Volume 3 of Biomembranes covers receptors of cell adhesion and cellular recognition. Proteins in the plasma membrane of cells are heavily involved in processes of cell adhesion, but such proteins were not actually isolated and characterized until the mid-1970s. Since then, application of the methods of molecular biology has led to the recognition of four major classes of cell adhesion molecule (CAMs), the immunoglobulin super family, the cadherins, the integrins, and the selecting. A convenient system in which to study the importance of cell adhesion is in blood platelets where aggregation eventually leads to thrombus formation in a process involving a range of surface glycoproteins. Interaction with the extracellular matrix is exemplified by CD44, the receptor for hyaluronan, and a complex carbohydrate that is a major component of the extracellular matrix surrounding migrating and proliferating cells. Membrane-associated mucins have a variety of effects on cell adhesion. The super family of immunoglobulin related proteins also include the T cell receptors and the major histocompatibility complex (MHC), which, together with the receptors for immunoglobulins (the Fc receptors), are of fundamental importance in the processes of immunity. Volume 3 of Biomembranes explores the structures and functions of the molecules involved in these important functions of the cell.

Sugar chains (glycans) are often attached to proteins and lipids and have multiple roles in the organization and function of all organisms. "Essentials of Glycobiology" describes their biogenesis and function and offers a useful gateway to the understanding of glycans.

Medical Cell Biology, Third Edition, focuses on the scientific aspects of cell biology important to medical students, dental students, veterinary students, and prehealth undergraduates. With its National Board-type questions, this book is specifically designed to prepare students for this exam. The book maintains a concise focus on eukaryotic cell biology as it relates to human and animal disease, all within a manageable 300-page format. This is accomplished by explaining general cell biology principles in the context of organ systems and disease. This updated version contains 60% new material and all new clinical cases. New topics include apoptosis and cell death from a neural perspective; signal transduction as it relates to normal and abnormal heart function; and cell cycle and cell division related to cancer biology. - 60% New Material! - New Topics include: - Apoptosis and cell dealth from a neural perspective - Signal transduction as it relates to normal and abnormal heart function - Cell cycle and cell division related to cancer biology - All new clinical cases - Serves as a prep guide to the National Medical Board Exam with sample board-style questions (using Exam Master(R) technology): www.exammaster.com - Focuses on eukaryotic cell biology as it related to human disease, thus making the subject more accessible to pre-med and pre-health students

Rheumatoid arthritis is a bewilderingly complex disease involving the interactions of many, and varied, cell populations and multiple families of low and high molecular mass mediators. We are only slowly beginning to understand the mechanisms that produce the local and systematic pathology clinically recognized as rheumatoid arthritis. Increasingly, use is being made of experimental models of this disease in an effort to test hypotheses about putative pathological mechanisms and to investigate the effect of novel therapeutic agents. A major section of this book covers these experimental models in great detail from their development through to reviews of the most recent information on each model.Mechanisms and Models in Rheumatoid Arthritis brings together a group of eminent researchers from the fields of clinical rheumatology, pathology, experimental pathology, immunology, connective tissue biochemistry, microbiology, pharmacology and developmental biology to describe the current views of the cellular and humoral mechanisms that drive the pathology of rheumatoid arthritis and experimental models of rheumatoid arthritis.Key Features:* The book is divided into five sections:* The clinical spectrum, aetiopathogenesis, the role of microbial superantigens in pathology and the present and future therapies for rheumatoid arthritis* The pathology of rheumatoid arthritis, the development and role of synovial pannus and the use of immunohistochemistry in defining synovial pathology* Cell populations involved in synovitis with chapters on synovial cells, chondrocytes, bone cells, leukocytes and leukocyte trafficking* Mediators, with coverage of: cytokines and cytokine inhibitors, growth factors, free radicals and inflammatory lipid mediators, neuropeptides and proteases* Current studies on experimental models of rheumatoid arthritis

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

Interdisciplinarity is more often invoked than practised. This is hardly surprising, considering the daunting vastness of modern biology. To reach a satisfactory understanding of a complex biological system, a wide spectrum of conceptual and experimental tools must be applied at different levels, from the molecular to the cellular, tissue and organismic. We believe the multifaceted regulatory interplay between integrin receptors and ion channels offers a rich and challenging field for researchers seeking broad biological perspectives. By mediating cell adhesion to the extracellular matrix, integrins regulate many developmental processes in the widest sense (from cell choice between differentiation and proliferation, to tissue remodeling and organogenesis). Rapidly growing evidence shows that frequent communication takes place between cell adhesion receptors and channel proteins. This may occur through formation of multiprotein membrane complexes that regulate ion fluxes as well as a variety of intracellular signaling pathways. In other cases, cross talk is more indirect and mediated by cellular messengers such as G proteins. These interactions are reciprocal, in that ion channel stimulation often controls integrin activation or expression. From a functional standpoint, studying the interplay between integrin receptors and ion channels clarifies how the extracellular matrix regulates processes as disparate as muscle excitability, synaptic plasticity and lymphocyte activation, just to mention a few. The derangement of these processes has many implications for pathogenesis processes, in particular for tumor invasiveness and some cardiovascular and neurologic diseases. This book provides a general introduction to the problems and methods of this blossoming field.