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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 余宏政,鄭劍廷 | |
| dc.contributor.author | Shiu-Dong Chung | en |
| dc.contributor.author | 鍾旭東 | zh_TW |
| dc.date.accessioned | 2021-06-16T13:12:50Z | - |
| dc.date.available | 2015-09-24 | |
| dc.date.copyright | 2013-09-24 | |
| dc.date.issued | 2013 | |
| dc.date.submitted | 2013-07-30 | |
| dc.identifier.citation | 1. Adams JM, Cory S.The Bcl-2 protein family: arbiters of cell survival. Science 1998; 281: 1322–1326
2. Al-Zi’abi MO, Bowolaksono A, Okuda K.Survival role of locally produced acetylcholine in the bovine corpus luteum. Biol Reprod 2009; 80:823–832 3. Anders HJ, Muruve DA.The inflammasomes in kidney disease. J Am Soc Nephrol 2011; 22: 1007–1018 4. Antonsson B, Montessuit S, Lauper S, Eskes R, Martinou JC. Bax oligomerization is required for channel-forming activity in liposomes and to trigger cytochrome c release from mitochondria. Biochem J 2000; 345: 271–278 5. Ashrafian H, Czibik G, Bellahcene M, Aksentijević D, Smith AC, et al. Fumarate is cardioprotective via activation of the Nrf2 antioxidant pathway. Cell Metab 2012;15: 361–371 6. Bray GA, Nielsen SJ, Popkin BM. Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity. Am J Clin Nutr 2004; 79:537–543 7. Bruey JM, Bruey-Sedano N, Luciano F, Zhai D, Balpai R, et al. Bcl-2 and Bcl-XL regulate proinflammatory caspase-1 activation by interaction with NALP1. Cell 2007; 129: 45–56 8. Burnstock G . Therapeutic potential of purinergic signalling for diseases of the urinary tract. BJU Int 2011;107:192–204 9. Chen MC, Blunt LW, Pins MR, Klumpp DJ. Tumor necrosis factor promotes differential trafficking of bladder mast cells in neurogenic cystitis. J Urol 2006;175:754–759 10. Chen Y, Gibson SB. Is mitochondrial generation of reactive oxygen species a trigger for autophagy? Autophagy 2008; 4: 246–248 11. Cheng X, Siow RC, Mann GE. Impaired redox signaling and antioxidant gene expression in endothelial cells in diabetes: a role for mitochondria and the nuclear factor-E2-related factor 2-Kelch-like ECH-associated protein 1 defense pathway. Antioxid Redox Signal 2011; 14: 469–487 12. Chien CT, Chang TC, Tsai CY, Shyue SK, Lai MK. Adenovirus-mediated bcl-2 gene transfer inhibits renal ischemia/reperfusion induced tubular oxidative stress and apoptosis. Am J Transplant 2005;5: 1194–1203 13. Chien CT, Chien HF, Cheng YJ et al. Renal afferent signaling diuretic response is impaired in streptozotocin-induced diabetic rats. Kidney Int 2000;57:203–214 14. Chien CT, Lee PH, Chen CF, Ma MC, Lai MK, et al. De novo demonstration and co-localization of free-radical production and apoptosis formation in rat kidney subjected to ischemia/reperfusion. J Am Soc Nephrol 2011; 12: 973–982 15. Chien CT, Shyue SK, Lai MK. Bcl-xL augmentation potentially reduces ischemia/reperfusion induced proximal and distal tubular apoptosis and autophagy. Transplantation 2007; 84: 1183–1190 16. Chien CT, Yu HJ, Lin TB, Chen CF. Neural mechanisms of impaired micturition reflex in rats with acute partial bladder outlet obstruction. Neuroscience 2000; 96:221–230 17. Chien CT, Yu HJ, Lin TB et al. Substance P via NK1 receptor facilitates hyperactive bladder afferent signaling via action of ROS. Am J Physiol Renal Physiol 2003;284:F840–F851 18. Cockayne DA, Hamilton SG, Zhu QM et al.Urinary bladder hyporeflexia and reduced pain-related behaviour in P2X(3)-deficient mice. Nature 2000; 407:1011–1015 19. Devarajan P.Update on mechanisms of ischemic acute kidney injury. J Am Soc Nephrol 2006; 17: 1503–1520 20. Fiala JL, Egner PA, Wiriyachan N, Ruchirawat M, Kensler KH, et al. Sulforaphane-mediated reduction of aflatoxin B1-N7-guanine in rat liver DNA: impacts of strain and sex. Toxicol Sci 2011; 121: 57–62 21. Fukagawa NK, Li M, Liang P et al.Aging and high concentrations of glucose potentiate injury to mitochondrial DNA. Free Radic Biol Med 1999;27:1437–1443 22. Gabella G. Structure of the intramural nerves of the rat bladder. J Neurocytol 1999;28:615–637 23. Girard A, Madani S, Boustani ESE et al. Changes in lipid metabolism and antioxidant defense status in spontaneously hypertensive rats and Wistar rats a diet enriched with fructose and saturated fatty acids. Nutrition 2005;21:240–248 24. Gross A, Jockel J, Wei MC, Korsmeyer SJ. Enforced dimerization of BAX results in its translocation, mitochondrial dysfunction and apoptosis. EMBO J 1998;17: 3878–3785 25. Ha JH, Noh HS, Shin IW, Hahm JR, Kim DR. Mitigation of H2O2-induced autophagic cell death by propofol in H9c2 cardiomyocytes. Cell Biol Toxicol 2012;28: 19–29 26. Haugen E, Nath KA. The involvement of oxidative stress in the progression of renal injury. Blood Purif 1999; 17: 58–65 27. Hegde SS, Mandel DA, Wilford MR et al. Evidence for purinergic neurotransmission in the urinary bladder of pithed rats. Eur J Pharmacol 1998;349:75–82 28. Huang YC, Shindel AW, Ning H et al. Adipose derived stem cells ameliorate hyperlipidemia associated detrusor overactivity in a rat model. J Urol 2010;183:1232–1240 29. Imhoff BR, Hansen JM. Tert-butylhydroquinone induces mitochondrial oxidative stress causing Nrf2 activation. Cell Biol Toxicol 2010; 26: 541–551 30. Isaka Y, Suzuki C, Abe T, Okumi M, Ichimaru N, et al. Bcl-2 protects tubular epithelial cells from ischemia/reperfusion injury by dual mechanisms. Transplant Proc 2009; 41: 52–54 31. Jiang T, Huang Z, Lin Y, Zhang Z, Fang D, et al. The protective role of Nrf2 in streptozotocin-induced diabetic nephropathy. Diabetes 2010;59: 850–860 32. Juan YS, Chuang SM, Kogan BA et al. Effect of ischemia/reperfusion on bladder nerve and detrusor cell damage. Int Urol Nephrol 2009;41:513–521 33. Kahn R, Buse J, Ferrannini E, Stern M.The metabolic syndrome: time for a critical appraisal: joint statement from the American Diabetes Association and the European Association for the Study of Diabetes. Diabetes Care 2005; 28:2289–2304 34. Kaspar JW, Niture SK, Jaiswal AK. Nrf2:INrf2 (Keap1) signaling in oxidative stress. Free Radic Biol Med 2009; 47: 1304–1309 35. Kathiria AS, Butcher LD, Feagins LA, Souza RF, Boland CR, et al. Prohibitin 1 modulates mitochondrial stress-related autophagy in human colonic epithelial cells. PLoS One 2012; 7: e31231 36. Kedi X, Ming Y, Yongping W, Yi Y, Xiaoxiang Z. Free cholesterol overloading induced smooth muscle cells death and activated both ER- and mitochondrial-dependent death pathway. Atherosclerosis 2009;207:123–130 37. Kivirikko KI, Koivusalo M, Laitinen O, Liesmaa M. Effect of thyroxine on the hydroxyproline in rat urine and skin. Acta Physiol Scand 1963; 57: 462–467 38. Latta M, Kunstle G, Leist M, Wendel A. Metabolic depletion of ATP by fructose inversely controls CD95- and tumor necrosis factor receptor 1-mediated hepatic apoptosis. J Exp Med 2000;191:1975–1985 39. Lawrence GW, Aoki KR, Dolly JO. Excitatory cholinergic and purinergic signaling in bladder are equally susceptible to botulinum neurotoxin a consistent with co-release of transmitters from efferent fibers. J Pharmacol Exp Ther 2010;334:1080–1086 40. Le KA, Tappy L. Metabolic effects of fructose. Curr Opin Clin Nutr Metab Care 2006; 9:469–475 41. Lee SY, Jo SK, Cho WY, Kim HK, Won NH. The effect of alpha-melanocyte-stimulating hormone on renal tubular cell apoptosis and tubulointerstitial fibrosis in cyclosporine A nephrotoxicity. Transplantation 2004;78: 1756–1764 42. Lee WC, Chien CT, Yu HJ, Lee SW. Bladder dysfunction in rats with metabolic syndrome induced by long-term fructose feeding. J Urol 2008;179:2470–2476 43. Lee WC, Chuang YC, Chiang PH et al. Pathophysiological studies of overactive bladder and bladder motor dysfunction in a rat model of metabolic syndrome. J Urol 2011;186:318–325 44. Lee WC, Wu CC, Wu HP, Tai TY. Lower urinary tract symptoms and uroflowmetry in women with type 2 diabetes mellitus with and without bladder dysfunction. Urology 2007; 69:685–690 45. Lin SL, Chen RH, Chen YM, Chiang WC, Lai CF, et al. Pentoxifylline attenuates tubulointerstitial fibrosis by blocking Smad3/4-activated transcription and profibrogenic effects of connective tissue growth factor. J Am Soc Nephrol 2005; 16: 2702–2713 46. Liu G, Daneshgari F.Alterations in neurogenically mediated contractile responses of urinary bladder in rats with diabetes. Am J Physiol Renal Physiol 2005;288:F1220–F1226 47. Liu M, Grigoryev DN, Crow MT, Haas M, Yamamoto M, et al. Transcription factor Nrf2 is protective during ischemic and nephrotoxic acute kidney injury in mice. Kidney Int 2009; 76: 277–285 48. Mao L, Wang HD, Wang XL, Tian L, Xu JY. Disruption of Nrf2 exacerbated the damage after spinal cord injury in mice. J Trauma Acute Care Surg 2012; 72: 189–198 49. Martin SA, Haren MT, Marshall VR et al. Members of the Florey Adelaide Male Ageing Study. Prevalence and factors associated with uncomplicated storage and voiding lower urinary tract symptoms in community-dwelling Australian men. World J Urol 2011;29:179–184 50. Mazzei LJ, Garcia IM, Altamirano L, Docherty NG, Manucha W. Rosuvastatin preserves renal structure following unilateral ureteric obstruction in the neonatal rat. Am J Nephrol 2012; 35: 103–113 51. Messier C, Whately K, Liang J et al.The effects of high fat, high fructose, and combination diet on learning, weight, and glucose regulation in 57BL/6 mice. Behav Brain Res 2007;178:139–145 52. Metcalfe PD, Leslie JA, Campbell MT, Meldrum DR, Hile KL, et al. Testosterone exacerbates obstructive renal injury by stimulating TNF-alpha production and increasing proapoptotic and profibrotic signaling. Am J Physiol Endocrinol Metab 2008; 294: E435–E443 53. Miao EA, Rajan JV, Aderem A.Caspase-1-induced pyroptotic cell death. Immunol Rev 2011; 243: 206–214 54. Moura RF, Ribeiro C, Oliveira JA et al.Metabolic syndrome signs in Wistar rats submitted to different high-fructose ingestion protocols. Br J Nutr 2009;101:1178–1184 55. Niture SK, Jaiswal AK. INrf2 (Keap1) targets Bcl-2 degradation and controls cellular apoptosis. Cell Death Differ 2011;18: 439–451 56. Niture SK, Jaiswal AK. Inhibitor of Nrf2 (INrf2 or Keap1) protein degrades Bcl-xL via phosphoglycerate mutase 5 and controls cellular apoptosis. J Biol Chem 2011;286: 44542–44556 57. Niture SK, Kaspar JW, Shen J, Jaiswal AK. Nrf2 signaling and cell survival. Toxicol Appl Pharmacol 2010;244: 37–42 58. Orrenius S, Nicotera P, Zhivotovsky B.Cell death mechanisms and their implications in toxicology. Toxicol Sci 2011; 119: 3–19 59. O’Reilly BA, Kosaka AH, Knight GF et al. P2X receptors and their role in female idiopathic detrusor instability. J Urol 2002;167:157–164 60. Palea S, Artibani W, Ostardo E et al. Evidence for purinergic neurotransmission in human urinary bladder affected by interstitial cystitis. J Urol 1993;150:2007–2012 61. Pi J, Bai Y, Reece JM, Williams J, Liu D, et al. Molecular mechanism of human Nrf2 activation and degradation: role of sequential phosphorylation by protein kinase CK2. Free Radic Biol Med 2007; 42: 1797–1806 62. Plesnila N, Zhu C, Culmsee C, Groger M, Moskowitz MA, et al. Nuclear translocation of apoptosis-inducing factor after focal cerebral ischemia. J Cereb Blood Flow Metab 2004; 24: 458–466 63. Qian H, Yang Y, Wang X. Curcumin enhanced adriamycin-induced human liver-derived Hepatoma G2 cell death through activation of mitochondria-mediated apoptosis and autophagy. Eur J Pharm Sci 2011;43: 125–131 64. Rao VA, Klein SR, Bonar SJ, Zielonka J, Mizuno N, et al. The antioxidant transcription factor Nrf2 negatively regulates autophagy and growth arrest induced by the anticancer redox agent mitoquinone. J Biol Chem 2010; 285: 34447–34459 65. Rinaldi Tosi ME, Bocanegra V, Manucha W, Gil Lorenzo A, Valles PG. The Nrf2-Keap1 cellular defense pathway and heat shock protein 70 (Hsp70) response. Role in protection against oxidative stress in early neonatal unilateral ureteral obstruction (UUO). Cell Stress Chaperones 2011; 16: 57–68 66. Rohrmann S, Smit E, Giovannucci E, Platz EA. Association between markers of the metabolic syndrome and lower urinary tract symptoms in the Third National Health and Nutrition Examination Survey (NHANES III). Int J Obes (Lond) 2005; 29:310–316 67. Sadananda P, Drake MJ, Paton JF, Pickering AE.An exploration of the control of micturition using a novel in situ arterially perfused rat preparation. Front Neurosci 2011;5:62 68. Sakai T, Kawamura T, Shirasawa T. Mizoribine improves renal tubulointerstitial fibrosis in unilateral ureteral obstruction (UUO)-treated rat by inhibiting the infiltration of macrophages and the expression of alpha-smooth muscle actin. J Urol 1997; 158: 2316–2322 69. Sheludiakova A, Rooney K, Boakes RA.Metabolic and behavioural effects of sucrose and fructose/glucose drinks in the rat. Eur J Nutr 2011; [Epub ahead of print] 70. Shen GX. Oxidative stress and diabetic cardiovascular disorders: roles of mitochondria and NADPH oxidase. Can J Physiol Pharmacol 2010; 88:241–248 71. Stępkowski TM, Kruszewski MK. Molecular cross-talk between the NRF2/KEAP1 signaling pathway, autophagy, and apoptosis. Free Radic Biol Med 2011;50: 1186–1195 72. Tong YC, Cheng JT.Alterations of M2,3-muscarinic receptor protein and mRNA expression in the bladder of the fructose fed obese rat. J Urol 2007; 178:1537–1542 73. Vincent AM, Hayes JM, McLean LL et al. Dyslipidemia-induced neuropathy in mice: the role of oxLDL/LOX-1. Diabetes 2009; 58:2376–2385 74. Whitehouse T, Stotz M, Taylor V, Stidwill R, Singer M. Tissue oxygen and hemodynamics in renal medulla, cortex, and corticomedullary junction during hemorrhage-reperfusion. Am J Physiol Renal Physiol 2006; 291: F647–F653 75. Wu MJ, Wen MC, Chiu YT, Chiou YY, Shu KH, et al. Rapamycin attenuates unilateral ureteral obstruction-induced renal fibrosis. Kidney Int 2006; 69: 2029–2036 76. Yeh CH, Chiang HS, Chien CT. Hyaluronic acid ameliorates bladder hyperactivity via the inhibition of H2O2-enhanced purinergic and muscarinic signaling in the rat. Neurourol Urodyn 2010;29:765–770 77. Yeh CH, Chiang HS, Lai TY, Chien CT. Unilateral ureteral obstruction evokes renal tubular apoptosis via the enhanced oxidative stress and endoplasmic reticulum stress in the rat. Neurourol Urodyn 2011; 30: 472–479 78. Yokota T, Yamaguchi O.Changes in cholinergic and purinergic neurotransmission in pathologic bladder of chronic spinal rabbit. J Urol 1996;156:1862–1866 79. Yoshida M, Miyamae K, Iwashita H et al. Management of detrusor dysfunction in the elderly: changes in acetylcholine and adenosine triphosphate release during aging. Urology 2004;63:17–23 80. Yoshimura N, Kaiho Y, Miyazato M et al. Therapeutic receptor targets for lower urinary tract dysfunction. Naunyn Schmiedebergs Arch Pharmacol 2008; 377:437–448 81. Yu HJ, Chien CT, Lai YJ et al. Hypoxia preconditioning attenuates bladder overdistension-induced oxidative injury by up-regulation of Bcl-2 in the rat. J Physiol 2004;554:815–828 82. Yu HJ, Lee WC, Liu SP et al. Unrecognized voiding difficulty in female type 2 diabetic patients in the diabetes clinic: a prospective case-control study. Diabetes Care 2004; 27:988–989 83. Zhang H, Qiu X, Shindel AW et al. Adipose tissue-derived stem cells ameliorate diabetic bladder dysfunction in a type II diabetic rat model. Stem Cells Dev 2011; [Epub ahead of print] 84. Zheng H, Whitman SA, Wu W, Wondrak GT, Wong PK, et al. Therapeutic potential of Nrf2 activators in streptozotocin-induced diabetic nephropathy. Diabetes 2011; 60: 3055–3066 85. Zhu W, Cowie A, Wasfy GW, Penn LZ, Leber B, et al.Bcl-2 mutants with restricted subcellular location reveal spatially distinct pathways for apoptosis in different cell types. EMBO J 1996;15: 4130–4141 | |
| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/61778 | - |
| dc.description.abstract | 排尿障礙 (voiding dysfunction) 以及阻塞性尿路病變 (Obstructive uropathy) 都可說是泌尿科最常見的疾病，也是泌尿科相當重視的研究與治療的主題。臨床上，因尿路結石導致尿路阻塞是最常見並容易造成腎臟的傷害甚至需血液透析治療後者則使得病人的生活品質大受影響並限制其社交活動參與。排尿功能異常 (voiding dysfunction) 在過去常被認為只是因為老化、前列腺增生導致之膀胱出口阻塞以及膀胱逼尿肌的收縮力下降所造成的頻尿、急尿、尿失禁、解尿困難、尿流細小及膀胱內餘尿增加，而近年來也有越來越多的臨床及基礎研究的證據認為代謝症候群是排尿功能異常重要的致病因子之一。這兩種疾病的致病機轉被認為是相當複雜的。近年來，由於分子生物學的進步，過去研究已指出輸尿管阻塞 (ureteral obstruction)造成腎臟損害的機轉與氧化壓力及發炎浸潤有關。此外，我們過去的臨床研究也指出糖尿病或是代謝症候群會明顯地惡化排尿功能，然而這部分的分子生物學層次的致病機轉尚不明確。
我的研究首先以高果糖餵食的動物模式探討代謝症候群所造成的膀胱功能障礙與骨盆神經，外括約肌收縮力及膀胱內壁上的神經傳導受體的變化相關性。這部分研究將有助於了解代謝症候群所改變的下泌尿神經環境在排尿功能異常的發生及進展中所扮演的角色，亦可做為日後發展藥物治療的方向之一。另外我的研究將以單側輸尿管阻塞 (unilateral ureteral obstruction, UUO) 的動物模式探討氧化壓力導致腎臟內活性氧化物增加導致細胞凋亡 (apoptosis) ，細胞自噬 (autophagy) 及細胞死亡 (pyroptosis)在阻塞性尿路病變致病機轉上的角色。也試著研究如何利用調節或抑制腎臟內活性氧化物增加在減緩尿路阻塞導致腎臟損傷機轉的研究。 | zh_TW |
| dc.description.abstract | Voiding dysfunction and obstructive uropathy are both the most common diseases in clinical urology. In our field, these two diseases are the important targets for exploring pathologic mechanisms and potential new drug development. In clinical practice, stone disease is the most common etiology for obstructive uropathy, which can result in further kidney damage even irreversible and make patients to receive maintenance hemodialysis. The quality of life among patients with end-stage renal disease at maintenance dialysis therapy will be impaired, and the patients will be limited to social activity. Voiding dysfunction can manifested as urinary frequency, urgency, incontinence, difficult in voiding weak urinary stream and increased post-void residual. In the past, voiding dysfunction was attributed to aging process, prostatic hyperplasia related bladder outlet obstruction and detrusor underactivity. Increasing evidence based on clinical and basic researches suggested that metabolic syndrome can contribute to the bladder dysfunction. In addition, it is reported that oxidative stress and inflammation infiltration are associated with the renal damage by molecular biological studies. Our previous study also found that type 2 diabetes mellitus and metabolic syndrome will further aggravate the bothersome symptoms of voiding dysfunction, however, the underlying pathophysiology remains unclear.
The aim of the doctoral thesis is first to investigate the role of metabolic syndrome in the pathophysiology of bladder dysfunction by understanding the disarrangements of pelvic nerves, external sphincter synergy and neurotransmitter receptors by a high-fructose fed animal model. The accomplishment of the studies will provide a comprehensive view of the metabolic syndrome related lower urinary tract neural environment and voiding dysfunction. It also provides the direction of development of new drugs to treat voiding dysfunction in the future. On the other hand, my study will use an animal model of unilateral ureteral obstruction (UUO) to examine the role of oxidative stress induced accumulation of reactive oxygen species (ROS) which result in apoptosis, autophagy and pyroptosis in the pathophysiology of obstructive uropathy and investigate how to modulate or inhibit the increase of ROS to attenuate the renal damage by obstructive uropathy. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-16T13:12:50Z (GMT). No. of bitstreams: 1 ntu-102-D97421009-1.pdf: 3257853 bytes, checksum: 9523c63abf1fa59c17cca33e5abb0188 (MD5) Previous issue date: 2013 | en |
| dc.description.tableofcontents | 口試委員會審定書 i
誌謝 ii 中文摘要 iii 英文摘要 iv 博士論文內容 第一章 緒論 1 第一部分：長時間果糖餵養引發代謝症候群之大鼠膀胱周邊嘌呤受體和蕈鹼型受體信號改變 2 第二部分：活化NRF-2信號以抑制單側輸尿管阻塞所引起的粒線體壓力及腎臟相關的細胞自噬、細胞凋亡和炎性細胞死亡 4 第二章 研究方法與材料 6 第一部分：長時間果糖餵養引發代謝症候群之大鼠膀胱周邊嘌呤受體和蕈鹼型受體信號改變 7 第二部分：活化NRF-2信號以抑制單側輸尿管阻塞所引起的粒線體壓力及腎臟相關的細胞自噬、細胞凋亡和炎性細胞死亡 12 第三章 結果 18 第一部分：長時間果糖餵養引發代謝症候群之大鼠膀胱周邊嘌呤受體和蕈鹼型受體信號改變 19 第二部分：活化NRF-2信號以抑制單側輸尿管阻塞所引起的粒線體壓力及腎臟相關的細胞自噬、細胞凋亡和炎性細胞死亡 22 第四章 討論 25 第一部分：長時間果糖餵養引發代謝症候群之大鼠膀胱周邊嘌呤受體和蕈鹼型受體信號改變 26 第二部分：活化NRF-2信號以抑制單側輸尿管阻塞所引起的粒線體壓力及腎臟相關的細胞自噬、細胞凋亡和炎性細胞死亡 30 第五章 展望 35 第六章 論文英文簡述 38 Part I. Alterations in peripheral purinergic and muscarinic signaling of rat bladder after long-term fructose-induced metabolic syndrome 38 Part II. Activating Nrf-2 Signaling Depresses Unilateral Ureteral Obstruction-Evoked Mitochondrial Stress-Related Autophagy, Apoptosis and Pyroptosis in Kidney 42 第七章 參考文獻 47 圖表 57 第一部分：長時間果糖餵養引發代謝症候群之大鼠膀胱周邊嘌呤受體和蕈鹼型受體信號改變 57 表1. 57 圖1. 58 圖2. 59 圖3. 60 圖4. 61 圖5. 62 圖6. 63 圖7. 64 第二部分：活化NRF-2信號以抑制單側輸尿管阻塞所引起的粒線體壓力及腎臟相關的細胞自噬、細胞凋亡和炎性細胞死亡 65 圖1. 65 圖2. 66 圖3. 67 圖4. 68 圖5. 69 圖6. 70 圖7. 71 附錄 73 | |
| dc.language.iso | zh-TW | |
| dc.subject | 排尿障礙 | zh_TW |
| dc.subject | 致病機轉 | zh_TW |
| dc.subject | 粒線體傷害 | zh_TW |
| dc.subject | 輸尿管阻塞 | zh_TW |
| dc.subject | 代謝症候群 | zh_TW |
| dc.subject | voiding dysfunction | en |
| dc.subject | ureteral obstruction | en |
| dc.subject | mitochondrial injury | en |
| dc.subject | metabolic syndrome | en |
| dc.subject | pathomechanism | en |
| dc.title | 代謝性與阻塞性傷害引起排尿及腎功能失調之機轉探究 | zh_TW |
| dc.title | The Pathophysiologic Mechanisms of Metabolic and Obstructive Damage Induced Voiding and Renal Dysfunction | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 101-2 | |
| dc.description.degree | 博士 | |
| dc.contributor.oralexamcommittee | 黃一勝,楊偉勛,陳冠州,孫家棟 | |
| dc.subject.keyword | 代謝症候群,輸尿管阻塞,粒線體傷害,致病機轉,排尿障礙, | zh_TW |
| dc.subject.keyword | metabolic syndrome,ureteral obstruction,mitochondrial injury,pathomechanism,voiding dysfunction, | en |
| dc.relation.page | 90 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2013-07-30 | |
| 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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