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Links from GEO DataSets

Items: 9

1.

Changes in mouse cognition and hippocampal gene expression observed in a mild physical- and blast-traumatic brain injury

(Submitter supplied) Warfare has long been associated with traumatic brain injury (TBI) in militarized zones. Common forms of TBI can be caused by a physical insult to the head-brain or by the effects of a high velocity blast shock wave generated by the detonation of an explosive device. While both forms of trauma are distinctly different regarding the mechanism of trauma induction, there are striking similarities in the cognitive and emotional status of survivors. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6885
16 Samples
Download data: TXT
Series
Accession:
GSE44625
ID:
200044625
2.

Blast traumatic brain injury induced cognitive deficits are attenuated by pre- or post-injury treatment with the glucagon-like peptide-1 receptor agonist, exendin-4

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6885
40 Samples
Download data
Series
Accession:
GSE71850
ID:
200071850
3.

Blast traumatic brain injury induced cognitive deficits are attenuated by pre- or post-injury treatment with the glucagon-like peptide-1 receptor agonist, exendin-4 [Day 3 dataset]

(Submitter supplied) Blast traumatic brain injury (B-TBI) affects military and civilian personnel. Presently there are no approved drugs for blast brain injury. Exendin-4, administered subcutaneously, was evaluated as a pre-treatment (48 hours) and post-injury treatment (2 hours) on neurodegeneration, behaviors and gene expressions in a murine open field model of blast injury. B-TBI induced neurodegeneration, changes in cognition and genes expressions linked to dementia disorders. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6885
24 Samples
Download data: TXT
Series
Accession:
GSE71846
ID:
200071846
4.

Exendin-4, a glucagon-like peptide-1 receptor agonist prevents mTBI-induced changes in hippocampus gene expression and memory deficits in mice

(Submitter supplied) Traumatic brain injury (TBI) is a global problem reaching near epidemic numbers that manifests clinically with cognitive problems that decades later may result in dementias like Alzheimer’s disease (AD). Presently, little can be done to prevent ensuing neurological dysfunctions by pharmacological means. Recently, it has become apparent that several CNS diseases share common terminal features of neuronal cell death. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6885
18 Samples
Download data: TXT
Series
Accession:
GSE41345
ID:
200041345
5.

Single cell sequencing of hippocampus tissues in traumatic brain injury

(Submitter supplied) A single cell suspension was generated from 24hr TBI and Sham mouse hippocampi, and single-cell mRNAseq libraries were generated with Drop-Seq.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
6 Samples
Download data: TXT
Series
Accession:
GSE101901
ID:
200101901
6.

Hippocampal gene expression after brain injury

(Submitter supplied) RNA samples were prepared from ipsilateral rat hippocampi 3 hr and 24 hr following lateral cortical impact injury and compared to samples from sham-operated controls. For details please see Matzilevich et al., J Neurosci Res 2002 Mar 1;67(5):646-63. Keywords = Brain injury Keywords: time-course
Organism:
Rattus norvegicus
Type:
Expression profiling by array
Platform:
GPL85
3 Samples
Download data
Series
Accession:
GSE1911
ID:
200001911
7.

Evidence for a rheostat that determines neuronal survival after traumatic brain injury

(Submitter supplied) To investigate the determinants of neuronal survival after traumatic brain injury, we compared the transcriptional profiles of dying (Fluoro-Jade-positive) and immediately adjacent surviving (Fluoro-Jade-negative) neurons from the CA3 subfield of the rat hippocampus 24 hours after experimental TBI. We found that hippocampal neurons that survive TBI invariably express high levels of genes that have cellular functions involved in survival, regeneration, development, proliferation, neuronal plasticity such as cAMP response element binding protein (CREB), brain-derived-neurotrophic factor (BDNF) and mitogen-activated protein kinase 1 (MAPK1). more...
Organism:
Rattus norvegicus
Type:
Expression profiling by array
Platform:
GPL7294
8 Samples
Download data: TXT
Series
Accession:
GSE16735
ID:
200016735
8.

Chronic Gene Expression after Traumatic Brain Injury

(Submitter supplied) This project continues our acute TBI studies and initiates chronic studies -- characterizing the temporal genomic profile of the injured brain up to 12 months post-TBI. Thus, the primary objective of this proposal is to determine the long-term effects of traumatic brain injury on gene expression in the hippocampus and cortex, two brain regions known to be particularly vulnerable to TBI.
Organism:
Rattus norvegicus
Type:
Expression profiling by array
Platforms:
GPL15084 GPL22740
113 Samples
Download data: TXT
Series
Accession:
GSE111452
ID:
200111452
9.

Meningeal lymphatic dysfunction exacerbates traumatic brain injury pathogenesis

(Submitter supplied) The goal of this study is to use bulk RNA-sequencing of the right brain hemisphere to observe the effects of TBI in the context of pre-existing meningeal lymphatic dysfunction in mice. We find that pre-existing meningeal lymphatic dysfunction potentiates the inflammatory response to TBI, suggesting an important role for the meningeal lymphatics in injury site drainage and proper recovery.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
32 Samples
Download data: TXT
Series
Accession:
GSE155063
ID:
200155063
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