Ontology highlight
ABSTRACT:
PROVIDER: PRJEB52147 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR9528550.fastq.gz | Fastqsanger.gz | |||
| ERR9528560.fastq.gz | Fastqsanger.gz | |||
| ERR9528570.fastq.gz | Fastqsanger.gz | |||
| ERR9528580.fastq.gz | Fastqsanger.gz | |||
| ERR9528590.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 288 |
Similar Datasets
Project description:Qiita ID 13241 - The Association Between Milk Feedings in the Preterm Population, the Microbiome and Risk of Atopic Disease: Microbiome, Atopic Disease, and Prematurity (MAP Study) - Data was acquired using a Bruker Maxis Impact and C18 RP-UHPLC. Positive polarity acquisition of LC-MS/MS.
2020-10-07 | MSV000086246 | GNPS
Project description:Children who grow up on farms have a lower risk of developing childhood atopic disease. Although human milk proteins are heavily glycosylated, there is a lack of studies investigating the milk glycoproteome. In this study, we have used label-free quantitative proteomics to analyze milk samples from Rochester and Older Order Mennonite mothers, two populations with different lifestyles, exposures, and risk of allergic disease. We identified multiple N-glycopeptides with significantly different abundances between the two communities and four N-glycopeptides that may have a protective effect against the development of atopic disease. The findings of this study indicate that the differential glycosylation of milk proteins may affect the development of atopic disease, something previously uninvestigated.
2022-06-09 | PXD026644 | Pride
Project description:Retinopathy of prematurity (ROP), a blinding condition affecting preterm infants, accounts for up to 40% of all childhood blindness worldwide. ROP is an interruption of retinal vascular maturation, which is physiologically complete at full term and thus ongoing at the time of preterm birth. Although ROP demonstrates delayed onset following preterm birth, representing a window for therapeutic intervention, we cannot cure or prevent this disease. The in-utero environment, including placental function, is increasingly recognized for contributions to preterm infant disease risk. Herein, we examine the clinical associations between presence and severity of acute placental inflammation to ROP risk. Using logistic regression, we find a protective relationship between presence and severity of acute placental inflammation and preterm infant development of ROP. This is most significant for infants born in the absence of maternal preeclampsia. Further, we examine the underlying molecular mediators that may inform this protective paradigm. Adopting a candidate approach analyzing proteins with described ROP risk associations, we find that placental HTRA1 and FABP4 protein expression is significantly decreased within placental tissues characterized by acute inflammation. Additionally, HTRA1 and VEGFA demonstrate inverse longitudinal trends within the peripheral circulation for infants born in the presence compared to absence of acute placental inflammation. An agnostic approach, including whole transcriptome and differential methylation placental analysis, identifies novel mediators and pathways that may underly protection. Taken together, these data build on emerging literature showing disparate associations between acute placental inflammation and ROP development within preeclamptic or non-preeclamptic preterm infant populations and identifies novel placental mechanisms that may inform postnatal risk associations in preterm infants.
2023-01-01 | GSE218039 | GEO
Project description:Spontaneous preterm birth (sPTB) is a leading cause of maternal and neonatal morbidity and mortality, yet its prevention and early risk stratification are limited. Previous investigations have suggested that vaginal microbes and metabolites may be implicated in sPTB. Here we performed untargeted metabolomics on 232 second-trimester vaginal samples, 80 from pregnancies ending preterm. We find multiple associations between vaginal metabolites and subsequent preterm birth, and propose that several of these metabolites, including diethanolamine and ethyl glucoside, are exogenous. We observe associations between the metabolome and microbiome profiles previously obtained using 16S ribosomal RNA amplicon sequencing, including correlations between bacteria considered suboptimal, such as Gardnerella vaginalis, and metabolites enriched in term pregnancies, such as tyramine. We investigate these associations using metabolic models. We use machine learning models to predict sPTB risk from metabolite levels, weeks to months before birth, with good accuracy (area under receiver operating characteristic curve of 0.78). These models, which we validate using two external cohorts, are more accurate than microbiome-based and maternal covariates-based models (area under receiver operating characteristic curve of 0.55-0.59). Our results demonstrate the potential of vaginal metabolites as early biomarkers of sPTB and highlight exogenous exposures as potential risk factors for prematurity.
2022-11-21 | MTBLS702 | MetaboLights
Project description:Preterm birth is an important unsolved clinical problem. Despite advanced treatments, infants who survive prematurity remain at increased risk for permanent disabilities. In approximately one-third of cases, prematurity is related to infection and/or inflammation, which renders hostile the normally receptive intrauterine environment. Proinflammatory cytokines provoke up-regulation of genes that promote uterine contractions. Using monolayer cultures of human decidual cells as a model, we profiled the global pattern of gene expression in response to cytokine challenge.
2016-01-01 | GSE58220 | GEO
Project description:Preterm birth is an important unsolved clinical problem. Despite advanced treatments, infants who survive prematurity remain at increased risk for permanent disabilities. In approximately one-third of cases, prematurity is related to infection and/or inflammation, which renders hostile the normally receptive intrauterine environment. Proinflammatory cytokines provoke up-regulation of genes that promote uterine contractions. Using monolayer cultures of human cervical fibroblast cells as a model, we profiled the global pattern of gene expression in response to cytokine challenge.
2020-07-30 | GSE154571 | GEO
Project description:Preterm birth is an important unsolved clinical problem. Despite advanced treatments, infants who survive prematurity remain at increased risk for permanent disabilities. In approximately one-third of cases, prematurity is related to infection and/or inflammation, which renders hostile the normally receptive intrauterine environment. Proinflammatory cytokines provoke up-regulation of genes that promote uterine contractions. Using monolayer cultures of human decidual cells as a model, we profiled the global pattern of gene expression in response to cytokine challenge. Decidualized human endometrial stromal cells were treated with 1 ng/ml of interleukin-1-beta for 6 hours, while control cells were treated with 0.1% PBS containing 0.1% bovine serum albumin (vehicle). The cells were subjected to RNA extraction, quantification, and evaluation, followed by hybridization on Affymetrix Human Gene 2.0 ST Arrays (Platform GPL16686). Three biological replicates were used (6 total samples).
2016-07-03 | E-GEOD-58220 | biostudies-arrayexpress
Project description:To further explore the underlying mechanisms of the protection functions of human milk exosmes, high throughput sequencings were used to identify differentially expressed lncRNA and mRNA profiles between human milk exosomes form term human breast milk (Term-Exos) and preterm human breast milk (Pre-Exos).
2022-11-15 | GSE217708 | GEO
Project description:Necrotizing enterocolitis (NEC) is a severe gastrointestinal complication of prematurity. Using small intestinal organoids derived from fetal tissue of a gestational age similar to an extremely preterm infant, this study aims to assess the effect of diet on intestinal epithelial growth and differentiation to elucidate the role nutrition type plays in intestinal development and modifies the risk for NEC. Organoids were cultured for 5 days in growth media and 5 days in differentiation media supplemented 1:40 with four different diets: maternal milk (MM), donor human milk (DHM), standard formula, or extensively hydrolyzed formula. Images were captured daily and organoids were quantified. Organoids were preserved for RNA sequencing and immunofluorescence staining with Ki67, cleaved caspase 3, and chromogranin-A. Media was saved for cytokine/chemokine and growth factor analysis.Human milk supplementation improved growth and differentiation of intestinal organoids generating larger organoids during the growth phase and organoids with longer and wider buds during differentiation compared to formula. Ki67 staining confirmed the proliferative nature of milk-supplemented organoids and chromogranin A staining proved that MM-supplemented organoids induced highest enteroendocrine differentiation. Human milk supplementation also upregulated genes involved in proliferation and promoted a homeostatic immune landscape while those supplemented with formula had a downregulation of cell-cycle-promoting genes and a more inflammatory immune signature. Our results show that MM, and to a lesser extent DHM, support robust intestinal epithelial proliferation and differentiation, suggesting a critical role for factors enriched in human milk in intestinal epithelial health.
2024-07-01 | GSE253501 | GEO