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TNF-alpha polymorphisms in Korean adult-onset Still's disease patients

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dc.contributor.authorSung, Yoon-Kyoung-
dc.contributor.authorSeong, Sang-Seokg-
dc.contributor.authorWoo, Jin-Hyun-
dc.contributor.authorLee, Myung-Ho-
dc.contributor.authorChung, Won-Tae-
dc.contributor.authorChoe, Jeong-Yoon-
dc.contributor.authorYoo, Dae-Hyun-
dc.date.accessioned2022-12-21T01:54:50Z-
dc.date.available2022-12-21T01:54:50Z-
dc.date.created2022-08-26-
dc.date.issued2008-07-
dc.identifier.issn1756-1841-
dc.identifier.urihttps://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/178162-
dc.description.abstractAim: To investigate the role of TNF-alpha promoter polymorphisms in the pathogenesis of Korean adult-onset Still's disease (AOSD) patients. Methods: DNA was isolated from blood samples collected from 58 patients with AOSD meeting Yamaguchi's criteria and 105 healthy controls. TNF-alpha promoter polymorphisms at positions -1013, -863, -857, -308 were analysed by polymerase chain reaction-restriction fragment length polymorphism method. Genotype, allele, and estimated haplotype frequencies were compared between the AOSD group and controls. Results: The genotype, allele distributions, and estimated haplotype frequencies of the TNF-alpha polymorphism between AOSD patients and controls were not significantly different. In addition, TNF-alpha polymorphisms did not appear to have an effect on the disease course of the Korean AOSD patients. Conclusion: Genetic polymorphisms of TNF-alpha do not play a significant role in the development or in their course of Korean AOSD patients.-
dc.language영어-
dc.language.isoen-
dc.publisherWILEY-
dc.titleTNF-alpha polymorphisms in Korean adult-onset Still's disease patients-
dc.typeArticle-
dc.contributor.affiliatedAuthorSung, Yoon-Kyoung-
dc.contributor.affiliatedAuthorYoo, Dae-Hyun-
dc.identifier.doi10.1111/j.1756-185X.2008.00351.x-
dc.identifier.scopusid2-s2.0-58049137453-
dc.identifier.wosid000266391300010-
dc.identifier.bibliographicCitationINTERNATIONAL JOURNAL OF RHEUMATIC DISEASES, v.11, no.2, pp.155 - 162-
dc.relation.isPartOfINTERNATIONAL JOURNAL OF RHEUMATIC DISEASES-
dc.citation.titleINTERNATIONAL JOURNAL OF RHEUMATIC DISEASES-
dc.citation.volume11-
dc.citation.number2-
dc.citation.startPage155-
dc.citation.endPage162-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaRheumatology-
dc.relation.journalWebOfScienceCategoryRheumatology-
dc.subject.keywordPlusNECROSIS-FACTOR-ALPHA-
dc.subject.keywordPlusSYSTEMIC-LUPUS-ERYTHEMATOSUS-
dc.subject.keywordPlusPROMOTER POLYMORPHISMS-
dc.subject.keywordPlusRHEUMATOID-ARTHRITIS-
dc.subject.keywordPlusANKYLOSING-SPONDYLITIS-
dc.subject.keywordPlusGENE POLYMORPHISMS-
dc.subject.keywordPlusASSOCIATION-
dc.subject.keywordPlusHLA-
dc.subject.keywordPlusMANIFESTATIONS-
dc.subject.keywordPlusSUSCEPTIBILITY-
dc.subject.keywordAuthoradult-onset Still&apos-
dc.subject.keywordAuthors disease-
dc.subject.keywordAuthorKorean-
dc.subject.keywordAuthorpolymorphism-
dc.subject.keywordAuthorTNF-alpha-
dc.identifier.urlhttps://onlinelibrary.wiley.com/doi/10.1111/j.1756-185X.2008.00351.x-
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