Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17629929.fastq.gz | Fastqsanger.gz | |||
| SRR17629930.fastq.gz | Fastqsanger.gz | |||
| SRR17629931.fastq.gz | Fastqsanger.gz | |||
| SRR17629932.fastq.gz | Fastqsanger.gz | |||
| SRR17629933.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:To investigate the expression profiles of circRNAs in colon tissues of the patients with Crohn’s Disease(CD) , ulcerative colitis (UC) and healthy controls (HC), we used circRNA microArray analysis form Arraystar to examine the expression of circRNAs in colon tissues of CD,UC and HC.
2019-05-30 | GSE131911 | GEO
Project description:Activation of inflammatory pathways in human IBD. Leukocyte recruitment pathways including those for eosiniphils are activated in the affected colon in IBD. However, the functional implications of this are not known. We hypothesized that pro-inflammatory eotaxin (CCL11) dependent networks would be up regulated in the colon of pediatric patients with Ulcerative Colitis (UC), and that these would regulate eosinophil recruitment to the gut. These experiments tested differential colon gene expression relative to these pathways in healthy and UC samples. Colon biopsy samples were obtained from UC patients at diagnosis, and healthy controls. The global pattern of gene expression was determined using GeneSpring software, and biological networks were identified using Ingenuity software. Data suggested that a leukocyte recruitment network which includeds CCL11 is up regulated in pediatric UC at diagnosis. The degree of up regulation of these genes compared to healthy controls was remarkably conserved within the UC patient group, suggesting common mechanisms of mucosal inflammation. These experiments tested differential colon gene expression relative to these pathways in healthy and UC samples. Keywords: Single time point in UC and healthy controls. Colon RNA was isolated from biopsies obtained from UC at diagnosis and healthy controls. Samples were obtained from the most proximal affected segment of colon. Microarray experiments were performed as described in the CCHMC microarray core, and data was analyzed as described above in the summary. The '107' internal control CEL files (for batches 1,2,4,5) used for ormalization of the Sample VALUEs are also contained within this data set.
2010-05-15 | E-GEOD-10191 | biostudies-arrayexpress
Project description:Activation of inflammatory pathways in human IBD. Leukocyte recruitment pathways including those for eosiniphils are activated in the affected colon in IBD. However, the functional implications of this are not known. We hypothesized that pro-inflammatory eotaxin (CCL11) dependent networks would be up regulated in the colon of pediatric patients with Ulcerative Colitis (UC), and that these would regulate eosinophil recruitment to the gut. These experiments tested differential colon gene expression relative to these pathways in healthy and UC samples. Colon biopsy samples were obtained from UC patients at diagnosis, and healthy controls. The global pattern of gene expression was determined using GeneSpring software, and biological networks were identified using Ingenuity software. Data suggested that a leukocyte recruitment network which includeds CCL11 is up regulated in pediatric UC at diagnosis. The degree of up regulation of these genes compared to healthy controls was remarkably conserved within the UC patient group, suggesting common mechanisms of mucosal inflammation. These experiments tested differential colon gene expression relative to these pathways in healthy and UC samples. Keywords: Single time point in UC and healthy controls.
2008-12-22 | GSE10191 | GEO
Project description:Analysis of miRNA expression in colon biopsies from Crohn's disease (CD), ulcerative colitis (UC), and non-inflammatory bowel disease (IBD) control subjects.
2014-12-31 | GSE53867 | GEO
Project description:Activation of inflammatory pathways in human IBD IL-6:STAT3 pathways are activated in the affected colon in IBD. However, the functional implications of this are not known. We hypothesized that pro-inflammatory IL-6:STAT3 dependent networks would be up regulated in the colon of pediatric patients with Crohn Disease (CD) and Ulcerative Colitis (UC), and that these would regulate leukocyte survival, proliferation, and recruitment to the gut. These experiments tested differential colon gene expression relative to these pathways in healthy, CD, and UC samples. Colon biopsy samples were obtained from CD and UC patients at diagnosis, CD patients during therapy, and healthy controls. The global pattern of gene expression was determined using GeneSpring software, and biological networks were identified using Ingenuity software. Data suggested that two IL-6:STAT3 dependent networks are up regulated in pediatric IBD both at diagnosis and during therapy which regulate leukocyte recruitment and survival. The degree of up regulation of these genes compared to healthy controls was remarkably conserved across the two CD groups and the UC groups, suggesting common mechanisms of mucosal inflammation. Colon RNA was isolated from biopsies obtained from CD at diagnosis and during therapy, UC at diagnosis, and healthy controls. Samples were obtained from the most proximal affected segment of colon. Microarray experiments were performed as described in the CCHMC microarray core, and data was analyzed as described above in the summary. The '107' internal control CEL files (for batches 1-4) used for normalization of the Sample VALUEs are linked below as supplementary files.
2010-05-27 | E-GEOD-9686 | biostudies-arrayexpress
Project description:Metastatic urothelial carcinoma (UC) of the bladder is associated with multiple somatic copy number alterations (SCNAs). We evaluated SCNAs to identify predictors of poor survival in patients with metastatic UC treated with platinum chemotherapy. We obtained overall survival (OS) and DNA copy number data from UC patients in a Spanish discovery cohort and three validation cohorts. GISTIC was used to identify altered regions, and associations between copy number gains/losses and OS were determined by a Cox proportional hazard model adjusting for performance status and visceral disease The output files of the GISTIC 2.0 software are linked as supplementary files on Series record along with readme.txt file describing the contents of each file/column.
2013-07-07 | E-GEOD-39280 | biostudies-arrayexpress
Project description:Metastatic urothelial carcinoma (UC) of the bladder is associated with multiple somatic copy number alterations (SCNAs). We evaluated SCNAs to identify predictors of poor survival in patients with metastatic UC treated with platinum chemotherapy. We obtained overall survival (OS) and DNA copy number data from UC patients in a Spanish discovery cohort and three validation cohorts. GISTIC was used to identify altered regions, and associations between copy number gains/losses and OS were determined by a Cox proportional hazard model adjusting for performance status and visceral disease The output files of the GISTIC 2.0 software are linked as supplementary files on Series record along with readme.txt file describing the contents of each file/column.
2013-07-07 | E-GEOD-39281 | biostudies-arrayexpress
Project description:BACKGROUND & AIMS: Ulcerative colitis (UC) is an inflammatory bowel disorder with unknown etiology, and given its complex nature, an in vivo model to study its pathophysiology is vital. Animal models play an important role in molecular profiling necessary to pinpoint mechanisms that contribute to human disease. Thus, we aim to identify common conserved gene expression signatures and differentially regulated pathways between human UC and a mouse model hereof, which can be used to identify UC patients from healthy individuals and to suggest novel treatment targets and biomarker candidates. METHODS: Therefore, we performed high-throughput total and small RNA sequencing to comprehensively characterize the transcriptome landscape of the most widely used UC mouse model, the dextran sodium sulfate (DSS) model. We used this data in conjunction with publicly available human UC transcriptome data to compare gene expression profiles and pathways. RESULTS: We identified differentially regulated protein-coding genes, long non-coding RNAs and microRNAs from colon and whole blood of UC mice and further characterized the involved pathways and biological processes through which these genes may contribute to disease development and progression. By integrating human and mouse UC datasets, we suggest a set of 51 differentially regulated genes in UC colon and blood that may improve molecular phenotyping, as well as aid in treatment decisions, drug discovery and the design of clinical trials. CONCLUSION: Global transcriptome analysis of the DSS-UC mouse model supports its use as an efficient high-throughput tool to discover new targets for therapeutic and diagnostic applications in human UC through identifying relationships between gene expression and disease phenotype.
2021-03-13 | GSE155302 | GEO