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.
Highly interconnected genes in disease-specific networks are enriched for disease-associated polymorphisms.
Specimen part, Subject
View SamplesIn this study, we evaluated global Mtb-induced gene expression in airway immune cells obtained by bronchoalveolar lavage of individuals with latent tuberculosis infection (LTBI) and in Mtb-naïve control subjects
<i>Mycobacterium tuberculosis</i>-Induced Bronchoalveolar Lavage Gene Expression Signature in Latent Tuberculosis Infection Is Dominated by Pleiotropic Effects of CD4<sup>+</sup> T Cell-Dependent IFN-γ Production despite the Presence of Polyfunctional T Cells within the Airways.
Specimen part, Disease
View SamplesAnalysis of GPR120 which play roles for the fatty acid sensor in adipose tissue. Results provide insight into the transcriptional effects caused by the loss of the GPR120 proteins and provide further insight into their functions.
Dysfunction of lipid sensor GPR120 leads to obesity in both mouse and human.
Specimen part, Treatment, Subject
View SamplesPurpose: 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.
Electrical stimulation modulates Wnt signaling and regulates genes for the motor endplate and calcium binding in muscle of rats with spinal cord transection.
Sex, Specimen part
View SamplesAim: 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
Limits of Peripheral Blood Mononuclear Cells for Gene Expression-Based Biomarkers in Juvenile Idiopathic Arthritis.
Specimen part, Disease stage, Subject
View SamplesAim: 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
Limits of Peripheral Blood Mononuclear Cells for Gene Expression-Based Biomarkers in Juvenile Idiopathic Arthritis.
Specimen part, Disease stage, Subject
View SamplesIn 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
Chromatin landscapes and genetic risk for juvenile idiopathic arthritis.
No sample metadata fields
View SamplesWe 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.
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.
No sample metadata fields
View SamplesTotal 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.
Disease-associated pathophysiologic structures in pediatric rheumatic diseases show characteristics of scale-free networks seen in physiologic systems: implications for pathogenesis and treatment.
No sample metadata fields
View SamplesSpinal 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.
The central nervous system (CNS)-independent anti-bone-resorptive activity of muscle contraction and the underlying molecular and cellular signatures.
Sex, Specimen part
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