Dynamics of Exposure, Phthalates, and Asthma in a Randomized Trial (DEPART)
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo Sapiens
TISSUE(S): Urine
DISEASE(S): Environmental Exposure,Asthma
PROVIDER: ST001317 | MetabolomicsWorkbench |
REPOSITORIES: MetabolomicsWorkbench
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| mwtab | Other |
Items per page: 5 1 - 1 of 1 |
Similar Datasets
Project description:Asthma is a complex syndrome associated with episodic decompensations provoked by aeroaller-gen exposures. The underlying pathophysiological states driving exacerbations are latent in the resting state and do not adequately inform biomarker-driven therapy. A better understanding of the pathophysiological pathways driving allergic exacerbations is needed. We hypothesized that disease-associated pathways could be identified in humans by unbiased metabolomics of bron-choalveolar fluid (BALF) during the peak inflammatory response provoked by a bronchial aller-gen challenge. We analyzed BALF metabolites in samples from 12 volunteers who underwent segmental bronchial antigen provocation (SBP-Ag). Metabolites were quantified using liquid chromatography-tandem mass spectrometry (LC–MS/MS) followed by pathway analysis and cor-relation with airway inflammation. SBP-Ag induced statistically significant changes in 549 fea-tures that mapped to 72 uniquely identified metabolites. From these features, two distinct induci-ble metabolic phenotypes were identified by the principal component analysis, partitioning around medoids (PAM) and k-means clustering. Ten index metabolites were identified that in-formed the presence of asthma-relevant pathways, including unsaturated fatty acid produc-tion/metabolism, mitochondrial beta oxidation of unsaturated fatty acid, and bile acid metabolism. Pathways were validated using proteomics in eosinophils. A segmental bronchial allergen chal-lenge induces distinct metabolic responses in humans, providing insight into pathogenic and pro-tective endotypes in allergic asthma.
2022-06-09 | PXD033172 | Pride
Project description:We evaluated whether targeted next-generation sequencing (NGS) using the Ion Torrent Personal Genome Sequencer of cfDNA could identify prognostic or predictive factors for overall survival (OS) or progression free survival (PFS) within a large cohort of patients with advanced lung adenocarcinoma enrolled in the GALAXY-1 trial.
2018-01-10 | E-MTAB-5749 | biostudies-arrayexpress
Project description:OBJECTIVE:To provide a comprehensive overview of common school exposures and the association between school exposures and pediatric asthma morbidity. DATA SOURCES:A comprehensive literature review was performed using PubMed. STUDY SELECTIONS:Full-length, peer-reviewed studies published in English were considered for review. In vivo, in vitro, and animal studies were excluded. Studies of school exposure to cockroach, mouse, dust mite, dog, cat, molds, pollution, and endotoxin associated with asthma and asthma morbidity were considered. RESULTS:The current literature establishes an association between school exposure and pediatric asthma morbidity. There is a need for ongoing research to evaluate the effects of school-based environmental interventions on asthma morbidity. CONCLUSION:It is evident that the indoor school environment is a significant reservoir of allergens, molds, pollutants, and endotoxin and that there is an association between school exposure and pediatric asthma morbidity. School-based interventions have the potential for substantial individual, community, and public health benefit. It is important that researchers continue to study the health effects associated with school exposures and assess cost-effectiveness of multifaceted school-based interventions.
| S-EPMC5942597 | biostudies-literature
Project description:MicroRNAs are important negative regulators of protein coding gene expression, and have been studied intensively over the last few years. To this purpose, different measurement platforms to determine their RNA abundance levels in biological samples have been developed. In this study, we have systematically compared 12 commercially available microRNA expression platforms by measuring an identical set of 20 standardized positive and negative control samples, including human universal reference RNA, human brain RNA and titrations thereof, human serum samples, and synthetic spikes from homologous microRNA family members. We developed novel quality metrics in order to objectively assess platform performance of very different technologies such as small RNA sequencing, RT-qPCR and (microarray) hybridization. We assessed reproducibility, sensitivity, quantitative performance, and specificity. The results indicate that each method has its strengths and weaknesses, which helps guiding informed selection of a quantitative microRNA gene expression platform in function of particular study goals.
2013-09-01 | E-MTAB-1815 | biostudies-arrayexpress
Project description:BackgroundSecondhand tobacco smoke exposure impairs the control of pediatric asthma. Evidence of the efficacy of interventions to reduce children's exposure and improve disease outcomes has been inconclusive.MethodsCaregivers of 519 children aged 3 to 12 years with asthma and reported smoke exposure attended two baseline assessment visits, which involved a parent interview, sampling of the children's urine (for cotinine assay), and spirometry (children≥5 years). The caregivers and children (n=352) with significant documented exposure (cotinine≥10 ng/mL) attended a basic asthma education session, provided a third urine sample, and were randomized to the Lowering Environmental Tobacco Smoke: LET'S Manage Asthma (LET'S) intervention (n=178) or usual care (n=174). LET'S included three in-person, stage-of-change-based counseling sessions plus three follow-up phone calls. Cotinine feedback was given at each in-person session. Follow-up visits at 6 and 12 months postrandomization repeated the baseline data collection. Multivariate regression analyses estimated the intervention effect on the natural logarithm of the cotinine to creatinine ratio (lnCCR), use of health-care services, and other outcomes.ResultsIn the sample overall, the children in the LET'S intervention had lower follow-up lnCCR values compared with the children in usual care, but the group difference was not significant (β coefficient=-0.307, P=.064), and there was no group difference in the odds of having>one asthma-related medical visit (β coefficient=0.035, P=.78). However, children with high-risk asthma had statistically lower follow-up lnCCR values compared with children in usual care (β coefficient=-1.068, P=.006).ConclusionsThe LET'S intervention was not associated with a statistically significant reduction in tobacco smoke exposure or use of health-care services in the sample as a whole. However, it appeared effective in reducing exposure in children at high risk for subsequent exacerbations.Trial registryClinicialTrials.gov; No.: NCT00217958; URL: clinicaltrials.gov.
| S-EPMC3047287 | biostudies-literature
Project description:Alpha-amanitin (α-AMA) is a cyclic peptide and is one of the most lethal mushroom amatoxins found in Amanita phalloides. α-AMA is known to cause hepatotoxicity through RNA polymerase II inhibition, which acts in RNA and DNA translocation. To investigate the toxic signature of α-AMA beyond known mechanisms, we used quantitative nanoflow liquid chromatography-tandem mass spectrometry analysis coupled with tandem mass tag labeling to examine proteome dynamics in Huh-7 human hepatoma cells treated with toxic concentrations of α-AMA. We identified 1,828 proteins, quantified 1,563 proteins, and found a decrease of four subunits in T-complex protein 1-ring complex protein that was dependent on the α-AMA concentration. We conducted bioinformatics analyses of the quantified proteins to characterize the toxic signature of α-AMA in hepatoma cells. This is the first report of global proteome abundance changes according to α-AMA concentration variations and suggests a possible novel molecular regulation mechanism for hepatotoxicity.
2021-09-09 | PXD018702 | Pride
Project description:Although asthma mortality has been declining for the past several decades, asthma morbidity is on the rise, largely due to deteriorating indoor air quality and comorbidities, such as allergies. Consumer products and building materials including paints emit volatile organic compounds (VOCs), such as propylene glycol (PG), which is shown to dehydrate respiratory tracts and can contributor to airway remodeling. We hypothesize that paint exposure increases the risk of asthma attacks among children because high levels of VOCs persist indoors for many weeks after painting. Children 1-15 years old visiting two of the University of Miami general pediatric clinics were screened for their history of asthma and paint exposure by interviewing their parents and/or guardians accompanying them to the clinic. They were also asked questions about asthma diagnosis, severity of asthma and allergies and their sociodemographics. The risk of asthma attack among asthmatic children was modeled with respect to paint exposure adjusting for potential confounders using multivariate logistic regressions. Of 163 children, 36 (22%) reported physician-diagnosed asthma and of these, 13 (33%) had an asthma attack during the last one year. Paint exposure was marginally significant in the univariate analysis (OR = 4.04; 95% CI = 0.90-18.87; p < 0.1). However, exposed asthmatic children were 10 times more likely to experience an asthma attack than unexposed asthmatic children (OR = 10.49; CI = 1.16-94.85, p < 0.05) when adjusted for other risk factors. Given paint is one of the sources of indoor VOCs, multiple strategies are warranted to manage the health effects of VOC exposure from paint, including the use of zero-VOC water-based paint, exposure avoidance and clinical interventions.
| S-EPMC8069823 | biostudies-literature
Project description:RationaleSevere asthma is a public health problem with limited information regarding preventable causes. Although occupational exposures have been implicated as important risk factors for asthma and asthma exacerbations, associations between occupational exposures and asthma severity have not been reported.ObjectiveTo examine associations between occupational exposures and asthma severity.MethodsThe Epidemiological Study on the Genetics and Environment of Asthma combines a case-control study with a family study of relatives of patients with asthma. Adult patients (n = 148) were recruited in chest clinics and control subjects without asthma (n = 228) were population-based. Occupational exposures to nonasthmogenic irritants and asthmogens (classified as "any asthmogen" including three broad groups: high-molecular-weight agents, low-molecular-weight agents, and mixed environments) were assessed by an asthma-specific job exposure matrix. Asthma severity was defined from an 8-grade clinical score (frequency of attacks, persistent symptoms, and hospitalization). Patients with severe (score >or= 2) and mild asthma were compared with control subjects using nominal logistic regression.Main resultsSignificant associations were observed between severe adult-onset asthma and exposure to any occupational asthmogen (odds ratio [OR], 4.0; 95% confidence interval [CI], 2.0-8.1), high-molecular-weight agents (OR, 3.7; CI, 1.3-11.1), low-molecular-weight agents (OR, 4.4; CI, 1.9-10.1), including industrial cleaning agents (OR, 7.2; CI, 1.3-39.9), and mixed environments (OR, 7.5; CI, 2.4-23.5). No significant associations were found between nonasthmogenic irritants and asthma severity, nor between asthmogens and childhood-onset asthma or mild adult-onset asthma.ConclusionsOur results suggested a strong deleterious role of occupational asthmogens in severe asthma. Clinicians should consider occupational exposures in patients with moderate to severe asthma.
| S-EPMC4710786 | biostudies-literature
Project description: Not available
| S-EPMC7159436 | biostudies-literature
Project description:Genome-wide identification of transcription factor (TF) binding sites in the genome of the fission yeast Schizosaccharomyces pombe. The ChIP-nexus method was used. TFs included were: Cbf11-TAP and Cbf12-TAP (and their DBM mutants with impaired DNA binding), TAP-Mga2, and Fkh2-TAP (as an irrelevant control TF). IPs from an untagged WT strain were also analyzed. Cbf11-related IPs were performed from exponential cultures, while Cbf12-related IPs were performed from stationary cultures. YES complex medium was used for all cultivations.
2024-04-05 | E-MTAB-13258 | biostudies-arrayexpress