Microbiome research on congenital heart disease
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB89730 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The early-life gut microbiome in children with congenital heart disease
| PRJEB89733 | ENA
Project description:We used Affymetrix CytoScan750K array to detect the pathogenic copy number variations in 7 Chinese children with congenital heart disease
2021-10-01 | E-MTAB-8315 | biostudies-arrayexpress
Project description:Kids First Pediatric Research Program in Congenital Heart Disease
| PRJNA324733 | ENA
Project description:Congenital heart disease (CHD) is the most frequent birth defect and affects nearly 1% of newborns. The etiology of CHD is largely unknown and only a small percentage can be assigned to environmental risk factors such as maternal diseases or exposure to mutagenic agents during pregnancy. Chromosomal imbalances have been identified in many forms of syndromic CHD, but next to nothing is known about the impact of DNA copy number changes in non-syndromic CHD. Here we present a sub-megabase resolution array CGH screen of a cohort with CHD as the sole abnormality at the time of diagnosis. Keywords: array CGH In this BAC array CGH study 104 patients with congenital heart disease and some of their parents were screened for DNA copy number changes at submegabase resolution. No dye swap was performed.
2008-05-11 | E-GEOD-7527 | biostudies-arrayexpress
Project description:Congenital heart disease (CHD) is the most common birth defect in newborns, often requiring cardiac surgery with concomitant thymectomy that is known to increase disease susceptibility later in life. Studies of γδ T cells, which are one of the dominant T cells in the early fetal human thymus, are rare. Here, we provide a comprehensive analysis of the γδ T cell compartment via flow cytometry and next-generation sequencing in children and infants with CHD, who underwent cardiac surgery shortly after birth. A perturbation of the γδ T cell repertoire is evident and Vδ1 T cell numbers are reduced. However, those cells that are present, do retain cytotoxicity. In contrast, GZMA+CD28+CD161hi innate effector Vγ9Vδ2 T cells are found in higher proportions. TCR-seq identifies an increase in TRDJ3+ γδ T cell clones in children with CHD, but not in a confirmatory group of neonates prior to CHD surgery, which overall points to a persistence of fetal-derived effector γδ T cells in children with CHD.
2024-08-06 | GSE274083 | GEO
Project description:Data-independent acquisition (DIA)-based proteome analysis in preterm infants and congenital heart disease infants
2024-12-20 | PXD047992 | JPOST Repository
Project description:Congenital heart disease (CHD) is a major global health problem. Although treatment has improved, children still face comorbidities that may shorten their life. Most studies of the immune system in people with CHD have focused on the quantitative analysis of lymphocyte subpopulations, maturation and T cell receptor repertoires, while knowledge of effector functions is limited. We analysed αβ T cell phenotypes, transcriptomes and functions in children with CHD who underwent cardiac surgery within a year of birth and were followed up five to ten years after thymectomy, in comparison to age-matched healthy controls. We show that children with CHD have immunological alterations, including reduced T cell populations, lower CD4+ or CD8+ T cell proportions, reduced proportions of recent thymic emigrants (RTEs) and naive cells, and an accumulation of memory T cell populations. Single-cell transcriptomics and functional assays revealed high activation states of T cells and higher granzyme and effector cytokine production in children with CHD. Our study provides a foundation for longitudinal studies in children, adults and the elderly to unravel the cause of increased morbidity and mortality in these patients.
2026-05-20 | GSE299265 | GEO
Project description:Mammalian heart development is built on highly conserved molecular mechanisms with polygenetic perturbations resulting in a spectrum of congenital heart diseases (CHD). However, the transcriptional landscape of cardiogenic ontogeny that regulates proper cardiogenesis remains largely based on candidate-gene approaches. Herein, we designed a time-course transcriptome analysis to investigate the genome-wide expression profile of innate murine cardiogenesis ranging from embryonic stem cells to adult cardiac structures. This comprehensive analysis generated temporal and spatial expression profiles, prioritized stage-specific gene functions, and mapped the dynamic transcriptome of cardiogenesis to curated pathways. Reconciling the bioinformatics of the congenital heart disease interactome, we deconstructed disease-centric regulatory networks encoded within this cardiogenic atlas to reveal stage-specific developmental disturbances clustered on epithelial-to-mesenchymal transition (EMT), BMP regulation, NF-AT signaling, TGFb-dependent induction, and Notch signaling. Therefore, this cardiogenic transcriptional landscape defines the time-dependent expression of cardiac ontogeny and prioritizes regulatory networks at the interface between health and disease. To interrogate the temporal and spatial expression profiles across the entire genome during mammalian heart development, we designed a time-course microarray experiment using the mouse model at defined stages of cardiogenesis, starting with embryonic stem cells (ESC, R1 stem cell line), early embryonic developmental stages: E7.5 whole embryos, E8.5 heart tubes, left and right ventricle tissues at E9.5, E12.5, E14.5, E18.5 to 3 days after birth (D3) and adult heart (Figure 1A). At each time point, microarray experiments were performed on triplicate biological samples. Starting at E9.5, tissue samples from left ventricles (LV) and right ventricles (RV) were microdissected for RNA purification and microarray analysis to determine spatially differential gene expression between LV and RV during heart development.
2014-05-19 | E-GEOD-51483 | biostudies-arrayexpress
Project description:To explore molecular mechanisms affecting nutritional risk and neurodevelopment in children with congenital heart disease (CHD) by combining transcriptome and metabolome analysis. In this study, transcriptomic and metabolomic analysis of blood and serum samples from 26 children with CHD was performed to search for key DEGs and DEMs, and explore molecular mechanisms affecting nutritional risk and neurodevelopment in children with CHD.
2024-08-28 | GSE267250 | GEO
Project description:PCGC: Congenital Heart Disease Genetic Network Study
| PRJNA183421 | ENA