Kooperativer Bibliotheksverbund

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Umfang: 1 online resource (374 pages)

Ausgabe: 1st ed.

ISBN: 9789811511851

Anmerkung: Intro -- Preface -- Contents -- Part I: Basic Science of Pulmonary Development and Pulmonary Arterial Disease -- 1: Perspective for Part I -- 2: The Alveolar Stem Cell Niche of the Mammalian Lung -- 2.1 Introduction: The Alveolar Type 2 Epithelial Stem Cell Niche -- 2.2 Evidence for Heterogeneity in the AT2 Population -- 2.3 Signaling Pathways in the Stem Cell Niche -- 2.4 The Role of Immune Cells and Stromal Cells in Alveolar Repair and Regeneration -- 2.5 Future Directions and Clinical Implications -- References -- 3: Lung Development and Notch Signaling -- 3.1 Introduction -- 3.2 Morphogenesis and Epithelial Progenitors -- 3.3 Notch Signaling Controls Both Epithelial Cell Fates and Distributions -- 3.4 Development of NE Cell Clusters on Bifurcating Area of Branching Airways -- 3.5 Notch-Hes1 Signaling Is Required for Restricted Differentiation of Solitary NE Cells -- 3.6 Directional Migration of NE Cells Toward Bifurcation Points Creates Nodal NEBs -- References -- 4: Specialized Smooth Muscle Cell Progenitors in Pulmonary Hypertension -- 4.1 Introduction -- 4.2 Hypoxia-Induced Distal Pulmonary Arteriole SMCs Derive from Specialized SMC Progenitors -- 4.3 Stereotyped Program of Distal Muscularization -- 4.4 Monoclonal Expansion of SMCs in PH -- 4.5 Signaling Pathways Regulating Primed Cells -- 4.6 Future Direction and Clinical Implications -- References -- 5: Diverse Pharmacology of Prostacyclin Mimetics: Implications for Pulmonary Hypertension -- 5.1 Introduction -- 5.2 Development of Prostacyclin Mimetics and Their Diverse Pharmacology -- 5.3 Prostanoid Synthesis and Receptor Expression -- 5.3.1 Bronchial Smooth Muscle -- 5.3.2 Pulmonary Blood Vessels -- 5.3.2.1 Endothelium -- 5.3.2.2 Pulmonary Artery -- 5.3.2.3 Differential Prostanoid Expression in Distal Pulmonary Artery and Veins -- 5.3.2.4 Distal Pulmonary Veins. , 5.3.3 Prostanoid Receptor Expression in PAH -- 5.3.3.1 Downregulation of IP Receptors in PAH -- 5.3.3.2 Robust Expression of EP2 and EP4 Receptors in PAH: Key Anti-Fibrotic Targets -- 5.3.3.3 EP3 Receptors May Contribute to Disease Pathology in PAH -- 5.3.3.4 Role of the Veins in PAH and Other Classified Groups of PH -- 5.4 BMPR2 and TGF-β Signalling in PAH and Impact of Prostacyclin Analogues -- 5.5 Regulation of TASK-1 By Prostacyclin Mimetics: Implications in PAH -- 5.6 Prostacyclin Effects on Vascular Remodelling In Vivo: Outstanding Issues -- 5.7 Future Work and Clinical Implications -- References -- 6: Endothelial-to-Mesenchymal Transition in Pulmonary Hypertension -- 6.1 Pulmonary Hypertension -- 6.2 Endothelial-to-Mesenchymal Transition -- 6.3 EndoMT in PAH Pathogenesis -- 6.3.1 EndoMT in PAH Vascular Remodeling -- 6.3.2 Molecular Pathways of EndoMT in PAH -- 6.4 Conclusion -- 6.5 Future Direction and Clinical Implications -- References -- 7: Extracellular Vesicles, MicroRNAs, and Pulmonary Hypertension -- 7.1 Extracellular Vesicles (EV) -- 7.2 EV in Pulmonary Hypertension (PH) -- 7.3 MicroRNA Transfer Through EV in PH -- 7.4 Future Direction and Clinical Implications -- References -- 8: Roles of Tbx4 in the Lung Mesenchyme for Airway and Vascular Development -- References -- 9: A lacZ Reporter Transgenic Mouse Line Revealing the Development of Pulmonary Artery -- References -- 10: Roles of Stem Cell Antigen-1 in the Pulmonary Endothelium -- References -- 11: Morphological Characterization of Pulmonary Microvascular Disease in Bronchopulmonary Dysplasia Caused by Hyperoxia in Newborn Mice -- References -- 12: Involvement of CXCR4 and Stem Cells in a Rat Model of Pulmonary Arterial Hypertension -- References. , 13: Ca2+ Signal Through Inositol Trisphosphate Receptors for Cardiovascular Development and Pathophysiology of Pulmonary Arterial Hypertension -- References -- Part II: Abnormal Pulmonary Circulation in the Developing Lung and Heart -- 14: Perspective for Part II -- 14.1 Idiopathic Pulmonary Arterial Hypertension (IPAH) -- 14.2 Pulmonary Hypertension with Congenital Heart Disease -- 14.3 Pulmonary Circulation in Patients with Congenital Heart Disease -- References -- 15: Pathophysiology of Pulmonary Circulation in Congenital Heart Disease -- 15.1 Introduction -- 15.2 Comprehensive Assessment of Integrated Pulmonary Circulation -- 15.2.1 Physiologic Components of Pulmonary Circulation -- 15.2.2 Impedance Analysis -- 15.3 Pathophysiological Characteristics of Pulmonary Circulation in Congenital Heart Disease -- 15.3.1 Abnormal Resistance Is the Main Pathophysiology -- 15.3.2 Right Ventricular Function and Coupling to PA Load -- 15.3.3 Abnormalities of Compliance Is the Main Pathophysiology -- 15.3.4 Non-pulsatile Pulmonary Flow Is the Main Pathophysiology -- References -- 16: Development of Novel Therapies for Pulmonary Hypertension by Clinical Application of Basic Research -- 16.1 Introduction -- 16.2 Endothelial Function in the Development of PAH -- 16.3 PASMCs in the Development of PAH -- 16.4 Selenoprotein P in the Development of PAH -- 16.5 Conclusion -- References -- 17: Using Patient-Specific Induced Pluripotent Stem Cells to Understand and Treat Pulmonary Arterial Hypertension -- 17.1 Introduction -- 17.2 Patient-Specific iPSC-Derived Endothelial Cells to Model PAH -- 17.2.1 iPSC-EC Recapitulates Native Pulmonary Arterial Endothelial Cell (PAEC) -- 17.2.2 Patient-Specific Drug Response in IPSC-EC and PAEC -- 17.3 Modeling Reduced Penetrance of BMPR2 Mutation in PAH. , 17.3.1 Preserved EC Function in Unaffected BMPR2 Mutation Carrier (UMC) -- 17.3.2 Preserved pP38 Signaling Pathway in Unaffected BMPR2 Mutation Carrier -- 17.4 Gene Editing in PAH IPSCs -- 17.4.1 Correction of the BMPR2 Mutation in PAH iPSCs -- 17.4.2 Generation of iPSC Line with BMPR2 Mutation -- 17.5 Future Directions and Clinical Implications -- References -- 18: Modeling Pulmonary Arterial Hypertension Using Induced Pluripotent Stem Cells -- 18.1 Heritable Pulmonary Arterial Hypertension -- 18.1.1 Insights into the Pathobiology of PAH -- 18.1.2 Reduced Penetrance of BMPR2 in PAH -- 18.2 Modeling Pulmonary Arterial Hypertension with Induced Pluripotent Stem Cells -- 18.2.1 Embryological Origins of the Pulmonary Vasculature -- 18.2.2 Current iPSC Models of PAH -- 18.3 Future Direction and Clinical Implications -- References -- 19: Dysfunction and Restoration of Endothelial Cell Communications in Pulmonary Arterial Hypertension: Therapeutic Implications -- 19.1 Introduction -- 19.2 Pulmonary Endothelial Dysfunction and the Pathobiology of PAH -- 19.3 Current Promising Strategies for Restoring Pulmonary Endothelial Dysfunction and Cell-Cell Communications -- 19.3.1 Restoring the Balance of Vasodilation and Vasoconstriction -- 19.3.2 Restitution of the Defective BMPR-2 Signaling System -- 19.3.3 Targeting Cell Proliferation and Cell accumulation -- 19.3.4 Restitution of an Adapted Extracellular Matrix (ECM) Remodeling -- 19.3.5 Targeting Metabolic Changes -- 19.3.6 Targeting the Vicious Cycle Between Endothelial Dysfunction and Immune Dysregulation -- 19.4 Future Directions and Clinical Implications -- References -- 20: Inflammatory Cytokines in the Pathogenesis of Pulmonary Arterial Hypertension -- 20.1 Background -- 20.2 IL-6 in the Pathogenesis of HPH -- 20.3 IL-21 in the Pathogenesis of HPH. , 20.4 Increased Expression of IL-21 and M2 Macrophage Markers in the Lungs of IPAH Patients -- References -- 21: Genotypes and Phenotypes of Chinese Pediatric Patients with Idiopathic and Heritable Pulmonary Arterial Hypertension: Experiences from a Single Center -- 21.1 Introduction -- 21.2 Methods -- 21.3 Selection of Patients -- 21.4 Genetic Studies -- 21.5 Statistical Analysis -- 21.6 Results -- 21.6.1 Clinical Characteristics -- 21.6.2 Targeted Drug Therapy -- 21.6.3 Outcome of Patients -- 21.7 Discussion -- References -- 22: Fundamental Insight into Pulmonary Vascular Disease: Perspectives from Pediatric PAH in Japan -- 22.1 Early Detection and Early Treatment of PAH: Mechanistic Insights -- 22.2 Pathological Basis of Atypical CHD-PAH: Clinical and Mechanistic Implications -- 23: Risk Stratification in Paediatric Pulmonary Arterial Hypertension -- 23.1 Why Risk Stratify? -- 23.2 Multidimensional Risk Stratification -- 23.3 Factors to Consider in Multidimensional Risk Stratification of children with Pulmonary Arterial Hypertension -- 23.4 Cause of Pulmonary Hypertension -- 23.5 Vascular Burden -- 23.6 Ventricular Function -- 23.7 Impact on the Patient -- 23.8 Summary -- References -- 24: The Adaptive Right Ventricle in Eisenmenger Syndrome: Potential Therapeutic Targets for Pulmonary Hypertension? -- 24.1 Introduction -- 24.2 Improved Survival in Eisenmenger Syndrome -- 24.3 Preserved Fetal Morphology in Eisenmenger Syndrome -- 24.4 Fetal Phenotype in Ovine CHD Model -- 24.5 The Adaptive RV Response to Acute Afterload-RV Anrep Effect -- 24.6 Potential Mechanisms of RV Anrep Effect -- 24.7 Future Directions and Clinical Implications -- References -- 25: Impaired Right Coronary Vasodilator Function in Pulmonary Hypertensive Rats Assessed by In Vivo Synchrotron Microangiography -- References. , 26: Relationship Between Mutations in ENG and ALK1 Genes and the Affected Organs in Hereditary Hemorrhagic Telangiectasia.

Weitere Ausg.: Print version: Nakanishi, Toshio Molecular Mechanism of Congenital Heart Disease and Pulmonary Hypertension Singapore : Springer Singapore Pte. Limited,c2020 ISBN 9789811511844

Sprache: Englisch

Schlagwort(e): Electronic books. ; Congress ; Conference papers and proceedings. ; Conference papers and proceedings. ; Actes de congrès.

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URL: ProQuest Ebook Central

URL: SpringerLink

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Umfang: 7,1 Min.

ISBN: 9783966351164

Inhalt: Mr & Mrs Smith - in superromantisch! Betty Dawsey weiß, dass sie mit Thom Schluss machen muss. Er ist zu nett, zu aufmerksam, zu berechenbar. Doch als plötzlich und ohne Vorwarnung ihre Wohnung in die Luft fliegt und Betty von Unbekannten entführt wird, stellt sich heraus, dass sie viel weniger über ihren Verlobten weiß, als sie dachte. Denn er ist nicht Thom, der Langweiler, sondern Thom, der Geheimagent - dessen einzige Mission es jetzt ist, Betty lebend aus den Fängen seiner Feinde zu befreien ... Der neue Roman von SPIEGEL-Bestseller-Autorin Kylie Scott!

Anmerkung: Kylie Scott ist ein großer Fan erotischer Liebesromane und zweitklassiger Horrorfilme. Sie verlangt immer ein Happy End - wenn Blut und Gemetzel auch noch vorkommen, umso besser! Mit ihren zwei Kindern und ihrem Ehemann lebt Kylie in Queensland, Australien. Sie war mit ihrer Stage-Dive-Reihe auf der New-York-Times-, der USA-Today- sowie der Spiegel-Bestseller-Liste vertreten.

Sprache: Deutsch