Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ABSTRACT: a gut microbiota study about children primary nephrotic syndrome

PROVIDER: PRJNA800190 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR17733000_1.fastq.gz	Fastqsanger.gz
	SRR17733000_2.fastq.gz	Fastqsanger.gz
	SRR17733001_1.fastq.gz	Fastqsanger.gz
	SRR17733001_2.fastq.gz	Fastqsanger.gz
	SRR17733002_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 170

Similar Datasets

Project description:A gut microbiota study about steroid children steroid-dependent primary nephrotic syndrome

| PRJNA800189 | ENA

Urinary sediment mRNA level of CREBBP and CYBA in children with steroid-resistant nephrotic syndrome

Project description:This study aimed to evaluate gene expression patterns in urinary sediment samples of children with steroid-resistant nephrotic syndrome (SRNS).

2022-02-23 | GSE189734 | GEO

Transcriptome profile of leukocyte RNA from children with steroid sensitive and resistant nephrotic syndrome

Project description:Glucocorticoid resistance complicates the treatment of ~20% of children with nephrotic syndrome, yet the molecular basis for resistance remains unclear. We generated the transcriptome profile by RNA sequencing of peripheral blood leukocytes from children obtained both at initial nephrotic syndrome presentation and after ~7 weeks of glucocorticoid therapy to identify genes or a gene panel able to differentiate steroid sensitive from steroid resistant nephrotic syndrome. RNA -seq analysis was followed by in-silico algorithm-based approaches and subsequent biochemical analyses on relevant candidate gene with important roles in podocyte and glomerular pathophysiology, using both patient samples and experimental models of nephrotic syndrome and podocyte injury.

2021-02-16 | GSE145969 | GEO

mWGS analysis of the fecal microbiota of WT and TCRb-/- mice

Project description:The gut microbiota plays an important role in host health. Microbiota dysbiosis has been implicated in the global epidemic of Metabolic Syndrome (MetS) and could impair host metabolism by noxious metabolites. It has been well established that the gut microbiota is shaped by host immune factors. However, the effect of T cells on the gut microbiota is yet unknown. Here, we performed a metagenomic whole-genome shotgun sequencing (mWGS) study of the microbiota of TCRb-/- mice, which lack alpha/beta T cells.

2024-05-06 | GSE262397 | GEO

Glomerular voom-transformed RNAseq counts from the Neptune Cohort and healthy living donors [re-analysis of GSE197307]

Project description:Glomerular Transcriptome in the Nephrotic Syndrome study network cohort

2024-02-07 | GSE254957 | GEO

The Nephrotic Syndrome Study Network (NEPTUNE)

Project description:The Nephrotic Syndrome Study Network (NEPTUNE)

| PRJNA935856 | ENA

The Nephrotic Syndrome Study Network (NEPTUNE)

Project description:The Nephrotic Syndrome Study Network (NEPTUNE)

| PRJNA935855 | ENA

The gut microbiota downregulates renal MAS1 through H3K9bu in high-fat diet-induced obesity-related hypertensive rats

Project description:Obesity is a leading cause of primary hypertension in children, and a high-fat intake and the gut microbiota may be involved in the pathogenesis of obesity-related hypertension (OrHTN), but the underlying mechanisms are not fully understood. Here, we show that high-fat diet (HFD) feeding alters the gut microbiota composition in OrHTN rats, resulting in a reduced abundance of the butyrate-producing bacteria Ruminococcus and a subsequent decrease in plasma butyrate levels. Histone 3 lysine 9 butyrylation (H3K9bu) levels decreased in the kidneys of OrHTN rats, which downregulates the expression of the hypertension-related MAS1 gene. Furthermore, sodium butyrate affected H3K9bu modification levels in a concentration-dependent manner, with decreased H3K9bu and downregulated MAS1 expression at low concentrations in human proximal tubular epithelial cells. Our results suggest that a HFD contributes to the development of OrHTN by altering the gut microbiota and its metabolites, leading to the downregulation of H3K9bu and hypertension-related gene expression.

2024-06-27 | GSE235898 | GEO

The effect of serum from children with nephrotic syndrome on transcriptome of human immortalized podocytes cultured in vitro

Project description:Nephrotic syndrome (NS) is an unfavorable disease with heterogeneous causes and variable prognosis. One of the clinically crucial prognostic feature is the response to initial glucocorticoid treatment. Whereas in some children with steroid-sensitive nephrotic syndrome (SSNS) the treatment may induce long-term remission of the disease, steroid-resistant cases (SRNS) are at risk of renal failure requiring renal replacement therapy. The aim of this project was to explore whether sera from children with the two main clinically defined types of NS induce changes in transcriptome of in-vitro cultures of immortalized human podocytes. After 3 days of culture, total RNA was isolated and then library from polyadenylated RNA was prepared and RNA sequencing was performed. Log2 (fold-changes) were calculated to describe differential gene expression. Within the Reactome online tool, Camera methodology was implemented to identify functionally linked gene groups (pathways) that could distinguish the two patient groups. Significant transcriptome differences were found between samples from children with SSNS and SRNS. This may help to reveal the molecular mechanisms of the disease and open up for an effective individualized treatment.

2022-10-14 | GSE215231 | GEO

Gut Microbiota from Human Autism Spectrum Disorder Induces Behavioral Deficits in Mice

Project description:We transplanted gut microbiota via fecal transfer from TD and ASD children into germ-free wild-type mice, and reveal that colonization with ASD microbiomes induces hallmark changes in sociability, vocalization, and stereotypies. The brains of mice receiving gut microbiota from ASD individuals display alternative splicing patterns for genes dysregulated in the human ASD brain.

2019-02-01 | GSE109827 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data