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GSE37476
Rattus norvegicus
33 Downloadable Samples
Affymetrix Rat Gene 1.0 ST Array (ragene10st)
Description
Purpose: The goal of this study was to determine the gene expression changes that occur over 7 days in parralyzed muscle in response to isometric contraction elicited by electrical stimulation initiated 4 months after spinal cord injury and to compare such changes to those observed in a normal muscle subjected to overload.
Publication Title
Electrical stimulation modulates Wnt signaling and regulates genes for the motor endplate and calcium binding in muscle of rats with spinal cord transection.
Sample Metadata Fields
Sex, Specimen part
View Samples- Homo sapiens
- 90 Downloadable Samples
Illumina HiSeq 2500
Description
Aim: To discovery biomarkers in JIA base on gene expression from RNA sequencing on PBMC Method: Paired-end Ilumina sequencing to capture gene expression of PBMC from JIA individuals and healthy controls Results:sample heterogeneity makes RNA sequencing on PBMC unsuitable as a first-step method for screening biomarker candidates in JIA Overall design: RNA sequencing on PBMC of 3 independent cohorts consist of JIA patients and healthy controls
Publication Title
Limits of Peripheral Blood Mononuclear Cells for Gene Expression-Based Biomarkers in Juvenile Idiopathic Arthritis.
Sample Metadata Fields
Specimen part, Disease stage, Subject
View Samples- Homo sapiens
- 21 Downloadable Samples
- Illumina HiSeq 2500
Description
Aim: To discovery biomarkers in JIA base on gene expression from RNA sequencing on CD4+ T Cells Method: Paired-end Ilumina sequencing to capture gene expression of CD4+ T cells from JIA individuals with active disease and patients in clinical remission on medication. Overall design: RNA sequencing on CD4+T cells consist of JIA patients
Publication Title
Limits of Peripheral Blood Mononuclear Cells for Gene Expression-Based Biomarkers in Juvenile Idiopathic Arthritis.
Sample Metadata Fields
Specimen part, Disease stage, Subject
View Samples- Homo sapiens
- 8 Downloadable Samples
- Illumina HiSeq 2000
Description
In this study, we explored transcriptional complexity in human neutrophils from juvenile idiopathis arthritis and healthy control. We obtained differentially expressed genes among 3 ADU (active disease, untreated), 3 ADT (active disease, treated) and 2 HC (healthy control) samples using Cuffdiff2 software. Overall design: 3 ADU (active disease, untreated), 3 ADT (active disease, treated) and 2 HC (healthy control) samples were carried out RNA-Seq by next-generation sequencing strategy
Publication Title
Chromatin landscapes and genetic risk for juvenile idiopathic arthritis.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 3 Downloadable Samples
- IlluminaHiSeq2500
Description
We sequenced mRNA from 3 neutrophil cells taken from 3 male adult to generate the gene expression profile of human neutrophil cells Overall design: Examination of mRNA levels in human neutrophils.
Publication Title
Disease-Associated Single-Nucleotide Polymorphisms From Noncoding Regions in Juvenile Idiopathic Arthritis Are Located Within or Adjacent to Functional Genomic Elements of Human Neutrophils and CD4+ T Cells.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 80 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Total RNA from peripheral blood mononuclear cells (PBMC) and neutrophils from children with juvenile dermatomyositis (JDM) and juvenile idiopathic arthritis (JIA) were separately compared to pediatric control samples.
Publication Title
Disease-associated pathophysiologic structures in pediatric rheumatic diseases show characteristics of scale-free networks seen in physiologic systems: implications for pathogenesis and treatment.
Sample Metadata Fields
No sample metadata fields
View Samples- Rattus norvegicus
- 12 Downloadable Samples
- Illumina ratRef-12 v1.0 expression beadchip
Description
Spinal cord injury (SCI) causes severe bone loss and disrupts connections between higher centers in the central nervous system (CNS) and bone. Muscle contraction elicited by functional electrical stimulation (FES) partially protects against loss of bone but cellular and molecular events by which this occurs are unknown. Here, using a rat model, we characterized effects of 7 days of contraction-induced loading of tibia and fibula due to FES when begun 16 weeks after SCI. SCI reduced tibial and femoral BMD by 12-17% and promoted bone resorption, as indicated by increased serum CTX; SCI-related changes in CTX were reversed by FES. In cultures of bone marrow cell-derived cells, SCI increased the number of osteoclasts and mRNA levels of the several osteoclast differentiation markers; these changes were significantly reversed by FES. The number of osteoblasts was also reduced by SCI as was the ratio of OPG/RANKL mRNAs therein; the unfavorable change in OPG/RANKL ratio was partially reversed by FES. cDNA microarray analysis revealed that alterations in genes involved in signaling through Wnt, FSH/LH, PTH and calcineurin/NFAT pathways may be linked to the favorable action of FES on SCI-induced bone resorption. In particular, SCI increased levels of the Wnt inhibitors DKK1, sFRP2 and SOST in osteoblasts, These effects were completely or partially reversed by FES. Our results demonstrate an anti-bone resorptive activity of acute FES in bone loss after SCI and suggest potential underlying mechanisms, among them involving increased Wnt signaling to cause more favorable ratios of OPG and RANKL for the inhibition of osteoclastogenesis. The present study indicates that the effects of bone reloading on SCI- related bone remodeling occurred independently of the effects of higher CNS centers on bone.
Publication Title
The central nervous system (CNS)-independent anti-bone-resorptive activity of muscle contraction and the underlying molecular and cellular signatures.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 23 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
As a critical cellular stress sensor, p53 mediates a variety of defensive processes including cell-cycle arrest, apoptosis, and senescence to prevent propagation of hyperproliferative cells or cells with a damaged genome, hence the formation of neoplasia. Transactivation of downstream genes plays an important while sometimes controversial role in regulating these cellular processes. To evaluate the dependence on transcriptional activation in p53s activities, we generated genetically-modified mouse lines carrying mutations in the transactivation domains (TADs) of p53. These transactivatio-deficient mutants serve as unique reagents to probe the dependence on robust transactivation in p53-mediated cellular functions, as well as the underneath mechanisms. To identify genes differentially regulated by these p53 mutants, we performed gene expression profiling analysis on mouse embryonic fibroblast cells (MEFs) from these mice in the context of oncogenic Ras-induced premature cellular senescence.
Publication Title
Distinct p53 transcriptional programs dictate acute DNA-damage responses and tumor suppression.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 39 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Identify biomarkers to predict response to therapy in polyarticular juvenile idiopathic arthritis (JIA) using gene expression microarrays.
Publication Title
The meaning of clinical remission in polyarticular juvenile idiopathic arthritis: gene expression profiling in peripheral blood mononuclear cells identifies distinct disease states.
Sample Metadata Fields
Specimen part, Disease, Disease stage
View Samples- Homo sapiens
- 6 Downloadable Samples
- Sentrix Human-6 Expression BeadChip
Description
Seasonal allergic rhinitis (SAR) is a complex disease that is caused by many interacting genes and environmental factors. It is also an excellent model disease for clinical studies; it is common, it is seasonal, and since it takes place in the nasal cavity it can be studied in vivo non-invasively. Furthermore, the key disease cell, the Th2 cell is known. We study SAR using allergen-challenged CD4+ cells from allergic patients.
Publication Title
Highly interconnected genes in disease-specific networks are enriched for disease-associated polymorphisms.
Sample Metadata Fields
Specimen part, Subject
View Samples