Data-Gouv-ML/pcri-informations-sur-les-projets-laureats huggingface dataset:
Tidal Demonstration for Energy Scheme (TIDES)

Framework: FP7 — Cooperation
Programme: Energy
Destination: Renewable electricity generation
Action type: Collaborative project
Countries involved: Ireland,Sweden,United Kingdom,United Kingdom,Ireland,United Kingdom,Belgium
Call:  (FP7-ENERGY-2012-2, 2012)
Start date: 2013-04-15
End date: 2018-04-14
Duration (months): 60.0
Total project cost (EUR): 13432209.8
EU funding (EUR): 8002735.15
Participants: 7
Project status: CLOSED

A full tidal array has not been installed anywhere, commercially to date. A number of the leading turbine manufacturers have part or full scale working prototypes which are under-going testing in various sites the majority of which are enclosed in semi-test environments. In order to move this nascent technology into the commercial arena and expedite market deployment, it is necessary to establish an array of turbines in one site to verify the performance capability and environmental characteristics of a full array. The demonstration will also enable developers to make critical investment decisions based on the cost to market of deploying the technology, and manufacturers to establish likely interaction effects between machines which will inform their design. As with other technologies, notably wind, the manufacture and installation costs will drop as the technology matures. The SPV will deliver one of the first operating tidal energy farms, located 2km off the coast of Antrim in Northern Ireland by 2017. Critically the Fair Head site is a scalable (to 100MW) open sea real site representative of a significant percentage of the near future exploitable tidal resource. The TIDES project will produce many specific results which will benefit the industry as a whole:- 1. Prove the energy conversion potential of a tidal array in a real sea environment. 2. Develop viable financial models to support commercial exploitation. 3. Identify potential future energy cost reduction techniques including innovative installation methodologies. 4. De-risk tidal energy projects and make them more bankable. The S&T objectives include addressing technical problems associated with the environment, demonstrating the deployment of an array, environmental assessment, generation and yield assessment. The proposed consortium has an appropriate and replicable site, market leading technology and sufficient financial backing to ensure the project is built.

Keywords: energy,tidal,power,renewable,grid,electricity,ocean,connectivity
Demonstration of more reliable innovative designs on a 2MW Wind turbine (WINDTRUST)

Framework: FP7 — Cooperation
Programme: Energy
Destination: Renewable electricity generation
Action type: Collaborative project
Countries involved: Spain,Denmark,Germany,Denmark,United Kingdom,Greece,United Kingdom,Belgium
Call:  (FP7-ENERGY-2012-2, 2012)
Start date: 2013-09-01
End date: 2016-08-31
Duration (months): 36.0
Total project cost (EUR): 11483537.4
EU funding (EUR): 6247264.3
Participants: 9
Project status: CLOSED

The objective of the WINDTRUST project is to demonstrate the technical and economic feasibility of innovative and more reliable solutions for multi MW wind turbines in order to improve the competitiveness of wind energy technologies. The selected components of the wind turbine are the rotor (specifically the blade), power electronics (specifically the converter) and Control and communication system (specifically the controller system). The project will demonstrate the reliability of the proposed solution on an onshore 2MW prototype turbine and will also extrapolate conclusion to larger wind turbine and off-shore locations. To reach such objectives, the project will join a 9 partnership European consortium, led by key industrial stakeholders of the wind turbine industry, GAMESA, LM and SEMIKRON, in cooperation with a group of R&D centres and SMEs with complementary skills and expertise to support design, testing and dissemination activities. The project partners are strongly committed to work together and to include all the necessary resources to deal with the scheduled project work plan.

Keywords: multi-mw wind turbine,reliability,cost of energy,demonstration
Systems analysis of pancreatic tumor cell phenotype dependence on the spatial regulation of oncogenic Ras signaling (SPATONC)

Framework: FP7 — Ideas
Programme: European Research Council
Theme: European research council
Destination: Advanced grants
Action type: Support for frontier research (ERC)
Panel: Cellular and Developmental Biology
Countries involved: Germany
Call:  (ERC-2012-ADG_20120314, 2012)
Start date: 2013-04-01
End date: 2018-03-31
Duration (months): 60.0
Total project cost (EUR): 2442400.0
EU funding (EUR): 2442400.0
Participants: 1
Project status: CLOSED

Over the last several years me and my team have uncovered the reaction cycles that dynamically maintain the spatial organization of the Ras proto-oncogene products on cellular membranes. The quantitative microscopic imaging approaches in close iteration with computational systems dynamic analysis that we developed in the course of these studies were key to understand these reaction systems which were termed “spatial cycles”. Recent exciting results from my laboratory show that interference with spatial cycles, that normally maintain all major Ras isoforms on the plasma membrane, affects the signaling output from oncogenic Ras and thereby inhibits the growth and survival of KRas transformed murine pancreatic cancer cells. The purpose of the proposed multi-disciplinary project is to quantitatively assess in situ how the spatial organization of KRas affects the state of intracellular growth factor signaling networks and thereby maintains the phenotype of murine pancreatic cancer cells. A major objective that integrates the multiple levels of research in this proposal is whether and how the pharmacological inhibition of spatial cycles affects the growth of oncogenic KRas driven pancreatic tumors.

Keywords: oncogenic signaling,spatial organization,microscopic imaging,network biology,phenotypic response,cancer
The vascular stem cell niche and the neurovascular unit (VASNICHE)

Framework: FP7 — Ideas
Programme: European Research Council
Theme: European research council
Destination: Advanced grants
Action type: Support for frontier research (ERC)
Panel: Physiology, Pathophysiology and Endocrinology
Countries involved: Israel
Call:  (ERC-2012-ADG_20120314, 2012)
Start date: 2013-03-01
End date: 2018-02-28
Duration (months): 60.0
Total project cost (EUR): 2499980.0
EU funding (EUR): 2499980.0
Participants: 1
Project status: CLOSED

Recent evidence suggests that VEGF and the vasculature play multiple roles in organ homeostasis, functions extending far beyond their traditional roles in tissue perfusion. The proposed study represents a vascular-centred approach to the neurovascular unit thriving to gain further insights on the many ways by which blood vessels may affect proper brain functioning. Major focus is on the vascular stem cell niche, i.e. the contention that blood vessels are a key component of adult stem cell niches, including a niche securing proper function of neuronal stem cells (NSCs). Further insights on the niche are also critical for contemplated implementation of stem-cell based therapy. In this multidisciplinary study combining the fields of vascular biology, neurobiology, stem cell biology, and aging research, we harness unique transgenic methodologies to conditionally manipulate (via VEGF) the vasculature within the stem cell niches. We provide a first compelling proof that blood vessels at the niche indeed control stem cells properties and behaviour, evidenced by showing that mere expansion of the niche vasculature and independently of VEGF) increases dramatically adult hippocampal neurogenesis, a process known to be associated with improved cognitive performance. We will determine what aspects of stem cell biology are controlled by juxtaposed, directly contacting blood vessels and will identify signalling systems mediating the vascular/stem cell cross-talk. Adult neurogenesis is known to rapidly decline with age and ways to sustain the process are highly desired. We hypothesize and, in fact, provide initial evidence that expanding and 'rejuvenating' the niche vasculature can override the natural age-dependent decline of adult neurogenesis. Proposed experiments will extend this exciting finding and thrive to uncover the underlying mechanisms.

Keywords: neurovascular,vegf,stem cell vascular niche,neurogenesis,aging
Strengthening adaptive immunity via innate immunity: enhancing the CD8 T cell response by using the NKG2D ligand expressed in a herpesvirus vector (STADVINN)

Framework: FP7 — Ideas
Programme: European Research Council
Theme: European research council
Destination: Advanced grants
Action type: Support for frontier research (ERC)
Panel: Immunity and infection
Countries involved: Croatia
Call:  (ERC-2012-ADG_20120314, 2012)
Start date: 2013-05-01
End date: 2018-04-30
Duration (months): 60.0
Total project cost (EUR): 1754897.0
EU funding (EUR): 1754897.0
Participants: 1
Project status: CLOSED

CD8+ T cells play a key role in the control of infections by intracellular pathogens. Recently, several top-notch studies provided ample evidence that NK cells are important in the regulation of CD8+ T cell response. NKG2D is an activating NK cell receptor which plays a role in the adaptive immune response by co-stimulating CD8+ T cells. Due to unique pattern of immune response, live attenuated CMVs are attractive candidates as vaccine vectors for a number of clinically relevant infections. The main idea behind this project stems from our preliminary data which suggest that a recombinant CMV vector expressing NKG2D ligand has a tremendous potential for subverting viral immunoevasion and boosting the efficiency of CD8 T cell response. During the project we plan to systematically investigate the impact of all major innate immunity players on the CD8+ T cell response. A special focus will be given in obtaining new knowledge on the maintenance of memory CD8+ T cells during latent infection. This study will also provide novel insights on the role of NKG2D in both NK and T cell immunity. In order to test our hypothesis in vivo, we will employ state-of-the-art technology used in herpesvirus genetics coupled with high-end immune monitoring. Ultimately, we will translate our results to a human CMV vector, in order to gauge the impact of NKG2D signaling on immune response in a humanized mouse model. We believe that the significance of the proposed study is enormous since stimulating CD8+ T cells has been widely recognized as a method of choice for vaccine development. There are relatively large number of pathogens for which the immunity acquired post-infection does not fully shelter against re-infection and disease. Therefore, we are in a desperate need for vaccines which offer superior protection compared to the one following natural infection. This study will provide groundbreaking information which will set the stage for the development of new vaccines and vaccine vectors.

Keywords: nk cells,cd8 t cells,nkg2d,protective immunity
The nanomechanical mechanism of exocytotic fusion pore formation (THE FUSION MACHINE)

Framework: FP7 — Ideas
Programme: European Research Council
Theme: European research council
Destination: Advanced grants
Action type: Support for frontier research (ERC)
Panel: Neurosciences and neural disorders
Countries involved: Germany
Call:  (ERC-2012-ADG_20120314, 2012)
Start date: 2013-04-01
End date: 2018-03-31
Duration (months): 60.0
Total project cost (EUR): 2165200.0
EU funding (EUR): 2165200.0
Participants: 1
Project status: CLOSED

Cells release neurotransmitters, hormones and other compounds stored in secretory vesicles by a process called exocytosis. In this process, the molecules are released upon stimulation by a nanomachine forming a fusion pore that connects the vesicular lumen to the extracellular space. Similar fusion events are also essential for intracellular transport mechanisms and virus-induced fusion. Here I propose a multidisciplinary approach using highly innovative techniques to determine the nanomechanical mechanism of fusion pore formation. The proposal is based on the hypothesis that the vesicle fusion nanomachine is formed by the mechanical interactions of the SNARE proteins synaptobrevin, syntaxin, and SNAP-25 and that the fusion pore is opened by intra-membrane movement of the transmembrane domains. I will combine fluorescence resonance energy transfer microscopy with detection of individual fusion events using microfabricated electrochemical detector arrays to demonstrate that fusion pore formation is produced directly by a conformational change in the SNARE complex. I will estimate the energies that are needed to pull the synaptobrevin C terminus into the hydrophobic membrane core and the forces that are generated by the SNARE complex for wild type and a set of specific mutations using molecular dynamics simulations. I will determine how these energies and forces relate to inhibition and facilitation of experimentally observed fusion, performing patch clamp capacitance measurements of vesicle fusion in chromaffin cells expressing wild type and mutated SNARE proteins. Based on these results I will develop a detailed picture of the molecular steps, the energies, and the forces exerted by the molecular nanomachine of fusion pore formation and will ultimately generate a molecular movie of this fundamental biological process. Understanding cellular and viral fusion events will likely lead to novel treatments from spasms and neurodegeneration to cancer and infectious disease

Keywords: transmitter release,membrane fusion,molecular dynamics,patch clamp
LEARNING TO SURVIVE IN A CHANGING WORLD (EARLYLIFE)

Framework: FP7 — Ideas
Programme: European Research Council
Theme: European research council
Destination: Advanced grants
Action type: Support for frontier research (ERC)
Panel: Evolutionary, population and environmental biology
Countries involved: France
Call:  (ERC-2012-ADG_20120314, 2012)
Start date: 2013-03-01
End date: 2018-08-31
Duration (months): 66.0
Total project cost (EUR): 2484000.0
EU funding (EUR): 2484000.0
Participants: 1
Project status: CLOSED

This project has the ambitious goal of providing new groundbreaking information on a poorly known, yet critical stage of the life of any animal, the EARLYLIFE. The originality and novelty of EARLYLIFE is to combine two fields in ecology generally considered independently: foraging ecology and demography.With the data obtained for a range of marine predators with contrasted life histories I will be in a position to test several long lasting hypotheses in ecology, in particular on the causes of mortality of young animals, learning abilities, as well as on the significance of delayed maturity in long lived animals. Ultimately the project will allow a robust evaluation of the potential effects of global changes on young animals, and its consequences for population dynamics and conservation of marine air breathing predators. I will carry out EARLYLIFE in three steps, with my CNRS research group that brings together top researchers with complementary specialties and skills in animal tracking, foraging ecology, demographic modeling. First, using newly developed state of the art developments in bio-telemetry, bio-logging and biochemical markers, I will study for the first time the foraging ecology (movement, habitat, energetic, diet) of 13 species of seabirds and seals during their first years of life at sea after independence. This will allow estimating critical parameters such as the timing and causes of death, the spatial variation in mortality, as well as the extent of improvement in foraging skills at early stages. Second I will model the ontogenic changes occurring during the early stage of life, and contrast them with the foraging abilities of mature animals using our tracking data base. Finally, using our unique long term demographic data base I will examine to what extent, and how, environmental variability affects juvenile mortality, and models the potential effects of climate change and human activities on population dynamics.
DEsigning new Paths in The differentiation Hyperspace (DEPTH)

Framework: FP7 — Ideas
Programme: European Research Council
Theme: European research council
Destination: Advanced grants
Action type: Support for frontier research (ERC)
Panel: Genetics, Genomics, Bioinformatics and Systems Biology
Countries involved: Italy
Call:  (ERC-2012-ADG_20120314, 2012)
Start date: 2013-04-01
End date: 2018-09-30
Duration (months): 66.0
Total project cost (EUR): 2639804.0
EU funding (EUR): 2639804.0
Participants: 1
Project status: CLOSED

The adult human organism contains heterogeneous reservoirs of pluripotent stem cells characterized by a diversified differentiation potential. Understanding their biology at a system level would advance our ability to selectively activate and control their differentiation potential. Aside from the basic implications this would represent a substantial progress in regenerative medicine by providing a rational framework for using small molecules to control cell trans-determination and reprogramming. Here we propose a combined experimental and modelling approach to assemble a predictive model of mesoderm stem cell differentiation. Different cell states are identified by a vector in the differentiation hyperspace, the coordinates of the vector being the activation levels of a large number of nodes of a logic model linking the cell signalling network to the transcription regulatory network. The premise of this proposal is that differentiation is equivalent to rewiring the cell regulatory network as a consequence of induced perturbation of the gene expression program. This process can be rationally controlled by perturbing specific nodes of the signalling network that in turn control transcription factor activation. We will develop this novel strategy using the mesoangioblast ex vivo differentiation system. Mesoangioblasts are one of the many different types of mesoderm stem/progenitor cells that exhibit myogenic potential. Ex vivo, they readily differentiate into striated muscle. However, under appropriate conditions they can also differentiate, into smooth muscle and adipocytes, albeit less efficiently. We will start by assembling, training and optimizing different predictive models for the undifferentiated mesoangioblast. Next by a combination of experiments and modelling approaches we will learn how, by perturbing the signalling models with different inhibitors and activators we can rewire the cell networks to induce trans-determination or reprogramming.

Keywords: high content screening,perturbation analysis
Eco-evolutionary dynamics of community self-organization through ontogenetic asymmetry (ECOEVODEVO)

Framework: FP7 — Ideas
Programme: European Research Council
Theme: European research council
Destination: Advanced grants
Action type: Support for frontier research (ERC)
Panel: Evolutionary, population and environmental biology
Countries involved: Netherlands
Call:  (ERC-2012-ADG_20120314, 2012)
Start date: 2013-06-01
End date: 2018-05-31
Duration (months): 60.0
Total project cost (EUR): 1779634.0
EU funding (EUR): 1779634.0
Participants: 1
Project status: CLOSED

Classical theory on community ecology models dynamics as interplay between top-down and bottom-up effects of population abundances only and considers population composition irrelevant. It ignores food-dependent ontogenetic development, in particular somatic growth, which characterizes most species and uniquely distinguishes organisms from fundamental units in physical or chemical multi-particle systems. Similarly, evolutionary theory has ignored the potential population feedback on food-dependent ontogenetic development. Classic theory has been shown to apply in case of ontogenetic symmetry in energetics, when dynamics of population abundance and composition are independent. Ontogenetic symmetry stipulates that mass-specific rates of net biomass turnover are independent of individual body size. Ontogenetic symmetry only represents a limiting, structurally unstable case, separating two stable domains with ontogenetic asymmetry in energetics, when either juveniles or adults have higher mass-specific net-biomass production. In case of ontogenetic asymmetry the dynamics of population abundance and composition become intimately linked, ultimately resulting in the emergence of positive feedbacks between densities of predators and their main prey. This transforms consumer-resource interactions into indivisible units, whose behavior can no longer be predicted from its constituting parts (the species). Ontogenetic asymmetry in energetics is thus a potent driver of self-organization in ecological communities. This research project aims at unraveling the eco-evolutionary dynamics of ontogenetic asymmetry in energetics, focusing on (1) the likelihood that ontogenetic asymmetry in energetics evolves as mechanism of self-organization in ecological communities, (2) the conditions that may have promoted or inhibited this evolution and (3) the extent to which ontogenetic asymmetry in energetics has contributed to the diversity of life and the development of complex life cycles.

Keywords: ontogenetic development,ontogenetic niche shifts,complex life cycles,growth in body size,population size structure,multi-species communities,eco-evolutionary dynamics,life history evolution
Molecular Plasticity of Inhibitory Synapses (PLASTINHIB)

Framework: FP7 — Ideas
Programme: European Research Council
Theme: European research council
Destination: Advanced grants
Action type: Support for frontier research (ERC)
Panel: Neurosciences and neural disorders
Countries involved: France
Call:  (ERC-2012-ADG_20120314, 2012)
Start date: 2013-05-01
End date: 2018-04-30
Duration (months): 60.0
Total project cost (EUR): 2429640.0
EU funding (EUR): 2429640.0
Participants: 1
Project status: CLOSED

Neurons maintain a precise organization of their membrane into sub-domains with specific molecular compositions, together with the capacity to change it in response to plasticity events. However, as seen with the tracking of single molecules, receptors in the plasma membrane continuously exchange between synaptic and extrasynaptic locations. Interactions between neurotransmitter receptors and postsynaptic scaffold proteins control the distribution of receptors at synaptic and extrasynaptic sites. This mechanism is modulated at many levels, and contributes to the regulation of the synaptic strength of excitatory and inhibitory synapses in physiological and pathological conditions. This project will address the gap in knowledge between the molecular instability of randomly diffusing receptors and the stable functional architecture of synapses. It will provide new insights into fundamental issues related to the cellular basis of neuronal information processing. Focusing on inhibitory Glycine and GABAA receptors (GlyR, GABAAR) I will have 3 main objectives: Objective 1: to determine key aspects of the relationship between the synapse microstructure, molecular dynamics, and molecular interactions. Objective 2: characterize the mechanisms by which receptor diffusion contributes to the adaptation of inhibitory synapses to excitatory activity. Objective 3: understand how non-neuronal glial cells modulate inhibitory receptor diffusion-trapping and ultimately impact on neuronal excitability. For this research, single molecule methods and super-resolution microscopy give access to molecular dynamics (tracking), the morphology at high resolution, and quantitative data such as dwell times and absolute numbers of molecules, thus identifying new cellular mechanisms accounting for the regulation of inhibitory synaptic strength.

Keywords: molecular imaging,synapse,inhibition,plasticity