Exposure to high levels of arsenic in drinking water is associated with several types of cancers including lung, bladder and skin, as well as vascular disease and diabetes. Drinking water standards are based primarily on epidemiology and extrapolation from higher dose experiments, rather than measurements of phenotypic changes associated with chronic exposure to levels of arsenic similar to the current standard of 10ppb, and little is known about the difference between arsenic in food as opposed to arsenic in water. Measurement of phenotypic changes at low doses may be confounded by the effect of laboratory diet, in part because of trace amounts of arsenic in standard laboratory chows, but also because of broad metabolic changes in response to the chow itself. Finally, this series contrasts 8hr, 1mg/kg injected arsenic with the various chronic exposures, and also contrasts the acute effects of arsenic, dexamethasone or their combination. Male C57BL/6 mice were fed on two commercially available laboratory diets (LRD-5001 and AIN-76A) were chronically exposed, through drinking water or food, to environmentally relevant concentrations of sodium arsenite, or acutely exposed to dexamethasone.
Laboratory diet profoundly alters gene expression and confounds genomic analysis in mouse liver and lung.
No sample metadata fields
View SamplesExposure to high levels of arsenic in drinking water is associated with several types of cancers including lung, bladder and skin, as well as vascular disease and diabetes. Drinking water standards are based primarily on epidemiology and extrapolation from higher dose experiments, rather than measurements of phenotypic changes associated with chronic exposure to levels of arsenic similar to the current standard of 10ppb, and little is known about the difference between arsenic in food as opposed to arsenic in water. Measurement of phenotypic changes at low doses may be confounded by the effect of laboratory diet, in part because of trace amounts of arsenic in standard laboratory chows, but also because of broad metabolic changes in response to the chow itself. Finally, this series contrasts 8hr, 1mg/kg injected arsenic with the various chronic exposures, and also contrasts the acute effects of arsenic, dexamethasone or their combination. Male C57BL/6 mice were fed on two commercially available laboratory diets (LRD-5001 and AIN-76A) were chronically exposed, through drinking water or food, to environmentally relevant concentrations of sodium arsenite, or acutely exposed to dexamethasone.
Chronic exposure to arsenic in the drinking water alters the expression of immune response genes in mouse lung.
No sample metadata fields
View SamplesTo define the characteristics of human oral mucosa fibroblasts (hOFs), we analyzed the gene expression of hOFs compared with that of human dermal fibroblasts (hDFs), and that of hOF-derived induced pluripotent stem cells (hOF-iPSCs).
Gene Signature of Human Oral Mucosa Fibroblasts: Comparison with Dermal Fibroblasts and Induced Pluripotent Stem Cells.
Sex, Age, Specimen part
View SamplesThe putative trancriptional regulator PA2449 was found to be essential for both glycine/serine metabolism and the production of phenazines in P. aeruignosa PAO1.
Gene PA2449 is essential for glycine metabolism and pyocyanin biosynthesis in Pseudomonas aeruginosa PAO1.
No sample metadata fields
View SamplesWe did transcription profiling on the effect of rlm1 (MAPK Slt2 transcription factor) deletion and swi3 (component of SWI/SNF complex involved in chromatin remodeling) deletion in genes involved in cell wall stress (Congo Red) response.
Chromatin remodeling by the SWI/SNF complex is essential for transcription mediated by the yeast cell wall integrity MAPK pathway.
No sample metadata fields
View SamplesThe transcriptome of P. aeruginosa PAO1 in the presence of extracelluar 2-oxoglutarate at a concentration of 20 mM.
Genetic analysis of the assimilation of C5-dicarboxylic acids in Pseudomonas aeruginosa PAO1.
No sample metadata fields
View SamplesTo understand the molecular mechanism underlying inflammatory reaction in vascular system post exposure to ionizing radiation, we carried out microarray analysis in HUVEC exposed with X-ray
Comprehensive and computational analysis of genes in human umbilical vein endothelial cells responsive to X-irradiation.
Specimen part
View SamplesSkeletal muscle mass is an important determinant of whole-body glucose disposal. We here show that mice (M-PDK1KO mice) with skeletal muscle–specific deficiency of 3'-phosphoinositide–dependent kinase 1 (PDK1), a key component of the phosphatidylinositol 3-kinase (PI3K) signaling pathway, manifest a reduced skeletal muscle mass under the static condition as well as impairment of exercise load–induced muscle hypertrophy.
Role of PDK1 in skeletal muscle hypertrophy induced by mechanical load.
Sex, Specimen part
View SamplesWild-type cells were cultured at 30 deg and cells were harvested. Total RNAs were purified from 3 populations.
Mapping of long-range associations throughout the fission yeast genome reveals global genome organization linked to transcriptional regulation.
No sample metadata fields
View SamplesInfliximab (IFX) has been reported as the further therapy in intravenous immunoglobulin G (IVIG)-resistant Kawasaki disease (KD) patients. IFX is a monoclonal antibody that blocks the pro-inflammatory cytokine tumor necrosis factor (TNF)-, but how IFX affect KD vasculitis is unknown. We investigated expression profiling of whole blood cells to elucidate the molecular mechanisms of the effectiveness of IFX therapy and to find characteristic biomarker and an important target in refractory KD. Methods: Refractory KD patients who failed to respond to repeated intravenous immunoglobulin G (IVIG) infusions had received a single infusion of IFX as third therapy. To validate specifically transcripts abundance for IFX therapy, we detected the altered transcripts expression and signaling pathways of whole blood mRNA in these IFX-responsive patients (n=8) using Affymetrix array, comparing initial IVIG-responsive patients (n=6).Results: A total of 1,388 transcripts abundance were significantly altered before and after IFX treatment. These transcripts abundance in IFX had Nucleotide-binding oligomerization domain pathway that play a role in activation of NFB and IL-1 signaling pathway outside the field of TNF- signaling pathway. Fifty transcripts including Peptidase inhibitor-3 (PI3), Matrix metalloproteinase-8 (MMP8), Chemokine (C-C motif) receptor-2 (CCR2) and Pentraxin-3 (PTX3) were significantly down-regulated in IFX. Conclusion: We demonstrated that the inhibition of TNF- by IFX have affected various molecular mechanism materially for IVIG-resistant KD patients.
Transcriptional regulation by infliximab therapy in Kawasaki disease patients with immunoglobulin resistance.
Specimen part, Disease, Disease stage, Treatment, Subject
View Samples