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.
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.
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
Project description:Heart RNA-seq of therapeutic RBM20 antisense oligonucleotide (ASO) treatment in a mouse model of heart failure with preserved ejection fraction (HFpEF)
Project description:Transcription profiling of spontaneously hypertensive heart failure rats (SHHF) and a reference strain to identify heart failure susceptibility genes
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.
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
