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Angiogenesis is the growth of new blood vessels and is an important natural process in the body. A healthy body maintains a perfect balance of angiogenesis modulators. In many serious disease states, however, the body loses control over angiogenesis. Diseases that are angiogenesis-dependent result when blood vessels either grow excessively or insufficiently. Understanding how angiogenesis "works" and how to control it, will have massive implications on the management, treatments, and ultimately the prevention of many common (and not so common) diseases. Angiogenesis cuts across virtually every discipline. The Angiogenesis Foundation identified angiogenesis as a "common denominator" in our most serious diseases. Excessive angiogenesis occurs in diseases such as cancer, diabetic blindness, age-related macular degeneration, rheumatoid arthritis, psoriasis, and many other conditions. Insufficient angiogenesis occurs in diseases such as coronary artery disease, stroke, and delayed wound healing. Tried-and-tested techniques written by researchers that developed them, used them, and brought them to fruition Provides the "builder's manual" for essential techniques. This is a one-stop shop that eliminates needless searching among untested techniques Includes step-by-step methods for understanding the cell and molecular basis of wound healing, vascular integrin signaling, mechanical signaling in blood vessels, and vascular proteomics
Angiogenesis, the development of new blood vessels from the existing vasculature, is essential for physiological growth and over 18,000 research articles have been published describing the role of angiogenesis in over 70 different diseases, including cancer, diabetic retinopathy, rheumatoid arthritis and psoriasis. One of the most important technical challenges in such studies has been finding suitable methods for assessing the effects of regulators of eh angiogenic response. While increasing numbers of angiogenesis assays are being described both in vitro and in vivo, it is often still necessary to use a combination of assays to identify the cellular and molecular events in angiogenesis and the full range of effects of a given test protein. Although the endothelial cell - its migration, proliferation, differentiation and structural rearrangement - is central to the angiogenic process, it is not the only cell type involved. the supporting cells, the extracellular matrix and the circulating blood with its cellular and humoral components also contribute. In this book, experts in the use of a diverse range of assays outline key components of these and give a critical appraisal of their strengths and weaknesses. Examples include assays for the proliferation, migration and differentiation of endothelial cells in vitro, vessel outgrowth from organ cultures, assessment of endothelial and mural cell interactions, and such in vivo assays as the chick chorioallantoic membrane, zebrafish, corneal, chamber and tumour angiogenesis models. These are followed by a critical analysis of the biological end-points currently being used in clinical trials to assess the clinical efficacy of anti-angiogenic drugs, which leads into a discussion of the direction future studies should take. This valuable book is of interest to research scientists currently working on angiogenesis in both the academic community and in the biotechnology and pharmaceutical industries. Relevant disciplines include cell and molecular biology, oncology, cardiovascular research, biotechnology, pharmacology, pathology and physiology.
In Vivo Models to Study Angiogenesis provides the latest information and an overview of the most common assays for studying angiogenesis in vivo. Under physiological conditions, angiogenesis is tightly controlled, whereas increased production of angiogenic stimuli and/or reduced production of angiogenic inhibitors leads to abnormal neovascularization, such as occurs in cancer, chronic inflammatory disease, diabetic retinopathy, macular degeneration and cardiovascular disorders. Several genetic and epigenetic mechanisms are involved in the early development of the vascular system. This book presents the latest information from the extensive literature and research available. Evidence is now emerging that blood vessels themselves have the ability to provide instructive regulatory signals to surrounding non-vascular target cells during organ development. Thus, endothelial cell signaling is currently believed to promote fundamental cues for cell fate specification, embryo patterning, organ differentiation and postnatal tissue remodeling. - Provides information on the most common assays to study angiogenesis in vivo - Presents an ideal reference for those interested in angiogenesis as a normal and vital process in growth and development - Covers wound healing, the formation of granulation tissue, and the transition of tumors from benign to malignant
Understanding how angiogenesis "works" and how to control it will have massive implications on the management, treatments, and ultimately the prevention of many common (and not so common) diseases. Angiogenesis is the growth of new blood vessels and is an important natural process in the body. A healthy body maintains a perfect balance of angiogenesis modulators. In many serious disease states, however, the body loses control over angiogenesis. Diseases that are angiogenesis-dependent result when blood vessels either grow excessively or insufficiently. - Tried-and-tested techniques written by researchers that developed them, used them, and brought them to fruition - Provides the "builder's manual" for essential techniques--a one-stop shop that eliminates needless searching among untested techniques - Includes step-by-step methods for understanding the cell and molecular basis of wound healing, vascular integrin signaling, mechanical signaling in blood vessels, and vascular proteomics
Angiogenesis is the growth of blood vessels from the existing vasculature. The field of angiogenesis has grown enormously in the past 30 years, with only 40 papers published in 1980 and nearly 6000 in 2010. Why has there been this explosive growth in angiogenesis research? Angiogenic therapies provide a potential to conquer cancer, heart diseases, and more than 70 of life's most threatening medical conditions. The lives of at least 1 billion people worldwide could be improved with angiogenic therapy, according to the Angiogenesis Foundation. In this little book, we provide a simple approach to understand the essential elements of the angiogenic process, we critique the most powerful angiogenesis assays that are used to discover proangiogenic and antiangiogenic substances, and we provide an in-depth physiological perspective on how angiogenesis is regulated in normal, healthy tissues of the human body. All tissues of the body require a continuous supply of oxygen to burn metabolic substrates that are needed for energy. Oxygen is conducted to these tissues by blood capillaries: more capillaries can improve tissue oxygenation and thus enhance energy production; fewer capillaries can lead to hypoxia and even anoxia in the tissues. This means that angiogenic therapies designed to control the growth and regression of blood capillaries can be used to improve the survival of poorly perfused tissues that are essential to the body (heart, brain, skeletal muscle, etc.) and to rid the body of unwanted tissues (tumors). Table of Contents: Overview of Angiogenesis / Angiogenesis Assays / Regulation: Metabolic Factors / Regulation: Mechanical Factors / Glossary / References / Author Biographies
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
In this second of two new volumes covering mitochondria, methods developed to assess the number and function of nuclear-encoded proteins in the mitochondrion are presented. Chapters focus on the regulation of mitochondrial function and mitochondrial diseases, with a section emphasizing the mitochondrial defects associated with type 2 diabetes. The critically acclaimed laboratory standard for 40 years, Methods in Enzymology is one of the most highly respected publications in the field of biochemistry. With more than 450 volumes published, each volume presents material that is relevant in today's labs, truly an essential publication for researchers in all fields of life sciences. - New methods focusing on the examination of normal and abnormal mitochondrial function are presented in an easy-to-follow format by the researchers who developed them - Along with a companion volume covering topics including mitochondrial electron transport chain complexes and reactive oxygen species, provides a comprehensive overview of modern techniques in the study of mitochondrial malfunction - Provides a "one-stop shop" for tried and tested essential techniques, eliminating the need to wade through untested or unreliable methods
This is the companion volume to Daniel Klionsky's Autophagy: Lower Eukaryotes, which features the basic methods in autophagy covering yeasts and alternative fungi. Klionsky is one of the leading authorities in the field. He is the editor-in-chief of Autophagy. The November 2007 issue of Nature Reviews highlighted his article, "Autophagy: from phenomenology to molecular understanding in less than a decade. He is currently editing guidelines for the field, with 230 contributing authors that will publish in Autophagy.Particularly in times of stress, like starvation and disease, higher organisms have an internal mechanism in their cells for chewing up and recycling parts of themselves. The process of internal "house-cleaning in the cell is called autophagy – literally self-eating. Breakthroughs in understanding the molecular basis of autophagy came after the cloning of ATG1 in yeast. These ATG genes in yeast were the stepping stones to the explosion of research into the molecular analysis of autophagy in higher eukaryotes. In the future, this research will help to design clinical approaches that can turn on autophagy and halt tumor growth. - Establishes the functional roles of specific cellular proteins in selective and nonselective autophagy in mammalian cells, which aides researchers in determining why autophagy is shut down in neoplastia (growth of abnormal tissue mass) and turned on during bacterial invasion - Includes methods to evaluate the role of autophagy in the drug-induced cell death of cancer cells in culture, which helps researchers design clinical approaches that can turn on autophagy and halt tumor growth - Covers higher eukaryotes including lifespan in C.elegans to marine organisms and bridging into the clinical aspects, including autophagy in chronic myelogenous leukemia (CML is one of four types of leukemia), lung cancer, prostate cancer, and cardiac cells
Multicellular organisms must be able to adapt to cellular events to accommodate prevailing conditions. Sensory-response circuits operate by making use of a phosphorylation control mechanism known as the "two-component system." This volume, the third in a three-volume treatment edited by the same group of editors, includes a wide range of methods, including those dealing with the Sln-1 kinase pathway, triazole sensitivity in C. albicans, and histidine kinases in cyanobacteria circadian clock. - Includes time-tested core methods and new innovations applicable to any researcher studing two-component signaling systems or histidine kinases - Methods included are useful to both established researchers and newcomers to the field - Relevant background and reference information given for procedures can be used as a guide to developing protocols in a number of disciplines
This is the companion volume to Daniel Klionsky's Autophagy: Lower Eukaryotes, which features the basic methods in autophagy covering yeasts and alternative fungi (aspergillus, podospora, magnaporthe). Klionsky is one of the leading authorities in the field. He is the editor-in-chief of Autophagy. The November 2007 issue of Nature Reviews highlighted his article, "Autophagy: From phenomenology to molecular understanding in less than a decade. He is currently editing guidelines for the field, with 230 contributing authors, that will publish in Autophagy.Particularly in times of stress, like starvation and disease, higher organisms have an internal mechanism in their cells for chewing up and recycling parts of themselves. The process of internal "house cleaning in the cell is called autophagy – literally self-eating. Breakthroughs in understanding the molecular basis of autophagy came after the cloning of ATG1 (autophagy-related gene 1) in yeast. (To date, 30 additional yeast genes have been identified.) These ATG genes in yeast were the stepping stones to the explosion of research into the molecular analysis of autophagy in higher eukaryotes. In the future, this research will help to design clinical approaches that can turn on autophagy and halt tumor growth.