GeneVenn - A web application for comparing gene lists using Venn diagrams-1

<p><b>Copyright information:</b></p><p>Taken from "GeneVenn - A web application for comparing gene lists using Venn diagrams"</p><p>Bioinformation 2007;1(10):420-422.</p><p>Published online 10 Apr 2007</p><p>PMCID:PMC1899164.</p><p></p

GeneVenn - A web application for comparing gene lists using Venn diagrams-0

<p><b>Copyright information:</b></p><p>Taken from "GeneVenn - A web application for comparing gene lists using Venn diagrams"</p><p>Bioinformation 2007;1(10):420-422.</p><p>Published online 10 Apr 2007</p><p>PMCID:PMC1899164.</p><p></p

A comparative study of different machine learning methods on microarray gene expression data-2

classification methods<p><b>Copyright information:</b></p><p>Taken from "A comparative study of different machine learning methods on microarray gene expression data"</p><p>http://www.biomedcentral.com/1471-2164/9/S1/S13</p><p>BMC Genomics 2008;9(Suppl 1):S13-S13.</p><p>Published online 20 Mar 2008</p><p>PMCID:PMC2386055.</p><p></p

Results of 10-fold cross validation of the classification methods applied to all datasets without performing any feature selection

<p><b>Copyright information:</b></p><p>Taken from "A comparative study of different machine learning methods on microarray gene expression data"</p><p>http://www.biomedcentral.com/1471-2164/9/S1/S13</p><p>BMC Genomics 2008;9(Suppl 1):S13-S13.</p><p>Published online 20 Mar 2008</p><p>PMCID:PMC2386055.</p><p></p

A comparative study of different machine learning methods on microarray gene expression data-3

And classification methods<p><b>Copyright information:</b></p><p>Taken from "A comparative study of different machine learning methods on microarray gene expression data"</p><p>http://www.biomedcentral.com/1471-2164/9/S1/S13</p><p>BMC Genomics 2008;9(Suppl 1):S13-S13.</p><p>Published online 20 Mar 2008</p><p>PMCID:PMC2386055.</p><p></p

Gene Expression Analysis of CL-20-Induced Reversible Neurotoxicity Reveals GABA_A Receptors as Potential Targets in the Earthworm <i>Eisenia fetida</i>

The earthworm <i>Eisenia fetida</i> is one of the most used species in standardized soil ecotoxicity tests. End points such as survival, growth, and reproduction are eco-toxicologically relevant but provide little mechanistic insight into toxicity pathways, especially at the molecular level. Here we apply a toxicogenomic approach to investigate the mode of action underlying the reversible neurotoxicity of hexanitrohexaazaisowurtzitane (CL-20), a cyclic nitroamine explosives compound. We developed an <i>E. fetida</i>-specific shotgun microarray targeting 15119 unique <i>E. fetida</i> transcripts. Using this array we profiled gene expression in <i>E. fetida</i> in response to exposure to CL-20. Eighteen earthworms were exposed for 6 days to 0.2 μg/cm² of CL-20 on filter paper, half of which were allowed to recover in a clean environment for 7 days. Nine vehicle control earthworms were sacrificed at days 6 and 13, separately. Electrophysiological measurements indicated that the conduction velocity of earthworm medial giant nerve fiber decreased significantly after 6-day exposure to CL-20, but was restored after 7 days of recovery. Total RNA was isolated from the four treatment groups including 6-day control, 6-day exposed, 13-day control, and 13-day exposed (i.e., 6-day exposure followed by 7-day recovery), and was hybridized to the 15K shotgun oligo array. Statistical and bioinformatic analyses suggest that CL-20 initiated neurotoxicity by noncompetitively blocking the ligand-gated GABA_A receptor ion channel, leading to altered expression of genes involved in GABAergic, cholinergic, and Agrin-MuSK pathways. In the recovery phase, expression of affected genes returned to normality, possibly as a result of autophagy and CL-20 dissociation/metabolism. This study provides significant insights into potential mechanisms of CL-20-induced neurotoxicity and the recovery of earthworms from transient neurotoxicity stress

Gene Expression Analysis of CL-20-Induced Reversible Neurotoxicity Reveals GABA_A Receptors as Potential Targets in the Earthworm <i>Eisenia fetida</i>

The earthworm <i>Eisenia fetida</i> is one of the most used species in standardized soil ecotoxicity tests. End points such as survival, growth, and reproduction are eco-toxicologically relevant but provide little mechanistic insight into toxicity pathways, especially at the molecular level. Here we apply a toxicogenomic approach to investigate the mode of action underlying the reversible neurotoxicity of hexanitrohexaazaisowurtzitane (CL-20), a cyclic nitroamine explosives compound. We developed an <i>E. fetida</i>-specific shotgun microarray targeting 15119 unique <i>E. fetida</i> transcripts. Using this array we profiled gene expression in <i>E. fetida</i> in response to exposure to CL-20. Eighteen earthworms were exposed for 6 days to 0.2 μg/cm² of CL-20 on filter paper, half of which were allowed to recover in a clean environment for 7 days. Nine vehicle control earthworms were sacrificed at days 6 and 13, separately. Electrophysiological measurements indicated that the conduction velocity of earthworm medial giant nerve fiber decreased significantly after 6-day exposure to CL-20, but was restored after 7 days of recovery. Total RNA was isolated from the four treatment groups including 6-day control, 6-day exposed, 13-day control, and 13-day exposed (i.e., 6-day exposure followed by 7-day recovery), and was hybridized to the 15K shotgun oligo array. Statistical and bioinformatic analyses suggest that CL-20 initiated neurotoxicity by noncompetitively blocking the ligand-gated GABA_A receptor ion channel, leading to altered expression of genes involved in GABAergic, cholinergic, and Agrin-MuSK pathways. In the recovery phase, expression of affected genes returned to normality, possibly as a result of autophagy and CL-20 dissociation/metabolism. This study provides significant insights into potential mechanisms of CL-20-induced neurotoxicity and the recovery of earthworms from transient neurotoxicity stress

Gene Expression Analysis of CL-20-Induced Reversible Neurotoxicity Reveals GABA_A Receptors as Potential Targets in the Earthworm <i>Eisenia fetida</i>

The earthworm <i>Eisenia fetida</i> is one of the most used species in standardized soil ecotoxicity tests. End points such as survival, growth, and reproduction are eco-toxicologically relevant but provide little mechanistic insight into toxicity pathways, especially at the molecular level. Here we apply a toxicogenomic approach to investigate the mode of action underlying the reversible neurotoxicity of hexanitrohexaazaisowurtzitane (CL-20), a cyclic nitroamine explosives compound. We developed an <i>E. fetida</i>-specific shotgun microarray targeting 15119 unique <i>E. fetida</i> transcripts. Using this array we profiled gene expression in <i>E. fetida</i> in response to exposure to CL-20. Eighteen earthworms were exposed for 6 days to 0.2 μg/cm² of CL-20 on filter paper, half of which were allowed to recover in a clean environment for 7 days. Nine vehicle control earthworms were sacrificed at days 6 and 13, separately. Electrophysiological measurements indicated that the conduction velocity of earthworm medial giant nerve fiber decreased significantly after 6-day exposure to CL-20, but was restored after 7 days of recovery. Total RNA was isolated from the four treatment groups including 6-day control, 6-day exposed, 13-day control, and 13-day exposed (i.e., 6-day exposure followed by 7-day recovery), and was hybridized to the 15K shotgun oligo array. Statistical and bioinformatic analyses suggest that CL-20 initiated neurotoxicity by noncompetitively blocking the ligand-gated GABA_A receptor ion channel, leading to altered expression of genes involved in GABAergic, cholinergic, and Agrin-MuSK pathways. In the recovery phase, expression of affected genes returned to normality, possibly as a result of autophagy and CL-20 dissociation/metabolism. This study provides significant insights into potential mechanisms of CL-20-induced neurotoxicity and the recovery of earthworms from transient neurotoxicity stress

Genome-wide Methyl-Seq analysis of blood-brain targets of glucocorticoid exposure

<p>Chronic exposure to glucocorticoids (GCs) can lead to psychiatric complications through epigenetic mechanisms such as DNA methylation (DNAm). We sought to determine whether epigenetic changes in a peripheral tissue can serve as a surrogate for those in a relatively inaccessible tissue such as the brain. DNA extracted from the hippocampus and blood of mice treated with GCs or vehicle solution was assayed using a genome-wide DNAm platform (Methyl-Seq) to identify differentially methylated regions (DMRs) induced by GC treatment. We observed that ∼70% of the DMRs in both tissues lost methylation following GC treatment. Of the 3,095 DMRs that mapped to the same genes in both tissues, 1,853 DMRs underwent DNAm changes in the same direction. Interestingly, only 209 DMRs (<7%) overlapped in genomic coordinates between the 2 tissues, suggesting tissue-specific differences in GC-targeted loci. Pathway analysis showed that the DMR-associated genes were members of pathways involved in metabolism, immune function, and neurodevelopment. Also, changes in cell type composition of blood and brain were examined by fluorescence-activated cell sorting. Separation of the cortex into neuronal and non-neuronal fractions and the leukocytes into T-cells, B-cells, and neutrophils showed that GC-induced methylation changes primarily occurred in neurons and T-cells, with the blood tissue also undergoing a shift in the proportion of constituent cell types while the proportion of neurons and glia in the brain remained stable. From the current pilot study, we found that despite tissue-specific epigenetic changes and cellular heterogeneity, blood can serve as a surrogate for GC-induced changes in the brain.</p

Power estimates for multiple genes case-control studies with causal variants from disease etiologies randomly sampled from nine multinomial distributions (Figure S3).

<p>Power estimates for BOMP, VT, SKAT, KBAC (KBAC1P = minor allele frequency defined as , KBAC5P = minor allele frequency defined as ). Each vertical line represents power estimates for each method, based on 250 simulated case-control studies. The genomic individuals each had nine genes, of which three contained causal variants and six did not. The disease etiologies for the three genes with causal variants were randomly sampled from nine multinomial distributions (<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1003224#pgen.1003224.s003" target="_blank">Figure S3</a>). AA = African-American simple bottleneck demographic model. EA = European-American exponential growth demographic model.</p