Significantly lower Ca2+ levels were found among the seizure (+) group (9.22 +/- 0.50 vs 9.66 +/- 0.46 mg/dL, P = .01). Although Ca2+ levels were within normal ranges and did not directly cause the seizures, our results provide preliminary evidence for a relationship between Ca2+ homeostasis disruption and seizures in rotavirus patients.-
dc.format.extent5-
dc.language영어-
dc.language.isoENG-
dc.publisherSAGE PUBLICATIONS INC-
dc.titleRole of Ca2+ Homeostasis Disruption in Rotavirus-Associated Seizures-
dc.typeArticle-
dc.publisher.location미국-
dc.identifier.doi10.1177/0883073812469052-
dc.identifier.scopusid2-s2.0-84894501342-
dc.identifier.wosid000331512300006-
dc.identifier.bibliographicCitationJOURNAL OF CHILD NEUROLOGY, v.29, no.3, pp 331 - 335-
dc.citation.titleJOURNAL OF CHILD NEUROLOGY-
dc.citation.volume29-
dc.citation.number3-
dc.citation.startPage331-
dc.citation.endPage335-
dc.type.docTypeArticle-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClasssci-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaNeurosciences & Neurology-
dc.relation.journalResearchAreaPediatrics-
dc.relation.journalWebOfScienceCategoryClinical Neurology-
dc.relation.journalWebOfScienceCategoryPediatrics-
dc.subject.keywordPlusAGE-DEPENDENT DIARRHEA-
dc.subject.keywordPlusACUTE GASTROENTERITIS-
dc.subject.keywordPlusAFEBRILE SEIZURES-
dc.subject.keywordPlusINFECTION-
dc.subject.keywordPlusCONVULSIONS-
dc.subject.keywordPlusANTIGENEMIA-
dc.subject.keywordPlusMANIFESTATIONS-
dc.subject.keywordPlusPATHOGENESIS-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusINCREASE-
dc.subject.keywordAuthorrotavirus-
dc.subject.keywordAuthorseizure-
dc.subject.keywordAuthorcalcium-
dc.subject.keywordAuthorenterotoxin-
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