請用此 Handle URI 來引用此文件:
http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/64726
完整後設資料紀錄
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.advisor | 彭福佐(Fu-Chou Peng) | |
dc.contributor.author | Shih-Yi Lin | en |
dc.contributor.author | 林師儀 | zh_TW |
dc.date.accessioned | 2021-06-16T22:58:07Z | - |
dc.date.available | 2017-09-19 | |
dc.date.copyright | 2012-09-19 | |
dc.date.issued | 2012 | |
dc.date.submitted | 2012-08-09 | |
dc.identifier.citation | Afzali, S., and M. Gholyaf. 2008. The effectiveness of combined treatment with methylprednisolone and cyclophosphamide in oral paraquat poisoning. Archives of Iranian medicine 11: 387-391.
Auphan, N., J. A. DiDonato, C. Rosette, A. Helmberg, and M. Karin. 1995. Immunosuppression by glucocorticoids: inhibition of NF-kappa B activity through induction of I kappa B synthesis. Science 270: 286-290. Barnes, P. J., and I. M. Adcock. 2009. Glucocorticoid resistance in inflammatory diseases. Lancet 373: 1905-1917. Bescol-Liversac, J., A. Paquelin, and C. Guillam. 1975. [Ultrastructural study of a renal biopsy in a patient poisoned by paraquat]. European journal of toxicology and environmental hygiene. Journal europeen de toxicologie 8: 236-246. Bi, B., R. Schmitt, M. Israilova, H. Nishio, and L. G. Cantley. 2007a. Stromal cells protect against acute tubular injury via an endocrine effect. Journal of the American Society of Nephrology 18: 2486-2496. Bi, B., R. Schmitt, M. Israilova, H. Nishio, and L. G. Cantley. 2007b. Stromal cells protect against acute tubular injury via an endocrine effect. Journal of the American Society of Nephrology : JASN 18: 2486-2496. Birchmeier, C., and E. Gherardi. 1998. Developmental roles of HGF/SF and its receptor, the c-Met tyrosine kinase. Trends in cell biology 8: 404-410. Bismuth, C., R. Garnier, S. Dally, P. E. Fournier, and J. M. Scherrmann. 1982. Prognosis and Treatment of Paraquat Poisoning - a Review of 28 Cases. J Toxicol-Clin Toxic 19: 461-474. Bismuth, C., J. M. Scherrmann, R. Garnier, F. J. Baud, and P. G. Pontal. 1987. Elimination of Paraquat. Hum Toxicol 6: 63-67. Bolignano, D. et al. 2008. Neutrophil gelatinase-associated lipocalin (NGAL) as a marker of kidney damage. American journal of kidney diseases : the official journal of the National Kidney Foundation 52: 595-605. Bullivant, C. M. 1966. Accidental poisoning by paraquat: Report of two cases in man. British medical journal 1: 1272-1273. Bus, J. S., S. D. Aust, and J. E. Gibson. 1975. Lipid peroxidation: a possible mechanism for paraquat toxicity. Research communications in chemical pathology and pharmacology 11: 31-38. Bus, J. S., J. E. Gibson, and S. D. Aust. 1974. Superoxide-Catalyzed and Singlet Oxygen-Catalyzed Lipid Peroxidation as a Possible Mechanism for Paraquat (Methyl Viologen) Toxicity. Biochemical and biophysical research communications 58: 749-755. Calderbank, A. 1968. The bipyridylium herbicides. Advances in pest control research 8: 127-235. Camici, M. 2007. Urinary detection of podocyte injury. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 61: 245-249. Cao, H. L. et al. 2010. Mesenchymal stem cells derived from human umbilical cord ameliorate ischemia/reperfusion-induced acute renal failure in rats. Biotechnol Lett 32: 725-732. Cappelletti, G., M. G. Maggioni, and R. Maci. 1998. Apoptosis in human lung epithelial cells: triggering by paraquat and modulation by antioxidants. Cell biology international 22: 671-678. Carrillo-Esper, R., F. M. Castillo-Albarran, and J. Perez-Jauregui. 2011. Neutrophil gelatinase-associated lipocalin: a novel biomarker in acute kidney injury. Cirugia y cirujanos 79: 577-581. Chan, B. S., J. P. Seale, and G. G. Duggin. 1997a. The mechanism of excretion of paraquat in rats. Toxicol Lett 90: 1-9. Chan, B. S. H., J. P. Seale, and G. G. Duggin. 1997b. The mechanism of excretion of paraquat in rats. Toxicol Lett 90: 1-9. Chen, Y. A. et al. 2011. Hepatocyte Growth Factor Modification Promotes the Amelioration Effects of Human Umbilical Cord Mesenchymal Stem Cells on Rat Acute Kidney Injury. Stem Cells Dev 20: 103-113. Clark, D. G., T. F. McElligott, and E. W. Hurst. 1966. The toxicity of paraquat. Br J Ind Med 23: 126-132. Cornacchia, F. et al. 2001a. Glomerulosclerosis is transmitted by bone marrow-derived mesangial cell progenitors. The Journal of clinical investigation 108: 1649-1656. Cornacchia, F. et al. 2001b. Glomerulosclerosis is transmitted by bone marrow-derived mesangial cell progenitors. Journal of Clinical Investigation 108: 1649-1656. Dai, C., and Y. Liu. 2004. Hepatocyte growth factor antagonizes the profibrotic action of TGF-beta1 in mesangial cells by stabilizing Smad transcriptional corepressor TGIF. Journal of the American Society of Nephrology : JASN 15: 1402-1412. Dinis-Oliveira, R. J. et al. 2007. Signalling pathways involved in paraquat-induced apoptosis in the rat lung: Evidence of complete remission by sodium salicylate. Toxicol Lett 172: S65-S65. Durvasula, R. V., and S. J. Shankland. 2006. Podocyte injury and targeting therapy: an update. Current opinion in nephrology and hypertension 15: 1-7. Dwenger, A., F. Rosenthal, M. Machein, C. Waller, and A. Spyridonidis. 2004. Transplanted bone marrow cells preferentially home to the vessels of in situ generated murine tumors rather than of normal organs. Stem Cells 22: 86-92. Ecker, J. L., J. B. Hook, and J. E. Gibson. 1975. Nephrotoxicity of paraquat in mice. Toxicol Appl Pharmacol 34: 178-186. Ekert, P. G., and D. L. Vaux. 2005. The mitochondrial death squad: hardened killers or innocent bystanders? Current opinion in cell biology 17: 626-630. Eliopoulos, N. et al. 2010. Human marrow-derived mesenchymal stromal cells decrease cisplatin renotoxicity in vitro and in vivo and enhance survival of mice post-intraperitoneal injection. Am J Physiol-Renal 299: F1288-F1298. Elmore, S. 2007. Apoptosis: A review of programmed cell death. Toxicol Pathol 35: 495-516. Fabisiak, J. P., V. E. Kagan, V. B. Ritov, D. E. Johnson, and J. S. Lazo. 1997. Bcl-2 inhibits selective oxidation and externalization of phosphatidylserine during paraquat-induced apoptosis. The American journal of physiology 272: C675-684. Farringt.Ja, M. Ebert, E. J. Land, and K. Fletcher. 1973. Bipyridylium Quaternary-Salts and Related Compounds .5. Pulse-Radiolysis Studies of Reaction of Paraquat Radical with Oxygen - Implications for Mode of Action of Bipyridyl Herbicides. Biochimica et biophysica acta 314: 372-381. Faul, C., K. Asanuma, E. Yanagida-Asanuma, K. Kim, and P. Mundel. 2007. Actin up: regulation of podocyte structure and function by components of the actin cytoskeleton. Trends in cell biology 17: 428-437. Fei, Q., A. L. McCormack, D. A. Di Monte, and D. W. Ethell. 2008. Paraquat neurotoxicity is mediated by a Bak-dependent mechanism. Journal of Biological Chemistry 283: 3357-3364. Fisher, D. A., E. C. Salido, and L. Barajas. 1989. Epidermal Growth-Factor and the Kidney. Annu Rev Physiol 51: 67-80. Fisher, H. K., J. A. Clements, D. F. Tierney, and R. R. Wright. 1975. Pulmonary effects of paraquat in the first day after injection. The American journal of physiology 228: 1217-1223. Fisher, H. K., M. Humphries, and R. Bails. 1971. Paraquat poisoning. Recovery from renal and pulmonary damage. Annals of internal medicine 75: 731-736. Floege, J. et al. 1995. Basic fibroblast growth factor augments podocyte injury and induces glomerulosclerosis in rats with experimental membranous nephropathy. The Journal of clinical investigation 96: 2809-2819. Flower, D. R., A. C. North, and C. E. Sansom. 2000. The lipocalin protein family: structural and sequence overview. Biochimica et biophysica acta 1482: 9-24. Fowler, B. A., and R. E. Brooks. 1971. Effects of the herbicide paraquat on the ultrastructure of mouse kidney. Am J Pathol 63: 505-520. Galani, V. et al. 2010. The role of apoptosis in the pathophysiology of Acute Respiratory Distress Syndrome (ARDS): An up-to-date cell-specific review. Pathology Research and Practice 206: 145-150. Garovic, V. D. et al. 2007. Urinary podocyte excretion as a marker for preeclampsia. American journal of obstetrics and gynecology 196: 320 e321-327. Gegg, M. E., J. M. Cooper, A. H. V. Schapira, and J. W. Taanman. 2009. Silencing of PINK1 Expression Affects Mitochondrial DNA and Oxidative Phosphorylation in DOPAMINERGIC Cells. Plos One 4. Geiger, F. et al. 2007. VEGF producing bone marrow stromal cells (BMSC) enhance vascularization and resorption of a natural coral bone substitute. Bone 41: 516-522. Gerber, H. P. et al. 2002. VEGF regulates haematopoietic stem cell survival by an internal autocrine loop mechanism. Nature 417: 954-958. Gil, H. W., J. O. Yang, E. Y. Lee, and S. Y. Hong. 2009. Clinical implication of urinary neutrophil gelatinase-associated lipocalin and kidney injury molecule-1 in patients with acute paraquat intoxication. Clin Toxicol (Phila) 47: 870-875. Giri, S. N. et al. 1982. Pharmacokinetics of [14C]-paraquat and associated biochemical and pathologic changes in Beagle dogs following intravenous administration. Fundamental and applied toxicology : official journal of the Society of Toxicology 2: 261-269. Gonzalez-Polo, R. A. et al. 2009. Silencing DJ-1 reveals its contribution in paraquat-induced autophagy. J Neurochem 109: 889-898. Goransson, V. et al. 2004. Renal hyaluronan accumulation and hyaluronan synthase expression after ischaemia-reperfusion injury in the rat. Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 19: 823-830. Hampson, E. C., D. J. Effeney, and S. M. Pond. 1990. Efficacy of single or repeated hemoperfusion in a canine model of paraquat poisoning. The Journal of pharmacology and experimental therapeutics 254: 732-740. Hawksworth, G. M., P. N. Bennett, and D. S. Davies. 1981. Kinetics of Paraquat Elimination in the Dog. Toxicol Appl Pharm 57: 139-145. Hayakawa, M. et al. 2005a. Role of bone marrow cells in the healing process of mouse experimental glomerulonephritis. Pediatr Res 58: 323-328. Hayakawa, M. et al. 2005b. Role of bone marrow cells in the healing process of mouse experimental glomerulonephritis. Pediatr Res 58: 323-328. Herrera, M. B. et al. 2004a. Mesenchymal stem cells contribute to the renal repair of acute tubular epithelial injury. Int J Mol Med 14: 1035-1041. Herrera, M. B. et al. 2004b. Mesenchymal stem cells contribute to the renal repair of acute tubular epithelial injury. Int J Mol Med 14: 1035-1041. Herrera, M. B. et al. 2007a. Exogenous mesenchymal stem cells localize to the kidney by means of CD44 following acute tubular injury. Kidney international 72: 430-441. Herrera, M. B. et al. 2007b. Exogenous mesenchymal stem cells localize to the kidney by means of CD44 following acute tubular injury. Kidney international 72: 430-441. Hertzman, C., M. Wiens, D. Bowering, B. Snow, and D. Calne. 1990. Parkinsons-Disease - a Case-Control Study of Occupational and Environmental Risk-Factors. Am J Ind Med 17: 349-355. Hill, E. S., and L. Michaelis. 1933. The Effect of Iron on the Establishment of the Oxidation-Reduction Potential of Alloxantin. Science 78: 485-486. Hohenstein, B. et al. 2010. Enhanced progenitor cell recruitment and endothelial repair after selective endothelial injury of the mouse kidney. American journal of physiology. Renal physiology 298: F1504-1514. Honczarenko, M. et al. 2006. Human bone marrow stromal cells express a distinct set of biologically functional chemokine receptors. Stem Cells 24: 1030-1041. Honore, P., P. Hantson, J. P. Fauville, A. Peeters, and P. Manieu. 1994. Paraquat poisoning. 'State of the art'. Acta clinica Belgica 49: 220-228. Hughes, J. T. 1988. The Edwin Smith Surgical Papyrus: an analysis of the first case reports of spinal cord injuries. Paraplegia 26: 71-82. Huh, C. G. et al. 2004. Hepatocyte growth factor/c-met signaling pathway is required for efficient liver regeneration and repair. Proceedings of the National Academy of Sciences of the United States of America 101: 4477-4482. Humes, H. D., D. A. Cieslinski, T. M. Coimbra, J. M. Messana, and C. Galvao. 1989. Epidermal Growth-Factor Enhances Renal Tubule Cell Regeneration and Repair and Accelerates the Recovery of Renal-Function in Postischemic Acute Renal-Failure. Journal of Clinical Investigation 84: 1757-1761. Hung, S. C., R. R. Pochampally, S. C. Chen, S. C. Hsu, and D. J. Prockop. 2007a. Angiogenic effects of human multipotent stromal cell conditioned medium activate the PI3K-Akt pathway in hypoxic endothelial cells to inhibit apoptosis, increase survival, and stimulate angiogenesis. Stem Cells 25: 2363-2370. Hung, S. C. et al. 2007b. Short-Term Exposure of Multipotent Stromal Cells to Low Oxygen Increases Their Expression of CX3CR1 and CXCR4 and Their Engraftment In Vivo. Plos One 2. Ikarashi, K. et al. 2005a. Bone marrow cells contribute to regeneration of damaged glomerular endothelial cells. Kidney international 67: 1925-1933. Ikarashi, K. et al. 2005b. Bone marrow cells contribute to regeneration of damaged glomerular endothelial cells. Kidney international 67: 1925-1933. Imasawa, T. et al. 2001a. The potential of bone marrow-derived cells to differentiate to glomerular mesangial cells. Journal of the American Society of Nephrology 12: 1401-1409. Imasawa, T. et al. 2001b. The potential of bone marrow-derived cells to differentiate to glomerular mesangial cells. Journal of the American Society of Nephrology : JASN 12: 1401-1409. Imberti, B. et al. 2007. Insulin-like growth factor-1 sustains stem cell-mediated renal repair. Journal of the American Society of Nephrology 18: 2921-2928. Inoue, T. et al. 2002. TGF-beta1 and HGF coordinately facilitate collagen turnover in subepithelial mesenchyme. Biochemical and biophysical research communications 297: 255-260. Ito, T., A. Suzuki, E. Imai, M. Okabe, and M. Hori. 2001. Bone marrow is a reservoir of repopulating mesangial cells during glomerular remodeling. Journal of the American Society of Nephrology 12: 2625-2635. Ji, J. F., B. P. He, S. T. Dheen, and S. S. Tay. 2004. Interactions of chemokines and chemokine receptors mediate the migration of mesenchymal stem cells to the impaired site in the brain after hypoglossal nerve injury. Stem Cells 22: 415-427. Kale, S. et al. 2003. Bone marrow stem cells contribute to repair of the ischemically injured renal tubule. The Journal of clinical investigation 112: 42-49. Keeling, P. L., and L. L. Smith. 1982a. Relevance of Nadph Depletion and Mixed Disulfide Formation in Rat Lung to the Mechanism of Cell-Damage Following Paraquat Administration. Biochemical pharmacology 31: 3243-3249. Keeling, P. L., and L. L. Smith. 1982b. Relevance of NADPH depletion and mixed disulphide formation in rat lung to the mechanism of cell damage following paraquat administration. Biochemical pharmacology 31: 3243-3249. Kerjaschki, D. 2001. Caught flat-footed: podocyte damage and the molecular bases of focal glomerulosclerosis. The Journal of clinical investigation 108: 1583-1587. Kim, S. J., H. W. Gil, J. O. Yang, E. Y. Lee, and S. Y. Hong. 2009. The clinical features of acute kidney injury in patients with acute paraquat intoxication. Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 24: 1226-1232. Kollet, O. et al. 2003. HGF, SDF-1, and MMP-9 are involved in stress-induced human CD34+ stem cell recruitment to the liver. The Journal of clinical investigation 112: 160-169. Lange, C. et al. 2005. Administered mesenchymal stem cells enhance recovery from ischemia/reperfusion-induced acute renal failure in rats. Kidney international 68: 1613-1617. Lee, H. C., and Y. H. Wei. 2009. Mitochondrial DNA Instability and Metabolic Shift in Human Cancers. Int J Mol Sci 10: 674-701. Lee, S. R. et al. 2010a. Repeated administration of bone marrow-derived mesenchymal stem cells improved the protective effects on a remnant kidney model. Renal failure 32: 840-848. Lee, S. R. et al. 2010b. Repeated administration of bone marrow-derived mesenchymal stem cells improved the protective effects on a remnant kidney model. Renal failure 32: 840-848. Li, L. R., E. Sydenham, B. Chaudhary, and C. You. 2010. Glucocorticoid with cyclophosphamide for paraquat-induced lung fibrosis. Cochrane Database Syst Rev: CD008084. Li, X., and A. Y. Sun. 1999. Paraquat induced activation of transcription factor AP-1 and apoptosis in PC12 cells. J Neural Transm 106: 1-21. Lin, J. L., M. L. Leu, Y. C. Liu, and G. H. Chen. 1999. A prospective clinical trial of pulse therapy with glucocorticoid and cyclophosphamide in moderate to severe paraquat-poisoned patients. American journal of respiratory and critical care medicine 159: 357-360. Lin, J. L., D. T. Lin-Tan, K. H. Chen, and W. H. Huang. 2006. Repeated pulse of methylprednisolone and cyclophosphamide with continuous dexamethasone therapy for patients with severe paraquat poisoning. Crit Care Med 34: 368-373. Lin, J. L. et al. 2011. Improved survival in severe paraquat poisoning with repeated pulse therapy of cyclophosphamide and steroids. Intensive Care Med 37: 1006-1013. Lock, E. A. 1979. The effect of paraquat and diquat on renal function in the rat. Toxicol Appl Pharmacol 48: 327-336. Lock, E. A., and J. Ishmael. 1979. The acute toxic effects of paraquat and diquat on the rat kidney. Toxicol Appl Pharmacol 50: 67-76. Lowenberg, M. et al. 2005. Rapid immunosuppressive effects of glucocorticoids mediated through Lck and Fyn. Blood 106: 1703-1710. Matthew, H., A. Logan, M. F. Woodruff, and B. Heard. 1968. Paraquat poisoning--lung transplantation. British medical journal 3: 759-763. Mayer, H. et al. 2005. Vascular endothelial growth factor (VEGF-A) expression in human mesenchymal stem cells: autocrine and paracrine role on osteoblastic and endothelial differentiation. J Cell Biochem 95: 827-839. Mizuno, S., K. Matsumoto, T. Kurosawa, Y. Mizuno-Horikawa, and T. Nakamura. 2000. Reciprocal balance of hepatocyte growth factor and transforming growth factor-beta 1 in renal fibrosis in mice. Kidney international 57: 937-948. Molck, A. M., and C. Friis. 1998. Transport of paraquat by isolated renal proximal tubular segments from rabbits. Pharmacol Toxicol 83: 208-213. Mori, K. et al. 2005. Endocytic delivery of lipocalin-siderophore-iron complex rescues the kidney from ischemia-reperfusion injury. The Journal of clinical investigation 115: 610-621. Morigi, M. et al. 2004a. Mesenchymal stem cells are renotropic, helping to repair the kidney and improve function in acute renal failure. Journal of the American Society of Nephrology 15: 1794-1804. Morigi, M. et al. 2004b. Mesenchymal stem cells are renotropic, helping to repair the kidney and improve function in acute renal failure. Journal of the American Society of Nephrology : JASN 15: 1794-1804. Murray, R. E., and J. E. Gibson. 1974. Paraquat disposition in rats, guinea pigs and monkeys. Toxicol Appl Pharmacol 27: 283-291. Mussap, M., A. Noto, M. Fravega, and V. Fanos. 2011. Urine neutrophil gelatinase-associated lipocalin (uNGAL) and netrin-1: are they effectively improving the clinical management of sepsis-induced acute kidney injury (AKI)? The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstet 24 Suppl 2: 15-17. Nagata, T., I. Kono, T. Masaoka, and F. Akahori. 1992. Acute toxicological studies on paraquat: pathological findings in beagle dogs following single subcutaneous injections. Vet Hum Toxicol 34: 105-112. Niso-Santano, M. et al. 2010. Activation of apoptosis signal-regulating kinase 1 is a key factor in paraquat-induced cell death: modulation by the Nrf2/Trx axis. Free radical biology & medicine 48: 1370-1381. Olson, D. P., J. A. Diaz, and J. D. Jereda. 2010. A fatal case of paraquat ingestion: clinical course and review of pathophysiology. Medical science monitor : international medical journal of experimental and clinical research 16: CS153-156. Oreopoulos, D. G. et al. 1968. Acute renal failure in case of Paraquat poisoning. British medical journal 1: 749-750. Pavenstadt, H., W. Kriz, and M. Kretzler. 2003. Cell biology of the glomerular podocyte. Physiological reviews 83: 253-307. Peng, J., X. O. Mao, F. F. Stevenson, M. Hsu, and J. K. Andersen. 2004. The herbicide paraquat induces dopaminergic nigral apoptosis through sustained activation of the JNK pathway. The Journal of biological chemistry 279: 32626-32632. Petermann, A. T. et al. 2003. Podocytes that detach in experimental membranous nephropathy are viable. Kidney international 64: 1222-1231. Petermann, A. T. et al. 2004. Viable podocytes detach in experimental diabetic nephropathy: potential mechanism underlying glomerulosclerosis. Nephron. Experimental nephrology 98: e114-123. Pitchford, S. C., R. C. Furze, C. P. Jones, A. M. Wengner, and S. M. Rankin. 2009. Differential Mobilization of Subsets of Progenitor Cells from the Bone Marrow. Cell Stem Cell 4: 62-72. Pond, S. M. 1990a. Manifestations and management of paraquat poisoning. The Medical journal of Australia 152: 256-259. Pond, S. M. 1990b. Toxicology .5. Manifestations and Management of Paraquat Poisoning. Med J Australia 152: 256-259. Ponte, A. L. et al. 2007. The in vitro migration capacity of human bone marrow mesenchymal stem cells: comparison of chemokine and growth factor chemotactic activities. Stem Cells 25: 1737-1745. Prashad, D. N., D. Chambers, and D. J. Beadle. 1981. Changes in renal function associated with paraquat dichloride toxicity in the domestic fowl. General pharmacology 12: 291-293. Proskuryakov, S. Y., A. G. Konoplyannikov, and V. L. Gabai. 2003. Necrosis: a specific form of programmed cell death? Experimental cell research 283: 1-16. Proudfoot, A. T., M. S. Stewart, T. Levitt, and B. Widdop. 1979. Paraquat poisoning: significance of plasma-paraquat concentrations. Lancet 2: 330-332. Purser, D. A., and M. S. Rose. 1979. The toxicity and renal handling of paraquat in cynomolgus monkeys. Toxicology 15: 31-41. Raff, M. C. et al. 1993. Programmed cell death and the control of cell survival: lessons from the nervous system. Science 262: 695-700. Rookmaaker, M. B. et al. 2003. Bone-marrow-derived cells contribute to glomerular endothelial repair in experimental glomerulonephritis. Am J Pathol 163: 553-562. Rose, M. S., L. L. Smith, and I. Wyatt. 1974. Evidence for Energy-Dependent Accumulation of Paraquat into Rat Lung. Nature 252: 314-315. Samai, M., M. A. Sharpe, P. R. Gard, and P. K. Chatterjee. 2007. Comparison of the effects of the superoxide dismutase mimetics EUK-134 and tempol on paraquat-induced nephrotoxicity. Free Radical Bio Med 43: 528-534. Semedo, P. et al. 2009. Early modulation of inflammation by mesenchymal stem cell after acute kidney injury. Int Immunopharmacol 9: 677-682. Semedo, P. et al. 2007. Mesenchymal stem cells ameliorate tissue damages triggered by renal ischemia and reperfusion injury. Transplantation proceedings 39: 421-423. Smith, L. L. 1988. The Toxicity of Paraquat. Adverse Drug React T 7: 1-17. Stratta, P., G. Mazzucco, S. Griva, C. Tetta, and G. Monga. 1988. Immune-Mediated Glomerulonephritis after Exposure to Paraquat. Nephron 48: 138-141. Togel, F. et al. 2009. Autologous and Allogeneic Marrow Stromal Cells Are Safe and Effective for the Treatment of Acute Kidney Injury. Stem Cells Dev 18: 475-485. Togel, F. et al. 2005a. Administered mesenchymal stem cells protect against ischemic acute renal failure through differentiation-independent mechanisms. Am J Physiol-Renal 289: F31-F42. Togel, F., J. Isaac, Z. Hu, K. Weiss, and C. Westenfelder. 2005b. Renal SDF-1 signals mobilization and homing of CXCR4-positive cells to the kidney after ischemic injury. Kidney international 67: 1772-1784. Ueki, T. et al. 1999. Hepatocyte growth factor gene therapy of liver cirrhosis in rats. Nature medicine 5: 226-230. Van Cruchten, S., and W. Van den Broeck. 2002. Morphological and biochemical aspects of apoptosis, oncosis and necrosis. Anat Histol Embryol 31: 214-223. van Loo, G. et al. 2002. The role of mitochondrial factors in apoptosis: a Russian roulette with more than one bullet. Cell Death Differ 9: 1031-1042. van Timmeren, M. M. et al. 2007. Tubular kidney injury molecule-1 (KIM-1) in human renal disease. The Journal of pathology 212: 209-217. Vermes, I. et al. 1997. Apoptosis and secondary necrosis of lymphocytes in culture. Acta Haematol-Basel 98: 8-13. Vogelmann, S. U., W. J. Nelson, B. D. Myers, and K. V. Lemley. 2003. Urinary excretion of viable podocytes in health and renal disease. American journal of physiology. Renal physiology 285: F40-48. Wang, Y. J., R. Singh, J. H. Lefkowitch, R. M. Rigoli, and M. J. Czaja. 2006. Tumor necrosis factor-induced toxic liver injury results from JNK2-dependent activation of caspase-8 and the mitochondrial death pathway. Journal of Biological Chemistry 281: 15258-15267. Wise, A. F., and S. D. Ricardo. 2012. Mesenchymal stem cells in kidney inflammation and repair. Nephrology (Carlton) 17: 1-10. Wyllie, A. H., J. F. Kerr, and A. R. Currie. 1980. Cell death: the significance of apoptosis. International review of cytology 68: 251-306. Xiao, G. H. et al. 2001. Anti-apoptotic signaling by hepatocyte growth factor/Met via the phosphatidylinositol 3-kinase/Akt and mitogen-activated protein kinase pathways. Proceedings of the National Academy of Sciences of the United States of America 98: 247-252. Yonemitsu, K. 1986. Pharmacokinetic Profile of Paraquat Following Intravenous Administration to the Rabbit. Forensic science international 32: 33-42. Yoon, S. P. et al. 2011. Protective effects of chitosan oligosaccharide on paraquat-induced nephrotoxicity in rats. Food and Chemical Toxicology 49: 1828-1833. Yuan, L. et al. 2011. VEGF-modified human embryonic mesenchymal stem cell implantation enhances protection against cisplatin-induced acute kidney injury. Am J Physiol-Renal 300: F207-F218. Zhuang, S. G., Y. J. Dang, and R. G. Schnellmann. 2004. Requirement of the epidermal growth factor receptor in renal epithelial cell proliferation and migration. Am J Physiol-Renal 287: F365-F372. | |
dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/64726 | - |
dc.description.abstract | 巴拉刈(Paraquat, PQ)又稱百草枯,其化學名為 1,1’-dimethyl-4,4’-bipyridylium dichloride,分子式為 C 12 H 14 C l2 N 2 ,屬於聯嘧啶(bypyridiniums)類的化合物,目前已超過一百三十個國家正式登記並使用,為全球使用最廣泛的除草劑之一。巴拉刈中毒大多由口服途徑引起,進入體內後,最早達到最高組織濃度的器官為腎臟,同時它也是最主要的排泄器官。若腎臟功能正常,在口服後6小時內約有百分之八十至九十的巴拉刈以原型型態從尿液中排出體外,在24小時內幾乎為百分之百會由腎臟排出。若腎功能不正常,則組織中(尤其是肺)的巴拉刈濃度將增高,且其濃度頂點將延到 15 至 20 小時之後。當巴拉刈進到腎臟細胞內後,隨即進行氧化還原循環(redox cycling),消耗NADPH,產生大量的超氧化物 (superoxide anion, O 2.-)等自由基,導致腎臟的傷害。根據 2001 到 2002 年的統計資料指出,在台灣所有農藥中毒事件中,巴拉刈中毒佔了 18.9 %,造成的死亡率為 72.1 %。
過去文獻顯示,高劑量巴拉刈中毒後,會引發多重器官衰竭,其中包括急性腎損傷(acute kidney injury, AKI),在 24 至 96 小時內出現的蛋白尿(proteinuria)、膿尿(pyuria)、氮血(azotemia)、血尿(hematuria)等較輕微症狀會出現,一旦出現寡尿或無尿,則代表更嚴重的急性腎小管壞死,也會發生腎絲球腎炎的情況。 傳統的治療方法包括洗胃(gastric lavage)、給予口服吸附劑如活性碳(active charcoal)、血液灌流(charcoal haemoperfusion)及糖質皮質固醇類(glucocorticoid)藥物治療,但這些治療往往無法有效提高存活率。急性腎損傷(AKI)目前仍然為高死亡率的疾病之一,主要是因為在臨床治療上有抗藥性的問題而造成治療無效的結果。因此在血管內移植骨髓間葉幹細胞(bone marrow mesenchymal stem cells,BM-MSCs)對於治療AKI是一種新穎且有希望的方法,過去已有研究利用BM-MSCs治療 AKI 模式小鼠,觀察到BM-MSCs會在受傷的腎臟上,修復腎小管及改善腎臟功能,且會分化成腎小管上皮細胞、腎小球系膜細胞(mesangial cells)及腎絲球上皮細胞。因此,本實驗利用雄鼠骨髓細胞對於巴拉刈中毒的雌鼠進行細胞處理,觀察是否能減少傷害並提高其存活率,接著探討其中的調節機制。 為了建立巴拉刈所造成的急性腎臟損傷,首先利用八週大雌性 C57BL/6小鼠以腹腔注射給予 55 mg/kg BW劑量的巴拉刈,使C57BL/6 小鼠腎功能指數與對照組相比有顯著上升的趨勢,隨著暴露巴拉刈後的天數增加,腎功能指數也有增加的趨勢。由組織切片中觀察到腎小管刷狀緣失去、細胞排列不規則且細胞因為毒性死亡而掉落,足細胞結構不完整及核掉落等現象。而在給予三次小鼠骨髓細胞 進行細胞治療後,可將C57BL/6小鼠存活率由20%提高至60%,但利用 dexamethasone (DEX)進行治療無法有效提升小鼠存活率。實驗結果也顯示細胞治療可改善巴拉刈對小鼠引起的腎臟組織傷害,並減少腎功能的破壞,且在處理後第六天可使腎功能恢復到與控制組相似,同時,可減少細胞凋亡及嗜中性白血球浸潤的現象。 綜合以上結論,實驗結果顯示在高劑量 55 mg/kg BW 巴拉刈處理後的 C57BL/6小鼠,以骨髓細胞進行細胞治療,恢復小鼠腎臟功能,減少腎臟傷害並且提高其存活率。而這樣的恢復的現象,或許是藉由骨髓細胞分泌出的細胞激素及生長因子作為免疫抑制的調節以改善巴拉刈對腎臟造成的傷害。本實驗是首先探討巴拉刈對腎臟足細胞造成傷害的研究。 | zh_TW |
dc.description.abstract | Paraquat(1,1’-dimethyl-4,4’-bipyridylium dichloride, PQ),a potent nephrotoxicant, belongs to the class of bipyridylium quaternary ammonium herbicides. Paraquat mainly excrete by kidney and undergoes a process of redox-cycling and finally leads to reactive oxygen species (ROS) production at the expense of NADPH. This alters the normal cell functions and causes kidney toxicity. Paraquat poisoning is the most common cause of fulminated and fatal herbicide intoxication. From 2001 to 2002, paraquat intoxication contributed to 18.9 % of all pesticide poisonings in Taiwan.
Studies showed that high doses of paraquat lead to multiple organ failure such as lung, kidney, liver and so on. Kidney has the most highest concentration compare to the other organs at any detection time. Paraquat-induced acute kidney injury (AKI) caused proteinuria, pyuria, azotemia, uremia and other minor symptoms within 24-96 hours and this can be used as a predict marker of AKI. Despite severe tubular necrosis, paraquat may also cause glomerular damage and eventually lead to glomerulonephritis. The conventional clinical therapies for the patients of fulminant paraquat poisoning are ineffective. On the other hand, AKI patients remain high mortality after clinical treatment due to drug-resistance. Recently, bone marrow mesenchymal stem cells(BM-MSCs) have been reported to have the ability to repair injured kidney and improve survival rate of mice. Therefore, this study aim to evaluate the treatment efficacy of mouse bone marrow cells(mBMCs)on mice with acute kidney paraquat poisoning. In animal model,to mimic AKI, 8 weeks female C57BL/6 mice were intraperitoneally administered with 55 mg/kg BW paraquat. Histopathologically, kidneys showed tubular brush border lost, irregular cell arrangement and inflammatory cells infiltration. Furthermore, kidney functions evaluation also revealed significant differences in BUN, SCr, urine total protein and urine Cr compared to the control group. After three times co-treatment with mBMCs, paraquat-induced AKI mice showed an increased survival rate from 20% to 60%. One time treatment with mBMCs or dexamethasone, however, did not elevate the survival rate of mice. Histopathologically, three times mBMCs co-treatment repaired the injury caused by paraquat and the structure of renal tubular and podocytes seemed to be similar as control group. Renal functions study also suggested that three times mBMCs co-treatment would restore the physiological functions of kidney and results showed that there was no differences between treatment group and control group on Day 6. As a conclusion, the results of this study demonstrated that mBMCs co-treatment could decrease kidney damage,repair kidney functions and increase the survivalrate of mice with acute kidney paraquat poisoning. Besides, this is also the first study to evaluate the damage of podocytes that caused by paraquat. | en |
dc.description.provenance | Made available in DSpace on 2021-06-16T22:58:07Z (GMT). No. of bitstreams: 1 ntu-101-R99447002-1.pdf: 3074136 bytes, checksum: 8f2d98afddd0c423fa8b51caa22946da (MD5) Previous issue date: 2012 | en |
dc.description.tableofcontents | 圖表目錄………………………………………………………II
中文摘要………………………………………………………IV 英文摘要………………………………………………………VI 縮寫表 ………………………………………………………VIII 第一章 緒論……………………………………………………1 第二章 材料與方法……………………………………………16 第三章 結果……………………………………………………23 第四章 討論……………………………………………………29 第五章 參考文獻………………………………………………39 圖表集 …………………………………………………………56 | |
dc.language.iso | zh-TW | |
dc.title | 以動物模式探討小鼠骨髓細胞對巴拉刈造成急性腎損傷的再生潛能 | zh_TW |
dc.title | The Study on Regeneration Potential of Mouse Bone Marrow Cells for Paraquat-Induced Acute Kidney Injury in C57BL/6 Mice | en |
dc.type | Thesis | |
dc.date.schoolyear | 100-2 | |
dc.description.degree | 碩士 | |
dc.contributor.oralexamcommittee | 林國煌,陳惠文 | |
dc.subject.keyword | 巴拉刈,急性腎損傷,骨髓細胞,細胞治療,足細胞, | zh_TW |
dc.subject.keyword | paraquat,acute kidney injury,bone marrow cells,cell therapy,podocyte, | en |
dc.relation.page | 74 | |
dc.rights.note | 有償授權 | |
dc.date.accepted | 2012-08-09 | |
dc.contributor.author-college | 醫學院 | zh_TW |
dc.contributor.author-dept | 毒理學研究所 | zh_TW |
顯示於系所單位: | 毒理學研究所 |
文件中的檔案:
檔案 | 大小 | 格式 | |
---|---|---|---|
ntu-101-1.pdf 目前未授權公開取用 | 3 MB | Adobe PDF |
系統中的文件,除了特別指名其著作權條款之外,均受到著作權保護,並且保留所有的權利。