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This timely and most comprehensive reference available on the topic covers all the different aspects vital in the fight against the global obesity epidemic. Following a look at adipose tissue development and morphology, the authors go on to examine its metabolic and endocrine functions and its role in disease. The final section deals with comparative and evolutionary aspects of the tissue. The result is an essential resource for cell and molecular biologists, physiologists, biochemists, pharmacologists, and those working in the pharmaceutical industry.
Abstract: The proceedings of a 1982 international conference covers 33 review articles on research findings and the current state of knowledge of various metabolic and mechanistic aspects of the associations between the adipocyte fat cell and obesity. The articles address various facets of adipose cell growth and development; insulin action; lipid assimilation and lipoprotein and cholesterol metabolism in adipose tissue; lipolysis in adipocytes; and energy expenditure. The role of adipose tissue as a model system for the study of mechanisms of insulin action is highlighted by evidence of new cellular mediators. Recent insights in triglyceride assimilation regulation by lipoprotein lipase and fatty acid release through the lipolytic cascade are discussed. Other topics include the role of lipocytes in cholesterol turnover, the relationship of cholesterol metabolism to lipoprotein turnover and catabolism, and aspects of energy balance and thermoregulation in obesity. (wz).
This book highlights the important role free fatty acids (FFA) play as potential drug targets. While FFA have long been considered byproducts of cell metabolism, they are now recognized as ligands that regulate cell and tissue function via G-protein-coupled receptors. At least three receptors have been identified for which FFA appear to be the endogenous ligands.
This book focuses on host–pathogen interactions at the metabolic level. It explores the metabolic requirements of the infectious agents, the microbial metabolic pathways that are dedicated to circumvent host immune mechanisms as well as the molecular mechanisms by which pathogens hijack host cell metabolism for their own benefit. Finally, it provides insights on the possible clinical and immunotherapeutic applications, as well as on the available experimental and analytical methods. The contributions break new ground in understanding the metabolic crosstalk between host and pathogen.
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.
Methods in Toxicology, Volume 2: Mitochondrial Dysfunction provides a source of methods, techniques, and experimental approaches for studying the role of abnormal mitochondrial function in cell injury. The book discusses the methods for the preparation and basic functional assessment of mitochondria from liver, kidney, muscle, and brain; the methods for assessing mitochondrial dysfunction in vivo and in intact organs; and the structural aspects of mitochondrial dysfunction are addressed. The text also describes chemical detoxification and metabolism as well as specific metabolic reactions that are especially important targets or indicators of damage. The methods for measurement of alterations in fatty acid and phospholipid metabolism and for the analysis and manipulation of oxidative injury and antioxidant systems are also considered. The book further tackles additional methods on mitochondrial energetics and transport processes; approaches for assessing impaired function of mitochondria; and genetic and developmental aspects of mitochondrial disease and toxicology. The text also looks into mitochondrial DNA synthesis, covalent binding to mitochondrial DNA, DNA repair, and mitochondrial dysfunction in the context of developing individuals and cellular differentiation. Microbiologists, toxicologists, biochemists, and molecular pharmacologists will find the book invaluable.
Stroke is a major cause of death and the major cause of adult neurological disability in most of the world. Despite its importance on a population basis, research into the genetics of stroke has lagged behind that of many other disorders. However, the situation is now changing. An increasing number of single gene disorders causing stroke are being described, and there is growing evidence that polygenic factors are important in the risk of apparently "sporadic" stroke. Stroke Genetics provides an up-to-date review of the area, suitable for clinicians treating stroke patients, and both clinical and non-clinical researchers in the field of cerebrovascular disease. The full range of monogenic stroke disorders causing cerebrovascular disease, including ischaemic stroke, intracerebral haemorrhage, aneurysms and arteriovenous malformations, are covered. For each, clinical features, diagnosis, and genetics are described. Increasing evidence suggest that genetic factors are also important for the much more common multifactorial stroke; this evidence is reviewed along with the results of genetic studies in this area. Optimal and novel strategies for investigating multifactorial stroke, including the use of intermediate phenotypes such as intima-media thickness and MRI detected small vessel disease are reviewed. The book concludes by describing a practical approach to investigating patients with stroke for underlying genetic disorders. Also included is a list of useful websites.