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  (19)
  • 2005-2009  (2)
Document type
Language
Year
  • 1
    Keywords: Ecology -- Australia. ; Electronic books.
    Description / Table of Contents: Written from an interdisciplinary perspective, this volume examines the patterns of demographic change in Australia's rural landscapes. The text uses case studies to illustrate the driving factors behind these changes, and outlines the impact they have on society and the environment.
    Type of Medium: Online Resource
    Pages: 1 online resource (396 pages)
    Edition: 1st ed.
    ISBN: 9789048196548
    Series Statement: Landscape Series ; v.12
    DDC: 304.60994091734
    Language: English
    Note: Intro -- Foreword by the Series Editors -- Preface -- Contents -- Contributors -- About the Authors -- 1 Patterns, Drivers and Implications of Demographic Change in Rural Landscapes -- 1.1 Introduction -- 1.2 Patterns of Demographic Change in Rural Landscapes -- 1.2.1 Population Decline -- 1.2.2 Population Growth -- 1.3 The Drivers of Demographic Change -- 1.3.1 Population Decline -- 1.3.2 Population Growth -- 1.4 The Implications of Demographic Change in Rural Landscapes -- 1.5 Signs of a Contested Landscape -- 1.6 Natural Resource Management in Multi-Functional Landscapes -- 1.7 Conclusion -- References -- 2 Amenity-Led Migration in Rural Australia: A New Driver of Local Demographic and Environmental Change? -- 2.1 Introduction -- 2.2 Amenity-Led Migration into Rural Areas: A Review -- Box 2.1 Rural Amenity and Agricultural Restructuring -- 2.3 In-Migration to Rural Australia -- 2.4 Ex-metropolitan Migration -- 2.5 The Role of Rural Amenity -- 2.6 Ecological Consequences of Amenity-Led Migration -- 2.7 Conclusion -- References -- 3 Sea- and Tree-Change Phenomena in Far North Queensland, Australia: Impacts of Land Use Change and Mitigation Potential -- 3.1 Introduction -- 3.1.1 Sea- and Tree-Change Phenomena in Far North Queensland -- 3.2 Methods -- 3.2.1 The Wet Tropics Case Study Region -- 3.2.2 A Mixed Methods Approach -- 3.3 Results -- 3.3.1 Why Do Sea- and Tree-Changers Choose to Move to the Wet Tropics? -- Box 3.1 Increasing Property Prices Result fromTree-Change Migration -- Box 3.2 Classic Sea-Change Push and Pull Factors -- Box 3.3 The Beach as a Pull Factor for Sea-Changers -- Box 3.4 The Landscape as a Pull Factor for Tree-Changers -- Box 3.5 Tree-Change as a Life Style Choice -- Box 3.6 Tree-Change to Escape the Coastal Heat -- Box 3.7 Complexity of Factors Leading to Sea- and Tree-Change Migration. , 3.3.2 Types of Sea- and Tree-Change Areas in the Wet Tropics -- 3.3.3 Where Do Sea- and Tree-Changers Live in the Wet Tropics? -- 3.3.4 What Do Sea- and Tree-Changers Do and How Do They Manage Their Properties? -- 3.3.5 Environmental Effects of the Sea- and Tree-Change Phenomena -- 3.3.6 Social, Cultural and Economic Effects of the Sea- and Tree-Change Phenomena -- 3.4 Governance of Sea- and Tree-Change Landscapes -- 3.4.1 Planning Strategies to Protect Sea- and Tree-Change Growth Areas -- 3.4.1.1 Urban Growth Boundary -- 3.4.1.2 Rural Fragmentation -- 3.4.1.3 Transferable Development Rights -- 3.4.1.4 Master Planning -- 3.4.1.5 Conservation Partnerships and Incentives -- 3.5 Recommendations -- References -- 4 Seeking Trees or Escaping Traffic? Socio-Cultural Factors and 'Tree-Change' Migration in Australia -- 4.1 Introduction -- 4.1.1 Perceptions and Realities of the Australian Lifestyle: An Historical View -- 4.1.2 Migration in Australia: Historical and Contemporary Experiences -- 4.2 Research Methodology -- 4.3 Research Findings -- 4.3.1 Tree-Change: Media-Driven Stereotypes and the Creation of a Property Market -- Box 4.1 Marketing Campaign: Riverina Regional Development Board -- Box 4.2 Marketing Campaign: North East Victoria -- 4.3.1.1 Stereotype 1: Tree-Changers Are Cashed up Baby Boomers -- Box 4.3 Example of Media Inconsistency: The Australian -- Box 4.4 Academic Response to Popular Sea-Change and Tree-Change Imagery -- 4.3.1.2 Stereotype 2: Tree-Changers Are Poor Young Families in Search of Affordable Housing -- 4.3.2 Regional Growth, Rural Suburbanisation -- 4.3.2.1 Tree-Changers: An Insider's Perspective -- Box 4.5 Reasons for Tree-Changing from Sydney -- 4.3.2.2 Tree-Changers ? What Do They Want? -- Box 4.6 Air Pollution: One Reason for Tree-Changing from Melbourne -- 4.4 Conclusion -- References -- 5 Demographic Change and Rural Nature. , 5.1 Introduction -- 5.2 Spatial Patterns of People and Nature Across Broad Scales -- 5.3 The Lure of Natural Amenities -- 5.4 Conservation Challenges and Opportunities in Developing Rural Landscapes -- 5.4.1 Challenges -- 5.4.2 Opportunities -- 5.5 The Vast Interior: Implications of Agricultural Land Abandonment -- 5.6 Managing Rural Environments for Conservation and Production -- 5.6.1 Business-as-Usual Is Not an Option -- 5.6.2 The Challenges of Managing Australia's New Bush -- 5.6.3 A Way Forward -- 5.7 Conclusion -- References -- 6 Agricultural Areas Under Metropolitan Threats: Lessons for Perth from Barcelona -- 6.1 Introduction -- 6.2 Population Pressures at the Urban Fringes: Barcelona and Perth -- 6.2.1 Population Growth Pressures in Barcelona -- 6.2.2 Population Growth Pressures in Perth -- 6.3 Peri-Urban Agricultural Spaces: Planning and Management -- 6.3.1 A Review of Peri-Urban Agricultural Research -- 6.3.2 Planning and Managing Peri-Urban Agricultural Spaces -- 6.4 Case Study Area One: Peri-Urban Agriculture in Barcelona -- 6.4.1 Barcelona's Agricultural Fringe: A General Overview -- 6.4.2 The Baix Llobregat Agrarian Park -- 6.5 Case Study Area Two: Peri-Urban Issues in Perth -- 6.5.1 Perth's Agricultural Fringe: A General Overview -- 6.5.2 The Chittering Valley: A Peri-Urban Locality Near Perth -- 6.6 Discussion and Conclusion: Lessons from Barcelona for Perth -- References -- 7 Agricultural Land Ownership Change and Natural Resource Management: Comparing Australian and US Case Studies -- 7.1 Introduction -- 7.2 Conceptualising Rural and Agricultural Landscape Change -- 7.3 Rural Change in Australia and the American West -- 7.4 Methodology -- 7.4.1 Australian Case Studies -- 7.4.2 American West Case Studies -- 7.5 Trends in Rural Property Turnover -- 7.5.1 Rates of Ownership Change -- 7.5.2 New Owners. , Box 7.1 Working Landscapes in Transition -- Box 7.2 Motivations of Newer Owners -- 7.6 Implications of Property Turnover -- 7.6.1 Differences Between New and Longer-Term Landholders -- Box 7.3 Conservation and Recreation Goals of NewerOwners -- Box 7.4 Production Goals of Newer and Longer-Term Owners -- Box 7.5 Investment Goals of Newer Owners in the GYE -- Box 7.6 Differing Attitudes TowardsWildlife Managementin the GYE -- Box 7.7 Leaving the Property in Better Condition -- Box 7.8 Learning and Knowledge About NRM -- Box 7.9 Challenges Engaging Newer Owners in CoordinatedNRM -- Box 7.10 Learning from Others -- 7.6.2 Land Management Practices -- Box 7.11 Passive Management Due to Time Constraintsand a Learning Period -- Box 7.12 Constraints Affecting Active Management Efforts -- Box 7.13 The Role of Owner-Manager Relations in NRM in the GYE -- 7.7 Discussion -- 7.8 Conclusion -- References -- 8 Land-Use Planning and Demographic Change: Mechanisms for Designing Rural Landscapes and Communities -- 8.1 Introduction -- 8.2 Demographic Change in Rural Landscapes: Challenges for Land-Use Planners -- 8.2.1 Planning Challenges for Areas with Net Out-Migration -- 8.2.2 Planning Challenges for Areas with Net In-Migration -- 8.3 Land-Use Planning Policies and Mechanisms: Are They Addressing the Challenges? -- 8.4 Developing Mechanisms for Managing the Impacts of Demographic Change -- 8.4.1 Regulatory Planning Mechanisms -- 8.4.2 Voluntary Planning Mechanisms -- 8.5 Taking Control: Using the Right Mix of Planning Mechanisms to Design Preferred Rural Landscapes and Communities -- References -- 9 Demographic Change and the Implications for Commercial Forestry: Lessons from South-East Australia -- 9.1 Introduction -- 9.2 Research Methods -- 9.2.1 Selection of Case Studies -- 9.2.2 Sources of Data and Methods of Collection. , 9.2.3 Regional Settings for the Case Studies -- 9.3 Characteristics of Socio-Economic Changes and Factors Influencing the Changes -- 9.3.1 Population Changes -- 9.3.2 Employment Dynamics -- 9.3.2.1 Employment in Primary Industry -- 9.3.2.2 Off-Farm Employment -- 9.3.3 Purchase of Rural Property -- 9.3.3.1 The Value of Land for Agriculture -- 9.3.3.2 Spatial Distribution of Persons Who Purchased Rural Property -- 9.3.3.3 Patterns of Property Purchase in North-East Victoria -- 9.4 Impacts of Socio-Economic Changes in Rural Landscapes for Plantation Expansion -- 9.4.1 Introduction -- 9.4.2 Market Dynamics and Regional Expansion Targets -- 9.4.2.1 Regional Markets -- 9.4.2.2 Regional Targets for Plantation Expansion -- 9.4.3 The Supply of Land for Plantations -- 9.4.3.1 Studies of Land for Plantation Forestry in the Murray Valley -- 9.4.4 Recent Experiences of Companies Seeking to Expand Plantations -- 9.4.4.1 A Project to Develop Hardwood Plantations Within 200 km of Melbourne -- 9.4.4.2 Projects to Develop Radiata Pine Plantations -- 9.4.5 The Affordability of Land for Forestry -- 9.5 The Social Acceptability of Plantation Forestry -- 9.5.1 Forestry Land-Use Determination Under the Planning System -- 9.5.2 Impacts of New Landowners on the Management of Existing Plantations -- 9.6 Discussion and Conclusion -- References -- 10 Why Farming Families Decide to Maintain Native Biodiversity on Their Farms and the Implications of Demographic Change for Conservation Policies -- 10.1 Introduction -- 10.2 Decision-Systems Theory (DST) -- Box 10.1 A Farming Career -- 10.3 The 4-Group-Stakeholder Model -- 10.4 Policy Implications -- 10.4.1 Policies Implications in Relation to Farming Families -- Box 10.2 Farms as Homes and Businesses -- 10.4.2 Policies for Professional Managers of Corporate Farms -- 10.4.3 Policies for Families with Smaller Holdings of Farmland. , 10.4.4 Landholdings and Biodiversity Conservation.
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 2
    Online Resource
    Online Resource
    Berlin, Heidelberg :Springer Berlin / Heidelberg,
    Keywords: Metals -- Effect of radiation on. ; Electronic books.
    Description / Table of Contents: This book presents the results of time-dependent tight-binding simulations of radiation damage. It explores the effects of electronic excitations in collision cascades and ion channeling, and presents a new model.
    Type of Medium: Online Resource
    Pages: 1 online resource (309 pages)
    Edition: 1st ed.
    ISBN: 9783642154393
    Series Statement: Springer Theses Series
    Language: English
    Note: Intro -- The Modelling of Radiation Damage in Metals Using Ehrenfest Dynamics -- Supervisor's Foreword -- Acknowledgements -- Contents -- Part I Introductory Material -- 1 Introduction -- 1.1…Why Simulate Radiation Damage? -- 1.2…Semi-classical Simulation as a Link in the Multi-scale Chain -- 1.3…How to Read this Thesis -- References -- 2 A Radiation Damage Cascade -- 2.1…The Early Stages -- 2.1.1 Ion Channelling -- 2.1.2 Sub-cascade Branching -- 2.2…The Displacement Phase -- 2.3…The Thermal Spike -- References -- 3 The Treatment of Electronic Excitations in Atomistic Simulations of Radiation Damage---A Brief Review -- 3.1…The Theoretical Treatment of Radiation Damage -- 3.2…The Electronic Stopping Regime -- 3.2.1 General Concepts -- 3.2.2 Models of Fast, Light Particle Stopping -- 3.2.2.1 Early Models -- 3.2.2.2 The Bohr Formula -- 3.2.2.3 The Bethe Formula -- 3.2.3 Expanding the Realm of Stopping Power Theory -- 3.2.4 Models of Fast, Heavy Particle Stopping -- 3.2.4.1 The Effective Charge of the Projectile -- 3.2.4.2 Non-Perturbative Models of Heavy Ion Stopping -- 3.2.4.3 Empirical Models of Stopping Power -- 3.2.5 Models of Slow, Heavy Particle Stopping -- 3.2.5.1 Binary Models of Slow Particle Stopping -- 3.2.5.2 Electron Gas models of Slow Particle Stopping -- 3.2.5.3 Non-Linear Calculations of Electron Gas Stopping -- 3.2.6 The Gaps in Stopping Power Theory -- 3.3…The Electron--Phonon Coupling Regime -- 3.3.1 The Importance of Electron--Phonon Coupling in Radiation Damage -- 3.3.2 Two-Temperature Models -- 3.3.3 Representing the Electron--Phonon Coupling -- 3.3.4 Models of Electron--Phonon Coupling -- 3.4…Electronic Effects in Atomistic Models of Radiation Damage -- 3.4.1 The Binary Collision Approximation -- 3.4.2 Molecular Dynamics Models -- 3.4.2.1 Molecular Dynamics with Electronic Drag -- 3.4.2.2 Electrons as a Heat Bath. , 3.5…Improving the Models: Incorporating Electrons Explicitly -- References -- 4 Theoretical Background -- 4.1…Overview -- 4.2…The Semi-Classical Approximation -- 4.2.1 The Ehrenfest Approximation -- 4.2.2 The Approximations in Ehrenfest Dynamics -- 4.3…The Independent Electron Approximation -- 4.3.1 Density Functional Theory -- 4.3.2 Time-Dependent Density Functional Theory -- 4.4…Tight-Binding Models -- 4.4.1 Ab-Initio Tight-Binding -- 4.4.2 Semi-Empirical Tight-Binding -- 4.4.3 The Harris--Foulkes Functional -- 4.4.4 Towards Semi-Empirical Tight-Binding -- 4.4.5 Self-Consistent Tight-Binding -- 4.5…Time-Dependent Tight-Binding -- 4.5.1 The Description of the System -- 4.5.2 The Evolution of our System -- 4.5.2.1 The Evolution of the Density Matrix -- 4.5.2.2 The Evolution of the Ionic System -- 4.6…Ehrenfest Dynamics -- 4.6.1 Ehrenfest Dynamics versus Surface Hopping -- 4.6.2 Energy Transfer in Ehrenfest Dynamics -- 4.7…Conclusions -- References -- Part II Simulating Radiation Damage in Metals -- 5 A Framework for Simulating Radiation Damage in Metals -- 5.1…A Simple Model Metal -- 5.1.1 The Parameters of the Model -- 5.1.2 The Electronic Structure of the Model -- 5.1.3 A Note on the Truncation of the Hopping Integrals -- 5.2…Ehrenfest Dynamics -- 5.3…spICED: Our Simulation Software -- References -- 6 The Single Oscillating Ion -- 6.1…Simulations of a Single Oscillating Ion -- 6.2…Simulation Results -- 6.2.1 Frequency and Temperature Dependence of Energy Transfer -- 6.2.2 Position and Direction Dependence -- 6.3…Theoretical Analysis of the System -- 6.4…Explaining the Results -- 6.4.1 High Frequency Cut-off -- 6.4.2 Isotropic Damping About Equilibrium Lattice Site -- 6.4.3 Absence of Energy Transfer at Some Frequencies -- 6.4.4 Frequency Independence of beta at High Temperature -- 6.5…Conclusions -- References. , 7 Semi-classical Simulations of Collision Cascades -- 7.1…The Evolution of a Cascade -- 7.1.1 Thermalization of the Initial Distribution -- 7.1.2 The Evolution of the Ions -- 7.2…The Electronic Subsystem -- 7.2.1 The Evolving Electronic System -- 7.2.1.1 The Non-crossing Theorem -- 7.2.2 Adiabaticity, Non-Adiabaticity and Electronic Excitations -- 7.2.2.1 A Toy Model of an Avoided Crossing -- 7.2.3 Achieving Adiabatic Evolution by Altering the Electron--Ion Mass Ratio -- 7.2.3.1 Some Cascade Simulations at High Ion Mass -- 7.2.4 The Irreversible Energy Transfer -- 7.3…Conclusions -- References -- 8 The Nature of the Electronic Excitations -- 8.1…Patterns of Excitation in Collision Cascades -- 8.1.1 Fitting a Pseudo-temperature -- 8.1.2 Why do We Obtain Hot Electrons? -- 8.1.3 The Importance of the Result -- 8.1.4 Thermalization or Thermal Excitation? -- 8.2…Electronic Entropy in Ehrenfest Simulations -- 8.2.1 Two Definitions of Electronic Entropy -- 8.2.2 Reconciling the Two Entropies -- 8.2.3 A Thought Experiment -- 8.3…Conclusions -- References -- 9 The Electronic Forces -- 9.1…Understanding the Electronic Force -- 9.2…The Effect of Electronic Excitations on the 'Conservative' Force -- 9.2.1 The Importance of the Reduction in the Attractive Electronic Force -- 9.2.1.1 The Effective Strain Due to Electronic Heating -- 9.2.2 Replacement Collision Sequences -- 9.2.2.1 Does the Non-adiabatic Force Have an Effect on RCS Dynamics? -- 9.3…Conclusions -- References -- 10 Channelling Ions -- 10.1…Semi-Classical Simulations of Ion Channelling -- 10.1.1 The Simulation Set-Up -- 10.1.2 The Evolution of a Channelling Simulation -- 10.1.3 Challenges in Simulating Ion Channelling -- 10.2…Steady State Charge -- 10.2.1 Results for a Non-Self-Consistent Model -- 10.2.2 A Perturbation Theory Analysis. , 10.2.2.1 A More Detailed Look at the Perturbation Theory Expression -- 10.2.2.2 A Toy Model -- 10.2.3 The Effect of Channelling Direction -- 10.2.4 The Effect of Charge Self-Consistency Parameters U and V -- 10.3…Electronic Stopping Power for a Channelling Ion -- 10.3.1 Results -- 10.3.2 The Origin of the Stopping Power: A Tight-Binding Perspective -- 10.3.2.1 Bond-Orders in Channelling Simulations -- 10.3.3 The 'Knee' in the Stopping Power for U = V = 0 -- 10.3.4 Effect of Onsite Charge Self-Consistency -- 10.3.4.1 A U-Dependent Mechanism for Suppressing the Bond-Orders -- 10.4…Conclusions -- References -- 11 The Electronic Drag Force -- 11.1…Is a Simple Drag Model Good Enough? -- 11.1.1 An Investigation of Damping Models for Total Energy Loss in Collision Cascades -- 11.2…The Microscopic Behaviour of the Non-Adiabatic Force -- 11.2.1 The Non-Adiabatic Force in Ehrenfest Dynamics -- 11.2.2 The Character of the Non-Adiabatic Force -- 11.3…An Improved Model of the Non-Adiabatic Force -- 11.3.1 A ''Non-Adiabatic Bond Model'' -- 11.3.2 The Performance of Our Proposed Model -- 11.3.2.1 The Irreversible Energy Transfer -- 11.3.2.2 The Non-Adiabatic Force -- 11.3.2.3 Model Performance at the Cascade Level -- 11.4…Conclusions -- References -- 12 Concluding Remarks -- 12.1…Our Aims -- 12.2…Our Results -- 12.2.1 The Nature of the Electronic Excitations -- 12.2.2 The Effect of Electronic Excitations on the Conservative Forces -- 12.2.3 Non-Adiabatic Effects on Channelling Ions -- 12.2.4 The Non-Adiabatic Force in Collision Cascades -- 12.3…Possible Directions for Further Research -- References -- 13 Appendices -- 13.1…Appendix A: Selected proofs -- 13.1.1 Proof of Equation (4.10)-(i) -- 13.1.2 Proof of Equation (4.10)-(ii) -- 13.1.3 Proof of Equation (4.12) -- 13.1.4 Proof of Equation (4.28) -- 13.1.5 Proof of Equation (4.85) -- 13.1.6 Proof of Equation (4.86). , 13.1.7 Proof of Equation (4.102) -- 13.1.8 Proof of Equation (4.131) -- 13.1.9 Proof of Equation (4.135) -- 13.1.10 Proof of Equation (4.137) -- 13.1.11 Proof of Equation (4.141): The Conservation of Total Energy -- 13.1.12 Proof of Increase of Pseudo-Entropy (8.16) -- 13.1.13 Proof of Equation (9.4) -- 13.1.14 Proof that Im{f4} = 0 -- 13.1.15 Proof of Equation (11.9) -- 13.1.16 Proof of Equation (11.12) -- 13.1.17 Proof of Equation (11.18) -- 13.2…Appendix B: Perturbation Theory -- 13.2.1 A Periodic Perturbation -- 13.2.2 The Effect of a Sinusoidal Perturbation on an Electronic System -- 13.2.2.1 The Irreversible Energy Transfer -- 13.2.2.2 Charge Transfer -- 13.2.2.3 First-Order Perturbation Theory Approximations -- The Time Dependence of the Energy and Charge Transfer -- Interpreting the Perturbation Theory Expressions -- Can We Neglect the Off-Diagonal Elements of \hat{\rho} in our Expression for {\Updelta }q_{\alpha}? -- Some Numerical Results -- 13.2.3 A Quantum Mechanical Oscillator -- 13.3…Appendix C: The Coupling Matrix for a Single Oscillating Ion -- 13.4…Appendix D: Some Features of the Electronic Excitation Spectrum in Collision Cascades -- 13.4.1 Anomalous Excitations Early in the Cascade -- 13.4.2 The Width of the Temperature Fitting Window -- 13.4.3 The Sommerfeld Expression for the Heat Capacity of Our Model -- 13.4.4 Behaviour of the Fitted Temperature Early in the Cascade -- 13.5…Appendix E: The Strain on an Inclusion due to Electronic Heating -- References -- Index.
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 3
    Publication Date: 2019-10-01
    Repository Name: EPIC Alfred Wegener Institut
    Type: Book , peerRev
    Format: application/pdf
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 4
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Neurodegenerative diseases such as Alzheimer's, Parkinson's and the transmissible spongiform encephalopathies (TSEs) are characterized by abnormal protein deposits, often with large amyloid fibrils. However, questions have arisen as to whether such fibrils or smaller subfibrillar ...
    Type of Medium: Electronic Resource
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 5
    Publication Date: 2012-10-07
    Description: Mammalian prions are thought to consist of misfolded aggregates (protease-resistant isoform of the prion protein [PrP res ]) of the cellular prion protein (PrP C ). Transmissible spongiform encephalopathy (TSE) can be induced in animals inoculated with recombinant PrP (rPrP) amyloid fibrils lacking mammalian posttranslational modifications, but this induction is inefficient in hamsters or transgenic mice overexpressing glycosylphosphatidylinositol (GPI)-anchored PrP C . Here we show that TSE can be initiated by inoculation of misfolded rPrP into mice that express wild-type (wt) levels of PrP C and that synthetic prion strain propagation and selection can be affected by GPI anchoring of the host's PrP C . To create prions de novo , we fibrillized mouse rPrP in the absence of molecular cofactors, generating fibrils with a PrP res -like protease-resistant banding profile. These fibrils induced the formation of PrP res deposits in transgenic mice coexpressing wt and GPI-anchorless PrP C (wt/GPI – ) at a combined level comparable to that of PrP C expression in wt mice. Secondary passage into mice expressing wt, GPI – , or wt plus GPI – PrP C induced TSE disease with novel clinical, histopathological, and biochemical phenotypes. Contrary to laboratory-adapted mouse scrapie strains, the synthetic prion agents exhibited a preference for conversion of GPI – PrP C and, in one case, caused disease only in GPI – mice. Our data show that novel TSE agents can be generated de novo solely from purified mouse rPrP after amplification in mice coexpressing normal levels of wt and anchorless PrP C . These observations provide insight into the minimal elements required to create prions in vitro and suggest that the PrP C GPI anchor can modulate the propagation of synthetic TSE strains.
    Print ISSN: 0022-538X
    Electronic ISSN: 1098-5514
    Topics: Medicine
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 6
    Publication Date: 2012-09-11
    Description: Neurodegenerative diseases are typically associated with an activation of glia and an increased level of cytokines. In our previous studies of prion disease, the cytokine response in the brains of clinically sick scrapie-infected mice was restricted to a small group of cytokines, of which IL-12p40, CCL2, and CXCL10 were present at the highest levels. The goal of our current research was to determine the relationship between cytokine responses, gliosis, and neuropathology during prion disease. Here, in time course studies of C57BL/10 mice intracerebrally inoculated with 22L scrapie, abnormal protease-resistant prion protein (PrPres), astrogliosis, and microgliosis were first detected at 40 days after intracerebral scrapie inoculation. In cytokine studies, IL-12p40 was first elevated by 60 days; CCL3, IL-1β, and CXCL1 were elevated by 80 days; and CCL2 and CCL5 were elevated by 115 days. IL-12p40 showed the most extensive increase throughout disease and was 30-fold above control levels at the terminal stage. Because of the early onset and dramatic elevation of IL-12p40 during scrapie, we investigated whether IL-12p40 contributed to the development of prion disease neuropathogenesis by using three different scrapie strains (22L, RML, 79A) to infect knockout mice in which the gene encoding IL-12p40 was deleted. We also studied knockout mice lacking IL-12p35, which combines with IL-12p40 to form active IL-12 heterodimers. In all instances, knockout mice did not differ from control mice in survival time, clinical tempo, or levels of spongiosis, gliosis, or PrPres in the brain. Thus, neither IL-12p40 nor IL-12p35 molecules were required for prion disease-associated neurodegeneration or neuroinflammation.
    Print ISSN: 0022-538X
    Electronic ISSN: 1098-5514
    Topics: Medicine
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 7
    Publication Date: 2012-10-11
    Description: Astrobiology , Vol. 0, No. 0.
    Print ISSN: 1531-1074
    Electronic ISSN: 1557-8070
    Topics: Biology , Physics
    Published by Mary Ann Liebert
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 8
    Publication Date: 2013-07-24
    Description: Analytical Chemistry DOI: 10.1021/ac400737z
    Print ISSN: 0003-2700
    Electronic ISSN: 1520-6882
    Topics: Chemistry and Pharmacology
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 9
    Publication Date: 2013-08-28
    Description: Organic Letters DOI: 10.1021/ol4023112
    Print ISSN: 1523-7060
    Electronic ISSN: 1523-7052
    Topics: Chemistry and Pharmacology
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 10
    Publication Date: 2011-11-30
    Description: Prions are unconventional infectious agents that cause transmissible spongiform encephalopathy (TSE) diseases, or prion diseases. The biochemical nature of the prion infectious agent remains unclear. Previously, using a protein misfolding cyclic amplification (PMCA) reaction, infectivity and disease-associated protease-resistant prion protein (PrPres) were both generated under cell-free conditions, which supported a nonviral hypothesis for the agent. However, these studies lacked comparative quantitation of both infectivity titers and PrPres, which is important both for biological comparison with in vivo-derived infectivity and for excluding contamination to explain the results. Here during four to eight rounds of PMCA, end-point dilution titrations detected a 〉320-fold increase in infectivity versus that in controls. These results provide strong support for the hypothesis that the agent of prion infectivity is not a virus. PMCA-generated samples caused the same clinical disease and neuropathology with the same rapid incubation period as the input brain-derived scrapie samples, providing no evidence for generation of a new strain in PMCA. However, the ratio of the infectivity titer to the amount of PrPres (specific infectivity) was much lower in PMCA versus brain-derived samples, suggesting the possibility that a substantial portion of PrPres generated in PMCA might be noninfectious.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    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...