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2,375 results for “Antibiotics”

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zenodo36/100

Expanding the host-range of functional metagenomics reveals resistance threats to novel antibiotics

<p>Expanding the host-range of functional metagenomics reveals resistance threats to novel antibiotics. Sequences.</p>

opencc-by-4.0Dec 2022View details →
zenodo36/100

Antibiotic versus surgery in the treatment of acute appendicitis in the pregnant population: A systematic review and meta-analysis

<p>Antibiotic versus surgery in the treatment of acute appendicitis in the pregnant population: A systematic review and meta-analysis</p>

opencc-by-4.0Jan 2023View details →
zenodo36/100

Dataset of paper "Growth and prevalence of antibiotic-resistant bacteria in microplastic biofilm from wastewater treatment plant effluents"

<p>Dataset of paper &quot;Growth and prevalence of antibiotic-resistant bacteria in microplastic biofilm from wastewater treatment plant effluents&quot;:</p> <ul> <li>Raw 16srRNA forward and reverse sequence data</li> <li>16srRNA partial sequence data for submission to public database</li> <li>Nucleotide BLAST result from National Centre of Biotechnology Information (NCBI) database</li> <li>Summary of sample metadata and bacterial colony forming units (CFUs)</li> <li>Summary of sample metadata and quantified genes</li> </ul>

opencc-by-4.0Feb 2023View details →
zenodo36/100

Data for Whole-cell modeling of E. coli colonies enables quantification of single-cell heterogeneity in the antibiotic response

<p>Data from simulations used to generate the figures in the paper <em>Whole-cell modeling of E. coli colonies enables quantification of single-cell heterogeneity in the antibiotic response</em>.</p> <p>To reproduce analyses, extract <em>colony_data.zip</em> in the <em>data</em> folder after cloning the <em>vivarium-ecoli</em> repository.</p> <p>The extracted folder contains the following items:</p> <ul> <li><em>sim_dfs</em>: a folder containing the CSV files that represent a subset of the raw simulation data used for downstream analyses.</li> <li><em>glc_10000_fluxome.csv</em>: Each row represents a reaction in central carbon metabolism (in same order as listed in <em>validation/ecoli/flat/toya_2010_central_carbon_fluxes.tsv</em>). Each column represents a single time point for a single cell in a baseline glucose simulation (seed 10000). Each value is a flux (mmol/L/hr). Provided as input to <em>ecoli/analysis/centralCarbonMetabolism.py </em>script to reproduce fluxome validation plot.</li> <li><em>glc_10000_proteome_avgs.csv</em>: Each row represents a protein monomer (in same order as <em>sim_data.translation.monomer_data[&quot;id&quot;]</em> where <em>sim_data</em> is <em>reconstruction/sim_data/kb/validationData.cPickle</em>). Each column represents a cell in a baseline glucose simulation (seed 10000). Each row represents a protein monomer. Each value represents the average count of a given protein monomer for a given cell. Provided as input to <em>ecoli/analysis/proteinCountsValidation.py</em> script to reproduce proteome validation plot.</li> <li><em>glc_10000_expressome.csv</em>: Each column represents a gene (with the exception of the final two metadata columns: &quot;Time&quot; and &quot;Agent ID&quot;). Each row represents a specific cell (agent) at a specific time in a baseline glucose simulation (seed 10000). Each value represents the number of new RNA transcripts for a given gene in a given cell at a given time. Provided as input to <em>ecoli/analysis/antibiotics_colony/subgen_gene_plots/count_subgen.py</em> script to calculate number of sub-generational genes among all genes and antibiotic response genes.</li> <li><em>glc_10000_total_mrna.json</em>: Mapping of agent IDs for all cells in a baseline glucose simulation (seed 10000) to their average total mRNA count. Used by <em>ecoli/analysis/antibiotics_colony/plot.py </em>to generate Fig. 2C,D.</li> <li><em>jenner_2013.csv</em>: Data extracted from Fig. 2C of <a href="https://doi.org/10.1073/pnas.1216691110">10.1073/pnas.1216691110</a>. Used by <em>ecoli/analysis/antibiotics_colony/plot.py </em>to generate Fig. S6A.</li> <li><em>olson_2006.csv</em>: Data extracted from Fig. 2D of <a href="https://doi.org/10.1128%2FAAC.01499-05">10.1128/AAC.01499-05</a>. Used by <em>ecoli/analysis/antibiotics_colony/plot.py </em>to generate Fig. S6A.</li> <li><em>lysis_ratios.csv</em>: Data extracted from Fig. 2 of <a href="https://doi.org/10.1099/00221287-31-3-339">10.1099/00221287-31-3-339</a>. Used by <em>ecoli/analysis/antibiotics_colony/plot.py </em>to generate Fig. 4N.</li> </ul>

opencc-by-4.0Feb 2023View details →
zenodo36/100

Gut microbiota inter-species interactions shape the response of Clostridioides difficile to clinically relevant antibiotics

<p>In the human gut, the growth of <em>Clostridioides difficile </em>is impacted by a complex web of inter-species interactions with members of human gut microbiota. We investigate the contribution of inter-species interactions on the antibiotic response of <em>C. difficile </em>to clinically relevant antibiotics using bottom-up assembly of human gut communities. We discover two classes of microbial interactions that alter <em>C. </em>difficile&rsquo;s antibiotic susceptibility: infrequent increases in tolerance at high antibiotic concentrations and frequent growth enhancements at low antibiotic concentrations. Based on genome-wide transcriptional profiling data, we demonstrate that metal sequestration due to hydrogen sulfide production by the prevalent gut species <em>Desulfovibrio piger </em>increases metronidazole tolerance of <em>C. difficile</em>. Competition with species that display higher sensitivity to the antibiotic than <em>C. difficile </em>leads to enhanced growth of <em>C. difficile </em>at low antibiotic concentrations. A dynamic computational model identifies the ecological design principles driving this effect. Our results provide a deeper understanding of ecological and molecular principles shaping <em>C. difficile</em>&rsquo;s response to antibiotics, which could inform therapeutic interventions.</p>

opencc-by-4.0Sep 2022View details →
dryad36/100

Intensified livestock farming increases antibiotic resistance genotypes and phenotypes in animal feces

<p class="MsoNormal"><span>Animal feces from livestock farming can be a major source of antibiotic resistance to the environment, but a clear gap exists on how the resistance reservoir in feces alters as farming activities intensify. Here, we sampled feces from eight Chinese farms, where yak, sheep, pig, and horse were reared under free-range to intensive conditions, and determined fecal resistance using both genotype and phenotype approaches. </span><span>A</span><span>nimals reared </span><span><span>intensively</span></span><span> exhibited increased </span><span><span>diversity</span></span><span> of antibiotic resistance genes (ARGs) and greater resistance phenotypes in feces, which were cross-correlated. Furthermore, a</span><span>t the metagenome contig level, ARGs</span><span> </span><span>were </span><span><span>co-located</span></span><span> with </span><span>mobile genetic elements </span><span>at a higher frequency (27.38%) </span><span>as farming intensified, </span><span>with</span><span> associated resistance phenotyp</span><span><span>e</span></span><span>s </span><span>being less coupled with bacterial phylogeny. </span><span>I</span><span>ntensified farming also expanded the multidrug resistance preferentially carried on pathogens in fecal microbi</span><span>omes</span><span><span>.</span></span><span> Overall, </span><span><span>farming intensification </span></span><span>can </span><span><span>increase </span></span><span>antibiotic resistance</span><span> <span>genotypes and phenotypes in </span></span><span>domestic animal </span><span><span>feces</span></span><span>, with implications for environmental health.</span></p> <p> </p>

opencc-zeroMar 2023View details →
dryad36/100

Data for: Antibiotic-degrading resistance changes bacterial community structure via species-specific responses

<p>Some bacterial resistance mechanisms degrade antibiotics, potentially protecting neighbouring susceptible cells from antibiotic exposure. We do not yet understand how such effects influence bacterial communities of more than two species, which are typical in nature. Here, we used experimental multispecies communities to test the effects of clinically important pOXA-48-plasmid-encoded resistance on community-level responses to antibiotics. We found that resistance in one community member reduced antibiotic inhibition of other species, but some benefitted more than others. Further experiments with supernatants and pure-culture growth assays showed the susceptible species profiting most from detoxification were those that grew best at degraded antibiotic concentrations (greater than zero, but lower than the starting concentration). This pattern was also observed on agar surfaces, and the same species also showed relatively high survival compared to most other species during the initial high-antibiotic phase. By contrast, we found no evidence of a role for higher-order interactions or horizontal plasmid transfer in community-level responses to detoxification in our experimental communities. Our findings suggest carriage of an antibiotic-degrading resistance mechanism by one species can drastically alter community-level responses to antibiotics, and the identities of the species that profit most from antibiotic detoxification are predicted by their intrinsic ability to survive and grow at changing antibiotic concentrations.</p>

opencc-zeroJun 2023View details →
zenodo36/100

Green Synthesis of Copper Oxide Nanoparticles and its Efficiency in Degradation of Rifampicin Antibiotic

<p>The datasets came from synthesizing copper oxide nanoparticles from <em>Parthenium hysterophorus </em>aqueous extract, their characterization, and application in the degradation of rifampicin antibiotic. The data is presented in images&nbsp;and Microsoft Office Excel data sheets.</p>

opencc-by-4.0Jul 2023View details →
dryad36/100

Data from: Phenotypic plasticity of antibiotic resistance, metabolism byproduct utilization and the evolution of mutually beneficial cooperation in Escherichia coli

<p><span>Although tag-based donation and recognition have well explained how the cooperative individuals are positively assorted if the cooperative individuals possess some signals and are also able to detect such signals, an additional mechanism is required to explain why some individuals pay the costs of evolving such a tag that may not be rewarded subsequently, and how such tag-based cooperative individuals will meet other similar individuals with a very low mutation rate. Here, we show that many and even all<em> Escherichia coli </em>bacteria cells in the increased antibiotic concentration will plastically evolve to be antibiotic resistant individuals who could protect antibiotic sensitive strain from the attack of antibiotics, and the antibiotic resistant strain could reversibly evolve to be antibiotic sensitive in non-antibiotic supplement medium but in a harsher environment with low glucose. A further experiment showed that antibiotic-sensitive <em>E. coli </em>strain could in turn help reduce the concentration of indole produced by the resistant strain. This metabolic product is harmful to the growth of the antibiotic-resistant strain but benefits the antibiotic-sensitive strain by helping turn on the multi-drug exporter to discharge the antibiotic. The utilization of metabolism byproduct indole produced by antibiotic-resistant cells benefits antibiotic-sensitive cells, while the indole-absorbing service of antibiotic sensitive cells unconsciously help in nullifying the indole side effect on antibiotic resistant strain, and a mutual benefit cooperation could therefore evolve.</span></p>

opencc-zeroJul 2023View details →
dryad36/100

Phage-antibiotic synergy: cell filamentation is a key driver of successful phage predation

<div class="t-landing__text-wall "> <p><span>Phages are promising tools to fight antibiotic-resistant bacteria, and as for now, phage therapy is essentially performed in combination with antibiotics. Interestingly, combined treatments including phages and a wide range of antibiotics lead to an increased bacterial killing, a phenomenon called phage-antibiotic synergy (PAS), suggesting that antibiotic-induced changes in bacterial physiology alter the dynamics of phage propagation. Using single-phage and single-cell techniques, each step of the lytic cycle of phage HK620 was studied in <em>E. coli</em> cultures treated with either ciprofloxacin or cephalexin, two filamentation-inducing antibiotics. In the presence of sublethal doses of antibiotics, multiple stress tolerance and DNA repair pathways are triggered following activation of the SOS response. One of the most notable effects is the inhibition of bacterial division. As a result, a significant fraction of cells forms filaments that stop dividing but have higher rates of mutagenesis. Antibiotic-induced filaments become easy targets for phages due to their enlarged surface areas, as demonstrated by fluorescence microscopy and flow cytometry techniques. Adsorption, infection and lysis occur more often in filamentous cells compared to regular-sized bacteria. In addition, the reduction in bacterial numbers caused by impaired cell division may account for the faster elimination of bacteria during PAS. We developed a mathematical model to capture the interaction between sublethal doses of antibiotics and exposition to phages. This model shows that the induction of filamentation by sublethal doses of antibiotics can amplify the replication of phages and therefore yield PAS. We also use this model to study the consequences of PAS on the emergence of antibiotic resistance. A significant percentage of hyper-mutagenic filamentous bacteria are effectively killed by phages due to their increased susceptibility to infection. As a result, the addition of even a very low number of bacteriophages produced a strong reduction of the mutagenesis rate of the entire bacterial population. We confirm this prediction experimentally using reporters for bacterial DNA repair. Our work highlights the multiple benefits associated with the combination of sublethal doses of antibiotics with bacteriophages.</span></p> </div>

opencc-zeroAug 2023View details →
dryad36/100

Quantum chemical investigation of the predominant conformation of the antibiotic azithromycin in water and DMSO solutions: an integrated thermodynamic and NMR analysis

<p><span>Azithromycin (AZM) is a macrolide-type antibiotic used to prevent and treat serious infection</span><span>s (mycobacteria or MAC) that significantly inhibit bacterial growth. Knowledge of the predominant conformation in solution is of fundamental importance for advancing our understanding of the intermolecular interactions of AZM with biological targets. We report an extensive density functional theory (DFT) study of plausible AZM structures in solution considering implicit and explicit solvent effects. The best match between the experimental and theoretical nuclear magnetic resonance (NMR) profiles was used to assign the preferred conformer in solution, which was supported by the thermodynamic analysis. Among the 15 distinct AZM structures, conformer M14, having a short intramolecular C6-OH…N H-bond, is predicted to be dominant in water and DMSO solutions. The results indicated that the X-ray structure backbone is mostly conserved in solution, showing that large flexible molecules with several possible conformations may assume a preferential spatial orientation in solution, which is the molecular structure that ultimately interacts with biological targets.</span></p>

opencc-zeroSep 2023View details →
dryad36/100

Data from: Clinical antibiotic-resistance plasmids have small effects on biofilm formation and population growth in Escherichia coli in vitro

<div> <div> <div> <p>Antimicrobial resistance (AR) mechanisms encoded on plasmids can affect other phenotypic traits in bacteria, including biofilm formation. These effects may be important contributors to the spread of AR and the evolutionary success of plasmids, but it is not yet clear how common such effects are for clinical plasmids/bacteria, and how they vary among different plasmids and host strains. Here, we used a combinatorial approach to test the effects of clinical AR plasmids on biofilm formation and population growth in clinical and laboratory Escherichia coli strains. In most of the 25 plasmid-bacterium combinations tested, we observed no significant change in biofilm formation upon plasmid introduction, contrary to the notion that plasmids frequently alter biofilm formation. In a few cases we detected altered biofilm formation, and these effects were specific to particular plasmid-bacterium combinations. By contrast, we found a relatively strong effect of a chromosomal streptomycin-resistance mutation (in rpsL) on biofilm formation. Further supporting weak and host-strain- dependent effects of clinical plasmids on bacterial phenotypes in the combinations we tested, we found growth costs associated with plasmid carriage (measured in the absence of antibiotics) were moderate and varied among bacterial strains. These findings suggest some key clinical resistance plasmids cause only mild phenotypic disruption to their host bacteria, which may contribute to the persistence of plasmids in the absence of antibiotics.</p> </div> </div> </div>

opencc-zeroOct 2023View details →
zenodo36/100

Antibiotic Prescribing Adherence in Treatment of Uncomplicated Cellulitis

<p><strong>Authors:</strong></p><p><strong>* Talha Rizwan, Adnan Khan</strong></p><p>Our Lady's Hospital Navan, Republic of Ireland</p><p><strong>*Corresponding Author</strong>:* Talha Rizwan, Our Lady's Hospital Navan, Republic of Ireland</p>

opencc-by-4.0Oct 2023View details →
ClinicalTrials.gov36/100

Early Antibiotics After Aspiration in ICU Patients

ClinicalTrials.gov study NCT05079620. IPD Sharing: NO. Countries: 1. Publications: 12.

closedIPD-NOFeb 2026View details →
ClinicalTrials.gov36/100

Measuring the Influence of Kefir on Children's Stools on Antibiotics (MILK)

ClinicalTrials.gov study NCT00481507. IPD Sharing: Not stated. Countries: 1. Publications: 1.

restrictedIPD-UNDECIDEDFeb 2026View details →
ClinicalTrials.gov36/100

Partial Oral Antibiotic Treatment for Bacterial Brain Abscess

ClinicalTrials.gov study NCT04140903. IPD Sharing: YES. Countries: 1. Publications: 1.

controlledIPD-YESFeb 2026View details →
ClinicalTrials.gov36/100

Bacterial Pneumonia Score (BPS) Guided Antibiotic Use in Children With Pneumonia and Pneumococcal Vaccine

ClinicalTrials.gov study NCT01875731. IPD Sharing: NO. Countries: 1. Publications: 2.

closedIPD-NOFeb 2026View details →
ClinicalTrials.gov36/100

Placebo-Controlled Trial of Antibiotic Therapy in Adults With Suspect Lower Respiratory Tract Infection (LRTI) and a Procalcitonin Level

ClinicalTrials.gov study NCT03341273. IPD Sharing: Not stated. Countries: 1. Publications: 1.

restrictedIPD-UNDECIDEDFeb 2026View details →
ClinicalTrials.gov36/100

A Clinical Study to Evaluate the Tolerability of a Topical Antibiotic and Retinoid Used in a Combined Regimen With a BPO Wash

ClinicalTrials.gov study NCT00891982. IPD Sharing: Not stated. Countries: 1. Publications: 1.

restrictedIPD-UNDECIDEDFeb 2026View details →
ClinicalTrials.gov36/100

Comparison Between Carbapenems and Noncarbapenem Beta-lactam Antibiotics in Septic Burn Patients

ClinicalTrials.gov study NCT07096310. IPD Sharing: NO. Countries: 1. Publications: 6.

closedIPD-NOFeb 2026View details →

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International Brain Laboratory public data

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Last verified 2026-04-29Open record