Project description:This study examined the miRNA expression level in exosomal derived from the plasma of first episode schizophrenia (FOS) patients and Healthy controls (HC), and explored the the potential of exosomes as biomarkers for schizophrenia. This study examined the lncRNA expression level in exosomal derived from the plasma of first episode schizophrenia (FOS) patients and Healthy controls (HC), and explored the the potential of exosomes as biomarkers for schizophrenia. This study examined the mRNA expression level in exosomal derived from the plasma of first episode schizophrenia (FOS) patients and Healthy controls (HC), and explored the the potential of exosomes as biomarkers for schizophrenia.
2023-08-30 | GSE228881 | GEO
Project description:Gut Virome in First-Episode Schizophrenia
| PRJNA1135500 | ENA
Project description:eccDNA in plasma from first-episode schizophrenia
Project description:Genome-wide patterns of DNA methylation were quantified using the Illumina Infinium HumanMethylation450K BeadChip (“450K array”) in DNA samples isolated from blood for schizophrenia cases, first episode psychosis patients and controls. These samples were profiled as part of a wider study where they were meta-analysed with other cohorts.
Project description:Genome-wide patterns of DNA methylation were quantified using the Illumina Infinium HumanMethylationEPIC BeadChip (“EPIC array”) in DNA samples isolated from blood for schizophrenia cases, first episode psychosis patients and controls. These samples were profiled as part of a wider study where they were meta-analysed with other cohorts.
2021-04-07 | GSE152026 | GEO
Project description:Gut microbiome in first-episode, drug-naive patients with Schizophrenia
Project description:To explore the genomic architecture of schizophrenia symptomatology, we analysed blood co-expression modules, i.e. clusters of genes with highly correlated expression, in a cohort of remitted first-episode schizophrenia patients with less than 5 years of evolution, and their association with clinical data, including global functioning, clinical symptomatology and premorbid adjustment.
Project description:The imbalance of intestinal flora can affect the immune function and structural integrity of the intestinal barrier, leading to the colonization and reproduction of opportunistic pathogenic bacteria in the intestine to become the dominant flora, eventually inducing enteritis. This study aimed to investigate whether fecal microbiota transplantation (FMT) could improve the gut barrier in Nile tilapia (Oreochromis niloticus). The experiment involved administering normal saline (NS group) and fecal microbiota (FMT group) (from the negative control group (C group)) to tilapia that had been treated with oxytetracycline hydrochloride (OTC) (M group) by gavage. A total of 300 male tilapia (mean body weight 596.65 ± 47.18 g) were used, with 180 of them being fed OTC (120 mg/kg body weight/day) for 7 days to induce intestinal oxidative stress, while the rest served as the control group. After confirmation of mild chronic enteritis, the tilapia were treated in different ways.
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.
Project description:Mental health profoundly impacts inflammatory responses in the body. This is particularly apparent in inflammatory bowel disease (IBD), where psychological stress is associated with disease flares. Here, we discover a critical role for the enteric nervous system (ENS) in mediating the aggravating effect of chronic stress on intestinal inflammation. We find that chronically elevated levels of glucocorticoids drive the generation of an inflammatory subset of enteric glia that promotes monocyte- and TNF-mediated colitis via CSF1. Additionally, glucocorticoids cause transcriptional immaturity in enteric neurons, acetylcholine deficiency, and dysmotility via TGFβ2. We verify the connection between the psychological state, intestinal inflammation, and dysmotility in two cohorts of human IBD patients. Together, these findings offer a mechanistic explanation for the impact of the brain on peripheral inflammation, define the ENS as a relay between psychological stress and gut inflammation, and suggest that stress management could serve as a valuable component of IBD care.