Schizophrenia metagenome
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ABSTRACT:
PROVIDER: PRJEB29415 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Metagenome data from soil samples were collected at 0 to 10cm deep from 2 avocado orchards in Channybearup, Western Australia, in 2024. Amplicon sequence variant (ASV) tables were constructed based on the DADA2 pipeline with default parameters.
2025-06-15 | GSE298403 | GEO
Project description:Schizophrenia is a severe psychiatric disorder. Another study in BD has shown an aberrant pro-inflammatory status of monocytes/macrophages. Therefore, this study aimed at studying the monocyte compartment in schizophrenia, by transcription profiling of CD14+ monocytes in patients and controls.
2010-11-20 | E-MEXP-2998 | biostudies-arrayexpress
Project description:A large portion of common variant loci associated with genetic risk for schizophrenia reside within non-coding sequence of unknown function. Here, we demonstrate promoter and enhancer enrichment in schizophrenia variants associated with expression quantitative trait loci (eQTL). The enrichment is greater when functional annotations derived from human brain are used relative to peripheral tissues. Regulatory trait concordance analysis ranked genes within schizophrenia genome-wide significant loci, based on co-localization of a risk SNP, eQTL and regulatory element sequence. These include physical interactions of non-contiguous gene-proximal and distal elements bypassing the linear genome, which was verified in prefrontal cortex and human induced pluripotent stem cell derived neurons for the L-type calcium channel (CACNA1C) risk locus. Our findings point to a functional link between schizophrenia-associated non-coding SNPs and 3-dimensional genome architecture associated with chromosomal loopings and transcriptional regulation in the brain. Examination of H3K4me3 histone modifications in 3 samples.
2014-10-17 | E-GEOD-62391 | biostudies-arrayexpress
Project description:Schizophrenia Targeted Sequencing
| PRJEB9045 | ENA
Project description:Despite of multiple systematic studies of schizophrenia pathogenesis, reconstruction of the mechanism established on proteomics, metabolomics, and genome-wide significant loci is still a challenging task. We suggested that advanced data for quantitative proteomics, metabolomics, and genome-wide association study (GWAS) may enhance the current evidence and fundamental knowledge about molecular pathogenesis of schizophrenia. Liquide chromatography and ultra-high-resolution mass-spectrometry were utilized for proteomic and metabolomic assay, and high throughput genotyping for the GWAS study. Proteomic and metabolomic results were quantitatively evaluated and overlayed on the GWAS data. After statistical analysis using R-package, the resulting features were associated in a multilayer mode with adjusted biological processes in a reconstructed unified map of molecular events. We have identified 20 DFE proteins that were validated on an independent cohort of patients that are significant for schizophrenia, including ALS, A1AG1, PEDF, VTDB, CERU, APOB, APOH, FASN, GPX3, etc. Almost half of them are new for schizophrenia. The metabolomic survey revealed 18 compounds most of which were the part transformation of tyrosine and steroids with the incline to androgens (androsterone sulfate, thyroliberin, thyroxine, dihydrotestosterone, androstenedione, cholesterol sulfate, metanephrine, dopaquinone, etc.) which were extracted as group-specific determinants that permits to isolate patients with schizophrenia. The GWAS assay revealed 52 loci were integrated into proteome-metabolome data as significantly implicated in schizophrenia. We integrated three layers of omics science (proteomics, metabolomics and GWAS) and quantitative analysis utilized systematic approach to reconstruct the proposed map of molecular events associated with the considered psychopathology. The resulting interplay between different layers emphasized strict implication of lipids metabolism, oxidative stress, imbalance in steroidogenesis and associated impartments of thyroid hormones and sex hormones interconnection. The proposed interplay map can give opportunity in the understanding how the regulation of distinct metabolic axis is achieved and what happens in proteome arrangements to produce a schizophrenia-specific pattern of pathology condition.
2023-02-08 | PXD035863 | Pride
Project description:Genome-wide association study (GWAS) was performed in 120 patient-parents trio samples from Japanese schizophrenia pedigrees ABSTRACT: Schizophrenia is a devastating neuropsychiatric disorder with genetically complex traits. Genetic variants should explain a considerable portion of the risk for schizophrenia, and genome-wide association study (GWAS) is a potentially powerful tool for identifying the risk variants that underlie the disease. Here, we report the results of a three-stage analysis of three independent cohorts consisting of a total of 2,535 samples from Japanese and Chinese populations for searching schizophrenia susceptibility genes using a GWAS approach. Firstly, we examined 115,770 single nucleotide polymorphisms (SNPs) in 120 patient-parents trio samples from Japanese schizophrenia pedigrees. In stage II, we evaluated 1,632 SNPs (1,159 SNPs of p < 0.01 and 473 SNPs of p < 0.05 that located in previously reported linkage regions). The second sample consisted of 1,012 case-control samples of Japanese origin. The most significant p value was obtained for the SNP in the ELAVL2 [(embryonic lethal, abnormal vision, Drosophila)-like 2] gene located on 9p21.3 (p = 0.00087). In stage III, we scrutinized the ELAVL2 gene by genotyping gene-centric tagSNPs in the third sample set of 293 family samples (1,163 individuals) of Chinese descent and the SNP in the gene showed a nominal association with schizophrenia in Chinese population (p = 0.026). The current data in Asian population would be helpful for deciphering ethnic diversity of schizophrenia etiology.
2011-06-13 | GSE27923 | GEO
Project description:Schizophrenia is a severe psychiatric disease with complex etiology, affecting approximately one percent of the general population. Most genetic studies so far focused on disease association with common genetic variation such as single nucleotide polymorphisms, but recently it has become apparent that large-scale genomic copy number variants (CNVs) are involved in disease development as well. To assess the role of rare CNVs in schizophrenia, we screened 54 patients with deficit schizophrenia using Affymetrix’ GeneChip 250K SNP arrays. Keywords: genomic hybridisation
2008-10-22 | GSE12714 | GEO
Project description:Schizophrenia is a severe psychiatric illness that affects ~1% of the population and has a strong genetic underpinning. Recently, genome wide analysis of copy number variation (CNV) has implicated rare and de novo events as important in schizophrenia. Here we report a genome-wide analysis of 245 schizophrenia cases and 490 controls, all of Ashkenazi Jewish descent. Since many studies have found an excess burden of large, rare deletions in cases, we limited our analysis to deletions over 500 kb in size. We observed seven large, rare deletions in cases with 57% of these being de novo. We focused on one 836 kb de novo deletion at chromosome 3q29 that falls within a 1.3–1.6 Mb deletion previously identified in children with intellectual disability (ID) and autism, as increasing evidence suggests an overlap of specific rare CNVs between autism and schizophrenia. By combining our data with prior CNV studies of schizophrenia and analysis of the data of the Genetic Association Information Network (GAIN), we identified six 3q29 deletions among 7,545 schizophrenic subjects and one among 39,748 controls, resulting in a statistically significant association with schizophrenia (p = 0.02) and an odds ratio estimate of 17 (95% CI: 1.36–1198.4). Moreover, this 3q29 deletion region contains two linkage peaks from prior schizophrenia family studies, and the minimal deletion interval implicates 20 annotated genes, including PAK2 and DLG1, both paralogous to X-linked ID genes and now strong candidates for schizophrenia susceptibility.
2010-08-06 | GSE23201 | GEO
Project description:Dietary intake of fruits and vegetables (FV) has been inversely associated with lower risk of ulcerative colitis. A pig model was used to evaluate the impact of feeding FV on the host response to dextran sulfate sodium (DSS)-induced colitis. Methods: Six-week-old pigs were fed a grower diet alone or supplemented with lyophilized FV equivalent to the half (half-FV) or full (full-FV) daily levels recommended for humans by the Dietary Guidelines for Americans (DGA). Pigs were fed a 1) grower diet alone (negative control), 2) grower diet and orally treated with 4% DSS for 10 days to induce colitis (positive control), 3) half-FV diet treated with 4% DSS or 4) full-FV diet treated with 4% DSS. Pigs were monitored for the development of clinical signs of colitis. Proximal colon (PC) contents and mucosa (PCM) were collected for gut metagenome, tissue transcriptome and histopathological analysis. Results: Pigs fed the full-FV diet did not exhibit diarrhea, showed less fecal occult blood (FOB), PCM crypt hyperplasia but with no differential expressed genes (DEG) or changes in PC microbiome diversity (p < 0.05). Pigs within the half-FV group exhibited increased group FOB and DEG associated with tissue remodeling, crypt and goblet cell hyperplasia in the PCM and no changes in PC microbiome diversity and two pigs exhibiting diarrhea (p < 0.05). Pigs within the DSS positive control group exhibited a reduced DEG involved with intestinal immune response and PC microbiome diversity with altered metagenome, increased group PCM erosion and FOB with persistent diarrhea in one pig (p < 0.05) Conclusions: Overall, our results showed that pigs fed a three-week full-FV supplemented diet, were resistant to DSS-induced colitis with a differential dose-dependent protective effect on host intestinal tissue and gut metagenome when exposed to an inflammatory challenge.
2026-04-01 | GSE317287 | GEO