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完整後設資料紀錄
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.advisor | 龔秀妮 | zh_TW |
dc.contributor.advisor | Hsiu-Ni Kung | en |
dc.contributor.author | 王佑辰 | zh_TW |
dc.contributor.author | You-Chen Wang | en |
dc.date.accessioned | 2021-07-11T15:21:05Z | - |
dc.date.available | 2024-08-16 | - |
dc.date.copyright | 2019-03-11 | - |
dc.date.issued | 2019 | - |
dc.date.submitted | 2002-01-01 | - |
dc.identifier.citation | 1. Marchesini, G., et al. (2001). "Nonalcoholic fatty liver disease: a feature of the metabolic syndrome." 50(8): 1844-1850.
2. VIDELA, L. A., et al. (2004). "Oxidative stress-related parameters in the liver of non-alcoholic fatty liver disease patients." Clinical science 106(3): 261-268. 3. 袁本治(2016)。生理學。臺北市:五南圖書。 4. JOHN E. HALL(2008)。小GUYTON生理學手冊(Pocket companion to Guyton & Hall textbook of medical physiology 11th ed.,樓迎統譯)。臺北市 : 合記 5. Glen, J., Floros, L., Day, C., & Pryke, R. J. B. (2016). Non-alcoholic fatty liver disease (NAFLD): summary of NICE guidance. 354, i4428. 6. Rinella, M. E. J. J. (2015). Nonalcoholic fatty liver disease: a systematic review. 313(22), 2263-2273. 7. 李建瑩、巫櫻桃、蕭如君(2018)。非酒精性脂肪肝病治療介紹。THE JOURNAL OF TAIWAN PHARMACY Vol.34 No.2 Jun. 30 2018,27-32。 8. Chalasani et al. (2012). The diagnosis and management of non‐alcoholic fatty liver disease: Practice Guideline by the American Association for the Study of Liver Diseases, American College of Gastroenterology, and the American Gastroenterological Association. 55(6), 2005-2023. 9. 張天鈞(2004)。內科學。臺北市:橘井文化。 10. Harraan, D. (1955). Aging: a theory based on free radical and radiation chemistry. 11. 王淑卿(2014)。自由基與活性氧化物 ─ 上。上網日期:2018年12月30日,檢自http://highscope.ch.ntu.edu.tw/wordpress/?p=53230。 12. Carr, A. C., McCall, M. R., Frei, B. J. A., thrombosis,, & biology, v. (2000). Oxidation of LDL by myeloperoxidase and reactive nitrogen species: reaction pathways and antioxidant protection. 20(7), 1716-1723. 13. 黎孝韻、曾國慶(2008)。自由基及抗氧化物功能的探討。藥學雜誌,95,27-32。 14. Weyemi, U., & Dupuy, C. (2012). The emerging role of ROS-generating NADPH oxidase NOX4 in DNA-damage responses. Mutation Research/Reviews in Mutation Research, 751(2), 77-81. 15. Dai, Dao-Fu et al. (2011). Mitochondrial targeted antioxidant peptide ameliorates hypertensive cardiomyopathy. 58(1), 73-82. 16. Dai, W., Wang, H., Fang, J., Zhu, Y., Zhou, J., Wang, X., . . . Zhou, M. J. B. r. b. (2018). Curcumin provides neuroprotection in model of traumatic brain injury via the Nrf2-ARE signaling pathway. 140, 65-71. 17. Zhang, D. D. J. D. m. r. (2006). Mechanistic studies of the Nrf2-Keap1 signaling pathway. 38(4), 769-789. 18. Wang, X.-J., Sun, Z., Villeneuve, N. F., Zhang, S., Zhao, F., Li, Y., . . . Wondrak, G. T. J. C. (2008). Nrf2 enhances resistance of cancer cells to chemotherapeutic drugs, the dark side of Nrf2. 29(6), 1235-1243. 19. Itoh, K., Wakabayashi, N., Katoh, Y., Ishii, T., Igarashi, K., Engel, J. D., . . . development. (1999). Keap1 represses nuclear activation of antioxidant responsive elements by Nrf2 through binding to the amino-terminal Neh2 domain. 13(1), 76-86. 20. Rolo, A. P., Teodoro, J. S., Palmeira, C. M. J. F. R. B., & Medicine. (2012). Role of oxidative stress in the pathogenesis of nonalcoholic steatohepatitis. 52(1), 59-69. 21. Lettéron, P., Fromenty, B., Benoît, T., Degott, C., & Pessayre, D. J. J. o. h. (1996). Acute and chronic hepatic steatosis lead to in vivo lipid peroxidation in mice. 24(2), 200-208. 22. Teli, M. R., James, O. F., Burt, A. D., Bennett, M. K., & Day, C. P. J. H. (1995). The natural history of nonalcoholic fatty liver: a follow‐up study. 22(6), 1714-1719. 23. Day, C. P., & James, O. F. (1998). Steatohepatitis: a tale of two “hits”? In: Elsevier. 24. Manco, M., Marcellini, M., Giannone, G., & Nobili, V. (2007). Correlation of serum TNF-α levels and histologic liver injury scores in pediatric nonalcoholic fatty liver disease. American journal of clinical pathology, 127(6), 954-960. 25. Anstee, Q. M., Targher, G., Day, C. P. J. N. r. G., & hepatology. (2013). Progression of NAFLD to diabetes mellitus, cardiovascular disease or cirrhosis. 10(6), 330. 26. Atzori, L., Poli, G., Perra, A. J. T. i. j. o. b., & biology, c. (2009). Hepatic stellate cell: a star cell in the liver. 41(8-9), 1639-1642. 27. 顏銘宏(2017)。生藥在肝纖維化的分子生物學作用機轉新研究。臺灣臨床藥學雜誌,3,86-91。 28. Matsuoka, M., & Tsukamoto, H. (1990). Stimulation of hepatic lipocyte collagen production by Kupffer cell‐derived transforming growth factor β: Implication for a pathogenetic role in alcoholic liver fibrogenesis. Hepatology, 11(4), 599-605. 29. Gastaldelli, A., Baldi, S., Pettiti, M., Toschi, E., Camastra, S., Natali, A., . . . Ferrannini, E. (2000). Influence of obesity and type 2 diabetes on gluconeogenesis and glucose output in humans: a quantitative study. Diabetes, 49(8), 1367-1373. 30. Sunny, N. E., Parks, E. J., Browning, J. D., & Burgess, S. C. (2011). Excessive hepatic mitochondrial TCA cycle and gluconeogenesis in humans with nonalcoholic fatty liver disease. Cell Metab, 14(6), 804-810. 31. Chen, Z., Ding, L., Yang, W., Wang, J., Chen, L., Chang, Y., . . . Yang, J. J. D. (2017). Hepatic activation of the FAM3C-HSF1-CaM pathway attenuates hyperglycemia of obese diabetic mice. db160993. 32. Kahn, S. E., Hull, R. L., & Utzschneider, K. M. J. N. (2006). Mechanisms linking obesity to insulin resistance and type 2 diabetes. 444(7121), 840. 33. Sanyal, A. J., Campbell–Sargent, C., Mirshahi, F., Rizzo, W. B., Contos, M. J., Sterling, R. K., . . . Clore, J. N. J. G. (2001). Nonalcoholic steatohepatitis: association of insulin resistance and mitochondrial abnormalities. 120(5), 1183-1192. 34. Yoneda, M., Mawatari, H., Fujita, K., Endo, H., Iida, H., Nozaki, Y., . . . Kobayashi, N. (2008). Noninvasive assessment of liver fibrosis by measurement of stiffness in patients with nonalcoholic fatty liver disease (NAFLD). Digestive and Liver Disease, 40(5), 371-378. 35. Gressner, A., & Weiskirchen, R. (2006). Modern pathogenetic concepts of liver fibrosis suggest stellate cells and TGF‐β as major players and therapeutic targets. Journal of cellular and molecular medicine, 10(1), 76-99. 36. Milagro, F. I., Campión, J., & Martínez, J. A. J. O. (2006). Weight gain induced by high‐fat feeding involves increased liver oxidative stress. 14(7), 1118-1123. 37. Yang, D. K., Jo, D.-G. J. E.-B. C., & Medicine, A. (2018). Mulberry Fruit Extract Ameliorates Nonalcoholic Fatty Liver Disease (NAFLD) through Inhibition of Mitochondrial Oxidative Stress in Rats. 2018. 38. Browning, J. D., & Horton, J. D. (2004). Molecular mediators of hepatic steatosis and liver injury. The Journal of clinical investigation, 114(2), 147-152. 39. Yan, J., Wang, C., Jin, Y., Meng, Q., Liu, Q., Liu, Z., . . . Sun, H. J. R. A. (2017). Catalpol prevents alteration of cholesterol homeostasis in non-alcoholic fatty liver disease via attenuating endoplasmic reticulum stress and NOX4 over-expression. 7(2), 1161-1176. 40. Banerjee, R. R., Rangwala, S. M., Shapiro, J. S., Rich, A. S., Rhoades, B., Qi, Y., . . . Scherer, P. E. J. S. (2004). Regulation of fasted blood glucose by resistin. 303(5661), 1195-1198. 41. Cusi, K. (2018). Diagnosis and Treatment of Nonalcoholic Fatty Liver Disease (NAFLD) in Type 2 Diabetes. In Diabetes and Exercise (pp. 47-69): Springer. 42. Wei, Y., Rector, R. S., Thyfault, J. P., & Ibdah, J. A. (2008). Nonalcoholic fatty liver disease and mitochondrial dysfunction. World journal of gastroenterology: WJG, 14(2), 193. 43. Estes, C., Razavi, H., Loomba, R., Younossi, Z., & Sanyal, A. J. (2018). Modeling the epidemic of nonalcoholic fatty liver disease demonstrates an exponential increase in burden of disease. Hepatology, 67(1), 123-133. 44. Chalasani, N., Younossi, Z., Lavine, J. E., Diehl, A. M., Brunt, E. M., Cusi, K., . . . Sanyal, A. J. J. H. (2012). The diagnosis and management of non‐alcoholic fatty liver disease: Practice Guideline by the American Association for the Study of Liver Diseases, American College of Gastroenterology, and the American Gastroenterological Association. 55(6), 2005-2023. 45. 蘇慶豐、陳亮仁(2015)。非酒精性脂肪肝疾病的診斷與治療。家庭醫學與基層醫療,30(9),255-260。 46. Wang, Z., & Gleichmann, H. (1998). GLUT2 in pancreatic islets: crucial target molecule in diabetes induced with multiple low doses of streptozotocin in mice. Diabetes, 47(1), 50-56. 47. Surwit, R. S., Kuhn, C. M., Cochrane, C., McCubbin, J. A., & Feinglos, M. N. (1988). Diet-induced type II diabetes in C57BL/6J mice. Diabetes, 37(9), 1163-1167. 48. Zhang, M., Lv, X.-Y., Li, J., Xu, Z.-G., & Chen, L. (2009). The characterization of high-fat diet and multiple low-dose streptozotocin induced type 2 diabetes rat model. Experimental diabetes research, 2008. 49. Ratziu, V., Bellentani, S., Cortez-Pinto, H., Day, C., & Marchesini, G. (2010). A position statement on NAFLD/NASH based on the EASL 2009 special conference. Journal of hepatology, 53(2), 372-384. 50. Anstee, Q. M., Targher, G., & Day, C. P. (2013). Progression of NAFLD to diabetes mellitus, cardiovascular disease or cirrhosis. Nature reviews Gastroenterology & hepatology, 10(6), 330. 51. Targher, G., Bertolini, L., Padovani, R., Rodella, S., Tessari, R., Zenari, L., . . . Arcaro, G. (2007). Prevalence of nonalcoholic fatty liver disease and its association with cardiovascular disease among type 2 diabetic patients. Diabetes care, 30(5), 1212-1218. 52. Ryysy, L., Häkkinen, A.-M., Goto, T., Vehkavaara, S., Westerbacka, J., Halavaara, J., & Yki-Järvinen, H. (2000). Hepatic fat content and insulin action on free fatty acids and glucose metabolism rather than insulin absorption are associated with insulin requirements during insulin therapy in type 2 diabetic patients. Diabetes, 49(5), 749-758. 53. Adams, L. A., Waters, O. R., Knuiman, M. W., Elliott, R. R., & Olynyk, J. K. (2009). NAFLD as a risk factor for the development of diabetes and the metabolic syndrome: an eleven-year follow-up study. The American journal of gastroenterology, 104(4), 861. 54. Ricchi, M., Odoardi, M. R., Carulli, L., Anzivino, C., Ballestri, S., Pinetti, A., . . . Banni, S. (2009). Differential effect of oleic and palmitic acid on lipid accumulation and apoptosis in cultured hepatocytes. Journal of gastroenterology and hepatology, 24(5), 830-840. 55. Hensley, K., Kotake, Y., Sang, H., Pye, Q. N., Wallis, G. L., Kolker, L. M., . . . Nakae, D. J. C. (2000). Dietary choline restriction causes complex I dysfunction and increased H2O2 generation in liver mitochondria. 21(5), 983-989. 56. Seki, S., Kitada, T., Yamada, T., Sakaguchi, H., Nakatani, K., & Wakasa, K. J. J. o. h. (2002). In situ detection of lipid peroxidation and oxidative DNA damage in non-alcoholic fatty liver diseases. 37(1), 56-62. 57. Lieber, C. S. J. H. r. (2004). Cyp2e1: from ash to nash. 28(1), 1-11. 58. Bergamini, C. M., Gambetti, S., Dondi, A., & Cervellati, C. J. C. p. d. (2004). Oxygen, reactive oxygen species and tissue damage. 10(14), 1611-1626. 59. Prosser, C. C., Yen, R. D., & Wu, J. (2006). Molecular therapy for hepatic injury and fibrosis: where are we? World J Gastroenterol, 12(4), 509-515. 60. Hasegawa, T., Yoneda, M., Nakamura, K., Makino, I., Terano, A. J. A. p., & therapeutics. (2001). Plasma transforming growth factor‐β1 level and efficacy of α‐tocopherol in patients with non‐alcoholic steatohepatitis: a pilot study. 15(10), 1667-1672. 61. George, J., Pera, N., Phung, N., Leclercq, I., Hou, J. Y., & Farrell, G. J. J. o. h. (2003). Lipid peroxidation, stellate cell activation and hepatic fibrogenesis in a rat model of chronic steatohepatitis. 39(5), 756-764. 62. 譚淑萍、吳曉東(2006)。肝纖維化與TGF-β和以其為靶位點的治療策略。世界華人消化雜誌,14(32),3126-3130。 63. Takaki, A., Kawai, D., & Yamamoto, K. J. I. j. o. m. s. (2013). Multiple hits, including oxidative stress, as pathogenesis and treatment target in non-alcoholic steatohepatitis (NASH). 14(10), 20704-20728. 64. Heldin, C.-H., Miyazono, K., & ten Dijke, P. (1997). TGF-β signalling from cell membrane to nucleus through SMAD proteins. Nature, 390, 465. 65. Gentile, C. L., & Pagliassotti, M. J. J. T. J. o. n. b. (2008). The role of fatty acids in the development and progression of nonalcoholic fatty liver disease. 19(9), 567-576. 66. Pessayre, D. J. J. o. g., & hepatology. (2007). Role of mitochondria in non‐alcoholic fatty liver disease. 22, S20-S27. 67. Aronis, A., Madar, Z., Tirosh, O. J. F. R. B., & Medicine. (2005). Mechanism underlying oxidative stress-mediated lipotoxicity: exposure of J774. 2 macrophages to triacylglycerols facilitates mitochondrial reactive oxygen species production and cellular necrosis. 38(9), 1221-1230. 68. Houstis, N., Rosen, E. D., & Lander, E. S. J. N. (2006). Reactive oxygen species have a causal role in multiple forms of insulin resistance. 440(7086), 944. 69. Evans, J. L., Maddux, B. A., Goldfine, I. D. J. A., & signaling, r. (2005). The molecular basis for oxidative stress-induced insulin resistance. 7(7-8), 1040-1052. 70. Boden, G., Chen, X., Capulong, E., & Mozzoli, M. (2001). Effects of free fatty acids on gluconeogenesis and autoregulation of glucose production in type 2 diabetes. Diabetes, 50(4), 810-816. 71. Biddinger, S. B., & Kahn, C. R. J. A. R. P. (2006). From mice to men: insights into the insulin resistance syndromes. 68, 123-158. 72. Tzivion, G., Dobson, M., & Ramakrishnan, G. J. B. e. B. A.-M. C. R. (2011). FoxO transcription factors; Regulation by AKT and 14-3-3 proteins. 1813(11), 1938-1945. 73. Chen, Z., Wang, J., Yang, W., Chen, J., Meng, Y., Feng, B., . . . Cui, Q. (2017). FAM3C activates HSF1 to suppress hepatic gluconeogenesis and attenuate hyperglycemia of type 1 diabetic mice. Oncotarget, 8(62), 106038. | - |
dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/78811 | - |
dc.description.abstract | 非酒精性脂肪肝病(Non-alcoholic fatty liver disease, NAFLD)在歐美地區已經成為主要的肝臟疾病病之一,據估計,在美國和其他西方國家高達30%的成年人都有NAFLD。近年來由於飲食及生活習慣的改變,台灣NAFLD病人有逐漸增加的趨勢。NAFLD目前的治療方式有限,除了改變生活習慣外,多種藥物的使用都會有副作用,因此,尋找新的治療藥物刻不容緩。而這個疾病常被報導是由於因為肝臟內氧化壓力過高所引發,若能尋得抗氧化的藥物,也許對於NAFLD的治療能有助益。HN242為一種樹皮萃取出的天然物,已知能提高抗氧化能力,我們試圖了解其是否能保護肝細胞。
本實驗使用高脂飲食引發NAFLD,測量血清中的AST/ALT,高脂組小鼠的肝功能確實降低,切片染色後,觀察到有大量脂肪及纖維化的組織堆積在高脂組的小鼠的肝臟中;本研究證實不同模式的HN242餵食可以經由提升抗氧化能力達到減緩胰島素阻抗與抑制發炎等作用,在肝臟組織達到預防及治療大量脂肪堆積在肝臟的效果,同時也能防止肝臟出現纖維化的現象,對於NAFLD所產生的糖質新生也有抑制的效果,雖然治療效果不如預防顯著,但仍證實HN242能對肝臟產生實質的保護;在細胞實驗中使用HepG2肝細胞處理Palmitic acid來模擬高脂環境,結果發現自由基ROS (H2O2、O2-)的增加且細胞產生胰島素阻抗,胰島素傳訊路徑中的p-IRS及p-Akt均降低,加入HN242的組別可以減緩胰島素阻抗及降低ROS;現階段結果證實HN242具有治療及預防NAFLD極高的潛力。 | zh_TW |
dc.description.abstract | Non-alcoholic fatty liver disease (NAFLD) has become one of the major liver disease worldwide. It is estimated that up to 30% of adults have NAFLD in the United States and other Western countries. Due to changes in diet and lifestyle in Taiwan in recent years, there has been a dramatic increase number of NAFLD patients. Current treatment for NAFLD is limited. In addition to lifestyle changes developing new drugs for preventing or treating NAFLD is necessary and urgent. Since oxidative stress in the liver is reported to be the main cause of NAFLD, drugs with anti-oxidative ability may have potential to treat NAFLD. HN242 is a natural plant extraction that is known to enhance the antioxidant capacity in organism. We try to understand whether it can protect liver from damages of NAFLD.
In the in vivo study, high-fat-diet (HF) was used to induce NAFLD, and serum ALT/AST was measured. The liver function of the mice in HF group was indeed reduced, and a large amount of fat and fibrotic tissue was observed in livers. Two kinds of HN242 feeding were set up: (HF+HN242) HN242 was feed with HF for 70 days, and (HF-HN242) HN242 was feed with HF for 35 days after 35 days of HFD feeding. This study demonstrated that both two kinds of HN242 feeding ways can inhibit insulin resistance and decrease inflammation by increasing antioxidant capacity, thus slow down the fat accumulation and fibrosis in the livers. It also has an inhibitory effect on the gluconeogenesis produced by NAFLD. Although the therapeutic effect is not as obvious as prevention, it is confirmed that HN242 can provide substantial protection to the liver. In the in vitro experiment, Palmitic acid were used to treat HepG2 hepatocytes to mimic the high-fat environment. The results showed that the free radical (reactive oxidative species, ROS: H2O2、O2-) increased and the insulin resistance, also increased, with the insulin signaling pathway decreased. The addition of HN242 reduced ROS and slowed insulin resistance. Current results confirmed that HN242 has great potential as the preventing and treating drug for NAFLD. | en |
dc.description.provenance | Made available in DSpace on 2021-07-11T15:21:05Z (GMT). No. of bitstreams: 1 ntu-108-R04446005-1.pdf: 4055847 bytes, checksum: 6314e1365b41e38689b3cd0b27ab550d (MD5) Previous issue date: 2019 | en |
dc.description.tableofcontents | 第一章、緒論 1
一、引言 1 二、肝臟簡介 1 三、非酒精性脂肪性肝病概況及簡介 3 四、非酒精性脂肪性肝病診斷 4 五、非酒精性脂肪性肝病與氧化壓力 4 六、脂肪肝內氧化壓力與發炎的關係 5 七、脂肪肝纖維化的過程 6 八、肝臟的糖質新生 7 九、研究目的 8 第二章、實驗材料與方法 9 一、實驗藥品、動物與試劑來源 9 二、動物實驗流程 11 三、HN242配製及餵食方式 11 四、高脂飼料配方 12 五、IPITT與 IPPPT 12 六、石蠟組織包埋法 13 七、冷切包埋法 14 八、油紅O染色(Oil Red O Stain) 15 九、AST/ALT 分析kit 15 十、組織化學免疫染色法(Immunohistochemistry,IHC) 16 十一、蘇木精-伊紅染色(hematoxylin and eosin stain) 17 十二、Trichrome stain: 18 十三、西方墨點法分析(Western blot) 20 十四、流式細胞儀分析 23 十五、統計分析 23 第三章、實驗結果 24 一、以高脂飼料餵食C57BL/6 小鼠引發體重增加及胰島素阻抗的產生 24 二、HN2424減緩老鼠肝臟胰島素阻抗的發生 24 三、高脂飼料餵食C57BL/6小鼠脂肪肝產生 25 四、HN2424降低老鼠肝臟脂肪堆積以保護肝臟組織 25 五、HN242抑制老鼠NAFLD所產生的發炎反應 26 六、HN242抑制老鼠NAFLD所產生的纖維化 26 七、HN242降低肝臟內氧化壓力 26 八、HN2424促進抗氧化酵素在老鼠肝臟中增加 27 九、HN242抑制Palmitic acid 在HepG2肝細胞中引起的氧化壓力 27 十、HN2424促進抗氧化酵素在肝細胞中增加 28 十一、HN2424藉由降低氧化壓力減緩肝細胞胰島素阻抗的發生 29 十二、HN2424減緩老鼠肝臟糖質新生的發生 29 第四章、 討論 31 一、簡述 31 二、近代非酒精性脂肪性肝病藥物治療與研究 31 三、高脂飲食與第二型糖尿病 32 四、糖尿病與非酒精性脂肪性肝病之間的關聯 33 五、非酒精性脂肪性肝病的病變 33 六、Palmitic acid模擬高脂飲食環境 34 七、非酒精性脂肪性肝病與氧化壓力之間的關聯 34 八、非酒精性脂肪性肝病導致纖維化 35 九、氧化壓力與發炎反應的聯繫 36 十、氧化壓力與胰島素阻抗之間的探討 36 十一、非酒精性脂肪性肝病導致異常的糖質新生 36 第五章、結論 38 第六章、附圖 40 第七章、參考文獻 70 | - |
dc.language.iso | zh_TW | - |
dc.title | HN242透過抑制氧化壓力減緩高脂飲食所誘導的非酒精性脂肪肝病 | zh_TW |
dc.title | HN242 ameliorates high fat diet induced NAFLD through inhibiting oxidative stress | en |
dc.type | Thesis | - |
dc.date.schoolyear | 107-1 | - |
dc.description.degree | 碩士 | - |
dc.contributor.oralexamcommittee | 王淑慧;陳瀅 | zh_TW |
dc.contributor.oralexamcommittee | Shu-Huei Wang;Ying Chen | en |
dc.subject.keyword | HN242,非酒精性脂肪肝病,高脂飲食,氧化壓力,抗氧化, | zh_TW |
dc.subject.keyword | HN242,NAFLD,high-fat-diet,oxidative stress,anti-oxidative, | en |
dc.relation.page | 75 | - |
dc.identifier.doi | 10.6342/NTU201900595 | - |
dc.rights.note | 未授權 | - |
dc.date.accepted | 2019-02-14 | - |
dc.contributor.author-college | 醫學院 | - |
dc.contributor.author-dept | 解剖學暨細胞生物學研究所 | - |
dc.date.embargo-lift | 2024-03-11 | - |
顯示於系所單位: | 解剖學暨細胞生物學科所 |
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ntu-107-1.pdf 目前未授權公開取用 | 3.96 MB | Adobe PDF |
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