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Metabolic Syndrome (MS) is a highly prevalent condition in developed countries and is a cluster of several risk factors for type 2 diabetes and cardiovascular disease that includes increased body mass index/waist circumference, visceral obesity, insulin resistance, hyperclycaemia, dyslipidaemia and hypertension, which are all major causes of morbidity and death. This volume provides a critical review and discussion of the knowledge gathered on MS and analyzes the interplay between oxidative stress, chronic inflammation and angiogenesis features. There is a special focus on recent discoveries and progress toward possible therapeutic strategies, such as the role of glucose transporters within MS; the effects of polyphenols as anti-oxidant, anti-inflammatory and anti-angiogenic compounds. The role of NFkB, nitric oxide synthases, hypoxia-inducible factors, and many other molecules that play a part in the development of oxidative stress and inflammation as well as angiogenesis is also covered. This book fills the gap between basic science and medical care, and provides the reader with the skills to apply rigorous basic science to clinical settings of metabolic syndrome-associated disorders.
In the 2001 Surgeon General's Call to Action to Prevent and Decrease Overweight and Obesity, former Surgeon General David Satcher, MD, PhD, warned of the negative effects of the increasing weight of American citizens and outlined a public health response to reverse the trend. The Surgeon General plans to strengthen and expand this blueprint for action created by her predecessor. Although the country has made some strides since 2001, the prevalence of obesity, obesity-related diseases, and premature death remains too high.
Angiogenesis has recently played a critical role in regulation of adipose tissue expansion and regression. Like most other tissues in the body, adipose expansion and regression is accompanied by alteration of blood vessel density and structures. The vascular alteration plays an active role in regulation of adipose tissue size and functions. Targeting blood vessels in the adipose tissue have demonstrated to be a novel approach for possibly treatment of cancer, obesity and other metabolic diseases. This book provides the most updated information on this type research and discusses future opportunities for therapy..
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.
The endothelium, a monolayer of endothelial cells, constitutes the inner cellular lining of the blood vessels (arteries, veins and capillaries) and the lymphatic system, and therefore is in direct contact with the blood/lymph and the circulating cells. The endothelium is a major player in the control of blood fluidity, platelet aggregation and vascular tone, a major actor in the regulation of immunology, inflammation and angiogenesis, and an important metabolizing and an endocrine organ. Endothelial cells controls vascular tone, and thereby blood flow, by synthesizing and releasing relaxing and contracting factors such as nitric oxide, metabolites of arachidonic acid via the cyclooxygenases, lipoxygenases and cytochrome P450 pathways, various peptides (endothelin, urotensin, CNP, adrenomedullin, etc.), adenosine, purines, reactive oxygen species and so on. Additionally, endothelial ectoenzymes are required steps in the generation of vasoactive hormones such as angiotensin II. An endothelial dysfunction linked to an imbalance in the synthesis and/or the release of these various endothelial factors may explain the initiation of cardiovascular pathologies (from hypertension to atherosclerosis) or their development and perpetuation. Table of Contents: Introduction / Multiple Functions of the Endothelial Cells / Calcium Signaling in Vascular Cells and Cell-to-Cell Communications / Endothelium-Dependent Regulation of Vascular Tone / Conclusion / References
The endothelium enables communication between blood and tissues and is actively involved in cardiovascular homeostasis. Endothelial dysfunction has been recognized as an early step in the development of cardiovascular diseases: respectively, endothelium represents a potential therapeutic niche with multiple targets. The purpose of the book is to point out some recent findings of endothelial physiology and pathophysiology emphasizing various aspects of endothelial dysfunction connected to the body's internal and external environment. While basic features of the endothelium are presented in an introductory chapter, the authors of the following 17 chapters have provided extensive insight into some selected topics of endothelial (dys)function. The book would hopefully be useful for anyone interested in recapitulating endothelial (patho)physiology and expanding knowledge of molecular mechanisms involved in endothelial dysfunction, relevant also for further clinical investigations.
Atherosclerosis, the underlying cause of heart attacks, strokes and peripheral vascular disease, is one of the major killers in the world. By 2020 WHO statistics indicate that it will be the most common cause of morbidity and mortality in both the industrialised world and the underdeveloped world. The disease develops slowly over many years in the innermost layer of large and medium-sized arteries (Fig. 1) (Scott, 1995; Ross, 1999; Naumova and Scott, 2000; Glass and Witztum, 2001; Libby, 2001). It does not usually become manifest before the fourth of fifth decade, but then often strikes with devas tating suddenness. Fifty per cent of individuals still die (25 per cent immedi ately) from their first heart attack; and morbidity from coronary heart disease and stroke is very significant. The disease has a profound impact on health care services and on industrial economies. The lesions of atherosclerosis Autopsy studies show that in humans atherosclerosis begins in the first and second decade of life. A similar disease can be produced in experimental animals, where diet and genetics can be manipulated to produce identical lesions. The earliest lesions are fatty streaks. These consist of an accumulation of lipid-engorged macrophages (foam cells) and T and B lymphocytes in the arterial intima. With time, the fatty streaks progress to intermediate lesions, composed of foam cells and smooth muscle cells.
The book addresses controversies related to the origins of cancer and provides solutions to cancer management and prevention. It expands upon Otto Warburg's well-known theory that all cancer is a disease of energy metabolism. However, Warburg did not link his theory to the "hallmarks of cancer" and thus his theory was discredited. This book aims to provide evidence, through case studies, that cancer is primarily a metabolic disease requring metabolic solutions for its management and prevention. Support for this position is derived from critical assessment of current cancer theories. Brain cancer case studies are presented as a proof of principle for metabolic solutions to disease management, but similarities are drawn to other types of cancer, including breast and colon, due to the same cellular mutations that they demonstrate.
Is it advisable to go back from bedside to the bench? During the last decade, few topics encountered such a broad interest in bio- gy and medicine as angiogenesis. The amazing ability of the body to restore blood flow by induction of blood vessel growth as part of an adaptive process has alarmed physicians dealing with diseases in which angiogenesis is either exaggerated (as in tumors) or too slow (as in ischemic diseases of heart and brain). Not surprisingly, pro- and antiangiogenic strategies have found their way into clinical trials. For instance, for the USA, the NIH website in early 2004 displayed 38 clinical studies involving either pro- or antiangiogenic th- apies. Given the expected overwhelming wealth of clinical data, the question may be asked whether further exploration of biological mechanisms is required or whether results from the bedside are instructive enough to proceed. This question depends also on the progress of pro- and antiangiogenic clinical trials. In the following, I give a short overview about some of the progress that has been made in this field. Since Judah Folkman proposed antiangiogenic tumor therapy thirty years ago, it has become increasingly evident that agents which interfere with blood vessel formation also block tumor progression. Accordingly, antiangiogenic therapy has gained much attention as a potential adjunct to conventional c- cer therapy.
This book bridges the gap between fundamental and translational research in the area of heart disease. It describes a multidisciplinary approach, and demonstrates biochemical mechanisms associated with dysregulation of redox signaling, which leads heart disease. Presenting recent studies on improved forms of ROS scavenging enzymes; specific inhibitors for different ROS generating enzymes; and oxidant induced signaling pathways and their antagonists that allow subtle modulation of redox signaling, it also discusses the spatial and temporal aspects of oxidative stress in the cardiovascular system, which are of vital importance in developing better strategies for treating heart disease. Each chapter offers researchers valuable insights into identifying targets for drug development for different types of heart disease.