Chung Hwa University of Medical Technology

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    1453 research outputs found

    Design and Application Analysis of the Novel Energy Harvesting Devices with Phononic Crystal

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    研究領域:機械工程

    A Study of Impact on Governmental Is Staff upon Adopting Is Outsourcing by the Government

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    研究領域:管理科

    Gazed Performance---Gakugeikai and Kokugoenshukai of Primary Indigenous Educational Institution in Japanese Colonial Period

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    研究領域:教育學 計畫編號:NSC98-2410-H273-003[[abstract]]在歷經荷西、明鄭與清代三個時期的殖民統治,1895 年後的台灣原住民又見識到一位新的殖民統治者----日本。日本人為原住民帶來全新的教育方式,也帶來新的「學校行事」,其中「學藝會」與「國語演習會」對於原住民而言,是未曾經歷過的嶄新經驗。「學藝會」與「國語演習會」除了是學校行事活動的一環外,重要的是殖民者透過如此的活動,進而掌握原住民學習的狀況,特別是國(日)語的嫻熟程度如何。此外,這兩項活動所匯集的眾多參加人數,以及跨部落的集會活動,讓原住民的心理空間隨之加大,不再侷限於部落之內。因此,本研究將試著探討這背後所隱含的殖民者意圖,以及「學藝會」與「國語演習會」對於原住民部落社會的影響。研究者先前已完成論文〈本土化vs.荷蘭化----荷蘭時期臺灣教會的語言使用〉、〈教育菁英vs.傳統菁英:日治時期教育影響下原住民領導機制的轉變〉,〈國(日)語作為一種溝通的工具:日治時期旗山郡的教育所〉、〈日治時期蕃童教育所的教師角色分析〉、與〈國家vs.部落:日治時期官方原住民教育策略的變革〉,而博士論文則是《台灣原住民教育史研究〈1624-1895〉----從外來者的殖民教化談起》。為求研究之完整性,實在有必要針對日治時期之原住民教育作一持續研究,特別是就日本式教育對原住民的影響做深入的探討,尤其是這種新教育的形式與活動,對於原住民個人,以及部落社會的衝擊為何。研究者設計以一年的時間,從民國98 年8 月至99 年7 月止。研究者期待透過此研究,能對日治時期的原住民教育的影響層面,能有進一步的瞭解,並提供未來原住民教育改革之參考。 Since 1985, Taiwan indigenous people met a new colonial governor—Japanese, after through Dutch-Spanish, Ming-Cheng, Ching dynasty periods. Japanese gave indigenous people new educational institutions and activities, also established new school schedule. Among these activities both Gakugeikai and Kokugoenshukai were new experiences for the indigenous children. Gakugeikai and Kokugoenshukai were a part of the school schedule, it meat for Japanese colonizer to grasp the real situation and effect of the education set by them, especially the learning of Japanese language. Besides, these two activities could assemble masses of pan-tribal indigenous people, and enlarge their cognitive space, no long limited in a tribal society. The research will be trying to inquire what Japanese colonial true intention was, and the influence of Gakugeikai and Kokugoenshukai on indigenous tribal societies. The researcher has finished six pilot studies, “Indigenization vs. Dutchification: The Missionaries’ Linguistic Practice during the Dutch Colonial Period” ,” Educational Elites vs. Traditional Elites: the Transformation of Taiwan Aboriginal Leadership Institution under the Colonial Education in Japanese Colonial Period”, “Two Peoples Met:The Indigenous Primary Educational Institutions of Chishan County in Japanese Colonial Period “,“The Teachers’ Role of Indigenous Education in Japanese Colonial Period “, and” Nation vs. Tribe: The Evolution of Japanese Educational Strategies on Taiwan Indigenous People During 1895-1945” and doctoral dissertation “A study on educational history of Taiwan aboriginal people----focused on the colonial education”. It needs a continuing study to achieve a more complete study, therefore, the discussion is directed to focus on the relationship between Japanese colonial education and Taiwan indigenous people, and especially on the way new Japanese educational institutions and activities affected themselves and indigenous tribal society. The researcher hopes that the study may improve our understanding of the colonial education in Japanese period, and provide some suggestions for the future reforms of Taiwan indigenous people’s education

    探討CXCL12基因在大腸直腸癌基因多型性之研究

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    [[note]]合作廠商:永康榮民醫院合約期間:98.1.1~98.12.3

    穀類加工食品創新保健功效研發診斷計畫

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    [[note]]合作廠商:金屬中心+邱瑞隆行合約期間:98.4.1~98.9.3

    協助福記食品股份有限公司提升製程技術計畫

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    [[note]]合作廠商:福記食品股份有限公司合約期間:98.6.1~98.11.3

    從電鍍廢水回收貴重金屬之新型技術開發評估

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    [[note]]合作廠商:金屬中心+東岳環境工程有限公司合約期間:98.4.1~98.9.3

    聖邦不動產仲介員工健康管理計畫

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    [[note]]合作廠商:聖邦不動產仲介經紀有限公司合約期間:98.7.10~98.12.1

    Elucidation of the underlying mechanism that albumin induced cellular fibrosis in mesangial cells.

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    目錄 中文摘要………………………………………………………………………i 英文摘要……………………………………………………………………iii 致 謝…………………………………………………………………………v 縮 寫 表.…………………………………………………………………vii 第一章 前言………………………………………………………………1 第一節 腎臟功能的簡介…………………………………………………2 第二節 糖尿病腎病變的發展與其病理機轉……………………………6 第三節 TGF-β1與糖尿病腎病變…………………………………………9 第四節 泛素所調控的蛋白質降解反應…………………………………14 第二章 實驗背景……………………………………………………………17 第三章 研究目的……………………………………………………………20 第四章 材料與方法…………………………………………………………23 第五章 結果…………………………………………………………………31 第六章 討論…………………………………………………………………36 第七章 圖表…………………………………………………………………42 第八章 參考文獻........................................54 阿部信一著,徐家杰譯,腎、泌尿疾病護理,第一版,五南圖書出版公司,2000。 藤山順豐著,張佳微譯,活化腎機能,第一版,晨星出版有限公司,2001。 大野丞二著,楊鴻儒譯,第一版,腎臟病診療室,書泉出版社,1991。 蔡崇章等著,第一版,惱人的泌尿系疾病,健康世界雜誌社,1999。 蔡淳娟著,第一版,談腎臟及尿路疾病,旺文社股份有限公司,2004。 Bautista LE, Oróstegui M, Vera LM, Prada GE, Orozco LC, Herrán OF. Eur J Cardiovasc Prev Rehabil. (2006). 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(2002). TGF-beta signaling in renal disease. J Am Soc Nephrol 13, 2600–10. Cárcamo J, Weis FM, Ventura F, Wieser R, Wrana JL, Attisano L, Massagué J. (1994). Type I receptors specify growth-inhibitory and transcriptional responses to transforming growth factor beta and activin. Mol Cell Biol 14(6),3810-21. Cuhaci B, Kumar MS, Bloom RD, Pratt B, Haussman G, Laskow DA, Alidoost M, Grotkowski C, Cahill K, Butani L, Sturgill BC, Pankewycz OG. (1999). Transforming growth factor-beta levels in human allograft chronic fibrosis correlate with the rate of decline in renal function. Transplantation 68, 785–790. Dworkin LD, Ichikawa I, Brenner BM. (1983). Hormonal modulation of glomerular function. Am J Physiol 244(2), F95-104. Ebner R, Chen RH, Lawler S, Zioncheck T, Derynck R. (1993). Determination of type I receptor specificity by the type II receptors for TGF-beta or activin. Science 262, 900-02. Eddy AA. (1996). Serine proteases, inhibitors and receptors in renal fibrosis. J Am Soc Nephrol 12, 2495-508. Franzén P, Ten Dijke P, Ichijo H, Yamashita H, Schulz P, Heldin CH, Miyazono K. (1993). Cloning of a TGF beta type I receptor that forms a heteromeric complex with the TGF beta type II receptor. Cell 75.681-92. Fukasawa H, Yamamoto T, Togawa A, Ohashi N, Fujigaki Y, Oda T, Uchida C, Kitagawa K, Hattori T, Suzuki S, Kitagawa M, Hishida A. (2004). Down-regulation of Smad7 expression by ubiquitin-dependent degradation contributes to renal fibrosis in obstructive nephropathy in mice. Proc Natl Acad Sci U S A 101 , 8687-92. Gambaro, G., D'Angelo, A., Fabris, A., Tosetto, E., Anglani, F., and Lupo, A. (2004). Crystals, Randall's plaques and renal stones: do bone and atherosclerosis teach us something ? J. Nephrol 17,774-77. Giordano M, De Feo P, Lucidi P, dePascale E, Giordano G, Infantone L, Zoccolo AM, Castellino P. (2001). Increased albumin and fibrinogen synthesis in hemodialysis patients with normal nutritional status. J Am Soc Nephrol 12, 349-54. Guh JY, Yang ML, Yang YL, et al. (1996). Captopril reverses high-glucoseinduced growth effects on LLC-PK1 cells partly by decreasing transforming growth factor- beta receptor protein expressions. J Am Soc Nephrol 7, 1207–15. Grande JP, Warner GM, Walker HJ, et al. (2002). TGF-beta1 is an autocrine mediator of renal tubular epithelial cell growth and collagen IV production. Exp Biol Med 227, 171–81. Heldin CH, Miyazono K, ten Dijke P. (1997). TGF-beta signalling from cell membrane to nucleus through SMAD proteins. Nature 390, 465-71. Jørgensen JP, Lauridsen AM, Kristensen P, Dissing K, Johnsen AH, Hendil KB, Hartmann-Petersen R. (2006). Adrm1, a putative cell adhesion regulating protein, is a novel proteasome-associated factor. J Mol Biol 360, 1043-52. Kamata K, Mizutani K. (1999). Changes in angiotensin converting enzyme activity in the renal vascular bed of streptozotocin-induced diabetic rat. Res Commun Mol Pathol Pharmacol 104, 181-92. Kasinath BS.(1993). Glomerular endothelial cell proteoglycans-regulation by TGF-beta 1. Arch Biochem Biophys 305, 370-77. Kavsak P, Rasmussen RK, Causing CG, Bonni S, Zhu H, Thomsen GH, Wrana JL. (2000). Smad7 binds to Smurf2 to form an E3 ubiquitin ligase that targets the TGF beta receptor for degradation. Mol Cell 6, 1365-75. Kreisberg JI, Venkatachalam M, Troyer D. Am J Physiol. (1985) Contractile properties of cultured glomerular mesangial. Cell 249, 457-63. Lin X, Liang M, Feng XH. (2000). Smurf2 is a ubiquitin E3 ligase mediating proteasome-dependent degradation of Smad2 in transforming growth factor-beta signaling. J Biol Chem 275, 36818-22. López-Casillas F, Wrana JL, Massagué J. (1993) Betaglycan presents ligand to the TGF beta signaling receptor. Cell 73, 1435-44. Liu FY, Li XZ, Liu H, Liu YH. (2007) Arkadia-Smad7-mediated positive regulation of TGF-beta signaling in a rat model of tubulointerstitial fibrosis. Am J Nephrol.; 27(2):176-83. 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Sharma HS, Westman J, Navarro JC, Dey PK, Nyberg F. (1995). Probable involvement of serotonin in the increased permeability of the blood-brain barrier by forced swimming. An experimental study using Evans blue and 131I-sodium tracers in the rat. Behav Brain Res 72, 189-96. Sharma VK, Bologa RM, Li B, Xu GP, Lagman M, Hiscock W, Mouradian J, Wang J, Serur D, Rao VK, Suthanthiran M. (1996). Molecular executors of cell death-differential intrarenal expression of Fas ligand, Fas, granzyme B, and perforin during acute and/or chronic rejection of human renal allografts. Transplantation 62, 1860-66. Stone M, Hartmann-Petersen R, Seeger M, Bech-Otschir D, Wallace M, Gordon C. (2004). Uch2/Uch37 is the major deubiquitinating enzyme associated with the 26S proteasome in fission yeast. J Mol Biol 344, 697-706. Wicks SJ, Haros K, Maillard M, Song L, Cohen RE, Dijke PT, Chantry A. (2005). The deubiquitinating enzyme UCH37 interacts with Smads and regulates TGF-beta signalling. Oncogene 54, 8080-4. Wrana JL. (2000) Regulation of Smad activity. Cell 100, 189-92. Review. Wrana JL, Attisano L, Cárcamo J, Zentella A, Doody J, Laiho M, Wang XF, Massagué J. (1992) TGF beta signals through a heteromeric protein kinase receptor complex. Cell 71, 1003-14. Ziyadeh FN. (1993). The extracellular matrix in diabetic nephropathy. Am J Kidney Dis 22, 736-44. Review.[[abstract]]糖尿病腎病變 (diabetic nephropathy,DN) 是糖尿病患嚴重的併發症以及死因之ㄧ,其病理現象包含腎臟細胞的細胞肥大和細胞外間質增生;最後導致腎臟纖維化及末期腎病變 (end-stage renal disease,ESRD)。高糖、高度糖化終產物 (advanced glycation end products,AGE) 、尤其以乙型轉型生長因子 (transforming growth factor β,TGF-β) 所造成的生物效應已有相當程度的證據顯示會影響糖尿病腎病變。 白蛋白尿 (Albuminuria) 是腎臟纖維化病變指標之一,在腎臟功能中,腎絲球間質細胞與白蛋白尿有著相當關聯性。白蛋白不僅是DN的危險因素,也是治療的目標。因此,科學家們一直在尋求如何澄清白蛋白與糖尿病腎病之間的相互作用。在以前的研究中,TGF-β腎纖維化扮演重要的作用。在相關路徑中,TGF-β與其受器結合也是非常重要啟動因子。然而,卻少有研究的重點是針對白蛋白與 TGF -β1 receptors(TβRI)在腎小球纖維化中相關作用做探討。 首先,使用白蛋白進行劑量性 (0、0.1、1、10mg/ml) 刺激之下,我們發現腎絲球細胞內與纖維化最為相關的因子 (TGF-β1) 被大量表現,連帶誘導纖維蛋白 (fibronectin) 大量分泌。且細胞生理效應驗證了先前的研究而有細胞肥大的現象產生。在細胞內的蛋白質測定發現到高劑量白蛋白 (10mg/ml) 會促使細胞內fibronectin大量表現,且TGF-β1第一型受器表現也顯著增加。利用免疫沉澱法我們發現到在高劑量白蛋白 (10mg/ml) 刺激之下,TGF-β1受器上的泛素 (ubiquitin)的標記減少了,無法正常將受器帶到蛋白質酶體 (proteasome) 代謝。同時,白蛋白也影響了 TGF-β1受器上的 Smad-泛素調控因子1/2(Smurf-1/2) 的表現降低。此外,白蛋白進行劑量性 (0、0.1、1、10mg/ml) 刺激之下也發現到使得TGF-β1第一型受器的半衰期增加。綜合以上的研究,大概可以釐清了白蛋白對腎病變中腎絲球的損害程度。了解到這些相關效應可能有助於腎絲球纖維化。 Diabetic nephropathy (DN) is a major cause of end-stage renal disease (ESRD) and an important cause of morbidity and mortality in diabetic patients. The pathology of DN consists of cell proliferation, hypertrophy and accumulation of extracellular matrix, leading to renal fibrosis and finally ESRD. The pathogenesis of DN includes : hyperglycemia, advanced glycation end-product (AGE), renin-angiotensin system, cell cycle derangements, transforming growth factor β (TGF β) and oxidative stress, etc. Additionally, tubulointerstitial changes are as important as glomerulopathy in DN. Albuminuria is indicative of nephropathy. Albumin is not only a risk factor for DN, but also a therapeutic target. Hence, scientists have long sought ways to elucidate the interactions between albumin and diabetic nephropathy. In previous study, type I receptor of transforming growth factor-β plays an important role in renal fibrosis. It's a switch for TGF-β 1cascade pathway by ligand binding to its receptors. However, little literature has focused on the interactions of albumin with TGF-β 1receptors (TβRI) in renal glomerular fibrosis. We examined the effect of albumin in MES13 cell line (a mesangial cell), on the expression and secretion of TβRI. Fibronectin expressed was measured by western blot and Enzyme-linked immunoassay (ELISA). Ubiquitination on TβRI was assayed by immunoprecipitation. We demonstrated that treatment of BSA (0, 0.1, 1, or 10 mg/mL) for 24h could induce an increase in the protein level of TβRI and fibronectin. Moreover, we found that BSA dose-dependently and significantly decreased 60% the level of ubiquitin and Smurf 1/2, an ubiquitin ligase, on TβRI. In addition, BSA significantly increased half-life of type I TGF-β1 receptors. In conclusion, we suggest that BSA might enhance fibrotic sensitivity by decreasing the ubiquitination and increased the half-life of type I receptors of TGF-β1 in mesangial cells. These combinational effects might contribute to the pathogenesis of diabetic renal glomerular fibrosis

    Genetic polymorphism of CXCL12 gene on human colorectal cancer in Taiwan

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    目錄 口試委員會審定書 授權書 中文摘要 i 英文摘要 ii 誌謝 iv 目錄 vi 第一章 文獻資料回顧 - 1 - 第一節 趨化激素(chemokine) - 1 - 第二節Chemokine C-X-C motif ligand 12(CXCL12) - 3 - 第三節 CXC chemokine Receptor 4(CXCR4) - 4 - 第四節 CXCL12/CXCR4 結合作用(CXCL12/CXCR4 axis) - 5 - 第五節 CXCL12-G801A - 7 - 第二章 研究目的 - 8 - 第三章 實驗流程 - 9 - 第四章 實驗方法 - 10 - 第一節 對照質體的建構 - 10 - 第二節 解離式高效能液相層析儀(Denaturing High Performance Liquid Chromatography;DHPLC)分析 - 23 - 第五章 實驗結果 - 31 - 第一節 陽性對照質體製備 - 31 - 第二節 以PCR確認實驗樣本所需之CXCL12-801片段 - 31 - 第三節 以DHPLC分析健康成人CXCL12-801之基因多型性 - 32 - 第四節 以DHPLC分析大腸直腸癌病患CXCL12-801之基因多型性 - 32 - 第六章 討論與結論 - 34 - 參考文獻 - 39 - 圖表 - 47 -[[abstract]]大腸癌是世界性惡性腫瘤中造成死亡原因之一,在臺灣的盛行率也是佔其它惡性腫瘤之冠。但是,影響的大腸直腸癌發生或致死遺傳因子尚未瞭解清楚。趨化激素之一的CXCL12,又稱為基質細胞衍生因子-1(SDF-1),本身是小分子蛋白,主要調控白血球的遷移,在正常的或腫瘤組織會有不同的表現。它在血球生成過程扮演重要角色,因為它與造血幹細胞的移動、歸巢和存活有極大的關聯。CXCL12和它的受器CXCR4已經被證實與大腸直腸癌的進程有所牽連,包含血管生成及轉移。 CXCL12-G801A ,一個位於CXCL12基因β mRNA上第801個核苷酸3'未轉譯區(3' untranslated regions)位置的單一核苷酸多型性,已經在國外的文獻報告指出與乳癌和肺癌有關聯性。本研究比較它和臺灣大腸直腸癌族群的相關性。我們運用PCR及DHPLC兩種方法來分析基因多型性。根據分析結果,此點單一核苷酸多型性在病患群分佈有40(40/97)個,在控制組有20(20/99)個,P值為0.0014。進一步分析對偶基因分佈頻率(allelic frequencies),G allele 在病患群是153 (78.9%),在控制組是178 (89.9%),而 A allele 的分佈是41 (21.1%),控制組是20 (10.1%),明顯為病患群大於正常族群,其P值為0.0026。由以上數據,我們可以推論CXCL12-G801A此點單一核苷酸多型性與臺灣的大腸直腸癌族群具有一定的相關性。 Colon cancer is the major cause of malignancy-related deaths worldwide, and the most prevalent cancers in Taiwan. However, the genetic factors influencing its appearance remain far from being fully characterized. The chemokine(CXCL12),also known as stromal cell-derived factor-1 (SDF-1),is a small protein that regulates leukocyte trafficking and it is variably expressed in a number of normal and tumor tissues. CXCL12 plays a key role in hematopoiesis, and it is involved in migration, homing, and survival of hematopoietic progenitors . CXCL12 is identified as ligand and its receptor CXCR4 have been implicated in colorectal cancer progression , including angiogenesis and metastasis. CXCL12-G801A , a single nucleotide polymorphism(SNP) in the 3' untranslated region, had been previously reported to correlate with breast and lung cancer in Iran. In this study we compared to colorectal cancer patients from a Taiwan series. The results from an independent analysis of CXCL12-G801A in colorectal cancer series of Taiwan origin in order to analyse the robustness of this association within a same population. The polymorphism was analysed with PCR and DHPLC(denaturing high performance liquid chromatography )methods. There was significant difference in SNP distribution between colorectal cancer patients (n=40) and controls (n=20), P=0.0014. Furthermore, the analysis of allelic frequencies in both groups revealed that the frequency of G allele in patients and controls were 153 (78.9%) and 178 (89.9%), respectively. While the frequency of A allele in patients and controls were 41 (21.1%) and 20 (10.1%), respectively. Therefore it was revealed that patients had more A allele than controls. These differences were statistically significant (P=0.0026). Based on the above observation CXCL12-G801A can be considered as genotypes associated with colorectal cancer in Taiwan patients

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