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1,943 results for “pulmonary disease”
Supplementary material: Prophylactic antibiotics for adults with chronic obstructive pulmonary disease: a network meta-analysis
<p>Supplementary material for Cochrane review: Janjua S , Mathioudakis AG , Fortescue R , Walker RAE , Sharif S , Threapleton CJD , Dias S . Prophylactic antibiotics for adults with chronic obstructive pulmonary disease: a network meta-analysis. Cochrane Database of Systematic Reviews 2021, Issue 1. Art. No.: <a href="https://archie.cochrane.org/sections/documents/CD013198">CD013198</a>. DOI: <a href="https://archie.cochrane.org/sections/documents/10.1002/14651858.CD013198.pub2">10.1002/14651858.CD013198.pub2</a>.</p>
Experiment data in support of "Segmentation analysis and the recovery of queuing parameters via the Wasserstein distance: a study of administrative data for patients with chronic obstructive pulmonary disease"
<p>This archive contains a ZIP archive, `data.zip`, that itself contains the data used in the final sections of the paper. The remainder of the paper's supporting files are available at <a href="https://github.com/daffidwilde/copd-paper/">github.com/daffidwilde/copd-paper/</a></p> <p>The ZIP archive is structured as follows:</p> <ul> <li>There is a directory, `wasserstein`, for the parameter sweep described in the model construction section of the paper. Its contents are: (i) a file, `main.csv`, describing each parameter and their maximal Wasserstein distance to the observed data, and (ii) three directories, `best`, `median` and `worst`, each containing the simulated queuing results (in `main.csv`) from that sweep with the best, median and worst found parameter sets, respectively (in `params.txt`).</li> <li>The remaining three directories correspond to the experiments conducted in the final section of the paper. Each directory contains two files: (i) `system_times.csv` which holds trial parameters and system time records for every patient to pass through the model in that experiment, and (ii) `utilisations.csv` which holds trial parameters and utilisations for each server in the model for that experiment.</li> </ul>
Outdoor air pollution impacts chronic obstructive pulmonary disease deaths in South Asia and China: a systematic review and meta-analysis
<p><strong>Background: </strong>Chronic obstructive pulmonary disease (COPD) is among leading causes of death globally. Exposure to outdoor pollution is an important cause for increased mortality and morbidity. This study presents a systemic review regarding the impact of outdoor pollution on COPD mortality in South Asia and China.</p> <p><strong>Methods: </strong>A systematic search was conducted from 1990 to June 30<sup>th</sup> 2020 in English electronic databases: PubMed, Google Scholar and CDSR (Cochrane Database of Systematic Reviews) following Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. The following terms were used: Chronic Obstructive Pulmonary disease OR COPD OR Chronic Bronchitis OR Emphysema OR COPD Deaths OR Chronic Obstructive Lung Disease OR Airflow Obstruction OR Chronic Airflow Obstruction OR Airflow Obstruction, Chronic OR Bronchitis, Chronic AND Mortality OR Death OR Deceased AND Outdoor pollution, ambient pollution was conducted.</p> <p><strong>Results:</strong> Out of 1899 papers screened only 17 were found eligible to be included. Subjects with COPD exposed to higher levels of outdoor air pollution had a 49% higher risk of death as compared to COPD subjects exposed to lower levels of outdoor air pollution. When taking common air pollutants individually into consideration, PM10 had an odds ratio (OR) of 1.99 respectively at CI 95%, whereas SO2 had OR of 1.8 at 95% CI, and NO2 had an OR of 1.23 OR at 95% CI. These values suggest that there is an effect of outdoor pollution on COPD but not to a significant level.</p> <p><strong>Conclusion: </strong>Despite heterogeneity across selected studies, individuals exposed to outdoor pollutants were found to be at risk of COPD mortality. Though it appears to have risk, COPD mortality was not significantly associated with outdoor pollutants. Controlling air pollution can substantially decrease the risk of COPD in South Asia and China. Further researches including more prospective and longitudinal studies are urgently needed in COPD sub-groups.</p>
Fig. 2. Pulmonary hydatid cyst from a 3 year old female water buffalo from a in The first report of hydatid disease (Echinococcus granulosus) in an Australian water buffalo (Bubalus bubalis)
Fig. 2. Pulmonary hydatid cyst from a 3 year old female water buffalo from a farm in New South Wales, Australia.
Whole blood RNA-seq demonstrates an increased host immune response in individuals with cystic fibrosis who develop nontuberculous mycobacterial pulmonary disease
<p><strong>Background </strong></p> <p>Individuals with cystic fibrosis have an elevated lifetime risk of colonization, infection, and disease caused by nontuberculous mycobacteria. A prior study involving non-cystic fibrosis individuals reported a gene expression signature associated with susceptibility to nontuberculous mycobacteria pulmonary disease (NTM-PD). In this study, we determined whether people living with cystic fibrosis who progress to NTM-PD have a gene expression pattern similar to the one seen in the non-cystic fibrosis population. <strong> </strong></p> <p><strong>Methods</strong></p> <p>We evaluated whole blood transcriptomics using bulk RNA-seq in a cohort of cystic fibrosis patients with samples collected closest in timing to the first isolation of nontuberculous mycobacteria. The study population included patients who did (n = 12) and did not (n = 30) develop NTM-PD following the first mycobacterial growth. Progression to NTM-PD was defined by a consensus of two expert clinicians based on reviewing clinical, microbiological, and radiological information. Differential gene expression was determined by DESeq2.</p> <p><strong>Results</strong></p> <p>No differences in demographics or composition of white blood cell populations between groups were identified at baseline. Out of 213 genes associated with NTM-PD in the non-CF population, only two were significantly different in our cystic fibrosis NTM-PD cohort. Gene set enrichment analysis of the differential expression results showed that CF individuals who developed NTM-PD had higher expression levels of genes involved in the interferon (α and γ), tumor necrosis factor, and IL6-STAT3-JAK pathways. <strong> </strong></p> <p><strong>Conclusion</strong></p> <p>In contrast to the non-cystic fibrosis population, the gene expression signature of patients with cystic fibrosis who develop NTM-PD is characterized by increased innate immune responses.</p>
E-Cigarette Effects on Markers of Cardiovascular and Pulmonary Disease
ClinicalTrials.gov study NCT03863509. IPD Sharing: YES. Countries: 1. Publications: 1.
Proof-of-Concept Study to Assess the Efficacy, Safety and Tolerability of SAR440340 (Anti-IL-33 mAb) in Patients With Moderate-to-severe Chronic Obstructive Pulmonary Disease (COPD)
ClinicalTrials.gov study NCT03546907. IPD Sharing: YES. Countries: 10. Publications: 1.
Whole blood RNA-seq demonstrates an increased host immune response in individuals with cystic fibrosis who develop nontuberculous mycobacterial pulmonary disease
Open the record for dataset details and reuse information.
Identifying biomarkers for chronic obstructive pulmonary disease in the salivary metabolome.
<p><strong><span>Background:</span></strong><span> The lack of specificity in spirometry and accuracy in ‘pre-disease states’, and elderly indicates the need for other accurate, inexpensive and non-invasive tests for diagnosis, triage severity and particularly for choosing and monitoring response to treatments in chronic obstructive pulmonary disease (COPD). We compared salivary metabolomic signatures from patients with COPD and controls across a range of severity of airflow obstruction. </span></p> <p><a name="_61k4y1plsv5"></a><strong><span>Methods</span></strong></p> <p><span>45 people with COPD (mean age 66.1 ± 23 years, forced expiratory volume [FEV<sub>1</sub>] 47<u>+</u>15% predicted) and 48 healthy controls (mean age 56.0 <u>+</u>16.2 years, FEV<sub>1</sub> 90<u>+</u>23 % predicted) provided saliva that was assessed by flow infusion electrospray mass spectrometry (FIE-MS). Spectra were interrogated using an online library package. Data (patient data and metabolomic outputs) are available from this site. </span></p> <p><a name="_j99pcjszp0an"></a><strong><span>Results</span></strong></p> <p><span>Four potential biomarkers identified the presence of COPD with a sensitivity of 73%, specificity of 72%.<span> </span>Six metabolites predicted FEV1 % in the COPD cohort (<em>P </em>< 0.001, R<sup>2</sup> > 0.3, AUC > 0.7) whilst a range of multivariate approaches targeted six metabolites linked to GOLD stage (<em>P </em>< 0.001, AUC > 0.7). Identification of the metabolites suggested changes in pterin biosynthesis, lipid processing, nucleotide metabolism and melatonin in COPD patients. </span></p> <p><a name="_2n4ucvxs4l1n"></a><strong><span>Conclusions</span></strong></p> <p><span>Metabolic fingerprinting of saliva samples could differentiate COPD from age matched controls and inform COPD severity of airflow obstruction. Potential biomarkers are suggested which could inform the diagnosis and monitoring of COPD.</span></p> <p><span> </span></p> <h2><span> </span></h2>
data set regarding to project Optimal assessment of nutritional status in older subjects with the chronic obstructive pulmonary disease
<p>data set regarding to project Optimal assessment of nutritional status in older subjects with the chronic obstructive pulmonary disease</p>
data set regarding to project Optimal assessment of nutritional status in older subjects with the chronic obstructive pulmonary disease – a comparison of three screening tools used in the GLIM diagnostic algorithm
<p>data set regarding to project Optimal assessment of nutritional status in older subjects with the chronic obstructive pulmonary disease – a comparison of three screening tools used in the GLIM diagnostic algorithm </p>
Figure 1 in Detection of respiratory viruses and expression of inflammatory cytokines in patients with acute exacerbation chronic obstructive pulmonary disease in Mongolia China
Figure 1. Distribution of Viruses.
Identification of early genes in the pathophysiology of fibrotic interstitial lung disease in a new model of pulmonary fibrosis
<p>Some interstitial lung diseases involve pulmonary fibrosis, which is a process that is characterized by the excessive and abnormal accumulation of extracellular matrix in the pulmonary interalveolar space. Although the current anti-fibrotic therapy aims at slowing down the progression of pulmonary fibrosis, it does not reverse it, and many of the drugs that were identified in basic-research studies failed in clinical phases, mainly because of the lack of a model that can recapitulate the pathophysiological mechanisms of human pulmonary fibrosis. We developed a novel experimental model of pulmonary fibrosis induced by a cocktail of molecules on an air/liquid interface culture of mouse embryonic lung explants. Histological analyses revealed a pattern of usual interstitial pneumonia, the worst-prognosis form of pulmonary fibrosis. We performed a transcriptomics analysis at the single-cell level after the induction of fibrosis and before any histological signs of fibrosis could be observed. The results revealed increased expression of several gene families that are involved in early inflammation, fibrosis and iron homeostasis, as well as potential new genetic targets.</p> <p>This Zenodo repository includes original datasets of single cell RNA sequencing, analysis R scripts, final dataset/markers, and HTML codes for the interactive 3D UMAP and VolcanoPlot.</p>
The gut microbiota in chronic obstructive pulmonary disease varies by CT-verified emphysema status
<p><strong><span>Background and aim</span> </strong></p> <p><span>The association of the gut microbiota to </span><span>chronic obstructive pulmonary disease (COPD)</span><span> phenotypes is underexplored. We aimed to compare</span><span> stool samples from COPD patients and healthy controls and relate findings to common COPD phenotypes. </span></p> <p><strong><span>Methods</span></strong></p> <p><span>Single-centre case-control study with 62 current and former smoking COPD patients and 49 controls. DNA was extracted from stool samples, and the V3V4-region of the bacterial 16S-rRNA gene was sequenced. Emphysema was defined based on thoracic computed tomography (CT thorax) low attenuating areas ≥/<10% at threshold -950 and -910 Hounsfield units respectively. Microbial data were analysed with QIIME 2 and R.</span></p> <p><strong><span>Results</span></strong></p> <p><span>The genus Veillonella was decreased and a genus belonging to class Clostridia was increased in COPD compared to healthy controls. Beta diversity measure Bray Curtis differed in emphysema compared to controls, and 27 genera were differentially abundant in emphysema vs. controls. Nine of these genera belonged to the family Lachnospiraceae. Lung function, blood counts and COPD assessment test scores were correlated with the relative abundance of several genera. Some of the genera showing the strongest correlation to lung function belonged to the family Lachnospiraceae. </span></p> <p><strong><span>Conclusion</span></strong></p> <p><span>We found small but statistically significant differences in the gut microbiota of COPD versus controls. Larger differences were seen in the gut microbiota according to CT-verified emphysema status. Correlations between the gut microbiota and lung function, blood cell counts, and CAT score were found. </span></p>
Sildenafil for Chronic Obstructive Pulmonary Disease
ClinicalTrials.gov study NCT00104637. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Association Between Increased Oxidative Stress, Anti-Inflammatory Fatty Acid Formation, and Airway Infection in People With Asthma and Chronic Obstructive Pulmonary Disease
ClinicalTrials.gov study NCT00595114. IPD Sharing: Not stated. Countries: 1. Publications: 1.
24-week Trial Comparing GSK573719/GW642444 With GSK573719 and With Tiotropium in Chronic Obstructive Pulmonary Disease
ClinicalTrials.gov study NCT01316913. IPD Sharing: YES. Countries: 10. Publications: 2.
A 12-week Study to Evaluate the Efficacy and Safety of Umeclidinium Compared With Tiotropium in Subjects With Chronic Obstructive Pulmonary Disease
ClinicalTrials.gov study NCT02207829. IPD Sharing: YES. Countries: 13. Publications: 2.
Boston Early-Onset Chronic Obstructive Pulmonary Disease (COPD) Study
ClinicalTrials.gov study NCT01177618. IPD Sharing: YES. Countries: 1. Publications: 7.
Evaluate Onset of Effect in Patients With Chronic Obstructive Pulmonary Disease (COPD) Treated With Formoterol Turbuhaler®
ClinicalTrials.gov study NCT01048333. IPD Sharing: Not stated. Countries: 3. Publications: 1.
ScienceDex guides
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These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
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.