Rattus norvegicus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA100329 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcription profiling by array of human duodenal mucosa from healthy subjects after treatment with the non-steroidal anti-inflammatory drug idomethacin or a placebo
2025-01-22 | E-MEXP-1337 | ExpressionAtlas
Project description:Non-steroidal anti-inflammatory drugs (NSAIDs) are used extensively as therapeutic agents, despite their well-documented gastrointestinal (GI) toxicity. Presently, the mechanisms responsible for NSAID-associated GI damage are incompletely understood. In this study, we used Microarray analysis to generate a novel hypothesis about cellular mechanisms that underlie the GI toxicity of NSAIDs. Monolayers of intestinal epithelial; cells (IEC-6) were treated with NSAIDs that either exhibit indomethacin, NS-398) or lack (SC-560) inhibitory effects on intestinal epithelial cell migration. Bioinformatic analysis of array data suggested that NSAIDs with adverse GI effects either decrease the gene expression of the calpains or increase the gene expression of the calpain engodenous; inhibitor, calpastatin. Calpains have been shown previously to modulate the migration of a variety of cells in different physiological contexts. Our experimental results suggest that the altered expression of calpain genes may contribute to the adverse effects of NSAIDs on intestinal; epithelial restitution. Microarray analysis has generated the novel hypothesis that the GI toxicity of NSAIDs may be attributed in part to drug-induced changes in the expression and activity of calpains. Experiment Overall Design: Monolayers of intestinal epithelial cells (IEC-6) were treated with NSAIDs that either exhibit (indomethacin, NS-398) or lack (SC-560) inhibitory effects on intestinal epithelial cell migration. Samples were then pooled to obtain sufficient material for gene array analysis. The pooled samples were used to hybridize 4 gene array chips for each biological sample.
2009-03-27 | E-GEOD-7584 | biostudies-arrayexpress
Project description:Indomethacin is a non-steroidal anti-inflammatory drug. It is widely used in clinical practice. In scientific intervention studies, it is applied as a methodology to inflict reversible damage to gastrointestinal epithelium. The exact pathogenesis is not well understood. The present study aimed to obtain a better understanding of indomathacin-induced pathogenesis by determining its effects on gene expression in duodenal mucosa in healthy subjects. Tissue samples from the horizontal part of the duodenum were obtained by standard flexible gastroduodenoscopy, and Affymetrix microarrays were used to determine genome-wide gene expression profiles.
2008-11-15 | E-MEXP-1337 | biostudies-arrayexpress
Project description:Gene expression patterns following unilateral traumatic brain injury reveals a local pro-inflammatory and remote anti-inflammatory response
| PRJNA196846 | ENA
Project description:Mechanisms of pparγ activation by non-steroidal anti-inflammatory drugs and GQ16.
| PRJNA270064 | ENA
Project description:Non-steroidal anti-inflammatory drugs (NSAIDs) are used extensively as therapeutic agents, despite their well-documented gastrointestinal (GI) toxicity. Presently, the mechanisms responsible for NSAID-associated GI damage are incompletely understood. In this study, we used Microarray analysis to generate a novel hypothesis about cellular mechanisms that underlie the GI toxicity of NSAIDs. Monolayers of intestinal epithelial cells (IEC-6) were treated with NSAIDs that either exhibit indomethacin, NS-398) or lack (SC-560) inhibitory effects on intestinal epithelial cell migration. Bioinformatic analysis of array data suggested that NSAIDs with adverse GI effects either decrease the gene expression of the calpains or increase the gene expression of the calpain engodenous inhibitor, calpastatin. Calpains have been shown previously to modulate the migration of a variety of cells in different physiological contexts. Our experimental results suggest that the altered expression of calpain genes may contribute to the adverse effects of NSAIDs on intestinal epithelial restitution. Microarray analysis has generated the novel hypothesis that the GI toxicity of NSAIDs may be attributed in part to drug-induced changes in the expression and activity of calpains. Keywords: dose response
2009-03-21 | GSE7584 | GEO
Project description:The Norway rat has important impacts on our life. They are amongst the most used research subjects, resulting in ground-breaking advances. At the same time, wild rats live in close association with us, leading to various adverse interactions. In face of this relevance, it is surprising how little is known about their natural behaviour. While recent laboratory studies revealed their complex social skills, little is known about their social behaviour in the wild. An integration of these different scientific approaches is crucial to understand their social life, which will enable us to design more valid research paradigms, develop more effective management strategies, and to provide better welfare standards. Hence, I first summarise the literature on their natural social behaviour. Second, I provide an overview of recent developments concerning their social cognition. Third, I illustrate why an integration of these areas would be beneficial to optimise our interactions with them.
| S-EPMC7145424 | biostudies-literature
Project description:BackgroundMurine kobuviruses (MuKV) are newly recognized picornaviruses first detected in murine rodents in the USA in 2011. Little information on MuKV epidemiology in murine rodents is available. Therefore, we conducted a survey of the prevalence and genomic characteristics of rat kobuvirus in Guangdong, China.ResultsFecal samples from 223 rats (Rattus norvegicus) were collected from Guangdong and kobuviruses were detected in 12.6% (28) of samples. Phylogenetic analysis based on partial 3D and complete VP1 sequence regions showed that rat kobuvirus obtained in this study were genetically closely related to those of rat/mouse kobuvirus reported in other geographical areas. Two near full-length rat kobuvirus genomes (MM33, GZ85) were acquired and phylogenetic analysis of these revealed that they shared very high nucleotide/amino acids identity with one another (95.4%/99.4%) and a sewage-derived sequence (86.9%/93.5% and 87.5%/93.7%, respectively). Comparison with original Aichivirus A strains, such human kobuvirus, revealed amino acid identity values of approximately 80%.ConclusionOur findings indicate that rat kobuvirus have distinctive genetic characteristics from other Aichivirus A viruses. Additionally, rat kobuvirus may spread via sewage.
| S-EPMC7161169 | biostudies-literature
Project description:microRNA expression in rat lung receiving chemopreventive agents and attenuation of cigarette smoke-induced alterations
| PRJNA122317 | ENA