請用此 Handle URI 來引用此文件:
http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/15867完整後設資料紀錄
| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 余佳慧 | |
| dc.contributor.author | Yi-An Shih | en |
| dc.contributor.author | 施怡安 | zh_TW |
| dc.date.accessioned | 2021-06-07T17:54:04Z | - |
| dc.date.copyright | 2012-09-19 | |
| dc.date.issued | 2012 | |
| dc.date.submitted | 2012-08-17 | |
| dc.identifier.citation | 1. Reya, T. and H. Clevers, Wnt signalling in stem cells and cancer. Nature, 2005. 434(7035): p. 843-50.
2. Hall, P.A., et al., Regulation of cell number in the mammalian gastrointestinal tract: the importance of apoptosis. J Cell Sci, 1994. 107 ( Pt 12): p. 3569-77. 3. Fontaine, R.N., et al., Liver and intestinal fatty acid binding proteins in control and TGF beta 1 gene targeted deficient mice. Mol. Cell. Biochem., 1996. 159(2): p. 149-153. 4. Garcia, M.A., N. Yang, and P.M. Quinton, Normal mouse intestinal mucus release requires cystic fibrosis transmembrane regulator-dependent bicarbonate secretion. J Clin Invest, 2009. 119(9): p. 2613-22. 5. Heyman, M., A.M. Crain-Denoyelle, and J.F. Desjeux, Endocytosis and processing of protein by isolated villus and crypt cells of the mouse small intestine. J Pediatr Gastroenterol Nutr, 1989. 9(2): p. 238-45. 6. Farquhar, M.G. and G.E. Palade, Junctional Complexes in Various Epithelia. J. Cell Biol, 1963. 17(2): p. 375-&. 7. Blikslager, A.T., et al., Restoration of barrier function in injured intestinal mucosa. Physiological Reviews, 2007. 87(2): p. 545-564. 8. Hollander, D., The intestinal permeability barrier. A hypothesis as to its regulation and involvement in Crohn's disease. Scand J Gastroenterol, 1992. 27(9): p. 721-6. 9. Diamond, G., et al., The roles of antimicrobial peptides in innate host defense. Curr Pharm Des, 2009. 15(21): p. 2377-92. 10. Ouellette, A.J., et al., Mouse Paneth cell defensins: primary structures and antibacterial activities of numerous cryptdin isoforms. Infect Immun, 1994. 62(11): p. 5040-7. 11. Lehrer, R.I., A.K. Lichtenstein, and T. Ganz, Defensins: antimicrobial and cytotoxic peptides of mammalian cells. Annu Rev Immunol, 1993. 11: p. 105-28. 12. Frank, D.N. and N.R. Pace, Gastrointestinal microbiology enters the metagenomics era. Curr Opin Gastroenterol, 2008. 24(1): p. 4-10. 13. Frank, D.N., et al., Molecular-phylogenetic characterization of microbial community imbalances in human inflammatory bowel diseases. Proc Natl Acad Sci U S A, 2007. 104(34): p. 13780-5. 14. Bik, E.M., Composition and function of the human-associated microbiota. Nutrition Reviews, 2009. 67 Suppl 2: p. S164-71. 15. Kleessen, B., et al., Mucosal and invading bacteria in patients with inflammatory bowel disease compared with controls. Scand J Gastroenterol, 2002. 37(9): p. 1034-41. 16. Yu, L.C., et al., Host-microbial interactions and regulation of intestinal epithelial barrier function: From physiology to pathology. World J Gastrointest Pathophysiol, 2012. 3(1): p. 27-43. 17. Seksik, P., [Gut microbiota and IBD]. Gastroenterol Clin Biol, 2010. 34 Suppl 1: p. S44-51. 18. Marteau, P., Bacterial flora in inflammatory bowel disease. Dig Dis, 2009. 27 Suppl 1: p. 99-103. 19. Yang, L. and Z. Pei, Bacteria, inflammation, and colon cancer. World J Gastroenterol, 2006. 12(42): p. 6741-6. 20. Turnbaugh, P.J., et al., An obesity-associated gut microbiome with increased capacity for energy harvest. Nature, 2006. 444(7122): p. 1027-31. 21. Liu, C.H., et al., [Allergic airway response associated with the intestinal microflora disruption induced by antibiotic therapy]. Zhonghua Er Ke Za Zhi, 2007. 45(6): p. 450-4. 22. Sekirov, I., et al., Antibiotic-induced perturbations of the intestinal microbiota alter host susceptibility to enteric infection. Infect Immun, 2008. 76(10): p. 4726-36. 23. Dethlefsen, L. and D.A. Relman, Incomplete recovery and individualized responses of the human distal gut microbiota to repeated antibiotic perturbation. Proc Natl Acad Sci U S A, 2011. 108 Suppl 1: p. 4554-61. 24. Antonopoulos, D.A., et al., Reproducible community dynamics of the gastrointestinal microbiota following antibiotic perturbation. Infect Immun, 2009. 77(6): p. 2367-75. 25. Hill, D.A., et al., Metagenomic analyses reveal antibiotic-induced temporal and spatial changes in intestinal microbiota with associated alterations in immune cell homeostasis. Mucosal Immunol, 2010. 3(2): p. 148-58. 26. Toleman, M.A., et al., Molecular characterization of SPM-1, a novel metallo-beta-lactamase isolated in Latin America: report from the SENTRY antimicrobial surveillance programme. J Antimicrob Chemother, 2002. 50(5): p. 673-9. 27. Bhatia, R. and J.P. Narain, The growing challenge of antimicrobial resistance in the South-East Asia Region--are we losing the battle? Indian J Med Res, 2010. 132: p. 482-6. 28. Kotilainen, P., et al., Elimination of epidemic methicillin-resistant Staphylococcus aureus from a university hospital and district institutions, Finland. Emerg Infect Dis, 2003. 9(2): p. 169-75. 29. Tenover, F.C., et al., Vancomycin-resistant Staphylococcus aureus isolate from a patient in Pennsylvania. Antimicrob Agents Chemother, 2004. 48(1): p. 275-80. 30. Staphylococcus aureus resistant to vancomycin--United States, 2002. MMWR Morb Mortal Wkly Rep, 2002. 51(26): p. 565-7. 31. Endimiani, A., et al., In Vitro Activity of Fosfomycin against bla(KPC)-Containing Klebsiella pneumoniae Isolates, Including Those Nonsusceptible to Tigecycline and/or Colistin. Antimicrob. Agents Chemother., 2010. 54(1): p. 526-529. 32. Seema, K., et al., Dissemination of the New Delhi metallo-beta-lactamase-1 (NDM-1) among Enterobacteriaceae in a tertiary referral hospital in north India. J. Antimicrob. Chemother. , 2011. 66(7): p. 1646-1647. 33. Kumarasamy, K.K., et al., Emergence of a new antibiotic resistance mechanism in India, Pakistan, and the UK: a molecular, biological, and epidemiological study. Lacent Infect Dis, 2010. 10(9): p. 597-602. 34. Poirel, L., et al., Emergence of Metallo-beta-Lactamase NDM-1-Producing Multidrug-Resistant Escherichia coli in Australia. Antimicrob. Agents Chemother., 2010. 54(11): p. 4914-4916. 35. Raghunath, D., New metallo beta-lactamase NDM-1. Indian J Med Res, 2010. 132(5): p. 478-481. 36. Nordmann, P., G. Cuzon, and T. Naas, The real threat of Klebsiella pneumoniae carbapenemase-producing bacteria. Lacent Infect Dis, 2009. 9(4): p. 228-236. 37. Perez, F., et al., Effect of antibiotic treatment on establishment and elimination of intestinal colonization by KPC-producing Klebsiella pneumoniae in mice. Antimicrob Agents Chemother, 2011. 55(6): p. 2585-9. 38. Brandl, K., et al., Vancomycin-resistant enterococci exploit antibiotic-induced innate immune deficits. Nature, 2008. 455(7214): p. 804-7. 39. Kinnebrew, M.A., et al., Bacterial flagellin stimulates Toll-like receptor 5-dependent defense against vancomycin-resistant Enterococcus infection. J Infect Dis, 2010. 201(4): p. 534-43. 40. Ubeda, C., et al., Vancomycin-resistant Enterococcus domination of intestinal microbiota is enabled by antibiotic treatment in mice and precedes bloodstream invasion in humans. J Clin Invest, 2010. 120(12): p. 4332-41. 41. Barman, M., et al., Enteric salmonellosis disrupts the microbial ecology of the murine gastrointestinal tract. Infect and Immun, 2008. 76(3): p. 907-915. 42. Backhed, F., et al., Host-bacterial mutualism in the human intestine. Science, 2005. 307(5717): p. 1915-1920. 43. Amann, R.I., et al., Combination of 16S rRNA-targeted oligonucleotide probes with flow cytometry for analyzing mixed microbial populations. Appl Environ Microbiol, 1990. 56(6): p. 1919-25. 44. Rakoff-Nahoum, S., et al., Recognition of commensal microflora by toll-like receptors is required for intestinal homeostasis. Cell, 2004. 118(2): p. 229-241. 45. Leatham, M.P., et al., Precolonized Human Commensal Escherichia coli Strains Serve as a Barrier to E-coli O157:H7 Growth in the Streptomycin-Treated Mouse Intestine. Infect Immun, 2009. 77(7): p. 2876-2886. 46. Jankowska, A., et al., Competition of Lactobacillus paracasei with Salmonella enterica for adhesion to Caco-2 cells. J Biomed Biotechnol, 2008. 47. Ubeda, C., et al., Vancomycin-resistant Enterococcus domination of intestinal microbiota is enabled by antibiotic treatment in mice and precedes bloodstream invasion in humans. J Clin Invest, 2010. 120(12): p. 4332-4341. 48. Wells, C.L., et al., Role of Intestinal Anaerobic-Bacteria in Colonization Resistance. European Journal of Clinical Microbiol Infect Dis, 1988. 7(1): p. 107-113. 49. Wells, C.L., et al., Role of Anaerobic Flora in the Translocation of Aerobic and Facultatively Anaerobic Intestinal Bacteria. Infect Immun, 1987. 55(11): p. 2689-2694. 50. Snel, J., et al., Interactions between gut-associated lymphoid tissue and colonization levels of indigenous, segmented, filamentous bacteria in the small intestine of mice. Can J Microbiol, 1998. 44(12): p. 1177-1182. 51. Talham, G.L., et al., Segmented filamentous bacteria are potent stimuli of a physiologically normal state of the murine gut mucosal immune system. Infect Immun, 1999. 67(4): p. 1992-2000. 52. Jiang, H.Q., N.A. Bos, and J.J. Cebra, Timing, localization, and persistence of colonization by segmented filamentous bacteria in the neonatal mouse gut depend on immune status of mothers and pups. Infect Immun, 2001. 69(6): p. 3611-3617. 53. Croswell, A., et al., Prolonged Impact of Antibiotics on Intestinal Microbial Ecology and Susceptibility to Enteric Salmonella Infection. Infect Immun, 2009. 77(7): p. 2741-2753. 54. Leatham, M.P., et al., Precolonized human commensal Escherichia coli strains serve as a barrier to E. coli O157:H7 growth in the streptomycin-treated mouse intestine. Infect Immun, 2009. 77(7): p. 2876-86. 55. Gustafsson, B.E., The Physiological Importance of the Colonic Microflora. Scand J Gastroentero, 1982. 17: p. 117-131. 56. Wostmann, B.S., The germfree animal in nutritional studies. Annu Rev Nutr, 1981. 1: p. 257-79. 57. O'Hara, A.M. and F. Shanahan, The gut flora as a forgotten organ. Embo Reports, 2006. 7(7): p. 688-693. 58. Abad, C.L. and N. Safdar, The Role of Lactobacillus Probiotics in the Treatment or Prevention of Urogenital Infections - A Systematic Review. J Chemother, 2009. 21(3): p. 243-252. 59. Lin, Y.P., et al., Probiotic Lactobacillus reuteri suppress proinflammatory cytokines via c-Jun. Inflamm Bowel Dis, 2008. 14(8): p. 1068-1083. 60. Lupp, C., et al., Host-mediated inflammation disrupts the intestinal microbiota and promotes the Overgrowth of Enterobacteriaceae. Cell Host & Microbe, 2007. 2(2): p. 119-129. 61. Stecher, B., et al., Salmonella enterica serovar typhimurium exploits inflammation to compete with the intestinal microbiota. Plos Biol, 2007. 5(10): p. 2177-2189. 62. Lawley, T.D., et al., Antibiotic Treatment of Clostridium difficile Carrier Mice Triggers a Supershedder State, Spore-Mediated Transmission, and Severe Disease in Immunocompromised Hosts. Infect Immun, 2009. 77(9): p. 3661-3669. 63. Chowdhury, T.T., et al., Signal transduction pathways involving p38 MAPK, JNK, NFkappaB and AP-1 influences the response of chondrocytes cultured in agarose constructs to IL-1beta and dynamic compression. Inflamm Res, 2008. 57(7): p. 306-13. 64. Malago, J.J., J.F. Koninkx, and J.E. van Dijk, The heat shock response and cytoprotection of the intestinal epithelium. Cell Stress Chaperon, 2002. 7(2): p. 191-9. 65. Cowan, K.J. and K.B. Storey, Mitogen-activated protein kinases: new signaling pathways functioning in cellular responses to environmental stress. J Exp Biol, 2003. 206(Pt 7): p. 1107-15. 66. Muza-Moons, M.M., E.E. Schneeberger, and G.A. Hecht, Enteropathogenic Escherichia coli infection leads to appearance of aberrant tight junctions strands in the lateral membrane of intestinal epithelial cells. Cell Microbiol, 2004. 6(8): p. 783-793. 67. Shifflett, D.E., et al., Enteropathogenic E-coli disrupts tight junction barrier function and structure in vivo. Lab Invest, 2005. 85(10): p. 1308-1324. | |
| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/15867 | - |
| dc.description.abstract | 對beta-內酰胺有抗藥性的超級細菌,例如擁有新德里金屬beta-內酰胺酶(NDM)-1的超級細菌,對公眾健康有極大的威脅。腸道內的共生菌叢促進腸道屏障功能的穩固,並且與外來病菌競爭。而目前已知道抗生素會擾亂腸道共生菌叢。 目的:了解由抗生素造成的腸道菌叢擾亂,是否會促進超級細菌在腸道內生長和轉移。 方法: BALB/c小鼠給予正常飲水或是抗生素飲水七天,抗生素水去除之後,每隻小鼠灌食109CFU抗氨芐青黴素的大腸桿菌進行感染,在感染後的第0, 1, 3, 7, 和14天進行犧牲。利用蘇木紫-伊紅染色分析腸道的結構,並計數在腸道、脾臟、肝臟的細菌數量。被腸道上皮細胞內吞的細菌數量,則由慶大黴素耐藥檢測分離出來。利用螢光原位雜交,了解細菌入侵到黏膜層的情形。結果: 在第0天,抗生素組的腸道菌叢數量比正常飲水組的低。抗氨芐青黴素的細菌在正常飲水組的腸道中,每個時間點都沒有生長的現象。相反地,抗生素組的小鼠腸道中,在感染後第1, 3天都有抗氨芐青黴素的細菌出現在空腸、盲腸和結腸。抗氨芐青黴素的大腸桿菌在第7和14天被從腸道清除。此外,抗生素組小鼠在感染後第1天,出現盲腸腫脹並且有組織充血及白血球浸潤造成的水腫現象。另外,感染後第三天有細菌入侵空腸腺窩,空腸和結腸也有細菌被腸道上皮細胞內吞的情形。感染後第1和3天,有細菌在脾臟和肝臟轉移的現象。 結論: 正常的腸道菌叢具有屏障功能,可保護腸道不受抗藥性細菌感染。腸道菌叢受到干擾則會促進抗藥性細菌之定殖,並造成腸道共生菌和超級細菌都會體內的散布。 | zh_TW |
| dc.description.abstract | Superbugs that are resistant to beta-lactams antibiotics, such as those with New Delhi metallo-beta-lactamase (NDM)-1, pose major threats to public health. Enteric commensal microflora is involved in mucosal barrier fortification and pathogen competition. Antibiotics are known to disrupt intestinal flora. Aim: The aim is to evaluate whether antibiotic-induced intestinal dysbiosis may promote enteric colonization and translocation of superbug. Methods: BALB/c mice were drinking normal water (NW) or antibiotic water (AW) for 7 days. Ampicillin-resistant (Amp-r) E. coli BL21 (109 CFU) was administered by oral gavage after antibiotic withdrawal. Animals were sacrificed at 0, 1, 3, 7 and 14 days after inoculation. The structure of intestine was determined by H&E staining. Bacterial colony forming units in intestine, liver and spleen were assessed. The amount of intracellular bacteria in purified enterocytes was determined using a gentamicin resistance assay. Bacterial invasion to mucosa was determined by fluorescent in situ hybridization. Results: The enteric bacterial counts were reduced in AW mice compared to NW groups on day 0. After inoculation of Amp-r E.coli, no sign of bacterial colonization and translocation was seen in NW mice throughout all time points. In contrast, AW mice showed Amp-r E. coli in the jejunum, cecum and colon after inoculation for 1 and 3 days. Clearance of Amp-r E. coli was associated with recovery of commensal bacterial numbers after 7 and 14 days. Moreover, cecal flatulence and tissue edema associated with hyperemia and leukocyte infiltraton were observed in AW mice on day 1 post-infection. Furthermore, bacterial invasion to jejunal crypts, bacterial endocytosis in jejunal and colonic enterocytes, and bacterial translocation to liver and spleen were observed on day 1 and 3 post-infection in AW mice. Conclusions: The normal commensals served as a barrier to protect the intestine from antibiotic-resistant bacterial colonization. Enteric dysbiosis predisposes antibiotic-resistant bacteria to colonize, leading to systemic dissemination of both commensals and superbug. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-07T17:54:04Z (GMT). No. of bitstreams: 1 ntu-101-R99441003-1.pdf: 2908367 bytes, checksum: 9c878e04230c7ca16c48c3d7c51b3022 (MD5) Previous issue date: 2012 | en |
| dc.description.tableofcontents | 致謝................................................................................................................................I
中文摘要.......................................................................................................................II 英文摘要......................................................................................................................Ⅲ 中英文縮寫名詞對照................................................................................................. .V 一、前言.......................................................................................1 1.腸道組織結構.............................................................................................................1 1.1小腸絨毛結構..................................................................................................1 2.腸道生理功能.............................................................................................................2 2.1物理性屏障......................................................................................................2 2.2化學性屏障......................................................................................................3 2.3免疫性屏障......................................................................................................3 3.腸腔內常生細菌.........................................................................................................4 4.抗生素造成常生菌相失衡.........................................................................................5 5.超級細菌的演進史.....................................................................................................6 6. 實驗目的...................................................................................................................8 二、材料與方法..........................................................................9 1. 實驗動物................................................................................................................9 2. 實驗用細菌............................................................................................................9 2.1含與不含氨芐青黴素的Luria-Bertani培養基瓊脂平板 (LB agar plate) 和培養液 (LB broth) 製備.............................................................................................9 2.1.1 氨芐青黴素儲存液 (Ampicillin stock) 的製備..............................9 2.1.2 LB培養液(LB broth)的製備..............................................................9 2.1.3 LB培養基瓊脂平板(LB agar plate)的製備.......................................10 2.2大腸桿菌生長曲線(growth curve)製作方式.................................................10 2.3餵食小鼠之細菌製備方法............................................................................11 3. 實驗動物分組......................................................................................................11 3.1正常水組 (Normal Water, NW) 飲用水配法..............................................11 3.2抗生素水組(Antibiotic Water, AW)飲用水配法...........................................11 4. 實驗動物感染流程..............................................................................................12 5. 腸道細菌數目變化分析......................................................................................12 5.1腸段總細菌量 (total bacteria) 量分析.........................................................12 5.2細菌轉移數量的分析 (bacteria translocation).............................................12 5.3腸道上皮細胞內吞細菌(endocytosed bacteria in enterocytes)分析........13 6. 組織固定、切片及染色......................................................................................14 6.1石蠟包埋檢體的製備作組織染色(固定液為4%三聚甲醛).................14 6.2石蠟包埋檢體的製備作螢光原位雜交實驗(固定液為Carnoy's Solution) 6.3 冷凍切片包埋檢體的製備作緊密連結螢光染色.......................................15 6.4 蘇木紫-伊紅染色(Haematoxylin and Eosin Staining)............................15 6.5 螢光原位雜交(Fluorescence in situ hybridization, FISH)......................16 6.6緊密連結免疫螢光染色 (Tissue immunofluorescence for ZO-1) .........16 7. 西方轉漬法 (Western blotting)........................................................................17 7.1 黏膜層蛋白質萃取.......................................................................................17 7.2 蛋白質定量...................................................................................................18 7.3蛋白質電泳....................................................................................................18 7.4蛋白質分析....................................................................................................18 8.腸道屏障功能分析................................................................................................20 8.1腸道組織離子通透性(ion permeability)分析..........................................20 8.2腸道組織大分子通透性(macromolecular permeability)分析.................21 三、實驗結果............................................................................22 1. Amp-r E.coli之生長曲線...................................................................................22 2. 抗生素處理與Amp-r E.coli感染對BALB/c小鼠腸道生理的影響................22 2.1小鼠腹腔外觀與消化道外觀變化................................................................22 2.2 腸道組織外觀結構的變化...........................................................................23 3. 腸段總細菌量(total bacteria number)的變化.............................................23 4. 腸道細菌在組織中分布情形..............................................................................24 5. 腸道上皮細胞內吞細菌量(endocytosed bacteria in enterocytes)..............24 6. 細菌轉移至肝臟及脾臟以及血液 (bacteria translocation) 的情形..............25 7. 腸道組織緊密連結ZO-1 和occludin 結構變化.............................................26 8. 小鼠空腸、盲腸及結腸的通透性變化..............................................................26 9. 抗生素水組MAPKs (p38、Erk1/2、JNK) 和I-kappa-B-alpha磷酸化程度的變化......27 四、討論....................................................................................28 五、圖表....................................................................................33 六、參考文獻...........................................................................57 表目錄 表1、腸道共生菌叢的功能.........................................................................................33 表2、正常水組與抗生素水組小鼠在day 0腸道常氧總細菌量的比較...................34 表3、正常水組與抗生素水組小鼠在day 0腸道厭氧總細菌量的比較...................35 圖目錄 圖1、腸道組織結構...................................................................................................36 圖2、腸道腺窩-絨毛軸..............................................................................................37 圖3、Ampicillin resistant E.coli (Amp-r E.coli) 之質體基因圖...........................38 圖4、Amp-r E.coli生長曲線中活菌數量與分光光度計讀數之關係....................39 圖5、正常水組 (Normal water, NW) 和抗生素水組 (antibiotic water, AW)小鼠在灌食Amp-r E.coli之後,腹腔內以及腸道的外觀變化......................................40 圖6-1、空腸組織外觀結構的變化..............................................................................41 圖6-2、盲腸組織外觀結構的變化..............................................................................42 圖6-3、結腸組織外觀結構的變化..............................................................................43 圖7、腸段需氧菌總量(total aerobic bacteria)的變化.......................................44 圖8、腸段厭氧菌總量(total anaerobic bacteria)的變化....................................45 圖9-1、螢光原位雜交分析細菌和E.coli在空腸組織內分佈的情形......................46 圖9-2、螢光原位雜交分析細菌和E.coli在盲腸組織內分佈的情形.....................47 圖9-3、螢光原位雜交分析細菌和E.coli在結腸組織內分佈的情形......................48 圖10、腸道上皮細胞內吞細菌(endocytosed bacteria in enterocytes)變化.........49 圖11、細菌轉移數量的變化 .....................................................................................50 圖12-1、空腸組織緊密連結ZO-1結構變化..............................................................51 圖12-2、盲腸組織緊密連結ZO-1結構變化..............................................................52 圖12-3、結腸組織緊密連結ZO-1結構變化..............................................................53 圖13、抗生素水組腸道黏膜組織中occludin之表現................................................54 圖14、小鼠腸道電生理值和通透性的變化...............................................................55 圖15、抗生素水組小鼠空腸與結腸在MAPKs (p38、ERK、JNK) 和Ikappka B alpha磷酸化程度的變化..............................................................................................................56 | |
| dc.language.iso | zh-TW | |
| dc.subject | 上皮屏障功能 | zh_TW |
| dc.subject | 抗生素 | zh_TW |
| dc.subject | 超級細菌 | zh_TW |
| dc.subject | 腸道菌叢擾亂 | zh_TW |
| dc.subject | 定殖 | zh_TW |
| dc.subject | 入侵 | zh_TW |
| dc.subject | antibiotic | en |
| dc.subject | epithelial barrier function | en |
| dc.subject | invasion | en |
| dc.subject | colonization | en |
| dc.subject | dysbiosis | en |
| dc.subject | superbug | en |
| dc.title | 抗生素引起之共生菌相失衡促使超級細菌在小鼠腸道定殖和入侵 | zh_TW |
| dc.title | Antibiotic-induced enteric commensal dysbiosis favours superbug colonization and bacterial invasion in mice | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 100-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 張上淳,倪衍玄,盧俊良,賈景山 | |
| dc.subject.keyword | 抗生素,超級細菌,腸道菌叢擾亂,定殖,入侵,上皮屏障功能, | zh_TW |
| dc.subject.keyword | antibiotic,superbug,dysbiosis,colonization,invasion,epithelial barrier function, | en |
| dc.relation.page | 61 | |
| dc.rights.note | 未授權 | |
| dc.date.accepted | 2012-08-17 | |
| dc.contributor.author-college | 醫學院 | zh_TW |
| dc.contributor.author-dept | 生理學研究所 | zh_TW |
| 顯示於系所單位: | 生理學科所 | |
文件中的檔案:
| 檔案 | 大小 | 格式 | |
|---|---|---|---|
| ntu-101-1.pdf 未授權公開取用 | 2.84 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。
