Data-Gouv-ML/pcri-informations-sur-les-projets-laureats huggingface dataset:
Distributed Cloud product specification and supply chain manufacturing execution infrastructure (MANUCLOUD)

Framework: FP7 — Cooperation
Programme: Nanosciences, Nanotechnologies, Materials and new Production Technologies - NMP
Destination: New production
Action type: Collaborative project
Countries involved: Germany,Germany,Germany,Hungary,United Kingdom,Austria,Austria,Germany
Call:  (FP7-2010-NMP-ICT-FoF, 2010)
Start date: 2010-08-01
End date: 2013-07-31
Duration (months): 36.0
Total project cost (EUR): 5102913.2
EU funding (EUR): 3593945.0
Participants: 9
Project status: CLOSED

The objective of the ManuCloud project is the development of the service-oriented IT infrastructure “ManuCloud” as basis for the next level of manufacturing networks by enabling inter-enterprise integration down to shop floor level. R&amp;D Approach The ManuCloud IT infrastructure will consist of a set of services providing knowledge-based product specification based on the actual available manufacturing capabilities of the network, inter- enterprise data exchange, and inter-enterprise quality assurance. Additionally a highly agile intra-fab integration environment capable to automatically propagate manufacturing capabilities and manufacturing process data to the ManuCloud infrastructure will be developed. ManuCloud aims at bringing impact in the broad field of industrial manufacturing. Therefore ManuCloud does not targeting a specific industry, the concept will be applicable to all types of networked manufacturing. Impact and relevance of the project for a specific use case, but also in general, will be demonstrated by an industrial proof-of-concept. Industrial relevance is guaranteed by involving a strong industrial European key player, the Robert Bosch AG, as driver of the development and as end-user . The company has lately entered the photovoltaic industry and is actually investing in multiple companies in this domain. Several manufactures of innovative organic semiconductors are taking part in the project and will serve as testbed for the proof-of-concept ACP-IT and nxtControl will provide their knowledge in shop floor IT technologies. The scientific relevance is ensured by bringing together leading European institutes from the manufacturing engineering and automation, the organic semiconductor manufacturing, the supply chain management, the knowledge-based product specification domain and their implementation in applications.

Keywords: photovoltaic,organic lightning,intgrated manufacturing network
Syndromic approach to Neglected Infectious Diseases (NID) at primary health care level: an international collaboration on integrated diagnostic-treatment platforms (NIDIAG)

Framework: FP7 — Cooperation
Programme: Health
Destination: Translating research for human health
Action type: Collaborative project
Countries involved: Belgium,France,Switzerland,United Kingdom,Congo, The Democratic Republic of the,Indonesia,Mali,Sudan,Belgium,India,Nepal,United States
Call:  (FP7-HEALTH-2010-single-stage, 2010)
Start date: 2010-11-01
End date: 2016-04-30
Duration (months): 66.0
Total project cost (EUR): 6446506.3
EU funding (EUR): 5000000.0
Participants: 13
Project status: CLOSED

Neglected Infectious Diseases (NID) such as trypanosomiasis, leishmaniasis, schistosomiasis and soil-transmitted helminthiasis receive less than 5% of the global investment for tropical diseases research. Clinical praxis in disease-endemic countries (DEC) is rarely evidence based and does not make use of the latest innovations in diagnostic technology. NID–related research on diagnostics is particularly underfunded, and diagnostic tools are lacking for a number of NID. The aim of this proposal is to bridge the gap between existing technological innovation in diagnostics and clinical care practice for NID in resource-poor settings. The specific objectives are to develop simple, cost-effective diagnosis-treatment algorithms for three NID-related clinical syndromes: the persistent fever, the neurological and the digestive syndromes. Evidence-based algorithms for the primary care level will be designed with a patient-centred approach, following guidance from DEC stakeholders and making the best possible use of existing assays and treatments. Relevant diagnostic technology and diagnostic platforms will be introduced according to the specific epidemiological contexts in Africa and South-Asia. The research consortium brings together a network of clinical epidemiologists, a diagnostics development group, several partners from academia and SMEs. The consortium further includes workpackages on reference laboratory, economic evaluation, quality assurance and translation to policy. By developing accurate and affordable diagnostic platforms and by optimizing diagnostic-treatment algorithms, this project will rationalise treatment use, circumvent progression to severe presentations and thereby reduce NID morbidity/mortality and hinder the emergence of resistances. The project will result in two main deliverables: policy recommendation for health authorities in DEC, and a series of innovative diagnostic platforms.

Keywords: neglected infectious diseases,diagnostic,syndromic,health,developing countries,primary health care,clinical algorithms,icpc
Molecular mechanisms of autophagosome formation (MMAF)

Framework: FP7 — Ideas
Programme: European Research Council
Theme: European research council
Destination: Starting grants
Action type: Support for frontier research (ERC)
Panel: Cellular and Developmental Biology
Countries involved: Austria
Call:  (ERC-2010-StG_20091118, 2010)
Start date: 2011-03-01
End date: 2016-02-29
Duration (months): 60.0
Total project cost (EUR): 1163832.0
EU funding (EUR): 1163832.0
Participants: 1
Project status: CLOSED

During autophagy initially small double membrane-bound structures expand and adopt cup-like shapes. These cup-shaped structures fuse at their rims to give rise to autophagosomes within which cytoplasmic material is enclosed. Subsequently autophagosomes fuse with endosomes and lysosomes and the content and the inner membrane are degraded. Autophagy serves to recycle essential building blocks during starvation, to degrade damaged organelles, to clear cells of protein aggregates and to kill intracellular microorganisms. Little is known about the mechanisms by which cells bend and remodel membranes into autophagosomes. The action of a complex containing type III PI3K activity is essential for the initiation of autophagosome formation. During expansion of the initial double membrane bound structure the Atg8 and Atg12 conjugation systems play important roles. A further protein that is essential for autophagosome formation is the transmembrane protein Atg9. We will investigate the impact of individual PI3K complex subunits, the Atg8 and Atg12 conjugation systems and Atg9 on membrane morphology in vitro. We will analyse membrane shape changes and micro-domain formation using artificial small and giant liposomes by electron and light microscopy. We will introduce targeted mutations that are designed to interfere with membrane shape changes or micro-domain formation. Furthermore, where necessary, we will solve the structure of individual subunits or complexes by x-ray crystallography. We will further verify our in vitro findings in cell culture systems. Our results will give important insights into autophagy and organelle formation in general.

Keywords: autophagy,atg8,atg9,atg12,pi3k,membrane curvature
microRNA function in homeostatic plasticity in the mammalian brain (NEUROMIR)

Framework: FP7 — Ideas
Programme: European Research Council
Theme: European research council
Destination: Starting grants
Action type: Support for frontier research (ERC)
Panel: Neurosciences and neural disorders
Countries involved: Germany
Call:  (ERC-2010-StG_20091118, 2010)
Start date: 2010-10-01
End date: 2015-09-30
Duration (months): 60.0
Total project cost (EUR): 1452720.0
EU funding (EUR): 1452720.0
Participants: 1
Project status: CLOSED

Neural circuits are constantly modified in response to experience and changes in the environment, a phenomenon known as plasticity. While classical Hebbian plasticity is crucial to encode information, a different set of mechanisms, commonly referred to as homeostatic plasticity, are used by neurons to stabilize their activity in the face of perturbations that alter excitability. Homeostatic plasticity plays a critical role during activity-dependent development of neural circuits, and it is frequently distorted in common psychiatric disorders, including autism, mental retardation and schizophrenia. However, in contrast to Hebbian plasticity, the molecular underpinnings of homeostatic plasticity are largely unknown. We hypothesize that microRNAs (miRNAs), a recently discovered class of regulatory small non-coding RNAs, might have a prominent role in homeostatic plasticity by fine-tuning the expression of critical synaptic proteins. Using a large activity-regulated miRNA cluster as a paradigm, we plan to identify functionally important miRNAs during homeostatic plasticity in vitro and in vivo, to elucidate their mode of regulation and to determine the relevance of perturbed expression of these miRNAs for psychiatric disease. Towards these aims, we plan to use a battery of innovative approaches, including miRNA loss-of-function screening, biological target discovery, time-lapse fluorescence imaging of miRNA activity, genetic manipulation of mouse models of psychiatric disease and systemic brain delivery of miRNA mimics. This project has far reaching implications for our understanding of homeostatic mechanisms in brain development and disease, and could open up new avenues for the treatment of prominent psychiatric disorders that arise from defective neural homeostasis.

Keywords: microrna,local translation,synaptic plasticity,homeostasis,schizophrenia
Neural and computational determinants of left cerebral dominance in speech and language (COMPUSLANG)

Framework: FP7 — Ideas
Programme: European Research Council
Theme: European research council
Destination: Starting grants
Action type: Support for frontier research (ERC)
Panel: Neurosciences and neural disorders
Countries involved: Switzerland,France
Call:  (ERC-2010-StG_20091118, 2010)
Start date: 2011-02-01
End date: 2016-01-31
Duration (months): 60.0
Total project cost (EUR): 1500000.0
EU funding (EUR): 1500000.0
Participants: 3
Project status: CLOSED

More than a century after Wernicke and Broca established that speech perception and production rely on temporal and prefrontal cortices of the left brain hemisphere, the biological determinants for this organization are still unknown. While functional neuroanatomy has been described in great detail, the neuroscience of language still lacks a physiologically plausible model of the neuro-computational mechanisms for coding and decoding of speech acoustic signal. We propose to fill this gap by testing the biological validity and exploring the computational implications of one promising proposal, the Asymmetric Sampling in Time theory. AST assumes that speech signals are analysed in parallel at multiple timescales and that these timescales differ between left and right cerebral hemispheres. This theory is original and provocative as it implies that a single computational difference, distinct integration windows in right and left auditory cortices could be sufficient to explain why speech is preferentially processed by the left brain, and possible even why the human brain has evolved toward such an asymmetric functional organization. Our proposal has four goals: 1/ to validate, invalidate or amend AST on the basis of physiological experiments in healthy human subjects including functional magnetic resonance imaging (fMRI), combined electroencephalography (EEG) and fMRI, magnetoencephalography (MEG) and subdural electrocorticography (EcoG), 2/ to use computational modeling to probe those aspects of the theory that currently remain inaccessible to empirical testing (evaluation, assessment), 3/ to apply AST to binaural artificial hearing with cochlear implants, 4/ to test for disorders of auditory sampling in autism and dyslexia, two language neurodevelopmental pathologies in which a genetic basis implicates the physiological underpinnings of AST, and 5/ to assess potential generalisation of AST to linguistic action in the context of speech production.

Keywords: speech,language,theory
Efficient and accurate simulation techniques for free energies, enthalpies and entropies (EASTFE3)

Framework: FP7 — Ideas
Programme: European Research Council
Theme: European research council
Destination: Starting grants
Action type: Support for frontier research (ERC)
Panel: ERC Starting Grant Interdisciplinary Panel
Countries involved: Austria
Call:  (ERC-2010-StG_20091118, 2010)
Start date: 2011-01-01
End date: 2015-12-31
Duration (months): 60.0
Total project cost (EUR): 1485615.0
EU funding (EUR): 1485615.0
Participants: 1
Project status: CLOSED

Computational, structure-based, drug design offers insight at an atomic resolution, which is commonly not attainable by experimental means. Detailed calculations on protein-ligand interactions help to rationalize and predict experimental findings. Accurate and efficient calculations of binding free energies is essential in this respect. In addition, knowledge concerning the enthalpic and entropic contributions are highly relevant to determine novel drug design strategies and to understand the underlying principles of ligand binding. Currently available methods to address ligand affinity either do not include all relevant contributions to the binding free energy, or are too computationally demanding to be applied straightforwardly. In addition, calculations on enthalpy and entropy for drug design purposes are very rare, due to the difficulty in calculating these accurately. This proposal describes the research that leads the way to new, standard applications to be used in drug design processes in academia and industry. Furthermore, we propose to investigate the enthalpic and entropic contributions to ligand binding. We define a ligand-surroundings enthalpy and entropy, which conveys more information than the experimentally accessible enthalpy and entropy of ligand binding. In support of this research, we will develop new enhanced sampling techniques which not only render the above calculations practically feasible, but which will also find their application in related research questions such as the protein folding problem or the elucidation of protein-protein interactions. The methods described are highly relevant for the pharmaceutical industry, where currently available computational approaches are insufficient to answer the questions of todays drug discovery programmes.

Keywords: free energy calculations,molecular simulation
Immune Functions of Myeloid Syk-coupled C-type Lectin Receptors Sensing Necrosis (CLR SENSING NECROSIS)

Framework: FP7 — Ideas
Programme: European Research Council
Theme: European research council
Destination: Starting grants
Action type: Support for frontier research (ERC)
Panel: Immunity and infection
Countries involved: Spain
Call:  (ERC-2010-StG_20091118, 2010)
Start date: 2010-12-01
End date: 2016-08-31
Duration (months): 69.0
Total project cost (EUR): 1297671.0
EU funding (EUR): 1297671.0
Participants: 1
Project status: CLOSED

Necrosis triggers an inflammatory response driven by macrophages that normally contributes to tissue repair but, under certain conditions, can induce a state of chronic inflammation that forms the basis of many diseases. In addition, dendritic cell (DC)-mediated presentation of antigens from necrotic cells can trigger adaptive immunity in infection-free situations, such as autoimmunity or therapy-induced tumour rejection. Recently, we and others have identified the myeloid C-type lectin receptors (CLRs) CLEC9A (DNGR-1), in DC, and Mincle, in macrophages, as receptors for necrotic cells that can signal via the Syk kinase. Previous studies on similar Syk-coupled CLRs showed that Dectin-1 and Dectin-2 can induce innate and adaptive immune responses. We thus hypothesise that recognition of cell death by myeloid Syk-coupled CLRs is at the root of immune pathologies associated with accumulation of dead cells. The overall objective of this proposal is to investigate necrosis sensing by myeloid cells as a trigger of immunity and to study the underlying molecular mechanisms. Our first goal is to characterise signalling and gene induction via CLEC9A as a model necrosis receptor in DCs. Second, we will investigate the role of myeloid Syk-coupled necrosis-sensing CLRs in animal models of atherosclerosis, lupus and immunity to chemotherapy-treated tumours. Our preliminary data suggest that additional receptors can couple necrosis recognition to the Syk pathway in DC; thus, our third aim is to identify novel myeloid Syk-coupled receptors for necrotic cells. Characterisation of the outcomes of sensing necrosis by myeloid Syk-coupled receptors and their effect on the proposed pathologies promises to identify new mechanisms and targets for the treatment of these diseases.

Keywords: necrosis dendritic-cell macrophage c-type-lectin syk lupus atherosclerosis tumors danger
Crimean Congo Hemorrhagic Fever; Modern Approaches to Diagnostics, Surveillance, Prevention, Therapy and Preparedness. (CCH FEVER)

Framework: FP7 — Cooperation
Programme: Health
Destination: Translating research for human health
Action type: Collaborative project
Countries involved: Sweden,France,Germany,Greece,Belgium,Türkiye,Albania,Bulgaria,South Africa,Belgium,Slovenia,United States,Israel,Germany,United Kingdom,Sweden
Call:  (FP7-HEALTH-2010-single-stage, 2010)
Start date: 2010-10-01
End date: 2015-03-31
Duration (months): 54.0
Total project cost (EUR): 3849249.25
EU funding (EUR): 3000000.0
Participants: 17
Project status: CLOSED

Over the last years, large outbreaks of Crimean Congo Hemorrhagic fever virus (CCHFV) in several European countries and neighbouring areas are on the rise. This disease poses a great threat to public health due to its high mortality rate, modes of transmission and geographical distribution. Climate changes and observation of the CCHFV vector in central Europe alarm the European community as we cannot exclude that future outbreaks will take place in non-endemic area of Europe. To date, there is no vaccine available and no selective antiviral drug for the management of the disease. The general knowledge of migration, epidemiology, re-assortment and recombination of the virus is very limited. To fill these gaps, the CCH Fever project proposes to create a multidisciplinary collaborative research environment by bringing together selected competitive advantages such as: operative capacity with appropriate high security research facilities, reference centers and clinical samples from endemic areas and an international network of experienced researchers. This multidisciplinary research consortium will facilitate the progress in several key research areas of the field. This program will mainly focus on (i) developing sensitive and biosafe state-of-art diagnostic tools for CCHFV, (ii) gathering the forces and resources in Europe to build a Biobank of clinical samples, (iii) building a comprehensive database consisting in clinical, laboratory and surveillance data, (iv) taking advantage of unique and state-of art tools to progress towards vaccine candidates and specific antivirals against this bio-threat and (v) disseminating the appropriate knowledge to the health care workers in endemic regions and contributing to capacity building. These achievements will provide tools for local and European public health authorities to prevent or counter future outbreaks and monitor the spread of the disease thanks to the established novel and unique tools and resources.

Keywords: crimean congo hemorrhagic fever,epidemiology,vaccine,antivirals,emerging,vlp,minireplicon
Dissecting the Central Stress Response: Bridging the Genotype-Phenotype Gap (EURO-NEUROSTRESS)

Framework: FP7 — Ideas
Programme: European Research Council
Theme: European research council
Destination: Starting grants
Action type: Support for frontier research (ERC)
Panel: Neurosciences and neural disorders
Countries involved: Israel
Call:  (ERC-2010-StG_20091118, 2010)
Start date: 2011-04-01
End date: 2016-03-31
Duration (months): 60.0
Total project cost (EUR): 1500000.0
EU funding (EUR): 1500000.0
Participants: 1
Project status: CLOSED

The biological response to stress is concerned with the maintenance of homeostasis in the presence of real or perceived challenges. This process requires numerous adaptive responses involving changes in the central nervous and neuroendocrine systems. When a situation is perceived as stressful, the brain activates many neuronal circuits linking centers involved in sensory, motor, autonomic, neuroendocrine, cognitive, and emotional functions in order to adapt to the demand. However, the details of the pathways by which the brain translates stressful stimuli into the final, integrated biological response are presently incompletely understood. Nevertheless, it is clear that dysregulation of these physiological responses to stress can have severe psychological and physiological consequences, and there is much evidence to suggest that inappropriate regulation, disproportional intensity, or chronic and/or irreversible activation of the stress response is linked to the etiology and pathophysiology of anxiety disorders and depression. Understanding the neurobiology of stress by focusing on the brain circuits and genes, which are associated with, or altered by, the stress response will provide important insights into the brain mechanisms by which stress affects psychological and physiological disorders. This is an integrated multidisciplinary project from gene to behavior using state-of-the-art moue genetics and animal models. We will employ integrated molecular, biochemical, physiological and behavioral methods, focusing on the generation of mice genetic models as an in vivo tool, in order to study the central pathways and molecular mechanisms mediating the stress response. Defining the contributions of known and novel gene products to the maintenance of stress-linked homeostasis may improve our ability to design therapeutic interventions for, and thus manage, stress-related disorders.

Keywords: neurobiology of stress,neuroendocrinology,anxiety,depression,homeostasis,allostasis,mouse genetics,crf/urocortins family