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accession-icon GSE29652
Microarray analysis of the astrocyte transcriptome in the ageing brain: relationship to Alzheimer's pathology and ApoE genotype
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Astrocyte dysfunction impacts their normal function, including neuronal support, thereby contributing to neurodegenerative pathologies including Alzheimer's disease (AD). Therefore to understand the role of astrocytes in the pathogenesis of age-related disorders we analysed the gene expression profile of astrocytes with respect to Alzheimer-type pathology.

Publication Title

Microarray analysis of the astrocyte transcriptome in the aging brain: relationship to Alzheimer's pathology and APOE genotype.

Alternate Accession IDs

E-GEOD-29652

Sample Metadata Fields

Specimen part

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accession-icon GSE66333
Neuronal DNA damage response-associated dysregulation of signalling pathways and cholesterol metabolism at th earliest stages of Alzheimer-type pathology
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

High levels of oxidative stress and an associated neuronal DDR occur at the earliest stages of Alzheimer pathology (low Braak stage), and is associated with cognitive impairment.

Publication Title

Neuronal DNA damage response-associated dysregulation of signalling pathways and cholesterol metabolism at the earliest stages of Alzheimer-type pathology.

Alternate Accession IDs

E-GEOD-66333

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE31622
Gene expression data from WT and Klf3 KO mouse CD19+ splenic B cells
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

To investigate the roles of Klf3 in B lymphopoiesis, CD19+ B cells were sorted from the spleens of WT and Klf3 KO mice (Molecular and Cellular Biology (2008); 28:39673978).

Publication Title

Impaired B cell development in the absence of Krüppel-like factor 3.

Alternate Accession IDs

E-GEOD-31622

Sample Metadata Fields

Specimen part

View Samples
accession-icon SRP090108
RNA Sequencing Quantitative Analysis of RNA editing sites of Wild Type and ADAR1 editing deficient (ADAR1E861A) murine fetal RNA of various tissues
  • organism-icon Mus musculus
  • sample-icon 43 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The Adar1 deaminase inactive mutant mouse tissue samples were obtain from the Walkley lab as described in http://www.ncbi.nlm.nih.gov/pubmed/26275108. We performed mmPCR-seq on the samples and measured the editing levels of. Overall design: Fetal mRNA profiles of E12.5 wild type (WT) and ADAR E861A mutant mice were generated by deep sequencing using Illumina HiSeq 2000.

Publication Title

Dynamic landscape and regulation of RNA editing in mammals.

Alternate Accession IDs

GSE87068

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE37025
Interleukin-1 receptor antagonist for recent-onset type 1 diabeties mellitus: a multicenter randomized, placebo-controlled trial
  • organism-icon Homo sapiens
  • sample-icon 228 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Background: Blocking the action of the pro-inflammatory cytokine interleukin-1 (IL-1) reduces beta-cell secretory dysfunction and apoptosis in vitro, diabetes incidence in animal models of Type 1 diabetes mellitus (T1D), and glycaemia via improved beta-cell function in patients with T2D. We hypothesised that anakinra, a recombinant human IL-1 receptor antagonist, improves beta-cell function in patients with new-onset T1D. Methods: In an individually randomised, two-group parallel trial involving 14 European tertiary referral centers, 69 patients aged 18-35 with T1D, < 12 weeks of symptoms, and standard mixed meal test (MMT) stimulated C-peptide 200 pM were enrolled between January, 2009 and July, 2011 and assigned by centralised computer-generated blocked randomisation with locked computer-file concealment to treatment with 100 mg anakinra (n=35) subcutaneously once daily or placebo (n=34) for 9 months as add-on to conventional therapy. Participants and care-givers, but not data monitoring unit, were masked to group assignment. The primary end-point was change in the two-hour area-under-the-curve C-peptide response to MMT, and secondary end-points changes in insulin requirements, glycaemia, and inflammatory markers at one, three, six, and nine months. Findings: The study was prematurely terminated due to slow accrual and is closed to follow-up. No interim analysis was performed. Ten patients withdrew in the anakinra and eight in the placebo arm, leaving 25 and 26 patients to be analysed, respectively. There was no statistical difference in adverse event category reporting between arms. Interpretation: Anakinra-treatment in T1D was safe, but the trial failed to meet primary and secondary outcome measures.

Publication Title

Interleukin-1 antagonism moderates the inflammatory state associated with Type 1 diabetes during clinical trials conducted at disease onset.

Alternate Accession IDs

E-GEOD-37025

Sample Metadata Fields

Subject, Time

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accession-icon GSE68049
Canakinumab treatment for recent-onset type 1 diabeties mellitus: a multicenter randomized, placebo-controlled trial
  • organism-icon Homo sapiens
  • sample-icon 187 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Background: Blocking the action of the pro-inflammatory cytokine interleukin-1 (IL-1) reduces beta-cell secretory dysfunction and apoptosis in vitro, diabetes incidence in animal models of Type 1 diabetes mellitus (T1D), and glycaemia via improved beta-cell function in patients with T2D. We hypothesised that canakinumab, a monoclonal antibody to IL-1B, improves beta-cell function in patients with new-onset T1D. Methods: In an individually randomised, two-group parallel trial involving 12 sites in US, 69 patients aged 6-45 with T1D, < 12 weeks of symptoms, and assigned by centralised computer-generated blocked randomisation with locked computer-file concealment to treatment with 2 mg/kg (maximum 300 mg) canakinumab (n=45) or placebo (n=22) monthly for 12 months as add-on to conventional therapy. Participants and care-givers, but not data monitoring unit, were masked to group assignment. The primary end-point was change in the two-hour area-under-the-curve C-peptide response to MMT 12 months.

Publication Title

Interleukin-1 antagonism moderates the inflammatory state associated with Type 1 diabetes during clinical trials conducted at disease onset.

Alternate Accession IDs

E-GEOD-68049

Sample Metadata Fields

Subject, Time

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accession-icon GSE7440
Early Response and Outcome in High-Risk Childhood Acute Lymphoblastic Leukemia: A Childrens Oncology Group Study
  • organism-icon Homo sapiens
  • sample-icon 96 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The cure rate for childhood ALL has improved considerably in part because therapy is routinely tailored to the predicted risk of relapse. Various clinical and laboratory variables are used in current risk-stratification schemes, but many children who fail therapy lack adverse prognostic factors at initial diagnosis. Using gene expression analysis, we have identified genes and pathways in a NCI high-risk childhood B-precursor ALL cohort at diagnosis that may play a role in early blast regression as correlated with the Day 7 marrow status. We have also identified a 47-probeset signature (representing 41 unique genes) that was predictive of long term outcome in our dataset as well as three large independent datasets of childhood ALL treated on different protocols.

Publication Title

Gene expression signatures predictive of early response and outcome in high-risk childhood acute lymphoblastic leukemia: A Children's Oncology Group Study [corrected].

Alternate Accession IDs

E-GEOD-7440

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE141381
Siponimod selectively enriched regulatory T and B lymphocytes in active secondary progressive multiple sclerosis patients
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.1 ST Array (hugene21st)

Description

Siponimod selectively enriched regulatory T and B lymphocytes in active secondary progressive multiple sclerosis patients: 20 SPMS baseline including 3 repeats, 19 treated with 5 placebo and 14 siponimod treated.

Publication Title

Siponimod enriches regulatory T and B lymphocytes in secondary progressive multiple sclerosis.

Alternate Accession IDs

E-GEOD-141381

Sample Metadata Fields

Sex, Age, Treatment

View Samples
accession-icon GSE53473
Standard of hygiene and immune adaptation in newborn infants
  • organism-icon Homo sapiens
  • sample-icon 128 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U219 Array (hgu219)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Standard of hygiene and immune adaptation in newborn infants.

Alternate Accession IDs

E-GEOD-53473

Sample Metadata Fields

Sex

View Samples
accession-icon GSE53471
Standard of hygiene and immune adaptation in newborn infants [113 cord blood RNA samples]
  • organism-icon Homo sapiens
  • sample-icon 113 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U219 Array (hgu219)

Description

The prevalence of immune-mediated diseases such as allergies and autoimmune diseases is on the rise in the developed world. Microbial exposure is known to modulate the risk for these diseases. In order to explore differences in the gene expression patterns induced in utero in infants born in contrasting standards of living and hygiene, we collected umbilical cord blood RNA samples from full-term newborn infants born with normal vaginal delivery in Finland (modern society), Estonia (rapidly developing society) and the Republic of Karelia, Russia (poor economical conditions). Transcriptomic profiles were analyzed using whole genome microarrays including gender, gestational age, birth month and HLA allele genotype as confounding variables in the analysis. The data revealed that the whole blood transcriptome of Finnish and Estonian neonates differ from their Karelian counterparts. Samples from Karelian infants had an increase in transcripts associated with LPS induction and bacterial sepsis observed in 1-year-old infants in earlier studies. The results suggest exposure to toll like receptor (TLR) ligands and a more matured immune response in infants born in Petrozavodsk compared to the Finnish and Estonian infants. These results further support the concept of a conspicuous plasticity in the developing immune system: the environmental factors that play a role in the susceptibility/protection towards immune-mediated diseases begin to shape the neonatal immunity already in utero and direct the maturation of both the adaptive and the innate immune responses in accordance with the surrounding microbial milieu.

Publication Title

Standard of hygiene and immune adaptation in newborn infants.

Alternate Accession IDs

E-GEOD-53471

Sample Metadata Fields

Sex

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Developed by the Childhood Cancer Data Lab

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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