中國醫藥大學機構典藏 China Medical University Repository, Taiwan:Item 310903500/29321
English  |  正體中文  |  简体中文  |  全文筆數/總筆數 : 29490/55136 (53%)
造訪人次 : 1998055      線上人數 : 435
RC Version 7.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
搜尋範圍 查詢小技巧:
  • 您可在西文檢索詞彙前後加上"雙引號",以獲取較精準的檢索結果
  • 若欲以作者姓名搜尋,建議至進階搜尋限定作者欄位,可獲得較完整資料
  • 進階搜尋
    主頁登入上傳說明關於CMUR管理 到手機版
    請使用永久網址來引用或連結此文件: http://ir.cmu.edu.tw/ir/handle/310903500/29321


    題名: Objective evidence of a high prevalence of renal damage in women with type 2 diabetes by technetium-99m DMSA renal cortex scan findings
    作者: Wu, HC;Huang, WS;Lin, CC;Lee, CC;Kao, A
    貢獻者: 附設醫院泌尿部;China Med Coll Hosp, Dept Urol, Taichung 404, Taiwan;China Med Coll Hosp, Dept Family Med, Taichung 404, Taiwan;China Med Coll Hosp, Dept Med Res, Taichung 404, Taiwan;China Med Coll Hosp, Dept Nucl Med, Taichung 404, Taiwan;Triserv Gen Hosp, Natl Def Med Ctr, Dept Nucl Med, Taipei, Taiwan
    日期: 2003
    上傳時間: 2010-09-24 14:31:56 (UTC+8)
    出版者: ELSEVIER SCIENCE INC
    摘要: Congenital heart disease (CHD) is a common cardiac defect found in infants and children. Despite advances in diagnosis and treatment, our understanding of the causative mechanism and etiology of CHD is limited. To determine the genetic etiology of CHD, we selected 11 consecutive short tandem-repeat polymorphic (STRP) markers located in the interval of the 22q11.2 region to perform genotype analysis on a large number of CHD patients (>120) and their normal relatives (>220). The results show that as regards the distribution of allelic size and frequency of these STRP markers, there were no significant differences between the CHD patients and the normal volunteers. This indicates that there is no linkage disequilibrium with these markers in CHD. In the level of heterozygosity for each marker in non-syndromic CHD and conotruncal heart defect (CTD), there were no significant differences between the two populations. In syndromic CHD, the level of heterozygosity for D22S1648 was significantly lower than that observed in the unaffected population (chi(2) = 11.25; P = 0.001). This suggests that there may be a deletion at the D22S1648 locus, and the low heterozygosity of D22S1648 indicates that this marker can be used as a genetic marker for detecting microdeletions in 22q11.2. With the use of fluorescence in situ hybridization (FISH) and real-time quantitative polymerase chain reaction (PCR) performed on syndromic patients, we confirmed the molecular results. (C) 2003 Wiley-Liss, Inc.
    關聯: UROLOGY 61(1):50-54
    顯示於類別:[台中附設醫院] 期刊論文

    文件中的檔案:

    沒有與此文件相關的檔案.



    在CMUR中所有的資料項目都受到原著作權保護.

    TAIR相關文章

     


    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - 回饋