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646 results for “Pseudomonas aeruginosa”
Long-term Impact of Inhaled Tobramycin for Pseudomonas Aeruginosa Eradication in Bronchiectasis (ERASE II)
ClinicalTrials.gov study NCT06760273. IPD Sharing: NO. Countries: 1. Publications: 4.
Azithromycin as a Quorum-Sensing Inhibitor for the Prevention of Pseudomonas Aeruginosa Ventilator-Associated Pneumonia
ClinicalTrials.gov study NCT00610623. IPD Sharing: Not stated. Countries: 6. Publications: 1.
Carbapenem-resistant Pseudomonas Aeruginosa: the SAMPAN Study.
ClinicalTrials.gov study NCT05282082. IPD Sharing: YES. Countries: 3. Publications: 0.
The evolution of virulence in Pseudomonas aeruginosa during chronic wound infection
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Data from: Mridha S and Kümmerli R (2022) Enforced specialization fosters mutual cheating and not division of labour in the bacterium Pseudomonas aeruginosa
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Application strategies by selective medium treated with entomopathogenic bacteria Serratia marcescens and Pseudomonas aeruginosa as potential biocontrol against Coptotermes curvignathus
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Periodically disturbing biofilms reduces expression of quorum sensing regulated virulence factors in Pseudomonas aeruginosa
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The effects of antibiotic combination treatments on Pseudomonas aeruginosa tolerance evolution and coexistence with Stenotrophomonas maltophilia
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Interactions between metabolism and growth can determine the co-existence of Staphylococcus aureus and Pseudomonas aeruginosa
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Pseudomonas aeruginosa biofilm killing beyond the spacer by antibiotic-loaded calcium sulfate beads: An in vitro study raw data
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A fully synthetic Golden Gate assembly system for engineering a <em>Pseudomonas aeruginosa</em> phiKMV-like phage
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Spatial structure affects phage efficacy in infecting dual-strain biofilms of Pseudomonas aeruginosa
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Data from: Spatial structure maintains diversity of pyocin inhibition in household Pseudomonas aeruginosa
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Arms-race and fluctuating-selection dynamics in Pseudomonas aeruginosa bacteria coevolving with phage OMKO1
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RAST annotation for Clinical Strain Pseudomonas aeruginosa NRD619
<p>The RAST annotation for Clinical Strain Pseudomonas aeruginosa NRD619. </p>
Data from: Evolutionary reversals of antibiotic resistance in experimental populations of Pseudomonas aeruginosa
Antibiotic resistance mutations are accompanied by a fitness cost, and two mechanisms allow bacteria to adapt to this cost once antibiotic use is halted. First, it is possible for resistance to revert; second, it is possible for bacteria to adapt to the cost of resistance by compensatory mutations. Unfortunately, reversion to antibiotic sensitivity is rare, but the underlying factors that prevent reversion remain obscure. Here, we directly study the evolutionary dynamics of reversion by experimentally mimicking reversion mutations—sensitives—in populations of rifampicin-resistant Pseudomonas aeruginosa. We show that, in our populations, most sensitives are lost due to genetic drift when they are rare. However, clonal interference from lineages carrying compensatory mutations causes a dramatic increase in the time to fixation of sensitives that escape genetic drift, and mutations surpassing the sensitives' fitness are capable of driving transiently common sensitive lineages to extinction. Crucially, we show that the constraints on reversion arising from clonal interference are determined by the potential for compensatory adaptation of the resistant population. Although the cost of resistance provides the incentive for reversion, our study demonstrates that both the cost of resistance and the intrinsic evolvability of resistant populations interact to determine the rate and likelihood of reversion.
Data from: High virulence sub-populations in Pseudomonas aeruginosa long-term cystic fibrosis airway infections
Background: Pseudomonas aeruginosa typically displays loss of virulence-associated secretions over the course of chronic cystic fibrosis infections. This has led to the suggestion that virulence is a costly attribute in chronic infections. However, previous reports suggest that overproducing (OP) virulent pathotypes can coexist with non-producing mutants in the CF lung for many years. The consequences of such within-patient phenotypic diversity for the success of this pathogen are not fully understood. Here, we provide in-depth quantification of within-host variation in the production of three virulence associated secretions in the Liverpool cystic fibrosis epidemic strain of P. aeruginosa, and investgate the effect of this phenotypic variation on virulence in acute infections of an insect host model. Results: Within-patient variation was present for all three secretions (pyoverdine, pyocyanin and LasA protease). In two out of three patients sampled, OP isolates coexisted with under-producing mutants. In the third patient, all 39 isolates were under-producers of all three secretions relative to the transmissible ancestor LESB58. Finally, this phenotypic variation translated into variation in virulence in an insect host model. Conclusions: Within population variation in the production of P. aeruginosa virulence-associated secretions can lead to high virulence sub-populations persisting in patients with chronic CF infections.
Data from: Spite and the scale of competition in Pseudomonas aeruginosa
Scale of competition has been shown to be an important factor in shaping the evolution of the social interactions. Although many theoretical and experimental studies have examined its impact upon altruistic cooperation, relatively little research effort has been focused upon spiteful behaviours: actions that harm both the actor and recipient. In this study, we expand upon the existing theory by investigating the importance of global frequency of spiteful alleles, and we determine experimentally how scale of competition affects selection for spite in the bacterial pathogen Pseudomonas aeruginosa, under high and intermediate spatial relatedness. Consistent with our theoretical results, we find in our experiments that spiteful genotypes are more favoured under local (rather than global) competition and intermediate (rather than high) spatial relatedness; conditions that have been shown to select against indiscriminate altruism.
Data from: Rapid diversification of Pseudomonas aeruginosa in cystic fibrosis lung-like conditions
Chronic infection of the cystic fibrosis (CF) airway by the opportunistic pathogen Pseudomonas aeruginosa is the leading cause of morbidity and mortality for adult CF patients. Prolonged infections are accompanied by adaptation of P. aeruginosa to the unique conditions of the CF lung environment, as well as marked diversification of the pathogen into phenotypically and genetically distinct strains that can coexist for years within a patient. Little is known, however, about the causes of this diversification and its impact on patient health. Here, we show experimentally that, consistent with ecological theory of diversification, the nutritional conditions of the CF airway can cause rapid and extensive diversification of P. aeruginosa. Mucin, the substance responsible for the increased viscosity associated with the thick mucus layer in the CF airway, had little impact on within-population diversification but did promote divergence among populations. Furthermore, in vitro evolution recapitulated traits thought to be hallmarks of chronic infection, including reduced motility and increased biofilm formation, and the range of phenotypes observed in a collection of clinical isolates. Our results suggest that nutritional complexity and reduced dispersal can drive evolutionary diversification of P. aeruginosa independent of other features of the CF lung such as an active immune system or the presence of competing microbial species. We suggest that diversification, by generating extensive phenotypic and genetic variation on which selection can act, may be a key first step in the development of chronic infections.
Data from: Fitness trade-offs explain low levels of persister cells in the opportunistic pathogen Pseudomonas aeruginosa
Microbial populations often contain a fraction of slow-growing persister cells that withstand antibiotics and other stress factors. Current theoretical models predict that persistence levels should reflect a stable state in which the survival advantage of persisters under adverse conditions is balanced with the direct growth cost impaired under favourable growth conditions, caused by the nonreplication of persister cells. Based on this direct growth cost alone, however, it remains challenging to explain the observed low levels of persistence (<<1%) seen in the populations of many species. Here, we present data from the opportunistic human pathogen Pseudomonas aeruginosa that can explain this discrepancy by revealing various previously unknown costs of persistence. In particular, we show that in the absence of antibiotic stress, increased persistence is traded off against a lengthened lag phase as well as a reduced survival ability during stationary phase. We argue that these pleiotropic costs contribute to the very low proportions of persister cells observed among natural P. aeruginosa isolates (3 × 10−8–3 × 10−4) and that they can explain why strains with higher proportions of persister cells lose out very quickly in competition assays under favourable growth conditions, despite a negligible difference in maximal growth rate. We discuss how incorporating these trade-offs could lead to models that can better explain the evolution of persistence in nature and facilitate the rational design of alternative therapeutic strategies for treating infectious diseases.
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Allen Brain Atlas
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DANDI Archive for NWB datasets
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International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.