Ontology highlight
ABSTRACT:
PROVIDER: PRJNA674334 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12972026_1.fastq.gz | Fastqsanger.gz | |||
| SRR12972026_2.fastq.gz | Fastqsanger.gz | |||
| SRR12972027_1.fastq.gz | Fastqsanger.gz | |||
| SRR12972027_2.fastq.gz | Fastqsanger.gz | |||
| SRR12972028_1.fastq.gz | Fastqsanger.gz |
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Project description:Using heterogeneous stock (HS) rats, we have identified a region on rat chromosome 1 that maps multiple diabetic traits. We sought to use global expression analysis to determine if genes within this region are differentially expressed between HS rats with normal glucose tolerance and those with glucose intolerance
2014-09-18 | GSE57117 | GEO
Project description:Using heterogeneous stock (HS) rats, we have identified a region on rat chromosome 1 that maps multiple diabetic traits. We sought to use global expression analysis to determine if genes within this region are differentially expressed between HS rats with normal glucose tolerance and those with glucose intolerance HS rats were euthanized at 17 weeks of age and tail sample was taken. Genomic DNA was extracted from tail of 23 HS rats with glucose intolerance and 23 HS rats with normal glucose. The Affymetrix 10K SNP array was used to genotype these animals.
2014-09-18 | E-GEOD-57117 | biostudies-arrayexpress
Project description:Using heterogeneous stock (HS) rats, we have identified a region on rat chromosome 1 that maps multiple diabetic traits. We sought to use global expression analysis to determine if genes within this region are differentially expressed between HS rats with normal glucose tolerance and those with glucose intolerance HS rats were euthanized at 17 weeks of age and liver was immediately frozen in liquid nitrogen. RNA was extracted from liver of 23 HS rats with glucose intolerance and 23 HS rats with normal glucose. The Affymetrix 230_2 array was used to probe transcript abundance levels.
2014-09-18 | E-GEOD-54935 | biostudies-arrayexpress
Project description:Using heterogeneous stock (HS) rats, we have identified a region on rat chromosome 1 that maps multiple diabetic traits. We sought to use global expression analysis to determine if genes within this region are differentially expressed between HS rats with normal glucose tolerance and those with glucose intolerance
2014-09-18 | GSE54935 | GEO
Project description:The etiology of trauma-hemorrhage shock-induced acute lung injury has been difficult to elucidate due, at least in part, to the inability of in vivo studies to separate the non-injurious pulmonary effects of trauma-hemorrhage from the tissue injurious ones. To circumvent this in vivo limitation, we utilized a model of trauma-hemorrhagic shock (T/HS) in which T/HS-lung injury was abrogated by dividing the mesenteric lymph duct. In this way, it was possible to separate the pulmonary injurious response from the non-injurious systemic response to T/HS by comparing the pulmonary molecular response of rats subjected to T/HS which did and did not develop lung injury as well as to non-shocked rats. Utilizing high-density oligonucleotide arrays and treatment group comparisons of whole lung tissue collected at 3 hours after the end of the shock or sham-shock period, 139 of the 8,799 assessed genes were differentially expressed. Experiment Overall Design: Four groups of rats (n=3) were studied in order to identify changes in pulmonary gene expression associated with T/HS, both in the presence and absence of lung injury. These included trauma-sham shock (T/SS) rats which had a laparotomy (trauma) but were not subjected to hemorrhagic shock. These rats had no lung injury and served as controls for rats which were subjected to T/HS (laparotomy plus 90 min of shock) and had lung injury. Differences in gene expression between these two groups would represent both the effects of hemorrhagic shock as well as lung injury. To distinguish the gene response of hemorrhagic shock from the gene response associated with lung injury, gene expression was also compared between T/HS rats (hemorrhage and lung injury) and rats subjected to T/HS plus lymph duct ligation (T/HS-LDL), since the T/HS-LDL rats experienced hemorrhagic shock but had no measurable lung injury. Lastly, to identify hemorrhagic shock- modified genes, the pulmonary gene response of T/HS-LDL (hemorrhage without lung injury) were compared to rats subjected to T/SS plus LDL (no hemorrhage or lung injury). Three hours after the end of the 90 min shock or sham-shock period (i.e. 4.5 hrs after the induction of T/HS), the rats were sacrificed and specimens harvested for genechip analysis and histology.
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2021-07-01 | GSE149006 | GEO
Project description:Intake of ergot alkaloids associated with endophyte-infected fescue (E+) has adverse effects on animal health and productivity, which is collectively, termed fescue toxicosis. These effects are exacerbated under hot and humid (summer) conditions. A rat model for this condition was used to evaluate the effect of endophytic toxins on hepatic gene expression under acute (three days) heat stress (HS). Core temperature (Tc) was monitored continuously in rats (n=12) implanted with telemetric transmitters. Rats were fed ad libitum an E+ diet and maintained under thermoneutral (TN) conditions (21 ˚C) for five days, followed by TN or HS conditions (31 ˚C) for three days. Feed intake (FI) and body weight (BW) were measured daily. Both E+ and HS induced alterations in hepatic genes were evaluated using DNA microarrays. Intake of E+ reduced FI and BW under TN and HS conditions from pretreatment level, with greater reduction occurring during HS period. Core temperature at TN did not change from pretreatment level, but increased during HS. Genes associated with ATP synthesis, immune function, chaperone activity, and antioxidant function were reduced in E+HS vs E+TN. Present findings suggest that rats respond to E+ during heat stress by inducing hepatic CYP3A4 expression and suppressing chaperone, antioxidant and immune systems, which could ultimately increase the stress resulting in various pathological abnormalities. Keywords: Stress response
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