Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12527043_subreads.fastq.gz | Fastqsanger.gz | |||
| SRR12527044_subreads.fastq.gz | Fastqsanger.gz | |||
| SRR12527045_subreads.fastq.gz | Fastqsanger.gz | |||
| SRR12527046_subreads.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Social anxiety disorder (SAD) is a psychiatric disorder characterized by severe fear in social situations and avoidance of these. Multiple genetic as well as environmental factors contribute to the etiopathology of SAD. One of the main risk factors for SAD is stress, especially during early periods of life (early life adversity; ELA). ELA leads to structural and regulatory alterations contributing to disease vulnerability. This includes the dysregulation of the immune response. However, the molecular link between ELA and the risk for SAD in adulthood remain largely unclear. Evidence is emerging that long-lasting changes of gene expression patterns play an important role in the biological mechanisms linking ELA and SAD. Therefore, we conducted a transcriptome study of SAD and ELA performing RNA sequencing in peripheral blood samples. Analyzing differential gene expression between individuals suffering from SAD with high or low levels of ELA and healthy individuals with high or low levels of ELA, 13 significantly differentially expressed genes (DEGs) were identified with respect to SAD whilst no significant differences in expression were identified with respect to ELA. The most significantly expressed gene was MAPK3 (p=0.003) being upregulated in the SAD group compared to control individuals. In contrary, weighted gene co-expression network analyses (WGCNA) identified only modules significantly associated with ELA (p≤0.05), not with SAD. Furthermore, analyzing interaction networks of the genes from the ELA-associated modules and the SAD-related MAPK3) revealed complex interactions of those genes. Gene functional enrichment analyses indicate a role of signal transduction pathways as well as inflammatory responses supporting an involvement of the immune system in the association of ELA and SAD. In conclusion, we did not identify a direct molecular link between ELA and adult SAD by transcriptional changes. However, our data indicate an indirect association of ELA and SAD mediated by the interaction of genes involved in immune-related signal transduction.
2023-04-16 | GSE228702 | GEO
Project description:We report here lead optimisation efforts for molecule GW861072X, one of 177 leads published in a GSK-led phenotypic screening campaign by Balell et al. (2013), generating the AX series. Along with the parent compound AX-35, four other derivatives with mild to no cytotoxicity showed potent in vitro and ex vivo activity in infected THP-1 macrophages against M. tuberculosis. Isolation of resistant mutants to AX compounds in M. tuberculosis revealed mutations in the QcrB of the cytochrome bc1 oxidase, one of two terminal oxidases of the mycobacterial electron transport chain. Cross-resistance studies, transcriptomic analyses and bioenergetics flux assays provide further evidence of QcrB as the target of the AX compounds, and that AX compounds likely interact differently with the quinol binding pocket compared to other QcrB inhibitors. The transcriptomic and bioenergetic profiles obtained when M. tuberculosis was treated with AX-35 are similar to transcriptomic and respiratory signatures of other cytochrome bc1 oxidase inhibitors, whereby the pronounced role of the alternate terminal oxidase cytochrome bd in the respiratory adaptation of M. tuberculosis could be observed. Genes involved in utilisation and synthesis of triacylglycerol (TAG) were also additionally observed to be up-regulated with AX treatment, indicating a switch induced towards lipid metabolism under this particular stress.
2018-04-26 | GSE113683 | GEO
Project description:Social anxiety disorder (SAD) is a psychiatric disorder characterized by extensive fear in social situations. Multiple genetic and environmental factors are known to contribute to its pathogenesis. One of the main environmental risk factors is early life adversity (ELA). Evidence is emerging that epigenetic mechanisms such as DNA methylation might play an important role in the biological mechanisms underlying SAD and ELA. To investigate the relationship between ELA, DNA methylation, and SAD, we performed an epigenome-wide association study for SAD and ELA examining DNA from whole blood of a cohort of 143 individuals using DNA methylation arrays. We identified two differentially methylated regions (DMRs) associated with SAD located within the genes SLC43A2 and TNXB. As this was the first epigenome-wide association study for SAD, it is worth noting that both genes have previously been associated with panic disorder. Further, we identified two DMRs associated with ELA within the SLC17A3 promoter region and the SIAH3 gene and several DMRs that were associated with the interaction of SAD and ELA. Of these, the regions within C2CD2L and MRPL28 showed the largest difference in DNA methylation. Lastly, we found that two DMRs were associated with both the severity of social anxiety and ELA, however, neither of them was found to mediate the contribution of ELA to SAD later in life. Future studies are needed to replicate our findings in independent cohorts and to investigate the biological pathways underlying these effects.
2021-01-31 | GSE164056 | GEO
Project description:Although exercise and dietary interventions on cognitive function have been investigated, synergistic interactions remain unclear. As tested on hippocampus-dependent functions, mild exercise (ME) or astaxanthin (AX), a naturally-occurring antioxidant and cognitive enhancer, each boost the hippocampus-related memory and neurogenesis. Here we show that leptin (LEP) is required for the synergistic enhancement of hippocampal function by a combination of ME and AX. In C57BL/6J mice, ME or AX alone enhanced spatial memory and neurogenesis, but the enhancement was greater with their combination. DNA microarray analysis showed that the up-regulation of the Lep gene by ME alone was further elevated when combined with AX. The combined interventions synergistically increased hippocampal LEP protein, which was positively correlated with memory enhancement. In LEP-deficient mice, the combined interventions did not enhance memory compared to ME alone, leading us to suggest that the brain-derived LEP has an essential role for the synergistic effect on hippocampal functions.
2017-11-25 | GSE107314 | GEO
Project description:Brassinosteroid (BR) and auxin co-regulate plant growth in a process termed cross-talking. Based on the assumption that their signal transductions are partially shared, inhibitory chemicals for both signal transductions were screened from a commercially-available library. A chemical designated as NJ15 (ethyl 2-[5-(3,5-dichlorophenyl)-1,2,3,4-tetrazole-2-yl]acetate) diminished the growth promotion of both adzuki bean epicotyls and Arabidopsis seedlings, by either the application of BR or auxin. To understand its target site(s), bioassays with a high dependence on either the signal transduction of BR (BR-signaling) or of auxin (AX-signaling), were performed. NJ15 inhibited photomorphogenesis of Arabidopsis seedlings grown in the dark, which mainly depends on BR-signaling, while NJ15 also inhibited their gravitropic responses mainly depending on AX-signaling. On the study for the structure-activity relationships of NJ15 analogues, they showed strong correlations on the inhibitory profiles between BR- and AX-signalings. These correlations imply that NJ15 targets the downstream pathway after the integration of BR- and AX-signals.
2014-11-03 | GSE57449 | GEO
Project description:Mesenchymal stromal cells from adipose tissue (AD-MSCs) exhibit favourable clinical traits for autologous transplantation and can develop a ‘Schwann-like’ phenotype (sAD-MSCs) to improve peripheral nerve regeneration, where severe injuries yield insufficient recovery. However, sAD-MSCs regress without biochemical stimulation and detach from conduits under unfavourable transplant conditions, negating their paracrine effects. Graphene-derived materials support AD-MSC attachment, regulating cell adhesion and function through physiochemistry and topography. We report graphene oxide (GO) as a suitable substrate for human sAD-MSCs incubation towards severe peripheral nerve injuries, through evaluating transcriptome changes, neurotrophic factor expression over a 7-day period, and cell viability in apoptotic conditions. Transcriptome changes from GO incubation across four patients were minor compared to biological variance.
2021-03-08 | E-MTAB-10078 | biostudies-arrayexpress
Project description:Using Multiome and previously published sc/snRNA-seq data, we studied eight anatomical regions of the human heart including left and right ventricular free walls (LV and RV), left and right atria (LA and RA), left ventricular apex (AX), interventricular septum (SP), sino-atrial node (SAN) and atrioventricular node (AVN). For the first time, we profile the cells of the human cardiac conduction system, revealing their distinctive repertoire of ion channels, G-protein coupled receptors and cell-cell interactions. We map the identified cells to spatial transcriptomic data to discover cellular niches within the eight regions of the heart.
2023-06-01 | E-MTAB-12975 | biostudies-arrayexpress