Drug interactions and the evolution of antibiotic resistance
暂无分享,去创建一个
Roy Kishony | Aviva Presser Aiden | Matthew J. Hegreness | R. Kishony | P. Yeh | A. P. Aiden | Pamela J. Yeh
[1] L. Hurst. Epistasis and the Evolutionary Process , 2000, Heredity.
[2] W. Greco,et al. The search for synergy: a critical review from a response surface perspective. , 1995, Pharmacological reviews.
[3] Sean R. Collins,et al. A tool-kit for high-throughput, quantitative analyses of genetic interactions in E. coli , 2008, Nature Methods.
[4] L. Reimer,et al. Antibiotics in laboratory medicine , 1987 .
[5] Remy Chait,et al. Drug interactions modulate the potential for evolution of resistance , 2008, Proceedings of the National Academy of Sciences.
[6] L. Martínez-Martínez,et al. Mutant Prevention Concentrations of Fluoroquinolones for Enterobacteriaceae Expressing the Plasmid-Carried Quinolone Resistance Determinant qnrA1 , 2007, Antimicrobial Agents and Chemotherapy.
[7] J. Bader,et al. A DNA Integrity Network in the Yeast Saccharomyces cerevisiae , 2013, Cell.
[8] H. Adam,et al. Mutant Prevention Concentrations of Levofloxacin Alone and in Combination with Azithromycin, Ceftazidime, Colistin (Polymyxin E), Meropenem, Piperacillin-Tazobactam, and Tobramycin against Pseudomonas aeruginosa , 2006, Antimicrobial Agents and Chemotherapy.
[9] D. Hartl,et al. Accelerated evolution of resistance in multidrug environments , 2008, Proceedings of the National Academy of Sciences.
[10] J. Domagala,et al. Effect of Fluoroquinolone Concentration on Selection of Resistant Mutants of Mycobacterium bovis BCG andStaphylococcus aureus , 1999, Antimicrobial Agents and Chemotherapy.
[11] P. Phillips. The language of gene interaction. , 1998, Genetics.
[12] Kalin H. Vetsigian,et al. Exposing the fitness contribution of duplicated genes , 2008, Nature Genetics.
[13] O. Cars,et al. Mutant prevention concentrations of ciprofloxacin for urinary tract infection isolates of Escherichia coli. , 2005, The Journal of antimicrobial chemotherapy.
[14] B. Levin,et al. The population dynamics of antimicrobial chemotherapy , 1997, Antimicrobial agents and chemotherapy.
[15] H. Eagle,et al. THE RATE OF BACTERICIDAL ACTION OF PENICILLIN IN VITRO AS A FUNCTION OF ITS CONCENTRATION, AND ITS PARADOXICALLY REDUCED ACTIVITY AT HIGH CONCENTRATIONS AGAINST CERTAIN ORGANISMS , 1948, The Journal of experimental medicine.
[16] H. Dowling,et al. Treatment of pneumococcic meningitis with penicillin compared with penicillin plus aureomycin; studies including observations on an apparent antagonism between penicillin and aureomycin. , 1951, A.M.A. archives of internal medicine.
[17] MV Blagosklonny,et al. Drug-resistance enables selective killing of resistant leukemia cells: exploiting of drug resistance instead of reversal , 1999, Leukemia.
[18] Infectious diseases: problems of antimicrobial therapy. , 1954, Annual review of medicine.
[19] S. Zinner,et al. Enrichment of Fluoroquinolone-Resistant Staphylococcus aureus: Oscillating Ciprofloxacin Concentrations Simulated at the Upper and Lower Portions of the Mutant Selection Window , 2008, Antimicrobial Agents and Chemotherapy.
[20] K. Drlica,et al. In Vitro Pharmacodynamic Evaluation of the Mutant Selection Window Hypothesis Using Four Fluoroquinolones against Staphylococcus aureus , 2003, Antimicrobial Agents and Chemotherapy.
[21] J. Smith. The mode of action of 4-quinolones and possible mechanisms of resistance. , 1986, The Journal of antimicrobial chemotherapy.
[22] L. Piddock,et al. Mutant prevention concentrations of ciprofloxacin and enrofloxacin for Salmonella enterica. , 2004, The Journal of antimicrobial chemotherapy.
[23] N. Lehn,et al. Mutant prevention concentration of nalidixic acid, ciprofloxacin, clinafloxacin, levofloxacin, norfloxacin, ofloxacin, sparfloxacin or trovafloxacin for Escherichia coli under different growth conditions. , 2004, The Journal of antimicrobial chemotherapy.
[24] M. Klein,et al. THE ROLE OF BACTERIAL RESISTANCE IN ANTIBIOTIC SYNERGISM AND ANTAGONISM , 1953, Journal of bacteriology.
[25] Sean R. Collins,et al. A comprehensive strategy enabling high-resolution functional analysis of the yeast genome , 2008, Nature Methods.
[26] A. Fraser,et al. Systematic mapping of genetic interactions in Caenorhabditis elegans identifies common modifiers of diverse signaling pathways , 2006, Nature Genetics.
[27] K. Drlica,et al. Quinolone-Resistant Haemophilus influenzae: Determination of Mutant Selection Window for Ciprofloxacin, Garenoxacin, Levofloxacin, and Moxifloxacin , 2004, Antimicrobial Agents and Chemotherapy.
[28] R. Kishony,et al. Functional classification of drugs by properties of their pairwise interactions , 2006, Nature Genetics.
[29] G. Church,et al. Modular epistasis in yeast metabolism , 2005, Nature Genetics.
[30] V. Lorian. Antibiotics in laboratory medicine , 2005 .
[31] S. Deeks,et al. Treatment of antiretroviral-drug-resistant HIV-1 infection , 2003, The Lancet.
[32] T R Fraser,et al. Lecture on the Antagonism between the Actions of Active Substances , 1872, British medical journal.
[33] Paul Shannon,et al. Derivation of genetic interaction networks from quantitative phenotype data , 2005, Genome Biology.
[34] Ben Lehner,et al. Evolutionary plasticity of genetic interaction networks , 2008, Nature Genetics.
[35] J. Blondeau,et al. Comparison of minimal inhibitory and mutant prevention drug concentrations of 4 fluoroquinolones against clinical isolates of methicillin-susceptible and -resistant Staphylococcus aureus. , 2004, International journal of antimicrobial agents.
[36] B. Kreiswirth,et al. Mutant Prevention Concentration as a Measure of Antibiotic Potency: Studies with Clinical Isolates ofMycobacterium tuberculosis , 2000, Antimicrobial Agents and Chemotherapy.
[37] Grant W. Brown,et al. Functional dissection of protein complexes involved in yeast chromosome biology using a genetic interaction map , 2007, Nature.
[38] Sean R. Collins,et al. Conservation and Rewiring of Functional Modules Revealed by an Epistasis Map in Fission Yeast , 2008, Science.
[39] Sean R. Collins,et al. Exploration of the Function and Organization of the Yeast Early Secretory Pathway through an Epistatic Miniarray Profile , 2005, Cell.
[40] Robert P. St.Onge,et al. Defining genetic interaction , 2008, Proceedings of the National Academy of Sciences.
[41] I. Morrissey,et al. The mode of action of quinolones: The paradox in activity of low and high concentrations and activity in the anaerobic environment , 1991, European Journal of Clinical Microbiology and Infectious Diseases.
[42] S. Loewe,et al. Die quantitativen Probleme der Pharmakologie , 1928 .
[43] R. Korona,et al. Epistatic buffering of fitness loss in yeast double deletion strains , 2007, Nature Genetics.
[44] M. Wade,et al. Epistasis and the Evolutionary Process , 2000 .
[45] F. Baquero. Resistance to quinolones in gram-negative microorganisms: mechanisms and prevention. , 1990, European urology.
[46] R. Kishony,et al. Antibiotic interactions that select against resistance , 2007, Nature.
[47] C. I. Bliss. THE TOXICITY OF POISONS APPLIED JOINTLY1 , 1939 .
[48] Xilin Zhao,et al. Restricting the selection of antibiotic-resistant mutant bacteria: measurement and potential use of the mutant selection window. , 2002, The Journal of infectious diseases.
[49] Gary D Bader,et al. Global Mapping of the Yeast Genetic Interaction Network , 2004, Science.
[50] P. Brasseur,et al. Combination therapy for malaria: the way forward? , 2002, Drugs.
[51] Ronald W. Davis,et al. Systematic pathway analysis using high-resolution fitness profiling of combinatorial gene deletions , 2007, Nature Genetics.
[52] Nevan J Krogan,et al. High-throughput genetic interaction mapping in the fission yeast Schizosaccharomyces pombe , 2007, Nature Methods.
[53] Jef D Boeke,et al. Analysis of genetic interactions on a genome-wide scale in budding yeast: diploid-based synthetic lethality analysis by microarray. , 2008, Methods in molecular biology.
[54] J. Cairns,et al. The centenary of the one-gene one-enzyme hypothesis. , 2003, Genetics.
[55] N. Schork,et al. Who's afraid of epistasis? , 1996, Nature Genetics.
[56] J. Blondeau,et al. Mutant Prevention Concentrations of Fluoroquinolones for Clinical Isolates of Streptococcus pneumoniae , 2001, Antimicrobial Agents and Chemotherapy.
[57] K. Drlica. The mutant selection window and antimicrobial resistance. , 2003, The Journal of antimicrobial chemotherapy.
[58] S. Leibler,et al. Environmental stresses can alleviate the average deleterious effect of mutations , 2003, Journal of biology.
[59] Trey Ideker,et al. Functional Maps of Protein Complexes from Quantitative Genetic Interaction Data , 2008, PLoS Comput. Biol..
[60] Roy Kishony,et al. Networks from drug–drug surfaces , 2007, Molecular systems biology.
[61] Sean R. Collins,et al. A strategy for extracting and analyzing large-scale quantitative epistatic interaction data , 2006, Genome Biology.
[62] Gary D Bader,et al. Systematic Genetic Analysis with Ordered Arrays of Yeast Deletion Mutants , 2001, Science.
[63] Rafael A Irizarry,et al. Global synthetic-lethality analysis and yeast functional profiling. , 2006, Trends in genetics : TIG.
[64] Rafael Sanjuán,et al. The contribution of epistasis to the architecture of fitness in an RNA virus. , 2004, Proceedings of the National Academy of Sciences of the United States of America.
[65] Brian D. Peyser,et al. Gene function prediction from congruent synthetic lethal interactions in yeast , 2005, Molecular systems biology.
[66] F. Baquero,et al. Strategies to minimize the development of antibiotic resistance. , 1997, Journal of chemotherapy.