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The acute inflammatory response is the body's first system of alarm signals that are directed toward containment and elimination of microbial invaders. Uncontrolled inflammation has emerged as a pathophysiologic basis for many widely occurring diseases in the general population that were not initially known to be linked to the inflammatory response, including cardiovascular disease, asthma, arthritis, and cancer. To better manage treatment, diagnosis, and prevention of these wide-ranging diseases, multidisciplinary research efforts are underway in both academic and industry settings. This book provides an introduction to the cell types, chemical mediators, and general mechanisms of the host's first response to invasion. World-class experts from institutions around the world have written chapters for this introductory text. The text is presented as an introductory springboard for graduate students, medical scientists, and researchers from other disciplines wishing to gain an appreciation and working knowledge of current cellular and molecular mechanisms fundamental to inflammation.
A new perspective on the link between inflammation and cancer Inflammation is the human body’s normal biological response to threats in the modern world, as well as a defense against the harmful influence of pathogens, the environment, and poor nutrition. But what happens when the inflammatory response is triggered repeatedly and sustained for long periods of time? Cancer and Inflammation Mechanisms: Chemical, Biological, and Clinical Aspects discusses the mechanisms by which chronic inflammation can lead to cancer, the various causative agents, and possible prevention methods. A compilation of the latest information coming out of the various fields of cancer research, this book provides a detailed look at inflammation-related carcinogenesis from the perspective of researchers at the forefront of the field. It takes an interdisciplinary approach to the topic, and provides comprehensive information about the major factors at work in inflammation, cancer, and the intersection of the two conditions. Topics include: A general overview of inflammation-related cancer The biochemistry of inflammation and its effects on DNA Molecular biology and the role of microRNA in carcinogenesis Specific causative agents including oncogenic viruses, asbestos, and nanomaterial Anti-inflammatories, nutraceuticals, and other preventative measures A deeper understanding of the mechanisms behind inflammation-related carcinogenesis can lead to better patient outcomes by improving diagnostics and prevention, as well as altering the approach to treatment. Cancer and Inflammation Mechanisms: Chemical, Biological, and Clinical Aspects provides the knowledge base researchers need to push the field forward.
Our understanding of inflammation has increased rapidly in recent years, due in large part to the impact of molecular biology and gene identification and cloning. This book brings together ideas from a number of different biochemical disciplines which are frequently not integrated. The first chapter gives a visual overview of the subject; the remaining chapters are organized into three themes: the affector molecules, the regulatory components and the processes of inflammation itself. This book is essential reading for the busy physician or pathologist who wants to be up-to-date with the latest developments in immunology as they affect the diagnosis and treatment of many conditions.
The microcirculation is highly responsive to, and a vital participant in, the inflammatory response. All segments of the microvasculature (arterioles, capillaries, and venules) exhibit characteristic phenotypic changes during inflammation that appear to be directed toward enhancing the delivery of inflammatory cells to the injured/infected tissue, isolating the region from healthy tissue and the systemic circulation, and setting the stage for tissue repair and regeneration. The best characterized responses of the microcirculation to inflammation include impaired vasomotor function, reduced capillary perfusion, adhesion of leukocytes and platelets, activation of the coagulation cascade, and enhanced thrombosis, increased vascular permeability, and an increase in the rate of proliferation of blood and lymphatic vessels. A variety of cells that normally circulate in blood (leukocytes, platelets) or reside within the vessel wall (endothelial cells, pericytes) or in the perivascular space (mast cells, macrophages) are activated in response to inflammation. The activation products and chemical mediators released from these cells act through different well-characterized signaling pathways to induce the phenotypic changes in microvessel function that accompany inflammation. Drugs that target a specific microvascular response to inflammation, such as leukocyte-endothelial cell adhesion or angiogenesis, have shown promise in both the preclinical and clinical studies of inflammatory disease. Future research efforts in this area will likely identify new avenues for therapeutic intervention in inflammation. Table of Contents: Introduction / Historical Perspectives / Anatomical Considerations / Impaired Vasomotor Responses / Capillary Perfusion / Angiogenesis / Leukocyte-Endothelial Cell Adhesion / Platelet-Vessel Wall Interactions / Coagulation and Thrombosis / Endothelial Barrier Dysfunction / Epilogue / References
"A subject collection from Cold Spring Harbor perspectives in biology."
This book provides readers with an up-to-date and comprehensive view on the resolution of inflammation and on new developments in this area, including pro-resolution mediators, apoptosis, macrophage clearance of apoptotic cells, possible novel drug developments.
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This book was prepared as extension of author’s accidental discoveries on experimental models of acute and chronic ocular inflammatory diseases that were established at the University of Pennsylvania in 1980’s. Analyses of original data suggest a series of first evidence for direct link between inflammation and developmental phases of immune dysfunction in multistep tumorigenesis and angiogenesis. The only evidence presented on initial events for interactions and synergies between activated host and recruiting cells toward tumorigenesis. Effective immunity was defined as balance between two highly regulated and biologically opposing arms, Yin and Yang of acute inflammation, an amazingly precise signal communications between immune and non-immune systems requiring differential bioenergetics. Unresolved inflammation is a common denominator mapping aging process and induction of ‘mild’, ‘moderate’ or ‘severe’ immune disorders including cancers. Our knowledge of the fascinating biology of immunity in health or chronic diseases is fragmentary, chaotic and confusing, particularly for cancer science. Lack of progress in curing majority of chronic diseases or cancer is primarily due to the fact that scientists work on isolated molecules/cells or topics that are funded and promoted by decision makers in medical/cancer establishment. Despite existence of over 25 million articles on cancer-related topics, cancer biology and cure remain mysteries to be solved. After a century of cancer research, the failure rates of therapies for solid tumors are 90% (+/-5). Current reductionist views on cancer science are irresponsible, shut-gun approaches and create chaos. Outcomes are loss of millions of precious lives and economic drain to society. Very little is known about initial events that disturb effective immunity whose function is to monitor and arrest growth of cancerous cells or defend against other external or internal hazardous agents that threaten body’s survival. The author demonstrates the serious need for systematic understanding of how immune disruptors and aging process would alter effective immunity. Outcomes of proposed orderly studies are expected to provide logical foundations for cost-effective strategies to promote immunity toward a healthier society. The policy makers and medical/cancer establishment are urged to return to the common sense that our Forefathers used to serve the public.