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完整後設資料紀錄
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.advisor | 曹永魁 | |
dc.contributor.author | I-Jung Tsai | en |
dc.contributor.author | 蔡宜蓉 | zh_TW |
dc.date.accessioned | 2021-06-13T07:55:46Z | - |
dc.date.available | 2005-08-02 | |
dc.date.copyright | 2005-08-02 | |
dc.date.issued | 2005 | |
dc.date.submitted | 2005-07-23 | |
dc.identifier.citation | Al-Eisa A, Haider MZ, Srivastava BS. Angiotensin converting enzyme gene insertion/deletion polymorphism in idiopathic nephrotic syndrome in Kuwait Arab children. Scand J Urol Nephrol 2001; 35: 239-42
Alfiler CA, Roy LP, Doran T, et al. HLA-DRW7 and steroid responsive nephrotic syndrome of childhood. Clin Nephrol 1980; 14: 71-74 Bagga A, Sharma A, Srivastava RN. Levamisole therapy in corticosteroid dependent nephrotic syndrome. Pediatr Nephrol 1997; 11: 415-7 Barratt TM, Clark AGB. Minimal change nephrotic syndrome amd focal segmental lomerulosclerosis. In: Holliday MA, Barratt TM, Avner ED, editors: Pediatric nephrology. Baltimore: Williams and Wilkins; 1994. p.767-87 Bohrer MP, Deen WM, Robertson CR, Brenner BM. Mechanism of angiotensin II-induced proteinuria in the rat. Am J Physiol 1977; 233: F13-F21 Bustos C, Gonzalez E, Muley R, et al. Increase of tumour necrosis factor alpha synthesis and gene expression in peripheral blood mononuclear cells of children. Eur J Clin Invest 1994; 24: 799-805 Butanin L. Remission of membranoproliferative nephritis with angiotensin converting enzyme inhibition and receptor blockade. Pediatr Nephrol 2003; 18: 1119 Cambien F, Poirier O, Lecerf L, Evans A, Cambou JP, Arveiler D, Luc G, Bard JM, Bara L, Ricard S. Deletion polymorphism in the gene for angiotensin-converting enzyme is a potent risk factor for myocardial infarction. Nature 1992; 359: 641-644 Clark AG, Vaughan RW, Stephens HA, et al. Gene encoding the beta-chains of HLA-DR7 and HLA-DRW2 define major susceptibility determinants for idiopathic nephritic syndrome. Clin Sci (Lond) 1990; 78: 391-397 de Mouzon-Cambon A. Bouissou F, Dutau G, et al. HLA-DR7 in children with idiopathic nephritic syndrome. Correlation with atopy. Tissue Antigen 1981; 17: 518-524 Dixit M, Mansur A, Dixit N, Gilman J, Santarina L, Glicklich D. The role of ACE gene polymorphism in rapidity of progression of focal segmental glomerulosclerosis. J Postgrad Med 2002; 48: 266-269 Eisenbach GM, Van Liew JB, Boylan JW, Manz N, Muir P. Effect of angiotensin on the filtration of protein in the rat kidney: a micropuncture study. Kidney Int 1975; 8: 80-87 Fodde, R. and M. Losekoot. Mutation detection by denaturing gradient gel electrophoresis (DGGE). Hum Mutat 1994;3(2): 83-94 Huber, C. G., P. J. Oefner and G. K. Bonn. High-resolution liquid chromatography of oligonucleotides on nonporous alkylated styrene-divinylbenzene copolymers. Anal Biochem 1993;212(2): 351-8 Fernandez-lama P, Poch E, Oriola J, Botey A. Angiotensin-converting enzyme gene I/D polymorphism in essential hypertension and nephroangiosclerosis. Kidney Int 1998; 53: 1743-1747 Fogo A, Hawkins EP, Berry PL, Glick AD, Chiang ML, MacDonell RC Jr, Ichikawa I. Glomerular hypertrophy in minimal change disease predicts subsequent progression to focal glomerulosclerosis. Kidney Int 1990; 38: 115-123 Frishberg Y, Becker-Cohen R, Halle D, Feigin E, Eisenstein B, Halevy R, Lotan D, Juabeh I, Ish-Shalom N, Magen D, Shvil Y, Sinai-Treiman L, Drukker A. Genetic polymorphisms of the renin-angiotensin system and the outcome of focal segmental glomerulosclerosis in children. Kidney Int 1998; 54: 1843-1849 Garin EH, Blanchard DK, Matsushima K, Djeu JY. IL-8 production by peripheral blood mononuclear cells in nephrotic patients. Kidney Int 1994; 45: 1311-1317 Giangiacomo J, Cleary TG, Cole BR, et al. Serum immunoglobulins in the nephrotic syndrome. A possible cause of minimal change nephritic syndrome. N Engl J Med 1975; 293: 8-12 Gross E, Arnold N, Goette J, Schwarz-Boeger U, Kiechle M. A comparison of BRCA1 mutation analysis by direct sequencing, SSCP and DHPLC. Hum Genet 1999; 105: 72-78 Haack D, Scharerk, Asam-Taushcer A, Vecesei P. Glucocorticoid receptors in idiopathic nephrotic syndrome. Pediatr Nephrol 1999; 13: 653-6 Harden PN, Geddes C, Rowe PA, McIlroy JH, Boulton-Jones M, Rodger RS, Junor BJ, Briggs JD, Connell JM, Jardine AG. Polymorphisms in angiotensin converting enzyme gene and progression of IgA nephropathy. Lancet 1995; 345: 1540-1542 Hisanaga S, Kawagoe H, Yamamoto, et al. Nephrotic syndrome associated with recombinant interleukin-2. Nephron 1990; 54: 277-278 Hobenfellner K, Hunley TE, Brezinska R, et al. ACE I/D gene polymorphism predicts renal damage in congenital uropathies. Pediatr Nephrol 1999; 13: 514-8 International Study of Kidney Disease in Children. Nephrotic syndrome in children. Prediction of histopathology from clinical and laboratory characteristics at time of diagnosis. KI 1978, 13:159-65 Kashgarian M, Haslett TP, Seigel NJ. Lipoid nephrosis and focal sclerosis: distinct entities or spectrum of disease. Nephron 1974; 13: 105-108 Kim MS, Grupe WE. The management of primary glomerular disease: alternatives to steroid terapy. In: Edelmann CM, editor. Pediatric kidney diseases. Boston: Little Brown; 1992. p. 1355-80 Korbet SM, Schwartz MM, Lewis EJ. Primary focal segmental glomerulosclerosis: Clinical course and response to therapy. Am J Kidney Dis 1994; 23: 773-783 Lagrue G, Branellec A, Blanc C, et al. A vascular permeability factor in lymphocyte culture supernatants from patients with nephrotic syndrome. II. Pharmacological and physicochemical properties. Biomedicine 1975; 23(2): 74-75 Liu, W., D. I. Smith, K. J. Rechtzigel, et al. Denaturing high performance liquid chromatography (DHPLC) used in the detection of germline and somatic mutations. Nucleic Acids Res 1998;26(6): 1396-400 Lee DY, Kim W, Kang SK, Koh GY, Park SK. Angiotensin converting enzyme gene polymorphism in patients with minimal change nephrotic syndrome and focal segmental glojerulonephritis. Nephron 1997; 77: 471-3 Markoff, A., A. Savov, V. Vladimirov, et al. Optimization of single-strand conformation polymorphism analysis in the presence of polyethylene glycol. Clin Chem 1997;43(1): 30-3. Markoff, A., H. Sormbroen, N. Bogdanova, et al. Comparison of conformation-sensitive gel electrophoresis and single- strand conformation polymorphism analysis for detection of mutations in the BRCA1 gene using optimized conformation analysis protocols. Eur J Hum Genet 1998;6(2): 145-50. Marian AJ, Yu QT, Workman R, Greve G, Roberts R. Angiotensin- converting enzyme polymorphism in hypertrophic cardiomyopathy and sudden cardiac death. Lancet 1993; 342: 1085-1086 Maruyama K, Yoshida M, Nishio H, Shirakawa T, Kawamura T, Tanaka R, Nakamura H, Iijima K, Yoshikawa N. Polymorphisms of renin-angiotensin system genes in childhood IgA nephropathy. Pediatr Nephrol 2001; 16: 350-355 Matusaka T, Hymes J, Ichikawa I. Angiotensin in progressive renal diseases: theory and practice. J Am Soc Nephrol 1996; 7: 2025-2043 McEnery PT, Strife CF. Nephrotic syndrome in childhood. Management and treatment in patients with minimal change disease, mesangial proliferation, or focal glomeruloscelrosis. Pediatr Clin North Am 1982; 29: 874-894 Montane B, Abitbol C, CHandar J, Strauss J, Zilleruelo G. Novel therapy of focal glomerulosclerosis with mycophenolate and angiotensin blockade. Pediatr Nephrol 2003; 18: 772-7 Navis G, van der Kleij FG, de Zeeuw D, de Jong PE. Angiotensin- converting enzyme gene I/D polymorphism and renal disease. J Mol Med 1999; 77: 781-791 O'Donovan MC, Oefner PJ, Roberts SC, Austin J, Hoogendoorn B, Guy C, Speight G, Upadhyaya M, Sommer SS, McGuffin P. Blind analysis of denaturing high-performance liquid chromatography as a tool for mutation detection. Genomics 1998; 52: 44-49 Oktem F, Sirin A, Bilge I, Emre S, Agachan B, Ispir T. ACE I/D gene polymorphism in primary FSGS and steroid-sensitive nephrotic syndrome. Pediatr Nephrol 2004; 19: 384-389 Papp F, Friedman AL, Bereczki C, et al. Renin-angiotensin gene polymorphism in children with uremia and essential hypertension. Pediatr Nephrol 2003; 18: 150-4 Pardo R, Malaga S, Coto E, et al. Renin-angiotensin system polymorphisms and renal scarring. Pediatr Nephrol 2003; 18: 110-4 Pullmann R Jr., Lukac J, Skerenova M, et al. Association between systemic lupus erythematosus and insertion/deletion polymorphism of the angiotensin converting enzyme (ACE) gene. Clin Exp Rheumatol 1999; 17: 593-6 Richter, S. and A. Seth. One step direct detection of recurrent mutations in the breast cancer susceptibility gene, BRCA1. Int J Oncol 1998;12(6): 1263-7 Rigat B, Hurbert C, Alhenec-Gelas F, Cambien F, Corvol P, Soubrier F. An I/D polymorphism in the ACE gene accounting for half the variance of serum enzyme levels. J Clin Invest 1990; 86: 1343-6 Roy S, Pitcock JA. Idiopathic nephrosis in identical twins. Am J Dis Child 1971; 121: 428-439 Sahali D, Paklak A, Le Gouvello S, et al. Transcriptional and post-transcriptional alterations of IkappaNalpha in active minimal-change nephritic syndrome. J Am Soc Nephrol 2001; 12: 1648-1658 Salsdelli M, Cagnoli L, Candi P, et al. Cell mediated immunity in idiopathic glomerulonephritis. Clin Exp Immunol 1981; 46: 27-34 Sambrook J, Fritisch F, Maniatis T. Molecular cloning: a laboratory manual. 2nd ed. New York: Cold Spring Harbor Laboratory. 1989 Schwartz MM, Korbet SM. Primary focal segmental glomeruloscelrosis: Pathology, hostologic variants, and pathogenesis. Am J Kidney Dis 1993; 22: 874-883 Shalhoub RJ. Pathogenesis of lipoid nephrosis: a disorder of T cell function. Lancet 1074; ii: 556-559 Sharples PM, Poulton K, White RHR. Steroid responsive nephritic syndrome is more common in Asians. Arch Dis Child 1985; 60: 1014-1017 Sobel AT, Brenellec AL, Blanc CJ, Largue GA. Physiochemical characterization of a vasculat permeability factor, produced by Con A stimulated human lymphocytes. J Immunol 1977; 119: 1230-1234 Srivastava RN, Mayekar G, Anand R, et al. Nephrotic syndrome in Indian children. Arch Dis Child 1975; 50: 626-680 Takeda A, Ohgushi H, Niimura F, Matsutani H. Long-term effects of immunosuppressants in steroid-dependent nephrotic syndrome. Pediatr Nephrol 1998; 12: 746-50 Taube D, Brown Z, Williams DG. Impaired lymphocyte and suppressor cell function in minimal change nephropathy, membranous nephropathy and focal glomeruloscelrosis. Clin Nephrol 1984; 22: 176-182 Traynor A, Kruzel T, Samuelson E, Kanwar Y. Minimal change glomerulopathy and glomerular visceral epithelial hyperplasia associated with alpha-interferon therapy for cutaneous T-cell lymphoma. Nephron 1994; 67: 94-100 Van Der Berg JG, Aten J, Chand MA, et al. Interleukin-4 and interleukin-13 act on glomerular visceral epithelial cells. J Am Soc Nephrol 2000; 11: 413-422 Van Den Berg JG, Aten J, Annink C, et al. Interleukin-4 and -13 promote basolateral secretion of H+ and cathepsin L by glomerular epithelial cells. Am J Physiol Renal Physiol 2002; 282: F26-F33 Villard E, Soubrier F. Molecular biology and genetic of the angiotensin-I-converting enzyme gene: potential implication in cardiovascular diseases. Cardiovasc Res 1996; 32: 999-1007 Vleming LJ, van Kooten C, van Dijk M, Hollander DA, Paape ME, Westendorp RG, van Es LA. The D-allele of the ACE gene polymorphism predicts a stronger antiproteinuric response to ACE inhibitors. Nephrology 1998; 4, 143-149 Wagner, T. M., R. A. Moslinger, D. Muhr, et al. BRCA1-related breast cancer in Austrian breast and ovarian cancer families: specific BRCA1 mutations and pathological characteristics. Int J Cancer 1998;77(3): 354-60 White CT, Macpheron CF, Hurley RM, Matsell DG. Antiproteinuric effects of enalapril and losartan: a pilot study. Pediatr Nephrol 2003; 18: 1038-43 White RHR. The familial nephrotic syndrome. A European survey. Clin Nephrol 1973; 1: 215-219 Wolf G, Neilson EG. Angiotensin II as a renal growth factor. J Am Soc Nephrol 1993; 3: 1531-40 Yan K, Nakahara K, Awa S, et al. The increase of memory T cell subsets in children with idiopathic nephritic syndrome. Nephron 1998; 79: 274-278 Yap HK, Cheumg W, Murugasu B, et al. Th1 and Th2 cytokine mRNA profiles in childhood nephritic syndrome: evidence for increased IL-13 mRNA expression in relapse. J Am Soc Nephrol 1999; 10: 529-537 Yokoyama H, Kida H, Abe T, et al. Impaired immunoglobulin G production in minimal change nephritic syndrome in adults. Clin Exp Immunol 1987; 70: 110-115 Xiao, W. and P. J. Oefner. Denaturing high-performance liquid chromatography: A review. Hum Mutat 2001;17(6): 439-74 | |
dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/36280 | - |
dc.description.abstract | 原發性腎病症候群(idiopathic nephrotic syndrome)為兒童常見的腎臟方面的疾病,主要的表現為蛋白尿(proteinuria)、白蛋白降低(hypoalbuminemia)、高血脂 (hyperlipidemia)以及水腫(edema)。根據International Study of Kidney Disease in Children,罹患腎病症候群的兒童中有76%在病理表現上為微小性變化(minimal change)。大部分在病理變化上呈現微小性變化的腎病症候群的兒童,對於類固醇 (prednisolone)的標準療程具有很好的反應以及預後。有80%的病童可以達到完全緩解的情形(complete remission),不過有40-50%的比例有frequent relapse的現象。而在治療的期間,隨著對類固醇反應不同,大致可以分為類固醇敏感(steroid sensitive)、依賴(steroid-dependent) 以及抗性(steroid-resistant)。而根據病理切片的結果,若為局部巢狀腎絲球硬化(focal segmental glomerulosclerosis, FSGS),則對於類固醇的治療反應不佳,並且有可能進行成末期腎病變(end-stage renal failure)。若病童屬於類固醇依賴(steroid-dependent)的情形,可能就需要高劑量的類固醇治療,甚至需要免疫抑制劑(immunosuppressant)的治療,才能改善蛋白尿的情形。腎絲球硬化(glomerulosclerosis)在某種程度上與動脈硬化相似,會造成腎臟功能逐漸喪失,而renin-angiotensin system (RAS)為引起動脈硬化的一個重要因子,其中以血管轉化酶 (angiotensin converting enzyme)的基因多重性佔了重要的一個角色。
Renin-angiotensin aldosterone system(RAAS)在心血管疾病和腎臟的生理病理學上具有關鍵性的角色,血管轉化酶(angiotensin converting enzyme)的基因多重性,對於circulating 和cellular ACE的濃度,有顯著的影響。血管轉化酶(ACE)由ACE gene轉譯而來,而ACE gene具有diallelic polymorphism,此gene位於chromosome 17q23處,在intron16的地方有287 bp DNA的變異。 一般認為,此種insertion/deletion polymorphism決定血液中50% ACE的level 。ACE 基因I/D多重性於孩童腎病症候之研究僅有極少數報告,韓國學者發現局部巢狀腎絲球硬化孩童較多具DD基因型,而認為可能是類固醇治療反應不佳及發展成慢性腎衰竭之危險因素,科威特學者則發現阿拉伯孩童的腎病症候群(包括微小變化者)有較多的DD基因型,因此,此基因型與疾病之嚴重度(如高血壓、血尿及腎衰竭)有相關性。 本實驗的目的在於探討血管轉化酶基因的多重性與腎病症候群和其對類固醇治療反應的關聯性,我們將利用較新、敏感度更高的方法變性高效能液態色層分析(automatic denaturing high performance liquid chromatography system, DHPLC),來取代傳統的電泳,對於血管轉化酶基因多重性去作更進一步的分析。 共有59位臨床上診斷為原發性腎病症候群的病童加入本實驗,我們另外收集80位正常國小學齡兒童(6歲-12歲),其無腎臟疾病以及其他病史的檢體,作為基因分析中控制組的比較與對照。我們將59位病童根據其臨床表現以及對類固醇的治療反應分成兩組:SS組主要以對類固醇反應有效的病童,包含不常反覆發作(infrequent)或是反覆發作 (frequent)的復發者(relapsers);而non-SS組則主要包含類固醇抗性以及類固醇依賴的病童。而利用變性高效能液態色層分析去分析血管轉化酶基因的多重性,其中基因型為DD佔31位、ID為6位、II為22位病童。而臨床上的表現方面,除了在non-SS組有三酸甘油酯顯著增高的情形之外,其他包括發病年齡、收縮壓與舒張壓的變化、腎臟功能、白蛋白以及補體C3等等在兩組比較上,並無顯著性的差異。在基因分析中,原發性腎病症候群的兒童在血管轉化酶多重性中DD基因型的表現顯著的較對照組多(DD vs. non-DD; p<0.001);具D-allele的基因型也較對照組多(D-allele + vs. D-allele -; p<0.001)。其中在次族群分析中,原發性腎病症候群的兒童具DD基因型比上具ID或II基因型也較對照組多(DD vs. ID; DD vs. II; p均<0.001)。在59位為原發性腎病症候群的病童中,DD基因型在non-SS組在比例上有顯著增高(p=0.026),而具有D-allele的表現在non-SS組亦有顯著增加的情形(p=0.024)。 我們發現在原發性腎病症候群的兒童在血管轉化酶多重性中DD基因型的表現及具D-allele的基因型顯著的較對照組多。而在類固醇抗性以及類固醇依賴的病童中,有較高比例具有DD基因型和D-allele。因此,我們認為在腎病症候群的病童中,具有DD基因型者較有可能為屬於類固醇抗性以及類固醇依賴,也因此血管張力素(angiotensin II)在腎病症候群的病童對類固醇治療反應上,可能扮演一重要角色。 | zh_TW |
dc.description.abstract | Nephrotic syndrome is a common renal disease in children and it is defined as proteinuria, hypolbuminemia, hyperlipidemia and edema. According to the study from International Study of Kidney Disease in Children, 76.6% showed minimal change disease in nephrotic syndrome in children. Most patients with minimal change proven by renal biopsy have a good response after a standard course of prednisolone treatment. A complete remission is induced in about 80% cases and 40-50% of these relapse frequently. According to the biopsy results, patients with focal segmental glomerulosclerosis (FSGS) respond poorly to steroid therapy and tend to progress end-stage renal failure compared with patients with minimal change nephrotic syndrome (MCNS). In patients with steroid-dependent nephrotic syndrome (SDNS), in addition to high dosage of steroid therapy, some patients may need immunosuppressants to improve proteinuria. Glomerulosclerosis, leading to progressive loss of renal function in various kidney diseases, is analogous in some aspects of atherosclerosis including a regulatory role of the renin-angiotensin system (RAS), especially in angiotensin-converting enzyme (ACE) gene polymorphism.
The variable steroid response of children with idiopathic nephrotic syndrome has not been explained. Angiotensin II may induce proteinuria, while angiotensin converting enzyme (ACE) inhibitors may reduce proteinuria and even get remission in nephrotic syndrome. Whether angiotensin II related to steroid threshold in difficult steroid dependent and steroid resistant nephrotic syndrome remains undetermined. The genotypes in ACE gene polymorphism can influence plasma and tissue angiotensin II levels. ACE gene insertion/deletion (I/D) polymorphism with DD genotype is a risk factor for cardiovascular disease and renal disease. ACE gene has been identified I/D polymorphism on the ACE locus on chromosome 17q23 of a 287-basepair fragment on intron 16. Lee et al. reported a markedly different distribution of ACE genotypes in FSGS and MCNS in their Korean patients in which the DD genocypte was significantly associated with FSGS. Al-Eisa et al. described that an association of the D-allele of the ACE gene I/D polymorphism with the clinical manifestation in nephrotic syndrome in Kuwaiti children. The purpose of this study was to examine the association between the ACE I/D genotype distribution in children with nephrotic syndrome and the response to steroid therapy. We used the newly developed automatic denaturing high performance liquid chromatography system (DHPLC) instead of gel electrophoresis to analyze PCR amplicons. A total of 59 children diagnosed as nephrotic syndrome at the age of 1 to 10 year-old were recruited in this study. Eighty children without renal diseases were also recruited as control group in genetic analysis. The patients were divided into 2 groups according to their clinical response to steroid: SS group including infrequent and frequent relapsers and non-SS group including steroid resistant (SR) and steroid dependent (SD) patients. Clinical parameters including the age of onset, systolic and diastolic blood pressure, renal function, albumin and C3 level showed no difference between two groups except for significantly elevated triglyceride in the non-SS group. In genetic study for ACE I/D genotype distribution, patients had significantly higher percentage to have DD genotype (DD vs. non-DD; p<0.001) and D-allele (D-allele + vs. D-allele -; p<0.001) than control group. Furthermore, patients also had significantly higher percentage to have DD genotype than ID or II genotype than control group. Among 59 patients with nephritic syndrome, the distribution of DD, ID and II genotype was 52.5% (31/59), 10.2% (6/59) and 37.3% (22/59), respectively. DD genotype showed significantly higher in the non-SS group than SS group (p=0.026). And non-SS group also had significantly higher incidence in D-allele presentation than SS group (p=0.024). Our data shows that patients with nephrotic syndrome had higher rate to have DD genotype and D allele than control group. Among these patients, SD and SR patients had higher percentage of D-allele and DD genotype in ACE gene polymorphism. This finding suggests that DD genotype may indeed be a risk factor for steroid dependence and steroid resistance, and angiotensin II may be involved in the steroid response of idiopathic nephrotic syndrome. | en |
dc.description.provenance | Made available in DSpace on 2021-06-13T07:55:46Z (GMT). No. of bitstreams: 1 ntu-94-P92421009-1.pdf: 635013 bytes, checksum: 1f004afc61a40bf07c798727fb910bab (MD5) Previous issue date: 2005 | en |
dc.description.tableofcontents | 目錄 (Contents)
一、中文摘要 (Chinese Abtract)----------------3-4 二、緒論 (Introduction)---------------------5-12 三、研究方法與材料 (Methods and Materials)--13-18 四、結果 (Results)-------------------------19-20 五、討論 (Discussion)----------------------21-22 六、展望 (Perspection)------------------------23 七、英文摘要 (English Abtract)-------------24-25 八、參考文獻 (References)------------------26-31 九、表目錄及圖目錄 (Tables and Figures Index)-------------32-39 十、附錄 (Appendix)------------------------40-48 | |
dc.language.iso | zh-TW | |
dc.title | 原發性腎病症候群與血管轉化酶基因多重性之關聯 | zh_TW |
dc.title | Angiotensin converting enzyme gene polymorphism in idiopathic nephrotic syndrome | en |
dc.type | Thesis | |
dc.date.schoolyear | 93-2 | |
dc.description.degree | 碩士 | |
dc.contributor.coadvisor | 謝豐舟 | |
dc.contributor.oralexamcommittee | 江伯倫 | |
dc.subject.keyword | 血管轉化酶,基因的多重性,腎病症候群,類固醇依賴, | zh_TW |
dc.subject.keyword | ACE gene polymorphism,nephrotic syndrome,steroid dependent, | en |
dc.relation.page | 48 | |
dc.rights.note | 有償授權 | |
dc.date.accepted | 2005-07-25 | |
dc.contributor.author-college | 醫學院 | zh_TW |
dc.contributor.author-dept | 臨床醫學研究所 | zh_TW |
顯示於系所單位: | 臨床醫學研究所 |
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