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베체트병 환자에서 TNF-α와 TNF 수용체 유전자의 다양성
서욱장 ( Wook Jang Seo ),김용길 ( Yong Gil Kim ),양석균 ( Suk Kyun Yang ),박경숙 ( Kyung Sook Park ),이창근 ( Chang Keun Lee ),유빈 ( Bin Yoo ),문희범 ( Hee Bum Mon ) 대한류마티스학회 2007 대한류마티스학회지 Vol.14 No.2
Objective: TNF-α has a pivotal role in the development of inflammation on mucous lesion in Behcet`s disease like Crohn`s disease. We examined three single nucleotide polymorphisms (SNPs) of TNF receptor gene of intestinal Behcet`s disease and Behcet`s disease without gastrointestinal involvement. Methods: DNA of peripheral blood samples was obtained from 43 patients with intestinal Behcet`s disease, 59 patients with Behcet`s disease without gastrointestinal involvement and 60 healthy controls. After polymerase chain reaction (PCR), we examined SNPs of TNF-α gene (-308, -238) and TNF receptor gene (-1493, -196, -1466) by SNaPshot assay. We also analyzed reconstruction of haplotypes of three TNF receptor genes. Results: No significant difference was observed in the distribution of TNF-α gene (-308, -238) and TNF receptor gene (-1493, -196, -1466) polymorphisms among the groups. Haplotype reconstruction analysis of three TNF receptor genes showed difference in allele group of (T-T-G) (-1493/-196/-1493) between patients with intestinal Behcet`s disease and Behcet`s disease without gastrointestinal involvement (p<0.05). However, other allele groups revealed no difference among the groups. Conclusion: The role of TNF-α gene (-308, -238) polymorphisms and TNF receptor gene (-1493, -196, -1466) polymorphisms in the pathogenesis of Behcet`s disease is not supported by this data. Haplotype reconstruction analysis showed that haplotype of T-T-G (TNFR2, -1493/-196/-1466) in Behcet`s disease may have protective effect on gastrointestinal involvement of this disease.
서욱장,정선미,고수진,이창근,김재승,임주혁,유빈,문희범 대한핵의학회 2003 핵의학 분자영상 Vol.37 No.5
Purpose: We describe a 54-year-old woman with systemic lupus erythematosus (SLE) who suddenly presented with chorea and had positive antiphospholipid antibodies. F-18 FDG PET showed abnormally increased glucose metabolism in bilateral putamen and primary motor cotex. Tc-99m ECD SPECt also showed abnormally increased regional cerebral blood flow in bilateral putamen. She was treated with corticosteroid and aspirin after which the symptoms improved. Four months later, follow up F-18 FDG PET showed improvement with resolution of hypermetabolism in bilateral putamen. This case suggests that striatal hypermetabolism is associated with chorea in SLE.