Rotavirus infection is the single most important cause of severe diarrhea in young children worldwide. We used Affymetrix Human U95Av2 high density oligonucleotide arrays to compare gene expression profiles in peripheral blood mononuclear cells (PBMC) of 10 children with acute rotavirus diarrhea and 8 age-matched healthy children. We also examined patterns of gene expression in 5 convalescent-phase PBMC samples from rotavirus patients. For data analysis, we imported .cel files generated by Affymetrix MAS5.0 into Genetraffic 3.1 software (Iobion) and performed robust multi-chip analysis. We considered a gene in patients differentially expressed if its level of expression was at least 1.5-fold higher or lower than the baseline (arithmetic mean) of the corresponding gene in 8 controls and if its pattern of elevated or repressed expression was observed in at least 7 of the 10 patients. Using these criteria, we identified ~1% up- and ~2% down-regulated genes in acute-phase PBMC of patients. Up-regulated genes included those involved in the differentiation, maturation, activation, and survival of B cells, as well as an array of genes with function in inflammatory and antiviral activities. We observed a pattern of repressed expression of a number of genes involved in the various stages of T-cell development and activation. On the basis of these results, we conclude that rotavirus infection induces robust inflammatory response and B-cell activation but represses T-cell response.
Rotavirus infection alters peripheral T-cell homeostasis in children with acute diarrhea.
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View Samples-chloroprene (2-chloro-1,3-butadiene), a monomer used in the production of neoprene elastomers, is of regulatory interest due to the production of multi-organ tumors in mouse and rat cancer bioassays. A significant increase in female mouse lung tumors was observed at the lowest exposure concentration of 12.8 ppm while a small, but not statistically significant, increase was observed in female rats only at the highest exposure concentration of 80 ppm. The metabolism of chloroprene results in the generation of reactive epoxides and the rate of overall chloroprene metabolism is highly species dependent. To identify potential key events in the mode-of-action of chloroprene lung tumorigenesis, dose response and time course gene expression microarray measurements were made in the lungs of female mice and female rats. The gene expression changes were analyzed using both a traditional analysis of variance approach followed by pathway enrichment analysis and a pathway-based benchmark dose (BMD) analysis approach. Pathways related to glutathione biosynthesis and metabolism were the primary pathways consistent with cross-species differences in tumor incidence and transcriptional BMD values for the pathway were more similar to differences in tumor response than were estimated target tissue dose surrogates based on the total amount of chloroprene metabolized per unit mass of lung tissue per day. The closer correspondence of the transcriptional changes with the tumor response are likely due to their reflection of the overall balance between metabolic activation and detoxication reactions whereas the current tissue dose surrogate reflects only oxidative metabolism.
Cross-species transcriptomic analysis of mouse and rat lung exposed to chloroprene.
Sex, Age, Specimen part, Subject
View SamplesExposure to vanadium pentoxide (V2O5) is a cause of occupational bronchitis. We evaluated gene expression profiles in cultured human lung fibroblasts exposed to V2O5 in vitro in order to identify candidate genes that could play a role in airway remodeling associated with V2O5-induced bronchitis. Gene expression was measured at various time points over a 24 hr period using the Affymetrix Human Genome U133A 2.0 Array. Expression data were preprocessed using RMA with a log2 transformation. Statistical analysis was performed in R using the affylmGUI package using a linear model with contrasts between untreated control and V2O5-exposed fibroblasts. Genes identified as statistically significant were filtered by selecting only those genes that exhibited a > 2-fold change. Quantitative real-time RT-PCR was utilized to confirm expression of selected genes. More than 2000 genes were significantly changed in response to V2O5 over the time course of our experiment. Genes altered by V2O5 were involved in biologic processes related to cell growth and differentiation, oxidative stress responses, immune regulation, and interferon signaling and apoptosis. In particular, V2O5 induced genes that encode growth factors involved in epithelial repair (HB-EGF) or angiogenesis (VEGF), peroxide generating enzymes (SOD2), pro-inflammatory enzymes (PGHS2), while suppressing genes involved in growth arrest (GAS1, STAT-1) and cell cycle inhibition (CDKN1B). Our study also identified a variety of novel genes that could be used as biomarkers of V2O5-induced bronchitis or could serve as candidate genes for disease progression.
Genomic analysis of human lung fibroblasts exposed to vanadium pentoxide to identify candidate genes for occupational bronchitis.
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View SamplesProvided later
No associated publication
Sex, Age, Disease, Disease stage
View SamplesGene expression analysis in cattle embryos derived from mtDNA depleted cells in the presence and absence of Trichostatin A
No associated publication
Sex, Specimen part
View SamplesHepatitis E virus (HEV) is an important causative pathogen of acute hepatitis. Because of the absence of an in vitro culture system for HEV, research has been greatly impeded. And interaction between HEV and host cells was mainly studied by tansfection/transinfection system, such as Adeno virus transinfection system. We developed an in vitro culture system for HEV in PLC/PRF/5 cells. With this in vitro culture system, we studied the gene expression profile change by HEV infection.
Hepatitis E genotype 4 virus from feces of monkeys infected experimentally can be cultured in PLC/PRF/5 cells and upregulate host interferon-inducible genes.
Cell line, Treatment
View SamplesThe present study was designed using MT knockout mice in concert with genomic approaches to explore the possible molecular and cellular mechanisms involved in the protective effects of MT against DOX cardiotoxicity. MT-/ null (MT-/-) mice and corresponding wild-type mice (MT+/+) were administrated with a single dose of DOX (15 mg/kg, i.p.) or an equal volume of saline. Animals were sacrificed on the 4th day after DOX administration and samples were collected for further analyses. Global gene expression profiles of cardiac mRNA from two genotype mice revealed that 381 characteristically MT-responsive genes were identified between MT+/+ mice and MT-/- mice in response to DOX, including fos, ucp3, car3, atf3, map3k6, etc.. Functional analysis implied MAPK signaling pathway, p53 signaling pathway, Jak-STAT signaling pathway, PPAR signaling pathway, Wnt signaling pathway, etc. might be involved to mediate the protection of DOX cardiomyopathy by MT. Results from the present study not only validated the previously reported possible mechanisms of MT protection against DOX toxicity, but also provided new clues into the molecular mechanisms involved in this process.
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Specimen part
View SamplesTo induce a differentiated phenotype, primary pancreatic TIC cultures were grown in 10% FBS containing conditions. To analyze gene expression changes upon induction of a differentiated phenotype, total RNA of cells cultured in FBS containing conditions and parallel control cells cultured under serum-free conditions was isolated and comparative gene expression profiling was performed.
No associated publication
No sample metadata fields
View SamplesIn order to determine the effect of ArhGAP30 on the gene expression profile of colorectal cancer cells, Lovo cells were infected with either ArhGAP30 or the control pcDNA3.1 empty vector.
ArhGAP30 promotes p53 acetylation and function in colorectal cancer.
Cell line
View SamplesTranscriptome analysis of total RNA samples from HEK293-PIGS-KO and HEK293-PIGS-UBE2J1-DKO cells. To check whether KO of UBE2J1 upregulates genes of GPI biosthesis pathway, we used microarrays to analyze gene expression change by KO of UBE2J1 and comfirmed that known GPI pathway genes are not changed by ERAD-deficiency.
Cross-talks of glycosylphosphatidylinositol biosynthesis with glycosphingolipid biosynthesis and ER-associated degradation.
Cell line
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