Advances in Biochemistry in Health and Disease – serie

Signal Transduction in Cardiovascular System Health and Disease highlights the major contributions of different signaling systems in modulating normal cardiovascular functions and how a perturbation in these signaling events leads to abnormal cell functions and cardiovascular disorders.This title is volume 3 in the new Springer series, Advances in Biochemistry in Health and Disease.

At its present rate of growth, atherosclerosis will be the major cause of death from disease by the year 2020. Atherosclerosis is an extremely complex, biochemical, multifactorial process. This book will cover many aspects of atherogenesis, with particular emphasis on lipid and lipoprotein metabolism. We will cover all aspects of the regulation of cholesterol homeostasis and the importance of each pathway. This book will explore the role of nuclear hormone receptors on lipid and lipoprotein metabolism and their complex roles in atherogenesis. Finally, how the use of genetic studies can help sort out the immense complexities that mediate these aspects of atherogenesis will be discussed.

The term mitochondrion is derived from Latin, with mitos meaning thread and chondrion meaning granules. Indeed, under the light microscope, mitochondria often appear as rods or granules within the cytoplasm. For decades after initial visualization of mitochondria by light microscopy, mitochondrial function remained clouded. However, with the development of differential centri- gation and electron microscopy, it was discovered that a chief function of the mitochondria was the generation of ATP for the remainder of the cell. For many years, the energy generating function of the mitochondria was considered the primary, if not the sole function of the mitochondria. During that period, inves- gators attempted to obtain information on the mechanism of ATP synthesis and the regulation of electron transport. In the first chapter of the book, Dr. Hassinen summarizes those studies, providing clear pictures on the transformation of reducing equivalents into a proton gradient and the mechanism by which the F F 1 0 ATPase utilizes the proton gradient to generate ATP. He also summarizes the key regulatory steps of the citric acid cycle, which is the major source of reducing equivalents for the electron transport chain. In the heart, most of the carbon that feeds into the citric acid cycle is derived from fatty acid metabolism. Although fatty acid utilization provides most of the ATP for contraction, a proper balance must be maintained between the utilization of fatty acids and that of glucose. In the second chapter, Drs.

The term mitochondrion is derived from Latin, with mitos meaning thread and chondrion meaning granules. Indeed, under the light microscope, mitochondria often appear as rods or granules within the cytoplasm. For decades after initial visualization of mitochondria by light microscopy, mitochondrial function remained clouded. However, with the development of differential centri- gation and electron microscopy, it was discovered that a chief function of the mitochondria was the generation of ATP for the remainder of the cell. For many years, the energy generating function of the mitochondria was considered the primary, if not the sole function of the mitochondria. During that period, inves- gators attempted to obtain information on the mechanism of ATP synthesis and the regulation of electron transport. In the first chapter of the book, Dr. Hassinen summarizes those studies, providing clear pictures on the transformation of reducing equivalents into a proton gradient and the mechanism by which the F F 1 0 ATPase utilizes the proton gradient to generate ATP. He also summarizes the key regulatory steps of the citric acid cycle, which is the major source of reducing equivalents for the electron transport chain. In the heart, most of the carbon that feeds into the citric acid cycle is derived from fatty acid metabolism. Although fatty acid utilization provides most of the ATP for contraction, a proper balance must be maintained between the utilization of fatty acids and that of glucose. In the second chapter, Drs.

At its present rate of growth, atherosclerosis will be the major cause of death from disease by the year 2020. Atherosclerosis is an extremely complex, biochemical, multifactorial process. This book will cover many aspects of atherogenesis, with particular emphasis on lipid and lipoprotein metabolism. We will cover all aspects of the regulation of cholesterol homeostasis and the importance of each pathway. This book will explore the role of nuclear hormone receptors on lipid and lipoprotein metabolism and their complex roles in atherogenesis. Finally, how the use of genetic studies can help sort out the immense complexities that mediate these aspects of atherogenesis will be discussed.

This book summarizes present knowledge of different mechanisms involved in the development of positive and negative consequences of cardiac adaptation. Particular attention is paid to the still underestimated adaptive cardiac responses during development, to adaptation to the frequently occurring pressure and volume overload as well as to cardiac changes, induced by enduring exercise and chronic hypoxia.  Cardiac Adaptations will be of great value to cardiovascular investigators, who will find this book highly useful in their cardiovascular studies for finding solutions in diverse pathological conditions; it will also appeal to students, fellows, scientists, and clinicians interested in cardiovascular abnormalities.

The main objective of Cardiac Remodeling: Molecular Mechanisms is to summarize the major research advances in molecular, biochemical and translational aspects of cardiac remodeling over the last 2 to 3 decades under one cover and touch on future directions. It provides a high profile and valuable publication resource on molecular mechanisms of cardiac remodeling for both the present and future generations of researchers, teachers, students and trainees. This book should stimulate future translational research targeted towards discovery and development for preventing, limiting and reversing bad remodeling over the next few decades, with the ultimate goal of preventing progression to systolic and/or diastolic heart failure. The chapters suggest potential novel strategies that should receive attention for translating basic research knowledge to application in patients at the bedside.

It is now well known that proteases are found everywhere, in viruses and bacteria as well as in all human, animal and plant cells, and play a role in a variety of biological functions ranging from digestion, fertilization, development to senescence and death. Under physiological conditions the ability of proteases is regulated by endogenous inhibitors. However, when the activity of proteases is not regulated appropriately, disease processes can result, as seen in Alzheimer’s disease, cancer metastasis and tumor progression, inflammation and atherosclerosis. Thus it is evident that there is an absolute need for a tighter control of proteolytic activities in different cells and tissues.Aimed at graduate students and researchers with an interest in cellular proteolytic events, Role of Proteases in Cellular Dysfunctions is the second book on Proteases in this series. The book consists of three parts in specified topics based on current literatures for a better understanding for the readers with respect to their subject-wise interests. The first section of this book covers a brief idea about the neuronal disorders and the involvement of proteases such as calpains, caspases and matrix metalloproteases (MMPs). The second section covers the deadly disease cancer and its relation to ubiquitin-proteasome system, MMPs and serine proteases. The last section is about the role of proteases such as calpains, MMPs and serine protease as well as urokinase type plasminogen activator receptor (uPAR) in causing cardiovascular defects.

In view of rapidly growing research in the deregulation of proteases and their impact in human health and diseases, this book will highlight existing and emerging research in this exciting area. In-depth critical state-of-the-art reviews will be written by established investigators on proteases dysfunctions associated with pathogenesis of different diseases that are known to occur due to deregulation of proteolytic systems. Multidisciplinary approaches demonstrating biochemical and signal transduction mechanisms associated with deregulation of proteases leading to manifestation of the diseases will be discussed. The book highlights the roles of both intracellular and extracellular proteases in health and disease.

Diabetes has long been recognized as a disease of high blood sugar, and there has been a continuous search of the exact reason for its development and effective treatment. In 2005, the World Health Organization had estimated that more than 180 million people worldwide suffer from diabetes mellitus and indicated that this figure is likely to double within the next 20 years. Among the 3.8 million deaths each year associated with diabetes, about two thirds are attributable to cardiovascular complications, and diabetes is now considered to be a major metabolic risk factor for the occurrence of heart disease.Diabetic Cardiomyopathy: Biochemical and Molecular Mechanisms is a compilation of review articles devoted to the study on the topic with respect to biochemical and molecular mechanisms of hyperglycaemia. The wide range of areas covered here is of interest to basic research scientists, clinicians and graduate students, who are devoted to study the pathogenesis of diabetes-induced cardiovascular dysfunction. Furthermore, some chapters are directed towards increasing our understanding of novel ways for the prevention/treatment of cardiomyopathy.Twenty five articles in this book are organized in three sections. The first section discusses general aspects of the metabolic derangements in diabetic cardiomyopathy including metabolic alterations and substrate utilization as well as cardiac remodelling in the heart; role of diet in the development of metabolic syndrome in the heart; effect of hyperglycaemia in terms of biochemical and structural alterations in heart. In the second section, several cellular and molecular mechanisms are discussed indicating that diabetic cardiomyopathy is a multifactorial and complex problem. The third section discusses the prevention and treatment of diabetes using appropriate diet, proper supplements including antioxidants, angiotensin inhibitors and some other drugs. All in all, this book discusses the diverse mechanisms of diabetic cardiomyopathy with some information on new therapeutic approaches for finding solutions to prevent or reverse the development of cardiac dysfunction.

The main objective of Cardiac Remodeling: Molecular Mechanisms is to summarize the major research advances in molecular, biochemical and translational aspects of cardiac remodeling over the last 2 to 3 decades under one cover and touch on future directions. It provides a high profile and valuable publication resource on molecular mechanisms of cardiac remodeling for both the present and future generations of researchers, teachers, students and trainees. This book should stimulate future translational research targeted towards discovery and development for preventing, limiting and reversing bad remodeling over the next few decades, with the ultimate goal of preventing progression to systolic and/or diastolic heart failure. The chapters suggest potential novel strategies that should receive attention for translating basic research knowledge to application in patients at the bedside.

Signal Transduction in Cardiovascular System Health and Disease highlights the major contributions of different signaling systems in modulating normal cardiovascular functions and how a perturbation in these signaling events leads to abnormal cell functions and cardiovascular disorders.This title is volume 3 in the new Springer series, Advances in Biochemistry in Health and Disease.

This book summarizes present knowledge of different mechanisms involved in the development of positive and negative consequences of cardiac adaptation. Particular attention is paid to the still underestimated adaptive cardiac responses during development, to adaptation to the frequently occurring pressure and volume overload as well as to cardiac changes, induced by enduring exercise and chronic hypoxia.  Cardiac Adaptations will be of great value to cardiovascular investigators, who will find this book highly useful in their cardiovascular studies for finding solutions in diverse pathological conditions; it will also appeal to students, fellows, scientists, and clinicians interested in cardiovascular abnormalities.

Phospholipases generate lipid signaling molecules through their hydrolytic action on phospholipids and are known to regulate function of a variety of cells under normal and diseased conditions. While several physiological, biochemical and molecular techniques have identified key players involved in different disease processes, phospholipases have also emerged as critical players in the pathogenesis of a number of different diseases including cancer and heart disease. In addition, phospholipases are also implicated in such conditions as brain disorder/injury, kidney and immune cell dysfunction.Phospholipases in Health and Disease is a compilation of review articles dedicated to the study of the field with respect to biochemical and molecular mechanisms of normal and abnormal cell function. The wide range of area covered here is of interest to basic research scientists, clinicians and graduate students, who are engaged in studying pathophysiological basis of a variety of diseases. Furthermore, this book highlights the potential of the different phospholipases as therapeutic targets as well as part of prevention strategies. Twenty three articles in this book are organized in four sections that are designed to emphasize the most characterized forms of the phospholipases in mammalian cells. The first section discusses general aspect of phospholipases. Section two covers the role and function of phospholipase A in different pathophysiological conditions. The third section is focussed on phospholipase C which is believed to play a central role in transmembrane signaling. The final section covers phospholipase D which is present in a variety of different cells. The book illustrates that the activation of phospholipases is of fundamental importance in signal transduction affecting cell function. Overall, this book discusses the diverse mechanisms of phospholipase mediated signal transduction in different pathophysiological conditions and raises the possibility of specific forms of phospholipases serving as novel targets for drug development.

The heart has a very high energy demand but very little energy reserves. In order to sustain contractile function, the heart has to continually produce a large amount of ATP. The heart utilizes free fatty acids mainly and carbohydrates to some extent as substrates for making energy and any change in this energy supply can seriously compromise cardiac function. It has emerged that alterations in cardiac energy metabolism are a major contributor to the development of a number of different forms of heart disease. It is also now known that optimizing energy metabolism in the heart is a viable and important approach to treating various forms of heart disease.Cardiac Energy Metabolism in Health and Disease describes the research advances that have been made in understanding what controls cardiac energy metabolism at molecular, transcriptional and physiological levels. It also describes how alterations in energy metabolism contribute to the development of heart dysfunction and how optimization of energy metabolism can be used to treat heart disease. The topics covered include a discussion of the effects of myocardial ischemia, diabetes, obesity, hypertrophy, heart failure, and genetic disorders of mitochondrial oxidative metabolism on cardiac energetics. The treatment of heart disease by optimizing energy metabolism is also discussed, which includes increasing overall energy production as well as increasing the efficiency of energy production and switching energy substrate preference of the heart. This book will be a valuable source of information to graduate students, postdoctoral fellows, and investigators in the field of experimental cardiology as well as biochemists, physiologists, pharmacologists, cardiologists, cardiovascular surgeons and other health professionals.

It is now well known that proteases are found everywhere, in viruses and bacteria as well as in all human, animal and plant cells, and play a role in a variety of biological functions ranging from digestion, fertilization, development to senescence and death. Under physiological conditions the ability of proteases is regulated by endogenous inhibitors. However, when the activity of proteases is not regulated appropriately, disease processes can result, as seen in Alzheimer’s disease, cancer metastasis and tumor progression, inflammation and atherosclerosis. Thus it is evident that there is an absolute need for a tighter control of proteolytic activities in different cells and tissues.Aimed at graduate students and researchers with an interest in cellular proteolytic events, Role of Proteases in Cellular Dysfunctions is the second book on Proteases in this series. The book consists of three parts in specified topics based on current literatures for a better understanding for the readers with respect to their subject-wise interests. The first section of this book covers a brief idea about the neuronal disorders and the involvement of proteases such as calpains, caspases and matrix metalloproteases (MMPs). The second section covers the deadly disease cancer and its relation to ubiquitin-proteasome system, MMPs and serine proteases. The last section is about the role of proteases such as calpains, MMPs and serine protease as well as urokinase type plasminogen activator receptor (uPAR) in causing cardiovascular defects.

Phospholipases generate lipid signaling molecules through their hydrolytic action on phospholipids and are known to regulate function of a variety of cells under normal and diseased conditions. While several physiological, biochemical and molecular techniques have identified key players involved in different disease processes, phospholipases have also emerged as critical players in the pathogenesis of a number of different diseases including cancer and heart disease. In addition, phospholipases are also implicated in such conditions as brain disorder/injury, kidney and immune cell dysfunction.Phospholipases in Health and Disease is a compilation of review articles dedicated to the study of the field with respect to biochemical and molecular mechanisms of normal and abnormal cell function. The wide range of area covered here is of interest to basic research scientists, clinicians and graduate students, who are engaged in studying pathophysiological basis of a variety of diseases. Furthermore, this book highlights the potential of the different phospholipases as therapeutic targets as well as part of prevention strategies. Twenty three articles in this book are organized in four sections that are designed to emphasize the most characterized forms of the phospholipases in mammalian cells. The first section discusses general aspect of phospholipases. Section two covers the role and function of phospholipase A in different pathophysiological conditions. The third section is focussed on phospholipase C which is believed to play a central role in transmembrane signaling. The final section covers phospholipase D which is present in a variety of different cells. The book illustrates that the activation of phospholipases is of fundamental importance in signal transduction affecting cell function. Overall, this book discusses the diverse mechanisms of phospholipase mediated signal transduction in different pathophysiological conditions and raises the possibility of specific forms of phospholipases serving as novel targets for drug development.

The heart has a very high energy demand but very little energy reserves. In order to sustain contractile function, the heart has to continually produce a large amount of ATP. The heart utilizes free fatty acids mainly and carbohydrates to some extent as substrates for making energy and any change in this energy supply can seriously compromise cardiac function. It has emerged that alterations in cardiac energy metabolism are a major contributor to the development of a number of different forms of heart disease. It is also now known that optimizing energy metabolism in the heart is a viable and important approach to treating various forms of heart disease.Cardiac Energy Metabolism in Health and Disease describes the research advances that have been made in understanding what controls cardiac energy metabolism at molecular, transcriptional and physiological levels. It also describes how alterations in energy metabolism contribute to the development of heart dysfunction and how optimization of energy metabolism can be used to treat heart disease. The topics covered include a discussion of the effects of myocardial ischemia, diabetes, obesity, hypertrophy, heart failure, and genetic disorders of mitochondrial oxidative metabolism on cardiac energetics. The treatment of heart disease by optimizing energy metabolism is also discussed, which includes increasing overall energy production as well as increasing the efficiency of energy production and switching energy substrate preference of the heart. This book will be a valuable source of information to graduate students, postdoctoral fellows, and investigators in the field of experimental cardiology as well as biochemists, physiologists, pharmacologists, cardiologists, cardiovascular surgeons and other health professionals.

Diabetes has long been recognized as a disease of high blood sugar, and there has been a continuous search of the exact reason for its development and effective treatment. In 2005, the World Health Organization had estimated that more than 180 million people worldwide suffer from diabetes mellitus and indicated that this figure is likely to double within the next 20 years. Among the 3.8 million deaths each year associated with diabetes, about two thirds are attributable to cardiovascular complications, and diabetes is now considered to be a major metabolic risk factor for the occurrence of heart disease.Diabetic Cardiomyopathy: Biochemical and Molecular Mechanisms is a compilation of review articles devoted to the study on the topic with respect to biochemical and molecular mechanisms of hyperglycaemia. The wide range of areas covered here is of interest to basic research scientists, clinicians and graduate students, who are devoted to study the pathogenesis of diabetes-induced cardiovascular dysfunction. Furthermore, some chapters are directed towards increasing our understanding of novel ways for the prevention/treatment of cardiomyopathy.Twenty five articles in this book are organized in three sections. The first section discusses general aspects of the metabolic derangements in diabetic cardiomyopathy including metabolic alterations and substrate utilization as well as cardiac remodelling in the heart; role of diet in the development of metabolic syndrome in the heart; effect of hyperglycaemia in terms of biochemical and structural alterations in heart. In the second section, several cellular and molecular mechanisms are discussed indicating that diabetic cardiomyopathy is a multifactorial and complex problem. The third section discusses the prevention and treatment of diabetes using appropriate diet, proper supplements including antioxidants, angiotensin inhibitors and some other drugs. All in all, this book discusses the diverse mechanisms of diabetic cardiomyopathy with some information on new therapeutic approaches for finding solutions to prevent or reverse the development of cardiac dysfunction.

​According to the World Health Organization, the epidemic of global obesity has nearly tripled since 1975. In 2016, more than 1.9 billion adults were overweight, over 650 million of which were obese. Being overweight and obese has been linked to a  number of non-communicable, chronic diseases. Pathophysiology of Obesity-Induced Health Complications is a compilation of review articles dedicated to describe co-morbidities associated with obesity. The wide range that is covered is of significant interest to basic research scientists, clinicians and graduate students who are engaged in studying obesity-induced health complications. Furthermore, this book highlights the potential of novel approaches for the prevention and treatment of obesity and its related illnesses. Nineteen articles in this book are organized in four sections that are designed to provide an overview of obesity-induced health complications. The firstsection serves as an introductory section on the prevalence, causes, consequences, treatments and preventive approaches for obesity. Section two covers the metabolic disturbances and inflammation due to obesity. The third section is focused on neurological and visceral complications as a consequence of obesity. The final section covers strategies for the prevention of obesity-induced complications. The book illustrates that obesity can result in a diverse range of pathophysiological conditions that adversely affect health.

​According to the World Health Organization, the epidemic of global obesity has nearly tripled since 1975. In 2016, more than 1.9 billion adults were overweight, over 650 million of which were obese. Being overweight and obese has been linked to a  number of non-communicable, chronic diseases. Pathophysiology of Obesity-Induced Health Complications is a compilation of review articles dedicated to describe co-morbidities associated with obesity. The wide range that is covered is of significant interest to basic research scientists, clinicians and graduate students who are engaged in studying obesity-induced health complications. Furthermore, this book highlights the potential of novel approaches for the prevention and treatment of obesity and its related illnesses. Nineteen articles in this book are organized in four sections that are designed to provide an overview of obesity-induced health complications. The firstsection serves as an introductory section on the prevalence, causes, consequences, treatments and preventive approaches for obesity. Section two covers the metabolic disturbances and inflammation due to obesity. The third section is focused on neurological and visceral complications as a consequence of obesity. The final section covers strategies for the prevention of obesity-induced complications. The book illustrates that obesity can result in a diverse range of pathophysiological conditions that adversely affect health.

Obesity is an independent risk factor for cardiovascular disease (CVD) in adults as well as in obese children. This book will provide a description of the impact of obesity on the cardiovascular system and increased predisposition to CVD. It will identify the major biochemical mechanisms that lead to the occurrence of myocardial abnormalities and vascular alterations in obesity. We will also have some discussion on the biochemistry of the so-called obesity paradox in relation to CVD. The contributors to this book are international experts on obesity and associated cardiovascular complications. This book is also uniquely positioned as it focuses on the biochemistry of obesity-induced cardiovascular dysfunction. There are 20 chapters in 2 different parts in this book, comprising of Part A: Pathophysiology of Cardiovascular Complications in Obesity (11 chapters) and Part B: Modification of Cardiovascular Dysfunction in obesity (9 chapters).   Theintent of this volume is to provide current and basic understanding of the biochemical mechanisms of obesity induced cardiovascular dysfunction that will be of value not only to cardiologists and other allied health professionals, but will also stimulate and motivate biomedical researchers and scientists to find the way to prevent the epidemic of obesity associated cardiovascular abnormalities. Furthermore, this book will serve as a highly useful resource for medical students, fellows, residents and graduate students with an interest in the cardiovascular system.In summary, this book covers a broad range of biochemical mechanisms of obesity-induced cardiovascular complications. We hope that the reader will understand that obesity is linked to an increase in the risk and occurrence of fatal CVD. Furthermore, the underlying message presented in the book is that the cause of obesity related disorders is complex and that understanding the biochemistry of cardiovascular dysfunction may contribute to the development of novel interventions for the prevention and treatment of obesity associated comorbidities.

Obesity is an independent risk factor for cardiovascular disease (CVD) in adults as well as in obese children. This book will provide a description of the impact of obesity on the cardiovascular system and increased predisposition to CVD. It will identify the major biochemical mechanisms that lead to the occurrence of myocardial abnormalities and vascular alterations in obesity. We will also have some discussion on the biochemistry of the so-called obesity paradox in relation to CVD. The contributors to this book are international experts on obesity and associated cardiovascular complications. This book is also uniquely positioned as it focuses on the biochemistry of obesity-induced cardiovascular dysfunction. There are 20 chapters in 2 different parts in this book, comprising of Part A: Pathophysiology of Cardiovascular Complications in Obesity (11 chapters) and Part B: Modification of Cardiovascular Dysfunction in obesity (9 chapters).   Theintent of this volume is to provide current and basic understanding of the biochemical mechanisms of obesity induced cardiovascular dysfunction that will be of value not only to cardiologists and other allied health professionals, but will also stimulate and motivate biomedical researchers and scientists to find the way to prevent the epidemic of obesity associated cardiovascular abnormalities. Furthermore, this book will serve as a highly useful resource for medical students, fellows, residents and graduate students with an interest in the cardiovascular system.In summary, this book covers a broad range of biochemical mechanisms of obesity-induced cardiovascular complications. We hope that the reader will understand that obesity is linked to an increase in the risk and occurrence of fatal CVD. Furthermore, the underlying message presented in the book is that the cause of obesity related disorders is complex and that understanding the biochemistry of cardiovascular dysfunction may contribute to the development of novel interventions for the prevention and treatment of obesity associated comorbidities.

Cardiovascular diseases are the leading cause of mortality in men and women. Unfortunately, women have traditionally been excluded from clinical trials, and female animals have been used less or sex was not reported in basic research studies. Until recently, consideration of both sexes was not required in clinical and preclinical studies focusing on cardiovascular diseases. However, the number of clinical and experimental papers dealing with sex differences and heart disease significantly increases during the last years. This trend is obviously the result of at least two facts: the number of examples of different behavior of the male and female heart under physiological and pathological conditions is steadily increasing and there were controversial reports on the beneficial and adverse effect of hormonal replacement therapy. Detailed molecular and cellular mechanisms of these differences are still unknown but one is clear already today: sex differences are so important that they should be considered by the selection of optimum diagnostic and therapeutic procedures in clinical practice.The book presents 16 manuscripts on sex differences of heart disease, as developed by several investigators; the volume is organized in four parts. Part I, dealing with sex differences in cardiac ischemic injury, includes 5 chapters on experimental aspects of cardiac ischemia/reperfusion injury, the role of testosterone, and clinical aspects of ischemic heart disease. Part II is devoted to sex differences in heart failure and includes four chapters. Discussion in this part of the book is centered around the sex differences in heart failure due to volume overload. Part III of this volume includes four papers on risk factors of cardiovascular diseases, namely hypertension and obesity, and, finally, three chapters in part IV deal with sex differences of cardiac mitochondria under different pathological conditions. We believe this book will be very useful forcardiovascular scientists, graduate students, postdoctoral fellows and other health professionals.

Cardiovascular diseases are the leading cause of mortality in men and women. Unfortunately, women have traditionally been excluded from clinical trials, and female animals have been used less or sex was not reported in basic research studies. Until recently, consideration of both sexes was not required in clinical and preclinical studies focusing on cardiovascular diseases. However, the number of clinical and experimental papers dealing with sex differences and heart disease significantly increases during the last years. This trend is obviously the result of at least two facts: the number of examples of different behavior of the male and female heart under physiological and pathological conditions is steadily increasing and there were controversial reports on the beneficial and adverse effect of hormonal replacement therapy. Detailed molecular and cellular mechanisms of these differences are still unknown but one is clear already today: sex differences are so important that they should be considered by the selection of optimum diagnostic and therapeutic procedures in clinical practice. The book presents 16 manuscripts on sex differences of heart disease, as developed by several investigators; the volume is organized in four parts. Part I, dealing with sex differences in cardiac ischemic injury, includes 5 chapters on experimental aspects of cardiac ischemia/reperfusion injury, the role of testosterone, and clinical aspects of ischemic heart disease. Part II is devoted to sex differences in heart failure and includes four chapters. Discussion in this part of the book is centered around the sex differences in heart failure due to volume overload. Part III of this volume includes four papers on risk factors of cardiovascular diseases, namely hypertension and obesity, and, finally, three chapters in part IV deal with sex differences of cardiac mitochondria under different pathological conditions. We believe this book will be very useful forcardiovascular scientists, graduate students, postdoctoral fellows and other health professionals.

One of the most intriguing and compelling issues to impact contemporary biology to date is the concept that cell death is genetically regulated. Observations by Kerr and Wyllie, made more than 30 years ago on the basis of distinct morphological criteria, markedly distinguished apoptosis from classical cell death by necrosis. Apoptosis is a highly regulated, evolutionary conserved, genetic program of cell death essential for normal development and tissue homeostasis. The discovery of apoptosis as a regulated event and potentially amenable to therapeutic interventions has generated considerable excitement because it meant that disease entities resulting from either too much, or too little, apoptosis could be potentially cured with new therapies that target apoptosis.While there is little doubt that necrosis induced by massive cellular trauma is likely an unregulated event, several lines of investigation have challenged the dogma that necrotic cell death ismerely unregulated. Emerging data has shifted the paradigm in our thinking about necrosis as a regulated event.Autophagy is another cellular process that has received considerable attention over the past two decades and its remarkable involvement in the processes of cell survival, death and tumorigenesis. Macro autophagy is a catabolic process that involves the selective and targeted removal of oxidized proteins, macromolecular structures and organelles through an elaborate cellular process involving a lysosome mediated pathway. Other forms of autophagy involving adapter proteins, commonly referred to as chaperone mediated autophagy, involves the selective removal of cellular cargo by the ubiquitin-proteasome pathway.The book will serve as a reference guide for basic and clinical scientists who are interested in understanding how these critical cellular processes impact the pathogenesis of human disease.

One of the most intriguing and compelling issues to impact contemporary biology to date is the concept that cell death is genetically regulated. Observations by Kerr and Wyllie, made more than 30 years ago on the basis of distinct morphological criteria, markedly distinguished apoptosis from classical cell death by necrosis. Apoptosis is a highly regulated, evolutionary conserved, genetic program of cell death essential for normal development and tissue homeostasis. The discovery of apoptosis as a regulated event and potentially amenable to therapeutic interventions has generated considerable excitement because it meant that disease entities resulting from either too much, or too little, apoptosis could be potentially cured with new therapies that target apoptosis.While there is little doubt that necrosis induced by massive cellular trauma is likely an unregulated event, several lines of investigation have challenged the dogma that necrotic cell death ismerely unregulated. Emerging data has shifted the paradigm in our thinking about necrosis as a regulated event.Autophagy is another cellular process that has received considerable attention over the past two decades and its remarkable involvement in the processes of cell survival, death and tumorigenesis. Macro autophagy is a catabolic process that involves the selective and targeted removal of oxidized proteins, macromolecular structures and organelles through an elaborate cellular process involving a lysosome mediated pathway. Other forms of autophagy involving adapter proteins, commonly referred to as chaperone mediated autophagy, involves the selective removal of cellular cargo by the ubiquitin-proteasome pathway.The book will serve as a reference guide for basic and clinical scientists who are interested in understanding how these critical cellular processes impact the pathogenesis of human disease.

Global health has been challenged with the dawning of the era of the obesity epidemic, and thus as a consequence, strategies to reduce obesity have become public health priorities. According to the United Nations, obesity has been identified as a concern for achieving Sustainable Development Goals. Obesity is a serious health problem with an increased risk of several common diseases including diabetes, cardiovascular disease, and cancer. Although the fundamental cause of obesity and overweight is an imbalance between calorie intake and calorie expenditure, the underlying biochemical and metabolic processes that cause obesity are not fully understood.Two earlier volumes dedicated to the subject of obesity, published in the series “Advances in Biochemistry in Health and Disease” focused on the pathophysiology of obesity-induced health complications and the biochemistry of cardiovascular dysfunction in obesity. This book brings together contributions from international experts in the field to describe advancements on the mechanisms leading to development of obesity and related complications. There are 21 chapters in two different parts in this book, comprising of Part I: Pathophysiologic Mechanisms of Obesity (11 chapters) and Part II: Therapeutic Mechanisms of Obesity (10 chapters). This book will serve as a resource and be of interest to health professionals, medical students, fellows, residents and graduate students. It will also evoke innovative research and effective approaches for the prevention of obesity. This volume will accentuate that obesity is a major health hazard in its own right and that appropriate public health measures should be implemented to prevent or reduce or even reverse the impact of this global chronic disease.

Global health has been challenged with the dawning of the era of the obesity epidemic, and thus as a consequence, strategies to reduce obesity have become public health priorities. According to the United Nations, obesity has been identified as a concern for achieving Sustainable Development Goals. Obesity is a serious health problem with an increased risk of several common diseases including diabetes, cardiovascular disease, and cancer. Although the fundamental cause of obesity and overweight is an imbalance between calorie intake and calorie expenditure, the underlying biochemical and metabolic processes that cause obesity are not fully understood.Two earlier volumes dedicated to the subject of obesity, published in the series “Advances in Biochemistry in Health and Disease” focused on the pathophysiology of obesity-induced health complications and the biochemistry of cardiovascular dysfunction in obesity. This book brings together contributions from international experts in the field to describe advancements on the mechanisms leading to development of obesity and related complications. There are 21 chapters in two different parts in this book, comprising of Part I: Pathophysiologic Mechanisms of Obesity (11 chapters) and Part II: Therapeutic Mechanisms of Obesity (10 chapters). This book will serve as a resource and be of interest to health professionals, medical students, fellows, residents and graduate students. It will also evoke innovative research and effective approaches for the prevention of obesity. This volume will accentuate that obesity is a major health hazard in its own right and that appropriate public health measures should be implemented to prevent or reduce or even reverse the impact of this global chronic disease.