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[PMID]:28988110
[Au] Autor:Fadel MA; El-Gebaly RH; Mohamed SA; Abdelbacki AMM
[Ad] Endereço:Biophysics Department, Faculty of Science, Cairo University, Egypt.
[Ti] Título:Biophysical control of the growth of Agrobacterium tumefaciens using extremely low frequency electromagnetic waves at resonance frequency.
[So] Source:Biochem Biophys Res Commun;494(1-2):365-371, 2017 Dec 09.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Isolated Agrobacterium tumefaciens was exposed to different extremely low frequencies of square amplitude modulated waves (QAMW) from two generators to determine the resonance frequency that causes growth inhibition. The carrier was 10 MHz sine wave with amplitude ±10 Vpp which was modulated by a second wave generator with a modulation depth of ± 2Vpp and constant field strength of 200 V/m at 28 °C. The exposure of A. tumefaciens to 1.0 Hz QAMW for 90 min inhibited the bacterial growth by 49.2%. In addition, the tested antibiotics became more effective against A. tumefaciens after the exposure. Furthermore, results of DNA, dielectric relaxation and TEM showed highly significant molecular and morphological changes due to the exposure to 1.0 Hz QAMW for 90 min. An in-vivo study has been carried out on healthy tomato plants to test the pathogenicity of A. tumefaciens before and after the exposure to QAMW at the inhibiting frequency. Symptoms of crown gall and all pathological symptoms were more aggressive in tomato plants treated with non-exposed bacteria, comparing with those treated with exposed bacteria. We concluded that, the exposure of A. tumefaciens to 1.0 Hz QAMW for 90 min modified its cellular activity and DNA structure, which inhibited the growth and affected the microbe pathogenicity.
[Mh] Termos MeSH primário: Agrobacterium tumefaciens/efeitos da radiação
Antibacterianos/farmacologia
DNA Bacteriano/efeitos da radiação
Radiação Eletromagnética
[Mh] Termos MeSH secundário: Agrobacterium tumefaciens/efeitos dos fármacos
Agrobacterium tumefaciens/genética
Agrobacterium tumefaciens/crescimento & desenvolvimento
Amicacina/farmacologia
Carbenicilina/farmacologia
Cefaclor/farmacologia
Cloranfenicol/farmacologia
Ciprofloxacino/farmacologia
DNA Bacteriano/efeitos dos fármacos
Fluoroquinolonas/farmacologia
Gentamicinas/farmacologia
Lycopersicon esculentum/microbiologia
Tumores de Planta/microbiologia
Rifampina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (DNA, Bacterial); 0 (Fluoroquinolones); 0 (Gentamicins); 5E8K9I0O4U (Ciprofloxacin); 66974FR9Q1 (Chloramphenicol); 69K7K19H4L (Cefaclor); 84319SGC3C (Amikacin); G42ZU72N5G (Carbenicillin); L4618BD7KJ (gatifloxacin); VJT6J7R4TR (Rifampin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171009
[St] Status:MEDLINE


  2 / 1816 MEDLINE  
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[PMID]:28749949
[Au] Autor:Jeon AB; Obregón-Henao A; Ackart DF; Podell BK; Belardinelli JM; Jackson M; Nguyen TV; Blackledge MS; Melander RJ; Melander C; Johnson BK; Abramovitch RB; Basaraba RJ
[Ad] Endereço:Mycobacteria Research Laboratories, Department of Microbiology, Immunology, and Pathology, Colorado State University, Fort Collins, Colorado, United States of America.
[Ti] Título:2-aminoimidazoles potentiate ß-lactam antimicrobial activity against Mycobacterium tuberculosis by reducing ß-lactamase secretion and increasing cell envelope permeability.
[So] Source:PLoS One;12(7):e0180925, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:There is an urgent need to develop new drug treatment strategies to control the global spread of drug-sensitive and multidrug-resistant Mycobacterium tuberculosis (M. tuberculosis). The ß-lactam class of antibiotics is among the safest and most widely prescribed antibiotics, but they are not effective against M. tuberculosis due to intrinsic resistance. This study shows that 2-aminoimidazole (2-AI)-based small molecules potentiate ß-lactam antibiotics against M. tuberculosis. Active 2-AI compounds significantly reduced the minimal inhibitory and bactericidal concentrations of ß-lactams by increasing M. tuberculosis cell envelope permeability and decreasing protein secretion including ß-lactamase. Metabolic labeling and transcriptional profiling experiments revealed that 2-AI compounds impair mycolic acid biosynthesis, export and linkage to the mycobacterial envelope, counteracting an important defense mechanism reducing permeability to external agents. Additionally, other important constituents of the M. tuberculosis outer membrane including sulfolipid-1 and polyacyltrehalose were also less abundant in 2-AI treated bacilli. As a consequence of 2-AI treatment, M. tuberculosis displayed increased sensitivity to SDS, increased permeability to nucleic acid staining dyes, and rapid binding of cell wall targeting antibiotics. Transcriptional profiling analysis further confirmed that 2-AI induces transcriptional regulators associated with cell envelope stress. 2-AI based small molecules potentiate the antimicrobial activity of ß-lactams by a mechanism that is distinct from specific inhibitors of ß-lactamase activity and therefore may have value as an adjunctive anti-TB treatment.
[Mh] Termos MeSH primário: Anti-Infecciosos/farmacologia
Permeabilidade da Membrana Celular/efeitos dos fármacos
Imidazóis/farmacologia
Mycobacterium tuberculosis/citologia
Mycobacterium tuberculosis/enzimologia
beta-Lactamases/secreção
beta-Lactamas/farmacologia
[Mh] Termos MeSH secundário: Carbenicilina/farmacologia
Corantes/química
Lipídeos/análise
Testes de Sensibilidade Microbiana
Mycobacterium tuberculosis/efeitos dos fármacos
Mycobacterium tuberculosis/crescimento & desenvolvimento
Ácidos Nucleicos/metabolismo
Penicilina V/farmacologia
Dodecilsulfato de Sódio/farmacologia
Coloração e Rotulagem
Transcrição Genética/efeitos dos fármacos
Vancomicina/farmacologia
beta-Lactamases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Infective Agents); 0 (Coloring Agents); 0 (Imidazoles); 0 (Lipids); 0 (Nucleic Acids); 0 (beta-Lactams); 368GB5141J (Sodium Dodecyl Sulfate); 6Q205EH1VU (Vancomycin); 7720-39-0 (2-aminoimidazole); EC 3.5.2.6 (beta-Lactamases); G42ZU72N5G (Carbenicillin); Z61I075U2W (Penicillin V)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180925


  3 / 1816 MEDLINE  
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[PMID]:27190289
[Au] Autor:Lee K; Lee KM; Go J; Ryu JC; Ryu JH; Yoon SS
[Ad] Endereço:Department of Microbiology and Immunology, Yonsei University College of Medicine, Seoul, 120-752, Korea Brain Korea 21 PLUS Project for Medical Sciences, Yonsei University College of Medicine, Seoul, 120-752, Korea.
[Ti] Título:The ferrichrome receptor A as a new target for Pseudomonas aeruginosa virulence attenuation.
[So] Source:FEMS Microbiol Lett;363(11), 2016 06.
[Is] ISSN:1574-6968
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Pseudomonas aeruginosa is an opportunistic pathogen, known to develop robust biofilms. Its biofilm development increases when antibiotics are presented at subminimal inhibitory concentrations (MICs) for reasons that remain unclear. In order to identify genes that affect biofilm development under such a sublethal antibiotic stress condition, we screened a transposon (Tn) mutant library of PAO1, a prototype P. aeruginosa strain. Among ∼5000 mutants, a fiuA gene mutant was verified to form very defective biofilms in the presence of sub-MIC carbenicillin. The fiuA gene encodes ferrichrome receptor A, involved in the iron acquisition process. Of note, biofilm formation was not decreased in the ΔpchΔpvd mutant defective in the production of pyochelin and pyoverdine, two well-characterized P. aeruginosa siderophore molecules. Moreover, ΔfiuA, a non-polar fiuA deletion mutant, produced a significantly decreased level of elastase, a major virulence determinant. Mouse airway infection experiments revealed that the mutant expressed significantly less pathogenicity. Our results suggest that the fiuA gene has pleiotropic functions that affect P. aeruginosa biofilm development and virulence. The targeting of FiuA could enable the attenuation of P. aeruginosa virulence and may be suitable for the development of a drug that specifically controls the virulence of this important pathogen.
[Mh] Termos MeSH primário: Proteínas da Membrana Bacteriana Externa/genética
Ferricromo/metabolismo
Pseudomonas aeruginosa/patogenicidade
Fatores de Virulência/genética
[Mh] Termos MeSH secundário: Animais
Proteínas da Membrana Bacteriana Externa/metabolismo
Biofilmes/efeitos dos fármacos
Biofilmes/crescimento & desenvolvimento
Carbenicilina/farmacologia
Elementos de DNA Transponíveis
Biblioteca Gênica
Ferro/metabolismo
Pulmão/microbiologia
Camundongos
Testes de Sensibilidade Microbiana
Oligopeptídeos/biossíntese
Elastase Pancreática/biossíntese
Fenóis/metabolismo
Pseudomonas aeruginosa/química
Pseudomonas aeruginosa/genética
Deleção de Sequência
Tiazóis/metabolismo
Fatores de Virulência/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bacterial Outer Membrane Proteins); 0 (DNA Transposable Elements); 0 (Oligopeptides); 0 (Phenols); 0 (Thiazoles); 0 (Virulence Factors); 15630-64-5 (Ferrichrome); 69772-54-9 (pyochelin); 8062-00-8 (pyoverdin); E1UOL152H7 (Iron); EC 3.4.21.36 (Pancreatic Elastase); G42ZU72N5G (Carbenicillin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160519
[St] Status:MEDLINE


  4 / 1816 MEDLINE  
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[PMID]:27159970
[Au] Autor:Hoerr V; Duggan GE; Zbytnuik L; Poon KK; Große C; Neugebauer U; Methling K; Löffler B; Vogel HJ
[Ad] Endereço:Institute of Medical Microbiology, Jena University Hospital, Erlanger Allee 101, D-07747, Jena, Germany. verena.hoerr@uni-jena.de.
[Ti] Título:Characterization and prediction of the mechanism of action of antibiotics through NMR metabolomics.
[So] Source:BMC Microbiol;16:82, 2016 May 10.
[Is] ISSN:1471-2180
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The emergence of antibiotic resistant pathogenic bacteria has reduced our ability to combat infectious diseases. At the same time the numbers of new antibiotics reaching the market have decreased. This situation has created an urgent need to discover novel antibiotic scaffolds. Recently, the application of pattern recognition techniques to identify molecular fingerprints in 'omics' studies, has emerged as an important tool in biomedical research and laboratory medicine to identify pathogens, to monitor therapeutic treatments or to develop drugs with improved metabolic stability, toxicological profile and efficacy. Here, we hypothesize that a combination of metabolic intracellular fingerprints and extracellular footprints would provide a more comprehensive picture about the mechanism of action of novel antibiotics in drug discovery programs. RESULTS: In an attempt to integrate the metabolomics approach as a classification tool in the drug discovery processes, we have used quantitative (1)H NMR spectroscopy to study the metabolic response of Escherichia coli cultures to different antibiotics. Within the frame of our study the effects of five different and well-known antibiotic classes on the bacterial metabolome were investigated both by intracellular fingerprint and extracellular footprint analysis. The metabolic fingerprints and footprints of bacterial cultures were affected in a distinct manner and provided complementary information regarding intracellular and extracellular targets such as protein synthesis, DNA and cell wall. While cell cultures affected by antibiotics that act on intracellular targets showed class-specific fingerprints, the metabolic footprints differed significantly only when antibiotics that target the cell wall were applied. In addition, using a training set of E. coli fingerprints extracted after treatment with different antibiotic classes, the mode of action of streptomycin, tetracycline and carbenicillin could be correctly predicted. CONCLUSION: The metabolic profiles of E. coli treated with antibiotics with intracellular and extracellular targets could be separated in fingerprint and footprint analysis, respectively and provided complementary information. Based on the specific fingerprints obtained for different classes of antibiotics, the mode of action of several antibiotics could be predicted. The same classification approach should be applicable to studies of other pathogenic bacteria.
[Mh] Termos MeSH primário: Antibacterianos/farmacologia
Escherichia coli/efeitos dos fármacos
Metabolômica/métodos
Espectroscopia de Prótons por Ressonância Magnética/métodos
[Mh] Termos MeSH secundário: Carbenicilina/farmacologia
Descoberta de Drogas
Escherichia coli/classificação
Testes de Sensibilidade Microbiana
Análise Multivariada
Projetos Piloto
Estreptomicina/farmacologia
Tetraciclina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); F8VB5M810T (Tetracycline); G42ZU72N5G (Carbenicillin); Y45QSO73OB (Streptomycin)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160511
[St] Status:MEDLINE
[do] DOI:10.1186/s12866-016-0696-5


  5 / 1816 MEDLINE  
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[PMID]:26854955
[Au] Autor:Thoppil AA; Choudhary S; Kishore N
[Ad] Endereço:Department of Chemistry, Indian Institute of Technology Bombay, Powai, Mumbai 400076, India.
[Ti] Título:Competitive binding of anticancer drugs 5-fluorouracil and cyclophosphamide with serum albumin: Calorimetric insights.
[So] Source:Biochim Biophys Acta;1860(5):917-929, 2016 May.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Isothermal titration calorimetry (ITC) has emerged as an excellent method to characterize drug-protein interactions. 5-Fluorouracil and cyclophosphamide have been used in combination for the treatment of breast carcinoma, though individually these drugs have also been useful in treating other types of cancer. A quantitative understanding of binding of these drugs with the transport protein under different conditions is essential for optimizing recognition by the protein and delivery at the target. METHODS: The values of binding constant, enthalpy, and entropy of binding have been determined by using ITC. Fluorescence and circular dichroism spectroscopies have been used to obtain further support to calorimetric observations, monitor conformational changes in the protein and establishing stoichiometry of association. RESULTS: The thermodynamic parameters have enabled a quantitative understanding of the affinity of 5-fluorouracil and cyclophosphamide with bovine serum albumin. The nature of binding has been unraveled based on effect of ionic strength, tetrabutyl-ammonium bromide, and sucrose which interfere in ionic, hydrophobic, and hydrogen bonding interactions. The binding site has been identified by using site marker warfarin in combination with 5-fluorouracil and cyclophosphamide. Further, the experiments have been done to establish whether both the drugs share the same binding site, and the effect of antibiotic drug carbenecillin and anti-inflammatory drug naproxen on their association. GENERAL SIGNIFICANCE: Tuning optimum association of drugs with the transport vehicles for effective drug delivery requires identification of the nature of interacting groups in terms of energetics of interactions. Such studies employing ITC have direct significance in rational drug design.
[Mh] Termos MeSH primário: Antineoplásicos/química
Ciclofosfamida/química
Fluoruracila/química
Soroalbumina Bovina/química
[Mh] Termos MeSH secundário: Animais
Sítios de Ligação
Ligação Competitiva
Calorimetria
Carbenicilina/química
Bovinos
Dicroísmo Circular
Ligações de Hidrogênio
Interações Hidrofóbicas e Hidrofílicas
Cinética
Naproxeno/química
Concentração Osmolar
Ligação Proteica
Compostos de Amônio Quaternário/química
Estereoisomerismo
Sacarose/química
Termodinâmica
Varfarina/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Quaternary Ammonium Compounds); 27432CM55Q (Serum Albumin, Bovine); 57-50-1 (Sucrose); 57Y76R9ATQ (Naproxen); 5Q7ZVV76EI (Warfarin); 8N3DW7272P (Cyclophosphamide); CBU2X6BBJR (tetrabutylammonium); G42ZU72N5G (Carbenicillin); U3P01618RT (Fluorouracil)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160209
[St] Status:MEDLINE


  6 / 1816 MEDLINE  
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[PMID]:26831117
[Au] Autor:Li L; Wang Q; Zhang H; Yang M; Khan MI; Zhou X
[Ad] Endereço:Department of Pathobiology and Veterinary Science, University of Connecticut, Storrs, CT 06269-3089;
[Ti] Título:Sensor histidine kinase is a ß-lactam receptor and induces resistance to ß-lactam antibiotics.
[So] Source:Proc Natl Acad Sci U S A;113(6):1648-53, 2016 Feb 09.
[Is] ISSN:1091-6490
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:ß-Lactams disrupt bacterial cell wall synthesis, and these agents are the most widely used antibiotics. One of the principle mechanisms by which bacteria resist the action of ß-lactams is by producing ß-lactamases, enzymes that degrade ß-lactams. In Gram-negative bacteria, production of ß-lactamases is often induced in response to the antibiotic-associated damage to the cell wall. Here, we have identified a previously unidentified mechanism that governs ß-lactamase production. In the Gram-negative enteric pathogen Vibrio parahaemolyticus, we found a histidine kinase/response regulator pair (VbrK/VbrR) that controls expression of a ß-lactamase. Mutants lacking either VbrK or VbrR do not produce the ß-lactamase and are no longer resistant to ß-lactam antibiotics. Notably, VbrK autophosphorylation is activated by ß-lactam antibiotics, but not by other lactams. However, single amino acid substitutions in the putative periplasmic binding pocket of VbrK leads its phosphorylation in response to both ß-lactam and other lactams, suggesting that this kinase is a ß-lactam receptor that can directly detect ß-lactam antibiotics instead of detecting the damage to cell wall resulting from ß-lactams. In strong support of this idea, we found that purified periplasmic sensor domain of VbrK binds penicillin, and that such binding is critical for VbrK autophosphorylation and ß-lactamase production. Direct recognition of ß-lactam antibiotics by a histidine kinase receptor may represent an evolutionarily favorable mechanism to defend against ß-lactam antibiotics.
[Mh] Termos MeSH primário: Antibacterianos/farmacologia
Resistência Microbiana a Medicamentos/efeitos dos fármacos
Proteínas Quinases/metabolismo
beta-Lactamas/metabolismo
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Proteínas de Bactérias/química
Proteínas de Bactérias/metabolismo
Carbenicilina/farmacologia
Sequência Conservada
Regulação Bacteriana da Expressão Gênica/efeitos dos fármacos
Histidina Quinase
Proteínas de Membrana/química
Proteínas de Membrana/metabolismo
Dados de Sequência Molecular
Mutação/genética
Fosforilação/efeitos dos fármacos
Ligação Proteica/efeitos dos fármacos
Estrutura Terciária de Proteína
Análise de Sequência de RNA
Especificidade por Substrato/efeitos dos fármacos
Transcrição Genética/efeitos dos fármacos
Vibrio parahaemolyticus/efeitos dos fármacos
Vibrio parahaemolyticus/genética
beta-Lactamases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Bacterial Proteins); 0 (Membrane Proteins); 0 (beta-Lactams); EC 2.7.- (Protein Kinases); EC 2.7.13.1 (Histidine Kinase); EC 3.5.2.6 (beta-Lactamases); G42ZU72N5G (Carbenicillin)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160203
[St] Status:MEDLINE
[do] DOI:10.1073/pnas.1520300113


  7 / 1816 MEDLINE  
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[PMID]:26758525
[Au] Autor:El Meouche I; Siu Y; Dunlop MJ
[Ad] Endereço:School of Engineering, University of Vermont, Burlington, VT USA 05405.
[Ti] Título:Stochastic expression of a multiple antibiotic resistance activator confers transient resistance in single cells.
[So] Source:Sci Rep;6:19538, 2016 Jan 13.
[Is] ISSN:2045-2322
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Transient resistance can allow microorganisms to temporarily survive lethal concentrations of antibiotics. This can be accomplished through stochastic mechanisms, where individual cells within a population display diverse phenotypes to hedge against the appearance of an antibiotic. To date, research on transient stochastic resistance has focused primarily on mechanisms where a subpopulation of cells enters a dormant, drug-tolerant state. However, a fundamental question is whether stochastic gene expression can also generate variable resistance levels among growing cells in a population. We hypothesized that stochastic expression of antibiotic-inducible resistance mechanisms might play such a role. To investigate this, we focused on a prototypical example of such a system: the multiple antibiotic resistance activator MarA. Previous studies have shown that induction of MarA can lead to a multidrug resistant phenotype at the population level. We asked whether MarA expression also has a stochastic component, even when uninduced. Time lapse microscopy showed that isogenic cells express heterogeneous, dynamic levels of MarA, which were correlated with transient antibiotic survival. This finding has important clinical implications, as stochastic expression of resistance genes may be widespread, allowing populations to hedge against the sudden appearance of an antibiotic.
[Mh] Termos MeSH primário: Proteínas de Ligação a DNA/genética
Farmacorresistência Bacteriana Múltipla
Proteínas de Escherichia coli/genética
Escherichia coli/efeitos dos fármacos
Escherichia coli/genética
Regulação Bacteriana da Expressão Gênica
[Mh] Termos MeSH secundário: Antibacterianos/farmacologia
Carbenicilina/farmacologia
Escherichia coli/crescimento & desenvolvimento
Expressão Gênica
Testes de Sensibilidade Microbiana
Viabilidade Microbiana/efeitos dos fármacos
Viabilidade Microbiana/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (DNA-Binding Proteins); 0 (Escherichia coli Proteins); 0 (MarA protein, E coli); G42ZU72N5G (Carbenicillin)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160114
[St] Status:MEDLINE
[do] DOI:10.1038/srep19538


  8 / 1816 MEDLINE  
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[PMID]:26603913
[Au] Autor:Gholipourmalekabadi M; Sameni M; Hashemi A; Zamani F; Rostami A; Mozafari M
[Ad] Endereço:Biotechnology Department, School of Advanced Technologies in Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran; Cellular and Molecular Biology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Electronic address: mazaher.gholipour@gmail.com.
[Ti] Título:Silver- and fluoride-containing mesoporous bioactive glasses versus commonly used antibiotics: Activity against multidrug-resistant bacterial strains isolated from patients with burns.
[So] Source:Burns;42(1):131-140, 2016 Feb.
[Is] ISSN:1879-1409
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The wound healing process is frequently associated with a number of major clinical challenges, due to the failure of commonly used antibiotics as a remedy for wounds. There have always been fascinating questions about the novel applications of bioactive glasses (BGs) and it is expected that in the next few years these types of materials may play an important role in many aspects of soft tissue regeneration. This research focuses on the feasibility of using silver- and fluoride-containing BGs against multidrug-resistant bacterial strains isolated from patients with burns. According to the results obtained, fluoride did not exhibit antibacterial activity against the tested bacteria, while both 1% and 2% silver-containing BGs inhibited the bacterial growth. It is an important finding that 1% silver-containing BGs showed a potential antibacterial activity without any toxicity against fibroblasts, suggesting that this class of BGs could play a key role in the prevention of infection, reduction of pain, and removal of excessive exudates.
[Mh] Termos MeSH primário: Antibacterianos/farmacologia
Queimaduras/microbiologia
Farmacorresistência Bacteriana Múltipla
Fluoretos/farmacologia
Vidro
Pseudomonas aeruginosa/efeitos dos fármacos
Prata/farmacologia
Infecção dos Ferimentos/microbiologia
[Mh] Termos MeSH secundário: Amicacina/farmacologia
Animais
Aztreonam/farmacologia
Carbenicilina/farmacologia
Ceftazidima/farmacologia
Ceftriaxona/farmacologia
Sobrevivência Celular/efeitos dos fármacos
Cefalosporinas/farmacologia
Ciprofloxacino/farmacologia
Gentamicinas/farmacologia
Seres Humanos
Imipenem/farmacologia
Camundongos
Testes de Sensibilidade Microbiana
Células NIH 3T3
Ácido Penicilânico/análogos & derivados
Ácido Penicilânico/farmacologia
Piperacilina/farmacologia
Tienamicinas/farmacologia
Tobramicina/farmacologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Cephalosporins); 0 (Gentamicins); 0 (Thienamycins); 157044-21-8 (piperacillin, tazobactam drug combination); 3M4G523W1G (Silver); 5E8K9I0O4U (Ciprofloxacin); 71OTZ9ZE0A (Imipenem); 75J73V1629 (Ceftriaxone); 807PW4VQE3 (cefepime); 84319SGC3C (Amikacin); 87-53-6 (Penicillanic Acid); 9M416Z9QNR (Ceftazidime); FV9J3JU8B1 (meropenem); G2B4VE5GH8 (Aztreonam); G42ZU72N5G (Carbenicillin); Q80VPU408O (Fluorides); VZ8RRZ51VK (Tobramycin); X00B0D5O0E (Piperacillin)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170912
[Lr] Data última revisão:
170912
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151126
[St] Status:MEDLINE


  9 / 1816 MEDLINE  
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[PMID]:26530864
[Au] Autor:Liu X; Li Y; Guo Y; Zeng Z; Li B; Wood TK; Cai X; Wang X
[Ad] Endereço:Key Laboratory of Tropical Marine Bio-resources and Ecology, Guangdong Key Laboratory of Marine Materia Medica, RNAM Center for Marine Microbiology, South China Sea Institute of Oceanology, Chinese Academy of Sciences, Guangzhou 510301, PR China.
[Ti] Título:Physiological Function of Rac Prophage During Biofilm Formation and Regulation of Rac Excision in Escherichia coli K-12.
[So] Source:Sci Rep;5:16074, 2015 Nov 04.
[Is] ISSN:2045-2322
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Rac or rac-like prophage harbors many genes with important physiological functions, while it remains excision-proficient in several bacterial strains including Escherichia coli, Salmonella spp. and Shigella spp. Here, we found that rac excision is induced during biofilm formation, and the isogenic stain without rac is more motile and forms more biofilms in nutrient-rich medium at early stages in E. coli K-12. Additionally, the presence of rac genes increases cell lysis during biofilm development. In most E. coli strains, rac is integrated into the ttcA gene which encodes a tRNA-thioltransferase. Rac excision in E. coli K-12 leads to a functional change of TtcA, which results in reduced fitness in the presence of carbenicillin. Additionally, we demonstrate that YdaQ (renamed as XisR) is the excisionase of rac in E. coli K-12, and that rac excision is induced by the stationary sigma factor RpoS through inducing xisR expression. Taken together, our results reveal that upon rac integration, not only are new genes introduced into the host, but also there is a functional change in a host enzyme. Hence, rac excision is tightly regulated by host factors to control its stability in the host genome under different stress conditions.
[Mh] Termos MeSH primário: Biofilmes/crescimento & desenvolvimento
DNA Nucleotidiltransferases/metabolismo
Escherichia coli K12/crescimento & desenvolvimento
Prófagos/metabolismo
Proteínas Virais/metabolismo
Ativação Viral/genética
Liberação de Vírus/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Proteínas de Bactérias/genética
Carbenicilina/farmacologia
DNA Nucleotidiltransferases/genética
Escherichia coli K12/efeitos dos fármacos
Escherichia coli K12/genética
Escherichia coli K12/virologia
Proteínas de Escherichia coli/genética
Regulação Bacteriana da Expressão Gênica/genética
Regulação Viral da Expressão Gênica/genética
Dados de Sequência Molecular
Prófagos/genética
Alinhamento de Sequência
Fator sigma/genética
Sulfurtransferases/genética
Proteínas Virais/genética
Ativação Viral/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Escherichia coli Proteins); 0 (Sigma Factor); 0 (Viral Proteins); 0 (sigma factor KatF protein, Bacteria); EC 2.7.7.- (DNA Nucleotidyltransferases); EC 2.7.7.- (excisionase); EC 2.8.1.- (Sulfurtransferases); EC 2.8.1.- (TtcA protein, E coli); G42ZU72N5G (Carbenicillin)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151105
[St] Status:MEDLINE
[do] DOI:10.1038/srep16074


  10 / 1816 MEDLINE  
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Texto completo
[PMID]:26475574
[Au] Autor:Georgiou P; Zanos P; Garcia-Carmona JA; Hourani S; Kitchen I; Kieffer BL; Laorden ML; Bailey A
[Ad] Endereço:Sleep, Chronobiology & Addiction Group, School of Biosciences and Medicine, Faculty of Health and Medical Sciences, University of Surrey, Guildford, GU2 7XH Surrey, UK.
[Ti] Título:The oxytocin analogue carbetocin prevents priming-induced reinstatement of morphine-seeking: Involvement of dopaminergic, noradrenergic and MOPr systems.
[So] Source:Eur Neuropsychopharmacol;25(12):2459-64, 2015 Dec.
[Is] ISSN:1873-7862
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Relapse to illicit drug-seeking following abstinence is a major challenge for the treatment of addiction as no effective pharmacotherapy is available. We have recently shown that activating the central oxytocinergic system prevents emotional impairment and stress-induced reinstatement associated with opioid withdrawal. Here, we investigated whether the oxytocin analogue carbetocin (CBT) is able to reverse morphine-primed reinstatement of conditioned-place preference (CPP) in mice. The mechanism underlining the behavioural effect of CBT was investigated by assessing the involvement of the striatal noradrenergic and dopaminergic systems in CBT reversal of priming- and stress-induced reinstatement of opioid CPP. In addition, given recent evidence suggesting the presence of oxytocin receptor (OTR)-µ-opioid receptor (MOPr) interactions in the brain, we further explored these interactions by carrying out OTR autoradiographic binding in brain of mice lacking MOPr. CBT administration prevented priming-induced reinstatement of morphine CPP. While an acute effect of CBT in enhancing dopamine turnover was observed following stress- and priming-induced reinstatement, CBT significantly decreased striatal noradrenaline turnover only following priming-induced reinstatement. Moreover, a significant brain region- specific increase in OTR binding was observed in MOPr knockout mice, indicating the presence of a possible OTR-MOPr interaction, which may be involved in the modulation of relapse. These results support the oxytocinergic system as a promising target for the prevention of relapse to opioid use and highlight the differential involvement of monoaminergic systems on the effects of OTR stimulation in preventing stress- and priming-induced reinstatement of opioid CPP behaviour.
[Mh] Termos MeSH primário: Carbenicilina/farmacologia
Dopamina/metabolismo
Comportamento de Procura de Droga/efeitos dos fármacos
Morfina/administração & dosagem
Norepinefrina/metabolismo
Receptores Opioides mu/metabolismo
[Mh] Termos MeSH secundário: Análise de Variância
Animais
Condicionamento Operante/efeitos dos fármacos
Corticosterona/sangue
Locomoção/efeitos dos fármacos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Ligação Proteica/efeitos dos fármacos
Receptores de Ocitocina/metabolismo
Análise de Regressão
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Opioid, mu); 0 (Receptors, Oxytocin); 76I7G6D29C (Morphine); G42ZU72N5G (Carbenicillin); VTD58H1Z2X (Dopamine); W980KJ009P (Corticosterone); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151018
[St] Status:MEDLINE



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