یادداشتهای مربوط به کتابنامه ، واژه نامه و نمایه های داخل اثر
متن يادداشت
Includes bibliographical references.
یادداشتهای مربوط به مندرجات
متن يادداشت
Intro; Preface; Contents; Part I: Pathophysiology; Chapter 1: Genetics in Asthma; 1.1 Introduction; 1.2 Association Studies; 1.2.1 Candidate Gene Association Studies; 1.2.2 Genome-Wide Association Studies; 1.3 Phenotypic Heterogeneity, Epistasis, Gene-Environment Interactions, and Epigenetics; 1.4 Conclusion; References; Chapter 2: Group 2 Innate Lymphoid Cells and Asthma; 2.1 Introduction; 2.1.1 Two Distinct Type-2 Immune Responses; 2.1.2 Group 2 Innate Lymphoid Cells (ILC2s); 2.2 ILC2s in Patients with Asthma (Table 2.1)
متن يادداشت
2.2.1 ILC2s Are Increased in the Peripheral Blood and Airways of Patients with Asthma2.2.2 Increased ILC2 Numbers and Activation in More Severe Forms of Asthma; 2.2.3 ILC2s Are Increased in Eosinophilic Asthma; 2.3 Corticosteroid Sensitivity of ILC2s; 2.3.1 Corticosteroid Sensitivity of Murine and Human ILC2s; 2.3.2 Murine and Human ILC2s Isolated from Asthmatic Airways Are Corticosteroid-Resistant; 2.3.3 Mechanism of Corticosteroid Resistance Induction in Murine and Human ILC2s; 2.4 Asthma Exacerbation due to Viral Infection and ILC2s
متن يادداشت
2.4.1 Airway IL-33/IL-25/TSLP Production During Viral Infection2.4.2 IL-33/IL-25/TSLP-Mediated Exacerbation of Airway Inflammation During Viral Infection; 2.4.3 IFN Response in Healthy and Asthmatic Airways During Viral Infection; 2.5 Conclusion; References; Chapter 3: Cellular Mechanisms of Allergic Airway Inflammation; 3.1 Introduction; 3.2 Airway Structural Cells; 3.2.1 Airway Epithelial Cells; 3.2.2 Airway Smooth Muscle Cells; 3.3 Innate and Adaptive Immune Cells; 3.3.1 Dendritic Cells (DCs) (Fig. 3.2); 3.3.2 CD4+ T cells; 3.3.2.1 Th2 Cells (Fig. 3.3); 3.3.2.2 Th1 Cells
متن يادداشت
3.3.2.3 Th17 Cells3.3.2.4 Regulatory T cells (Tregs); 3.3.3 Group 2 Lymphoid Cell, Innate Lymphoid Cells (ILCs) (Fig. 3.3); 3.4 Conclusion; References; Chapter 4: Mechanisms for Non-eosinophilic Asthma; 4.1 Introduction; 4.2 Cellular Profiles of Eosinophilic and Non-eosinophilic Asthma; 4.3 Clinical Characteristics of Non-eosinophilic Asthma; 4.4 Evidence for Neutrophil Activation in Asthma; 4.5 Mechanisms of Eosinophilic and Non-eosinophilic Asthma; 4.5.1 Mechanisms of Neutrophilic Asthma; 4.5.2 Mechanisms of Paucigranulocytic Asthma
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یادداشتهای مربوط به خلاصه یا چکیده
متن يادداشت
This book provides discussions on bronchial asthma from a clinical perspective, focusing on the recent studies on its pathophysiology, diagnosis and treatment. It also explores the lastest findings regarding the phenotypes and endotypes of asthmatic patients, making it of particular interest to those involved with non-eosinophilic asthma and eosinophilic asthma. Further, it discusses the importance of ILC 2 in eosinophilic asthma, and the accumulated results from the forced oscilliation technique and periostin that are actively practiced in Japan. As some aspects of diagnosis and treatment are different in Western and Asian countries, it is important that the data is disseminated around the globe. The clinical questions addressed by the authors are critical and thought provoking, while the questions raised by the editors are instructive, informative and provide new perspectives on unresolved issues. This book appeals to wide readership from beginning learners to physicians in clinical practice and scholars engaging in basic research.
یادداشتهای مربوط به سفارشات
منبع سفارش / آدرس اشتراک
Springer Nature
شماره انبار
com.springer.onix.9789811327902
ویراست دیگر از اثر در قالب دیگر رسانه
عنوان
Advances in Asthma : Pathophysiology, Diagnosis and Treatment.