Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA225678 | ENA |
REPOSITORIES: ENA
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Project description:Several studies have shown the importance of immune and inflammatory mediators in the pathogenesis of heart failure. In clinical practice has been observed that many conventional drugs can modulate circulating levels of these mediators. Despite, there is poor understanding of the precise mechanisms of these drugs in regulating immune and inflammatory systems. Blood monocytes were isolated from 6 hospitalized patients in Intensive Cardiology Care Unit (ICCU) with symptomatic acute congestive heart failure (ACHF) (NYHA Class III-IV) before and after treatment with conventional drugs (ARBs, ACEIs, diuretics, and beta-blockers). Gene expression analysis (n=11) using whole human genome microarray showed that pharmacological treatment abrogate inflammatory activation of monocytes. The inflammatory response network constructed with Ingenuity Pathway Analysis (IPA) indicates the M-bM-^@M-^\TNFR1 signalingM-bM-^@M-^] as the most significantly modulated after pharmacological treatment and the pro-inflammatory cytokine TNF-alpha associated with more than a fifth of genes considered. In this study, we analyzed the expression profiles of 6 biological replicates of blood monocytes from ACHF patients pre- and post-treatment with conventional drugs (ARBs, ACEIs, diuretics, and beta-blockers). All RNAs from pre-treatment monocytes were hybridized against RNAs from post-treatment RNAs. We performed a total of 11 technical replicates.
2013-10-31 | E-GEOD-51888 | biostudies-arrayexpress
Project description:Several studies have shown the importance of immune and inflammatory mediators in the pathogenesis of heart failure. In clinical practice has been observed that many conventional drugs can modulate circulating levels of these mediators. Despite, there is poor understanding of the precise mechanisms of these drugs in regulating immune and inflammatory systems. Blood monocytes were isolated from 6 hospitalized patients in Intensive Cardiology Care Unit (ICCU) with symptomatic acute congestive heart failure (ACHF) (NYHA Class III-IV) before and after treatment with conventional drugs (ARBs, ACEIs, diuretics, and beta-blockers). Gene expression analysis (n=11) using whole human genome microarray showed that pharmacological treatment abrogate inflammatory activation of monocytes. The inflammatory response network constructed with Ingenuity Pathway Analysis (IPA) indicates the “TNFR1 signaling” as the most significantly modulated after pharmacological treatment and the pro-inflammatory cytokine TNF-alpha associated with more than a fifth of genes considered.
2013-10-31 | GSE51888 | GEO
Project description:Molecular analysis of the effect left ventricular assist device (LVAD) support has on congestive heart failure patients. Keywords = Congestive heart failure, left ventricular assist device, eNOS, gene, dimethylarginine dimethylaminohydrolase Keywords: other
2003-09-01 | GSE430 | GEO
Project description:Molecular analysis of the effect left ventricular assist device (LVAD) support has on congestive heart failure patients.
2007-12-13 | E-GEOD-430 | biostudies-arrayexpress
Project description:Terminalia arjuna (Roxb.) Wight & Arn., a well known Traditional medicine an. popularly known as Arjuna, has a long antiquity of its role as a cardiac stimulant, and has been stipulated in the treatment of hypercholesterolemia, heart failure and atherosclerosis. The present study was carried out to access the effects of Terminalia arjuna as an adjuvant therapy in angiographically proven patients with stable coronary artery disease who were on conventional medications. The goal of the study was to establish whether Terminalia arjuna exerts beneficial effects in targetting disease signatures which remain unresponsive to the standard therapies currently employed in the clinics. The present study scientifically validates the therapeutic effects of this medicinal plant as an adjuvant therapy along with conventional drugs routinely used in the clinics for prevention and treatment of coronary artery disease.
2015-04-16 | GSE56886 | GEO
Project description:Canine tachycardia-induced cardiomyopathy caused by several weeks of rapid ventricular pacing is a well-established animal model of congestive heart failure. However, little is known about the underlying changes in gene expression that occur in the canine myocardium after the induction of heart failure. This project aims to compare expression profiles in left ventricular free wall samples from control dogs and dogs with pacing-induced heart failure on the custom MuscleChip. Keywords: other
2003-07-16 | GSE472 | GEO
Project description:Rosiglitazone is a member of the thiazolidinedione class of drugs, an anti-diabetic drug known for being a ligand of peroxisome proliferation activating receptors γ (PPARγ), a group of nuclear hormone receptors that are involved in the regulation of genes related to glucose and lipid metabolism. The use of Rosiglitazone has been shown to increase the risk of congestive heart failure in type II diabetes patients due to increased fluid retention and plasma volume. Our data show that the effects of Rosiglitazone on cardiomyocytes occur really early within a great increase in magnitude in time but consistent in the pathways affected. Also, the initial deleterious effect triggers a protective molecular response at 24 hours of exposure that is maintained at 48h but also accompanied by further activation of the system that can damage the heart.
2020-02-26 | GSE117198 | GEO
Project description:This project contains a Modelica implementation of the model of the human baroreflex developed by H. Seidel in his PhD thesis (Seidel 1997) under the supervision of H. Herzel. We published and presented this implementation at the 2015 International Modelica Conference.
The Seidel-Herzel model (SHM) describes the autonomic control of the heart rate in humans at a high level of abstraction as a hybrid (discrete and continuous), deterministic, quantitative, macro-level model. All effects are described on the organ level, including the time course of systemic arterial blood pressure generated by the pumping of the heart; the Windkessel effect of the expanding arteries dampening the initial rise in blood pressure; the arterial baroreceptors generating a neural signal depending on the absolute value and the increase in blood pressure; the autonomic nervous system emitting norepinephrine and acetylcholine as hormone and neurotransmitter based on signals from the baroreceptor and the lungs; and the cardiac conduction system with the SA node as main pacemaker and the AV node as a fallback system.
The model is able to simulate several relevant disease conditions such as first and second degree atrioventricular block (Seidel 1997), carotid sinus hypersensitivity (Seidel and Herzel 1998), congestive heart failure (Kotani et al. 2005), and primary autonomic failure (Kotani et al. 2005) as well as treatment options such as the administration of atropine or metoprolol (Kotani et al. 2005). It is also especially interesting with regard to its dynamical properties such as the emergence of Mayer waves (Seidel 1997), bifurcations (Seidel and Herzel 1998) and cardiorespiratory synchronization (Kotani et al. 2002).
The current version of the model can also be found at https://github.com/CSchoel/shm.
2021-01-29 | MODEL2101280001 | BioModels