Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Presence of bacterial infection in brains of patients with Huntington's disease (HD)

ABSTRACT: Bacterial isolation in infected brains in patients with Huntington's disease. Here we used next generation sequencing of 16S ribosomal RNA gene PCR amplicons (NGS 16S amplicon analysis)

PROVIDER: EGAS00001003678 | EGA |

REPOSITORIES: EGA

ACCESS DATA

Json Xml

Similar Datasets

Presence of bacterial infection in brains of patients with Parkinson's disease (PD)

Project description:Isolation of bacteria in infected brains in patients with Parkinson's disease. Here we used next generation sequencing of 16S ribosomal RNA gene PCR amplicons (NGS 16S amplicon analysis).

| EGAS00001003643 | EGA

ena-DATASET-CBMSO-21-02-2020-14:26:33:100-537 - samples

Project description:Bacterial isolation in infected brains in patients with Huntington's disease. Here we used next generation sequencing of 16S ribosomal RNA gene PCR amplicons (NGS 16S amplicon analysis)

| EGAD00001005996 | EGA

ena-DATASET-CBMSO-08-05-2019-14:24:52:838-538 - samples

| EGAD00001005003 | EGA

3′ sequencing from human Huntington's disease and control motor cortex and cerebellum.

Project description:Purpose: We applied polyA site sequencing (Passeq) to human Huntington's disease and control motor cortex and cerebellum to test if any genes change 3′UTR isoforms abundance. Methods: 3′ sequencing was performed on 6 motor cortices from grade 1 Huntington's patient brains, 4 motor cortices from grade 2 Huntington's patient brains, and 5 motor cortices from control brains. Cerebellum samples included 9 cerebella from grade 2-3 Huntington's patient brains, and 7 cerebella from control brains. To verify HTT isoforms in mice, sequencing was performed on 5 Q140 mouse striata and 3 wild-type mouse striata. Results: We report 11% of genes from Huntington's disease patient motor cortex exhibit a change in at least one of their 3′UTR isoforms, commensurate with the 11% of genes which show different total expression in HD motor cortex versus control. In contrast, gene isoform and expression changes are minimal (<5%) in Huntington's disease cerebellum versus controls. In the motor cortex, we show isoform and gene expression differs between between grade 1 and grade 2 brains. We identify a novel isoform of huntingtin mRNA which is conserved in wild-type and Huntington's model mice. Conclusions: This is the first study characterizing widespread alterations in 3′UTR isoform abundance in Huntington's disease. Alterations in isoform abundance may affect mRNA metabolism in Huntington's disease brains.

2017-09-21 | GSE96099 | GEO

A phylogenetic microarray targeting 16S rRNA genes from the bacterial division Acidobacteria

Project description:Investigation of the phylogenetic diversity of Acidobacteria taxa using PCR amplicons from positive control 16S rRNA templates and total genomic DNA extracted from soil and a soil clay fraction A ten chip study using PCR amplicons from cloned 16S rRNA genes and from diverse soil 16S rRNAs, with PCR primers specific to the Division Acidobacteria. Each chip measures the signal from 42,194 probes (in triplicate) targeting Acidobacteria division, subdivision, and subclades as well as other bacterial phyla. All samples except one (GSM464591) include 2.5 M betaine in the hybridization buffer. Pair files lost due to a computer crash.

2010-06-24 | E-GEOD-18711 | biostudies-arrayexpress

A phylogenetic microarray targeting 16S rRNA genes from the bacterial division Acidobacteria

2010-01-01 | GSE18711 | GEO

Quantitative Proteomic Analysis Reveals Similarities between Huntington's Disease (HD) and Huntington's Disease-Like 2 (HDL2) Human Brains.

Project description:The pathogenesis of HD and HDL2, similar progressive neurodegenerative disorders caused by expansion mutations, remains incompletely understood. No systematic quantitative proteomics studies, assessing global changes in HD or HDL2 human brain, were reported. To address this deficit, we used a stable isotope labeling-based approach to quantify the changes in protein abundances in the cortex of 12 HD and 12 control cases and, separately, of 6 HDL2 and 6 control cases. The quality of the tissues was assessed to minimize variability due to post mortem autolysis. We applied a robust median sweep algorithm to quantify protein abundance and performed statistical inference using moderated test statistics. 1211 proteins showed statistically significant fold changes between HD and control tissues; the differences in selected proteins were verified by Western blotting. Differentially abundant proteins were enriched in cellular pathways previously implicated in HD, including Rho-mediated, actin cytoskeleton and integrin signaling, mitochondrial dysfunction, endocytosis, axonal guidance, DNA/RNA processing, and protein transport. The abundance of 717 proteins significantly differed between control and HDL2 brain. Comparative analysis of the disease-associated changes in the HD and HDL2 proteomes revealed that similar pathways were altered, suggesting the commonality of pathogenesis between the two disorders.

| S-EPMC5555151 | biostudies-literature

Neurobiological Predictors of Huntington's Disease Onset (Predict-HD)

Project description:Neurobiological Predictors of Huntington's Disease Onset (Predict-HD)

| PRJNA75985 | ENA

Metagenomic analysis Huntington's disease patients

Project description:Presence of bacterial infection in brains of patients with Huntington's disease

| PRJEB32814 | ENA

Microbiome characterization using transfer RNA sequencing

Project description:Here we report a direct tRNA sequencing protocol and software to simultaneously examine the composition and biological activity of naturally occurring microbial communities. Our analysis of mouse gut microbiome with tRNA-seq and 16S ribosomal RNA gene amplicons revealed comparable microbial community structures, and additional physiological insights into the microbiome through tRNA abundance and modifications.

2018-11-09 | GSE100263 | 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