Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA245878 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Hepatic encephalopathy (HE) is a frequent complication of liver cirrhosis and is seen as the clinical manifestation of a low grade cerebral edema associated with oxidative-nitrosative stress, however, comprehensive data on HE-associated molecular derangements in human brain are lacking. In the present study we used a whole human genome micro-array approach for gene expression profiling in post mortem brain samples from cirrhotic patients with or without HE and non-cirrhotic controls. Altered expression levels were found for a total of 1012 genes in liver cirrhotic patients without and with HE and HE-characteristic gene expression changes were identified. Genes with altered expression pattern in HE were related oxidative stress, microglia activation, inflammatory signalling pathways, cellular proliferation and apoptosis. Despite an up-regulation of genes associated with microglia activation, pro-inflammatory cytokine mRNA profiles remained unchanged in the brain of patients with liver cirrhosis and HE as compared to controls. Interestingly, many genes counteracting pro-inflammatory signalling and inflammatory cytokine expression were up-regulated in the cerebral cortex of patients with liver cirrhosis and HE. It is concluded that pathogenetic mechanisms of HE deduced from cell culture and animal experiments, such as oxidative stress, altered Zn2+-homeostasis and microglia activation also apply to human brain from cirrhotic patients with HE. The study also revealed a not yet recognized increased expression of genes antagonizing pro-inflammatory signalling and inflammatory cytokine expression. The dataset comprises 19 samples divided into three sample groups each representing a certain liver disease condition of humans.
2013-05-01 | E-GEOD-41919 | biostudies-arrayexpress
Project description:Hepatic encephalopathy (HE) is a frequent complication of liver cirrhosis and is seen as the clinical manifestation of a low grade cerebral edema associated with oxidative-nitrosative stress, however, comprehensive data on HE-associated molecular derangements in human brain are lacking. In the present study we used a whole human genome micro-array approach for gene expression profiling in post mortem brain samples from cirrhotic patients with or without HE and non-cirrhotic controls. Altered expression levels were found for a total of 1012 genes in liver cirrhotic patients without and with HE and HE-characteristic gene expression changes were identified. Genes with altered expression pattern in HE were related oxidative stress, microglia activation, inflammatory signalling pathways, cellular proliferation and apoptosis. Despite an up-regulation of genes associated with microglia activation, pro-inflammatory cytokine mRNA profiles remained unchanged in the brain of patients with liver cirrhosis and HE as compared to controls. Interestingly, many genes counteracting pro-inflammatory signalling and inflammatory cytokine expression were up-regulated in the cerebral cortex of patients with liver cirrhosis and HE. It is concluded that pathogenetic mechanisms of HE deduced from cell culture and animal experiments, such as oxidative stress, altered Zn2+-homeostasis and microglia activation also apply to human brain from cirrhotic patients with HE. The study also revealed a not yet recognized increased expression of genes antagonizing pro-inflammatory signalling and inflammatory cytokine expression.
2013-05-01 | GSE41919 | GEO
Project description:Gene expression profiling in the cerebral cortex of patients with cirrhosis with and without hepatic encephalopathy
| PRJNA178532 | ENA
Project description:Hepatic Encephalopathy is the brain disorder caused by liver damage, characterized by cognitive and motor impairments. Glutamate a predominant excitatory neurotransmitter over activate post-synaptic neuron via NMDAR receptors leads to neuronal derangement. NMDAR as a therapeutic target is not viable option due to its crucial role in brain physiology. In order to discover new non-NMDAR therapeutic targets high resolution mass spectrometry (HRMS) technique was used for proteomic profiling of the hippocampal proteins in Moderate hepatic encephalopathy (MoHE) rat model.
2024-05-27 | PXD036723 | Pride
Project description:In this study, we performed the first genome-wide expression profiling of post-mortem brains of a cohort of patients deceased from SVD and compared them to age-matched normal controls. Normal-appearing frontal temporal and occipital cortical and subcortical brain samples were dissected at autopsy from 5 patients diagnosed with pure SVD and 5 control patients without neurological disease and immediately frozen.
2015-03-11 | E-MTAB-3408 | biostudies-arrayexpress
Project description:Patients with liver cirrhosis may develop minimal hepatic encephalopathy (MHE) which affects their quality of life and life span. It has been proposed that a shift in peripheral inflammation triggers the appearance of MHE. However, the mechanisms involved in this immune system shift remain unknown. In this work we studied the broad molecular changes involved in the induction of MHE with the goal of identifying (1) altered genes and pathways in peripheral blood cells associated to the appearance of MHE, (2) serum metabolites and cytokines with modified levels in MHE patients and (3) MHE-regulated immune response processes related to changes in specific serum molecules. We adopted a multi-omic approach to profile the transcriptome, metabolome and a panel of cytokines of blood samples taken from cirrhotic patients with or without MHE.
2021-01-27 | GSE149741 | GEO
Project description:Patients with liver cirrhosis may have minimal hepatic encephalopathy (MHE) with cognitive and motor impairments that reduce life quality and span. MHE onset is associated with a shift in peripheral inflammation in which CD4+ lymphocytes play a key role but the underlying mechanisms remain unclear. We aimed to identify in CD4+ lymphocytes from patients with and without MHE: (1) gene expression changes and associated biological pathways using RNA-seq; (2) alterations in miRNA levels using miRNA-seq; (3) miRNAs and transcription factors regulating key mRNAs and (4) signalling pathways contributing to the peripheral inflammation shift associated to MHE onset. Additionally, we recovered T-cell receptor (TCR) repertoires from RNA-seq dataset to understand the immune status of control patients and cirrhotic patients with or without MHE.
2022-04-01 | GSE184200 | GEO
Project description:Cirrhosis, advanced liver disease, affects 2-5 million Americans. While most patients have compensated cirrhosis and may be fairly asymptomatic, many decompensate and experience life-threatening complications such as gastrointestinal bleeding, confusion (hepatic encephalopathy), and ascites, reducing life expectancy from 12 to less than 2 years. Among the patients with compensated cirrhosis, identifying patients at high risk of decompensation is critical to optimize care, reduce morbidity and mortality. This is important to preferentially direct them towards specialty care which cannot be provided to all patients with cirrhosis. We used discovery Top-down Proteomics (TDP) to detect differentially expressed proteoforms (DEPs) in the plasma of patients with cirrhosis with the goal to identify candidate biomarkers of disease progression. 663 DEPs were identified across three stages of cirrhosis (compensated, compensated with portal hypertension, and decompensated), of which 115 derived from proteins enriched in the liver at a transcriptional level and discriminated the progressive stages of cirrhosis. Enrichment analyses demonstrated DEPs are involved in numerous metabolic, oxidative, immunological, and hematological processes known to be impacted by cirrhosis progression. We have preliminarily defined the plasma proteoform signatures of cirrhosis patients, setting the stage for ongoing discovery and validation of biomarkers for early diagnosis, risk stratification, and disease monitoring.
2024-03-13 | MSV000094311 | MassIVE
Project description:Gut microbiota dysbiosis in Cirrhosis and hepatic encephalopathy
| PRJEB65440 | ENA
Project description:Genome wide DNA methylation profiling of post-mortem human brain samples from both autistic individuals and nonautistic individuals. Samples of the frontal cortex (BA10) and cingulate cortex (BA24) were examined from each individual.
2014-09-03 | GSE53924 | GEO