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Cardiomyopathy means "heart (cardio) muscle (myo) disease (pathy)". Currently, cardiomyopathies are defined as myocardial disorders in which the heart muscle is structurally and/or functionally abnormal in the absence of a coronary artery disease, hypertension, valvular heart disease or congenital heart disease sufficient to cause the observed myocardial abnormalities. This book provides a comprehensive, state-of-the-art review of the current knowledge of cardiomyopathies. Instead of following the classic interdisciplinary division, the entire cardiovascular system is presented as a functional unity, and the contributors explore pathophysiological mechanisms from different perspectives, including genetics, molecular biology, electrophysiology, invasive and non-invasive cardiology, imaging methods and surgery. In order to provide a balanced medical view, this book was edited by a clinical cardiologist.
Myocardium --- Diseases. --- Cardiomyopathies --- Cardiomyopathy --- Myocardial diseases --- Myocardiopathies --- Myocardiopathy --- Cardiovascular medicine
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The disease of the heart muscle may occur secondarily to common diseases, such as ischemic, hypertensive and valvular, among others. However, there is a group of conditions with intrinsic myocardial involvement from gene or multifactorial etiology, and high morbidity and mortality that represent a diagnostic and therapeutic challenge for the physician. The book is focused on these cardiomyopathies, its features, its pathophysiology and its relation to sudden death. Mention is made also on general aspects, like ecocardiographic findings and myocardial contractile reserve, specific as pathophysiology and molecular mechanisms and cardiomyopathies in special populations. Special attention was deserved to cardiomyopathies in pediatrics, diabetic patients and women, as well as to the cases of chronic heart failure and dilated cardiomyopathy.
Myocardium --- Diseases. --- Cardiomyopathies --- Cardiomyopathy --- Myocardial diseases --- Myocardiopathies --- Myocardiopathy --- Cardiovascular medicine
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Poised at the convergence of most catabolic and anabolic pathways, mitochondria are the center of heterotrophic aerobic life, representing a hub in the overall metabolic network of cells. The energetic functions performed by mitochondria face the unavoidable redox hurdle of handling huge amounts of oxygen while keeping its own as well as the cellular redox environment under control. Reactive oxygen species (ROS) are produced in the respiratory chain as a result of the energy supplying function of mitochondria. Originally considered an unavoidable by-product of oxidative phosphorylation, ROS have become crucial signaling molecules when their levels are kept within physiological range. This occurs when their production and scavenging are balanced within mitochondria and cells. Mitochondria-generated hydrogen peroxide can act as a signaling molecule within mitochondria or in the cytoplasm, affecting multiple networks that control, for example, cell cycle, stress response, cell migration and adhesion, energy metabolism, redox balance, cell contraction, and ion channels. However, under pathophysiological conditions, excessive ROS levels can happen due to either overproduction, overwhelming of antioxidant defenses, or both. Under oxidative stress, detrimental effects of ROS include oxidation of protein, lipids, and nucleic acids; mitochondrial depolarization and calcium overload; and cell-wide oscillations mediated by ROS-induced ROS release mechanisms. Mitochondrial dysfunction is central in the pathogenesis of numerous human maladies including cardiomyopathies and neurodegeneration. Diseases characterized by altered nutrient metabolism, such as diabetes and cancer, exhibit elevated ROS levels. These may contribute to pathogenesis by increasing DNA mutation, affecting regulatory signaling and transcription, and promoting inflammation. Under metabolic stress, several ionic channels present in the inner and outer mitochondrial membranes can have pro-life and -death effects. In the present E-book, based on the Frontiers Research Topic entitled: "Mitochondria: Hubs of cellular signaling, energetics and redox balance", we address one of the fundamental questions that the field of ROS biology faces today: how do mitochondria accomplish a reliable energy provision and at the same time keep ROS levels within physiological, non-harming, limits but crucial for cellular signaling function? Additionally, and within the perspective of mitochondria as signaling-energetic hubs in the extensive cellular metabolic network, we ask how can their collective dynamics scale from the subcellular to the cellular, tissue and organ levels to affect function in health and disease.
redox and energetic compartmentation --- light- and anesthetics-induced cardioprotection --- redox metabolism and signaling --- hypertrophic and diabetic cardiomyopathies --- skeletal-cardiac muscle and brain protection --- ketone bodies --- post-translational modifications --- redox aging --- lipid catabolism --- necroptosis
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Mathematical modelling in biomedicine is a rapidly developing scientific discipline at the intersection of medicine, biology, mathematics, physics, and computer science. Its progress is stimulated by fundamental scientific questions and by the applications to public health. This book represents a collection of papers devoted to mathematical modelling of various physiological problems in normal and pathological conditions. It covers a broad range of topics including cardiovascular system and diseases, heart and brain modelling, tumor growth, viral infections, and immune response. Computational models of blood circulation are used to study the influence of heart arrhythmias on coronary blood flow and on operating modes for left-ventricle-assisted devices. Wave propagation in the cardiac tissue is investigated in order to show the influence of tissue heterogeneity and fibrosis. The models of tumor growth are used to determine optimal protocols of antiangiogenic and radiotherapy. The models of viral hepatitis kinetics are considered for the parameter identification, and the evolution of viral quasi-species is investigated. The book presents the state-of-the-art in mathematical modelling in biomedicine and opens new perspectives in this passionate field of research.
virus density distribution --- genotype --- virus infection --- immune response --- resistance to treatment --- nonlocal interaction --- quasi-species diversification --- mathematical oncology --- spatially distributed modeling --- reaction-diffusion-convection equations --- computer experiment --- spiral wave --- heterogeneity --- heart modeling --- myocardium --- left ventricle --- neural field model --- integro-differential equation --- waves --- brain stimulation --- mathematical modeling --- cardiac mechanics --- multiscale simulation --- cardiomyopathies --- left ventricle remodeling --- spatially-distributed modeling --- gradient descent --- 1D haemodynamics --- systole variations --- coronary circulation --- cardiac pacing --- tachycardia --- bradycardia --- interventricular asynchrony --- long QT syndrome --- premature ventricular contraction --- rotary blood pump --- lumped heart model --- cardiac fibrosis --- excitable media --- wave break --- elongated obstacle --- lymph flow --- mathematical modelling --- lymphatic vessels --- lymph nodes --- parameter estimation --- constrained optimization --- derivative free optimization --- multiscale models --- differential equations --- viral hepatitis
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