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完整後設資料紀錄
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.advisor | 楊偉勛(Wei-Shiung Yang) | |
dc.contributor.author | Hui-Hsuan Hsieh | en |
dc.contributor.author | 謝慧萱 | zh_TW |
dc.date.accessioned | 2021-06-16T02:35:36Z | - |
dc.date.available | 2015-12-17 | |
dc.date.copyright | 2015-09-25 | |
dc.date.issued | 2015 | |
dc.date.submitted | 2015-07-27 | |
dc.identifier.citation | 1. Weetman, A.P., Graves' disease. New England Journal of Medicine, 2000. 343(17): p. 1236-1248.
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Huber, The etiology of autoimmune thyroid disease: a story of genes and environment. Journal of autoimmunity, 2009. 32(3): p. 231-239. 42. Brix, T.H., et al., Evidence for a Major Role of Heredity in Graves’ Disease: A Population-Based Study of Two Danish Twin Cohorts 1. The Journal of Clinical Endocrinology & Metabolism, 2001. 86(2): p. 930-934. 43. Barlow, A., et al., Association of HLA‐DQA1* 0501 with Graves’ disease in English Caucasian men and women. Clinical endocrinology, 1996. 44(1): p. 73-77. 44. Yanagawa, T., et al., Human histocompatibility leukocyte antigen-DQA1* 0501 allele associated with genetic susceptibility to Graves' disease in a Caucasian population. The Journal of Clinical Endocrinology & Metabolism, 1993. 76(6): p. 1569-1574. 45. Chen, P.-L., et al., Comprehensive genotyping in two homogeneous Graves' disease samples reveals major and novel HLA association alleles. PLoS One, 2011. 6(1): p. e16635. 46. 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Zaletel, K., et al., The influence of the exon 1 polymorphism of the cytotoxic T lymphocyte antigen 4 gene on thyroid antibody production in patients with newly diagnosed Graves' disease. Thyroid, 2002. 12(5): p. 373-376. 53. Zaletel, K., et al., Thyroid autoantibody production is influenced by exon 1 and promoter CTLA‐4 polymorphisms in patients with Hashimoto's thyroiditis. International journal of immunogenetics, 2006. 33(2): p. 87-91. 54. Vieland, V.J., et al., A multilocus model of the genetic architecture of autoimmune thyroid disorder, with clinical implications. The American Journal of Human Genetics, 2008. 82(6): p. 1349-1356. 55. Armitage, R.J., et al., Human B cell proliferation and Ig secretion induced by recombinant CD40 ligand are modulated by soluble cytokines. The Journal of Immunology, 1993. 150(9): p. 3671-3680. 56. Arpin, C., et al., Generation of memory B cells and plasma cells in vitro. Science, 1995. 268(5211): p. 720-722. 57. Tomer, Y., et al., A New Graves Disease–Susceptibility Locus Maps To Chromosome 20q11. 2. The American Journal of Human Genetics, 1998. 63(6): p. 1749-1756. 58. Tomer, Y., E. Concepcion, and D.A. Greenberg, AC/T single-nucleotide polymorphism in the region of the CD40 gene is associated with Graves' disease. Thyroid, 2002. 12(12): p. 1129-1135. 59. Pearce, S.H., et al., Further evidence for a susceptibility locus on chromosome 20q13. 11 in families with dominant transmission of Graves disease. American journal of human genetics, 1999. 65(5): p. 1462. 60. Kim, T.Y., et al., AC/T polymorphism in the 5'-untranslated region of the CD40 gene is associated with Graves' disease in Koreans. Thyroid, 2003. 13(10): p. 919-925. 61. Ban, Y., et al., Association of a C/T single-nucleotide polymorphism in the 5'untranslated region of the CD40 gene with Graves' disease in Japanese. Thyroid, 2006. 16(5): p. 443-446. 62. Kurylowicz, A., et al., Association of CD40 gene polymorphism (C-1T) with susceptibility and phenotype of Graves' disease. Thyroid, 2005. 15(10): p. 1119-1124. 63. MUKAI, T., et al., AC/T polymorphism in the 5'untranslated region of the CD40 gene is associated with later onset of Graves' disease in Japanese. Endocrine journal, 2005. 52(4): p. 471-477. 64. Cloutier, J.-F. and A. Veillette, Cooperative inhibition of T-cell antigen receptor signaling by a complex between a kinase and a phosphatase. The Journal of experimental medicine, 1999. 189(1): p. 111-121. 65. Velaga, M., et al., The codon 620 tryptophan allele of the lymphoid tyrosine phosphatase (LYP) gene is a major determinant of Graves’ disease. The Journal of Clinical Endocrinology & Metabolism, 2004. 89(11): p. 5862-5865. 66. Criswell, L.A., et al., Analysis of families in the multiple autoimmune disease genetics consortium (MADGC) collection: the PTPN22 620W allele associates with multiple autoimmune phenotypes. 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dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/53986 | - |
dc.description.abstract | 由甲狀腺亢進引起的葛瑞夫茲氏症,約佔了族群裡的1.0%-1.6%,抗甲狀腺藥物是最基本的治療,但藥物引發之顆粒性白血球低下則是一嚴重的副作用。在本篇論文中,我們以臺大醫院收案之服用抗甲狀腺藥物引發之顆粒性白血球低下患者共42人為研究對象,使用1208位葛瑞夫茲氏病患者做為對照組進行直接偵測人類白血球抗原基因分型及單一核甘酸多型性全基因體相關分析,結果發現到在HLA-B*38:02及HLA-DRB1*08:03兩個對偶基因對於引發顆粒性白血球低下具有高度相關性(Armitage trend Pcombined = 6.75 × 10-32)及(Pcombined = 1.83 × 10-9),全基因組相關分析也顯示出在此兩區域出現相同的訊號。評估帶有此兩個對偶基因比沒有帶有此對偶基因容易引發顆粒性白血球低下分別約為21.48倍(95%信賴區間=11.13-41.48)及6.13倍(95%信賴區間=3.28-11.46);研究顯示同時帶HLA-B*38:02及HLA-DRB1*08:03兩個對偶基因其引發顆粒性白血球低下的風險更增加至48.41倍(Pcombined = 3.32 × 10-21, 95% 信賴區間= 21.66-108.22)。此次研究結果對於因抗甲狀腺藥物引發之顆粒性白血球低下的淺在的致病風險將會有很大的幫助。 | zh_TW |
dc.description.abstract | Graves’ disease is the leading cause of hyperthyroidism affecting 1.0-1.6% of the population. Anti-thyroid drugs are the treatment cornerstone, but may causelife-threatening agranulocytosis.
Here we conduct a two-stage association study on two separate subject sets (in total 42 agranulocytosis cases and 1,208 Graves’ disease controls), using direct humanleukocyte antigen genotyping and SNP-based genome-wide association study. Wedemonstrate HLA-B*38:02 (Armitage trend Pcombined = 6.75 × 10-32) andHLA-DRB1*08:03 (Pcombined = 1.83 × 10-9) as independent susceptibility loci. The genome-wide association study identifies the same signals. Estimated odds ratios for these two loci comparing effective allele carriers to non-carriers are 21.48 (95% confidence interval = 11.13-41.48) and 6.13 (95% confidence interval = 3.28-11.46), respectively. Carrying both HLA-B*38:02 and HLA-DRB1*08:03 increases odds ratio to 48.41 (Pcombined = 3.32 × 10-21, 95% confidence interval = 21.66-108.22). Our results could be useful for anti-thyroid-induced agranulocytosis and potentially for agranulocytosis caused by other chemicals. | en |
dc.description.provenance | Made available in DSpace on 2021-06-16T02:35:36Z (GMT). No. of bitstreams: 1 ntu-104-P02448007-1.pdf: 3644027 bytes, checksum: 16e40b47ac3c56ebda0eaa4ddb5ce442 (MD5) Previous issue date: 2015 | en |
dc.description.tableofcontents | 論文口試委員審定書 i
中文摘要 ii 英文摘要 iii 目錄 iv 圖目錄 vi 表目錄 vii 第一章 緒論 1 1.1葛瑞夫茲氏病(Graves’ disease, GD) 1 1.1.1葛瑞夫茲氏病簡介 1 1.1.2 葛瑞夫茲氏病之臨床表徵 1 1.1.2.1葛瑞夫茲氏病典型表徵 2 1.1.2.2葛瑞夫茲氏病綜合性表徵 4 1.1.3葛瑞夫茲氏病之診斷 4 1.1.3.1 生化學檢驗 4 1.1.3.2影像學檢驗 4 1.1.4葛瑞夫茲氏病之治療 5 1.1.4.1口服抗甲狀腺藥物 5 1.1.4.1.1 藥物種類 5 1.1.4.1.2藥物化學結構 6 1.1.4.1.3 藥物作用機制 6 1.1.4.1.4 藥物副作用 6 1.1.4.2 甲狀腺機能亢進治療 7 1.1.4.3 症狀治療 7 1.2 抗甲狀腺藥物引發顆粒性白血球低下 8 1.2.1顆粒性白血球低之定義 8 1.2.2顆粒性白血球低下之臨床症狀 8 1.2.3顆粒性白血球低下之治療 8 1.3葛瑞夫茲氏病與基因 11 1.3.1免疫調節基因 11 1.3.2甲狀腺調控基因 12 1.4 研究動機 13 第二章 材料與方法 13 2.1研究材料 13 2.2 DNA 萃取 16 2.3 直接HLA基因定序 (Direct HLA genotyping) 16 2.3.1 Dynal RELI SSO typing 16 2.3.2 Gold SSP HLA-DPB1 High-resolution 17 2.3.3 LABType SSO 17 2.3.4 SeCore HLA Sequence-Based Typing 17 2.4 全基因體相關研究(genome-wide association study, GWAS ) 17 2.4.1 全基因體相關研究簡介 17 2.4.2 基因型鑑定(Genome-wide SNP genotyping) 18 2.4.3 品質管控(Quality control) 18 2.4.4 統計分析(Statistical analysis) 18 第三章 結果 21 3.1 直接HLA基因定序 21 3.1.1直接HLA 基因定序分析結果 21 3.1.2 HLA-B*38:02與HLA-DRB1*08:03為兩個獨立影響之對偶基因 21 3.2 全基因組相關分析結果 25 第四章 討論 29 參考文獻 31 附錄一 39 附錄二 45 | |
dc.language.iso | zh-TW | |
dc.title | 抗甲狀腺藥物引發顆粒性白血球低下之遺傳學研究 | zh_TW |
dc.title | Genetic Study of Anti thyroid Drug-Induced Agranulocytosis | en |
dc.type | Thesis | |
dc.date.schoolyear | 103-2 | |
dc.description.degree | 碩士 | |
dc.contributor.coadvisor | 陳沛隆(Pei-Lung Chen) | |
dc.contributor.oralexamcommittee | 張天鈞(Tien-Chun Chang) | |
dc.subject.keyword | 葛瑞夫茲氏病,抗甲狀腺藥物,顆粒性白血球低下,直接偵測 人類白血球抗原基因分型,全基因體相關研究, | zh_TW |
dc.subject.keyword | Grave’s disease,Anti-thyroid drugs,agranulocytosis,direct human leukocyte antigen genotyping,genome-wide association study, | en |
dc.relation.page | 48 | |
dc.rights.note | 有償授權 | |
dc.date.accepted | 2015-07-27 | |
dc.contributor.author-college | 醫學院 | zh_TW |
dc.contributor.author-dept | 分子醫學研究所 | zh_TW |
顯示於系所單位: | 分子醫學研究所 |
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