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重金屬生物有效性對於抗生素抗性基因在農地土壤的分佈與持續之影響

為了解決th-65gx900w的問題，作者鄧教毅 這樣論述：

近年來隨著抗生素的濫用與不當使用，已使得環境和臨床案例中感染具多重抗藥性的病原菌之案例逐年升高，由於大部分的致病菌已知多是透過環境中的一般微生物而獲得抗性基因，因此環境中抗生素抗藥性的加速發展所引發的公共衛生問題逐漸令人憂心。然而，減少抗生素的使用卻發現無法有效遏止抗藥性的擴散，代表環境中可能存有其他能持續對細菌造成壓力的物質；這當中，重金屬被視為極可能是維持抗生素抗性基因(antibiotic resistance genes, ARGs)在環境流佈存續的最關鍵因子，但此種非傳統抗生素抗性發展的途徑(即透過金屬的共選擇機制而誘發抗生素抗性)截至目前為止仍未得到廣泛的研究。有鑒於此，為瞭解重

金屬是否/如何影響抗生素抗性基因在本土土壤中的維持及傳播，本研究選擇桃園中壢工業區周圍受重金屬污染且具有濃度梯度的農地為場址，透過土壤採樣與序列萃取進行初步的相關性分析。調查結果發現：(1)桃園地區受污染的農地土壤中，銅主要分佈於鐵錳氧化態、有機態及殘餘態，鉻主要分佈於殘餘態，鋅、鎳和鉛主要分佈於鐵錳氧化態及殘餘態；(2)當利用最小共選擇濃度(minimum co-selective concentration, MCC)來評估共選擇的潛勢時，發現在重金屬濃度高於MCC的場址，其ARGs和Class 1 integron相對豐富度顯著高於低於MCC的場址；(3)不同的ARGs透過基因連鎖同時存

在於Class 1 integron，意指若有重金屬的環境壓力時，ARGs經由水平基因轉移而散佈；(4)重金屬全量濃度和移動相得到相似的結果，但移動相的結果顯示銅變為具有更強的驅動水平基因轉移潛勢，金屬移動相可能驅動水平基因轉移透過Class 1 integron將ARGs在環境中散佈，暗示著移動相可能適合作為生物有效性的代表，且當有數種重金屬的存在時更有助於誘發共選擇；(5) Class 1 integron同時對重金屬與ARGs具有顯著相關，代表其可能擁有應對重金屬與抗生素的能力，在受重金屬影響的農地種植，作物上可能發現同時擁有重金屬抗性和抗生素抗性的菌株，因而進入食物鏈之中。

調控型T細胞的功能探討

為了解決th-65gx900w的問題，作者楊維正 這樣論述：

長庚大學博士學位論文指導教授推薦書長庚大學博士學位論文口試委員會審定書Acknowledgements iiiChinese Abstract ivEnglish Abstract viTable of Contents viiiList of Figures xList of Tables xiiAbbreviations xiiiChapter 1 Introduction 11.1 Regulatory T cells 21.2 Tregs in autoimmune disease 91.3 Interleukin-4

151.4 Significance of the study 17Chapter 2 Materials and methods 202.1 Animal experiments 202.2 Flow cytometry 262.3 Cell culture medium and reagents 302.4 Suppression assay 312.5 Transcriptional analysis of protein expression 322.6 Enzyme linked immunosorbent assay (ELISA)

332.7 Hematoxylin and eosin staining (H&E staining) 342.8 Statistical analysis 35Chapter 3 Results 363.1 Instability of Foxp3 expression in Tregs from NZB mice might result in their functional incompetency in vitro 363.2 NZB Tregs were less potent in preventing AIHA progression particul

arly on regulating autoantibody production in vivo 383.3 To validate and track the efficacy of Treg cell therapy in the recipient NZB mice 403.4 Deficiency of IL-4 deteriorated Treg mediated immune suppression 413.5 The presence of physiological relevant amount of IL-4 was essential for Tre

g mediated immune suppression in vitro 423.6 Several factors contributed to IL-4 mediated maintenance of Treg function 44Chapter 4 Discussion 46Chapter 5 Conclusion 57Figures 59Tables 78Reference 81Appendix 105 List of FiguresFigure 1 Foxp3 expression is not stable in Tregs f

rom NZB mice after activation 59Figure 2 Hct values and Coombs' titers of nude mice at 4 and 8 weeks after receiving CD4 T cells from NZB or BALB/c mice 60Figure 3 AIHA progresses in mice receiving CD4 cells from NZB mice 61Figure 4 Hct values and Coombs' titers of nude mice at 4 and 8 week

s after receiving Treg cells from NZB or BALB/c mice with Tresp cells from NZB mice 62Figure 5 AIHA progresses in mice receiving Treg cells from both BALB/c and NZB mice 64Figure 6 AIHA progresses in mice receiving Tregs from both BALB/c and NZB mice 65Figure 7 BALB/c Tregs adoptive transfe

r does not rescue NZB mice from AIHA progression 66Figure 8 Adoptive transferring of BALB/c Tregs does not rescue NZB mice from AIHA progression 67Figure 9 Similar frequencies of Foxp3 expressing cells are identified in WT and IL-4 KO mice in the steady state 68Figure 10 Tregs from IL-4 def

icient host have inferior suppressive capabilities in suppressing autologous Tresps 69Figure 11 Removal of IL-4 deteriorates the suppressive immune response elicited by WT Tregs 70Figure 12 IL-4 supplement rescues the defective phenotype of IL-4 KO Tregs 71Figure 13 IL-4 KO Tregs are able t

o suppress WT Tresps 72Figure 14 WT Tregs lose their immune modulatory capacities when they are suppressing IL-4 KO Tresps 73Figure 15 IL-4 KO Tregs are incapable of suppressing antigen specific activated Tresps from OT2 mice 74Figure 16 Deprivation of IL-4 leads to increased cell death aft

er activation 75Figure 17 The relative changes of T cell anergy and tolerance related genes in Tregs with or without the presence of IL-4 during co-culturing with WT Tresps. 76Figure 18 The amount of IL-4 determines their differential acts on Treg mediated immune suppressive responses 77 Li

st of TablesTable 1 List of antibodies 78Table 2 List of primers 79Table 3 The amount of IL-4 produced by cells after stimulation 80