We exposed wild-type Vibrio cholerae E7496, multiple Vibrio cholerae virulence factor deleted genes with intact hemolysin A gene [CVD109] and without hemolysin A gene [CVD110] in E7946, and E.coli OP50 to wild-type C.elegans N2 for 18 hours. We used microarrays to detail the global gene expression and identified distinct classes of up-regulated and down-regulated genes during this process.
Genomic analysis of immune response against Vibrio cholerae hemolysin in Caenorhabditis elegans.
No sample metadata fields
View Sampleswe employed DNA microarray platform to compare the gene expression patterns in primary human cardiomyocytes treated with trastuzumab (50g/ml), trastuzumab (50g/ml) plus pertuzumab (50g/ml), T-DM1 (10 g/ml), or control (no treatment).
Type IIB DNA topoisomerase is downregulated by trastuzumab and doxorubicin to synergize cardiotoxicity.
Specimen part
View SamplesWe used microarrays to explore the global affect on gene expression in C. elegans after exposure to arsenic
No associated publication
No sample metadata fields
View SamplesThis study was initiated to characterize early DOX-induced changes in cardiac gene expression in order to identify potential additional areas for clinical intervention. Male spontaneously hypertensive rats (SHR) received 3 mg/kg DOX or vehicle (iv) 30 minutes following pretreatment with 50 mg/kg DZR or saline (ip) weekly for 1, 2 or 3 weeks.
No associated publication
Sex, Age, Specimen part, Disease, Disease stage, Treatment, Time
View SamplesAt one site (#10), three different batches of MTRRM (see E-TABM-16), were labeled with two different kits (Enzo and Affymetrix) and hybridized to two different Affymetrix Arrays (RAE230A and RAE230_2).
Use of diagnostic accuracy as a metric for evaluating laboratory proficiency with microarray assays using mixed-tissue RNA reference samples.
Sex, Age
View SamplesThe present study was constructed to confirm previous findings that mice on a high fat diet (HFD) treated by subcutaneous injection with exenatide (EXE) at 3g/kg once daily for 6 weeks develop exocrine pancreatic injury (Rouse et al. 2014). The present study included 12 weeks of EXE exposure at multiple concentrations (3, 10, or 30 g/kg) with multiple endpoints (histopathology evaluations, immunoassay for cytokines, immunostaining of the pancreas, serum chemistries and measurement of trypsin, amylase, and, lipase, and gene expression profiles). Time- and dose-dependent exocrine pancreatic injury was observed in mice associated with EXE exposure in a HFD environment. The time- and dose-dependent morphological changes identified in the pancreas involved acinar cell injury and death (autophagy, apoptosis, necrosis, and atrophy), cell adaptations (hypertrophy and hyperplasia), and cell survival (regeneration) accompanied with varying degrees of inflammatory response leading to secondary injury in pancreatic blood vessels, ducts, and adipose tissues. Gene expression profiles supported the presence of increased signaling for cell survival and altered lipid metabolism. The potential for EXE to cause acute or early chronic pancreatic injury was identified in a HFD environment. In human disease, the influence of pancreatitis risk factors or pre-existing chronic pancreatitis on this injury potential requires further investigation.
Extended exenatide administration enhances lipid metabolism and exacerbates pancreatic injury in mice on a high fat, high carbohydrate diet.
Sex, Specimen part
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