Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The Gut Microbiome of renal transplant recipients Ã¢Â€Â“ Cross-sectional

ABSTRACT: TransplantLines is designed as a single-center, prospective cohort study and biobank including all different types of solid organ transplant recipients as well as living organ donors. In the TransplantLines gut microbiome study the gut microbiome of solid organ transplant recipients is characterized and linked to clinical phenotypes. This batch contains the cross-sectional data from renal transplant recipients is.

PROVIDER: EGAS00001006257 | EGA |

REPOSITORIES: EGA

ACCESS DATA

Json Xml

Similar Datasets

The Gut Microbiome of liver transplant recipients Ã¢Â€Â“ Cross-sectional + Longitudinal (renal and liver)

Project description:TransplantLines is designed as a single-center, prospective cohort study and biobank including all different types of solid organ transplant recipients as well as living organ donors. In the TransplantLines gut microbiome study the gut microbiome of solid organ transplant recipients is characterized and linked to clinical phenotypes. This batch contains the cross-sectional data from liver transplant recipients and longitudinal data from renal and liver transplant recipients.

| EGAS00001006258 | EGA

4f116e53-e722-4a09-ad23-6833dda7688a - samples

Project description:The TransplantLines Gut Microbiome study includes raw data generated by shotgun metagenomic sequencing of fecal samples of solid organ transplant recipients and basic phenotypes (age and sex, BMI).

| EGAD00001008907 | EGA

Multi-omics of Bladder Cancers of Solid Organ Transplant Recipients

Project description:Multi-omics of Bladder Cancers of Solid Organ Transplant Recipients

| PRJNA865854 | ENA

Multi-omics of Bladder Cancers of Solid Organ Transplant Recipients

Project description:Multi-omics of Bladder Cancers of Solid Organ Transplant Recipients

| PRJNA865855 | ENA

Effect of gut microbiome transplant from neonates of particle-exposed mothers on the epigenome of dendritic cells

Project description:In our model the newborns of asthmatic mother mice or of mothers exposed to air pollutant particles are born with a predisposition to asthma. Gut microbiome of these pups is altered, and the transplant of the pups’ microbiome (GMT) has conferred the asthma predisposition to naïve recipients. We hypothesized that bacteria alter metabolomic profile in the gut, which polarizes the dendritic cells (DC) in the recipient by affecting epigenetic regulation in these key decision-maker cells. Here we examined DNA methylation profiles in the recipient host’s DCs to test the prediction that GMT confers alterations in DNA methylation (not seen with sterilized GMT).

2024-04-01 | GSE247470 | GEO

Project description:Background: Hepatitis E Virus (HEV) is a new causative agent of chronic hepatitis in solid organ transplant recipients in Europe. Factors associated with the occurrence and persistence of chronic HEV infection remain largely unknown but chronic evolution seems to be the consequence of hostM-bM-^@M-^Ys immunological factors rather than of viral factors. Method: In a prospective case-control study, we have determined in whole blood of chronically HEV-infected kidney-transplant recipients the host response using microarray technology. Results: Chronically HEV-infected kidney-transplant recipients exhibited a specific transcriptional program, in which interferon effectors were prominent. The intensity of expression of each signatureM-bM-^@M-^Ys gene was significantly lower in patients who were subsequently cleared of HEV than in patients who were not. Furthermore, in patients who were cleared of HEV, a higher expression of these genes was associated with a longer delay until HEV clearance. Conclusions: The specific transcriptional program determined in chronically HEV-infected kidney-transplant recipients suggests an activation of type I interferon response. Intensity of interferon-stimulated genes expression could be useful to forecast the outcome of infection. High expression of interferon-stimulated genes could signify a dysregulation in the interferon response that might favour the persistence of the HEV infection. TrialM-bM-^@M-^Ys registration number: NCT01090232; RegistryM-bM-^@M-^Ys URL: http://clinicaltrials.gov/ct2/show/study/NCT01090232?term=kidney+transplant+recipients&cntry1=EU%3AFR&rank=2 Total RNA was extracted from whole-blood sample or monocytes of kidney-transplant patients with or without chronic hepatitis E (CHE) infection. Control patients were matched up with CHE patients for age, sex, time since kidney transplant and immunosuppressive treatment.

2013-01-29 | E-GEOD-36539 | biostudies-arrayexpress

Project description:Whole genome profiling of lung microbiome in solid organ transplant recipients

| PRJNA806679 | ENA

Project description:Background: Hepatitis E Virus (HEV) is a new causative agent of chronic hepatitis in solid organ transplant recipients in Europe. Factors associated with the occurrence and persistence of chronic HEV infection remain largely unknown but chronic evolution seems to be the consequence of host’s immunological factors rather than of viral factors. Method: In a prospective case-control study, we have determined in whole blood of chronically HEV-infected kidney-transplant recipients the host response using microarray technology. Results: Chronically HEV-infected kidney-transplant recipients exhibited a specific transcriptional program, in which interferon effectors were prominent. The intensity of expression of each signature’s gene was significantly lower in patients who were subsequently cleared of HEV than in patients who were not. Furthermore, in patients who were cleared of HEV, a higher expression of these genes was associated with a longer delay until HEV clearance. Conclusions: The specific transcriptional program determined in chronically HEV-infected kidney-transplant recipients suggests an activation of type I interferon response. Intensity of interferon-stimulated genes expression could be useful to forecast the outcome of infection. High expression of interferon-stimulated genes could signify a dysregulation in the interferon response that might favour the persistence of the HEV infection. Trial’s registration number: NCT01090232; Registry’s URL: http://clinicaltrials.gov/ct2/show/study/NCT01090232?term=kidney+transplant+recipients&cntry1=EU%3AFR&rank=2

2013-01-29 | GSE36539 | GEO

Kidney transplant recipients

Project description:Kidney transplant recipients

| PRJNA1054489 | ENA

Fatal encephalitic Borna disease virus 1 infection cluster in solid organ transplant recipients

Project description:Fatal encephalitic Borna disease virus 1 infection cluster in solid organ transplant recipients

| PRJEB24346 | ENA