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http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/54991完整後設資料紀錄
| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 賴逸儒(I-Rue Lai) | |
| dc.contributor.author | Han-Chen Lin | en |
| dc.contributor.author | 林含貞 | zh_TW |
| dc.date.accessioned | 2021-06-16T03:43:40Z | - |
| dc.date.available | 2019-12-31 | |
| dc.date.copyright | 2015-03-12 | |
| dc.date.issued | 2015 | |
| dc.date.submitted | 2015-02-10 | |
| dc.identifier.citation | Chapter 1
References Argaud, L., Gateau-Roesch, O., Raisky, O., Loufouat, J., Robert, D., & Ovize, M. (2005). Postconditioning inhibits mitochondrial permeability transition. Circulation, 111, 194-197. Bajt, M. L., Farhood, A., & Jaeschke, H. (2001). Effects of CXC chemokines on neutrophil activation and sequestration in hepatic vasculature. Am.J.Physiol Gastrointest.Liver Physiol, 281, G1188-G1195. Bar, F. W., Tzivoni, D., Dirksen, M. T., Fernandez-Ortiz, A., Heyndrickx, G. R., Brachmann, J. et al. (2006). Results of the first clinical study of adjunctive CAldaret (MCC-135) in patients undergoing primary percutaneous coronary intervention for ST-Elevation Myocardial Infarction: the randomized multicentre CASTEMI study. Eur.Heart J., 27, 2516-2523. Bernardi, P. (1999). Mitochondrial transport of cations: channels, exchangers, and permeability transition. Physiol Rev., 79, 1127-1155. Bernardi, P., Vassanelli, S., Veronese, P., Colonna, R., Szabo, I., & Zoratti, M. (1992). Modulation of the mitochondrial permeability transition pore. Effect of protons and divalent cations. J.Biol.Chem., 267, 2934-2939. Bysani, G. K., Kennedy, T. P., Ky, N., Rao, N. V., Blaze, C. A., & Hoidal, J. R. (1990). Role of cytochrome P-450 in reperfusion injury of the rabbit lung. J.Clin.Invest, 86, 1434-1441. Caban, A., Oczkowicz, G., Abdel-Samad, O., & Cierpka, L. (2002). Influence of Kupffer cells on the early phase of liver reperfusion. Transplant.Proc., 34, 694-697. Camargo, C. A., Jr., Madden, J. F., Gao, W., Selvan, R. S., & Clavien, P. A. (1997). Interleukin-6 protects liver against warm ischemia/reperfusion injury and promotes hepatocyte proliferation in the rodent. Hepatology, 26, 1513-1520. Chan, P. H. (2005). Mitochondrial dysfunction and oxidative stress as determinants of cell death/survival in stroke. Ann.N.Y.Acad.Sci., 1042, 203-209. Chan, W., Taylor, A. J., Ellims, A. H., Lefkovits, L., Wong, C., Kingwell, B. A. et al. (2012). Effect of iron chelation on myocardial infarct size and oxidative stress in ST-elevation-myocardial infarction. Circ.Cardiovasc.Interv., 5, 270-278. Chavez-Cartaya, R. E., DeSola, G. P., Wright, L., Jamieson, N. V., & White, D. J. (1995). Regulation of the complement cascade by soluble complement receptor type 1. Protective effect in experimental liver ischemia and reperfusion. Transplantation, 59, 1047-1052. Chen, H., Xing, B., Liu, X., Zhan, B., Zhou, J., Zhu, H. et al. (2008). Ischemic postconditioning inhibits apoptosis after renal ischemia/reperfusion injury in rat. Transpl.Int., 21, 364-371. Chen, S., Chen, L., Wu, X., Lin, J., Fang, J., Chen, X. et al. (2012). Ischemia postconditioning and mesenchymal stem cells engraftment synergistically attenuate ischemia reperfusion-induced lung injury in rats. J.Surg.Res., 178, 81-91. Cohen, M. V. & Downey, J. M. (2008). Adenosine: trigger and mediator of cardioprotection. Basic Res.Cardiol., 103, 203-215. Cohen, M. V., Yang, X. M., & Downey, J. M. (2007). The pH hypothesis of postconditioning: staccato reperfusion reintroduces oxygen and perpetuates myocardial acidosis. Circulation, 115, 1895-1903. Colletti, L. M., Cortis, A., Lukacs, N., Kunkel, S. L., Green, M., & Strieter, R. M. (1998). Tumor necrosis factor up-regulates intercellular adhesion molecule 1, which is important in the neutrophil-dependent lung and liver injury associated with hepatic ischemia and reperfusion in the rat. Shock, 10, 182-191. Crenesse, D., Hugues, M., Ferre, C., Poiree, J. C., Benoliel, J., Dolisi, C. et al. (1999). Inhibition of calcium influx during hypoxia/reoxygenation in primary cultured rat hepatocytes. Pharmacology, 58, 160-170. Crompton, M. (1999). The mitochondrial permeability transition pore and its role in cell death. Biochem.J., 341 ( Pt 2), 233-249. Crompton, M. (2000). Mitochondrial intermembrane junctional complexes and their role in cell death. J.Physiol, 529 Pt 1, 11-21. Currin, R. T., Gores, G. J., Thurman, R. G., & Lemasters, J. J. (1991). Protection by acidotic pH against anoxic cell killing in perfused rat liver: evidence for a pH paradox. FASEB J., 5, 207-210. Duchen, M. R., McGuinness, O., Brown, L. A., & Crompton, M. (1993). On the involvement of a cyclosporin A sensitive mitochondrial pore in myocardial reperfusion injury. Cardiovasc.Res., 27, 1790-1794. Eldaif, S. M., Deneve, J. A., Wang, N. P., Jiang, R., Mosunjac, M., Mutrie, C. J. et al. (2010). Attenuation of renal ischemia-reperfusion injury by postconditioning involves adenosine receptor and protein kinase C activation. Transpl.Int., 23, 217-226. Fan, C., Zwacka, R. M., & Engelhardt, J. F. (1999). Therapeutic approaches for ischemia/reperfusion injury in the liver. J.Mol.Med.(Berl), 77, 577-592. Fang, J., Chen, L., Fan, L., Wu, L., Chen, X., Li, W. et al. (2011). Enhanced therapeutic effects of mesenchymal stem cells on myocardial infarction by ischemic postconditioning through paracrine mechanisms in rats. J.Mol.Cell Cardiol., 51, 839-847. Ferranti, R., da Silva, M. M., & Kowaltowski, A. J. (2003). Mitochondrial ATP-sensitive K+ channel opening decreases reactive oxygen species generation. FEBS Lett., 536, 51-55. Flaherty, J. T., Pitt, B., Gruber, J. W., Heuser, R. R., Rothbaum, D. A., Burwell, L. R. et al. (1994). Recombinant human superoxide dismutase (h-SOD) fails to improve recovery of ventricular function in patients undergoing coronary angioplasty for acute myocardial infarction. Circulation, 89, 1982-1991. Gateau-Roesch, O., Argaud, L., & Ovize, M. (2006). Mitochondrial permeability transition pore and postconditioning. Cardiovasc.Res., 70, 264-273. Gho, B. C., Schoemaker, R. G., van den Doel, M. A., Duncker, D. J., & Verdouw, P. D. (1996). Myocardial protection by brief ischemia in noncardiac tissue. Circulation, 94, 2193-2200. Gogvadze, V., Robertson, J. D., Zhivotovsky, B., & Orrenius, S. (2001). Cytochrome c release occurs via Ca2+-dependent and Ca2+-independent mechanisms that are regulated by Bax. J.Biol.Chem., 276, 19066-19071. Granger, D. N. (1999). Ischemia-reperfusion: mechanisms of microvascular dysfunction and the influence of risk factors for cardiovascular disease. Microcirculation., 6, 167-178. Halestrap, A. P., McStay, G. P., & Clarke, S. J. (2002). The permeability transition pore complex: another view. Biochimie, 84, 153-166. Hansen, P. R., Thibault, H., & Abdulla, J. (2010). Postconditioning during primary percutaneous coronary intervention: a review and meta-analysis. Int.J.Cardiol., 144, 22-25. Hausenloy, D. J., Boston-Griffiths, E. A., & Yellon, D. M. (2012). Cyclosporin A and cardioprotection: from investigative tool to therapeutic agent. Br.J.Pharmacol., 165, 1235-1245. Hisama, N., Yamaguchi, Y., Ishiko, T., Miyanari, N., Ichiguchi, O., Goto, M. et al. (1996). Kupffer cell production of cytokine-induced neutrophil chemoattractant following ischemia/reperfusion injury in rats. Hepatology, 24, 1193-1198. Hoffmeyer, M. R., Jones, S. P., Ross, C. R., Sharp, B., Grisham, M. B., Laroux, F. S. et al. (2000). Myocardial ischemia/reperfusion injury in NADPH oxidase-deficient mice. Circ.Res., 87, 812-817. Ishikawa, M., Cooper, D., Russell, J., Salter, J. W., Zhang, J. H., Nanda, A. et al. (2003). Molecular determinants of the prothrombogenic and inflammatory phenotype assumed by the postischemic cerebral microcirculation. Stroke, 34, 1777-1782. Iwakura, K., Ito, H., Okamura, A., Koyama, Y., Date, M., Higuchi, Y. et al. (2009). Nicorandil treatment in patients with acute myocardial infarction: a meta-analysis. Circ.J., 73, 925-931. Jaeschke, H. (1998). Mechanisms of reperfusion injury after warm ischemia of the liver. J.Hepatobiliary.Pancreat.Surg., 5, 402-408. Jaeschke, H., Farhood, A., Bautista, A. P., Spolarics, Z., & Spitzer, J. J. (1993). Complement activates Kupffer cells and neutrophils during reperfusion after hepatic ischemia. Am.J.Physiol, 264, G801-G809. Janicki, P. K., Wise, P. E., Belous, A. E., & Pinson, C. W. (2001). Interspecies differences in hepatic Ca(2+)-ATPase activity and the effect of cold preservation on porcine liver Ca(2+)-ATPase function. Liver Transpl., 7, 132-139. JENNINGS, R. B., SOMMERS, H. M., SMYTH, G. A., FLACK, H. A., & LINN, H. (1960). Myocardial necrosis induced by temporary occlusion of a coronary artery in the dog. Arch.Pathol., 70, 68-78. Jiang, B., Chen, Q., Liu, X., Kong, D., Kuang, Y., Weng, X. et al. (2012). Ischemic postconditioning protects renal function after 24 hours of cold preservation in a canine autotransplantation model. Transplant.Proc., 44, 1776-1781. Jordan, J. E., Zhao, Z. Q., & Vinten-Johansen, J. (1999). The role of neutrophils in myocardial ischemia-reperfusion injury. Cardiovasc.Res., 43, 860-878. Jurgensmeier, J. M., Xie, Z., Deveraux, Q., Ellerby, L., Bredesen, D., & Reed, J. C. (1998). Bax directly induces release of cytochrome c from isolated mitochondria. Proc.Natl.Acad.Sci.U.S.A, 95, 4997-5002. Kanazawa, H., Fujimoto, Y., Teratani, T., Iwasaki, J., Kasahara, N., Negishi, K. et al. (2011). Bone marrow-derived mesenchymal stem cells ameliorate hepatic ischemia reperfusion injury in a rat model. PLoS.One., 6, e19195. Kasama, S., Furuya, M., Toyama, T., Ichikawa, S., & Kurabayashi, M. (2008). Effect of atrial natriuretic peptide on left ventricular remodelling in patients with acute myocardial infarction. Eur.Heart J., 29, 1485-1494. Khalil, A. A., Aziz, F. A., & Hall, J. C. (2006). Reperfusion injury. Plast.Reconstr.Surg., 117, 1024-1033. Kis, B., Rajapakse, N. C., Snipes, J. A., Nagy, K., Horiguchi, T., & Busija, D. W. (2003). Diazoxide induces delayed pre-conditioning in cultured rat cortical neurons. J.Neurochem., 87, 969-980. Kitakaze, M., Asakura, M., Kim, J., Shintani, Y., Asanuma, H., Hamasaki, T. et al. (2007). Human atrial natriuretic peptide and nicorandil as adjuncts to reperfusion treatment for acute myocardial infarction (J-WIND): two randomised trials. Lancet, 370, 1483-1493. Lai, I. R., Chang, K. J., Chen, C. F., & Tsai, H. W. (2006). Transient limb ischemia induces remote preconditioning in liver among rats: the protective role of heme oxygenase-1. Transplantation, 81, 1311-1317. Lai, I. R., Chang, K. J., Tsai, H. W., & Chen, C. F. (2008). Pharmacological preconditioning with simvastatin protects liver from ischemia-reperfusion injury by heme oxygenase-1 induction. Transplantation, 85, 732-738. Lai, I. R., Ma, M. C., Chen, C. F., & Chang, K. J. (2004). The protective role of heme oxygenase-1 on the liver after hypoxic preconditioning in rats. Transplantation, 77, 1004-1008. Le Moine, O., Louis, H., Demols, A., Desalle, F., Demoor, F., Quertinmont, E. et al. (2000). Cold liver ischemia-reperfusion injury critically depends on liver T cells and is improved by donor pretreatment with interleukin 10 in mice. Hepatology, 31, 1266-1274. Lehmann, T. G., Koeppel, T. A., Munch, S., Heger, M., Kirschfink, M., Klar, E. et al. (2001). Impact of inhibition of complement by sCR1 on hepatic microcirculation after warm ischemia. Microvasc.Res., 62, 284-292. Lentsch, A. B., Yoshidome, H., Cheadle, W. G., Miller, F. N., & Edwards, M. J. (1998). Chemokine involvement in hepatic ischemia/reperfusion injury in mice: roles for macrophage inflammatory protein-2 and Kupffer cells. Hepatology, 27, 507-512. Lim, S. Y., Davidson, S. M., Hausenloy, D. J., & Yellon, D. M. (2007). Preconditioning and postconditioning: the essential role of the mitochondrial permeability transition pore. Cardiovasc.Res., 75, 530-535. Lim, S. Y., Yellon, D. M., & Hausenloy, D. J. (2010). The neural and humoral pathways in remote limb ischemic preconditioning. Basic Res.Cardiol., 105, 651-655. Lin, H. C., Liu, S. Y., Lai, H. S., & Lai, I. R. (2013). Isolated mitochondria infusion mitigates ischemia-reperfusion injury of the liver in rats. Shock, 39, 304-310. Llacuna, L., Mari, M., Lluis, J. M., Garcia-Ruiz, C., Fernandez-Checa, J. C., & Morales, A. (2009). Reactive oxygen species mediate liver injury through parenchymal nuclear factor-kappaB inactivation in prolonged ischemia/reperfusion. Am.J.Pathol., 174, 1776-1785. McAllister, S. E., Ashrafpour, H., Cahoon, N., Huang, N., Moses, M. A., Neligan, P. C. et al. (2008). Postconditioning for salvage of ischemic skeletal muscle from reperfusion injury: efficacy and mechanism. Am.J.Physiol Regul.Integr.Comp Physiol, 295, R681-R689. McCully, J. D., Cowan, D. B., Pacak, C. A., Toumpoulis, I. K., Dayalan, H., & Levitsky, S. (2009). Injection of isolated mitochondria during early reperfusion for cardioprotection. Am.J.Physiol Heart Circ.Physiol, 296, H94-H105. McCurry, K. R., Campbell, D. A., Jr., Scales, W. E., Warren, J. S., & Remick, D. G. (1993). Tumor necrosis factor, interleukin 6, and the acute phase response following hepatic ischemia/reperfusion. J. Surg. Res., 55, 49-54. Morigi, M., Rota, C., Montemurro, T., Montelatici, E., Lo, C., V, Imberti, B. et al. (2010). Life-sparing effect of human cord blood-mesenchymal stem cells in experimental acute kidney injury. Stem Cells, 28, 513-522. Murry, C. E., Jennings, R. B., & Reimer, K. A. (1986). Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium. Circulation, 74, 1124-1136. Nakagawa, T., Zhu, H., Morishima, N., Li, E., Xu, J., Yankner, B. A. et al. (2000). Caspase-12 mediates endoplasmic-reticulum-specific apoptosis and cytotoxicity by amyloid-beta. Nature, 403, 98-103. Piccotti, L., Marchetti, C., Migliorati, G., Roberti, R., & Corazzi, L. (2002). Exogenous phospholipids specifically affect transmembrane potential of brain mitochondria and cytochrome C release. J. Biol.Chem., 277, 12075-12081. Piot, C., Croisille, P., Staat, P., Thibault, H., Rioufol, G., Mewton, N. et al. (2008). Effect of cyclosporine on reperfusion injury in acute myocardial infarction. N. Engl. J. Med., 359, 473-481. Post, S., Post, M. C., van den Branden, B. J., Eefting, F. D., Goumans, M. J., Stella, P. R. et al. (2012). Early statin treatment prior to primary PCI for acute myocardial infarction: REPERATOR, a randomized placebo-controlled pilot trial. Catheter.Cardiovasc.Interv., 80, 756-765. Przyklenk, K., Darling, C. E., Dickson, E. W., & Whittaker, P. (2003). Cardioprotection 'outside the box'--the evolving paradigm of remote preconditioning. Basic Res.Cardiol., 98, 149-157. Reers, M., Smith, T. W., & Chen, L. B. (1991). J-aggregate formation of a carbocyanine as a quantitative fluorescent indicator of membrane potential. Biochemistry, 30, 4480-4486. Saad, S., Minor, T., Kotting, M., Fu, Z. X., Hagn, U., Paul, A. et al. (2001). Extension of ischemic tolerance of porcine livers by cold preservation including postconditioning with gaseous oxygen. Transplantation, 71, 498-502. Sanada, S., Komuro, I., & Kitakaze, M. (2011). Pathophysiology of myocardial reperfusion injury: preconditioning, postconditioning, and translational aspects of protective measures. Am.J.Physiol Heart Circ.Physiol, 301, H1723-H1741. Selzner, N., Rudiger, H., Graf, R., & Clavien, P. A. (2003). Protective strategies against ischemic injury of the liver. Gastroenterology, 125, 917-936. Shimizu, K., Lacza, Z., Rajapakse, N., Horiguchi, T., Snipes, J., & Busija, D. W. (2002). MitoK(ATP) opener, diazoxide, reduces neuronal damage after middle cerebral artery occlusion in the rat. Am.J.Physiol Heart Circ.Physiol, 283, H1005-H1011. Singer, N. G. & Caplan, A. I. (2011). Mesenchymal stem cells: mechanisms of inflammation. Annu.Rev.Pathol., 6, 457-478. Sun, K., Liu, Z. S., & Sun, Q. (2004). Role of mitochondria in cell apoptosis during hepatic ischemia-reperfusion injury and protective effect of ischemic postconditioning. World J.Gastroenterol., 10, 1934-1938. Tan, X., Zhang, L., Jiang, Y., Yang, Y., Zhang, W., Li, Y. et al. (2013). Postconditioning ameliorates mitochondrial DNA damage and deletion after renal ischemic injury. Nephrol.Dial.Transplant., 28, 2754-2765. Taskapilioglu, M. O., Alkan, T., Goren, B., Tureyen, K., Sahin, S., Taskapilioglu, O. et al. (2009). Neuronal protective effects of focal ischemic pre- and/or postconditioning on the model of transient focal cerebral ischemia in rats. J.Clin.Neurosci., 16, 693-697. Theroux, P., Chaitman, B. R., Danchin, N., Erhardt, L., Meinertz, T., Schroeder, J. S. et al. (2000). Inhibition of the sodium-hydrogen exchanger with cariporide to prevent myocardial infarction in high-risk ischemic situations. Main results of the GUARDIAN trial. Guard during ischemia against necrosis (GUARDIAN) Investigators. Circulation, 102, 3032-3038. Tsao, P. S., Aoki, N., Lefer, D. J., Johnson, G., III, & Lefer, A. M. (1990). Time course of endothelial dysfunction and myocardial injury during myocardial ischemia and reperfusion in the cat. Circulation, 82, 1402-1412. Urano, F., Wang, X., Bertolotti, A., Zhang, Y., Chung, P., Harding, H. P. et al. (2000). Coupling of stress in the ER to activation of JNK protein kinases by transmembrane protein kinase IRE1. Science, 287, 664-666. Wei, Y. H., Ding, W. H., & Wei, R. D. (1984). Biochemical effects of PR toxin on rat liver mitochondrial respiration and oxidative phosphorylation. Arch.Biochem.Biophys., 230, 400-411. Wu, L., Shen, F., Lin, L., Zhang, X., Bruce, I. C., & Xia, Q. (2006). The neuroprotection conferred by activating the mitochondrial ATP-sensitive K+ channel is mediated by inhibiting the mitochondrial permeability transition pore. Neurosci.Lett., 402, 184-189. Yandza, T., Tauc, M., Saint-Paul, M. C., Ouaissi, M., Gugenheim, J., & Hebuterne, X. (2012). The pig as a preclinical model for intestinal ischemia-reperfusion and transplantation studies. J.Surg.Res., 178, 807-819. Yellon, D. M. & Hausenloy, D. J. (2007). Myocardial reperfusion injury. N.Engl.J.Med., 357, 1121-1135. Yun, Y., Duan, W. G., Chen, P., Wu, H. X., Shen, Z. Q., Qian, Z. Y. et al. (2009). Ischemic postconditioning modified renal oxidative stress and lipid peroxidation caused by ischemic reperfusion injury in rats. Transplant.Proc., 41, 3597-3602. Zeng, Z., Huang, H. F., Chen, M. Q., Song, F., & Zhang, Y. J. (2010). Postconditioning prevents ischemia/reperfusion injury in rat liver transplantation. Hepatogastroenterology, 57, 875-881. Zhao, Z. Q. (2010). Postconditioning in reperfusion injury: a status report. Cardiovasc.Drugs Ther., 24, 265-279. Zhao, Z. Q., Corvera, J. S., Halkos, M. E., Kerendi, F., Wang, N. P., Guyton, R. A. et al. (2003). Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning. Am.J.Physiol Heart Circ.Physiol, 285, H579-H588. Zwacka, R. M., Zhang, Y., Halldorson, J., Schlossberg, H., Dudus, L., & Engelhardt, J. F. (1997). CD4(+) T-lymphocytes mediate ischemia/reperfusion-induced inflammatory responses in mouse liver. J.Clin.Invest, 100, 279-289. Chapter 2 References Ambros, V. (2004). The functions of animal microRNAs. Nature, 431, 350-355. Argaud, L., Gateau-Roesch, O., Raisky, O., Loufouat, J., Robert, D., & Ovize, M. (2005). Postconditioning inhibits mitochondrial permeability transition. Circulation, 111, 194-197. Bajt, M. L., Farhood, A., & Jaeschke, H. (2001). Effects of CXC chemokines on neutrophil activation and sequestration in hepatic vasculature. Am.J.Physiol Gastrointest.Liver Physiol, 281, G1188-G1195. Bar, F. W., Tzivoni, D., Dirksen, M. T., Fernandez-Ortiz, A., Heyndrickx, G. R., Brachmann, J. et al. (2006). Results of the first clinical study of adjunctive CAldaret (MCC-135) in patients undergoing primary percutaneous coronary intervention for ST-Elevation Myocardial Infarction: the randomized multicentre CASTEMI study. Eur.Heart J., 27, 2516-2523. Bartel, D. P. (2004). MicroRNAs: genomics, biogenesis, mechanism, and function. Cell, 116, 281-297. Bernardi, P. (1999). Mitochondrial transport of cations: channels, exchangers, and permeability transition. Physiol Rev., 79, 1127-1155. Bernardi, P., Vassanelli, S., Veronese, P., Colonna, R., Szabo, I., & Zoratti, M. (1992). Modulation of the mitochondrial permeability transition pore. Effect of protons and divalent cations. J.Biol.Chem., 267, 2934-2939. Brennecke, J., Hipfner, D. R., Stark, A., Russell, R. B., & Cohen, S. M. (2003). bantam encodes a developmentally regulated microRNA that controls cell proliferation and regulates the proapoptotic gene hid in Drosophila. Cell, 113, 25-36. Bysani, G. K., Kennedy, T. P., Ky, N., Rao, N. V., Blaze, C. A., & Hoidal, J. R. (1990). Role of cytochrome P-450 in reperfusion injury of the rabbit lung. J.Clin.Invest, 86, 1434-1441. Caban, A., Oczkowicz, G., Abdel-Samad, O., & Cierpka, L. (2002). Influence of Kupffer cells on the early phase of liver reperfusion. Transplant.Proc., 34, 694-697. Camargo, C. A., Jr., Madden, J. F., Gao, W., Selvan, R. S., & Clavien, P. A. (1997). Interleukin-6 protects liver against warm ischemia/reperfusion injury and promotes hepatocyte proliferation in the rodent. Hepatology, 26, 1513-1520. Chan, P. H. (2005). Mitochondrial dysfunction and oxidative stress as determinants of cell death/survival in stroke. Ann.N.Y.Acad.Sci., 1042, 203-209. Chan, W., Taylor, A. J., Ellims, A. H., Lefkovits, L., Wong, C., Kingwell, B. A. et al. (2012). Effect of iron chelation on myocardial infarct size and oxidative stress in ST-elevation-myocardial infarction. Circ.Cardiovasc.Interv., 5, 270-278. Chavez-Cartaya, R. E., DeSola, G. P., Wright, L., Jamieson, N. V., & White, D. J. (1995). Regulation of the complement cascade by soluble complement receptor type 1. Protective effect in experimental liver ischemia and reperfusion. Transplantation, 59, 1047-1052. Chen, H., Xing, B., Liu, X., Zhan, B., Zhou, J., Zhu, H. et al. (2008). Ischemic postconditioning inhibits apoptosis after renal ischemia/reperfusion injury in rat. Transpl.Int., 21, 364-371. Chen, Q., Kong, L., Xu, X., Geng, Q., Tang, W., & Jiang, W. (2013). Down-regulation of microRNA-146a in the early stage of liver ischemia-reperfusion injury. Transplant.Proc., 45, 492-496. Chen, S., Chen, L., Wu, X., Lin, J., Fang, J., Chen, X. et al. (2012). Ischemia postconditioning and mesenchymal stem cells engraftment synergistically attenuate ischemia reperfusion-induced lung injury in rats. J.Surg.Res., 178, 81-91. Cheng, Y., Zhu, P., Yang, J., Liu, X., Dong, S., Wang, X. et al. (2010). Ischaemic preconditioning-regulated miR-21 protects heart against ischaemia/reperfusion injury via anti-apoptosis through its target PDCD4. Cardiovasc.Res., 87, 431-439. Cohen, M. V. & Downey, J. M. (2008). Adenosine: trigger and mediator of cardioprotection. Basic Res.Cardiol., 103, 203-215. Cohen, M. V., Yang, X. M., & Downey, J. M. (2007). The pH hypothesis of postconditioning: staccato reperfusion reintroduces oxygen and perpetuates myocardial acidosis. Circulation, 115, 1895-1903. Colletti, L. M., Cortis, A., Lukacs, N., Kunkel, S. L., Green, M., & Strieter, R. M. (1998). Tumor necrosis factor up-regulates intercellular adhesion molecule 1, which is important in the neutrophil-dependent lung and liver injury associated with hepatic ischemia and reperfusion in the rat. Shock, 10, 182-191. Crenesse, D., Hugues, M., Ferre, C., Poiree, J. C., Benoliel, J., Dolisi, C. et al. (1999). Inhibition of calcium influx during hypoxia/reoxygenation in primary cultured rat hepatocytes. Pharmacology, 58, 160-170. Crompton, M. (1999). The mitochondrial permeability transition pore and its role in cell death. Biochem.J., 341 ( Pt 2), 233-249. Crompton, M. (2000). Mitochondrial intermembrane junctional complexes and their role in cell death. J.Physiol, 529 Pt 1, 11-21. Currin, R. T., Gores, G. J., Thurman, R. G., & Lemasters, J. J. (1991). Protection by acidotic pH against anoxic cell killing in perfused rat liver: evidence for a pH paradox. FASEB J., 5, 207-210. Dharap, A., Bowen, K., Place, R., Li, L. C., & Vemuganti, R. (2009). Transient focal ischemia induces extensive temporal changes in rat cerebral microRNAome. J.Cereb.Blood Flow Metab, 29, 675-687. Doench, J. G., Petersen, C. P., & Sharp, P. A. (2003). siRNAs can function as miRNAs. Genes Dev., 17, 438-442. Duchen, M. R., McGuinness, O., Brown, L. A., & Crompton, M. (1993). On the involvement of a cyclosporin A sensitive mitochondrial pore in myocardial reperfusion injury. Cardiovasc.Res., 27, 1790-1794. Eldaif, S. M., Deneve, J. A., Wang, N. P., Jiang, R., Mosunjac, M., Mutrie, C. J. et al. (2010). Attenuation of renal ischemia-reperfusion injury by postconditioning involves adenosine receptor and protein kinase C activation. Transpl.Int., 23, 217-226. Fan, C., Zwacka, R. M., & Engelhardt, J. F. (1999). Therapeutic approaches for ischemia/reperfusion injury in the liver. J.Mol.Med.(Berl), 77, 577-592. Fang, J., Chen, L., Fan, L., Wu, L., Chen, X., Li, W. et al. (2011). Enhanced therapeutic effects of mesenchymal stem cells on myocardial infarction by ischemic postconditioning through paracrine mechanisms in rats. J.Mol.Cell Cardiol., 51, 839-847. Fasanaro, P., Greco, S., Ivan, M., Capogrossi, M. C., & Martelli, F. (2010). microRNA: emerging therapeutic targets in acute ischemic diseases. Pharmacol.Ther., 125, 92-104. Feng, X., Wang, Z., Fillmore, R., & Xi, Y. (2014). MiR-200, a new star miRNA in human cancer. Cancer Lett., 344, 166-173. Ferranti, R., da Silva, M. M., & Kowaltowski, A. J. (2003). Mitochondrial ATP-sensitive K+ channel opening decreases reactive oxygen species generation. FEBS Lett., 536, 51-55. Filipowicz, W., Bhattacharyya, S. N., & Sonenberg, N. (2008). Mechanisms of post-transcriptional regulation by microRNAs: are the answers in sight? Nat.Rev.Genet., 9, 102-114. Flaherty, J. T., Pitt, B., Gruber, J. W., Heuser, R. R., Rothbaum, D. A., Burwell, L. R. et al. (1994). Recombinant human superoxide dismutase (h-SOD) fails to improve recovery of ventricular function in patients undergoing coronary angioplasty for acute myocardial infarction. Circulation, 89, 1982-1991. Gateau-Roesch, O., Argaud, L., & Ovize, M. (2006). Mitochondrial permeability transition pore and postconditioning. Cardiovasc.Res., 70, 264-273. Gho, B. C., Schoemaker, R. G., van den Doel, M. A., Duncker, D. J., & Verdouw, P. D. (1996). Myocardial protection by brief ischemia in noncardiac tissue. Circulation, 94, 2193-2200. Godwin, J. G., Ge, X., Stephan, K., Jurisch, A., Tullius, S. G., & Iacomini, J. (2010). Identification of a microRNA signature of renal ischemia reperfusion injury. Proc.Natl.Acad.Sci.U.S.A, 107, 14339-14344. Gogvadze, V., Robertson, J. D., Zhivotovsky, B., & Orrenius, S. (2001). Cytochrome c release occurs via Ca2+-dependent and Ca2+-independent mechanisms that are regulated by Bax. J.Biol.Chem., 276, 19066-19071. Granger, D. N. (1999). Ischemia-reperfusion: mechanisms of microvascular dysfunction and the influence of risk factors for cardiovascular disease. Microcirculation., 6, 167-178. Halestrap, A. P., McStay, G. P., & Clarke, S. J. (2002). The permeability transition pore complex: another view. Biochimie, 84, 153-166. Hansen, P. R., Thibault, H., & Abdulla, J. (2010). Postconditioning during primary percutaneous coronary intervention: a review and meta-analysis. Int.J.Cardiol., 144, 22-25. Hausenloy, D. J., Boston-Griffiths, E. A., & Yellon, D. M. (2012). Cyclosporin A and cardioprotection: from investigative tool to therapeutic agent. Br.J.Pharmacol., 165, 1235-1245. He, B., Xiao, J., Ren, A. J., Zhang, Y. F., Zhang, H., Chen, M. et al. (2011). Role of miR-1 and miR-133a in myocardial ischemic postconditioning. J.Biomed.Sci., 18, 22. He, S., Liu, P., Jian, Z., Li, J., Zhu, Y., Feng, Z. et al. (2013). miR-138 protects cardiomyocytes from hypoxia-induced apoptosis via MLK3/JNK/c-jun pathway. Biochem.Biophys.Res.Commun., 441, 763-769. Hisama, N., Yamaguchi, Y., Ishiko, T., Miyanari, N., Ichiguchi, O., Goto, M. et al. (1996). Kupffer cell production of cytokine-induced neutrophil chemoattractant following ischemia/reperfusion injury in rats. Hepatology, 24, 1193-1198. Hoffmeyer, M. R., Jones, S. P., Ross, C. R., Sharp, B., Grisham, M. B., Laroux, F. S. et al. (2000). Myocardial ischemia/reperfusion injury in NADPH oxidase-deficient mice. Circ.Res., 87, 812-817. Hsieh, C. H., Jeng, J. C., Jeng, S. F., Wu, C. J., Lu, T. H., Liliang, P. C. et al. (2010). MicroRNA profiling in ischemic injury of the gracilis muscle in rats. BMC.Musculoskelet.Disord., 11, 123. Hu, S., Huang, M., Li, Z., Jia, F., Ghosh, Z., Lijkwan, M. A. et al. (2010). MicroRNA-210 as a novel therapy for treatment of ischemic heart disease. Circulation, 122, S124-S131. Ishikawa, M., Cooper, D., Russell, J., Salter, J. W., Zhang, J. H., Nanda, A. et al. (2003). Molecular determinants of the prothrombogenic and inflammatory phenotype assumed by the postischemic cerebral microcirculation. Stroke, 34, 1777-1782. Iwakura, K., Ito, H., Okamura, A., Koyama, Y., Date, M., Higuchi, Y. et al. (2009). Nicorandil treatment in patients with acute myocardial infarction: a meta-analysis. Circ.J., 73, 925-931. Jaeschke, H. (1998). Mechanisms of reperfusion injury after warm ischemia of the liver. J.Hepatobiliary.Pancreat.Surg., 5, 402-408. Jaeschke, H., Farhood, A., Bautista, A. P., Spolarics, Z., & Spitzer, J. J. (1993). Complement activates Kupffer cells and neutrophils during reperfusion after hepatic ischemia. Am.J.Physiol, 264, G801-G809. Janicki, P. K., Wise, P. E., Belous, A. E., & Pinson, C. W. (2001). Interspecies differences in hepatic Ca(2+)-ATPase activity and the effect of cold preservation on porcine liver Ca(2+)-ATPase function. Liver Transpl., 7, 132-139. JENNINGS, R. B., SOMMERS, H. M., SMYTH, G. A., FLACK, H. A., & LINN, H. (1960). Myocardial necrosis induced by temporary occlusion of a coronary artery in the dog. Arch.Pathol., 70, 68-78. Jiang, B., Chen, Q., Liu, X., Kong, D., Kuang, Y., Weng, X. et al. (2012). Ischemic postconditioning protects renal function after 24 hours of cold preservation in a canine autotransplantation model. Transplant.Proc., 44, 1776-1781. Jiang, W., Kong, L., Ni, Q., Lu, Y., Ding, W., Liu, G. et al. (2014). miR-146a ameliorates liver ischemia/reperfusion injury by suppressing IRAK1 and TRAF6. PLoS.One., 9, e101530. Jordan, J. E., Zhao, Z. Q., & Vinten-Johansen, J. (1999). The role of neutrophils in myocardial ischemia-reperfusion injury. Cardiovasc.Res., 43, 860-878. Jurgensmeier, J. M., Xie, Z., Deveraux, Q., Ellerby, L., Bredesen, D., & Reed, J. C. (1998). Bax directly induces release of cytochrome c from isolated mitochondria. Proc.Natl.Acad.Sci.U.S.A, 95, 4997-5002. Kanazawa, H., Fujimoto, Y., Teratani, T., Iwasaki, J., Kasahara, N., Negishi, K. et al. (2011). Bone marrow-derived mesenchymal stem cells ameliorate hepatic ischemia reperfusion injury in a rat model. PLoS.One., 6, e19195. Kasama, S., Furuya, M., Toyama, T., Ichikawa, S., & Kurabayashi, M. (2008). Effect of atrial natriuretic peptide on left ventricular remodelling in patients with acute myocardial infarction. Eur.Heart J., 29, 1485-1494. Ke, B., Shen, X. D., Ji, H., Kamo, N., Gao, F., Freitas, M. C. et al. (2012). HO-1-STAT3 axis in mouse liver ischemia/reperfusion injury: regulation of TLR4 innate responses through PI3K/PTEN signaling. J.Hepatol., 56, 359-366. Khalil, A. A., Aziz, F. A., & Hall, J. C. (2006). Reperfusion injury. Plast.Reconstr.Surg., 117, 1024-1033. Kim, J., Inoue, K., Ishii, J., Vanti, W. B., Voronov, S. V., Murchison, E. et al. (2007). A MicroRNA feedback circuit in midbrain dopamine neurons. Science, 317, 1220-1224. Kis, B., Rajapakse, N. C., Snipes, J. A., Nagy, K., Horiguchi, T., & Busija, D. W. (2003). Diazoxide induces delayed pre-conditioning in cultured rat cortical neurons. J.Neurochem., 87, 969-980. Kitakaze, M., Asakura, M., Kim, J., Shintani, Y., Asanuma, H., Hamasaki, T. et al. (2007). Human atrial natriuretic peptide and nicorandil as adjuncts to reperfusion treatment for | |
| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/54991 | - |
| dc.description.abstract | 缺血再灌流傷害(ischemia-reperfusion injury)常發生在器官移植、心肌梗塞、腦中風、創傷等情況，恢復血流(或稱再灌流)對於缺血的組織而言是必要的，然而再灌流往往帶來缺血以外的傷害，因此研究減少缺血再灌流傷害對於提升器官移植的成功率以及心肌梗塞或腦中風的預後是相當重要的。目前主要研究減少缺血再灌流傷害的方法有下列幾種：1. 藥物2.幹細胞療法3.制約訓練4.胞器治療(例如粒線體)。制約訓練(conditioning)是給予短暫的缺血再灌流處理，又可分為前制約訓練、後制約訓練以及遠端制約訓練，依照實行的時間點以及是否直接實行於缺血器官來做為區分，其保護效果與機制也略有不同。本研究中，吾人以肝臟缺血再灌流的動物模式，來探討後制約訓練(ischemic postconditioning, iPoC)對於肝臟缺血再灌流的保護效應與機制。首先，Wistar大鼠肝臟經過45分鐘缺血，立即給予重複三個循環的1分鐘的肝臟缺血和1分鐘的再灌流處理(iPoC組)，跟只有肝臟缺血的組別(IR組)比較，血液中ALT的升高值、肝臟細胞的凋亡以及4-hydroxy-2- nonenal (4-HNE，脂質過氧化產物)的增加情形都減少。缺血再灌流會破壞粒線體的膜電位(mitochondrial membrane potential)而導致cytochrome c 釋放至細胞質，引發肝細胞的凋亡。在iPoC的組別中，細胞質cytochrome c 的表現有明顯下降的情形，且粒線體膜電位的破壞也比較輕微。粒線體膜電位的改變是跟mitochondria permeability transition (MPT)有關。對肝臟缺血的大鼠給予NIM811 (MPT抑制劑)可以模擬iPoC的保護效應，減少cytochrome c的釋放；若給予atractyloside (MPT誘發劑)則會破壞iPoC的保護效應，表示iPoC是透過調控MPT來減少肝臟缺血再灌流傷害。
進而以陣列分析與定量聚合脢反應比較iPoC組跟IR組肝臟的microRNA的變化，發現iPoC會明顯增加肝臟中miR-183的表現增加以軟體搜尋發現參與細胞凋亡過程的一個重要蛋白質，Apaf-1，是miR-183的作用標的。Dual luciferase assay證實miR-183會透過結合至Apaf-1 的3’-UTR來抑制其表現。吾人以氧氣及葡萄糖剝奪模式(oxygen-glucose deprivation, OGD)，驗證低氧後制約訓練(hypoxic postconditioining, HPoC)會使大鼠肝臟細胞株-Clone 9 cells的miR-183表現增加、減少細胞凋亡以及Apaf-1的表現；給予miR-183模擬物可以模擬HPoC的保護效果，但給予miR-183抑制劑則會破壞HPoC的保護效果。同時，觀察到miR-183模擬物會減少凋亡訊息中Apaf-1下游的active caspase-3、cleaved caspase-9的表現，但不會影響上游cytochrome c 的表現。顯示miR-183是透過對於Apaf-1的抑制而減少下游caspase signaling，達到保護效果。接著，以C57BL/6小鼠的肝臟缺血再灌流的模式，與IR組比較，發現後制約訓練 (iPoC)引起miR-183的表現有明顯上升，且減少了ALT的上升、肝臟細胞的傷害(TUNEL assay和Suzuki’s classification評估)以及Apaf-1的表現。經由小鼠脾臟輸注miR-183模擬物可以模擬iPoC的保護效果，輸注miR-183抑制劑則破壞iPoC的保護效應。綜合上述，吾人發現後制約訓練可以透過:(1)調控MPT，減少ROS產生，以及(2)引起miR-183表現上升，抑制其目標mRNA，Apaf-1，來達到對肝臟缺血再灌流的保護效果。 | zh_TW |
| dc.description.abstract | Ischemia-reperfusion injury (IR injury) happens during organ transplantation, cardiac infarct, stroke, and trauma. Recovery of the blood, which called reperfusion, is necessary for the ischemic tissues. However, reperfusion causes extra injury other than ischemia. Therefore, investigation of attenuating IR injury is essential for the success rate of organ transplantation and the prognosis of cardiac infarct and stroke. Therapies for reducing IR injury are as follows: 1. Drugs, 2.Cell therapy, 3. Conditioning, 4. Organelle therapy. Conditioning is a maneuver received a brief period of ischemia and reperfusion, and it can be divided into preconditioning, postconditioning, and remote conditioning according to the executive time point and tissues. The protective mechanisms are different between these maneuvers. In this study, we set up an animal model of hepatic IR injury to investigate the protective effects and mechanisms of ischemia postconditioning (iPoC) on hepatic IR injury. First, we discovered that three cycles of 1 min reperfusion by releasing the clip across the left hepatic artery followed by 1 min of ischemia of liver by clamping the left hepatic artery performed on Wistar rats (iPoC group) reduced the elevation of serum ALT, apoptosis of hepatocytes, and 4-hydroxy-2-nonenal (4-HNE, a product of lipid peroxidation) compare to that of IR goup. The cytosolic cytochrome c expression significantly decreased, and the mitochondrial membrane potential was also preserved in iPoC group. Mitochondria permeability transition (MPT) was responsible for changes of mitochondrial membrane potential. The protective effects of iPoC was reduced by mPTP opener with ATR and mimicked by the inhibitor of mPTP opening with NIM811. Furthermore, the miRNAs profiles in the rats’ livers with or without iPoC after IR injury was analyzed by microarray. The target of miRNA was identified by luciferase assay. MicroRNA mimics and inhibitors were used in oxygen-glucose deprivation (OGD) injury in Clone 9 cells and partial liver IR injury in mice to test the function of miR-183 in the postconditioning. The expression of miR-183 was increased in the iPoC livers, and miR-183 repressed Apaf-1 mRNA expression. Hypoxic postconditioning (HPoC) and miR-183 mimics significantly decreased cell death after OGD, but miR-183 inhibitors eliminated the protection of HPoC. The increased expression of Apaf-1 and downstream capsase 3 / 9 activations after OGD were mitigated by HPoC or the addition of miR-183, while miR-183 inhibitor diminished the effect of HPoC on Apaf-1-capsapse signaling. Ischemic postconditoining (iPoC) and agomiR-183 decreased the elevation of serum ALT after liver IR in the mice, but antagomiR-183 mitigated the effect of iPoC. The results of H&E and TUNEL staining were compatible with biochemical assay. Besides, iPoC and agomiR-183 decreased the expression of Apaf-1 after IR injury in mice’s livers, while antagomiR-mediated prevention of miR-183 expression led to an increased protein expression of Apaf-1 in the postischemic livers.
This study suggested that iPoC protected liver from IR injury through: (1). Modulating MPT and reducing the production of reactive oxygen species, (2). Up-regulating miR-183 to inhibit the expression of its target mRNA, Apaf-1. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-16T03:43:40Z (GMT). No. of bitstreams: 1 ntu-104-D99446001-1.pdf: 15740802 bytes, checksum: e9fe70737b586f935f5680cf0fe3a401 (MD5) Previous issue date: 2015 | en |
| dc.description.tableofcontents | 口試委員審定書…………………………………………………………….………i
致謝…………………………………………………………………………….……ii 中文摘要……………………………………………………………………….……iii 英文摘要………………………………………………………………….……….…v Chapter 1 ………………………………………………………………………….…1 Introduction ………………………………………………………………….…1 I. Ischemia-reperfusion injury (IR injury) ….……….1 II. Therapies for IR injury.………………………………….……………….9 i.Drugs…………………………………………………………………..........9 ii.Preconditioning……………………………………………………….11 iii.Postconditioning……………………………………………………..12 iv.Remote conditioning…………………………………………………13 v.Cell therapy…………………………………………………………...13 vi.Organelle therapy (mitochondria infusion).14 Aim……………………………………………………………………………...15 Materials and Methods.…………………………………………………………16 Results…………………………………………………………………………...22 Discussion……………………………………………………………………….26 Future work……………………………………………………………………...30 References……………………………………………………………………….31 Figures…………………………………………………………………………...48 Figure 1…………………………………………………………………..48 Figure 2…………………………………………………………………..49 Figure 3…………………………………………………………………..50 Figure 4…………………………………………………………………..51 Figure 5…………………………………………………………………..52 Figure 6…………………………………………………………………..53 Chapter 2 ……………………………………………………………………………...54 Introduction………………………………………………………………………54 I. MicroRNA………………………………….………………………………54 II. MicroRNAs and IR injury……………….……………………….55 III. MicroRNAs and conditionin……………………………………57 Aim………………………………………………………………………………..60 Materials and Methods.…………………………………………………………...61 Results…………………………………………………………………………….72 Discussion………………………………………………………………………...79 Future work…………………………………………………………………….....85 References……………………………………………………………..……….....86 Figures…………………………………………………………………………...110 Figure 1…………………………………………………………………..110 Figure 2…………………………………………………………………..111 Figure 3…………………………………………………………………..112 Figure 4…………………………………………………………………..113 Figure 5…………………………………………………………………..114 Figure 6…………………………………………………………………..115 Figure 7…………………………………………………………………..117 Figure 8…………………………………………………………………..118 Figure 9…………………………………………………………………..119 Figure 10………………………………………………………………...121 Figure 11………………………………………………………………...123 Figure 12………………………………………………………………...124 Figure 13………………………………………………………………...125 Figure 14………………………………………………………………...128 Figure 15………………………………………………………………...129 Table 1…………………………………………………………………...131 Appendix (published papers)………………………………………………………..133 Ischemic postconditioning protects liver from ischemia-reperfusion injury by modulating mitochondrial permeability transition………………………………133 Isolated mitochondria infusion mitigates ischemia-repefusion injury of the liver in rats……………………………………………………………………………….140 Postconditioning mitigates cell death following oxygen and glucose deprivation in PC12 cells and forebrain reperfusion injury in rats……………………………...147 | |
| dc.language.iso | en | |
| dc.title | 後制約訓練對肝臟缺血再灌流傷害的保護效應與機制 | zh_TW |
| dc.title | The protective effects and mechanisms of ischemic postconditioning on hepatic ischemia-reperfusion injury | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 103-1 | |
| dc.description.degree | 博士 | |
| dc.contributor.oralexamcommittee | 鄭劍廷(Chiang-Ting Chien),周逸鵬(Yat-Pang Chau),余佳慧(Chia-Hui Yu),陳玉怜(Yuh-Lien Chen) | |
| dc.subject.keyword | 缺血再灌流傷害,後制約訓練,粒線體膜電位,microRNA,氧氣及葡萄糖剝奪模式,Apaf-1, | zh_TW |
| dc.subject.keyword | Ischemia-reperfusion injury,postconditioning,mitochondrial membrane potential,microRNA,oxygen-glucose deprivation,Apaf-1, | en |
| dc.relation.page | 155 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2015-02-10 | |
| dc.contributor.author-college | 醫學院 | zh_TW |
| dc.contributor.author-dept | 解剖學暨細胞生物學研究所 | zh_TW |
| 顯示於系所單位： | 解剖學暨細胞生物學科所 | |
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