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The main goal of this book is to form a high-quality platform in which well-known and emerging pioneering basic, translational and clinical scientists can present their latest, exciting findings in the studies of redox signaling in the pulmonary vasculature. Content from outstanding investigators with unique expertise and skills of molecular and cell biology, biochemistry, physiology, pharmacology, biophysics, biotechnology and medicine will update our current out-of-date concepts with new knowledge. Rapidly increasing scientific studies have gathered a large volume of novel and important information on redox signaling in healthy and diseased pulmonary vasculature. This volume covers the need for a cohesive book to display state-of-the-art advances in the field. The second major aim of this book is to help direct future research. Redox signaling is a major molecular process involved in almost every physiologic cellular response in the pulmonary vasculature including energy metabolism, host defense, gene expression, contraction, proliferation, and migration. Aberrancy in this important signaling pathway leads to a critical role in the development of nearly all pulmonary diseases, such as pulmonary hypertension, cor pulmonale, pulmonary edema, and vasculitis, among others.
This report considers the biological and behavioral mechanisms that may underlie the pathogenicity of tobacco smoke. Many Surgeon General's reports have considered research findings on mechanisms in assessing the biological plausibility of associations observed in epidemiologic studies. Mechanisms of disease are important because they may provide plausibility, which is one of the guideline criteria for assessing evidence on causation. This report specifically reviews the evidence on the potential mechanisms by which smoking causes diseases and considers whether a mechanism is likely to be operative in the production of human disease by tobacco smoke. This evidence is relevant to understanding how smoking causes disease, to identifying those who may be particularly susceptible, and to assessing the potential risks of tobacco products.
Lung diseases are leading causes of death and disability globally, with about 65 million people suffering from COPD, and 334 million from asthma. Each year, tens of millions of people develop and can die from lung infections such as pneumonia and TB. Systemic inflammation may induce and exacerbate local inflammatory diseases in the lungs, and local inflammation can in turn cause systemic inflammation. There is increasing evidence of the coexistence of systemic and local inflammation in patients suffering from asthma, COPD, and other lung diseases, and the co-morbidity of two or more local inflammatory diseases often occurs. For example, rheumatoid arthritis frequently occurs together with, and promotes the development of, pulmonary hypertension. This co-morbidity significantly impacts quality of life, and can result in death for some patients. Current treatment options for lung disease are neither always effective, nor condition-specific; there is a desperate need for novel therapeutics in the field. Additionally, the molecular and physiological significance of most major lung diseases is not well understood, which further impedes development of new treatments, especially in the case of coexistent lung diseases with other inflammatory diseases. Great progress has been made in recent years in many areas of the field, particularly in understanding the molecular geneses, regulatory mechanisms, signalling pathways, and cellular processes within lung disease, as well as basic and clinical technology, drug discovery, diagnoses, treatment options, and predictive prognoses. This is the first text to aggregate these developments. In two comprehensive volumes, experts from all over the world present state-of-the-art advances in the study of lung inflammation in health and disease. Contributing authors cover well-known as well as emerging topics in basic, translational, and clinical research, with the aim of providing researchers, clinicians, professionals, and students with new perspectives and concepts. The editors hope these books will also help to direct future research in lung disease and other inflammatory diseases, and result in the development of novel therapeutics.
Respiratory diseases are leading causes of death and disability globally, with about 65 million people suffering from COPD, and 334 million from asthma, the most common chronic disease. Each year, tens of millions of people develop and can die from from respiratory infections such as pneumonia and TB. Systemic inflammation may induce and exacerbate local inflammatory diseases in the lungs, and local inflammation can in turn cause systemic inflammation. There is increasing evidence of the coexistence of systemic and local inflammation in patients suffering from asthma, COPD, and other lung diseases, and the co-morbidity of two or more local inflammatory diseases often occurs. For example, rheumatoid arthritis frequently occurs together with, and promotes the development of, pulmonary hypertension. This co-morbidity significantly impacts quality of life, and can result in death for those affected. Current treatment options for lung disease are neither effective, nor condition-specific; there is a desperate need for novel therapeutics in the field. Additionally, the molecular and physiological significance of most major lung diseases is not well understood, which further impedes development of new treatments, especially in the case of coexistent lung diseases with other inflammatory diseases. Great progress has been made in recent years in many areas of the field, particularly in understanding the molecular geneses, regulatory mechanisms, signalling pathways, and cellular processes within lung disease, as well as basic and clinical technology, drug discovery, diagnoses, treatment options, and predictive prognoses. This is the first text to aggregate these developments. In two comprehensive volumes, experts from all over the world present state-of-the-art advances in the study of lung inflammation in health and disease. Contributing authors cover well-known as well as emerging topics in basic, translational, and clinical research, with the aim of providing researchers, clinicians, professionals, and students with new perspectives and concepts. The editors hope these books will also help to direct future research in lung disease and other inflammatory diseases, and result in the development of novel therapeutics.
Platelets in Cardiovascular Disease provides an in-depth and current coverage of relevant platelet biology and antiplatelet therapy that is in clinical use today and potentially for the future. The book provides a succinct overview of the critical role of platelets in cardiovascular medicine. Cardiovascular disease is the leading cause of mortality worldwide, and recent research has found that the platelet is central to the genesis of heart attacks and stroke as well as many of the complications of angioplasty and bypass surgery. An explosion of knowledge of the biology of platelets has established their important role in the formation of blood clots and, perhaps more intriguingly, their role as inflammatory cells. This growth in information has been paralleled by the development of several drugs that can interfere with platelet action and thereby improve patient outcomes. Indeed, several antiplatelet drugs already in development may ultimately lead to marked advances in both the treatment and prevention of cardiovascular disease. Drawing upon a panel of international experts, Platelets in Cardiovascular Disease delivers a concise yet thorough review of the major developments in antiplatelet therapy. Practicing clinicians as well as those involved in the development of new antithrombotic therapies will find the book interesting and useful. Sample Chapter(s). Chapter 1: Platelet Biology the Role of Platelets in Hemostasis, Thrombosis and Inflammation (274 KB). Contents: Platelet Biology: The Role of Platelets in Hemostasis, Thrombosis and Inflammation (R C Becker); Thromboxane Antagonists (B R Dulin & S R Steinhubl); Glycoprotein IIb/IIIa Inhibitors (S J Lehman et al.); ADP Receptor Antagonists (J Karha & C P Cannon); Monitoring Antiplatelet Therapy (P Harrison & A D Michelson); Platelet Genomics (B K Jefferson et al.); Future Strategies for the Development of Antiplatelet Drugs (R A Harrington). Readership: Physicians: cardiologists, vascular medicine specialists, hematologists; physicians in training: fellows, residents, interns; pharmacists; pharmaceutical industry: scientists, sales representatives.
Many physiological conditions such as host defense or aging and pathological conditions such as neurodegenerative diseases, and diabetes are associated with the accumulation of high levels of reactive oxygen species and reactive nitrogen species. This generates a condition called oxidative stress. Low levels of reactive oxygen species, however, which are continuously produced during aerobic metabolism, function as important signaling molecules, setting the metabolic pace of cells and regulating processes ranging from gene expression to apoptosis. For this book we would like to recruit the experts in the field of redox chemistry, bioinformatics and proteomics, redox signaling and oxidative stress biology to discuss how organisms achieve the appropriate redox balance, the mechanisms that lead to oxidative stress conditions and the physiological consequences that contribute to aging and disease.
This book describes the methods of analysis and determination of oxidants and oxidative stress in biological systems. Reviews and protocols on select methods of analysis of ROS, RNS, oxygen, redox status, and oxidative stress in biological systems are described in detail. It is an essential resource for both novices and experts in the field of oxidant and oxidative stress biology.
This book highlights the multifaceted roles of Reactive Oxygen Species (ROS) in modulating normal cellular and molecular mechanisms during the development of different types of heart disease. Each chapter in the book deals with the role that altered redox homeostasis plays in the pathophysiology of heart disease. In addition, the book explains how reactive oxidant species interact with their targets and provides novel strategies for attenuating oxidative stress-induced types of heart disease. The book not only covers ROS-induced response in heart disease at the cellular level, but also demonstrates that an imbalance of redox states has its roots in our genes, and explains the ways gene expression is regulated. In turn, it reviews potential sources of ROS, their pathological effects on the heart, and potential sites for therapeutic interventions.
The focus of this collection of illustrated reviews is to discuss the systems biology of free radicals and anti-oxidants. Free radical induced cellular damage in a variety of tissues and organs is reviewed, with detailed discussion of molecular and cellular mechanisms. The collection is aimed at those new to the field, as well as clinicians and scientists with long standing interests in free radical biology. A feature of this collection is that the material also brings insights into various diseases where free radicals are thought to play a role. There is extensive discussion of the success and limitations of the use of antioxidants in several clinical settings.