Дисертації з теми "Multiple resistance mechanisms"
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Scott, F. M. "Drug resistance mechanisms in multiple myeloma." Thesis, University of Edinburgh, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.661665.
Повний текст джерелаDoherty, Catherine Jean. "Drug resistance mechanisms in multiple myeloma." Thesis, University of Edinburgh, 1997. http://hdl.handle.net/1842/22154.
Повний текст джерелаAbbaszadegan, Mohammad Reza. "Mechanisms of resistance to chemosensitizers in a multidrug resistant human multiple myeloma cell line." Diss., The University of Arizona, 1995. http://hdl.handle.net/10150/187140.
Повний текст джерелаBlackhall, William J. "Genetic variation and multiple mechanisms of anthelmintic resistance in Haemonchus contortus." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0034/NQ64519.pdf.
Повний текст джерелаBlackhall, William James. "Genetic variation and multiple mechanisms of anthelmintic resistance in Haemonchus contortus." Thesis, McGill University, 1999. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=37596.
Повний текст джерелаBaran, Yusuf. "Multiple Drug Resistance Mechanisms In Imatinib Resistat Human Chronic Myeloid Leukemia Cells." Phd thesis, METU, 2006. http://etd.lib.metu.edu.tr/upload/12607612/index.pdf.
Повний текст джерела#956
M imatinib resistant cells. Measurement of endogenous ceramide levels showed that treatment with Imatinib increased the generation of C18-ceramide significantly, which is mainly synthesized by the human longevity assurance gene 1 (hLASS1), in sensitive, but not in resistant cells. Mechanistically, analysis of mRNA and enzyme activity levels of hLASS1 in the absence or presence of Imatinib did not show any significant differences in the resistant cells when compared to its sensitive counterparts, suggesting that accumulation and/or metabolism, but not the synthesis of ceramide, might be altered in resistant cells. iv Indeed, further studies demonstrated that expression levels, and enzyme activity of sphingosine kinase-1 (SK-1), increased significantly in resistant K562 or Meg-1 cells. The expression levels of glucosyl ceramide synthase (GCS) also increased in resistant cells, comparing to the sensitive counterparts, which indicates conversion of pro-apoptotic ceramide to glucosyl ceramide. Expression analyses of BCR-ABL gene demonstrated that expression levels of BCR-ABL gene increased gradually as the cells acquired the resistance. However, Nucleotide sequence analyses of ABL kinase gene revealed that there was no mutation in Imatinib binding region of the gene in resistant cells. There was also an increase in expression levels of MDR1 gene in resistant cells, which transport the toxic substances outside of cells. In conclusion, these data show, for the first time, a role for endogenous ceramide synthesis via hLASS1 in Imatinib-induced apoptosis, and those alterations of the balance between the levels of ceramide and S1P. Mainly the overexpression of SK-1 seems to result in resistance to Imatinib in K562 cells. The cellular resistance may also result from conversion of ceramide to glucosyl ceramide, from overexpression of BCR-ABL and MDR1 genes but not due to mutations in Imatinib binding site of ABL kinase.
Parrish, Jason Thomas. "Investigations into Multiple–Herbicide-Resistant Ambrosia artemisiifolia (Common Ragweed) in Ohio and Glyphosate-Resistance Mechanisms." The Ohio State University, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=osu1420789335.
Повний текст джерелаDemirel, Kars Meltem. "Molecular Mechanisms Of Vincristine And Paclitaxel Resistance In Mcf-7 Cell Line." Phd thesis, METU, 2008. http://etd.lib.metu.edu.tr/upload/3/12610241/index.pdf.
Повний текст джерелаLembersky, Dmitry. "THE SECOND GENERATION PROTEASOME INHIBITOR CARFILZOMIB INTERACTS SYNERGISTICALLY WITH HDAC INHIBITORS IN DIFFUSE LARGE B-CELL LYMPHOMA CELLS THROUGH MULTIPLE MECHANISMS AND CIRCUMVENTS BORTEZOMIB RESISTANCE." VCU Scholars Compass, 2009. http://scholarscompass.vcu.edu/etd/1800.
Повний текст джерелаTong, Zhichao [Verfasser], Jürgen E. [Akademischer Betreuer] Gschwend, Jürgen E. [Gutachter] Gschwend, and Dieter [Gutachter] Saur. "Functional genomics identifies multiple clinically actionable resistance mechanisms to CDK4/6 inhibition in bladder cancer / Zhichao Tong ; Gutachter: Jürgen E. Gschwend, Dieter Saur ; Betreuer: Jürgen E. Gschwend." München : Universitätsbibliothek der TU München, 2019. http://d-nb.info/1189815451/34.
Повний текст джерелаIwakami, Satoshi. "Molecular mechanism of resistance in a multiple-herbicide resistant Echinochloa phyllopogon." Kyoto University, 2013. http://hdl.handle.net/2433/180368.
Повний текст джерела0048
新制・課程博士
博士(農学)
甲第17830号
農博第2015号
新制||農||1016(附属図書館)
学位論文||H25||N4787(農学部図書室)
30645
京都大学大学院農学研究科農学専攻
(主査)教授 稲村 達也, 教授 冨永 達, 教授 奥本 裕
学位規則第4条第1項該当
Hoffman, Mary M. "Mechanism of MDR protein mediated multidrug resistance /." Access full-text from WCMC, 1997. http://proquest.umi.com/pqdweb?did=733008491&sid=6&Fmt=2&clientId=8424&RQT=309&VName=PQD.
Повний текст джерелаNakka, Sridevi. "Physiological, biochemical and molecular characterization of multiple herbicide resistance in Palmer amaranth (Amaranthus palmeri)." Diss., Kansas State University, 2016. http://hdl.handle.net/2097/34474.
Повний текст джерелаDepartment of Agronomy
Mithila Jugulam
Palmer amaranth (Amaranthus palmeri) is one of the most aggressive, troublesome and damaging broadleaf weeds in many cropping systems including corn, soybean, cotton, and grain sorghum causing huge yield losses across the USA. As a result of extensive and intensive selection of pre- and -post emergence herbicides, Palmer amaranth has evolved resistance to multiple herbicide modes of action, microtubule-, 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS)-, acetolactate synthase (ALS)-, photosystem II (PS II)-, hydroxyphenylpyruvate dioxygenase (HPPD)- and more recently to protoporphyrinogen oxidase (PPO)-inhibitors. A Palmer amaranth population from Kansas was found resistant to HPPD-, PS II-, and ALS-inhibitors. The overall objective of this research was to investigate the target-site and/or non-target-site resistance mechanisms in Palmer amaranth from KS (KSR) to mesotrione (HPPD-inhibitor), atrazine (PS II-inhibitor), and chlorsulfuron (ALS-inhibitor) relative to known susceptible Palmer amaranth from Mississippi (MSS) and KS (KSS). Whole plant dose-response assays showed high level of resistance in KSR to mesotrione, atrazine and chlorsulfuron. KSR was 10-18, 178-237 and >275 fold more resistant to mesotrione, atrazine, and chlorsulfuron, respectively, compared to MSS and KSS. Metabolism studies using [¹⁴C] labeled mesotrione and atrazine demonstrated non-target-site resistance to both herbicides, particularly, enhanced metabolism of [¹⁴C] mesotrione likely mediated by cytochrome P450 monooxygenases and rapid degradation of [¹⁴C] atrazine by glutathione S-transferases (GSTs). In addition, molecular and biochemical basis of mesotrione resistance was characterized by quantitative PCR (qPCR) and immunoblotting. These results showed 4-12 fold increased levels of the HPPD transcript and positively correlated with the increased HPPD protein. Sequencing of atrazine and chlorsulfuron target genes, psbA and ALS, respectively, showed interesting results. The most common mutation (serine264glycine) associated with atrazine resistance in weeds was not found in KSR. On the other hand, a well-known mutation (proline197serine) associated with chlorsulfuron resistance was found in 30% of KSR, suggesting ~70% of plants might have a non-target-site, possibly P450 mediated metabolism based resistance. Over all, KSR evolved both non-target-site and target-site based mechanisms to mesotrione and chlorsulfuron with only non-target-site based mechanism of resistance to atrazine leaving fewer options for weed control, especially in no-till crop production systems. Such multiple herbicide resistant Palmer amaranth populations are a serious threat to sustainable weed management because metabolism-based resistance may confer resistance to other herbicides and even those that are yet to be discovered. The findings of this research are novel and valuable to recommend appropriate weed management strategies in the region and should include diversified tactics to prevent evolution and spread of multiple herbicide resistance in Palmer amaranth.
Nguyen, Albert Thu. "The molecular mechanism of action of bevirimat : a prototype HIV-1 maturation inhibitor /." Oklahoma City : [s.n.], 2009.
Знайти повний текст джерелаAndrawes, Bassem Onsi. "Seismic Response and Analysis of Multiple Frame Bridges Using Superelastic Shape Memory Alloys." Diss., Georgia Institute of Technology, 2005. http://hdl.handle.net/1853/6914.
Повний текст джерелаMousseau, Mireille. "Étude des mécanismes moléculaires de chimiorésistance intrinsèque des tumeurs cérébrales humaines." Grenoble 1, 1992. http://www.theses.fr/1992GRE10186.
Повний текст джерелаBostamam, Yazid. "Glyphosate resistance in annual ryegrass (Lolium rigidum Gaud.) with multiple resistance mechanisms." Thesis, 2010. http://hdl.handle.net/2440/64715.
Повний текст джерелаThesis (M.Ag.Sc.) -- University of Adelaide, School of Agriculture, Food and Wine, 2010
Coughlan, Kimberly A. "Inhibition of AMPK via phosphorylation at Ser485/491: multiple mechanisms of regulation." Thesis, 2015. https://hdl.handle.net/2144/13729.
Повний текст джерелаLeow, Benjamin Chia Sing. "Multiple Molecular Mechanisms Contribute Towards In Vitro Resistance to Tyrosine Kinase Inhibitors in Chronic Myeloid Leukaemia." Thesis, 2019. http://hdl.handle.net/2440/121613.
Повний текст джерелаThesis (Ph.D.) -- University of Adelaide, Adelaide Medical School, 2019
Aves, Charlotte Sarah. "Herbicide resistance in Conyza bonariensis (L.) Cronquist (flaxleaf fleabane) populations from northeast Victoria and its management in mixed farming systems." Thesis, 2018. http://hdl.handle.net/2440/114022.
Повний текст джерелаThesis (Ph.D.) -- University of Adelaide, School of Agriculture, Food and Wine, 2018.
"The anti-tumor activities of steroid saponin HK18 on human hepatocellular carcinoma cell line HepG2 and multidrug resistant human hepatocellular carcinoma cell line R-HepG2 and its action mechanisms." 2002. http://library.cuhk.edu.hk/record=b5891176.
Повний текст джерелаThesis (M.Phil.)--Chinese University of Hong Kong, 2002.
Includes bibliographical references (leaves 194-208).
Abstracts in English and Chinese.
Acknowledgement --- p.i
Abstract --- p.ii
摘要 --- p.iv
Contents --- p.vi
List of Figures --- p.xii
List of Tables --- p.xv
Abbreviations --- p.xvi
Chapter Chapter 1 --- Introduction --- p.1
Chapter 1 --- Introduction --- p.2
Chapter 1.1 --- Characteristic of Saponins --- p.3
Chapter 1.1.1 --- Occurrence of Saponins --- p.3
Chapter 1.1.2 --- General Properties of Saponins --- p.3
Chapter 1.1.2.1 --- Emulsifying Agents --- p.3
Chapter 1.2.2.2 --- Forming Complex with Cholesterol --- p.4
Chapter 1.1.2.3 --- Hemolytic Property --- p.4
Chapter 1.1.3 --- Structure of Saponins --- p.5
Chapter 1.1.3.1 --- Categories of Saponins --- p.5
Chapter 1.1.3.1.1 --- Triterpene Saponins --- p.5
Chapter 1.1.3.1.2 --- Steroid Saponins --- p.5
Chapter 1.1.3.2 --- Monodesmosidic and Bidesmosidic Saponins --- p.7
Chapter 1.1.4 --- Biological and Pharmacological Properties of Saponins --- p.9
Chapter 1.1.4.1 --- Anti-microbial Activity --- p.9
Chapter 1.1.4.1.1 --- Anti-fungal Activities --- p.9
Chapter 1.1.4.1.2 --- Anti-bacterial Activities --- p.10
Chapter 1.1.4.1.3 --- Anti-viral Activities --- p.10
Chapter 1.1.4.2 --- Insecticidal Activity --- p.10
Chapter 1.1.4.3 --- Molluscicidal Activity --- p.10
Chapter 1.1.4.4 --- Hypocholesterolemic Activity --- p.11
Chapter 1.1.4.5 --- Anti-ulcer Activity --- p.11
Chapter 1.1.4.6 --- Contraceptive Activity --- p.12
Chapter 1.1.4.7 --- Immunomodulatory Activities --- p.12
Chapter 1.1.4.7.1 --- Direct Immunostimulation --- p.12
Chapter 1.1.4.7.2 --- Acting as Immuno-adjuvants --- p.13
Chapter 1.1.4.8 --- Anti-tumor Activity --- p.14
Chapter 1.1.4.8.1 --- Anti-carcinogenesis --- p.15
Chapter 1.1.4.8.2 --- Suppression of Tumor Growth --- p.16
Chapter 1.1.5 --- Anti-tumor Activity of Steroid Saponins --- p.18
Chapter 1.1.5.1 --- Diosgenin Steroid Saponin --- p.18
Chapter 1.1.5.2 --- Hong Kong Compounds --- p.18
Chapter 1.1.5.3 --- Hong Kong18 --- p.21
Chapter 1.2 --- Human Hepatocellular Carcinoma (HCC) --- p.24
Chapter 1.2.1 --- The Incidence of Liver Cancer --- p.24
Chapter 1.2.2 --- Classification of Liver Cancer --- p.24
Chapter 1.2.3 --- Human Hepatocellular Carcinoma Cell Lines --- p.25
Chapter 1.2.3.1 --- Human Hepatocellular Carcinoma Cell Line HepG2 --- p.25
Chapter 1.2.3.2 --- Multidrug Resistant Human Hepatocellular Carcinoma Cell Line R-HepG2 --- p.27
Chapter 1.2.3.2.1 --- Mechanisms of Multidrug Resistance --- p.28
Chapter 1.2.3.2.2 --- Structure and Characteristics of P-glycoprotein --- p.29
Chapter 1.2.3.2.3 --- Methods in Dealing with P-glycoprotein Over-expressed MDR Cells --- p.31
Chapter 1.3 --- Objectives of the Project --- p.32
Chapter 1.3.1 --- Study of the Anti-tumor Activities of Hong Kong 18 on Human Hepatocellular Carcinoma Cell Line HepG2 and Unravel the Underlying Mechanisms --- p.32
Chapter 1.3.2 --- Study of the Anti-tumor Activities of Hong Kong 18on Multidrug Resistant Human Hepatocellular Carcinoma Cell Line R-HepG2 and Unravel the Underlying Mechanisms --- p.32
Chapter Chapter 2 --- Materials and Methods --- p.33
Chapter 2.1 --- Materials --- p.34
Chapter 2.1.1 --- Cell Culture --- p.34
Chapter 2.1.1.1 --- Cell Lines --- p.34
Chapter 2.1.1.2 --- Culture Media --- p.35
Chapter 2.1.2 --- Reagents and Buffers --- p.36
Chapter 2.1.2.1 --- Phosphate Buffered Saline (PBS) --- p.36
Chapter 2.1.2.2 --- Reagents and Buffers for DNA Fragmentation --- p.36
Chapter 2.1.2.3 --- Reagents and Buffers for Western Analysis --- p.37
Chapter 2.1.2.4 --- Reagents and Buffer for Caspases Activities --- p.39
Chapter 2.1.2.5 --- Fluorescent Dyes used for Flow Cytometry --- p.39
Chapter 2.1.3 --- Chemicals --- p.39
Chapter 2.2 --- Methods --- p.46
Chapter 2.2.1 --- MTT Assay --- p.46
Chapter 2.2.2 --- Determination of Cell Viability --- p.46
Chapter 2.2.3 --- Purification of Macrophages from balb/c Mice --- p.47
Chapter 2.2.4 --- Hemolysis Assay --- p.47
Chapter 2.2.5 --- In vivo Studies of the Toxicity of HK18 --- p.48
Chapter 2.2.6 --- DNA Fragmentation Assay --- p.50
Chapter 2.2.7 --- Detection of Apoptotic and Necrotic / Late Apoptotic Cells Death by Flow Cytometry with Annexin V-FITC / PI --- p.51
Chapter 2.2.8 --- Detection of Mitochondrial Membrane Potential by JC-1 Fluorescent Dye --- p.52
Chapter 2.2.9 --- Detection of Intracellular Ca Level by Flow Cytometry with Fluo-3 Fluorescent Dye --- p.52
Chapter 2.2.10 --- Detection of Intracellular Hydrogen Peroxide Level by Flow Cytometry with DCF Fluorescence Dye --- p.53
Chapter 2.2.11 --- Simultaneous Detection of Mitochondrial Membrane Potential and Intracellular Ca2+ or Mitochondrial Membrane Potential and Intracellular Hydrogen Peroxide --- p.54
Chapter 2.2.12 --- Western Analysis --- p.55
Chapter 2.2.12.1 --- Total Protein Extraction --- p.55
Chapter 2.2.12.2 --- Extraction of Cytosolic Proteins --- p.59
Chapter 2.2.13 --- Determination of Caspases Enzymatic Activity --- p.63
Chapter 2.2.14 --- Reverse Transcriptase Polymerase Chain Reaction (RT-PCR) --- p.67
Chapter 2.2.14.1 --- RNA Extraction by TRIzol Reagent --- p.67
Chapter 2.2.14.2 --- Reverse Transcription --- p.68
Chapter 2.2.14.3 --- Polymerase Chain Reaction --- p.68
Chapter 2.3 --- Statistic Analysis --- p.71
Chapter Chapter 3 --- Cytotoxicity of HK18 --- p.72
Chapter 3.1 --- Cytotoxicity of HK18 on HepG2 Cells --- p.73
Chapter 3.1.1 --- Study of the Cytotoxic Activity of HK18 on HepG2 Cells by MTT Assay --- p.73
Chapter 3.1.2 --- Study of the Cytotoxic Activity of HK18 on HepG2 Cells by Tryphan Blue Exclusion Assay --- p.76
Chapter 3.2 --- Cytotoxicity of HK18 on R-HepG2 Cells --- p.78
Chapter 3.2.1 --- Study of the Cytotoxic Activity of HK18 on R-HepG2 Cells by MTT Assay --- p.78
Chapter 3.2.2 --- Study of the Cytotoxic Activity of HK18 on R-HepG2 Cells by Tryphan Blue Exclusion Assay --- p.81
Chapter 3.3 --- Cytotoxicity of HK18 on Macrophages --- p.83
Chapter 3.4 --- Hemolytic Activity of HK18 --- p.85
Chapter 3.5 --- In vivo Study of the Toxicity of HK18 --- p.87
Chapter Chapter 4 --- Mechanistic Study of HK18 on HepG2 Cells --- p.90
Chapter 4.1 --- Hallmarks of Apoptosis Induced by HK18 on HepG2 Cells --- p.91
Chapter 4.1.1 --- Induction of Phosphatidylserine Externalization by HK18 on HepG2 Cells --- p.91
Chapter 4.1.2 --- Induction of DNA Fragmentation by HK18 of HepG2 Cells --- p.97
Chapter 4.2 --- Study of the Underlying Mechanisms of HK18 Induced Apoptosis in HepG2 Cells --- p.99
Chapter 4.2.1 --- The Role of Mitochondria in HK18 Induced Apoptosis of HepG2 Cells --- p.99
Chapter 4.2.1.1 --- HK18 Induced Mitochondrial Membrane Depolarization in HepG2 Cells --- p.101
Chapter 4.2.1.2 --- Addition of Bongkrekic Acid Reduced HK18 Cytotoxicity on HepG2 Cells --- p.105
Chapter 4.2.1.3 --- Elevation of Intracellular Hydrogen Peroxide Level in HK18 Treated HepG2 Cells --- p.108
Chapter 4.2.1.4 --- Elevation of Intracellular Ca2+ Level in HK18 Treated HepG2 Cells --- p.114
Chapter 4.2.1.5 --- HK18 Induced Cytochrome c and AIF Released from Mitochondria of HepG2 Cells --- p.120
Chapter 4.3 --- Downstream Biochemical Changes Induced by HK18 on HepG2 Cells --- p.123
Chapter 4.3.1 --- Activation of Caspase 3 of HepG2 Cells by HK18 as Demonstrated by Western Blot --- p.123
Chapter 4.3.2 --- Induction of Caspases Activities of HepG2 Cells by HK18 as Demonstrated by Enzymatic Activity Assays --- p.125
Chapter 4.4 --- Down-regulation of Anti-apoptotic Bcl-2 Family Members of HepG2 Cells by HK18 --- p.129
Chapter Chapter 5 --- Mechanistic Study of HK18 on R-HepG2 Cells --- p.133
Chapter 5.1 --- Hallmarks of Apoptosis Induced by HK18 on R-HepG2 Cells --- p.134
Chapter 5.1.1 --- Induction of Phosphatidylserine Externalization by HK18 on R-HepG2 Cells --- p.134
Chapter 5.1.2 --- Induction of DNA Fragmentation by HK18 of R-HepG2 Cells --- p.137
Chapter 5.2 --- Study of the Underlying Mechanisms of HK18 Induced Apoptosis in R-HepG2 Cells --- p.139
Chapter 5.2.1 --- The Role of Mitochondria in HK18 Induced Apoptosis of R-HepG2 Cells --- p.139
Chapter 5.2.1.1 --- HK18 Induced Mitochondrial Membrane Depolarization in R-HepG2 Cells --- p.139
Chapter 5.2.1.2 --- Addition of Bongkrekic Acid Reduced HK18 Cytotoxicity on R-HepG2 Cells --- p.142
Chapter 5.2.1.3 --- Elevation of Intracellular Hydrogen Peroxide Level in HK18 Treated R-HepG2 Cells --- p.144
Chapter 5.2.1.4 --- Elevation of Intracellular Ca2+ Level in HK18 Treated R-HepG2 Cells --- p.146
Chapter 5.3 --- Downstream Biochemical Changes Induced by HK18 on R-HepG2 Cells --- p.148
Chapter 5.3.1 --- Activation of Caspase 3 of R-HepG2 Cells by HK18 as Demonstrated by Western Blot --- p.148
Chapter 5.3.2 --- Induction of Caspases Activation of R-HepG2 Cells by HK18 as Demonstrated by Enzymatic Activity Assays --- p.150
Chapter 5.4 --- Down-regulation of the Anti-apoptotic Bcl-2 Protein of R-HepG2 Cells by HK18 --- p.154
Chapter 5.5 --- HK18 was Not a Substrate of P-glycoprotein Contents --- p.156
Chapter Chapter 6 --- Discussion --- p.158
Chapter 6.1 --- Cytotoxicity of HK18 --- p.159
Chapter 6.1.1 --- HK18 was Cytotoxic to the Human Hepatocellular Carcinoma Cell Line HepG2 and Multidrug Resistant Human Hepatocellular Carcinoma Cell Line R-HepG2 --- p.159
Chapter 6.1.2 --- Study of the Toxicity of HK18 --- p.160
Chapter 6.2 --- Mechanistic Studies of the Cytotoxic Effects of HK18 on HepG2 Cells --- p.161
Chapter 6.2.1 --- Apoptotic Cell Death Induction of HK18 on HepG2 Cells --- p.161
Chapter 6.2.2 --- Studies of the Underlying Mechanisms of HK18 Induced Apoptosis of HepG2 Cells --- p.162
Chapter 6.3 --- Mechanistic Studies of the Cytotoxic Effects of HK18 on R-HepG2 Cells --- p.181
Chapter 6.3.1 --- Apoptotic Cell Death Induction of HK18 on R-HepG2 Cells --- p.181
Chapter 6.3.2 --- Studies of the Underlying Mechanisms of HK18 Induced Apoptosis of HepG2 Cells --- p.181
Chapter Chapter 7 --- Future Perspectives --- p.190
Chapter Chapter 8 --- References --- p.193
Chang, Kai-Ming, and 張開明. "The molecular epidemiology, resistant mechanism and environment control of multiple drug resistant Acinetobacter baumannii." Thesis, 2012. http://ndltd.ncl.edu.tw/handle/03895117176036811177.
Повний текст джерела國立中興大學
生命科學系所
100
Acinetobacter baumannii is one of the most common pathogens causing nosocomial infection in recent decades. Increasing trends in multiple drug resistance and its rapid spread in hospitals have caused a serious impact on the treatment for A. baumannii nosocomial infections. Therefore, it is very important to study the molecular epidemiology of A.baumannii, including the outbreak of multiple drug resistant A.baumannii, the transfer and spread of drug resistant genes, and the control of multiple drug resistant A.baumannii. Nowadays pulsed-field gel electrophoresis (PFGE) is the best tool for studying molecular epidemiology. In order to obtain clear and consistent PFGE band patterns for inter-laboratory comparison and discussion, establishing a standard experiment model is necessary, and the restriction enzyme used to cut genomic DNA is critical, it should be cost-effective and discriminative. This study aimed to select a suitable rare-cutting restriction enzyme for analyzing A. baumannii genome with PFGE. Among the enzymes tested, ApaI, AscI and AsiSI exhibited similar discriminative indices. ApaI which has been used by some laboratory was the most cost-effective restriction enzyme for PFGE analysis for its low price, but it generated more than 40 fragments that were a little crowded and not easy to resolve, different laboratories would have less consistent results. AscI exhibited a very close discriminative ability to that of AsiSI, both enzymes generated 10 to 20 fragments that were easy to resolve, but AscI was at half of the cost of AsiSI for PFGE analysis, therefore AscI is a more suitable restriction enzyme for standardizing the PFGE analysis of A. baumannii and for inter-laboratory comparison. Recent researches have indicated that multiple drug resistant A. baumannii produce class D (OXA) carbapenemases to degrade antibiotic carbapenem. This study collected total 90 carbapenem resistant A. baumannii (CRAB) isolates from the clinical microbiological laboratory of three medical centers in northern, central, and southern Taiwan, their MIC of carbapenem were determined, and their genomes were screened the existence of OXA genes by multiplex PCR. It was found that all the 90 isolates had OXA-51-like gene, twenty-six out of 30 isolates (86.67%) from northern Taiwan had OXA-51-like gene only, 25 out of 30 isolates (83.33%) from central Taiwan had both OXA-51-like and OXA-23-like genes, and 23 out of 30 isolates (76.67%) from southern Taiwan had both OXA-51-like and OXA-24-like genes. It looked like different part of Taiwan had different distribution of CRAB producing specific OXA type carbapenemase. We also found the appearance of OXA gene types related to the resistant strength of CRAB isolates to carbapenem (MIC value). CRAB isolates harboring OXA-51-like gene has imipenem MIC50 value of 8 ug/mL, CRAB isolates harboring OXA-51-like and OXA-23-like genes has imipenem MIC50 value of 16 ug/mL, whereas CRAB isolates harboring OXA-51-like and OXA-24-like genes has imipenem MIC50 value of 64 ug/mL. All the 90 CRAB isolates were susceptible to colistin and tigecycline. As A.baumannii is difficult to be eradicated from hospital environment, we tried using bacteriophage for environment control. Ten phages infecting A.baumannii were isolated. We chose two hospitals with respiratory care ward (RCW) to sample from patients, beds and environments. The isolated A.baumannii were carried out MIC determination and PFGE analysis. Then the mixture of the ten phages was used for environment eradication. After spraying the phages mixture to the beds and environments previously sampled, no A.baumannii was isolated any more. This is the first study to use bacteriophage for controling A.baumannii in environments and the result suggested the eradication is effective.
Hsu, Chih Jung, and 許至榮. "Proposed Mechanism of Multiple Drug Resistance Cell Line Attenuates Apoptosis Induced by Proteasome Inhibitor." Thesis, 2008. http://ndltd.ncl.edu.tw/handle/88285788229708705979.
Повний текст джерела長庚大學
醫學生物技術研究所
96
Multiple drug resistance (MDR) is a major obstacle to attenuate the effectiveness of chemotherapy to many human malignancies. Despite extensively investigation, MDR inhibitors have been discovered unwanted severe side effects. Recently, scientists have reported that proteasome inhibition induced apoptosis in a variety of cancer cells and recognized as a novel anticancer therapy approach. Despite its success, some patients are resistant or become refractory to ongoing proteasome inhibitor-bortezomib treatment. These finding suggested that chemoresistant multiple myeloma may develop a novel mechanism to against proteasome inhibitor. To test hypotheses, we studied: (1) to evaluate proteasome inhibitor effect in MDR cell line model. (2) to investigate the potential mechanisms of MDR cell line attenuates apoptosis induced by proteasome inhibitor. Our results shown: compared to parental human uterus sarcoma cell line MES-SA cells, the Dx5-C5 cells with highly expressed P-glycoprotein was more resistant to MG132 and didn’t amend the proteasome inhibitor induced apoptosis pathway. Interestingly, when co-treatment of MDR inhibitor and MG132 together, the survival rates of Dx5-C5 cells shown significant declined compared with MES-SA cells. These data indicated that P-glycoprotein may play a role in efflux out MG132 from Dx5-C5 cells and reduced MG132 induced apoptosis. Furthermore, we also found that the Canonical Wnt pathway was only activated in Dx5-C5 cells through active β-catenin and its related transactivation activity. Western blot analysis demonstrated that Wnt targeting genes, including c-Myc and Cyclin D1, were up-regulated and relevant to inhibit the expression of p21, whereas MES-SA cells expressed the high level of p21 and down-regulated the Cyclin D1 and caused cell cycle arrest. In conclusion, our study demonstrated that existence of P-glycoprotein and Wnt pathway in MDR cell line would attenuate proteasome inhibitor induced apoptosis and may help us to develop a new strategy for treatment of multiple drug resistance cancer cells.
Crank, Michelle C. "Understand the mechanism of action of Rutuximab® in the reversal of multidrug resistance in a Non-Hodgkins Lymphoma cell line." 2006. http://edissertations.library.swmed.edu/pdf/CrankM030206/CrankMichelle.pdf.
Повний текст джерелаCHANG, TIEN-YAO, and 張天耀. "Investigating the regulatory mechanism of efflux pump and antibacterial activity of silver nanoparticles for multiple drug resistant Acinetobacter baumannii." Thesis, 2017. http://ndltd.ncl.edu.tw/handle/8a4qwn.
Повний текст джерела國防醫學院
醫學科學研究所
105
Part 1 Acinetobacter baumannii is an increasing threat of nosocomial infections in recent years, especially the emergence of multi-drug resistant strains (multi-drug resistant Acinetobacter baumannii; MDRAB). Infections caused by multi-drug resistant A. baumannii could cause longer hospital stay and higher treatment costs. Tigecycline, a board-spectrum tetracycline derivative, is considered as the last antibiotic choice for the MDRAB. However, resistance to Tigecycline was reported following the drug usage worldwide. These resistances are mainly associated with overexpression of efflux pump, especially AdeABC, which is regulated by a corresponding two-component system AdeRS. In the research, we found that the regulatory factor AdeR could recognize the direct repeat on intercistronic region between adeR and adeA. This interaction inhibits the downstream efflux pump expression. In addition, mutations on AdeR DNA binding domain show lower affinity to the direct repeat sequences, and elevate the expression level of efflux pump, leading to high resistance to tigecycline (MIC = 16 μg/mL). This result is very useful for understanding the mechanism of tigecycline resistance of A. baumannii. Part 2 We generate a silver nanoparticles using green synthesis. In this process, silver nitrate is used as a precursor of silver ions, and then glucose and trimethyl nitrate chitosan (TMCN) are used as a reducing agent and stabilizer, respectively. The whole reaction of silver nanoparticle synthesis could be done at room temperature after adding alkaline solution and mixing thoroughly. There is no need to consume energy or to use expensive equipment. Adjusting the concentration of sodium hydroxide, glucose and TMCN will affect the particle size, zeta potential and formation yield of silver nanoparticles. The average size of this silver nanoparticles (TMCN-AgNPs) is around 60 nm with positive surface charge. The physical and chemical properties of this nanoparticles were characterized by UV-Vis spectroscopy, X-ray diffraction and X-ray photoelectron spectroscopy. The catalytic activity of TMCN-AgNPs was determined by reduction of 4-nitrophenol using NaBH4 as a reducing agent. The antibacterial activity of TMCN-AgNPs was evaluated by broth microdilution method, and was proved to have antibacterial activity against Acinetobacter baumannii, Escherichia coli, Pseudomonas aeruginosa and Staphylococcus aureus. The minimum inhibitory concentration (MIC) was < 6.13 μg/mL. Moreover, TMCN-AgNPs also showed antibacterial activity against multidrug-resistant Acinetobacter baumannii from clinical isolated, and the MIC value was < 12.25 μg/mL.
Bolukaoto, Yenga John. "Incidence and mechanism of antibiotic resistance of Streptococcus Agalactiae isolates from pregnant women and their babies at Dr George Mukhari Academic Hospital, Pretoria." Diss., 2014. http://hdl.handle.net/10500/14402.
Повний текст джерелаHealth Studies
M.Sc. (Life Sciences (Microbiology))
Chiang, Yu Ling, and 蔣裕玲. "Bioactivity of active ingredient in dietary seasonings --Rosmarinic acid(I)Inhibition on invasive activity of human colorectal carcinoma cells(II)Inhibitory effect and mechanism on multiple-drug resistant Mycobacterium tuberculosis." Thesis, 2012. http://ndltd.ncl.edu.tw/handle/81873134553699820316.
Повний текст джерела台南應用科技大學
生活應用科學研究所
100
(I) Colorectal cancer is the leading cause of cancer mortality, and metastasis is responsible for approximately 40% of death in colon cancer patients. Matrix metalloproteinases (MMPs) are key enzymes in the degradation of extracellular matrix, and MMP-2 and -9 are critical for cell migration leading to invasion and metastasis of cancer. The inhibition of MMP-2 and -9 is therefore considered that might depress the occurrence of tumor invasion and metastasis. Rosmarinic acid (RA) is a bioactive polyphenol that widely presented in Rosmarinus officinalis L. However, the literature regarding the effect of RA on invasion of cancer cells is still limited. In this study, we investigated the anti-invasion activity of RA against human colorectal adenocarcinoma Colo205 and HT-29 cells. The cells were treated with 0, 10, 50, 100, or 200 M of RA at 37C for 24 h, and the MMP-2, -9, and uPA activities as well as cell-matrix adhesion, motility, and invasion activities were determined. The MMP-2, -9, TIMP-1 and -2 mRNA levels were assayed by RT-PCR. The molecular signaling was determined by Weastern blot. The results showed that the MMP-2 and uPA activities of Colo205 and HT-29 cells were significantly inhibited by RA at a concentration of > 50 μM. The migration and invasion activities of Colo205 and HT-29 cells were also suppressed after treating with RA at a concentration higher than 50 M. The mRNA level of MMP-2 in HT-29 and Colo205 were significantly inhibited by RA at a concentration of > 50 M. The mRNA levels of TIMP-1 and -2 in HT-29 and TIMP-1 in Colo205 were significantly increased by RA. The signaling of p-ERK and p-p38 in Colo205 and HT-29 were signigicantly inhibited by RA. Furthermore, the activations of NF-κB and AP-1 in colorectal cancer cells were also suppressed by RA. Our results suggest that RA might be a bioactive with potential anti-invasive activity against colorectal cancer cells by inhibiting uPA and MMP-2 activity and reducing motility capabilities through inhibiting the activations of MAPKs signaling pathways and NF-κB and AP-1 transcription factors. (II) Tuberculosis (TB) is a contagious disease which causes a serious public health risk. WHO estimates that there were approximately 9,400,000 new TB cases globally in 2008, and South-East Asia Region accounted for 34% of incident cases. Multidrug-resistant TB (MDR-TB) is a particularly dangerous form of TB, which is responsible for the majority of failures in TB therapy. Mycobacterium tuberculosis is the major pathogeny of TB, and uridine diphosphate-glucose pyrophosphorylase (UGPase; EC 2.7.7.9) is the major enzyme that involved to the synthesis of cell wall. The inhibition of UGPase might depress the proliferation of the bacilli. Rosmarinic acid (RA), a polyphenol which is widely presented in natural plants of Lamiaceae and Boraginaceae family, has been reported that possesses several biological activities such as anti-virus, anti-inflammation, and anti-bacteria. The aim of this study was to investigate the inhibitory effects of RA on the viability of multidrug-resistant M. tuberculosis, and their impact on UGPase was also evaluated. Because the biological activity of a bioactive sometimes having an association with their antioxidant power, we therefore first determined the antioxidant activity of RA by trolox equivalent antioxidant capacity (TEAC) method. The viability of the bacilli was measured by counting the colony growing on 7H11 agar plates, and the expression of UGPase was performed by RT-PCR. The results showed RA having a strong antioxidant activity, and the viability of M. tuberculosis was reduced by treating with RA at a concentration of > 250 g/ml for 24 h. Furthermore, the expression of UGPase was also decreased by treating with 250 g/ml RA for 24 h. Based on the data mentioned above, it is suggested that RA can be used to inhibit the proliferation of multidrug-resistant M. tuberculosis, and the anti-proliferous activity of RA might be through inhibiting the expression of UGPase.
Chiang, Yu-Ling, and 蔣裕玲. "Bioactivity of active ingredient in dietary seasonings --Rosmarinic acid(I) Inhibition on invasive activity of human colorectal carcinoma cells(II) Inhibitory effect and mechanism on multiple-drug resistant Mycobacterium tuberculosis." Thesis, 2012. http://ndltd.ncl.edu.tw/handle/35663803510360707953.
Повний текст джерела台南應用科技大學
生活應用科學研究所
100
(I) Colorectal cancer is the leading cause of cancer mortality, and metastasis is responsible for approximately 40% of death in colon cancer patients. Matrix metalloproteinases (MMPs) are key enzymes in the degradation of extracellular matrix, and MMP-2 and -9 are critical for cell migration leading to invasion and metastasis of cancer. The inhibition of MMP-2 and -9 is therefore considered that might depress the occurrence of tumor invasion and metastasis. Rosmarinic acid (RA) is a bioactive polyphenol that widely presented in Rosmarinus officinalis L. However, the literature regarding the effect of RA on invasion of cancer cells is still limited. In this study, we investigated the anti-invasion activity of RA against human colorectal adenocarcinoma Colo205 and HT-29 cells. The cells were treated with 0, 10, 50, 100, or 200 M of RA at 37C for 24 h, and the MMP-2, -9, and uPA activities as well as cell-matrix adhesion, motility, and invasion activities were determined. The MMP-2, -9, TIMP-1 and -2 mRNA levels were assayed by RT-PCR. The molecular signaling was determined by Weastern blot. The results showed that the MMP-2 and uPA activities of Colo205 and HT-29 cells were significantly inhibited by RA at a concentration of > 50 μM. The migration and invasion activities of Colo205 and HT-29 cells were also suppressed after treating with RA at a concentration higher than 50 M. The mRNA level of MMP-2 in HT-29 and Colo205 were significantly inhibited by RA at a concentration of > 50 M. The mRNA levels of TIMP-1 and -2 in HT-29 and TIMP-1 in Colo205 were significantly increased by RA. The signaling of p-ERK and p-p38 in Colo205 and HT-29 were signigicantly inhibited by RA. Furthermore, the activations of NF-κB and AP-1 in colorectal cancer cells were also suppressed by RA. Our results suggest that RA might be a bioactive with potential anti-invasive activity against colorectal cancer cells by inhibiting uPA and MMP-2 activity and reducing motility capabilities through inhibiting the activations of MAPKs signaling pathways and NF-κB and AP-1 transcription factors. (II) Tuberculosis (TB) is a contagious disease which causes a serious public health risk. WHO estimates that there were approximately 9,400,000 new TB cases globally in 2008, and South-East Asia Region accounted for 34% of incident cases. Multidrug-resistant TB (MDR-TB) is a particularly dangerous form of TB, which is responsible for the majority of failures in TB therapy. Mycobacterium tuberculosis is the major pathogeny of TB, and uridine diphosphate-glucose pyrophosphorylase (UGPase; EC 2.7.7.9) is the major enzyme that involved to the synthesis of cell wall. The inhibition of UGPase might depress the proliferation of the bacilli. Rosmarinic acid (RA), a polyphenol which is widely presented in natural plants of Lamiaceae and Boraginaceae family, has been reported that possesses several biological activities such as anti-virus, anti-inflammation, and anti-bacteria. The aim of this study was to investigate the inhibitory effects of RA on the viability of multidrug-resistant M. tuberculosis, and their impact on UGPase was also evaluated. Because the biological activity of a bioactive sometimes having an association with their antioxidant power, we therefore first determined the antioxidant activity of RA by trolox equivalent antioxidant capacity (TEAC) method. The viability of the bacilli was measured by counting the colony growing on 7H11 agar plates, and the expression of UGPase was performed by RT-PCR. The results showed RA having a strong antioxidant activity, and the viability of M. tuberculosis was reduced by treating with RA at a concentration of > 250 g/ml for 24 h. Furthermore, the expression of UGPase was also decreased by treating with 250 g/ml RA for 24 h. Based on the data mentioned above, it is suggested that RA can be used to inhibit the proliferation of multidrug-resistant M. tuberculosis, and the anti-proliferous activity of RA might be through inhibiting the expression of UGPase.