Project acronym ADAPT
Project Life in a cold climate: the adaptation of cereals to new environments and the establishment of agriculture in Europe
Researcher (PI) Terence Austen Brown
Host Institution (HI) THE UNIVERSITY OF MANCHESTER
Country United Kingdom
Call Details Advanced Grant (AdG), SH6, ERC-2013-ADG
Summary "This project explores the concept of agricultural spread as analogous to enforced climate change and asks how cereals adapted to new environments when agriculture was introduced into Europe. Archaeologists have long recognized that the ecological pressures placed on crops would have had an impact on the spread and subsequent development of agriculture, but previously there has been no means of directly assessing the scale and nature of this impact. Recent work that I have directed has shown how such a study could be carried out, and the purpose of this project is to exploit these breakthroughs with the goal of assessing the influence of environmental adaptation on the spread of agriculture, its adoption as the primary subsistence strategy, and the subsequent establishment of farming in different parts of Europe. This will correct the current imbalance between our understanding of the human and environmental dimensions to the domestication of Europe. I will use methods from population genomics to identify loci within the barley and wheat genomes that have undergone selection since the beginning of cereal cultivation in Europe. I will then use ecological modelling to identify those loci whose patterns of selection are associated with ecogeographical variables and hence represent adaptations to local environmental conditions. I will assign dates to the periods when adaptations occurred by sequencing ancient DNA from archaeobotanical assemblages and by computer methods that enable the temporal order of adaptations to be deduced. I will then synthesise the information on environmental adaptations with dating evidence for the spread of agriculture in Europe, which reveals pauses that might be linked to environmental adaptation, with demographic data that indicate regions where Neolithic populations declined, possibly due to inadequate crop productivity, and with an archaeobotanical database showing changes in the prevalence of individual cereals in different regions."
Summary
"This project explores the concept of agricultural spread as analogous to enforced climate change and asks how cereals adapted to new environments when agriculture was introduced into Europe. Archaeologists have long recognized that the ecological pressures placed on crops would have had an impact on the spread and subsequent development of agriculture, but previously there has been no means of directly assessing the scale and nature of this impact. Recent work that I have directed has shown how such a study could be carried out, and the purpose of this project is to exploit these breakthroughs with the goal of assessing the influence of environmental adaptation on the spread of agriculture, its adoption as the primary subsistence strategy, and the subsequent establishment of farming in different parts of Europe. This will correct the current imbalance between our understanding of the human and environmental dimensions to the domestication of Europe. I will use methods from population genomics to identify loci within the barley and wheat genomes that have undergone selection since the beginning of cereal cultivation in Europe. I will then use ecological modelling to identify those loci whose patterns of selection are associated with ecogeographical variables and hence represent adaptations to local environmental conditions. I will assign dates to the periods when adaptations occurred by sequencing ancient DNA from archaeobotanical assemblages and by computer methods that enable the temporal order of adaptations to be deduced. I will then synthesise the information on environmental adaptations with dating evidence for the spread of agriculture in Europe, which reveals pauses that might be linked to environmental adaptation, with demographic data that indicate regions where Neolithic populations declined, possibly due to inadequate crop productivity, and with an archaeobotanical database showing changes in the prevalence of individual cereals in different regions."
Max ERC Funding
2 492 964 €
Duration
Start date: 2014-02-01, End date: 2019-01-31
Project acronym AngioBone
Project Angiogenic growth, specialization, ageing and regeneration
of bone vessels
Researcher (PI) Ralf Heinrich Adams
Host Institution (HI) Westfälische Wilhelms-Universität Münster
Country Germany
Call Details Advanced Grant (AdG), LS3, ERC-2013-ADG
Summary The skeleton and the sinusoidal vasculature form a functional unit with great relevance in health, regeneration, and disease. Currently, fundamental aspects of sinusoidal vessel growth, specialization, arteriovenous organization and the consequences for tissue perfusion, or the changes occurring during ageing remain unknown. Our preliminary data indicate that key principles of bone vascularization and the role of molecular regulators are highly distinct from other organs. I therefore propose to use powerful combination of mouse genetics, fate mapping, transcriptional profiling, computational biology, confocal and two-photon microscopy, micro-CT and PET imaging, biochemistry and cell biology to characterize the growth, differentiation, dynamics, and ageing of the bone vasculature. In addition to established angiogenic pathways, the role of highly promising novel candidate regulators will be investigated in endothelial cells and perivascular osteoprogenitors with sophisticated inducible and cell type-specific genetic methods in the mouse. Complementing these powerful in vivo approaches, 3D co-cultures generated by cell printing technologies will provide insight into the communication between different cell types. The dynamics of sinusoidal vessel growth and regeneration will be monitored by two-photon imaging in the skull. Finally, I will explore the architectural, cellular and molecular changes and the role of capillary endothelial subpopulations in the sinusoidal vasculature of ageing and osteoporotic mice.
Technological advancements, such as new transgenic strains, mutant models or cell printing approaches, are important aspects of this proposal. AngioBone will provide a first conceptual framework for normal and deregulated function of the bone sinusoidal vasculature. It will also break new ground by analyzing the role of blood vessels in ageing and identifying novel strategies for tissue engineering and, potentially, the prevention/treatment of osteoporosis.
Summary
The skeleton and the sinusoidal vasculature form a functional unit with great relevance in health, regeneration, and disease. Currently, fundamental aspects of sinusoidal vessel growth, specialization, arteriovenous organization and the consequences for tissue perfusion, or the changes occurring during ageing remain unknown. Our preliminary data indicate that key principles of bone vascularization and the role of molecular regulators are highly distinct from other organs. I therefore propose to use powerful combination of mouse genetics, fate mapping, transcriptional profiling, computational biology, confocal and two-photon microscopy, micro-CT and PET imaging, biochemistry and cell biology to characterize the growth, differentiation, dynamics, and ageing of the bone vasculature. In addition to established angiogenic pathways, the role of highly promising novel candidate regulators will be investigated in endothelial cells and perivascular osteoprogenitors with sophisticated inducible and cell type-specific genetic methods in the mouse. Complementing these powerful in vivo approaches, 3D co-cultures generated by cell printing technologies will provide insight into the communication between different cell types. The dynamics of sinusoidal vessel growth and regeneration will be monitored by two-photon imaging in the skull. Finally, I will explore the architectural, cellular and molecular changes and the role of capillary endothelial subpopulations in the sinusoidal vasculature of ageing and osteoporotic mice.
Technological advancements, such as new transgenic strains, mutant models or cell printing approaches, are important aspects of this proposal. AngioBone will provide a first conceptual framework for normal and deregulated function of the bone sinusoidal vasculature. It will also break new ground by analyzing the role of blood vessels in ageing and identifying novel strategies for tissue engineering and, potentially, the prevention/treatment of osteoporosis.
Max ERC Funding
2 478 750 €
Duration
Start date: 2014-02-01, End date: 2019-01-31
Project acronym BETAIMAGE
Project An in vivo imaging approach to understand pancreatic beta-cell signal-transduction
Researcher (PI) Per-Olof Berggren
Host Institution (HI) KAROLINSKA INSTITUTET
Country Sweden
Call Details Advanced Grant (AdG), LS4, ERC-2013-ADG
Summary The challenge in cell physiology/pathology today is to translate in vitro findings to the living organism. We have developed a unique approach where signal-transduction can be investigated in vivo non-invasively, longitudinally at single cell resolution, using the anterior chamber of the eye as a natural body window for imaging. We will use this approach to understand how the universally important and highly complex signal Ca2+ is regulated in the pancreatic beta-cell, while localized in the vascularized and innervated islet of Langerhans, and how that affects the insulin secretory machinery in vivo. Engrafted islets in the eye take on identical innervation- and vascularization patterns as those in the pancreas and are proficient in regulating glucose homeostasis in the animal. Since the pancreatic islet constitutes a micro-organ, this imaging approach offers a seminal model system to understand Ca2+ signaling in individual cells at the organ level in real life. We will test the hypothesis that the Ca2+-signal has a key role in pancreatic beta-cell function and survival in vivo and that perturbation in the Ca2+-signal serves as a common denominator for beta-cell pathology associated with impaired glucose homeostasis and diabetes. Of special interest is how innervation impacts on Ca2+-dynamics and the integration of autocrine, paracrine and endocrine signals in fine-tuning the Ca2+-signal with regard to beta-cell function and survival. We aim to define key defects in the machinery regulating Ca2+-dynamics in association with the autoimmune reaction, inflammation and obesity eventually resulting in diabetes. Our imaging platform will be applied to clarify in vivo regulation of Ca2+-dynamics in both healthy and diabetic human beta-cells. To define novel drugable targets for treatment of diabetes, it is crucial to identify similarities and differences in the molecular machinery regulating the in vivo Ca2+-signal in the human and in the rodent beta-cell.
Summary
The challenge in cell physiology/pathology today is to translate in vitro findings to the living organism. We have developed a unique approach where signal-transduction can be investigated in vivo non-invasively, longitudinally at single cell resolution, using the anterior chamber of the eye as a natural body window for imaging. We will use this approach to understand how the universally important and highly complex signal Ca2+ is regulated in the pancreatic beta-cell, while localized in the vascularized and innervated islet of Langerhans, and how that affects the insulin secretory machinery in vivo. Engrafted islets in the eye take on identical innervation- and vascularization patterns as those in the pancreas and are proficient in regulating glucose homeostasis in the animal. Since the pancreatic islet constitutes a micro-organ, this imaging approach offers a seminal model system to understand Ca2+ signaling in individual cells at the organ level in real life. We will test the hypothesis that the Ca2+-signal has a key role in pancreatic beta-cell function and survival in vivo and that perturbation in the Ca2+-signal serves as a common denominator for beta-cell pathology associated with impaired glucose homeostasis and diabetes. Of special interest is how innervation impacts on Ca2+-dynamics and the integration of autocrine, paracrine and endocrine signals in fine-tuning the Ca2+-signal with regard to beta-cell function and survival. We aim to define key defects in the machinery regulating Ca2+-dynamics in association with the autoimmune reaction, inflammation and obesity eventually resulting in diabetes. Our imaging platform will be applied to clarify in vivo regulation of Ca2+-dynamics in both healthy and diabetic human beta-cells. To define novel drugable targets for treatment of diabetes, it is crucial to identify similarities and differences in the molecular machinery regulating the in vivo Ca2+-signal in the human and in the rodent beta-cell.
Max ERC Funding
2 499 590 €
Duration
Start date: 2014-03-01, End date: 2019-02-28
Project acronym BEYOND
Project METABOLIC BASIS OF NEURODEGENERATIVE DISEASE
Researcher (PI) Thomas Franz Erich Willnow
Host Institution (HI) MAX DELBRUECK CENTRUM FUER MOLEKULARE MEDIZIN IN DER HELMHOLTZ-GEMEINSCHAFT (MDC)
Country Germany
Call Details Advanced Grant (AdG), LS4, ERC-2013-ADG
Summary Alzheimer disease (AD) is the most common form of age-related dementia affecting millions of patients worldwide. Disturbingly, disorders of lipid and glucose metabolism emerge as major risk factors for onset and progression of neurodegeneration in the human population. Thus, an increasing life expectance combined with an observable rise in metabolic disturbances is expected to turn AD into one of the most serious health problems for future generations. Still, the molecular mechanisms whereby dysregulation of glucose and lipid homeostasis elicits noxious insults to the brain remain poorly understood. We characterized a novel class of intracellular sorting receptors, termed VPS10P domain receptors with dual roles in regulation of neuronal viability and function, but also in modulation of glucose and lipid homeostasis. Our proposal aims at elucidating an important yet poorly understood link between metabolism and neurodegeneration that converges on these receptors. Our approach is unique and novel in several ways. Thematically, our studies focus on a novel class of receptors previously not considered. Based on the receptors’ ability to act as sorting proteins, we propose faulty protein trafficking as a major unifying concept underlying neurodegenerative and metabolic disorders. Conceptually, our approach relies on the interdisciplinary effort of neuroscientists and metabolism researchers working jointly on pathophysiological pathways converging on these receptors. Through this effort, we are confident to gain important insights into the crosstalk between brain and peripheral tissues, and to elucidate pathways common to metabolic disturbances and dementia, two prevailing degenerative disorders inflicting our societies.
Summary
Alzheimer disease (AD) is the most common form of age-related dementia affecting millions of patients worldwide. Disturbingly, disorders of lipid and glucose metabolism emerge as major risk factors for onset and progression of neurodegeneration in the human population. Thus, an increasing life expectance combined with an observable rise in metabolic disturbances is expected to turn AD into one of the most serious health problems for future generations. Still, the molecular mechanisms whereby dysregulation of glucose and lipid homeostasis elicits noxious insults to the brain remain poorly understood. We characterized a novel class of intracellular sorting receptors, termed VPS10P domain receptors with dual roles in regulation of neuronal viability and function, but also in modulation of glucose and lipid homeostasis. Our proposal aims at elucidating an important yet poorly understood link between metabolism and neurodegeneration that converges on these receptors. Our approach is unique and novel in several ways. Thematically, our studies focus on a novel class of receptors previously not considered. Based on the receptors’ ability to act as sorting proteins, we propose faulty protein trafficking as a major unifying concept underlying neurodegenerative and metabolic disorders. Conceptually, our approach relies on the interdisciplinary effort of neuroscientists and metabolism researchers working jointly on pathophysiological pathways converging on these receptors. Through this effort, we are confident to gain important insights into the crosstalk between brain and peripheral tissues, and to elucidate pathways common to metabolic disturbances and dementia, two prevailing degenerative disorders inflicting our societies.
Max ERC Funding
2 415 229 €
Duration
Start date: 2014-02-01, End date: 2019-01-31
Project acronym CARDIOREDOX
Project Redox sensing and signalling in cardiovascular health and disease
Researcher (PI) Philip Eaton
Host Institution (HI) KING'S COLLEGE LONDON
Country United Kingdom
Call Details Advanced Grant (AdG), LS4, ERC-2013-ADG
Summary "We want to determine how oxidants are sensed and transduced into a biological effect within the cardiovascular system. The proposed work will focus on thiol-based redox sensors, defining their role in heart and blood vessel function during health and disease. Although this laboratory has studied the molecular basis of redox signaling for more than a decade, the subject is still in its relative infancy with considerable scope for major advances. Oxidant signaling remains a ‘hot topic’ with high profile studies confirming a fundamental role for redox control of protein and cellular function continuing to emerge. The molecular basis of redox sensing is the reaction of an oxidant with target proteins. This gives rise to oxidative post-translational modifications, most commonly of cysteinyl thiols, potentially altering the activity of proteins to regulate cell or tissue function. One of the reasons there are so many unanswered questions about redox sensing and signaling is the diversity of oxidant molecules produced by cells that can interact with sensor proteins to alter their function. This application is aimed at extending our knowledge of redox sensing and signalling, allowing us to define its importance in cardiovascular health and disease."
Summary
"We want to determine how oxidants are sensed and transduced into a biological effect within the cardiovascular system. The proposed work will focus on thiol-based redox sensors, defining their role in heart and blood vessel function during health and disease. Although this laboratory has studied the molecular basis of redox signaling for more than a decade, the subject is still in its relative infancy with considerable scope for major advances. Oxidant signaling remains a ‘hot topic’ with high profile studies confirming a fundamental role for redox control of protein and cellular function continuing to emerge. The molecular basis of redox sensing is the reaction of an oxidant with target proteins. This gives rise to oxidative post-translational modifications, most commonly of cysteinyl thiols, potentially altering the activity of proteins to regulate cell or tissue function. One of the reasons there are so many unanswered questions about redox sensing and signaling is the diversity of oxidant molecules produced by cells that can interact with sensor proteins to alter their function. This application is aimed at extending our knowledge of redox sensing and signalling, allowing us to define its importance in cardiovascular health and disease."
Max ERC Funding
2 255 659 €
Duration
Start date: 2013-12-01, End date: 2018-11-30
Project acronym CENFOR
Project Dissecting the mechanisms governing centriole formation
Researcher (PI) Pierre Goenczy
Host Institution (HI) ECOLE POLYTECHNIQUE FEDERALE DE LAUSANNE
Country Switzerland
Call Details Advanced Grant (AdG), LS3, ERC-2013-ADG
Summary "Centrioles are critical for the formation of cilia, flagella and centrosomes, as well as for human health. The mechanisms governing centriole formation constitute a long-standing question in cell biology. We will pursue an innovative multidisciplinary research program to gain further insight into these mechanisms, using human cells, C. elegans and Trichonympha as model systems. This program is expected to also have a major impact by contributing a novel cell free assay to the field, thus paving the way towards making synthetic centrioles. Six specific aims will be pursued:
1) Deciphering HsSAS-6/STIL distribution and dynamics. We will use super-resolution microscopy, molecular counting, photoconversion and FCS to further characterize these two key components required for centriole formation in human cells.
2) The SAS-6 ring model as a tool to redirect centriole organization. Utilizing predictions from the SAS-6 ring model, we will assay the consequences for centrioles and cilia of altering the diameter and symmetry of the structure.
3) Determining the architecture of C. elegans centrioles. We will conduct molecular counting and cryo-ET of purified C. elegans centrioles to determine if they contain a spiral or a cartwheel, as well as identify SAS-6-interacting components.
4) Comprehensive 3D map and proteomics of Trichonympha centriole. We will obtain a ~35 Å 3D map of the complete T. agilis centriole, perform proteomic analysis to identify its constituents and test their function using RNAi.
5) Regulation of cartwheel height and centriole length. We will explore whether cartwheel height is set by SAS-6 proteins and perform screens in human cells to identify novel components regulating cartwheel height and centriole length.
6) Novel cell free assay for cartwheel assembly and centriole formation. Using SAS-6 proteins on a lipid monolayer as starting point, we will develop and utilize a cell-free assay to reconstitute cartwheel assembly and centriole format"
Summary
"Centrioles are critical for the formation of cilia, flagella and centrosomes, as well as for human health. The mechanisms governing centriole formation constitute a long-standing question in cell biology. We will pursue an innovative multidisciplinary research program to gain further insight into these mechanisms, using human cells, C. elegans and Trichonympha as model systems. This program is expected to also have a major impact by contributing a novel cell free assay to the field, thus paving the way towards making synthetic centrioles. Six specific aims will be pursued:
1) Deciphering HsSAS-6/STIL distribution and dynamics. We will use super-resolution microscopy, molecular counting, photoconversion and FCS to further characterize these two key components required for centriole formation in human cells.
2) The SAS-6 ring model as a tool to redirect centriole organization. Utilizing predictions from the SAS-6 ring model, we will assay the consequences for centrioles and cilia of altering the diameter and symmetry of the structure.
3) Determining the architecture of C. elegans centrioles. We will conduct molecular counting and cryo-ET of purified C. elegans centrioles to determine if they contain a spiral or a cartwheel, as well as identify SAS-6-interacting components.
4) Comprehensive 3D map and proteomics of Trichonympha centriole. We will obtain a ~35 Å 3D map of the complete T. agilis centriole, perform proteomic analysis to identify its constituents and test their function using RNAi.
5) Regulation of cartwheel height and centriole length. We will explore whether cartwheel height is set by SAS-6 proteins and perform screens in human cells to identify novel components regulating cartwheel height and centriole length.
6) Novel cell free assay for cartwheel assembly and centriole formation. Using SAS-6 proteins on a lipid monolayer as starting point, we will develop and utilize a cell-free assay to reconstitute cartwheel assembly and centriole format"
Max ERC Funding
2 499 270 €
Duration
Start date: 2014-04-01, End date: 2019-03-31
Project acronym ChroNeuroRepair
Project Chromatin states in neurogenesis – from understanding chromatin loops to eliciting neurogenesis for repair
Researcher (PI) Magdalena Goetz
Host Institution (HI) HELMHOLTZ ZENTRUM MUENCHEN DEUTSCHES FORSCHUNGSZENTRUM FUER GESUNDHEIT UND UMWELT GMBH
Country Germany
Call Details Advanced Grant (AdG), LS3, ERC-2013-ADG
Summary The mechanisms regulating neural stem cells and their progression to neurogenesis are important not only to understand brain development and evolution, but also to elicit neurogenesis after brain injury. Our recent findings imply novel chromatin-associated proteins in the regulation of neural stem cell fate and neurogenesis. Therefore this project aims to understand the molecular mechanisms of how these factors regulate neurogenesis in developing and adult mice (Aim1) and implement this knowledge for reprogramming glia into neurons after brain injury (Aim2). This will be pursued in mouse models in vivo (2.1) and with human glial cells derived from patient brain resections in vitro (2.2). It is well known that transcription factors need to alter the chromatin structure to achieve transcriptional regulation, but the factors involved in this regulation in neural stem and progenitor cells are still ill understood. Therefore the molecular function of the novel chromatin interacting protein Trnp1 with essential roles in neural stem cell (NSC) fate and the chromatin conformation mediated at neurogenic target genes by Pax6/Brg1-containing BAF complexes will be addressed in Aim1. Combined with genome-wide approaches to determine changes in chromatin conformation at neurogenic target gene sites this will greatly further our understanding of key roles of chromatin conformation in neural stem cells and neurogenesis. In Aim2 Trnp1 promoting neural stem cells fate and later acting neurogenic transcription factors will be used to improve neuronal reprogramming after stab wound injury in the murine brain in vivo and in patient-derived glial cells in vitro. Together with novel strategies to induce chromatin looping in a sequence-specific manner this project will not only advance our knowledge at the frontier of transcriptional regulation in neurogenesis, but also implement highly innovative approaches to utilize this knowledge for neuronal repair by direct reprogramming.
Summary
The mechanisms regulating neural stem cells and their progression to neurogenesis are important not only to understand brain development and evolution, but also to elicit neurogenesis after brain injury. Our recent findings imply novel chromatin-associated proteins in the regulation of neural stem cell fate and neurogenesis. Therefore this project aims to understand the molecular mechanisms of how these factors regulate neurogenesis in developing and adult mice (Aim1) and implement this knowledge for reprogramming glia into neurons after brain injury (Aim2). This will be pursued in mouse models in vivo (2.1) and with human glial cells derived from patient brain resections in vitro (2.2). It is well known that transcription factors need to alter the chromatin structure to achieve transcriptional regulation, but the factors involved in this regulation in neural stem and progenitor cells are still ill understood. Therefore the molecular function of the novel chromatin interacting protein Trnp1 with essential roles in neural stem cell (NSC) fate and the chromatin conformation mediated at neurogenic target genes by Pax6/Brg1-containing BAF complexes will be addressed in Aim1. Combined with genome-wide approaches to determine changes in chromatin conformation at neurogenic target gene sites this will greatly further our understanding of key roles of chromatin conformation in neural stem cells and neurogenesis. In Aim2 Trnp1 promoting neural stem cells fate and later acting neurogenic transcription factors will be used to improve neuronal reprogramming after stab wound injury in the murine brain in vivo and in patient-derived glial cells in vitro. Together with novel strategies to induce chromatin looping in a sequence-specific manner this project will not only advance our knowledge at the frontier of transcriptional regulation in neurogenesis, but also implement highly innovative approaches to utilize this knowledge for neuronal repair by direct reprogramming.
Max ERC Funding
2 376 560 €
Duration
Start date: 2014-02-01, End date: 2019-01-31
Project acronym COCO2CASA
Project Modeling Stellar Collapse and Explosion: Evolving Progenitor Stars to Supernova Remnants
Researcher (PI) Hans-Thomas Janka
Host Institution (HI) MAX-PLANCK-GESELLSCHAFT ZUR FORDERUNG DER WISSENSCHAFTEN EV
Country Germany
Call Details Advanced Grant (AdG), PE9, ERC-2013-ADG
Summary "This project intends to make groundbreaking progress towards the solution of one of the most pestering and long-standing riddles of stellar astrophysics, namely the question how massive stars explode as supernovae (SNe).
State-of-the-art simulations in two dimensions (2D) now yield neutrino-powered (through underenergetic) explosions for a growing variety of progenitors and thus support the delayed neutrino-heating mechanism. However, sophisticated, fully self-consistent, 3D simulations are still lacking, the spherical symmetry of the progenitor star models is becoming a serious handicap, and better exploitation of observational constraints of the SN mechanism is urgently needed.
For these reasons we plan a novel, comprehensive modeling approach, in which 3D hydrodynamics including all relevant microphysics will not only be employed for the launch phase of the SN blast wave by neutrino-energy deposition. Different from previous initiatives, 3D hydrodynamics will also be applied to the final stages of convective shell burning in the progenitor core before collapse in order to derive --for the first time-- self-consistent, multidimensional progenitor data for adopting them as initial conditions in the SN modeling. Moreover, the 3D explosion simulations will be continued consistently through the long-time evolution of the SN outburst into the gaseous remnant phase. This challenging approach promises fundamentally new insights into the processes that trigger and shape SN explosions and will revise our understanding of how SNe depend on the properties of their progenitor stars. Moreover, heading for a direct comparison of the derived theoretical models with nearby young SN remnants like Crab, Cassiopeia A, and SN 1987A, whose 3D morphology and composition are currently unfolded in stunning detail by multiwavelength observations, the project will lay the foundations of a powerful, innovative, and so far not exploited way of probing the physics deep inside the SN core."
Summary
"This project intends to make groundbreaking progress towards the solution of one of the most pestering and long-standing riddles of stellar astrophysics, namely the question how massive stars explode as supernovae (SNe).
State-of-the-art simulations in two dimensions (2D) now yield neutrino-powered (through underenergetic) explosions for a growing variety of progenitors and thus support the delayed neutrino-heating mechanism. However, sophisticated, fully self-consistent, 3D simulations are still lacking, the spherical symmetry of the progenitor star models is becoming a serious handicap, and better exploitation of observational constraints of the SN mechanism is urgently needed.
For these reasons we plan a novel, comprehensive modeling approach, in which 3D hydrodynamics including all relevant microphysics will not only be employed for the launch phase of the SN blast wave by neutrino-energy deposition. Different from previous initiatives, 3D hydrodynamics will also be applied to the final stages of convective shell burning in the progenitor core before collapse in order to derive --for the first time-- self-consistent, multidimensional progenitor data for adopting them as initial conditions in the SN modeling. Moreover, the 3D explosion simulations will be continued consistently through the long-time evolution of the SN outburst into the gaseous remnant phase. This challenging approach promises fundamentally new insights into the processes that trigger and shape SN explosions and will revise our understanding of how SNe depend on the properties of their progenitor stars. Moreover, heading for a direct comparison of the derived theoretical models with nearby young SN remnants like Crab, Cassiopeia A, and SN 1987A, whose 3D morphology and composition are currently unfolded in stunning detail by multiwavelength observations, the project will lay the foundations of a powerful, innovative, and so far not exploited way of probing the physics deep inside the SN core."
Max ERC Funding
2 898 600 €
Duration
Start date: 2014-02-01, End date: 2019-01-31
Project acronym COORDINATINGforLIFE
Project Coordinating for life. Success and failure of Western European societies in coping with rural hazards and disasters, 1300-1800
Researcher (PI) Balthassar Jozef Paul (Bas) Van Bavel
Host Institution (HI) UNIVERSITEIT UTRECHT
Country Netherlands
Call Details Advanced Grant (AdG), SH6, ERC-2013-ADG
Summary Societies in past and present are regularly confronted with major hazards, which sometimes have disastrous effects. Some societies are successful in preventing these effects and buffering threats, or they recover quickly, while others prove highly vulnerable. Why is this?
Increasingly it is clear that disasters are not merely natural events, and also that wealth and technology alone are not adequate to prevent them. Rather, hazards and disasters are social occurrences as well, and they form a tough test for the organizational capacities of a society, both in mitigation and recovery. This project targets a main element of this capacity, namely: the way societies have organized the exchange, allocation and use of resources. It aims to explain why some societies do well in preventing or remedying disasters through these institutional arrangements and others not.
In order to do so, this project analyses four key variables: the mix of coordination systems available within that society, its degree of autarky, economic equity and political equality. The recent literature on historical and present-day disasters suggests these factors as possible causes of success or failure of institutional arrangements in their confrontation with hazards, but their discussion remains largely descriptive and they have never been systematically analyzed.
This research project offers such a systematic investigation, using rural societies in Western Europe in the period 1300-1800 - with their variety of socio-economic characteristics - as a testing ground. The historical perspective enables us to compare widely differing cases, also over the long run, and to test for the variables chosen, in order to isolate the determining factors in the resilience of different societies. By using the opportunities offered by history in this way, we will increase our insight into the relative performance of societies and gain a better understanding of a critical determinant of human wellbeing.
Summary
Societies in past and present are regularly confronted with major hazards, which sometimes have disastrous effects. Some societies are successful in preventing these effects and buffering threats, or they recover quickly, while others prove highly vulnerable. Why is this?
Increasingly it is clear that disasters are not merely natural events, and also that wealth and technology alone are not adequate to prevent them. Rather, hazards and disasters are social occurrences as well, and they form a tough test for the organizational capacities of a society, both in mitigation and recovery. This project targets a main element of this capacity, namely: the way societies have organized the exchange, allocation and use of resources. It aims to explain why some societies do well in preventing or remedying disasters through these institutional arrangements and others not.
In order to do so, this project analyses four key variables: the mix of coordination systems available within that society, its degree of autarky, economic equity and political equality. The recent literature on historical and present-day disasters suggests these factors as possible causes of success or failure of institutional arrangements in their confrontation with hazards, but their discussion remains largely descriptive and they have never been systematically analyzed.
This research project offers such a systematic investigation, using rural societies in Western Europe in the period 1300-1800 - with their variety of socio-economic characteristics - as a testing ground. The historical perspective enables us to compare widely differing cases, also over the long run, and to test for the variables chosen, in order to isolate the determining factors in the resilience of different societies. By using the opportunities offered by history in this way, we will increase our insight into the relative performance of societies and gain a better understanding of a critical determinant of human wellbeing.
Max ERC Funding
2 227 326 €
Duration
Start date: 2014-03-01, End date: 2019-02-28
Project acronym COS
Project "The Cult of Saints: a christendom-wide study of its origins, spread and development"
Researcher (PI) Bryan Ward-Perkins
Host Institution (HI) THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF OXFORD
Country United Kingdom
Call Details Advanced Grant (AdG), SH6, ERC-2013-ADG
Summary "An investigation of the origins and development of a central feature of late-antique, medieval and modern culture: the belief that dead saints can act as mediators between a distant God and humankind, and that they are active on earth in many different ways (such as healing the sick, punishing the irreverent, or even controlling the weather).
The project will investigate the emergence of this belief by systematically collecting all the available evidence - across several academic disciplines and six linguistic cultures (Latin, Greek, Syriac, Coptic, Armenian and Georgian), from the first stirrings of the phenomenon in the third century until around the year 700, by which time the cult of saints was fully developed and firmly rooted throughout the Christian world, from Ireland to Iran.
The work will be done by a team of researchers (under expert supervision for four of the eastern languages), closely co-ordinated by the PI. The project will operate concurrently at two levels. The individual researchers will produce free-standing regional studies on aspects of the cult of saints that are essential to the wider project, but at present under-researched. While doing this, they will collect the full range of evidence from their regions within a single searchable database. This will provide the basis for a christendom-wide monograph on the emergence of the cult of saints authored by the PI, and also the context essential to give breadth and depth to the regional studies.
For the first time it will be possible to tell the history of the emergence of the cult of saints across the full geographical and cultural range of early Christendom. Of great importance in itself, this will also link, and thereby enhance, the many pre-existing works of scholarship on aspects of the cult of saints.
The ‘Cult of Saints’ will result in a major summative monograph, a comprehensive international conference, a series of ground-breaking regional studies, and a freely-available database."
Summary
"An investigation of the origins and development of a central feature of late-antique, medieval and modern culture: the belief that dead saints can act as mediators between a distant God and humankind, and that they are active on earth in many different ways (such as healing the sick, punishing the irreverent, or even controlling the weather).
The project will investigate the emergence of this belief by systematically collecting all the available evidence - across several academic disciplines and six linguistic cultures (Latin, Greek, Syriac, Coptic, Armenian and Georgian), from the first stirrings of the phenomenon in the third century until around the year 700, by which time the cult of saints was fully developed and firmly rooted throughout the Christian world, from Ireland to Iran.
The work will be done by a team of researchers (under expert supervision for four of the eastern languages), closely co-ordinated by the PI. The project will operate concurrently at two levels. The individual researchers will produce free-standing regional studies on aspects of the cult of saints that are essential to the wider project, but at present under-researched. While doing this, they will collect the full range of evidence from their regions within a single searchable database. This will provide the basis for a christendom-wide monograph on the emergence of the cult of saints authored by the PI, and also the context essential to give breadth and depth to the regional studies.
For the first time it will be possible to tell the history of the emergence of the cult of saints across the full geographical and cultural range of early Christendom. Of great importance in itself, this will also link, and thereby enhance, the many pre-existing works of scholarship on aspects of the cult of saints.
The ‘Cult of Saints’ will result in a major summative monograph, a comprehensive international conference, a series of ground-breaking regional studies, and a freely-available database."
Max ERC Funding
2 499 240 €
Duration
Start date: 2014-01-01, End date: 2018-12-31
