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  1 / 310895 MEDLINE  
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[PMID]:29444073
[Au] Autor:Hall MT; Simms KT; Lew JB; Smith MA; Saville M; Canfell K
[Ad] Endereço:Cancer Research Division, Cancer Council NSW, Sydney, Australia.
[Ti] Título:Projected future impact of HPV vaccination and primary HPV screening on cervical cancer rates from 2017-2035: Example from Australia.
[So] Source:PLoS One;13(2):e0185332, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Many countries are transitioning from cytology-based to longer-interval HPV screening. Trials comparing HPV-based screening to cytology report an increase in CIN2/3 detection at the first screen, and longer-term reductions in CIN3+; however, population level year-to-year transitional impacts are poorly understood. We undertook a comprehensive evaluation of switching to longer-interval primary HPV screening in the context of HPV vaccination. We used Australia as an example setting, since Australia will make this transition in December 2017. METHODS: Using a model of HPV vaccination, transmission, natural history and cervical screening, Policy1-Cervix, we simulated the planned transition from recommending cytology every two years for sexually-active women aged 18-20 to 69, to recommending HPV screening every five years for women aged 25-74 years. We estimated rates of CIN2/3, cervical cancer incidence, and mortality for each year from 2005 to 2035, considering ranges for HPV test accuracy and screening compliance in the context of HPV vaccination (current coverage ~82% in females; ~76% in males). FINDINGS: Transient increases are predicted to occur in rates of CIN2/3 detection and invasive cervical cancer in the first two to three years following the screening transition (of 16-24% and 11-14% in respectively, compared to 2017 rates). However, by 2035, CIN2/3 and invasive cervical cancer rates are predicted to fall by 40-44% and 42-51%, respectively, compared to 2017 rates. Cervical cancer mortality rates are predicted to remain unchanged until ~2020, then decline by 34-45% by 2035. Over the period 2018-2035, switching to primary HPV screening in Australia is expected to avert 2,006 cases of invasive cervical cancer and save 587 lives. CONCLUSIONS: Transient increases in detected CIN2/3 and invasive cancer, which may be detectable at the population level, are predicted following a change to primary HPV screening. This is due to improved test sensitivity bringing forward diagnoses, resulting in longer term reductions in both cervical cancer incidence and mortality. Fluctuations in health outcomes due to the transition to a longer screening interval are predicted to occur for 10-15 years, but cervical cancer rates will be significantly reduced thereafter due to the impact of HPV vaccination and HPV screening. In order to maintain confidence in primary HPV screening through the transitional phase, it is important to widely communicate that an initial increase in CIN2/3 and perhaps even invasive cervical cancer is expected after a national transition to primary HPV screening, that this phenomenon is due to increased prevalent disease detection, and that this effect represents a marker of screening success.
[Mh] Termos MeSH primário: Infecções por Papillomavirus/diagnóstico
Vacinas contra Papillomavirus/administração & dosagem
Neoplasias do Colo do Útero/epidemiologia
[Mh] Termos MeSH secundário: Austrália/epidemiologia
Feminino
Seres Humanos
Modelos Biológicos
Infecções por Papillomavirus/prevenção & controle
Cooperação do Paciente
Neoplasias do Colo do Útero/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Papillomavirus Vaccines)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185332


  2 / 310895 MEDLINE  
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[PMID]:29431542
[Au] Autor:Smit C; De Hoogd S; Brüggemann RJM; Knibbe CAJ
[Ad] Endereço:a Department of Clinical Pharmacy , St. Antonius Hospital , Nieuwegein , The Netherlands.
[Ti] Título:Obesity and drug pharmacology: a review of the influence of obesity on pharmacokinetic and pharmacodynamic parameters.
[So] Source:Expert Opin Drug Metab Toxicol;14(3):275-285, 2018 Mar.
[Is] ISSN:1744-7607
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: The rising prevalence of obesity confronts clinicians with dosing problems in the (extreme) overweight population. Obesity has a great impact on key organs that play a role in the pharmacokinetics (PK) and pharmacodynamics (PD) of drugs, however the ultimate impact of these changes on how to adapt the dose may not always be known. Areas covered: In this review, physiological changes associated with obesity are discussed. An overview is provided on the alterations in absorption, distribution, drug metabolism and clearance in (morbid) obesity focusing on general principles that can be extracted from pharmacokinetic studies. Also, relevant pharmacodynamic considerations in obesity are discussed. Expert opinion: Over the last two decades, increased knowledge is generated on PK and PD in obesity. Future research should focus on filling in the knowledge gaps that remain, especially in connecting obesity-related physiological changes with changes in PK and/or PD and vice versa. Ultimately, this knowledge can be used to develop physiologically based PK and PD models on the basis of quantitative systems pharmacology principles. Moreover, efforts should focus on thorough prospective evaluation of developed model-based doses with subsequent implementation of these dosing recommendations in clinical practice.
[Mh] Termos MeSH primário: Obesidade Mórbida/metabolismo
Obesidade/metabolismo
Preparações Farmacêuticas/metabolismo
[Mh] Termos MeSH secundário: Animais
Relação Dose-Resposta a Droga
Seres Humanos
Modelos Biológicos
Preparações Farmacêuticas/administração & dosagem
Farmacocinética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Pharmaceutical Preparations)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180213
[St] Status:MEDLINE
[do] DOI:10.1080/17425255.2018.1440287


  3 / 310895 MEDLINE  
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[PMID]:29363349
[Au] Autor:Van Donge T; Mian P; Tibboel D; Van Den Anker J; Allegaert K
[Ad] Endereço:a Intensive Care and Department of Paediatric Surgery , Erasmus MC-Sophia Children's Hospital , Rotterdam , The Netherlands.
[Ti] Título:Drug metabolism in early infancy: opioids as an illustration.
[So] Source:Expert Opin Drug Metab Toxicol;14(3):287-301, 2018 Mar.
[Is] ISSN:1744-7607
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Drug dosing in infants frequently depends on body weight as a crude indicator for maturation. Fentanyl (metabolized by Cytochrome P450 3A4) and morphine (glucuronidated by UDP-glucuronosyltransferase-2B7) served as model drugs to provide insight in maturation patterns of these enzymes and provide understanding of the impact of non-maturational factors to optimize dosing in infants. Areas covered: Systematic searches on metabolism and population pharmacokinetic (Pop-PK) models for fentanyl and morphine were performed. Pre- and post-model selection criteria were applied to assess and evaluate the validity of these models. It was observed that maturational changes have been rather well investigated, be it with variability in the maturational function estimates. The same holds true for Pop-PK models, where non-maturational covariates have also been reported (pharmacogenetics, disease state or external influences), although less incorporated in the PK models and with limited knowledge on mechanisms involved. Expert opinion: PK models for fentanyl and morphine are currently available. Consequently, we suggest that researchers should not continue to develop new models, but should investigate whether collected data fit in already existing models and provide additional value concerning the impact of (non)-maturational factors like drug-drug interactions or pharmacogenetics.
[Mh] Termos MeSH primário: Analgésicos Opioides/administração & dosagem
Fentanila/administração & dosagem
Morfina/administração & dosagem
[Mh] Termos MeSH secundário: Fatores Etários
Analgésicos Opioides/farmacocinética
Peso Corporal
Citocromo P-450 CYP3A/metabolismo
Relação Dose-Resposta a Droga
Fentanila/farmacocinética
Glucuronosiltransferase/metabolismo
Seres Humanos
Lactente
Modelos Biológicos
Morfina/farmacocinética
Farmacogenética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Analgesics, Opioid); 76I7G6D29C (Morphine); EC 1.14.13.67 (CYP3A4 protein, human); EC 1.14.14.1 (Cytochrome P-450 CYP3A); EC 2.4.1.- (UGT2B7 protein, human); EC 2.4.1.17 (Glucuronosyltransferase); UF599785JZ (Fentanyl)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180125
[St] Status:MEDLINE
[do] DOI:10.1080/17425255.2018.1432595


  4 / 310895 MEDLINE  
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[PMID]:29339162
[Au] Autor:El-Lakkani A; Ibrahim EM
[Ad] Endereço:Biophysics Department, Faculty of Science, Cairo University, Giza, 12613, Egypt. Electronic address: lakkani@netscape.com.
[Ti] Título:A method to improve prediction of secondary structure for large single RNA sequences.
[So] Source:Biochem Biophys Res Commun;496(2):523-528, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The function of a particular RNA molecule within an organic system is principally determined by its structure. The current physical methods available for structure determination are time consuming and expensive. Hence, computational methods for structure prediction are often used. The prediction of the structure of a large single sequence of RNA needs a lot of research work. In the present work, a method is introduced to improve the prediction of large single sequence RNA secondary structure obtained by Mfold program using the concept of minimum free energy. The Mfold program contains a constraint option that allows forcing some helices in the predicted structure. In our method, some of the firstly formed hairpins that are expected, by a statistical study, to be present in the real structure are forced in the Mfold predicted structure. The results show improvement, toward the real structure, in the Mfold predicted structure and this gives evidence to the RNA kinetic folding.
[Mh] Termos MeSH primário: RNA/química
[Mh] Termos MeSH secundário: Cinética
Modelos Biológicos
Conformação de Ácido Nucleico
Software
Termodinâmica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
63231-63-0 (RNA)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE


  5 / 310895 MEDLINE  
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[PMID]:29031613
[Au] Autor:Majd H; King MS; Smith AC; Kunji ERS
[Ad] Endereço:Medical Research Council Mitochondrial Biology Unit, University of Cambridge, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK.
[Ti] Título:Pathogenic mutations of the human mitochondrial citrate carrier SLC25A1 lead to impaired citrate export required for lipid, dolichol, ubiquinone and sterol synthesis.
[So] Source:Biochim Biophys Acta;1859(1):1-7, 2018 01.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Missense mutations of the human mitochondrial citrate carrier, encoded by the SLC25A1 gene, lead to an autosomal recessive neurometabolic disorder characterised by neonatal-onset encephalopathy with severe muscular weakness, intractable seizures, respiratory distress, and lack of psychomotor development, often resulting in early death. Here, we have measured the effect of all twelve known pathogenic mutations on the transport activity. The results show that nine mutations abolish transport of citrate completely, whereas the other three reduce the transport rate by >70%, indicating that impaired citrate transport is the most likely primary cause of the disease. Some mutations may be detrimental to the structure of the carrier, whereas others may impair key functional elements, such as the substrate binding site and the salt bridge network on the matrix side of the carrier. To understand the consequences of impaired citrate transport on metabolism, the substrate specificity was also determined, showing that the human citrate carrier predominantly transports citrate, isocitrate, cis-aconitate, phosphoenolpyruvate and malate. Although D-2- and L-2 hydroxyglutaric aciduria is a metabolic hallmark of the disease, it is unlikely that the citrate carrier plays a significant role in the removal of hydroxyglutarate from the cytosol for oxidation to oxoglutarate in the mitochondrial matrix. In contrast, computer simulations of central metabolism predict that the export of citrate from the mitochondrion cannot be fully compensated by other pathways, restricting the cytosolic production of acetyl-CoA that is required for the synthesis of lipids, sterols, dolichols and ubiquinone, which in turn explains the severe disease phenotypes.
[Mh] Termos MeSH primário: Proteínas de Transporte de Ânions
Ácido Cítrico/metabolismo
Simulação por Computador
Dolicol
Proteínas Mitocondriais
Modelos Biológicos
Mutação de Sentido Incorreto
Esteróis
Ubiquinona
[Mh] Termos MeSH secundário: Proteínas de Transporte de Ânions/química
Proteínas de Transporte de Ânions/genética
Proteínas de Transporte de Ânions/metabolismo
Transporte Biológico Ativo/genética
Encefalopatias Metabólicas Congênitas/enzimologia
Encefalopatias Metabólicas Congênitas/genética
Domínio Catalítico
Dolicol/biossíntese
Dolicol/química
Dolicol/genética
Seres Humanos
Proteínas Mitocondriais/química
Proteínas Mitocondriais/genética
Proteínas Mitocondriais/metabolismo
Esteróis/biossíntese
Esteróis/química
Esteróis/metabolismo
Ubiquinona/biossíntese
Ubiquinona/química
Ubiquinona/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anion Transport Proteins); 0 (Mitochondrial Proteins); 0 (Slc25a1 protein, human); 0 (Sterols); 1339-63-5 (Ubiquinone); 2067-66-5 (Dolichol); 2968PHW8QP (Citric Acid)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171017
[St] Status:MEDLINE


  6 / 310895 MEDLINE  
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[PMID]:28455696
[Au] Autor:Mentis AA; Dardiotis E; Grigoriadis N; Petinaki E; Hadjigeorgiou GM
[Ad] Endereço:Department of Microbiology, University Hospital of Larissa, University of Thessaly, Larissa, Greece. amentis1@jhu.edu.
[Ti] Título:Viruses and Multiple Sclerosis: From Mechanisms and Pathways to Translational Research Opportunities.
[So] Source:Mol Neurobiol;54(5):3911-3923, 2017 Jul.
[Is] ISSN:1559-1182
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Viruses are directly or indirectly implicated in multiple sclerosis (MS). Here, we review the evidence on the virus-related pathophysiology of MS, introduce common experimental models, and explore the ways in which viruses cause demyelination. By emphasizing knowledge gaps, we highlight future research directions for effective MS diagnostics and therapies: (i) identifying biomarkers for at-risk individuals, (ii) searching for direct evidence of specific causative viruses, (iii) establishing the contribution of host genetic factors and viruses, and (iv) investigating the contribution of immune regulation at extra-CNS sites. Research in these areas is likely to be facilitated by the application of high-throughput technologies, the development of systems-based bioinformatic approaches, careful selection of experimental models, and the acquisition of high-quality clinical material for tissue-based research.
[Mh] Termos MeSH primário: Esclerose Múltipla/virologia
Pesquisa Médica Translacional
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Progressão da Doença
Seres Humanos
Modelos Biológicos
Esclerose Múltipla/patologia
Esclerose Múltipla/fisiopatologia
Células-Tronco/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE
[do] DOI:10.1007/s12035-017-0530-6


  7 / 310895 MEDLINE  
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[PMID]:28456463
[Au] Autor:Petrovskii S; Sekerci Y; Venturino E
[Ad] Endereço:Department of Mathematics, University of Leicester, University Road, Leicester LE1 7RH, U.K. Electronic address: sp237@le.ac.uk.
[Ti] Título:Regime shifts and ecological catastrophes in a model of plankton-oxygen dynamics under the climate change.
[So] Source:J Theor Biol;424:91-109, 2017 Jul 07.
[Is] ISSN:1095-8541
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:It is estimated that more than a half of the total atmospheric oxygen is produced in the oceans due to the photosynthetic activity of phytoplankton. Any significant decrease in the net oxygen production by phytoplankton is therefore likely to result in the depletion of atmospheric oxygen and in a global mass mortality of animals and humans. In its turn, the rate of oxygen production is known to depend on water temperature and hence can be affected by the global warming. We address this problem theoretically by considering a model of a coupled plankton-oxygen dynamics where the rate of oxygen production slowly changes with time to account for the ocean warming. We show that, when the temperature rises sufficiently high, a regime shift happens: the sustainable oxygen production becomes impossible and the system's dynamics leads to fast oxygen depletion and plankton extinction. We also consider a scenario when, after a certain period of increase, the temperature is set on a new higher yet apparently safe value, i.e. before the oxygen depletion disaster happens. We show that in this case the system dynamics may exhibit a long-term quasi-sustainable dynamics that can still result in an ecological disaster (oxygen depletion and mass extinctions) but only after a considerable period of time. Finally, we discuss the early warning signals of the approaching regime shift resulting in the disaster.
[Mh] Termos MeSH primário: Extinção Biológica
Aquecimento Global
Modelos Biológicos
Oceanos e Mares
Oxigênio/metabolismo
Plâncton/fisiologia
[Mh] Termos MeSH secundário: Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
S88TT14065 (Oxygen)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE


  8 / 310895 MEDLINE  
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[PMID]:28456461
[Au] Autor:Ose NJ; Ohmann PR
[Ad] Endereço:Department of Physics, University of Saint Thomas, St. Paul, MN 55105, USA.
[Ti] Título:The selfish herd: Noise effects in Local Crowded Horizon and Voronoi models.
[So] Source:J Theor Biol;424:84-90, 2017 Jul 07.
[Is] ISSN:1095-8541
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Randomness or noise in the motion of herding animals is more important than commonly assumed. We show through simulations that noise promotes the compactness of a herd by facilitating the breakup of small clusters in favor of a more compact whole, reducing the mean median distances to center (MMDC) for the herd. Adding noise to movement models can also decrease risk from predators emerging locally by reducing Domains of Danger (DODs); we specifically show that adding noise to the Voronoi (V) movement model gives favorable DOD results comparable to that of the Local Crowded Horizon (LCH) model. In addition, we show that adding noise to these models can significantly reduce risk from predators emerging outside the herding area through head-to-head competition in mixed herds, with effects that can be larger than the choice of model itself. Our results are consistent with recent observational studies in several different animal populations that suggest random motion plays a significant role in the movement of individuals within these groups. Because of its significance, noise must be considered whenever model effectiveness is discussed or comparisons between movement models are made.
[Mh] Termos MeSH primário: Aglomeração
Modelos Biológicos
[Mh] Termos MeSH secundário: Animais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE


  9 / 310895 MEDLINE  
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[PMID]:28456460
[Au] Autor:Sasaki A; Mizuno AN
[Ad] Endereço:Department of Evolutionary Studies of Biosystems, SOKENDAI (The Graduate University for Advanced Studies), Hayama, Kanagawa 240-0193, Japan; Evolution and Ecology Program, International Institute for Applied Systems Analysis, A-2361 Laxenburg, Austria. Electronic address: sasaki_akira@soken.ac.jp.
[Ti] Título:Partitioning light spectra: Adaptive stratification of phytobenthic communities in Antarctic lakes.
[So] Source:J Theor Biol;424:1-10, 2017 Jul 07.
[Is] ISSN:1095-8541
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Competition for light has an important influence for phototrophic community structures, especially, along the perpendicular axis. Here we develop a mathematical model for perpendicular community buildup of phototrophic species that differ in light absorption spectra and compete for incident light. Details of photon capture efficiencies and the roles of photoinhibition were taken into consideration to define species' fitness. Our theory showed that, if there is strong light irradiation due, for example, to the high transparency of the water in freshwater lakes in Antarctica, protective absorption of light should occur near the surface and photosynthetic absorption should gradually increase with depth. These results were then validated in comparison with observed vertical distributions of pigments in phytobenthic-mat communities from Antarctic lakes.
[Mh] Termos MeSH primário: Lagos
Luz
Modelos Biológicos
Fotossíntese/fisiologia
Fitoplâncton/fisiologia
[Mh] Termos MeSH secundário: Regiões Antárticas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE


  10 / 310895 MEDLINE  
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[PMID]:29458544
[Au] Autor:Aguilar-Ayala DA; Cnockaert M; Vandamme P; Palomino JC; Martin A; Gonzalez-Y-Merchand J
[Ad] Endereço:2​Laboratory of Microbiology, Department of Biochemistry and Microbiology, Ghent University, Ghent 9000, Belgium.
[Ti] Título:Antimicrobial activity against Mycobacterium tuberculosis under in vitro lipid-rich dormancy conditions.
[So] Source:J Med Microbiol;67(3):282-285, 2018 Mar.
[Is] ISSN:1473-5644
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Although tuberculosis treatment is dependent on drug-susceptibility testing (DST) and molecular drug-resistance detection, treatment failure and relapse remain a challenge. This could be partially due to the emergence of antibiotic-tolerant dormant mycobacteria, where host lipids have been shown to play an important role. This study evaluated the susceptibility of Mycobacterium tuberculosis to two antibiotic combinations - rifampicin, moxifloxacin, amikacin and metronidazole (RIF-MXF-AMK-MTZ), and rifampicin, moxifloxacin, amikacin and pretomanid (RIF-MXF-AMK-PA) - in a lipid-rich dormancy model. Although their effectiveness in in vitro cultures with dextrose as a carbon source has been proved, we observed that none of the antibiotic mixtures were bactericidal in the presence of lipids. The presence of lipids may confer tolerance to M. tuberculosis against the mixture of antibiotics tested and such tolerance could be even higher during the dormant stages. The implementation of lipids in DST on clinical isolates could potentially lead to a better treatment strategy.
[Mh] Termos MeSH primário: Antibacterianos/farmacologia
Lipídeos/farmacologia
Mycobacterium tuberculosis/efeitos dos fármacos
Mycobacterium tuberculosis/fisiologia
[Mh] Termos MeSH secundário: Amicacina/farmacologia
Antituberculosos/farmacologia
Tolerância a Medicamentos
Fluoroquinolonas/farmacologia
Aptidão Genética
Genótipo
Seres Humanos
Metabolismo dos Lipídeos
Testes de Sensibilidade Microbiana
Modelos Biológicos
Infecções por Micobactéria não Tuberculosa/microbiologia
Mycobacterium tuberculosis/genética
Mycobacterium tuberculosis/crescimento & desenvolvimento
Nitroimidazóis/farmacologia
Rifampina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-nitro-6-(4-(trifluoromethoxy)benzyloxy)-6,7-dihydro-5H-imidazo(2,1-b)(1,3)oxazine); 0 (Anti-Bacterial Agents); 0 (Antitubercular Agents); 0 (Fluoroquinolones); 0 (Lipids); 0 (Nitroimidazoles); 84319SGC3C (Amikacin); U188XYD42P (moxifloxacin); VJT6J7R4TR (Rifampin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180221
[St] Status:MEDLINE
[do] DOI:10.1099/jmm.0.000681



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