Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28406301_1.fastq.gz | Fastqsanger.gz | |||
| SRR28406301_2.fastq.gz | Fastqsanger.gz | |||
| SRR28406302_1.fastq.gz | Fastqsanger.gz | |||
| SRR28406302_2.fastq.gz | Fastqsanger.gz | |||
| SRR28406303_1.fastq.gz | Fastqsanger.gz |
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Project description:Aflatoxin B1 (AFB1) is a mutagen and IARC (International Agency for Research on Cancer) Group 1 carcinogen that causes hepatocellular carcinoma (HCC). Here we present the first whole genome data on the mutational signatures of AFB1 exposure from a total of > 40,000 mutations in four experimental systems: two different human cell lines, and in liver tumors in wild-type mice and in mice that carried a hepatitis B surface antigen transgene – this to model the multiplicative effects of aflatoxin exposure and hepatitis B in causing HCC. AFB1 mutational signatures from all four experimental systems were remarkably similar. We integrated the experimental mutational signatures with data from newly-sequenced HCCs from Qidong County, China, a region of well-studied aflatoxin exposure. This indicated that COSMIC mutational signature 24, previously hypothesized to stem from aflatoxin exposure, indeed likely represents AFB1 exposure, possibly combined with other exposures. Among published somatic mutation data, we found evidence of AFB1 exposure in 0.7% of HCCs treated in North America, 1% of HCCs from Japan, but 16% of HCCs from Hong Kong. Thus, aflatoxin exposure apparently remains a substantial public health issue in some areas. This aspect of our study exemplifies the promise of future widespread resequencing of tumor genomes in providing new insights into the contribution of mutagenic exposures to cancer incidence.
| EGAS00001002490 | EGA
Project description:Stress-induced tRNA fragmentation is an evolutionarily conserved molecular phenomenon. A variety of the resulting tRNA-derived small RNAs (tsRNAs) have been associated with a multitude of cellular processes including cell survival during adverse environmental conditions. However, application of experimental stressors under laboratory conditions often differs from stress encountered naturally. This raises important questions about the extent of experimental bias when studying stress biology including tRNA fragmentation, especially in cell culture. Here, we have revisited one of the most often used experimental paradigms for modeling oxidative stress and tRNA fragmentation, the exposure of cultured cells to sodium arsenite. These experiments revealed that transient exposure to sodium arsenite concentrations that caused robust tRNA fragmentation resulted in extensive cell death during the stress recovery. Importantly, released material from dying cells contained also tsRNA species, which were sufficiently stable against nuclease digestion.
2021-12-31 | GSE182334 | GEO
Project description:This dataset contains nanoLC-MS/MS results of heads of honey bee workers. All the heads were from 13 days old bees that were 11 days postinfection (DPI) that lasted 24 hours. Abdomens of bees were analyzed using qPCR to determine parasite load. Further, corresponding selected heads were subjected to a label-free proteomic analysis. Overall, five heads of bees were selected from each of the following experimental exposures performed: i) control without L. passim and IMI exposure and with confirmed no L. passim detected; ii) bees positive for L. passim from the experimental exposure of L. passim; and iii) bees positive for L. passim from the experimental exposure of L. passim combined with 2.5 uL IMI coexposure. This research was supported by project no. QK1910018 (NAZV) and Institutional Support for R&D no. MZE-RO0423 of the Ministry of Agriculture of the Czech Republic.
| MSV000092818 | MassIVE
Project description:Experimental asthma was induced in BALB/c mice by sensitization and challenge with the allergen ovalbumin. Control groups received PBS. To investigate the innate immune component of experimental asthma, we also analyzed recombinase activating gene (RAG) deficient mice following exposure to ovalbumin and control PBS Keywords: case control
2007-04-23 | GSE6858 | GEO
Project description:in vitro genomic analyses of clozapine response. Genome wide DNA methylation profiling was performed across several experimental conditions of clozapine exposure. LCLs were exposed to different concentrations of clozapine (vehicle (DMSO), 1x, 20x, 40x and 60 times clinical concentration) and exposure times were 24h and 96h.
2020-09-30 | GSE158716 | GEO
Project description:A multi-omic approach in a clinical experimental study identified circulating biomarkers reflecting glucocorticoid exposure. Background: Endogenous glucocorticoids (GC) are mechanistically linked to common diseases and are important as drugs in the treatment of many disorders. There is no marker that can measure and quantify GC action. Our aim was to identify circulating biomarkers of GC action using a clinical experimental study. Methods: In a randomized, crossover, single-blind trial, subjects with primary adrenal insufficiency received intravenous hydrocortisone infusion in a circadian pattern (physiological GC exposure) or isotonic saline (GC withdrawal) over 22 hours. Samples were collected at 7 AM (end of infusion). Integrated multi-omic analysis was used because of the complexity in GC action and the low number of subjects. The transcriptome in peripheral blood mononuclear cells (PBMCs) and adipose tissue, plasma miRNAomic, and serum metabolomics were compared between the interventions. Replication of the plasma miRNA findings was performed in three independent studies. Results: During GC withdrawal, overnight urinary cortisol and cortisone excretion were undetectable. Correlation and hypernetwork analyses identified a transcriptomic profile derived from PBMCs and adipose tissue predictive of GC exposure, and a multi-omic cluster predictive of GC exposure. From the circulating ‘omic data, decreased expression of plasma miR-122-5p was associated with increased GC exposure. This finding was reproduced in three independent studies. Conclusion: We developed a human experimental model for physiological GC exposure and withdrawal. The integrated multi-omic data identified circulating miRNAs and metabolites associated with GC-responsive genes. In independent studies, miR-122-5p was shown to be associated with GC exposure. Background: Endogenous glucocorticoids (GC) are mechanistically linked to common diseases and are important as drugs in the treatment of many disorders. There is no marker that can measure and quantify GC action. Our aim was to identify circulating biomarkers of GC action using a clinical experimental study.
2021-04-02 | GSE148640 | GEO
Project description:A multi-omic approach in a clinical experimental study identified circulating biomarkers reflecting glucocorticoid exposure. Background: Endogenous glucocorticoids (GC) are mechanistically linked to common diseases and are important as drugs in the treatment of many disorders. There is no marker that can measure and quantify GC action. Our aim was to identify circulating biomarkers of GC action using a clinical experimental study. Methods: In a randomized, crossover, single-blind trial, subjects with primary adrenal insufficiency received intravenous hydrocortisone infusion in a circadian pattern (physiological GC exposure) or isotonic saline (GC withdrawal) over 22 hours. Samples were collected at 7 AM (end of infusion). Integrated multi-omic analysis was used because of the complexity in GC action and the low number of subjects. The transcriptome in peripheral blood mononuclear cells (PBMCs) and adipose tissue, plasma miRNAomic, and serum metabolomics were compared between the interventions. Replication of the plasma miRNA findings was performed in three independent studies. Results: During GC withdrawal, overnight urinary cortisol and cortisone excretion were undetectable. Correlation and hypernetwork analyses identified a transcriptomic profile derived from PBMCs and adipose tissue predictive of GC exposure, and a multi-omic cluster predictive of GC exposure. From the circulating ‘omic data, decreased expression of plasma miR-122-5p was associated with increased GC exposure. This finding was reproduced in three independent studies. Conclusion: We developed a human experimental model for physiological GC exposure and withdrawal. The integrated multi-omic data identified circulating miRNAs and metabolites associated with GC-responsive genes. In independent studies, miR-122-5p was shown to be associated with GC exposure. Background: Endogenous glucocorticoids (GC) are mechanistically linked to common diseases and are important as drugs in the treatment of many disorders. There is no marker that can measure and quantify GC action. Our aim was to identify circulating biomarkers of GC action using a clinical experimental study.
2021-04-02 | GSE148639 | GEO