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Format: 1 Online-Ressource (XIII, 406 Seiten) , Illustrationen, Diagramme

ISBN: 9789811511851

Additional Edition: Erscheint auch als Druck-Ausgabe ISBN 978-981-151-184-4

Additional Edition: Erscheint auch als Druck-Ausgabe ISBN 978-981-151-186-8

Additional Edition: Erscheint auch als Druck-Ausgabe ISBN 978-981-151-187-5

Language: English

Subjects: Biology

Keywords: Medizin ; Innere Medizin ; Herz ; Lunge ; Pulmonale Hypertonie ; Herzfehler ; Angeborene Krankheit

DOI: 10.1007/978-981-15-1185-1

URL: Volltext  (kostenfrei)

URL: Volltext  (kostenfrei)

URL: Buchcover

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Format: 1 online resource (XIII, 406 p. 84 illus., 74 illus. in color.)

Edition: 1st ed. 2020.

ISBN: 981-15-1185-3

Content: This open access book focuses on the molecular mechanism of congenital heart disease and pulmonary hypertension, offering new insights into the development of pulmonary circulation and the ductus arteriosus. It describes in detail the molecular mechanisms involved in the development and morphogenesis of the heart, lungs and ductus arteriosus, covering a range of topics such as gene functions, growth factors, transcription factors and cellular interactions, as well as stem cell engineering technologies. The book also presents recent advances in our understanding of the molecular mechanism of lung development, pulmonary hypertension and molecular regulation of the ductus arteriosus. As such, it is an ideal resource for physicians, scientists and investigators interested in the latest findings on the origins of congenital heart disease and potential future therapies involving pulmonary circulation/hypertension and the ductus arteriosus.

Note: 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 -- 3 Lung development and Notch signalling -- 4 Specialized smooth muscle cell progenitors in pulmonary hypertension -- 5 Diverse Pharmacology of Prostacyclin Mimetics: Implications for Pulmonary Hypertension -- 6 Endothelial-to-mesenchymal transition in pulmonary hypertension -- 7 Extracellular vesicles, MicroRNAs and Pulmonary Hypertension -- 8 Roles of Tbx4 in the lung mesenchyme for airway and vascular development -- 9 A lacZ reporter transgenic mouse line revealing the development of pulmonary artery -- 10 Roles of stem cell antigen-1 in the pulmonary endothelium -- 11 Morphological characterization of pulmonary microvascular disease in bronchopulmonary dysplasia caused by hyperoxia in newborn mice -- 12 Involvement of CXCR4 and stem cells in a rat model of pulmonary arterial hypertension -- 13 Ca2+ signal through inositol trisphosphate receptors for cardiovascular development and pathophysiology of pulmonary arterial hypertension -- PART II: Abnormal pulmonary circulation in the developing lung and heart -- 14 Perspective for Part II -- 15 Pathophysiology of Pulmonary Circulation in Congenital Heart Disease -- 16 Development of Novel Therapies for Pulmonary Hypertension by Clinical Application of Basic Research -- 17 Using Patient-Specific Induced Pluripotent Stem Cells to Understand and Treat Pulmonary Arterial Hypertension -- 18 Modeling pulmonary arterial hypertension using induced pluripotent stem cells -- 19 Dysfunction and restoration of endothelial cell communications in Pulmonary Arterial Hypertension: Therapeutic implications -- 20 Inflammatory Cytokines in the Pathogenesis of Pulmonary Arterial Hypertension -- 21 Genotypes and Phenotypes of Chinese Pediatric Patients with Idiopathic and Heritable Pulmonary Arterial Hypertension- Experiences from A Single Center -- 22 Fundamental Insight into Pulmonary Vascular Disease : Perspectives from Pediatric PAH in Japan -- 23 Risk stratification in paediatric pulmonary arterial hypertension -- 24 The Adaptive Right Ventricle in Eisenmenger Syndrome: Potential Therapeutic Targets for Pulmonary Hypertension -- 25 Impaired right coronary vasodilator function in pulmonary hypertensive rat assessed by in vivo synchrotron microangiography -- 26 Relationship between mutations in ENG and ALK1 gene and the affected organs in hereditary hemorrhagic telangiectasia -- 27 A genetic analysis for patients with pulmonary arterial hypertension -- 28 Evaluation and visualization of right ventricle using three dimensional echocardiography -- 29 Pulmonary hypertension associated with post-operative Tetralogy of Fallot -- 30 Microscopic Lung Airway Abnormality and Pulmonary Vascular Disease Associated with Congenital Systemic to Pulmonary Shunt -- 31 Respiratory syncytial virus infection in infants with heart and lung diseases -- PART III: Ductus arteriosus: bridge over troubled vessels -- 32 Perspective for Part III -- 33 The ductus arteriosus, a vascular outsider, in relation to the pulmonary circulation -- 34 Molecular, genetic, and pharmacological modulation of the ductus arteriosus: KATP channels as novel drug targets -- 35 New mediators in the biology of the ductus arteriosus: Lessons from the chicken embryo -- 36 Constriction of the Ductus Arteriosus with KATP Channel Inhibitors -- 37 New insights on how to treat patent ductus arteriosus -- 38 Antenatal Administration of Betamethasone Contributes to Intimal thickening of the Ductus Arteriosus -- 39 Prostaglandin E-EP4-mediated fibulin-1 up-regulation plays a role in intimal thickening of the ductus arteriosus -- 40 Transcriptional profiles in the chicken ductus arteriosus during hatching -- 41 Inhibition of Cyclooxygenase Contracts Chicken Ductus Arteriosus -- 42 Prostaglandin E2 receptor EP4 inhibition constricts the rat ductus arteriosus -- 43 Dilatation of the Ductus Arteriosus by Diazoxide in Fetal and Neonatal Rats -- 44 The Effect of Long-term Administration of Plostaglandin E1 on Morphological Changes in Ductus Arteriosus -- 45 Significance of SGK1 as a protein kinase transcriptionally regulated by ALK1 signaling in vascular endothelial cells -- 46 Fabrication of Implantable Human Arterial Graft by Periodic Hydrostatic Pressure -- 47 Optimum preparation of Candida albicans cell wall extra (CAWE) for the mouse model of Kawasaki disease -- PART IV: Development and Regeneration of the Cardiovascular System -- 48 Perspective for Part IV -- 49 Advances in the second heart field -- 50 Novel cardiac progenitors for all components of the heart except for the right ventricle -- 51 Regional and TBX5-dependent gene expression in the atria: Implications for pulmonary vein development and atrial fibrillation -- 52 The Endocardium as a Master Regulator of Ventricular Trabeculation -- 53 The Role of Alternative mRNA Splicing in Heart Development -- 54 Progress in the Generation of Multiple Lineage Human-iPSC-derived 3D Engineered Cardiac Tissues for Cardiac Repair -- 55 Quantification of contractility in stem cell derived cardiomyocytes -- 56 A neurotrophic factor receptor GFRA2, a specific surface antigen for cardiac progenitor cells, regulates the process of myocardial compaction -- 57 Cardiac cell specification and differentiation by the defined factors -- 58 A Temporo-Spatial Regulation of Sema3c is Essential for Interaction of Progenitor Cells during Cardiac Outflow Tract Development -- 59 Spatiotemporally restricted developmental alterations in the anterior and secondary heart fields cause distinct conotruncal heart defects -- 60 Significance of transcription factors in the mechanisms of great artery malformations -- 61 The different c-kit expression in human induced pluripotent stem (iPS) cells between with feeder cells and without feeder cells -- 62 Establishment of induced pluripotent stem cells from immortalized B cell lines and their differentiation into cardiomyocytes -- 63 Establishment of an in vitro LQT3 model, using induced pluripotent stem cells from LQT3 patient-derived cardiomyocytes -- 64 Genetic Assessments for clinical courses of Left ventricle noncompaction -- 65 Elucidating the pathogenesis of congenital heart disease in the era of next-generation sequencing. , English

Additional Edition: ISBN 981-15-1184-5

Language: English

DOI: 10.1007/978-981-15-1185-1

UID:

Format: 1 online resource (374 pages)

Edition: 1st ed.

ISBN: 9789811511851

Note: 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.

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

Language: English

Keywords: Electronic books. ; Congress ; Conference papers and proceedings. ; Conference papers and proceedings. ; Actes de congrès.

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Format: 1 Online-Ressource

ISBN: 9784431546283 , 9783662488478

Content: Cardiology; Pediatrics

Note: English

Language: English

URL: kostenfrei

UID:

Format: 1 Online-Ressource (405 p.)

ISBN: 9789811511851

Content: This open access book focuses on the molecular mechanism of congenital heart disease and pulmonary hypertension, offering new insights into the development of pulmonary circulation and the ductus arteriosus. It describes in detail the molecular mechanisms involved in the development and morphogenesis of the heart, lungs and ductus arteriosus, covering a range of topics such as gene functions, growth factors, transcription factors and cellular interactions, as well as stem cell engineering technologies. The book also presents recent advances in our understanding of the molecular mechanism of lung development, pulmonary hypertension and molecular regulation of the ductus arteriosus. As such, it is an ideal resource for physicians, scientists and investigators interested in the latest findings on the origins of congenital heart disease and potential future therapies involving pulmonary circulation/hypertension and the ductus arteriosus

Note: English

Language: English

URL: kostenfrei

UID:

Format: 1 online resource (367 pages)

ISBN: 9784431546283

Note: Intro -- Preface -- Contents -- Part I: From Molecular Mechanism to Intervention for Congenital Heart Diseases, Now and the Future -- Perspective -- 1: Reprogramming Approaches to Cardiovascular Disease: From Developmental Biology to Regenerative Medicine -- 1.1 Introduction -- 1.2 Molecular Networks Regulate Cardiac Cell Fate -- 1.3 Cardiac Fibroblasts in the Normal and Remodeling Heart -- 1.4 Direct Cardiac Reprogramming In Vitro -- 1.5 Direct Cardiac Reprogramming In Vivo -- 1.6 Direct Cardiac Reprogramming in Human Fibroblasts -- 1.7 Challenges and Future Directions -- References -- 2: The Arterial Epicardium: A Developmental Approach to Cardiac Disease and Repair -- 2.1 Origin of the Epicardium -- 2.2 Epicardium-Derived Cells (EPDCs) -- 2.3 Heterogeneity of Epicardial Cells -- 2.3.1 The Cardiac Fibroblast -- 2.3.2 Arterial Smooth Muscle Cell -- 2.3.3 Endothelial Cells -- 2.3.4 Cardiomyocytes -- 2.3.5 The Purkinje Fiber -- 2.4 Congenital and Adult Cardiac Disease -- 2.4.1 Non-compaction -- 2.4.2 Conduction System Anomalies -- 2.4.3 Valvulopathies -- 2.4.4 Coronary Vascular Anomalies -- 2.5 Cardiovascular Repair -- 2.6 Future Directions and Clinical Applications -- References -- 3: Cell Sheet Tissue Engineering for Heart Failure -- 3.1 Introduction -- 3.2 Cell Sheet Engineering -- 3.3 Cardiac Tissue Reconstruction -- 3.4 Cell Sheet Transplantation in Small Animal Models -- 3.5 Cell Sheet Transplantation in Preclinical and Clinical Studies -- 3.6 Conclusions -- References -- 4: Future Treatment of Heart Failure Using Human iPSC-Derived Cardiomyocytes -- 4.1 Introduction -- 4.2 Cardiac Differentiation from Human iPSCs -- 4.3 Nongenetic Methods for Purifying Cardiomyocytes -- 4.4 Transplantation of Human PSC-Derived Cardiomyocytes -- 4.5 Future Directions -- References -- 5: Congenital Heart Disease: In Search of Remedial Etiologies. , 5.1 Introduction -- 5.1.1 Emerging Concepts -- 5.1.2 Hub Hypothesis -- 5.2 Searching for Candidate Signaling Hubs in Heart Development -- 5.2.1 Nodal Signaling Kinases -- 5.2.2 Filamin A -- 5.2.3 Relevance of Signaling Hubs to CHD -- 5.3 Lineage Is a Key to Remedial Therapy -- 5.3.1 Postnatal Origin of Cardiac Fibroblasts -- 5.3.2 A Strategy to Use Fibroblast Progenitors to Carry Genetic Payloads -- 5.3.2.1 This Strategy Calls for a Conceptual Revision in Our Thinking About Fibroblasts -- 5.4 Remedial Therapies: Delivering Genetic ``Payloads ́́-- 5.4.1 Preliminary Studies -- References -- Part II: Left-Right Axis and Heterotaxy Syndrome -- 6: Left-Right Asymmetry and Human Heterotaxy Syndrome -- 6.1 Introduction -- 6.2 Molecular and Cellular Mechanisms of Left-Right Determination -- 6.2.1 Node Cell Monocilia Create Leftward ``Nodal Flow ́́and Activate Asymmetry Signaling Around the Node -- 6.2.2 Asymmetry Signaling Transmits to the Left Lateral Plate Mesoderm -- 6.2.3 Genes Associated with the Human Heterotaxy Syndrome -- 6.3 Clinical Manifestation of the Heterotaxy Syndrome -- 6.3.1 Right Isomerism -- 6.3.2 Left Isomerism -- 6.4 Long-Term Prognosis of Heterotaxy Patients -- 6.4.1 Protein-Losing Enteropathy -- 6.4.2 Arrhythmias -- 6.4.3 Heart Failure -- 6.4.4 Hepatic Dysfunction -- 6.4.5 Management of Failing Fontan Patients -- 6.5 Future Direction and Clinical Implications -- References -- 7: Roles of Motile and Immotile Cilia in Left-Right Symmetry Breaking -- 7.1 Introduction -- 7.2 Symmetry Breaking by Motile Cilia and Fluid Flow -- 7.3 Sensing of the Fluid Flow by Immotile Cilia -- 7.4 Readouts of the Flow -- 7.5 Future Directions -- References -- 8: Role of Cilia and Left-Right Patterning in Congenital Heart Disease -- 8.1 Introduction -- 8.1.1 Heterotaxy, Primary Ciliary Dyskinesia, and Motile Cilia Defects. , 8.1.2 Motile Respiratory Cilia Defects in Other Ciliopathies -- 8.1.3 Ciliary Dysfunction in Congenital Heart Disease Patients with Heterotaxy -- 8.1.4 Respiratory Complications in Heterotaxy Patients with Ciliary Dysfunction -- 8.1.5 Left-Right Patterning and the Pathogenesis of Congenital Heart Disease -- 8.1.6 Ciliome Gene Enrichment Among Mutations Causing Congenital Heart Disease -- 8.1.7 Ciliary Dysfunction in Congenital Heart Disease Patients Without Heterotaxy -- 8.1.8 Future Directions and Clinical Implications -- References -- 9: Pulmonary Arterial Hypertension in Patients with Heterotaxy/Polysplenia Syndrome -- References -- Perspective -- Part III: Cardiomyocyte and Myocardial Development -- 10: Single-Cell Expression Analyses of Embryonic Cardiac Progenitor Cells -- 10.1 Introduction -- 10.2 CPCs of the Two Heart Fields -- 10.3 CPC Specification -- 10.4 The Potential of Single-Cell Transcriptomics in the Study of CPC Specification -- 10.5 Future Direction and Clinical Implication -- References -- 11: Meis1 Regulates Postnatal Cardiomyocyte Cell Cycle Arrest -- 11.1 Introduction -- 11.2 Results -- 11.2.1 Expression of Meis1 During Neonatal Heart Development and Regeneration -- 11.2.2 Cardiomyocyte Proliferation Beyond Postnatal Day 7 Following Meis1 Deletion -- 11.2.3 MI in Meis1 Overexpressing Heart Limits Neonatal Heart Regeneration -- 11.2.4 Regulation of Cyclin-Dependent Kinase Inhibitors by Meis1 -- 11.3 Future Direction and Clinical Implications -- References -- 12: Intercellular Signaling in Cardiac Development and Disease: The NOTCH pathway -- 12.1 Introduction -- 12.2 Left Ventricular Non-compaction (LVNC) -- 12.3 The NOTCH Signaling Pathway -- 12.4 NOTCH in Ventricular Chamber Development -- 12.5 Future Directions and Clinical Implications -- References. , 13: The Epicardium in Ventricular Septation During Evolution and Development -- 13.1 Introduction -- 13.2 Septum Components in the Completely Septated Heart -- 13.3 The Presence of the Epicardium in Amniotes -- 13.4 The Epicardium in the Avian Heart -- 13.5 Disturbance of the Epicardium -- 13.6 Septum Components in Reptilian Hearts -- 13.7 Tbx5 Expression Patterns -- 13.8 Discussion -- References -- 14: S1P-S1p2 Signaling in Cardiac Precursor Cells Migration -- References -- 15: Myogenic Progenitor Cell Differentiation Is Dependent on Modulation of Mitochondrial Biogenesis through Autophagy -- 16: The Role of the Thyroid in the Developing Heart -- References -- Perspective -- Part IV: Valve Development and Diseases -- 17: Atrioventricular Valve Abnormalities: From Molecular Mechanisms Underlying Morphogenesis to Clinical Perspective -- 17.1 Introduction -- 17.2 RV-TV Dysplastic Syndrome -- 17.2.1 Anatomic Features of the Heart in Ebsteinś Anomaly Patients -- 17.2.2 Morphogenetic Features of the Heart in Patients with Uhlś Anomaly -- 17.2.3 Absence of the TV -- 17.3 Bone Morphogenetic Proteins (BMPs) and Their Important Role in Cushion Formation -- 17.3.1 Role of BMP2 in Cushion Mesenchymal Cell (CMC) Migration -- 17.3.2 BMP2 Induces CMC Migration and Id and Twist Expression -- 17.3.3 BMP2 Induces Expression of ECM Proteins in the Post-EMT Cushion -- 17.4 The Role of BMP2 for Cardiomyocytes Formation -- 17.5 Future Direction -- References -- 18: Molecular Mechanisms of Heart Valve Development and Disease -- 18.1 Introduction -- 18.2 Heart Valve Development -- 18.3 Heart Valve Disease -- 18.3.1 Calcific Aortic Valve Disease (CAVD) -- 18.3.2 Myxomatous Valve Disease -- 18.4 Signaling Pathways in Heart Valve Development and Disease -- 18.5 Future Directions and Clinical Implications -- References. , 19: A Novel Role for Endocardium in Perinatal Valve Development: Lessons Learned from Tissue-Specific Gene Deletion of the Tie... -- 19.1 Introduction -- 19.2 Model for Valvar Endocardial-Specific Gene Deletion -- 19.3 Tie1 Is Required for Late-Gestational and Early Postnatal Aortic Valve Remodeling -- 19.4 Future Directions -- References -- 20: The Role of the Epicardium in the Formation of the Cardiac Valves in the Mouse -- 20.1 Introduction -- 20.1.1 The AV Valves and Their Leaflets -- 20.1.2 The Epicardium and Epicardially Derived Cells (EPDCs) -- 20.1.3 The Contribution of EPDCs to the Developing AV Valves -- 20.2 The Role of Bmp Signaling in Regulating the Contribution of EPDC to the AV Valves -- 20.2.1 Epicardial-Specific Deletion of the Bmp Receptor BmpR1A/Alk3 Leads to Disruption of AV Junction Development -- 20.2.2 Discussion -- 20.2.3 Future Direction and Clinical Implications -- References -- 21: TMEM100: A Novel Intracellular Transmembrane Protein Essential for Vascular Development and Cardiac Morphogenesis -- References -- 22: The Role of Cell Autonomous Signaling by BMP in Endocardial Cushion Cells in AV Valvuloseptal Morphogenesis -- References -- Perspective -- Part V: The Second Heart Field and Outflow Tract -- 23: Properties of Cardiac Progenitor Cells in the Second Heart Field -- 23.1 Introduction -- 23.2 Demarcating the First and Second Heart Fields and Their Contributions to the Heart -- 23.3 New Insights into the Role and Regulation of Noncanonical Wnt Signaling in the Second Heart Field and the Origins of Cono... -- 23.4 Involvement of the Second Heart Field in Atrial and Atrioventricular Septal Defects -- 23.5 Future Directions and Clinical Implications -- References -- 24: Nodal Signaling and Congenital Heart Defects -- 24.1 Introduction -- 24.2 The Nodal Signaling Pathway -- 24.3 Requirement for Nodal in Development. , 24.4 Congenital Heart Defects Associated with Perturbations in Nodal Signaling.

Additional Edition: Print version: Nakanishi, Toshio Etiology and Morphogenesis of Congenital Heart Disease Tokyo : Springer Japan,c2016 ISBN 9784431546276

Language: English

Keywords: Electronic books.

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Format: 28 ungez. Seiten , Illustrationen , 26 cm

Original writing title: 近代作家の回顧 : 富田渓仙, 太田聴雨, 佐藤玄 , 石井柏亭, 中西利雄 ; 昭和39年2月21日-3月29日, 国立近代美術館

Original writing publisher: 東京 : 東京国立近代美術館

Note: Exhibition held at the Museum, Feb. 21 - Mar. 29, 1964 , English and Japanese

Language: Japanese

Keywords: Ausstellungskatalog

UID:

Edition: 1st ed. 2016.

ISBN: 4-431-54628-6

Note: English

Additional Edition: ISBN 4-431-54627-8

Language: English

UID:

Edition: 1st ed. 2016.

ISBN: 4-431-54628-6

Note: English

Additional Edition: ISBN 4-431-54627-8

Language: English

UID:

Format: 1 online resource (xii, 383 pages) : , illustrations (some color)

ISBN: 9784431546283 , 4431546286 , 9783662488454 , 3662488450 , 9783662488478 , 3662488477

Content: This volume focuses on the etiology and morphogenesis of congenital heart diseases. It reviews in detail the early development and differentiation of the heart, and later morphologic events of the cardiovascular system, covering a wide range of topics such as gene functions, growth factors, transcription factors and cellular interactions that are implicated in cardiac morphogenesis and congenital heart disease. This book also presents recent advances in stem cell and cell sheet tissue engineering technologies which have the potential to provide novel in vitro disease models and to generate regenerative paradigms for cardiac repair and regeneration. This is the ideal resource for physician scientists and investigators looking for updates on recent investigations on the origins of congenital heart disease and potential future therapies.

Note: Part I. From molecular mechanism to intervention for congenital heart diseases, now and future -- Reprogramming approaches to cardiovascular disease: from developmental biology to regenerative medicine -- The arterial epicardium, a developmental approach to cardiac disease and repair -- Cell sheet tissue engineering for heart failure -- Future treatment of heart failure and pathophysiological analysis of various heart diseases using human iPS cell-derived cardiomyocytes -- Congenital heart disease: in search of remedial etiologies -- Part II. Left-right axis and heterotaxy syndrome -- Left-right asymmetry and human heterotaxy syndrome -- Roles of motile and immotile cilia in left-right symmetry breaking -- Role of cilia and left-right patterning in congenital heart disease -- Pulmonary arterial hypertension in patients with heterotaxy /polysplenia syndrome -- Part III. Cardiomyocyte and myocardial development -- Single cell expression analyses of embryonic cardiac progenitor cells -- Meis1 regulates post-natal cardiomyocyte cell cycle arrest -- Intercellular signalling in cardiac development and disease: NOTCH -- The epicardium in ventricular septation during evolution and development -- S1P-S1p2 signaling in cardiac precursor cells migration -- Myogenic progenitor cell differentiation is dependent on modulation of mitochondrial biogenesis through autophagy -- The role of the thyroid in the developing heart -- Part IV. Valve development and diseases -- Atrioventricular valve abnormalities: From molecular mechanisms underlying morphogenesis to clinical perspective -- Molecular mechanisms of heart valve development and disease -- A novel role for endocardium in perinatal valve development: Lessons learned from tissue specific gene deletion of the Tie1 receptor tyrosine kinase -- The role of the epicardium in the formation of the cardiac valves in the mouse -- TMEM100, a novel intracellular transmembrane protein essential for vascular development and cardiac morphogenesis -- Cell autonomous regulation of BMP-2 in endocardial cushion cells during AV valvuloseptal morphogenesis -- Part V. The second heart field and outflow tract -- Properties of cardiac progenitor cells in the second heart field -- Nodal signaling and congenital heart defects -- Utilizing zebrafish to understand second heart field development -- A history and interaction of outflow progenitor cells implicated in "Takao syndrome" -- The loss of Foxc2 expression in the outflow tract links the interrupted arch in the conditional Foxc2 knockout mouse -- Environmental modification for phenotype of truncus arteriosus in Tbx1 hypomorphic mice -- Part VI. Vascular development and diseases -- Extracellular matrix remodeling in vascular development and disease -- The "cardiac neural crest" concept revisited -- Roles of endothelial Hrt genes for vascular development -- Placental expression of type 1 and 3 inositol trisphosphate receptors is required for the extra-embryonic vascular development -- Tissue remodeling in vascular wall in Kawasaki disease-related vasculitis model mice -- Part VII. Ductus arteriosus -- Progerin expression during normal closure of the human ductus arteriosus: A case of premature ageing? -- The multiple roles of prostaglandin E2 in the regulation of the ductus arteriosus -- Developmental differences in the maturation of sarcoplasmic reticulum and contractile proteins in large blood vessels influences their contractility -- Fetal and neonatal ductus arteriosus is regulated with ATP-sensitive potassium channel -- Part VIII. Conduction system and arrhythmia -- Regulation of vertebrate conduction system development -- Cardiac Pacemaker Development from a Tertiary Heart Field -- Endothelin receptor type A expressing cell population in the inflow tract contributes to chamber formation -- Specific isolation of HCN4 positive cardiac pace-making cells derived from embryonic stem cell -- Part IX. Current molecular mechanism in cardiovascular development -- Combinatorial functions of transcription factors and epigenetic factors in heart development and disease -- Pcgf5 contributes to PRC1 (Polycomb repressive complex 1) in developing cardiac cells -- Non-coding RNAs in cardiovascular disease -- Part X. iPS cells and regeneration in congenital heart diseases -- Human pluripotent stem cells to model congenital heart disease -- Engineered cardiac tissues generated from immature cardiac and stem-cell derived cells: Multiple approaches and outcomes -- Dissecting the left heart hypoplasia by pluripotent stem cells -- Lentiviral gene transfer to iPS cells; toward the cardiomyocyte differentiation of Pompe disease-specific iPS cells -- Molecular analysis of long-term cultured cardiac stem cells for cardiac regeneration -- Epicardial contribution in neonatal heart regeneration -- Part XI. Current genetics in congenital heart diseases -- Genetic discovery for congenital heart defects -- Evidence that deletion of ETS-1, a gene in the Jacobsen syndrome (11q- ) cardiac critical region, causes congenital heart defects through impaired cardiac neural crest cell function -- Notch signaling in aortic valve development and disease -- To detect and explore mechanism of CITED2 mutation and methylation in children with congenital heart disease. , English.

Additional Edition: Print version: Etiology and morphogenesis of congenital heart disease. Tokyo : SpringerOpen, [2016] 9784431546276

Language: English

Keywords: Electronic books. ; Congress ; Electronic books.

DOI: 10.1007/978-4-431-54628-3

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