Project description:Cortical Dysplasia (CD) is the histopathological substrate in almost half of all drug-resistant epilepsy. Little is known about the gene expression profile of CD. As such information may help target therapeutics more effectively, our aim was to perform a gene expression analysis of an animal model of cortical dysplasia induced by in utero irradiation. THIS SERIES (GSE13676) INCLUDES ALL (AND ONLY) CONTROL SAMPLES (9).
Project description:Cortical Dysplasia (CD) is the histopathological substrate in almost half of all drug-resistant epilepsy. Little is known about the gene expression profile of CD. As such information may help target therapeutics more effectively, our aim was to perform a gene expression analysis of an animal model of cortical dysplasia induced by in utero irradiation. THIS SERIES (GSE13697) INCLUDES ALL (AND ONLY) EXPERIMENTAL SAMPLES--I.E. IRRADIATED/CORTICAL DYSPLASIA (9).
Project description:Cortical Dysplasia (CD) is the histopathological substrate in almost half of all drug-resistant epilepsy. Little is known about the gene expression profile of CD. As such information may help target therapeutics more effectively, our aim was to perform a gene expression analysis of an animal model of cortical dysplasia induced by in utero irradiation. THIS SERIES (GSE13697) INCLUDES ALL (AND ONLY) EXPERIMENTAL SAMPLES--I.E. IRRADIATED/CORTICAL DYSPLASIA (9). Nine offspring from irradiated animals, and nine age-matched controls were sacrificed at post-natal day 60. Cortex and hippocampal regions were separated, and total ribonucleic acid (RNA) was extracted using a commercially available kit (Qiagen®). RNA was then subjected to a gene expression analysis using an oligonucleotide microarray platform (Illumina®). After statistical analysis, genes were considered differentially expressed when a p value less than .001 was observed. Real-time, quantitative polymerase chain reaction (RT-qPCR) was used to confirm microarray results for three genes via the Livak method.
Project description:Cortical Dysplasia (CD) is the histopathological substrate in almost half of all drug-resistant epilepsy. Little is known about the gene expression profile of CD. As such information may help target therapeutics more effectively, our aim was to perform a gene expression analysis of an animal model of cortical dysplasia induced by in utero irradiation. THIS SERIES (GSE13676) INCLUDES ALL (AND ONLY) CONTROL SAMPLES (9). Nine offspring from irradiated animals, and nine age-matched controls were sacrificed at post-natal day 60. Cortex and hippocampal regions were separated, and total ribonucleic acid (RNA) was extracted using a commercially available kit (Qiagen®). RNA was then subjected to a gene expression analysis using an oligonucleotide microarray platform (Illumina®). After statistical analysis, genes were considered differentially expressed when a p value less than .001 was observed. Real-time, quantitative polymerase chain reaction (RT-qPCR) was used to confirm microarray results for three genes via the Livak method.
Project description:Analysis of hormone effects on irradiated LBNF1 rat testes, which contain only somatic cells except for a few type A spermatgogonia. Rats were treated for 2 weeks with either sham treatment (group X), hormonal ablation (GnRH antagonist and the androgen receptor antagonist flutamide, group XAF), testosterone supplementation (GnRH antagonist and testosterone, group XAT), and FSH supplementation ((GnRH antagonist, androgen receptor antagonist, and FSH, group XAFF). Results provide insight into identifying genes in the somatic testis cells regulated by testosterone, LH, or FSH.
Project description:Living organisms are intricate systems with dynamic internal processes. Their RNA, protein, and metabolite levels fluctuate in response to variations in health and environmental conditions. Among these, RNA expression is particularly accessible for comprehensive analysis, thanks to the evolution of high throughput sequencing technologies in recent years. This progress has enabled researchers to identify unique RNA patterns associated with various diseases, as well as to develop predictive and prognostic biomarkers for therapy response. Such cross-sectional studies allow for the identification of differentially expressed genes (DEGs) between groups, but they have limitations. Specifically, they often fail to capture the temporal changes in gene expression following individual perturbations and may lead to significant false discoveries due to inherent noise in RNA sequencing sample preparation and data collection. To address these challenges, our study hypothesized that frequent, longitudinal RNA sequencing (RNAseq) analysis of blood samples could offer a more profound understanding of the temporal dynamics of gene expression in response to drug interventions, while also enhancing the accuracy of identifying genes influenced by these drugs. In this research, we conducted RNAseq on 829 blood samples collected from 84 Sprague-Dawley lab rats. Excluding the control group, each rat was administered one of four different compounds known for liver toxicity: tetracycline, isoniazid, valproate, and carbon tetrachloride. We developed specialized bioinformatics tools to pinpoint genes that exhibit temporal variation in response to these treatments.