Rattus norvegicus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA312344 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3175220.fastq.gz | Fastqsanger.gz | |||
| SRR3175230.fastq.gz | Fastqsanger.gz | |||
| SRR3175240.fastq.gz | Fastqsanger.gz | |||
| SRR3175250.fastq.gz | Fastqsanger.gz | |||
| SRR3175260.fastq.gz | Fastqsanger.gz |
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Project description:Open lung approach with low tidal volume mechanical ventilation attenuates lung injury in rats with massive brain damage
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Project description:Scientific knowledge on the subjects: Injurious mechanical ventilation amplifies acute lung injury in a heterogeneous and regional fashion but the molecular mechanisms underlying regional lung injury and the protective effects of prone positioning are unclear. Regionally injurious ventilation is associated with discrete differential lung transcriptomic changes. Ventilating in the prone, compared with the supine position abrogates regional injury by depressing MKP-1.
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Project description:Scientific knowledge on the subjects: Injurious mechanical ventilation amplifies acute lung injury in a heterogeneous and regional fashion but the molecular mechanisms underlying regional lung injury and the protective effects of prone positioning are unclear. Regionally injurious ventilation is associated with discrete differential lung transcriptomic changes. Ventilating in the prone, compared with the supine position abrogates regional injury by depressing MKP-1. Adult rats were ventilated with high (18 mL/Kg, PEEP 0) tidal volume (Vt) in supine or prone position. Non ventilated rats were used as controls. Dorsal-caudal lung mRNA was analyzed by microarray.
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Project description:Molecular Signatures of Trauma Hemorrhagic Shock-Induced Lung Injury: Hemorrhage- and Injury-Associated Genes
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Project description:In the present study we seek to identify changes in lung gene expression under mechanical ventilation in uninjured as well as acutely and chronically injured lungs. A standard volume-controlled lung-protective ventilatory protocol is compared to a concept of mechanical ventilation using variable tidal volumes.
2017-02-17 | GSE78008 | GEO
Project description:Few studies have assessed the patterns of parasite populations of rodents over a longitudinal gradient in Chile. In this work, the gastrointestinal helminthic fauna of invasive rodents in Chile was examined to assess the association between their presence/absence and abundance with latitude, host sex, and host body condition, and to assess the coexistence and correlation of the abundance between parasite species. Rodents were obtained from 20 localities between 33 and 43°S. Helminths were extracted from the gastrointestinal tract and identified morphologically. Overall, 13 helminth taxa were obtained. The most frequently identified parasite species was Heterakis spumosa, and the most abundant was Syphacia muris, while Physaloptera sp. was the most widely distributed. No locality presented with a coexistence that was different from that expected by chance, while the abundance of five helminthic species correlated with the abundance of another in at least one locality, most likely due to co-infection rather than interaction. Host sex was associated with parasite presence or abundance, and female sex-biased parasitism was notably observed in all cases. Body condition and latitude presented either a positive or negative association with the presence or abundance of parasites depending on the species. It is notable that the likely native Physaloptera sp. is widely distributed among invasive rodents. Further, gravid females were found, suggesting spillback of this species to the native fauna. The low frequency and abundance of highly zoonotic hymenolepid species suggest that rodents are of low concern regarding gastrointestinal zoonotic helminths.
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Project description:Background: Mechanical ventilation causes ventilator-induced lung injury in animals and humans. Mitogen-activated protein kinases have been implicated in ventilator-induced lung injury though their functional significance remains incomplete. We characterize the role of p38 mitogen-activated protein kinase/ mitogen activated protein kinase kinase-3 and c-Jun-NH2-terminal kinase-1 in ventilator-induced lung injury and investigate novel independent mechanisms contributing to lung injury during mechanical ventilation. Methodology and Principle Findings: C57/BL6 wild-type mice and mice genetically deleted for mitogen-activated protein kinase kinase-3 (mkk-3-/-) or c-Jun-NH2-terminal kinase-1 (jnk1-/-) were ventilated, and lung injury parameters were assessed. We demonstrate that mkk3-/- or jnk1-/- mice displayed significantly reduced inflammatory lung injury and apoptosis relative to wild-type mice. Since jnk1-/- mice were highly resistant to ventilator-induced lung injury, we performed comprehensive gene expression profiling of ventilated wild-type or jnk1-/- mice to identify novel candidate genes which may play critical roles in the pathogenesis of ventilator-induced lung injury. Microarray analysis revealed many novel genes differentially expressed by ventilation including matrix metalloproteinase-8 (MMP8) and GADD45a. Functional characterization of MMP8 revealed that mmp8-/- mice were sensitized to ventilator-induced lung injury with increased lung vascular permeability. Conclusions: We demonstrate that mitogen-activated protein kinase pathways mediate inflammatory lung injury during ventilator-induced lung injury. C-Jun-NH2-terminal kinase was also involved in alveolo-capillary leakage and edema formation, whereas MMP8 inhibited alveolo-capillary protein leakage. Keywords: response to injury, genetically modified mouse
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Project description:Gene Expression Changes due to Rat Lung Ischemia-Reperfusion Injury
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