E-MTAB-1425
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: EGAD00010000383EGAC00000000014EGAS00000000137EGAD00010000385EGAD00010000381EGAO00000000131EGAO00000000110
PROVIDER: E-MTAB-1425 | ExpressionAtlas | 2025-01-23
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-MTAB-1425-analysis-methods.tsv | Tabular | |||
| E-MTAB-1425-atlasExperimentSummary.Rdata | Rdata | |||
| E-MTAB-1425-configuration.xml | Xml | |||
| E-MTAB-1425-configuration.xml.beforeQC | Xml | |||
| E-MTAB-1425-percentile-ranks.tsv | Tabular |
Items per page: 5 1 - 5 of 56 |
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Project description:We have created a global map of the effects of polymorphism on gene expression in 400 children from families recruited through a proband with asthma. We genotyped 408,273 SNPs and identified expression quantitative trait loci from measurements of 54,675 transcripts representing 20,599 genes in Epstein-Barr virusﾡﾧCtransformed lymphoblastoid cell lines. We executed genome-wide association scans for these traits.
2013-01-09 | E-MTAB-1425 | biostudies-arrayexpress
Project description:Asthma is caused by a combination of poorly understood genetic and environmental factors. We found multiple markers on chromosome 17q21 to be strongly and reproducibly associated with childhood onset asthma in family and case-referent panels with a combined P < 10-12. In independent replication studies the 17q21 locus showed strong association with diagnosis of childhood asthma in 2,320 subjects from a cohort of German children (P = 0.0003) and in 3,301 subjects from the British 1958 Birth Cohort (P = 0.0005). We systematically evaluated the relationships between markers of the 17q21 locus and transcript levels of genes in EBV-transformed lymphoblastoid cell lines from children in the asthma family panel used in our association study. The SNPs associated with childhood asthma were consistently and strongly associated (P <10-22) in cis with transcript levels of ORMDL3, a member of a gene family that encode transmembrane proteins anchored in the endoplasmic reticulum. The results indicate that genetic variants regulating ORMDL3 expression are determinants of susceptibility to childhood asthma. Experiment Overall Design: Gene expression levels were evaluated in 404 children. We then evaluated the relationship between SNPs in the 17q21 region (which show association to asthma in the same children) with gene expression levels. See http://www.sph.umich.edu/csg/liang/asthma/
2007-11-09 | E-GEOD-8052 | biostudies-arrayexpress
Project description:We determined whether we could identify clusters of children with critical asthma by plasma cytokine concentration. Differences in gene expression between the two clusters were analyzed using a targeted Nanostring immunology array. We performed a single-center, prospective, observational cohort study of 64 children ages 6 – 17 years admitted to a pediatric intensive care unit for an asthma attack between July 2019 to February 2021.
2022-07-15 | GSE208220 | GEO
Project description:Obesity is a risk factor for asthma severity and morbidity, displaying a distinct clinical phenotype that is less responsive to inhaled corticosteroids. CD4+ T-cells are central to the immunologic pathways of asthma and may contribute to the unique obese asthma phenotype. We sought to characterize the single cell CD4+ transcriptional profile among obese children with asthma compared to matched normal weight children with asthma.
2025-05-01 | GSE230024 | GEO
Project description:Background: Asthma is highly heterogeneous and severity evaluation is key to asthma management. DNA methylation (DNAm) contributes to asthma pathogenesis. This study aimed to identify nasal epithelial DNAm differences between severe and non-severe asthmatic children and evaluate the impact of environmental exposures. Methods: Thirty-three non-severe and 22 severe asthmatic African-American children were included in an epigenome-wide association study. Genome-wide nasal epithelial DNAm and gene expression were measured. CpG sites associated with asthma severity and environmental exposures and predictive of severe asthma were identified. DNAm was correlated with gene expression. Enrichment for transcription factor (TF) binding sites or histone modifications surrounding DNAm differences were determined. Results: We identified 816 differentially methylated CpG positions (DMPs) and 10 differentially methylated regions (DMRs) associated with asthma severity. Three DMPs exhibited discriminatory ability for severe asthma. Intriguingly, six DMPs were simultaneously associated with asthma, allergic asthma, total IgE, environmental IgE, and FeNO in an independent cohort of children. 27 DMPs were associated with traffic-related air pollution or secondhand smoke. DNAm at 22 DMPs were altered by diesel particles or allergen in human bronchial epithelial cells. DNAm levels at 39 DMPs were correlated with mRNA expression. Proximal to 816 DMPs, three histone marks and several TFs involved in asthma pathogenesis were enriched. Conclusions: Significant differences in nasal epithelial DNAm were observed between non-severe and severe asthma in African-American children, a subset of which may be useful to predict disease severity. These CpG sites are subject to the influences of environmental exposures and may regulate gene expression.
2022-04-15 | GSE161485 | GEO
Project description:CGH array for human cell lines
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Project description:Background: Around 5% of children with asthma suffer from chronic symptoms and/or severe exacerbations despite extensive treatment. The causes of severe therapy-resistant childhood asthma are poorly understood. Objectives: To define global patterns of gene expression in severe therapy-resistant vs. controlled asthma and healthy controls. Methods: Children with severe, therapy-resistant (SA, n=20) and controlled asthma (CA, n=20) were identified from a Swedish nation-wide study including extensive clinical and immunological characterisation. In addition, healthy controls were recruited (Ctrl, n=19). White blood cells were isolated and the global transcriptome profile was characterised using the Affymetrix Human Gene ST 1.0 chip. Results: 1378 genes were differentially expressed in one or several of the CA vs. Ctrl, SA vs. CA or SA vs. Ctrl contrasts. A large number could uniquely differentiate the SA group from the CA (n=351 genes) and Ctrl (n=315) groups, whereas fewer genes differentiated the CA from the Ctrl group (n=149). Several non-coding RNAs were found up-regulated in SA compared to CA or Ctrl. Three significantly enriched KEGG pathways were represented; bitter taste transduction, TAS2Rs (up-regulated mostly in SA), natural killer cell mediated cytotoxicity (up-regulated in CA) and N-Glycan biosynthesis (down-regulated in SA). An unsupervised hierarchical clustering of the 1378 genes could crudely separate the SA, CA and Ctrl individuals. Conclusion: Our data indicate a separation in gene expression patterns between children with severe, therapy-resistant asthma and controlled persistent asthma, and suggest novel pathways characterizing the severe therapy-resistant asthma phenotype. The transcriptomes of 59 subjects were assayed on the Affymetrix Human Gene ST 1.0 expression array. All samples passed pre-hybridisation quality control. After pre-processing and quality control of the post-hybridised arrays, five samples were regarded as outliers and removed (ctrl 510, MA 248, SA 141, SA 261, SA 41). The remaining sample set of 17 severe asthmatics (SA), 19 mild asthmatics (MA) and 18 controls (ctrl) were used for down-stream analysis.
2011-12-01 | E-GEOD-27011 | biostudies-arrayexpress
Project description:Asthma and postinfectious bronchiolitis obliterans (PIBO) are chronic lung diseases characterized by recurrent episodes of wheezing. Mycoplasma, adenovirus, and respiratory syncytial virus infections can trigger both asthma and PIBO. These two diseases have common etiologic mechanisms that cause airway epithelial injury. They are often difficult to differentiate clinically in preschool children because both are exacerbated by viral infections and respond similarly to steroids and β2 agonists. PIBO, which is occasionally observed in children, is diagnosed through characteristic findings of air trapping on computed tomography or in biopsy samples of lung tissue. However, researchers have not clearly identified the specific blood markers that can distinguish these diseases or the differences in the mechanisms of development. We performed proteomic analysis of plasma to identify specific biomarkers that can be helpful in differentiating asthma from PIBO. This study discovered plasma biomarker candidates by measuring plasma proteome sequential window acquisition of all theoretical mass spectra (SWATH-MS) and included 30 healthy children, 18 with asthma and 15 with PIBO. was used to measure proteins in plasma samples. We identified and quantified 354 proteins across all 63 samples in the SWATH-MS analysis.
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Project description:Asthma is caused by a combination of poorly understood genetic and environmental factors. We found multiple markers on chromosome 17q21 to be strongly and reproducibly associated with childhood onset asthma in family and case-referent panels with a combined P < 10-12. In independent replication studies the 17q21 locus showed strong association with diagnosis of childhood asthma in 2,320 subjects from a cohort of German children (P = 0.0003) and in 3,301 subjects from the British 1958 Birth Cohort (P = 0.0005). We systematically evaluated the relationships between markers of the 17q21 locus and transcript levels of genes in EBV-transformed lymphoblastoid cell lines from children in the asthma family panel used in our association study. The SNPs associated with childhood asthma were consistently and strongly associated (P <10-22) in cis with transcript levels of ORMDL3, a member of a gene family that encode transmembrane proteins anchored in the endoplasmic reticulum. The results indicate that genetic variants regulating ORMDL3 expression are determinants of susceptibility to childhood asthma. Keywords: association study, global gene expression, asthma, ORMDL3
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