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Animal models are indispensable for studies requiring an intact immune system, especially for studying the pathogenic mechanisms in atopic diseases, regulation of IgE production, and related biologic effects. Mice are particularly suitable and have been used extensively for such studies because their immune system is well characterized. Further, large numbers of mutants or inbred strains of mice are available that express deficiencies of individual immunologic processes, inflammatory cells, or mediator systems. By comparing reactions in such mice with appropriate control animals, the unique roles of individual cells or mediators may be characterized more precisely in the pathogenesis of atopic respiratory diseases including asthma. However, given that asthma in humans is characterized by the presence of airway hyperresponsiveness to specific and nonspecific stimuli, it is important that animal models of this disease exhibit similar physiologic abnormalities. In the past, the size of the mouse has limited its versatility in this regard. However, recent studies indicate the feasibility of measuring pulmonary responses in living mice, thus facilitating the physiologic evaluation of putative mouse models of human asthma that have been well charcterized at the immunologic and patholigic level. Future work will provide details of the morphometry of the methacholine-induced bronchoconstriction and will further seek to determine the relationship between cigarette smoke exposure and the development of NS-AHR in the transgenic mouse model.
For researchers using animals to investigate human asthma, explains physiological and pharmacological process in the lung in vivo, and reviews the animal models available for studying the bronchospasm and inflammation associated with human asthma. Also discusses such methodological aspects as administering drugs to animal airways and the mechanics of assessing lung function. Also considers the use of genetically altered animals as research models. The sixth volume in the Airways Smooth Muscle sub- series. Annotation copyright by Book News, Inc., Portland, OR
This landmark volume discusses the characteristics and impact of the remodeling process on airway function and clinical disease expression within the airway in asthma, covering pharmacological therapies and possible future targets relevant to regulating the remodeling process. Emphasizes the importance of treating underlying airway inflammation and the relevance of structural alterations to the airway wall, including glandular increases, enhanced collagen deposition within the submucosa, increased vasculature, smooth hypertrophy, and hyperplasias! Tracing the development and maintenance of bronchial hyperresponsiveness, decline in lung function, and loss of reversibility evident in chronic asthma, Airway Remodelingdescribes the contribution of inflammatory cells in the development of airway structural changes examines how pharmaceutical agents act and whether existing treatments modify or prevent remodeling in chronically inflamed asthmatic airways considers whether neural pathways initiate as well as contribute to the airway inflammatory cascade that leads to remodeling reviews the action of cytokines and growth factors on ASM signaling outlines novel approaches to regulating smooth muscle growth clarifies whether permanent ventilatory incapacity in asthma is caused by the uncoupling of the airway and the role of the lung parenchyma details high-resolution computerized tomography scan to measure the internal size of the airway at baseline, during challenge, or after bronchodilatation and more!Improving lung function and quality of life by reducing the need for emergency care, hospital admissions, and systemic steroid administration, Airway Remodeling is a superb reference for pulmonologists and respiratory system specialists; physiologists; pneumologists; allergists; pharmacologists; molecular, cellular, and lung biologists; and graduate and medical school students in these disciplines.
"The combination of scientific and institutional integrity represented by this book is unusual. It should be a model for future endeavors to help quantify environmental risk as a basis for good decisionmaking." â€"William D. Ruckelshaus, from the foreword. This volume, prepared under the auspices of the Health Effects Institute, an independent research organization created and funded jointly by the Environmental Protection Agency and the automobile industry, brings together experts on atmospheric exposure and on the biological effects of toxic substances to examine what is knownâ€"and not knownâ€"about the human health risks of automotive emissions.
Eosinophils represent approximately 1% of peripheral blood leukocytes and play a central proinflammatory and immunoregulatory role in various immune disorders. This volume provides the reader with a comprehensive survey of the major aspects of human eosinophilic biology and immunology as well as the most clinically relevant aspects of eosinophil-related disorders. Expert contributions cover the ultrastructural and phenotypic characteristics of human eosinophils, and their fundamental biochemical features including receptors for IgE and chemokines. The production of cytokines and their role in the activation of eosinophils are reviewed. Furthermore, the classic eosinophil-related disorders such as hypereosinophilia, drug reactions, allergic disorders and some cardiovascular diseases are described. Each of the chapters is written by an investigator actively engaged in research on the topic under consideration. The well-edited and stimulating material compiled in this volume will be of interest to all those working in allergology, immunology, biochemistry and pulmonary medicine.
Severe asthma is a form of asthma that responds poorly to currently available medication, and its patients represent those with greatest unmet needs. In the last 10 years, substantial progress has been made in terms of understanding some of the mechanisms that drive severe asthma; there have also been concomitant advances in the recognition of specific molecular phenotypes. This ERS Monograph covers all aspects of severe asthma – epidemiology, diagnosis, mechanisms, treatment and management – but has a particular focus on recent understanding of mechanistic heterogeneity based on an analytic approach using various ‘omics platforms applied to clinically well-defined asthma cohorts. How these advances have led to improved management targets is also emphasised. This book brings together the clinical and scientific expertise of those from around the world who are collaborating to solve the problem of severe asthma.
Viral respiratory tract infections are important and common causes of morbidity and mortality worldwide. In the past two decades, several novel viral respiratory infections have emerged with epidemic potential that threaten global health security. This Monograph aims to provide an up-to-date and comprehensive overview of severe acute respiratory syndrome, Middle East respiratory syndrome and other viral respiratory infections, including seasonal influenza, avian influenza, respiratory syncytial virus and human rhinovirus, through six chapters written by authoritative experts from around the globe.
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.
Asthma is a prevalent disease in all age groups that results from different pathogenic mechanisms, cells, and mediators engaged in innumerous clinical phenotypes and endotypes. This book exhaustively and didactically explores the biological expression of numerous cells and mediators involved in bronchial inflammation. The information provided aims at identifying the diversity and complexity of the interrelationships between the different players, drawing attention to critical mechanisms in asthma. It also highlights the requirement of new tools to identify strong biomarkers absolutely critical for managing asthma.