Impact of acute noise trauma on the gene expression profile of the hippocampus
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ABSTRACT:
PROVIDER: PRJNA588236 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To investigate the early changes in the hippocampus following noise-induced hearing loss, the gene expression profile of the hippocampus was evaluated using microarray analyses immediately after exposure to intense noise stimuli.
2020-10-17 | GSE140087 | GEO
Project description:In order to elucidate molecular mechanisms of noise-induced hearing loss and dexamethasone therapy in the cochlea (inner ear), transcriptome of cochlear samples was analyzed after induction of hearing loss by exposure to intense noise in mice. Dexamethasone was intraperitoneally injected immediately following the noise trauma. Cochlear transcriptome was analyzed at 12h and 24h following the noise trauma and dexamethasone administration.
2016-12-03 | GSE85290 | GEO
Project description: Not available
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Project description:Cochlear transcriptome at 3 hours post-noise trauma in mice
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Project description:In order to elucidate molecular mechanisms of noise-induced hearing loss in the cochlea (inner ear), transcriptome of the cochlear sample was analyzed after induction of hearing loss by exposure to intense noise in mice. Cochlear transcriptome was analyzed at 3 hours following the noise exposure.
2020-01-14 | GSE137817 | GEO
Project description:The cochlea possesses a robust circadian clock machinery that regulates auditory function. How the cochlear clock is influenced by the circadian system remains unknown. Here we show that cochlear rhythms are system-driven and require local Bmal1 as well as central input from the suprachiasmatic nuclei (SCN). SCN ablations disrupted the circadian expression of the core clock genes in the cochlea. Since the circadian secretion of glucocorticoids (GCs) is controlled by the SCN and that GCs are known to modulate auditory function, we assessed their influence on circadian gene expression. Removal of circulating GCs by adrenalectomy (ADX) did not have a major impact on core clock gene expression in the cochlea. Rather it abolished the transcription of clock-controlled genes involved in inflammation. ADX abolished the known differential auditory sensitivity to day and night noise trauma and prevented the induction of GABA-ergic and glutamate receptors mRNA transcripts. However, these improvements were unrelated to changes at the synaptic level suggesting other cochlear functions may be involved. Due to this circadian regulation of noise sensitivity by GCs, we evaluated the actions of the synthetic glucocorticoid dexamethasone (DEX) at different times of the day. DEX was effective in protecting from acute noise trauma only when administered during daytime, when circulating glucocorticoids are low, indicating that chronopharmacological approaches are important for obtaining optimal treatment strategies for hearing loss. GCs appear as a major regulator of the differential sensitivity to day or night noise trauma, a mechanism likely involving the circadian control of inflammatory responses.
2019-06-15 | GSE107086 | GEO
Project description:Using the RiboTag approach, we profiled the cell type-specific molecular landscape of the outer hair cells and supporting cells as well as the whole cochlea, both before and after noise trauma (6h and 24h) that induces a permanent hearing loss.
2021-09-03 | GSE168973 | GEO
Project description:Background. Coagulopathic bleeding is a major cause of mortality after trauma, and platelet dysfunction contributes to this problem. The causes of platelet dysfunction are relatively unknown, but a great deal can be learned from the plasma environment about the possible pathways involved.
Objective. Describe the changes in plasma proteomic profile associated with platelet dysfunction after trauma.
Methods. Citrated blood was collected from severely injured trauma patients at the time of their arrival to the Emergency Department. Samples were collected from 110 patients, and a subset of twenty-four patients was identified by a preserved (n=12) or severely impaired (n=12) platelet aggregation response to five different agonists. Untargeted proteomics was performed by nanoflow liquid chromatography tandem mass spectrometry. Protein abundance levels for each patient were normalized to total protein concentration to control for hemodilution by crystalloid fluid infusion prior to blood draw.
Results. Patients with platelet dysfunction were more severely injured but otherwise demographically similar to those with retained platelet function. Of 232 proteins detected, twelve were significantly different between groups. These proteins fall into several broad categories related to platelet function, including microvascular obstruction with platelet activation, immune activation, and protease activation.
Conclusions. This observational study provides a description of the change in proteomic profile associated with platelet dysfunction after trauma and identifies twelve proteins with the most profound changes. The pathways involving these proteins are salient targets for immediate investigation to better understand platelet dysfunction after trauma and identify targets for intervention.
2021-02-24 | MSV000086948 | MassIVE
Project description:Toxoplasma gondii is a protozoan parasite with a remarkable neuro-tropismneurotropic affinity. We recently showed that T. gondii infection can alter the global metabolism of the cerebral cortex of the mice. However, the impact of this infection on the metabolism of the hippocampus remains unclear. In this study, we compared the metabolomic profiles of mouse hippocampus following acute and chronic infection with T. gondii. Our data provide new insight into the neuropathogenesis of T. gondii infection and reveal new pathways and metabolites that mediate the interplay between T. gondii infection and the mouse hippocampus
2021-01-27 | MTBLS1890 | MetaboLights
Project description:Fuzziness and noise in nucleosomal architecture
| PRJEB4709 | ENA