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"This is a Ph.D. dissertation. Cardiac excitation-contraction (EC) coupling is the process from electrical excitation to contraction of the heart. Electrical stimulation of cardiac cells gives rise to an action potential, which triggers a systolic rise of the intracellular Ca2+ concentration, initiating a contraction. Contents include: Introduction, Excitation-contraction coupling in cardiac muscle, Excitation-contraction coupling in the failing heart, Aims, Methods, Animal models, Cell isolation, Experimental setup, Experimental protocols, Protein expression levels, Echocardiographic measurements, Data analysis, Results, Mechanisms underlying the frequency dependence of contraction and Ca2+i transients in mouse ventricular myocytes, Ca2+ handling and contractile dysfunction in ventricular myocytes of MLP, Ca2+ handling in the SERCA 2b/b mouse, General discussion, and Summary."
PROFILES POTENTIAL TREATMENT APPROACHES FOR CARDIAC ARRHYTHMIAS Cardiac arrhythmias of ventricular origin are responsible for the deaths of nearly half a million Americans each year while atrial fibrillation accounts for about 2.3 million cases per year, a rate that is projected to increase 2.5 fold over the next half century. Effectively managing these cardiac rhythm disorders remains a major challenge for both caregivers and the pharmaceutical industry. Filling a gap in the current literature, Novel Therapeutic Targets for Antiarrhythmic Drugs presents the latest treatments for cardiac arrhythmias alongside comprehensive presentations of basic cardiac physiology and pharmacology. Written b...
Under normal, healthy conditions, the contraction of cardiac myocytes, leading to the pump function of this organ, is driven by calcium-dependent mechanisms. Entry of calcium into the myocyte during the cardiac action potential causes activation of the ryanodine receptors and release of calcium from the sarcoplasmic reticulum. This process termed calcium-induced calcium release is essential for excitation-contraction coupling and enables each action potential to be transduced into a mechanical event. Indeed, in healthy myocytes, the calcium concentration in the cytosol of is elevated approximately 10-fold from a resting level of ∼100 nM to ∼1 μM. This process is finely orchestrated by a...
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This book reports the text of the lectures of the 6th International Conference on Sodium Calcium Exchange held in Lacco Ameno in the Island of Ischia in the Gulf of Naples, Italy, from October 1 to October 5, 2011. The present book uncovers the most striking new findings on NCX that emerged since the previous Conference on Sodium Calcium Exchange, such as the structural dissection of the molecular determinants of Ca2+ sensitivity of the exchanger, the epigenetic regulation of ncx1 gene, the molecular identification of the mitochondrial Sodium Calcium Exchanger, and the discovery of NCX in unexpected anatomical locations such as the female reproductive tract. The book is organized into 11 parts covering NCX structural aspects, genetic and epigenetic regulation, regulatory mechanisms, subcellular localization in mitochondria, involvement in neurodegenerative diseases and in immune regulation, and the role of the cardiovascular and endocrine systems, as well as diabetes in physiology and pathophysiology. Selected chapters of the book are also devoted to the interaction of NCKX and other ion channels and transporters with NCX, like ASICs, TRPM, and NHE.
The cardiovascular benefits of dietary omega-3 polyunsaturated fatty acids (n-3 PUFA) have been actively investigated for nearly 40 years. Beginning with the pioneering studies of Bang and Dyerberg, epidemiological data provide strong evidence for an inverse relationship between fatty fish consumption and cardiac mortality. In contrast to these observational studies, interventional studies using n-3 PUFAs for the secondary prevention of adverse cardiovascular events in patients with heart disease have yielded conflicting results; some studies have reported reduced sudden cardiac death or mortality, while other more recent studies have reported either no effect or an increase in adverse cardi...
This is a Ph.D. dissertation. Restenosis occurs in 10-50% of patients after PCI, thus remaining a major challenge. Restenosis after PCI is a complex, multifactorial, overlapping wound healing process involving a cascade of cellular and molecular events including platelet activation, inflammatory cell infiltration, smooth muscle cell proliferation, migration and extracellular matrix production. Recent evidence shows that inflammation, matrix metalloproteinases and free oxygen radicals all play a critical role in the restenosis process. Different approaches to prevent restenosis after PCI were studied in this work. Restenosis has been remarkably reduced in the last decade with the introduction...
"This is a Ph.D. dissertation. Role of Inflammation in the Pathogenesis of Restenosis, Local Drug Delivery Using Drug Eluting Stents, In Vitro Stent Implantation, Optimization of Local Methylprednisolone Delivery to Inhibit Inflammatory Reaction and Neointimal Hyperplasia of Coated Coronary Stents, Cytochalasin Polymer Coated Stents Reduce Neointimal Formation in a Porcine Coronary Model, Long-Term Biocompatibility Evaluation of a Biodegradable Polymer Coated Stent in a Porcine Coronary Stent Model, Methotrexate Loaded SAE-Coated Coronary Stents Reduce Neointimal Hyperplasia in a Porcine Coronary Model, Local Methylprednisolone Delivery Using a Biodivysio Phosphorycholone Coated Drug Delivery Stents Reduces Inflammation and Neointimal Hyperplasia in a Porcine Coronary Stent Model, Stent Based Dexamethasone Delivery: From Pre-Clinical Data to the Stride Trial, General Discussions and Conclusions."