Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Staphyloccocal food poisoning investigation in Luxembourg, 2014

ABSTRACT: Investigation of a staphylococcal food poisoning outbreak in Luxembourg using epidemiological case-control analysis, traditional typing and whole genome sequencing

PROVIDER: PRJEB7847 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	ERR863169_1.fastq.gz	Fastqsanger.gz
	ERR863169_2.fastq.gz	Fastqsanger.gz
	ERR863170_1.fastq.gz	Fastqsanger.gz
	ERR863170_2.fastq.gz	Fastqsanger.gz
	ERR863171_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 154

Similar Datasets

Dupond: Transcriptional analysis of a clinical case of acute dioxin poisoning.

Project description:Transcriptional analysis of a clinical case of acute dioxin poisoning. Tissue sampling : patient 5 months and patient 11 months : skin biopsieson the face under general anaesthesia; controls 1-4 : retroauricular skin biopsies under local anaesthesia

2012-03-30 | E-MTAB-617 | biostudies-arrayexpress

High-throughput CRISPR typing must not replace traditional phage typing for epidemiological surveillance and outbreak investigation of Salmonella Typhimurium

Project description:High-throughput CRISPR typing must not replace traditional phage typing for epidemiological surveillance and outbreak investigation of Salmonella Typhimurium

| PRJEB18673 | ENA

The transcriptional profile of deoxycholate-induced sporulation in Clostridium perfringens food poisoning isolate

2016-03-13 | GSE69649 | GEO

Staphylococcus

Project description:Genome analysis of staphylococcal food poisoning isolates

| PRJDB5453 | ENA

EPIDEMIOLOGICAL TYPING OF SERRATIA MARCESCENS

Project description:EPIDEMIOLOGICAL TYPING OF SERRATIA MARCESCENS

| PRJEB28358 | ENA

Human serum samples - Acute and chronic blood serum proteome changes in patients with methanol poisoning

Project description:We carried out a prospective, longitudinal, single-center, observational cohort study of patients with confirmed acute methanol poisoning that were treated in hospitals during a mass methanol poisoning outbreak in the Czech Republic in 2012. Venous blood for proteomic analysis was obtained from 24 patients with confirmed acute methanol poisoning upon admission to the hospital (group M (“Methanol”)) with heparin administration for hemodialysis and ethanol or fomepizole administration as the antidote to block ADH. In the follow-up group of survivors of methanol poisoning (group S (“Survivors”)), venous blood samples for proteomic analysis were obtained from 46 patients during the examination, which took place 4 years after discharge from the hospital. For the control group not exposed to methanol, 24 healthy subjects were recruited (group C, “Controls”). Blood samples were spun, the serum was separated, and the samples were frozen to −80 °C until the analyses. Blood serum samples were depleted of most abundant serum proteins using Agilent MARS 14 column, samples fractionated and fractions containing proteins of interest precipitated. Samples were analyzed using LC-MS/MS Thermo Orbitrap Fusion (UHPLC-ESI-Q-OT-qIT) and identified proteins with differential expression.

2022-12-12 | PXD035726 | Pride

miRNA-based liquid biopsy provides early prediction of lethal acetaminophene poisoning: a case study

Project description:miRNA-based liquid biopsy provides early prediction of lethal acetaminophene poisoning: a case study

| PRJNA436462 | ENA

Identification of biomarkers of central nervous system damage in mice of benzene poisoning based on TMT proteomics

Project description:Benzene is known to be a common toxic industrial chemical, and prolonged benzene exposure may cause nervous system damage. At present, there were few studies on benzene-induced neurological damage. This research aimed to identify protein biomarkers to predict central nervous system damage of benzene poisoning. We established a benzene poisoning model of C57 mice by gavage of benzene-peanut oil suspension and identified differentially expressed proteins (DEPs) in brain tissue using TMT proteomics. The results showed a significant weight loss and decrease in leukocyte and neutrophil counts in benzene poisoning mice compared to the control group. We also observed significant cerebral oedema and enhanced basophilic of neurons in the hippocampus in benzene poisoning group of mice. TMT proteomic results showed that a total 6985 proteins were quantified, with a Fold Change (FC) > 1.2 (or <1/1.2) and P value <0.05 were considered as DEPs. Compared with the control group, we identified 43 DEPs, comprising 14 upregulated and 29 downregulated proteins. KEGG pathway analysis showed that the candidate proteins were mainly involved in cholesterol metabolism, complement and coagulation cascades, african trypanosomiasis, PPAR signaling pathway and vitamin digestion and absorption. Three proteins, 2-hydroxyacylsphingosine 1-beta-galactosyltransferase (UGT8), Apolipoprotein A-I (APOA1) and Complement C3 (C3) were validated using immunoblotting and immunohistochemical. In conclusion, our results may provide some molecular biomarkers for identifying the nervous system damage of benzene poisoning.

2025-05-06 | PXD046028 | Pride

CLCF1/NF-κB signaling pathway regulates macrophage efferocytosis to ameliorate neurological damage and cognitive dysfunction following CO poisoning

Project description:Severe carbon monoxide (CO) poisoning can induce structural damage to the nervous system, leading to long-term cognitive dysfunction in patients. The proper termination of the inflammatory response caused by neuronal cell damage is a prerequisite for tissue repair. Macrophages can clear cell corpses/fragments caused by brain injury through efferocytosis and produce cytokines to coordinate immune responses, thereby promoting neuronal repair and regeneration. However, in the microenvironment of the nervous system affected by CO poisoning, the function of macrophages is inhibited. Our study found that CLCF1 can regulate the secretion of cytokines such as TNF-α, IL-1β, and IL-10 through the NF-κB signaling pathway, thereby affecting neuronal cell repair and regeneration.

2024-01-01 | GSE250190 | GEO

The transcriptional profile of deoxycholate-induced sporulation in Clostridium perfringens food poisoning isolate

Project description:Clostridium perfringens type A is a common source of food poisoning in humans. Vegetative cells sporulate in the small intestinal tract and produce a major pathogenic factor, C. perfringens enterotoxin (CPE) during sporulation. Although sporulation plays a critical role in the pathogenesis of food poisoning, the mechanisms to induce in vivo sporulation remain unclear. Bile salts had been identified to mediate sporulation, and we have confirmed deoxycholate (DCA)-induced sporulation in C. perfringens strain NCTC8239 co-cultured with human intestinal epithelial Caco-2 cells. In this study, we performed global transcriptome analysis of strain NCTC8239 to elucidate the mechanism to induce sporulation by DCA. From the 55 contigs of C. perfringens strain NCTC8239, 2778 coding sequences were extracted. We designed a DNA probe by utilizing eArray provided by Agilent Technologies. The custom 8Ã15K oligonucleotide array, containing 60 mer oligonucleotide probes for 2,778 genes in strain NCTC8239, 2 bacterial control genes: 16S rRNA and 23S rRNA, and 3 human control genes: beta-2-microglobulin, glucuronidase beta and 18S rRNA, were ordered to Agilent Technologies. Each probe was spotted in five-fold on each microarray. Each strain was run in triplicate or quadruplicate.

2016-03-13 | E-GEOD-69649 | biostudies-arrayexpress

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