Human subjects were randomized for treatment with a GnRH-analogue, Goserelin, which suppresses endogenous testosterone or placebo for 12 weeks. Strength training was performed during the last 8 weeks. The suppression of testosterone resulted in an attenuation of the normal muscle adaptation to strength training (increased muscle mass and strength). To identify molecular signals involved in the response to testosterone levels, biopsies were obtained 4 hours after the last training session and gene expression compared with Affymetrix 3' microarrays. This timepoint should capture goserelin effect on both constitutive expression, training induced changes as well as acute exercise induced (4 hours) differences in mRNA levels.
The activity of satellite cells and myonuclei following 8 weeks of strength training in young men with suppressed testosterone levels.
Sex, Age, Specimen part, Treatment
View SamplesWe analyzed mRNAs in transiliacal bone biopsies from 7 patients with primary hyperparathyroidism using Affymetrix HG-U133A Gene Chips Similar analyses of the global transcriptional activity were repeated in a second bone biopsy from the same patient taken one year after surgery and reversal of disease parameters.
Abnormal muscle and hematopoietic gene expression may be important for clinical morbidity in primary hyperparathyroidism.
Sex, Age, Specimen part, Disease, Subject
View SamplesLiver gene transcripts patterns were used to characterize toxicity from exposure to polybrominated diphenyl ethers (PBDEs), flame retardant components. In this study, Wistar Han dams were exposed by gavage to the PBDE mixture (DE71) starting at gestation day 6 (GD 6) and continuing to weaning on postnatal day 21 (PND 21). Offspring from the dams began PBDE direct dosing on PND 12 and were dosed daily through PND 21. After weaning, they were dosed 5 days per week for another 13 weeks. Liver samples were collected at PND 22 and week 13 for liver gene expression analysis and interrogated with the Affymetrix Rat Genome 230 2.0 Array.
Characterization of polybrominated diphenyl ether toxicity in Wistar Han rats and use of liver microarray data for predicting disease susceptibilities.
Sex, Specimen part
View SamplesTo identify nasal cavity transcripts differentially expressed due to treatment with N, N-dimethyl-p-toluidine (DMPT), we collected RNA during the from male F344/N rats exposed to 120 mg/kg DMPT, 5 days after DMPT exposure for animals 5-6 weeks of age. These samples were interrogated with the Affymetrix Rat Genome 230 2.0 GeneChip Array.
Molecular Changes in the Nasal Cavity after N, N-dimethyl-p-toluidine Exposure.
Sex
View SamplesTo identify liver transcripts differentially expressed due to treatment with N, N-dimethyl-p-toluidine (DMPT) and p-toluidine, we collected RNA during the from male F344/N rats exposed to 0, 1, 6, 20, 60 or 120 mg/kg DMPT (or p-toluidine), 5 days after exposure for animals 5-6 weeks of age. These samples were interrogated with the Affymetrix Rat Genome 230 2.0 GeneChip Array.
Hepatic transcriptomic alterations for N,N-dimethyl-p-toluidine (DMPT) and p-toluidine after 5-day exposure in rats.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Hepatic Transcriptomic Patterns in the Neonatal Rat After Pentabromodiphenyl Ether Exposure.
Sex, Specimen part, Treatment
View SamplesTo identify liver transcripts differentially expressed between control samples and animals exposed to PBDE-47, we collected RNA from male pups at postnatal day 4 (PND4) after the Wistar Han dams were exposed to 0, 0.1, 15, or 50 mg/kg PBDE-47. These samples were interrogated with the Affymetrix Rat Genome 230 2.0 GeneChip array.
Hepatic Transcriptomic Patterns in the Neonatal Rat After Pentabromodiphenyl Ether Exposure.
Sex, Specimen part, Treatment
View SamplesTo identify liver transcripts differentially expressed between control samples and animals exposed to DE-71, we collected RNA from male pups at postnatal day 4 (PND4) after the Wistar Han dams were exposed to 0, 0.1, 15, or 50 mg/kg DE-71. These samples were interrogated with the Affymetrix Rat Genome 230 2.0 GeneChip array
Hepatic Transcriptomic Patterns in the Neonatal Rat After Pentabromodiphenyl Ether Exposure.
Sex, Specimen part, Treatment
View SamplesThe plasma protein FHR1 induces release of inflammatory cytokines IL-1ß, IL-6, IL-18 or TNFa from blood-derived human monocytes. RNA sequencing was performed from RNA of BSA- or FHR1-treated monocytes from 4 different donors. In response to FHR1, 522 monocytic genes were upregulated (gene ontology enrichment analysis), including 35 inflammation related genes, e.g. TNF. Also, G protein-coupled receptors such as EMR2/ADGRE2 were upregulated in response to FHR1. Overall design: Blood-derived monocytes were treated with BSA or FHR1, after 4h RNA was isolated. RNA of 4 donors were combined and sequenced.
Serum FHR1 binding to necrotic-type cells activates monocytic inflammasome and marks necrotic sites in vasculopathies.
Specimen part, Treatment, Subject
View SamplesNeuronal function critically depends on coordinated subcellular distribution of mRNAs. Disturbed mRNA processing and axonal transport has been found in spinal muscular atrophy and could be causative for dysfunction and degeneration of motoneurons. Despite the advances made in characterizing the transport mechanisms of several axonal mRNAs, an unbiased approach to identify the axonal repertoire of mRNAs in healthy and degenerating motoneurons has been lacking. Here we used compartmentalized microfluidic chambers to investigate the somatodendritic and axonal mRNA content of cultured motoneurons by microarray analysis. In axons, transcripts related to protein synthesis and energy production were enriched relative to the somatodendritic compartment. Knockdown of Smn, the protein deficient in spinal muscular atrophy, produced a large number of transcript alterations in both compartments. Transcripts related to immune functions, including MHC class I genes, and with roles in RNA splicing were upregulated in the somatodendritic compartment. On the axonal side, transcripts associated with axon growth and synaptic activity were downregulated. These alterations provide evidence that subcellular localization of transcripts with axonal functions as well as regulation of specific transcripts with nonautonomous functions is disturbed in Smn-deficient motoneurons, most likely contributing to the pathophysiology of spinal muscular atrophy.
Subcellular transcriptome alterations in a cell culture model of spinal muscular atrophy point to widespread defects in axonal growth and presynaptic differentiation.
Specimen part
View Samples