帳號:guest(3.145.176.231)          離開系統
字體大小: 字級放大   字級縮小   預設字形  

詳目顯示

以作者查詢圖書館館藏以作者查詢臺灣博碩士論文系統以作者查詢全國書目
作者(中文):侯冠宇
作者(外文):Hou, Kuan-Yu
論文名稱(中文):利用微液滴系統觀察顆粒物質對金黃色葡萄球菌生長的影響
論文名稱(外文):Investigation of the Effects of Particular Matters on Staphylococcus aureus growth using a Microdroplet System
指導教授(中文):王翔郁
指導教授(外文):Wang, Hsiang-Yu
口試委員(中文):張晃猷
陳致真
高承源
口試委員(外文):Chang, Hwan-You
Chen, Chih-Chen
Kao, Cheng-Yuan
學位類別:碩士
校院名稱:國立清華大學
系所名稱:工程與系統科學系
學號:107011526
出版年(民國):110
畢業學年度:109
語文別:中文
論文頁數:191
中文關鍵詞:微液滴系統金黃色葡萄球菌顆粒物質多環芳香烴
外文關鍵詞:Microdroplet systemStaphylococcus aureusParticulate mattersPolycyclic Aromatic Hydrocarbons
相關次數:
  • 推薦推薦:0
  • 點閱點閱:61
  • 評分評分:*****
  • 下載下載:0
  • 收藏收藏:0
人體吸入空氣中的顆粒物質進而引發疾病的同時,體內微生物族群的平衡也會因此破壞。目前沒有文獻能夠明確解釋疾病的產生是顆粒物質改變體內環境,才導致微生物族群的破壞,還是顆粒物質影響微生物的生長速度導致平衡破壞,進而引發疾病。為了確認是否顆粒物質會直接影響著微生物的生長速度,本研究的目標在於探討顆粒物質是如何影響著人體內常見的致病菌(金黃色葡萄球菌)的生長。
  本研究分別利用巨觀與微觀的培養條件,分別探討顆粒物質的水溶性成分、油溶性成分、固體顆粒、以及未經處理顆粒物質對金黃色葡萄球菌生長的影響。實驗採用的兩種顆粒物質分別為SRM-1648a (都市室外收集)與SRM-2585 (室內收集),且1648a和2585含有成分相似但不含量的多環芳香烴(Polycyclic Aromatic Hydrocarbons,簡稱PAHs)。
  在巨觀實驗中將金黃色葡萄球菌培養於離心管內並以點盤定量細菌濃度,可得知1648a和2585的水溶性成分增加金黃色葡萄球菌的生長速度,分別是控制組的1.20倍、1.06倍,油溶性成分對生長速度的影響則不明顯,分別為控制組的0.92倍、0.96倍,可能原因為低分子量PAHs溶於水後被金黃色葡萄球菌降解形成碳源作為養分,留在油相中的高分子量PAHs因溶解於水溶液中的量極低,在離心管中與細菌接觸的機會相當低,只會發生在兩相交界面,因此沒有機會被細菌降解。另外,添加萃取過後的「固體顆粒」(不含PAHs及其他水溶/油溶性成分)後,金黃色葡萄球菌有了易附著的媒介而更容易團聚生長,生長速度分別是控制組的1.09倍、1.13倍。添加未萃取的顆粒物質後,多了水溶/油溶性成分的影響,影響程度反而比「固體顆粒」低,生長速度分別是1.07倍、1.06倍。油溶性成分中的高分子量PAHs單獨存在時雖然不會影響金黃色葡萄球菌的生長,但是當金黃色葡萄球菌團聚於顆粒物質上,群體感應(quorem sensing)會放大高分子量PAHs的毒性,而水溶性成分中的低分子量PAHs雖然會增加金黃色葡萄球菌的生長,但是油溶性成分中的高分子量PAHs含量較高,因此毒性的影響力大於額外養分。
  微觀實驗將金黃色葡萄球菌培養於微液滴之中,並利用DiI螢光標記細胞膜以定量細菌數。微液滴的形成利用flow-focusing微流道達成,菌液和dSURF分別作為分散相與連續相,並調整通入液體的壓力使液滴直徑控制在125um。1648a和2585的水溶性成分皆增加了液滴平均最大容忍細菌數量(κ),分別為控制組1.44、1.40倍,原因與巨觀實驗相同,低分子量的PAHs被降解後產生額外的養分而使得液滴中可容忍的細胞數增加。兩種顆粒物質的油溶性成分也增加金黃色葡萄球菌的最大生長速度(gr_max),分別為控制組的2.05、1.18倍,雖然高分子量的PAHs在巨觀環境下難以被降解,但是培養於液滴中,增加了每個細菌個體與油溶性成分接觸的機會,因此加速了降解過程,使高分子量的PAHs也被降解釋放出額外養分。
  本研究利用巨觀與微觀的培養條件,證實顆粒物質的水溶性成分及固體顆粒增加了金黃色葡萄球菌生長,並揭露顆粒物質影響金黃色葡萄球菌生長的可能途徑,長時間暴露在顆粒物質環境下,有可能增加金黃色葡萄球菌的生長而破壞了體內菌叢平衡,進而引發疾病。未來希望能夠採用特定含量較高的高環數、低環數PAHs,以確立本實驗認為PAHs能夠被金黃色葡萄球菌降解並提供養分的假設。
Past studies indicated that the occurrence of disease is oftenly accompanied with the inhalation of particulate matters (PMs) and the impaired balance of microbiota in vivo. Presently, an explicit explanation for the relationship between desease, PM, and microbiota has yet to be found. It is still unclear that whether PMs weakened the immune systems of human and lead to the impaired microbiota balance, or PMs impaired the microbiota balance and lead to the weakend immune system. In order to confirm whether PMs directly affect the balance of microbiota, this study aims to investigate how PM affects the growth rate of Staphylococcus aureus (S.aureus), one of the common pathogenic bacteria in the human body.
This study used macroscopic and microscopic culture conditions to explore the effects of hydrophilic, hydrophobic, stripped particulate matters, and untreated particulate matters on the growth of S. aureus. Two kinds of PMs were used :SRM-1648a (Urban Particulate Matter) and SRM-2585 (Organic Contaminants in House Dust). The compositions of polycyclic aromatic hydrocarbons (PAHs) were similar between these two PMs but SRM-1648a contains a higher total PAHs amount than SRM-2585.
Observed from macroscopic aspect, hydrophilic ingredients from SRM-1648a and SRM-2585 increased the growth rate of S. aureus to 1.20 and 1.06 folds respectively compared with the control. Hydrophobic ingredients had no significant effects on the growth rate. It was probably that low-ring PAHs had high solubilities in the aqueous phase and were able to be degraded by S. aureus, leading to the release of consumable organic matters for S. aureus. However, high-ring PAHs remained in the oil phase and only S. aureus at the water-oil interface had access to these PAHs, resulting in barely degraded PAHs. The ‘stripped PM’ increased the growth rate since it provided a medium for S. aureus to adhere, and the growth rate was 1.09 and 1.13 times for SRM-1648a and SRM-2585 compared to the control group. Adding untreated PM, influence of hydrophilic/hydrophobic elements was less than the stripped PM, and the growth rate was 1.07 and 1.06 times for SRM-1648a and SRM-2585 compared to the control group. Although the PAHs with more rings in hydrophobic elements alone did not affect the growth of S. aureus, when S. aureus aggregated on PM, quorem sensing amplified the toxicity of high-ring PAHs. This toxic effect evened out the enhanced effects of solid particle and low-ring PAHs on the growth rate of S. aureus.
Observed from microscopic aspect, hydrophilic ingredients from SRM-1648a and SRM-2585 increased the capacity of the droplets to 1.44 and 1.40 folds of the control, attributed to the same reasons as in the macroscopic experimets that the degradation of low-ring PAHs led to extra carbon sources. In contrast to the results in the macroscopic experiments, hydrophobic ingredients from SRM-1648a and SRM-2585 increased the growth rate of S. aureus considerable. In the droplet, every S. aureus cells had much higher chance and longer contact with high-ring PAHs and accelerated the degradation process of high-ring PAHs which released extra carbon sources for S. aureus.
This study revealed the possible pathways of how PMs affects human health. A long-term exposure to PM increases the growth rate of S. aureus and can disrupt the balance of the microbiota in the body, which may eventually lead to the occurrence of disease. Adding different amounts of specific high-ring and low-ring PAHs will be conducted in future studies to validate the hypothesis that PAHs can be degraded by S. aureus to provide carbon source.
摘要 i
Abstract iii
致謝 v
目錄 vi
表目錄 x
圖目錄 xiii
第 1 章 緒論 1
1.1介紹 1
1.2實驗目的與規劃 2
第 2 章 文獻回顧 4
2.1 空氣汙染對人體的影響 4
2.2微生物族群 11
2.2.1微生物對人體的影響 11
2.2.2微生物與疾病的關聯 13
2.3微液滴系統 16
2.3.1微流體系統的發展 16
2.3.2微液滴系統的優點 16
2.3.3控制液滴生成之微流道 18
2.3.4控制液滴大小參數 30
2.3.5微生物應用於液滴 35
2.4微流體系統中微生物檢測方法 41
2.4.1電訊號檢測 41
2.4.2光學檢測 44
第 3 章 實驗方法與材料 48
3.1不同稀釋液影響金黃色葡萄球菌的增長 48
3.1.1 微生物培養方法 49
3.1.1.1 LB溶液配置 50
3.1.1.2 Agar洋菜膠盤配置 50
3.1.2 微生物點盤法 51
3.1.2.1藥品配置 52
3.1.2.2序列稀釋實驗方法 53
3.2不同染劑影響金黃色葡萄球菌的增長 54
3.2.1染劑工作液置備 55
3.2.2 微生物染色方法 55
3.3利用點盤法與細胞計數器比較金黃色葡萄球菌的增長 57
3.4利用液滴培養金黃色葡萄球菌 58
3.4.1 微流道母模設計與製程 59
3.4.1.1微流道光罩圖形設計 59
3.4.1.2黃光顯影製程 60
3.4.2 微流道製程 65
3.4.2.1 PDMS翻模 66
3.4.2.2 玻片PDMS旋塗 68
3.4.3生成微液滴 68
3.4.3.1 微液滴直徑分析 70
3.4.5 液滴內細菌增長觀察方法 73
3.4.6半自動化分析方法 74
3.5兩種顆粒物質對金黃色葡萄球菌的影響 77
3.5.1 SRM-1648a Urban Particulate Matter 77
3.5.2 SRM-2585 Organic Contaminants in House Dust 79
3.5.3 顆粒物質配置方法 80
3.5.4 顆粒物質萃取方法 82
3.5.5水溶性成分對金黃色葡萄球菌的影響 83
3.5.6油溶性成分對金黃色葡萄球菌的影響 84
3.5.7 PAHs在兩相的濃度 85
3.5.8 統計數據分析 86
第 4 章 結果與討論 89
4.1 不同稀釋液影響金黃色葡萄球菌的增長 89
4.2 不同染劑影響金黃色葡萄球菌的增長 92
4.3 利用點盤法與細胞計數器比較金黃色葡萄球菌的增長 101
4.4 利用微液滴培養金黃色葡萄球菌 103
4.5 兩種顆粒物質對金黃色葡萄球菌的影響 113
4.5.1 利用點盤法觀察顆粒物質對金黃色葡萄球菌的影響 114
4.5.2 利用微液滴觀察顆粒物質的水溶性成分對金黃色葡萄球菌的影響 132
4.5.3 利用微液滴觀察顆粒物質的油溶性成分對金黃色葡萄球菌的影響 151
4.5.4綜合比較 170
第 5 章 結論與未來展望 175
5.1 結論 175
5.2 未來展望 177
參考資料 180
附錄A 實驗藥品 189
A.1微生物培養方法 189
A.2微生物點盤法 189
A.3 微生物染色方法 190
A.4微流道母模設計與製程 191
A.5 微流道製程 191

1. HOLLAND, W.W.J.A.J.o.E., Health effects of participate pollu-tion: reappraising the evidence. 1979. 110(5): p. 525-659.
2. Kelly, F.J. and J.C.J.A.e. Fussell, Size, source and chemical composition as determinants of toxicity attributable to ambient particulate matter. 2012. 60: p. 504-526.
3. Brown, J.S., et al., Thoracic and respirable particle definitions for human health risk assessment. 2013. 10(1): p. 12.
4. Lo, W.-C., et al., Burden of disease attributable to ambient fine particulate matter exposure in Taiwan. 2017. 116(1): p. 32-40.
5. Lima, A.L.C., J.W. Farrington, and C.M. Reddy, Combustion-derived polycyclic aromatic hydrocarbons in the environment—a review. Environmental forensics, 2005. 6(2): p. 109-131.
6. Kameda, Y., et al., Atmospheric polycyclic aromatic hydrocarbons: size distribution, estimation of their risk and their depositions to the human respiratory tract. Science of the Total Environment, 2005. 340(1-3): p. 71-80.
7. Kameda, T., Atmospheric chemistry of polycyclic aromatic hydrocarbons and related compounds. Journal of Health Science, 2011. 57(6): p. 504-511.
8. Unwin, J., et al., An assessment of occupational exposure to polycyclic aromatic hydrocarbons in the UK. Annals of Occupational Hygiene, 2006. 50(4): p. 395-403.
9. Olsson, A.C., et al., Occupational exposure to polycyclic aromatic hydrocarbons and lung cancer risk: a multicenter study in Europe. Occupational and environmental medicine, 2010. 67(2): p. 98-103.
10. Dockery, D.W. and C.A.J.A.r.o.p.h. Pope, Acute respiratory effects of particulate air pollution. 1994. 15(1): p. 107-132.
11. Dominici, F., et al., Fine particulate air pollution and hospital admission for cardiovascular and respiratory diseases. 2006. 295(10): p. 1127-1134.
12. Saldiva, P.H., et al., Association between air pollution and mortality due to respiratory diseases in children in São Paulo, Brazil: a preliminary report. 1994. 65(2): p. 218-225.
13. Ackermann-Liebrich, U., et al., Lung function and long term exposure to air pollutants in Switzerland. Study on Air Pollution and Lung Diseases in Adults (SAPALDIA) Team. 1997. 155(1): p. 122-129.
14. Schindler, C., et al., Short-term variation in air pollution and in average lung function among never-smokers: the Swiss Study on Air Pollution and Lung Diseases in Adults (SAPALDIA). 2001. 163(2): p. 356-361.
15. Schwartz, J.J.E., Air pollution and hospital admissions for heart disease in eight US counties. 1999: p. 17-22.
16. Ruckerl, R., et al., Air pollution and markers of inflammation and coagulation in patients with coronary heart disease. 2006. 173(4): p. 432-441.
17. Peters, A., et al., Increases in heart rate during an air pollution episode. 1999. 150(10): p. 1094-1098.
18. Kim, K.E., D. Cho, and H.J.J.L.s. Park, Air pollution and skin diseases: Adverse effects of airborne particulate matter on various skin diseases. 2016. 152: p. 126-134.
19. Puri, P., et al., Effects of air pollution on the skin: A review. 2017. 83(4): p. 415.
20. Ritz, B., et al., Ambient air pollution and risk of birth defects in Southern California. 2002. 155(1): p. 17-25.
21. Calderón-Garcidueñas, L., et al., Long-term air pollution exposure is associated with neuroinflammation, an altered innate immune response, disruption of the blood-brain barrier, ultrafine particulate deposition, and accumulation of amyloid β-42 and α-synuclein in children and young adults. 2008. 36(2): p. 289-310.
22. Asher, M.I., et al., Worldwide time trends in the prevalence of symptoms of asthma, allergic rhinoconjunctivitis, and eczema in childhood: ISAAC Phases One and Three repeat multicountry cross-sectional surveys. 2006. 368(9537): p. 733-743.
23. Thomsen, S.F.J.I.a., Atopic dermatitis: natural history, diagnosis, and treatment. 2014. 2014.
24. Lowe, A.J., et al., Do boys do the atopic march while girls dawdle? 2008. 121(5): p. 1190-1195.
25. Thyssen, J.P., L. Skov, and A.J.J.o.t.A.A.o.D. Egeberg, Cause-specific mortality in adults with atopic dermatitis. 2018. 78(3): p. 506-510.
26. Kim, J., et al., Symptoms of atopic dermatitis are influenced by outdoor air pollution. 2013. 132(2): p. 495-498. e1.
27. Ahn, K.J.J.o.A. and C. Immunology, The role of air pollutants in atopic dermatitis. 2014. 134(5): p. 993-999.
28. Byrd, A.L., et al., Staphylococcus aureus and Staphylococcus epidermidis strain diversity underlying pediatric atopic dermatitis. 2017. 9(397): p. eaal4651.
29. Rosenstein, B.J. and G.R.J.T.J.o.p. Cutting, The diagnosis of cystic fibrosis: a consensus statement. 1998. 132(4): p. 589-595.
30. Rosenfeld, M., et al., Gender gap in cystic fibrosis mortality. 1997. 145(9): p. 794-803.
31. Orenstein, D.M., G.B. Winnie, and H.J.T.J.o.p. Altman, Cystic fibrosis: a 2002 update. 2002. 140(2): p. 156-164.
32. Zemel, B.S., et al., Longitudinal relationship among growth, nutritional status, and pulmonary function in children with cystic fibrosis: analysis of the Cystic Fibrosis Foundation National CF Patient Registry. 2000. 137(3): p. 374-380.
33. Goss, C.H., et al., Effect of ambient air pollution on pulmonary exacerbations and lung function in cystic fibrosis. 2004. 169(7): p. 816-821.
34. Sender, R., S. Fuchs, and R.J.P.b. Milo, Revised estimates for the number of human and bacteria cells in the body. 2016. 14(8): p. e1002533.
35. Byrd, A.L., Y. Belkaid, and J.A.J.N.R.M. Segre, The human skin microbiome. 2018. 16(3): p. 143.
36. Koch, R., Investigations into the etiology of traumatic infective diseases. Vol. 88. 1880: New Sydenham Society.
37. Qin, J., et al., A human gut microbial gene catalogue established by metagenomic sequencing. 2010. 464(7285): p. 59.
38. Schroeder, B.O. and F.J.N.m. Bäckhed, Signals from the gut microbiota to distant organs in physiology and disease. 2016. 22(10): p. 1079.
39. Arnold, I.C., et al., Helicobacter pylori infection prevents allergic asthma in mouse models through the induction of regulatory T cells. 2011. 121(8): p. 3088-3093.
40. Lathrop, S.K., et al., Peripheral education of the immune system by colonic commensal microbiota. 2011. 478(7368): p. 250.
41. Ley, R.E., et al., Obesity alters gut microbial ecology. 2005. 102(31): p. 11070-11075.
42. Turnbaugh, P.J., et al., The effect of diet on the human gut microbiome: a metagenomic analysis in humanized gnotobiotic mice. 2009. 1(6): p. 6ra14-6ra14.
43. Cogen, A., V. Nizet, and R.J.B.J.o.D. Gallo, Skin microbiota: a source of disease or defence? 2008. 158(3): p. 442-455.
44. Grice, E.A. and J.A.J.N.R.M. Segre, The skin microbiome. 2011. 9(4): p. 244.
45. Bauernfeind, A., et al., Qualitative and quantitative microbiological analysis of sputa of 102 patients with cystic fibrosis. 1987. 15(4): p. 270-277.
46. Le, H.P.J.J.o.I.S. and Technology, Progress and trends in ink-jet printing technology. 1998. 42(1): p. 49-62.
47. Terry, S.C., J.H. Jerman, and J.B.J.I.t.o.e.d. Angell, A gas chromatographic air analyzer fabricated on a silicon wafer. 1979. 26(12): p. 1880-1886.
48. Manz, A., et al., Design of an open-tubular column liquid chromatograph using silicon chip technology. 1990. 1(1-6): p. 249-255.
49. Shoji, S., et al., Prototype miniature blood gas analyser fabricated on a silicon wafer. 1988. 14(2): p. 101-107.
50. Van Lintel, H., et al., A piezoelectric micropump based on micromachining of silicon. 1988. 15(2): p. 153-167.
51. Charlton, S.C., M.V. Rebec, and C. Ruetten, Self-metering fluid analysis device. 1993, Google Patents.
52. Lu, L.-H., K.S. Ryu, and C.J.J.o.m.s. Liu, A magnetic microstirrer and array for microfluidic mixing. 2002. 11(5): p. 462-469.
53. Kuswandi, B., J. Huskens, and W.J.A.c.a. Verboom, Optical sensing systems for microfluidic devices: a review. 2007. 601(2): p. 141-155.
54. Thorsen, T., et al., Dynamic pattern formation in a vesicle-generating microfluidic device. 2001. 86(18): p. 4163.
55. Teh, S.-Y., et al., Droplet microfluidics. 2008. 8(2): p. 198-220.
56. Guo, M.T., et al., Droplet microfluidics for high-throughput biological assays. 2012. 12(12): p. 2146-2155.
57. Agresti, J.J., et al., Ultrahigh-throughput screening in drop-based microfluidics for directed evolution. 2010. 107(9): p. 4004-4009.
58. Gensler, W.J., The Synthesis of Isoquinolines by the P omeranz‐F ritsch Reaction. Organic Reactions, 2004. 6: p. 191-206.
59. Banerjee, S. and R.N. Zare, Syntheses of isoquinoline and substituted quinolines in charged microdroplets. Angewandte Chemie, 2015. 127(49): p. 15008-15012.
60. Zhu, P. and L.J.L.o.a.C. Wang, Passive and active droplet generation with microfluidics: a review. 2017. 17(1): p. 34-75.
61. Nisisako, T., T. Torii, and T.J.L.o.a.C. Higuchi, Droplet formation in a microchannel network. 2002. 2(1): p. 24-26.
62. Umbanhowar, P., V. Prasad, and D.A.J.L. Weitz, Monodisperse emulsion generation via drop break off in a coflowing stream. 2000. 16(2): p. 347-351.
63. Yobas, L., et al., High-performance flow-focusing geometry for spontaneous generation of monodispersed droplets. 2006. 6(8): p. 1073-1079.
64. Anna, S.L., N. Bontoux, and H.A.J.A.p.l. Stone, Formation of dispersions using “flow focusing” in microchannels. 2003. 82(3): p. 364-366.
65. Schuler, F., et al., Centrifugal step emulsification applied for absolute quantification of nucleic acids by digital droplet RPA. 2015. 15(13): p. 2759-2766.
66. Sugiura, S., M. Nakajima, and M.J.L. Seki, Prediction of droplet diameter for microchannel emulsification. 2002. 18(10): p. 3854-3859.
67. Mine, Y., et al., Preparation and stabilization of simple and multiple emulsions using a microporous glass membrane. 1996. 6(4-5): p. 261-268.
68. Xu, J.H., et al., Correlations of droplet formation in T-junction microfluidic devices: from squeezing to dripping. 2008. 5(6): p. 711-717.
69. Gupta, A. and R.J.P.o.F. Kumar, Flow regime transition at high capillary numbers in a microfluidic T-junction: Viscosity contrast and geometry effect. 2010. 22(12): p. 122001.
70. Xu, J., et al., Shear force induced monodisperse droplet formation in a microfluidic device by controlling wetting properties. 2006. 6(1): p. 131-136.
71. Nossal, G.J.J.B.j.o.e.p., Antibody production by single cells. 1958. 39(5): p. 544.
72. Viret, C. and W.J.T.J.o.I. Gurr, The origin of the “one cell-one antibody” rule. 2009. 182(3): p. 1229-1230.
73. Kang, D.-K., et al., Rapid detection of single bacteria in unprocessed blood using Integrated Comprehensive Droplet Digital Detection. 2014. 5: p. 5427.
74. Iino, R., et al., A single-cell drug efflux assay in bacteria by using a directly accessible femtoliter droplet array. 2012. 12(20): p. 3923-3929.
75. Iino, R., et al., Design of a large-scale femtoliter droplet array for single-cell analysis of drug-tolerant and drug-resistant bacteria. 2013. 4: p. 300.
76. Jang, S., et al., On-chip analysis, indexing and screening for chemical producing bacteria in a microfluidic static droplet array. 2016. 16(10): p. 1909-1916.
77. Boedicker, J.Q., et al., Detecting bacteria and determining their susceptibility to antibiotics by stochastic confinement in nanoliter droplets using plug-based microfluidics. 2008. 8(8): p. 1265-1272.
78. Lewis, K.J.A.r.o.m., Persister cells. 2010. 64: p. 357-372.
79. Noble, R.T., S.B.J.J.o.w. Weisberg, and health, A review of technologies for rapid detection of bacteria in recreational waters. 2005. 3(4): p. 381-392.
80. Yao, L., et al., CMOS conductometric system for growth monitoring and sensing of bacteria. 2011. 5(3): p. 223-230.
81. Zelada-Guillén, G.A., et al., Real-time potentiometric detection of bacteria in complex samples. 2010. 82(22): p. 9254-9260.
82. Davey, H.M. and D.B.J.M.M.B.R. Kell, Flow cytometry and cell sorting of heterogeneous microbial populations: the importance of single-cell analyses. 1996. 60(4): p. 641-696.
83. Phinney, D. and T.J.C.T.J.o.t.I.S.f.A.C. Cucci, Flow cytometry and phytoplankton. 1989. 10(5): p. 511-521.
84. Steen, H., Flow cytometry instrumentation, in Particle analysis in oceanography. 1991, Springer. p. 3-29.
85. Button, D. and B.J.H.o.m.i.a.m.e. Robertson, Use of high-resolution flow cytometry to determine the activity and distribution of aquatic bacteria. 1993: p. 163-173.
86. Olson, R.J., E.R. Zettler, and M.D.J.H.o.m.i.a.m.e. DuRand, Phytoplankton analysis using flow cytometry. 1993: p. 175-186.
87. Hindson, B.J., et al., High-throughput droplet digital PCR system for absolute quantitation of DNA copy number. 2011. 83(22): p. 8604-8610.
88. Patterson, J.L., et al., Analysis of adherence, biofilm formation and cytotoxicity suggests a greater virulence potential of Gardnerella vaginalis relative to other bacterial-vaginosis-associated anaerobes. 2010. 156(Pt 2): p. 392.
89. Harf, C., et al., Flow cytometric determination of endocytosis of viable labelled Legionella pneumophila by Acanthamoeba palestinensis. 1997. 27(3): p. 269-274.
90. May, W.E., S.P. Wasik, and D.H. Freeman, Determination of the solubility behavior of some polycyclic aromatic hydrocarbons in water. Analytical Chemistry, 1978. 50(7): p. 997-1000.
91. Ma, Y.-G., et al., Critical review and recommended values for the physical-chemical property data of 15 polycyclic aromatic hydrocarbons at 25 C. Journal of Chemical & Engineering Data, 2010. 55(2): p. 819-825.
92. Adams, M.J.M.i.M.R., Bacterial viruses. 1950. 2.
93. Mackay, D. and W.Y. Shiu, Aqueous solubility of polynuclear aromatic hydrocarbons. Journal of Chemical and Engineering Data, 1977. 22(4): p. 399-402.
94. Šepič, E., M. Bricelj, and H. Leskovšek, Biodegradation studies of polyaromatic hydrocarbons in aqueous media. Journal of applied microbiology, 1997. 83(5): p. 561-568.
95. Joyce, G.H. and D.C. White, Effect of benzo (a) pyrene and piperonyl butoxide on formation of respiratory system, phospholipids, and carotenoids of Staphylococcus aureus. Journal of bacteriology, 1971. 106(2): p. 403-411.
96. Hussey, S.J., et al., Air pollution alters Staphylococcus aureus and Streptococcus pneumoniae biofilms, antibiotic tolerance and colonisation. Environmental microbiology, 2017. 19(5): p. 1868-1880.
97. Vasquez, J.K., et al., Simplified AIP-II peptidomimetics are potent inhibitors of Staphylococcus aureus AgrC quorum sensing receptors. Chembiochem: a European journal of chemical biology, 2017. 18(4): p. 413.
98. Guzman, A.R., et al., A three-dimensional electrode for highly efficient electrocoalescence-based droplet merging. Biomedical microdevices, 2015. 17(2): p. 35.
99. Flow Cytometry Guide. Retrieved May 24, 2020, from https://www.creative-diagnostics.com/flow-cytometry-guide.htm
100. LabMedica International staff writers (2019, April 10).Liquid Biopsy Potential Tested with ddPCR Technology. Retrieved May 24, 2020, from https://www.labmedica.com/molecular-diagnostics/articles/294777571/liquid-biopsy-potential-tested-with-ddpcr-technology.html
101. Steve Pawlizak (2009) Fluorescence Microscopy. Retrieved May 24, 2020, from https://home.uni-leipzig.de/pwm/web/?section=introduction&page=fluorescence

 
 
 
 
第一頁 上一頁 下一頁 最後一頁 top
* *