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完整後設資料紀錄
DC 欄位 | 值 | 語言 |
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dc.contributor.advisor | 李建南(Chien-Nan Lee) | |
dc.contributor.author | Ding-Ting Chen | en |
dc.contributor.author | 陳玎婷 | zh_TW |
dc.date.accessioned | 2021-07-09T15:53:35Z | - |
dc.date.available | 2024-08-28 | |
dc.date.copyright | 2019-08-28 | |
dc.date.issued | 2019 | |
dc.date.submitted | 2019-08-12 | |
dc.identifier.citation | 1. American Diabetes, A., 2. Classification and Diagnosis of Diabetes: Standards of Medical Care in Diabetes-2018. Diabetes Care, 2018. 41(Suppl 1): p. S13-S27.
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Sorlie, T., et al., Gene expression patterns of breast carcinomas distinguish tumor subclasses with clinical implications. Proc Natl Acad Sci U S A, 2001. 98(19): p. 10869-74. 45. Wierstra, I., & Alves, J. , FOXM1, a typical proliferation-associated transcription factor. Biological Chemistry,. 2007. 388(12). doi:10.1515/bc.2007.159 46. Krupczak-Hollis, K., et al., The mouse Forkhead Box m1 transcription factor is essential for hepatoblast mitosis and development of intrahepatic bile ducts and vessels during liver morphogenesis. Dev Biol, 2004. 276(1): p. 74-88. 47. Kim, I.M., et al., The forkhead box m1 transcription factor is essential for embryonic development of pulmonary vasculature. J Biol Chem, 2005. 280(23): p. 22278-86. 48. Ramakrishna, S., et al., Myocardium defects and ventricular hypoplasia in mice homozygous null for the Forkhead Box M1 transcription factor. Dev Dyn, 2007. 236(4): p. 1000-13. 49. Gregg, B.E., et al., Formation of a human beta-cell population within pancreatic islets is set early in life. J Clin Endocrinol Metab, 2012. 97(9): p. 3197-206. 50. Bonner-Weir, S., Life and Death of the Pancreatic  Cells. TEM, 2000. Vol. 11, No. 9,. 51. Zhang, H., et al., Gestational diabetes mellitus resulting from impaired beta-cell compensation in the absence of FoxM1, a novel downstream effector of placental lactogen. Diabetes, 2010. 59(1): p. 143-52. 52. Zhang, H., et al., The FoxM1 transcription factor is required to maintain pancreatic beta-cell mass. Mol Endocrinol, 2006. 20(8): p. 1853-66. 53. Reers, C., et al., Impaired islet turnover in human donor pancreata with aging. Eur J Endocrinol, 2009. 160(2): p. 185-91. 54. Ackermann Misfeldt, A., R.H. Costa, and M. Gannon, Beta-cell proliferation, but not neogenesis, following 60% partial pancreatectomy is impaired in the absence of FoxM1. Diabetes, 2008. 57(11): p. 3069-77. 55. Davis, D.B., et al., FoxM1 is up-regulated by obesity and stimulates beta-cell proliferation. Mol Endocrinol, 2010. 24(9): p. 1822-34. 56. Gasim, T., Gestational Diabetes Mellitus: Maternal and Perinatal Outcomes in 220 Saudi Women. Oman Medical Journal, 2012. Vol. 27, No. 2: 140-144. | |
dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/76514 | - |
dc.description.abstract | 研究背景:
在動物實驗中,foxm1基因被發現其對於懷孕的母鼠血糖恆定以及beta細胞質量擴增是必要的。人體懷孕的過程,母體胰島素阻抗會因為胎盤賀爾蒙分泌、孕期體重的增加、胎兒的負擔以及孕婦的飲食習慣而隨著孕期不斷增加,而妊娠糖尿病就會慢慢在無法順利平衡血糖的孕婦上發生。本研究假設人體在面對胰島素需求上升的情形時,一樣需要透過FOXM1基因相關的beta細胞的擴張過程來克服。另外,因母體患有妊娠糖尿病,而在高血糖環境下發育的胎兒可能會因為某些基因的表觀遺傳變化,而提升了其在日後得到肥胖、第二型糖尿病或是心血管相關疾病的風險。因此除了孕婦,胎兒也會是研究觀測的重點。 研究方法: 本研究共收錄166位孕婦及胎兒的血液檢體,並以real-time PCR相對定量法量測在妊娠糖尿病及非妊娠糖尿病孕婦的周邊血中FOXM1 mRNA表達量的倍數差異。胎兒部分則會比較妊娠糖尿病患的子代和非妊娠糖尿病患子代臍帶血中FOXM1 mRNA的表達量差異,並偵測兩組臍帶血血清中Glucose、insulin和C-peptide含量,並計算HOMA-IR。最後,研究數據皆以IBM SPSS statistic資料編輯器以適當的統計方式進行比較分析。 研究結果: 研究發現FOXM1 mRNA的表達量在胎兒臍帶血中較母體周邊血高約2.4倍,符合過去研究顯示FOXM1基因會在發育組織中高量表達的現象,但在第三孕期有無妊娠糖尿病孕婦以及在母體有無妊娠糖尿病的胎兒臍帶血樣本比較中皆未達統計上顯著差異。接著,將胎兒臍血FOXM1 ∆Ct與胎兒臨床變數進行線性關係 分析,結果在各變數間亦無發現明顯的線性關係。會造成以上研究結果的可能原因為組間樣本數不均、取樣時機及樣本種類而呈現的結果,每一個都是可以加以改善並進一步探討的方向。FOXM1基因與人類妊娠糖尿病的關係仍為未知,希望透過此研究可以做為一個開端,以期未來能針對此議題做更深入的研究。 | zh_TW |
dc.description.abstract | Background:
FOXM1(Forkhead box M1), known as a transcription activator, was reported to be essential for the beta-cell expansion and glucose homeostasis during the pregnant period in mice model. With the increasing of fetal burden, weight gain and the secretion of placental hormones through human gestation, maternal insulin resistance reaches its peak. Once pregnant woman fails to maintain glucose homeostasis under such circumstance, gestational diabetes mellitus(GDM)will be diagnosed at 24-28 gestational week by glucose tolerance test. In this assay, we assumed that human shared the same mechanism what animal model suggested. That is, human will overcome increased demand for insulin through FOXM1-associated beta cell expansion pathway. Method: To address this hypothesis, 166 subjects were recruited and collected maternal peripheral blood from the patients with GDM to test the FOXM1 mRNA relative expression level between control group and experimental group. Next, due to fetus developed in hyperglycemia environment reflects its higher insulin needs, we also harvested postpartum cord blood from the GDM to test the FOXM1 mRNA expression level, and test glucose、insulin and C-peptide protein concentration at the same time. Because the newborn umbilical cord blood was considered in the fasting status, the HOMA-IR then calculated by the serum glucose and insulin levels. Result: In this study, data showed that FOXM1 mRNA expression level in umbilical cord blood was 2.4 times higher than that of in the mother peripheral blood, this is consist with the role FOXM1 displays in the past research. However, as the result of unequal sample size、sampling timing and type of specimen, either in third trimester peripheral blood with/without GDM or in fetus umbilical cord blood from with/without GDM mother show no statistic significant. The relationship between FOXM1 and GDM still unknown, but hope this study can be a start for any possible further research. | en |
dc.description.provenance | Made available in DSpace on 2021-07-09T15:53:35Z (GMT). No. of bitstreams: 1 ntu-108-P06448006-1.pdf: 3478326 bytes, checksum: fca391859170ade9100fac408a351bd7 (MD5) Previous issue date: 2019 | en |
dc.description.tableofcontents | 口試委員會審定書………………………………………………………………… …i
誌謝……………………………………………………………………………………ii 中文摘要……………………………………………………………….... ………iii- iv Abstract……………………………………………………………………………. v-vi 第一章 研究背景與動機機 1.1妊娠糖尿病的介紹…………………………………………………………..1 1.2妊娠糖尿病的致病機轉…………………………………………………...1-2 1.3妊娠糖尿病的臨床症狀……………………………………………………..2 1.4妊娠糖尿病的診斷標準……………………………………………………..3 1.5妊娠糖尿病的疾病管理……………………………………………………..3 1.6 FOXM1(Forkhead box protein M1)基因介紹…………………………….3-6 1.7妊娠糖尿病與FOXM1可能的關係……………………………………….6-12 第二章 研究目的及動機……………………………………………………………13 第三章 研究方法 3.1研究對象 3.1.1受試者來源與收案標準……………………………………………...14 3.1.2同意書的簽署………………………………………………………...14 3.2檢體來源………………………………………….………………………14 3.3 研究方法 3.3.1白血球、血漿及血清的製備………………………………………14-15 3.3.2抽取總RNA…………………………………………………………..15 3.3.3確認RNA品質與定量……………………………………………15-16 3.3.4反轉錄作用…………………………………………………………...16 3.3.5引子的設計…………………………………………………………...17 3.3.6即時定量聚合酶連鎖反應(Real-time qPCR) ………………….17-18 3.3.7 相關檢驗數據………………………………………………………..18 3.3.8 數據統計方法………………………………………………………..19 第四章 研究結果 4.1研究結果的圖表 4.1.1孕婦與妊娠糖尿病相關的臨床參數特性…………………………...20 4.1.2 胎兒與妊娠糖尿病相關的臨床參數特性…………………………..20 4.1.3 母血與臍血中FOXM1 mRNA 相對表現量比較…………….........21 4.1.4 母血和臍血在有無妊娠糖尿病的狀態下相對表現量的比較……..23 4.1.5 臍血FOXM1 ∆Ct與各變項間的線性關係…………………………24 第五章 討論 5.1研究結果的討論 5.1.1孕婦與妊娠糖尿病相關的臨床參數特性…………………………...24 5.1.2 胎兒與妊娠糖尿病相關的臨床參數特性…………………………..24 5.1.3 母血與臍血中FOXM1 mRNA 相對表現量比較………………24-25 5.1.4 母血和臍血在有無妊娠糖尿病的狀態下相對表現量的比較……..25 5.1.5 臍血FOXM1 ∆Ct與各變項間的線性關係…………………………25 第六章 未來展望……………………………………………………………...…26-27 參考文獻……………………………………………………………………….…28-31 附錄 附錄一、受試者同意書……………………………………………….……32-36 | |
dc.language.iso | zh-TW | |
dc.title | FOXM1基因在妊娠糖尿病患者週邊血及臍帶血中之表現 | zh_TW |
dc.title | The expression of FOXM1 in peripheral blood and umbilical cord blood from patient with GDM. | en |
dc.type | Thesis | |
dc.date.schoolyear | 107-2 | |
dc.description.degree | 碩士 | |
dc.contributor.oralexamcommittee | 林芯?(Shin-Yu Lin),李弘元(Hung-Yuan Li) | |
dc.subject.keyword | 妊娠糖尿,FOXM1基因,孕婦周邊血,胎兒臍帶血, | zh_TW |
dc.subject.keyword | GDM,FOXM1,mother peripheral blood,fetus umbilical cord blood, | en |
dc.relation.page | 37 | |
dc.identifier.doi | 10.6342/NTU201903045 | |
dc.rights.note | 同意授權(全球公開) | |
dc.date.accepted | 2019-08-13 | |
dc.contributor.author-college | 醫學院 | zh_TW |
dc.contributor.author-dept | 分子醫學研究所 | zh_TW |
dc.date.embargo-lift | 2024-08-28 | - |
顯示於系所單位: | 分子醫學研究所 |
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