The Experts below are selected from a list of 189 Experts worldwide ranked by ideXlab platform
Nabil Elsherif - One of the best experts on this subject based on the ideXlab platform.
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differential expression of voltage gated k channel genes in left ventricular remodeled myocardium after Experimental Myocardial Infarction
Circulation Research, 1996Co-Authors: Madhavi Gidhjain, Boyu Huang, Praveer Jain, Nabil ElsherifAbstract:Left ventricular (LV) remodeling after Experimental Myocardial Infarction (MI) is associated with hypertrophy of noninfarcted myocardium and electrophysiological alterations. We have recently shown that post-MI hypertrophied LV myocytes have prolonged action potential duration (APD) and generate triggered activity from early afterdepolarizations. The prolonged APD was attributed to decreased density of the two outward K+ currents, Ito-fast (Ito-f) and Ito-slow (Ito-s), rather than changes in the density and/or kinetics of the L-type Ca2+ current. The changes in ionic current density may be related to alterations in the expression and levels of ion channel proteins. To test this hypothesis, rats underwent either left anterior descending coronary artery (LAD) ligation (post-MI group [n=10]) or sham surgery (sham group [n=10]). Three weeks later, transcripts from the noninfarcted LV myocardium in the post-MI group (n=6) and LV myocardium of the sham group (n=6) were analyzed by RNase protection assay. Expres...
Rinat Sharir - One of the best experts on this subject based on the ideXlab platform.
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Experimental Myocardial Infarction induces altered regulatory t cell hemostasis and adoptive transfer attenuates subsequent remodeling
PLOS ONE, 2014Co-Authors: Rinat Sharir, Jonathan Semo, Sara Shimoni, Tamar Benmordechai, Natalie Landarouben, Sofia MayselauslenderAbstract:BACKGROUND: Ischemic cardiac damage is associated with upregulation of cardiac pro-inflammatory cytokines, as well as invasion of lymphocytes into the heart. Regulatory T cells (Tregs) are known to exert a suppressive effect on several immune cell types. We sought to determine whether the Treg pool is influenced by Myocardial damage and whether Tregs transfer and deletion affect cardiac remodeling. METHODS AND RESULTS: The number and functional suppressive activity of Tregs were assayed in mice subjected to Experimental Myocardial Infarction. The numbers of splenocyte-derived Tregs in the ischemic mice were significantly higher after the injury than in the controls, and their suppressive properties were significantly compromised. Compared with PBS, adoptive Treg transfer to mice with Experimental Infarction reduced infarct size and improved LV remodeling and functional performance by echocardiography. Treg deletion with blocking anti-CD25 antibodies did not influence infarct size or echocardiographic features of cardiac remodeling. CONCLUSION: Treg numbers are increased whereas their function is compromised in mice with that underwent Experimental Infarction. Transfer of exogeneous Tregs results in attenuation of Myocardial remodeling whereas their ablation has no effect. Thus, Tregs may serve as interesting potential interventional targets for attenuating left ventricular remodeling.
Gary F. Baxter - One of the best experts on this subject based on the ideXlab platform.
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Adrenomedullin limits reperfusion injury in Experimental Myocardial Infarction
Basic Research in Cardiology, 2005Co-Authors: Shabaz A. Hamid, Gary F. BaxterAbstract:Adrenomedullin (AM) is a vascular–derived polypeptide that exerts numerous actions in cardiovascular homeostasis. Recent studies have demonstrated a cytoprotective action of exogenously applied or genetically over–expressed AM in Experimental Myocardial Infarction. The present studies were undertaken to test the hypothesis that AM exerts its effects through direct augmentation of NO generation in the myocardium during early reperfusion. Rat isolated hearts underwent 35 min left coronary artery occlusion followed by 120 min reperfusion. Infarct size (as percentage of ischaemic riskzone) was determined by Evans’ blue and tetrazolium double staining. AM 1 nM administered 5 min prior to and during the first 15 min of ischaemia did not significantly influence infarct size. However, the same concentration of AM given during the last 5 min ischaemia and first 15 min of reperfusion significantly limited infarct size (AM reperfusion 15.9 ± 3.5% vs control 31.4 ± 2.1%, P < 0.01). AM at reperfusion improved coronary flow and LV contractility. The protective effects of adrenomedullin were abolished in the presence of the NO synthase inhibitor, L–NAME 100 µM (infarct size 24.6 ± 5.7%, P > 0.05 vs control). AM treatment at reperfusion was associated with augmented phosphorylation of the pro–survival kinase, Akt, determined by immunoblotting of tissue sampled 30 min following reperfusion. These studies provide the first evidence that AM exerts its cytoprotective action specifically during early reperfusion through a NO–dependent mechanism.
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Adrenomedullin limits reperfusion injury in Experimental Myocardial Infarction
Basic Research in Cardiology, 2005Co-Authors: Shabaz A. Hamid, Gary F. BaxterAbstract:Adrenomedullin (AM) is a vascular–derived polypeptide that exerts numerous actions in cardiovascular homeostasis. Recent studies have demonstrated a cytoprotective action of exogenously applied or genetically over–expressed AM in Experimental Myocardial Infarction. The present studies were undertaken to test the hypothesis that AM exerts its effects through direct augmentation of NO generation in the myocardium during early reperfusion. Rat isolated hearts underwent 35 min left coronary artery occlusion followed by 120 min reperfusion. Infarct size (as percentage of ischaemic riskzone) was determined by Evans’ blue and tetrazolium double staining. AM 1 nM administered 5 min prior to and during the first 15 min of ischaemia did not significantly influence infarct size. However, the same concentration of AM given during the last 5 min ischaemia and first 15 min of reperfusion significantly limited infarct size (AM reperfusion 15.9 ± 3.5% vs control 31.4 ± 2.1%, P 0.05 vs control). AM treatment at reperfusion was associated with augmented phosphorylation of the pro–survival kinase, Akt, determined by immunoblotting of tissue sampled 30 min following reperfusion. These studies provide the first evidence that AM exerts its cytoprotective action specifically during early reperfusion through a NO–dependent mechanism.
Madhavi Gidhjain - One of the best experts on this subject based on the ideXlab platform.
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differential expression of voltage gated k channel genes in left ventricular remodeled myocardium after Experimental Myocardial Infarction
Circulation Research, 1996Co-Authors: Madhavi Gidhjain, Boyu Huang, Praveer Jain, Nabil ElsherifAbstract:Left ventricular (LV) remodeling after Experimental Myocardial Infarction (MI) is associated with hypertrophy of noninfarcted myocardium and electrophysiological alterations. We have recently shown that post-MI hypertrophied LV myocytes have prolonged action potential duration (APD) and generate triggered activity from early afterdepolarizations. The prolonged APD was attributed to decreased density of the two outward K+ currents, Ito-fast (Ito-f) and Ito-slow (Ito-s), rather than changes in the density and/or kinetics of the L-type Ca2+ current. The changes in ionic current density may be related to alterations in the expression and levels of ion channel proteins. To test this hypothesis, rats underwent either left anterior descending coronary artery (LAD) ligation (post-MI group [n=10]) or sham surgery (sham group [n=10]). Three weeks later, transcripts from the noninfarcted LV myocardium in the post-MI group (n=6) and LV myocardium of the sham group (n=6) were analyzed by RNase protection assay. Expres...
Boyu Huang - One of the best experts on this subject based on the ideXlab platform.
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differential expression of voltage gated k channel genes in left ventricular remodeled myocardium after Experimental Myocardial Infarction
Circulation Research, 1996Co-Authors: Madhavi Gidhjain, Boyu Huang, Praveer Jain, Nabil ElsherifAbstract:Left ventricular (LV) remodeling after Experimental Myocardial Infarction (MI) is associated with hypertrophy of noninfarcted myocardium and electrophysiological alterations. We have recently shown that post-MI hypertrophied LV myocytes have prolonged action potential duration (APD) and generate triggered activity from early afterdepolarizations. The prolonged APD was attributed to decreased density of the two outward K+ currents, Ito-fast (Ito-f) and Ito-slow (Ito-s), rather than changes in the density and/or kinetics of the L-type Ca2+ current. The changes in ionic current density may be related to alterations in the expression and levels of ion channel proteins. To test this hypothesis, rats underwent either left anterior descending coronary artery (LAD) ligation (post-MI group [n=10]) or sham surgery (sham group [n=10]). Three weeks later, transcripts from the noninfarcted LV myocardium in the post-MI group (n=6) and LV myocardium of the sham group (n=6) were analyzed by RNase protection assay. Expres...
