Project description:The study seeks to identify transcripts whose expression levels are significantly correlated with bedtime and awakening cortisol levels in healthy individuals.
Project description:CD4+ T cells, CD8+ T cells, CD14+ monocytes, and CD16+ neutrophils from the peripheral blood of 5 healthy individuals were isolated and their ex vivo transcriptomic profiles measured.
Project description:Total RNA from PBMCs isolated from TB patients and healthy individuals was subjected to RNASeq analysis. The samples among two groups were compared to analyze differentially expressed genes.
Project description:We performed whole-genome transcriptomic profiling of RNA from mononuclear cells from bone marrow aspirates taken from healthy individuals. This study complements GSE58335: transcriptomic profiling of peripheral blood mononuclear cells from healthy individuals.
Project description:DNA methylation likely plays a role in the regulation of human stress reactivity. In a genome-wide analysis of blood DNA methylation in 85 healthy individuals a locus in the Kit ligand (KITLG) gene (cg27512205) had the strongest association with cortisol stress reactivity (p=5.8x10-6). Replication was obtained in two independent samples, one using blood (N=45, p=0.001) and the other using buccal cells (N=255,p=0.004). KITLG methylation strongly mediated the relationship between childhood trauma and cortisol stress reactivity (32% mediation). Its genomic location (CpG island shore within an H3K27ac enhancer mark) provide further evidence that KITLG methylation is functionally relevant for the programming of stress reactivity. Our results extend preclinical evidence for epigenetic regulation of stress reactivity to humans and provide leads to enhance our understanding of the neurobiological pathways underlying stress vulnerability. Bisulphite converted DNA from whole blood of 85 healthy controls exposed to psychosocial stress task (TSST-G) was hybridised to the Illumina Infinium 450k Human Methylation Beadchip The DOI for this paper will be 10.1038/NCOMMS10967.
Project description:CD34+ cells from healthy individuals or those with primary myelofibrosis were cultured ex vivo under conditions to derive megakaryocytes. Following culture, megakaryocytes were purified by flow cytometry. The gene expression in these cells was determined by Illumina microarray analysis. Note that samples JC1-12 were run at a different time than JC13-24. Investigators may wish to perform the analysis of the two sets independently.
Project description:Chromothripsis in healthy individuals affects multiple protein-coding genes and can result in severe congenital abnormalities in offspring
Project description:DNA methylation likely plays a role in the regulation of human stress reactivity. In a genome-wide analysis of blood DNA methylation in 85 healthy individuals a locus in the Kit ligand (KITLG) gene (cg27512205) had the strongest association with cortisol stress reactivity (p=5.8x10-6). Replication was obtained in two independent samples, one using blood (N=45, p=0.001) and the other using buccal cells (N=255,p=0.004). KITLG methylation strongly mediated the relationship between childhood trauma and cortisol stress reactivity (32% mediation). Its genomic location (CpG island shore within an H3K27ac enhancer mark) provide further evidence that KITLG methylation is functionally relevant for the programming of stress reactivity. Our results extend preclinical evidence for epigenetic regulation of stress reactivity to humans and provide leads to enhance our understanding of the neurobiological pathways underlying stress vulnerability.
Project description:Comprehensively compare the transcriptional difference in PPD stimulated PBMCs from individuals with different tuberculosis infectious status: tuberculosis patients, latent infectious individuals and healthy controls using the microarray analysis.
Project description:Anti-nuclear antibody (ANA) positivity is a principal feature of individuals with an autoimmune disease, yet up to one in five healthy individuals are ANA+ and most will never develop clinical autoimmunity. Here, we show that immune profiles in ANA+ healthy individuals are altered, and differ by race. A suppressive immune signature distinguished by reduced T cell numbers and altered gene expression of HLA class I, IFN-associated, and apoptosis pathways, characterized European American (EA) ANA+ healthy individuals. In contrast, African American (AA) ANA+ healthy individuals had more elements of activation with increased CD69 gene expression on T cells and heightened pro-inflammatory cytokines. Increases in STAT4, IFNGR2 and STAT1 T cell transcripts and decreases in TGFBR1 gene expression in monocytes correlated with T cell expansion and clinical SLE. Thus, a suppressive immune signature in EA ANA+ healthy individuals may avert clinical autoimmune disease, which is associated with activation of Type I and II IFN pathways and T cell expansion.