Ontology highlight
ABSTRACT:
PROVIDER: PRJNA742541 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Human white blood cells from healthy, heart failure risk patients, asymptomatic left ventricular dysfunction patients, chronic heart failure, acute heart failure patients Common reference experiment, 9 replicates per group.
2012-05-02 | E-GEOD-21125 | biostudies-arrayexpress
Project description:Characterization of plasma metabolomic profile of 15 patients with advanced heart failure referred for heart transplantation (8 patients with chronic chagasic cardiomyopathy and 7 with idiopathic dilated cardiomyopathy) and 12 heart donor individuals using gas chromatography/quadrupole time-of-flight mass spectrometry.
2023-07-25 | MSV000092522 | GNPS
Project description:In this study, we compared the expression profiles of circulating miRNAs in blood samples from controls and patients with heart ailment. Subject with no past history of heart failure/disease are considered as controls. The patients were classified according to the percentage of left ventricular ejection fraction. Patients were grouped as heart failure with reduced (hfREF) and preserved (hfPEF) left ventricular ejection fraction. Employing miRNA microarray, we identified 'signature miRNAs' in peripheral blood samples that distinguished Heart failure from the non-heart failure controls, as well as those of hfREF and hfPEF groups.
2015-02-12 | GSE53437 | GEO
Project description:Human white blood cells from healthy, heart failure risk patients, asymptomatic left ventricular dysfunction patients, chronic heart failure, acute heart failure patients
2012-05-03 | GSE21125 | GEO
Project description:In current clinical practice care of diseased patients is often restricted to separated disciplines. However, such an organ-centered approach is not always suitable. For example, cognitive dysfunction is a severe burden in heart failure patients. Moreover, these patients have an increased risk for age-associated dementias. The underlying molecular mechanisms are presently unknown and thus corresponding therapeutic strategies to improve cognition in heart failure patients are missing. Using mice as model organisms we show that heart failure leads to specific changes in hippocampal gene-expression, a brain region intimately linked to cognition. These changes reflect increased cellular stress pathways which eventually lead to loss of neuronal euchromatin and reduced expression of a hippocampal gene cluster essential for cognition. Consequently, mice suffering from heart failure exhibit impaired memory function. These pathological changes are ameliorated via the administration of a drug that promotes neuronal euchromatin formation. Our study provides first insight to the molecular processes by which heart failure contributes to neuronal dysfunction and point to novel therapeutic avenues to treat cognitive defects in heart failure patients.
2020-12-01 | GSE159447 | GEO
Project description:In current clinical practice care of diseased patients is often restricted to separated disciplines. However, such an organ-centered approach is not always suitable. For example, cognitive dysfunction is a severe burden in heart failure patients. Moreover, these patients have an increased risk for age-associated dementias. The underlying molecular mechanisms are presently unknown and thus corresponding therapeutic strategies to improve cognition in heart failure patients are missing. Using mice as model organisms we show that heart failure leads to specific changes in hippocampal gene-expression, a brain region intimately linked to cognition. These changes reflect increased cellular stress pathways which eventually lead to loss of neuronal euchromatin and reduced expression of a hippocampal gene cluster essential for cognition. Consequently, mice suffering from heart failure exhibit impaired memory function. These pathological changes are ameliorated via the administration of a drug that promotes neuronal euchromatin formation. Our study provides first insight to the molecular processes by which heart failure contributes to neuronal dysfunction and point to novel therapeutic avenues to treat cognitive defects in heart failure patients.
2020-12-01 | GSE159436 | GEO
Project description:In current clinical practice care of diseased patients is often restricted to separated disciplines. However, such an organ-centered approach is not always suitable. For example, cognitive dysfunction is a severe burden in heart failure patients. Moreover, these patients have an increased risk for age-associated dementias. The underlying molecular mechanisms are presently unknown and thus corresponding therapeutic strategies to improve cognition in heart failure patients are missing. Using mice as model organisms we show that heart failure leads to specific changes in hippocampal gene-expression, a brain region intimately linked to cognition. These changes reflect increased cellular stress pathways which eventually lead to loss of neuronal euchromatin and reduced expression of a hippocampal gene cluster essential for cognition. Consequently, mice suffering from heart failure exhibit impaired memory function. These pathological changes are ameliorated via the administration of a drug that promotes neuronal euchromatin formation. Our study provides first insight to the molecular processes by which heart failure contributes to neuronal dysfunction and point to novel therapeutic avenues to treat cognitive defects in heart failure patients.
2020-12-01 | GSE159475 | GEO
Project description:MicroRNA profiling of myocardium of ovine comparing normal (Control), paced-induced heart failure (HF) and heart failure recovery (HF-R) after discontinuation of pacing.
2017-09-15 | GSE87449 | GEO
Project description:Gene expression in chronic heart failure patients
| PRJNA310098 | ENA