Macaca Fascicularis Differential Gene Expression Following Stroke: Control versus Tat-NR2B9c Treated Cortex at 1 hour and 6 hours following middle cerebral aretry occlusion (MCAO)
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ABSTRACT:
ORGANISM(S): Macaca fascicularis Macaca mulatta
PROVIDER: GSE35589 | GEO | 2012/02/08
SECONDARY ACCESSION(S): PRJNA152661
REPOSITORIES: GEO
Similar Datasets
Project description:Differential gene expression comparison between cortex of placebo and PSD-95 inhibitor (Tat-NR2B9c), treated cynomolgus macaques at 1 and 6 hours after middle cerebral artery occlusion. The purpose of this study was to identify changes in differential gene expression in the cortex of animals receiving strokes across the two time points and bewtwee the two treatment groups. Differential gene expression was defined as the ratio of fluroescene detected for expressed sequence tags in the left, unoperated cortex versus the contralateral, right, ischemic cortex at each time point. Two colour, Agilent, 4x44k whole genome macaca mulata microarrays with sample rna hybridized to Cy5 channel and universal macaca mulatta rna control on the Cy3 channel were obtained for each hemisphere. Comparisons between treatment groups at each time point and within in each treatment group across each time point were made to detect differential gene expression. Significant differential gene expression was defined as greater than 2-fold change and p<0.05 by T-test. Three condition experiment comparing the effect of treatment with placebo versus Tat-NR2B9c administered 5 min after MCAO with tissue samples collected 1h and 6h after MCAO and a second comparison of gene expression within each treatment group between 1h and 6h: 3 biological replicates in each group
2012-02-08 | E-GEOD-35589 | biostudies-arrayexpress
Project description:Purpose: The goal of this study is to understand the role of co-administred amiloride. This was derived through RNAseq of kidney cortex and determining differential genes in response to lithium, lithium+amiloride and control at 14 days, 28 days and 6 months. Methods: RNAseq of kidney cortex treated with either lithium alone, lithium+amiloride or control. Deseq2 was performed using contrast argument with Wald test to identify significant differentially expression genes at each time point individually. Result & Conclusion: Co-administration with amiloride at all time points contributed in the reduction of inflammation and fibrosis caused by lithium.
2022-08-31 | GSE178950 | GEO
Project description:Organophosphorus nerve agents irreversibly inhibit acetylcholinesterase, causing a toxic buildup of acetylcholine at muscarinic and nicotinic receptors. Current medical countermeasures to nerve agent intoxication increase survival if administered within a short period of time following exposure but may not fully prevent neurological damage. Therefore, there is a need to discover drug treatments that are effective when administered after the onset of seizures and secondary responses that lead to brain injury. Methods To determine potential therapeutic targets for such treatments, we analyzed gene expression changes in the rat piriform cortex following sarin (O-isopropyl methylphosphonofluoridate) exposure. Male Sprague-Dawley rats were challenged with 1.0 x LD50 sarin and subsequently treated with atropine sulfate, 2-pyridine aldoxime methylchloride (2-PAM), and the anticonvulsant diazepam. Control animals received an equivalent volume of vehicle and drug treatments. The piriform cortex, a brain region particularly sensitive to neural damage from sarin-induced seizures, was extracted at 0.25, 1, 3, 6, and 24 h after seizure onset, and total RNA was processed for microarray analysis. Principal component analysis identified sarin-induced seizure occurrence and time point following seizure onset as major sources of variability within the dataset. Based on these variables, the dataset was filtered and analysis of variance was used to determine genes significantly changed in seizing animals at each time point. The calculated p-value and geometric fold change for each probeset identifier were subsequently used for gene ontology analysis to identify canonical pathways, biological functions, and networks of genes significantly affected by sarin-induced seizure over the 24-h time course. Results A multitude of biological functions and pathways were identified as being significantly altered following sarin-induced seizure. Inflammatory response and signaling pathways associated with inflammation were among the most significantly altered across the five time points examined. Conclusions This analysis of gene expression changes in the rat brain following sarin-induced seizure and the molecular pathways involved in sarin-induced neurodegeneration will allow a better identification of potential therapeutic targets for the development of effective neuroprotectants to treat nerve agent exposure.
2011-12-31 | GSE28435 | GEO
Project description:This experiment set contains all of the arrays described in Baldwin et al., Genome Biology, 2002. All experiments are time courses, with the exception of multiple measurements for the zero time point in the parallel time course for the purpose of zero transformation. The parallel four hour time course was performed on a single day and three independent measurements were taken prior to infection. The eight hour time courses were each performed on different days, with single time zero measurements. Each array represents a measurement of human mRNA from cultured intestinal epithelial cells (red channel), relative to the control reference pool of mRNA (green channel), at different time points during the course of an infection by Listeria monocytogenes, or the mutants actA (defective in actin-based motility) and prfA (defective in virulence factor gene expression). Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set
2005-11-05 | GSE3567 | GEO
Project description:Stroke is a leading cause of mortality and long-term disability and ischemic stroke accounts for 87% of all strokes. Though timely recanalization of the occluded vessel is essential in the treatment of ischemic stroke, it is well known to cause ischemia-reperfusion (I/R) injury which result in neuronal cell death, brain tissue loss and severe neurological deficits. In this work, we employed a global proteomic approach to examine the changes of cerebral cortex proteins in rats undergoing acute and long-term I/R injury. In vivo middle cerebral artery occlusion (MCAO) model of focal cerebral I/R injury in rats was established. The animals were divided into three model groups with 2 h-MCAO followed with different reperfusion time, 1 day, 7 days and 14 days, respectively. For each model group a sham group was correspondingly set. Each group included four animals. For proteomic analysis, cerebral cortex proteins were extracted and analyzed by SDS-PAGE, whole-lane slicing, in-gel digestion and label-free quantitative LC-MS/MS. A total of 5621 proteins were identified and their quantities between the surgery and corresponding sham groups and across the three reperfusion time points were compared for mechanism investigation. This dataset includes all the raw files of the 840 LC-MS runs (6 groups x 4 animals x 35 gel squares/sample), as well as their identification and quantitation results at the levels of peptide fragments, peptides and proteins, respectively.
2019-07-03 | PXD012151 | Pride
Project description:Organophosphorus nerve agents irreversibly inhibit acetylcholinesterase, causing a toxic buildup of acetylcholine at muscarinic and nicotinic receptors. Current medical countermeasures to nerve agent intoxication increase survival if administered within a short period of time following exposure but may not fully prevent neurological damage. Therefore, there is a need to discover drug treatments that are effective when administered after the onset of seizures and secondary responses that lead to brain injury. Methods To determine potential therapeutic targets for such treatments, we analyzed gene expression changes in the rat piriform cortex following sarin (O-isopropyl methylphosphonofluoridate) exposure. Male Sprague-Dawley rats were challenged with 1.0 x LD50 sarin and subsequently treated with atropine sulfate, 2-pyridine aldoxime methylchloride (2-PAM), and the anticonvulsant diazepam. Control animals received an equivalent volume of vehicle and drug treatments. The piriform cortex, a brain region particularly sensitive to neural damage from sarin-induced seizures, was extracted at 0.25, 1, 3, 6, and 24 h after seizure onset, and total RNA was processed for microarray analysis. Principal component analysis identified sarin-induced seizure occurrence and time point following seizure onset as major sources of variability within the dataset. Based on these variables, the dataset was filtered and analysis of variance was used to determine genes significantly changed in seizing animals at each time point. The calculated p-value and geometric fold change for each probeset identifier were subsequently used for gene ontology analysis to identify canonical pathways, biological functions, and networks of genes significantly affected by sarin-induced seizure over the 24-h time course. Results A multitude of biological functions and pathways were identified as being significantly altered following sarin-induced seizure. Inflammatory response and signaling pathways associated with inflammation were among the most significantly altered across the five time points examined. Conclusions This analysis of gene expression changes in the rat brain following sarin-induced seizure and the molecular pathways involved in sarin-induced neurodegeneration will allow a better identification of potential therapeutic targets for the development of effective neuroprotectants to treat nerve agent exposure. Three animals were used for each experimental group (naM-CM-/ve, sarin-exposed non-seizure, non-seizure control [saline], sarin-exposed seizure, and seizure control [saline]) at each time point (0.25, 1, 3, 6, 24 h), with the exception of 1 h seizure control, 3 h sarin-exposed seizure, 24 h sarin-exposed non-seizure, and 24 h sarin-exposed seizure (n=4).
2011-12-31 | E-GEOD-28435 | biostudies-arrayexpress
Project description:CEA_SGF:E00007# This set of experiments was made in order to perform time series analyses. RNAs from sham-irradiated cells at each time point were pooled together. We then hybridized sham-irradiated samples at each time point versus cDNAs obtained from the pooled RNA. Each time point was assessed with two independent dye-swap hybridizations. Keywords: time-course
2004-11-01 | GSE1369 | GEO
Project description:Array Design; Mouse Compugen 22K Spotted Oligo Author; Sean Grimmond Common Reference (Yes/No, ID); Yes Mouse universal Reference (Stratagene) Concentration; 100 Data processing/normalization; Lowess Normalisation GeneSpring) Developmental Stage; embryonic Diseased/Normal; normal Dye Swap; red/green Experiment Type; time course Genetic Characteristic; Wild type Image Analysis Software; Imagene5.5 (Biodiscovery) Labeling Protocol; Amino Allyl Message Amp- Ambion Organ/Organism part; kidney Organism; Mus Musculus RNA type; aRNA Message Amp-ambion Tissue Type; Pool of whole organs Organization; IMB, Uni of QLD, Brisbane Australia Sample Source; primary tissue Sampling Method; Dissection of whole organ Sex; Pool of both sexes Strain/Cell-line; CD1 Series_overall_design: To account for dye swap, the signal channel and control channel measurements for each sample were reversed. A Lowess curve was fit to the log-intensity versus log-ratio plot. 20.0% of the data was used to calculate the Lowess fit at each point. This curve was used to adjust the control value for each measurement. If the control channel was lower than 10 then 10 was used instead. Specific samples were normalized to one another: sample(s) 1-38 were normalized against the median of the control sample(s) 1-38. Each measurement for each gene in those specific samples was divided by the median of that gene's measurements in the corresponding control samples. Keywords: time-course
2005-07-20 | GSE2282 | GEO
Project description:We performed genome-wide bisulfite capture sequencing in prefrontal cortex in male mice at four timepoints (one day, two weeks, six months, and one year) post-neuropathic injury in order to track and observe dynamics of DNA methylation and epigenetic regulation in response to the development of chronic pain. We identified hundreds of differentially methylated CpGs and genes at FDR < 0.1 and differential methylation > 5%. PFC DNA methylation rapidly and robustly responds to neuropathic injury and genes display time point specific patterns of differential methylation.
2020-05-26 | GSE146215 | GEO
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2022-11-05 | GSE217115 | GEO