GLORIA

GEOMAR Library Ocean Research Information Access

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • 2010-2014  (69)
  • 1990-1994  (31)
Document type
Keywords
Language
Years
Year
  • 1
    Online Resource
    Online Resource
    Paris :Springer Paris,
    Keywords: Neovascularization. ; Electronic books.
    Description / Table of Contents: This book reviews recent advances in understanding of the molecular and cellular mechanisms of angiogenesis, with a focus on how to integrate these observations into the context of developmental, post-natal and pathological neovascularization.
    Type of Medium: Online Resource
    Pages: 1 online resource (501 pages)
    Edition: 1st ed.
    ISBN: 9782817804668
    DDC: 612.13
    Language: English
    Note: Intro -- Contents -- Angiogenesis: An Ever-Challenging Research Field -- Acknowledgment -- References -- Part I: Angiogenesis During Embryonic Development -- Chapter 1: Emergence of Endothelial Cells During Vascular Development -- 1.1 Introduction -- 1.2 Vasculogenesis -- 1.3 Hemangioblast -- 1.4 Remodeling of the Primary Capillary Plexus into Arteries and Veins -- 1.5 Role of Hemodynamic Forces in Remodeling -- 1.6 Guidance of Capillaries by Endothelial Tip Cells -- 1.7 Circulating Endothelial Cells in the Embryo -- 1.8 Perspectives -- References -- Chapter 2: Lymphatic Vascular Morphogenesis -- 2.1 Early Steps of Lymphatic Vascular Development -- 2.1.1 Lymphatic Endothelial Cell Specification -- 2.1.2 Lymphatic Vessel Sprouting from the Veins -- 2.1.3 Separation of Lymphatic and Blood Vasculatures -- 2.1.4 Non-venous Origins of Lymphatic Vasculature -- 2.2 Lymphatic Vessel Remodelling -- 2.2.1 Sprouting and Growth of Lymphatic Vessels -- 2.2.2 Regulation of Lymphatic Endothelial Cell-Cell Junctions -- 2.2.3 Valve Morphogenesis -- 2.2.4 Smooth Muscle Cells Recruitment to Collecting Lymphatic Vessels -- 2.3 Lymphatic Vasculature and Diseases -- 2.3.1 Lymphoedema -- 2.3.2 Inflammation -- 2.3.3 Tumour Metastasis -- 2.3.4 Lipid Absorption -- 2.4 Concluding Remarks -- References -- Part II: The Physiological Angiogenic Signal: Cellular and Molecular Mechanisms -- Chapter 3: Finding New Partnerships: The Function of Individual Extracellular Receptor Domains in Angiogenic Signalling by VEGF Receptors -- 3.1 Biology of VEGF Family Growth Factors and Their Receptors -- 3.1.1 Introduction to VEGF -- 3.1.2 Structure-Function Relationship of VEGF and VEGF Receptors -- 3.1.2.1 Receptor Specificity of VEGFs -- 3.1.2.2 Structural Analysis of VEGF Binding to VEGFR-1, VEGFR-2 and VEGFR-3 -- 3.1.2.3 Activation of VEGF Receptors. , 3.2 VEGFR-2 as Part of a Signalling Platform -- 3.2.1 Neuropilins (NRPs) -- 3.2.2 Ephrin-B2 -- 3.2.3 VE-Cadherin -- 3.2.4 Dopamine Receptor D2 -- 3.2.5 CD146 -- 3.2.6 CD44 -- 3.3 Extracellular Components of the VEGF/VEGFR Signalling Cascade as Targets for Therapy and Functional Inhibition -- 3.3.1 VEGF/VEGFRs in Disease -- 3.3.2 VEGF/VEGFRs as Targets in Therapeutic Inhibition -- 3.3.2.1 VEGF-Neutralising Agents -- 3.3.2.2 Anti-VEGFR-1 Agents -- 3.3.2.3 Anti-VEGFR-2 D23 Agents -- 3.3.2.4 Anti-VEGFR-2 D4-7 Agents -- 3.3.3 Limitations to VEGF/VEGFR Targeted Therapy -- 3.3.4 Outlook and Conclusions -- References -- Chapter 4: Wnt/Frizzled Signaling in the Vasculature -- 4.1 Introduction -- 4.1.1 Wnt Signal Transduction -- 4.1.1.1 The Canonical Pathway: Wnt/β-Catenin -- 4.1.1.2 The Planar Cell Polarity Pathway -- 4.1.1.3 The Calcium-Mediated Pathway -- 4.1.2 Wnt Inhibitors and Modulators -- 4.1.3 Atypical Receptors Kinases -- 4.2 Role of the Wnt/Frizzled in Vascular Development -- 4.2.1 Evidence of Wnt/Fzd Expression and Signaling in Endothelial Cells -- 4.2.2 Placental Development -- 4.2.3 Postnatal Retinal Angiogenesis -- 4.2.4 Brain Vasculature -- 4.3 Role of Wnt Regulation in Vascular Pathology -- 4.3.1 Choroidal Neovascularization and Oxygen-Induced Retinopathy -- 4.3.2 Wound Healing -- 4.3.3 Hind Limb and Cardiac Ischemia -- 4.4 Conclusion -- 4.5 Online Databases -- References -- Chapter 5: BMP9, BMP10, and ALK1: An Emerging Vascular Signaling Pathway with Therapeutic Applications -- 5.1 Bone Morphogenetic Proteins (BMPs) -- 5.2 BMP9/BMP10/ALK1 Signaling Complex -- 5.3 The Role of BMP9 and BMP10 in Vascular Development -- 5.3.1 Knowledge from Human Vascular Diseases -- 5.3.2 Knowledge from Animal Models: Mice and Zebrafish -- 5.3.2.1 Mice -- 5.3.2.2 Zebrafish -- 5.3.3 In Vitro Roles of BMP9 and BMP10 in Endothelial Cells. , 5.4 Therapeutic Applications of the BMP9/BMP10/ALK1 Signaling Pathway -- 5.4.1 HHT -- 5.4.2 BMP9, BMP10, and ALK1 as Biomarkers in Cancer -- 5.4.3 Therapeutic Applications of the BMP9/BMP10/ALK1 Signaling Pathway in Tumor Angiogenesis -- 5.4.3.1 ALK1 Extracellular Domain (ALK1 ECD) -- 5.4.3.2 Anti-ALK1 Antibody (PF-03446962) -- 5.4.3.3 Anti-endoglin Antibody (TRC105) -- 5.5 Conclusions and Perspectives -- References -- Chapter 6: Apelin Signaling in Retinal Angiogenesis -- 6.1 Apelin Signaling -- 6.1.1 Receptor Discovery and Isolation of the Endogenous Ligand -- 6.1.2 Multiple Active Ligands and Receptor Heterodimers -- 6.1.3 Gene Transcription and Mode of Signaling -- 6.1.4 Physiological Functions of Apelin Signaling -- 6.2 The Retina -- 6.2.1 Anatomy and Development -- 6.2.2 Astrocyte: The Key Mediator of Neuron/Endothelial Cell Interactions -- 6.2.3 Developmental Patterning of Retinal Vessels -- 6.2.4 Subpopulations of Endothelial Cells -- 6.3 Apelin Signaling and Formation of Retinal Vessels -- 6.3.1 Apelin: A Bona Fide Angiogenic Factor -- 6.3.2 Vascular Phenotype of Apelin or APJ Gene Invalidation -- 6.3.3 Temporal Expression of Apelin Signaling Coincides with the Angiogenic Phase -- 6.3.4 Apelin Receptor Gene: An Early Marker of the Venous Phenotype -- 6.3.5 Receptor and Ligand Gene as Potential Markers of Tip or Stalk Phenotype -- 6.3.6 Apelin Signaling as a Linker Between VEGF-Secreting Astrocytes and Proliferating Stalk Cells -- 6.3.7 Apelin Signaling Regulates LIF Secretion and Controls Astrocyte Maturation -- 6.4 Apelin Signaling and Pathological Retinal Angiogenesis -- 6.4.1 The Retinopathy of Prematurity -- 6.4.2 Diabetic Retinopathy -- 6.4.3 Telangiectatic Vessels -- 6.5 Clinical Implications -- References -- Chapter 7: Emerging Role of the Two Related Basic Helix-Loop-Helix Proteins TAL1 and LYL1 in Angiogenesis -- 7.1 Introduction. , 7.2 Properties of LYL1 and TAL1 -- 7.3 Hematopoietic Functions of Tal1, Lyl1, and Lmo2 -- 7.4 Tal1 and Lmo2 Are Required for Cardiovascular Development -- 7.5 TAL1 Activity Is Required in the Early Steps of Angiogenesis -- 7.5.1 TAL1 and LMO2 Initiate Tubulogenesis Through VE-Cadherin Upregulation -- 7.5.2 TAL1-LMO2 Complexes Controls Angiopoietin-2 Expression -- 7.6 LYL1 Is Required for the Maturation of New Blood Vessels -- 7.6.1 Lyl1 Deficiency Leads to Increased Angiogenic Responses -- 7.6.2 LYL1 Contributes to Vessel Maturation and Stabilization -- 7.7 Coordinated Activity of TAL1 and LYL1 to Regulate Angiogenic Processes -- References -- Part III: Hypoxia, Ischemia and Angiogenesis -- Chapter 8: Hypoxia and Extracellular Matrix Remodeling -- 8.1 Hypoxia Induction of Angiogenesis -- 8.2 Establishment of the Vascular BM -- 8.3 Extracellular Matrix Proteolytic Degradation -- 8.4 Regulation of Hypoxia-Induced Growth Factor Sequestration in the Extracellular Matrix -- 8.5 Matricellular Proteins -- 8.5.1 Group A Thrombospondins -- 8.5.2 Group B Thrombospondins -- 8.6 Conclusion -- References -- Chapter 9: Sphingosine-1-Phosphate in Hypoxic Signaling -- 9.1 Hypoxia Significance and Impact on Clinical Outcome -- 9.2 The Hypoxia-Inducible Factors -- 9.3 Sphingosine 1-Phosphate Metabolism in Cancer -- 9.4 Sphingosine 1-Phosphate Signaling in Hypoxia -- 9.5 Sphingosine 1-Phosphate Signaling as a Target for Anti- hypoxic Strategy -- 9.6 Concluding Remarks -- References -- Chapter 10: Reciprocal Crosstalk Between Angiogenesis and Metabolism -- 10.1 Regulation of Angiogenesis by Oxygen and Metabolism -- 10.1.1 PHDs and HIF: The Molecular Players of Angiogenesis Are Regulated by Oxygen and Metabolic Intermediates -- 10.1.2 Modulators of HIF and PHDs by Nonhypoxic Stimuli -- 10.1.2.1 TCA Cycle and Other Metabolic Intermediates. , 10.1.2.2 Reactive Oxygen Species -- 10.1.3 Modulation of Angiogenesis by Metabolic Regulators -- 10.2 EC Metabolism Impacts Vessel Sprouting -- 10.2.1 EC Survival and Functions Are Dependent on Glycolysis -- 10.2.2 Metabolic Changes During Vascular Sprouting -- 10.3 Regulation of Metabolism by Angiogenesis -- Bibliography -- Chapter 11: Endothelial Progenitor Cells and Cardiovascular Ischemic Diseases: Characterization, Functions, and Potential Clinical Applications -- 11.1 Introduction -- 11.2 Cultured EPC -- 11.3 Recruitment of EPCs to the Ischemic Tissue -- 11.3.1 CXCL12/CXCR4 -- 11.3.2 Integrins and Selectins -- 11.3.3 Hemostatic Partners, Thrombospondin, and Thrombin Interaction with EPCs -- 11.3.4 Other Factors -- 11.4 Mechanisms of EPC-Related Effects on Postischemic Revascularization -- 11.4.1 Differentiation into Endothelial Cells -- 11.4.2 Paracrine Effects -- 11.4.3 Interaction with the Host Environment -- 11.5 EPCs as Diagnostic and Prognostic Tools -- 11.5.1 EPCs as Biomarkers of Cardiovascular Diseases -- 11.5.1.1 EPCs and Cardiovascular Risk Factors -- 11.5.1.2 EPCs and the Prevalence of CVDs -- 11.5.2 Are EPCs a Useful Prognostic Factor for Cardiovascular Diseases? -- 11.6 EPCs as Therapeutic Tools -- 11.6.1 Adult Stem/Progenitor Cells -- 11.6.2 Alternative Sources of EPCs -- 11.6.2.1 Embryonic Stem Cells (ESCs) -- 11.6.2.2 Induced Pluripotent Stem Cells (iPSCs) -- 11.6.2.3 Local Source of Stem/Progenitor Cells -- 11.7 Conclusion -- References -- Part IV: Tumor Angiogenesis -- Chapter 12: Endothelial Cell Reactions to Oxygen: Implications for Cancer -- 12.1 Overview of Oxygen-Mediated Pathways -- 12.2 Hypoxia-Inducible Factors Mediate Cellular Oxygen Signaling -- 12.3 The Function of Prolyl Hydroxylase Domain Proteins and Factor Inhibiting HIF as Oxygen Sensors. , 12.4 Role of Oxygen Signaling in Physiological and Pathophysiological Angiogenesis.
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 2
  • 3
    Book
    Book
    Barcelona : Instituto de Ciencias del Mar
    Type of Medium: Book
    Pages: 144 S. , zahlr. Ill
    Series Statement: Scientia Marina 56.1992,Suppl.1
    Language: Undetermined
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 4
    Electronic Resource
    Electronic Resource
    Woodbury, NY : American Institute of Physics (AIP)
    Applied Physics Letters 63 (1993), S. 3236-3237 
    ISSN: 1077-3118
    Source: AIP Digital Archive
    Topics: Physics
    Type of Medium: Electronic Resource
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 5
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Mathematical finance 2 (1992), S. 0 
    ISSN: 1467-9965
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Mathematics , Economics
    Notes: In the modern theory of finance, the valuation of derivative assets is commonly based on a replication argument. When there are transaction costs, this argument is no longer valid. In this paper, we try to address the general problem of finding the optimal portfolio among those which dominate a given derivative asset at maturity. We derive an interval for its price. the upper bound is the minimum amount one has to invest initially in order to obtain proceeds at least as valuable as the derivative asset. the lower bound is the maximum amount one can borrow initially against the proceeds of the derivative asset. We show that, in some instances, this interval may be strictly bounded above by the price of the replicating strategy. Prima facie, the cost of a dominating strategy should appear to be higher than that of the replicating one. But because trading is costly, it may pay to weigh the benefits of replication against those of potential savings on transaction costs.
    Type of Medium: Electronic Resource
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 6
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 7
    ISSN: 1365-246X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Geosciences
    Notes: The aim of the Couy experiment in the ‘Géologie Profonde de la France’ programme was to reach the source body of the magnetic anomaly of the ‘Bassin de Paris'. The drilling stopped at 3500 m. Magnetic field logging and susceptibility logging were undertaken to obtain as complete a description as possible of the magnetic parameters of rocks crossed by the borehole. Remanent magnetization and susceptibility measurements on the core were also carried out. The entire set of results is presented in this paper for both sedimentary layers and the basement. The values obtained for magnetic field variations and for susceptibility lead to the conclusion that the magnetic source body of the AMBP was not reached.
    Type of Medium: Electronic Resource
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 8
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Histopathology 20 (1992), S. 0 
    ISSN: 1365-2559
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 9
    ISSN: 1574-6968
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Notes: Abstract Immunocrossreactivity between the major outer membrane protein (MOMP) of Campylobacter jejuni 85H and the OmpC porin of Escherichia coli K-12 was observed. These results indicate that a common antigenic domain is conserved in both MOMP and OmpC. This antigenic region is detected only after a 96°C treatment suggesting that it is buried in the native conformation of the respective porins. In addition, differences were observed between the major outer membrane proteins from various C. jejuni strains tested contained a protein exhibiting a similar electrophoretic profile to the 85H porin.
    Type of Medium: Electronic Resource
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 10
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Molecular microbiology 4 (1990), S. 0 
    ISSN: 1365-2958
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: [125I]-colicin N binds to OmpF receptor sites (70000 per cell) with an average Kassoc of 3.2 × 106 M−1 at 23°C. Monoclonal antibody directed against a cell-surface-exposed epitope of OmpF is able to compete with the binding of the colicin in vitro and also to protect against colicin N in vivo. OmpF is an absolute requirement for colicin N uptake. OmpC cannot serve as a substitute for OmpF during translocation across the outer membrane under receptor bypass conditions, which is in contrast to colicin A. Colicin N does not cross-react with various monoclonal antibodies directed against colicin A.
    Type of Medium: Electronic Resource
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...