Data-Gouv-ML/pcri-informations-sur-les-projets-laureats huggingface dataset:
Measurement of the global characteristics of Relativistic Heavy Ion Collisions with the ATLAS detector at LHC. (GLOBALHIATLAS)

Framework: FP7 — People
Programme: Marie-Curie Actions
Theme: Marie Skłodowska-Curie
Destination: International Re-integration Grants
Action type: Support for training and career development of researchers (Marie Curie)
Countries involved: Israel
Call:  (FP7-PEOPLE-IRG-2008, 2008)
Start date: 2008-11-01
End date: 2012-10-31
Duration (months): 48.0
Total project cost (EUR): 100000.0
EU funding (EUR): 100000.0
Participants: 1
Project status: CLOSED

The Large Hadron Collider (LHC) soon to be commissioned at CERN opens a new energy frontier and a new era of quantitative understanding of the phase transition between hadronic nuclear matter and the Quark-Gluon Plasma. The primary and initial question for the relativistic heavy ion (RHI) program at the LHC is to establish whether the QGP formed at the LHC behaves like a strongly coupled perfect liquid as discovered at RHIC or whether it enters a new regime approaching the ideal QGP gas of weakly interacting quarks and gluons. The ATLAS detector has excellent capabilities to make a significant contribution to the LHC RHI program. This proposal deals with measurements of the centrality dependence of global characteristics of RHI collisions at LHC using the ATLAS detector. It focuses in particular on the measurements of charged particles and transverse energy pseudorapidity density, the inclusive particle spectra and the amount of the elliptic flow. These measurements can be carried out using the relatively small data samples expected in the first heavy ion runs at the LHC and they are likely to provide first answers on the nature of the matter formed in nuclear collisions at the LHC. A crucial pre-requisite for these measurements is to establish the methodology to define centrality and categorize the collisions according to the number of participating nucleons or the number of elementary collisions. Special effort will be devoted to determine centrality using the most reliable and universal approach based on the Glauber-inspired model of HI collisions and the statistics of the Negative Binomial Distribution.

Keywords: nuclear physics,relativistic heavy ions,global observables,spectra,centrality,ellipic flow
Electroactive Biofilms for Microbial Fuel Cells and Biosensors (EA-BIOFILMS)

Framework: FP7 — People
Programme: Marie-Curie Actions
Theme: Marie Skłodowska-Curie
Destination: International Re-integration Grants
Action type: Support for training and career development of researchers (Marie Curie)
Countries involved: Ireland
Call:  (FP7-PEOPLE-IRG-2008, 2008)
Start date: 2008-09-01
End date: 2012-08-31
Duration (months): 48.0
Total project cost (EUR): 100000.0
EU funding (EUR): 100000.0
Participants: 1
Project status: CLOSED

Electroactive biofilms are capable of extracellular electron transfer and are therefore relevant to geochemistry, biocatalysis, and energy production. Although electroactive biofilms are widely applied in microbial fuel cells (MFCs) for renewable electricity production, where they transfer electrons to solid electrodes, the extracellular electron transfer chain is not completely understood. This lack of knowledge is an obstacle to the development of efficient bioelectrochemical devices, such as biosensors, biocatalyst and innovative MFCs. In order to solve this problem, we will grow known electroactive biofilms in multiple electrochemical cells with potentiostat control and determine the limiting steps in the extracellular electron transfer chain. We will use a combination of electrochemical and biochemical methods to characterize the electrode-biofilm interface. We will then screen environmental samples from metal-contaminated subsurface environments using a combination of enrichment methods, metal-reduction assay and electrochemical methods. By this token, we expect to identify microbial consortia which possess higher efficiency in extracellular electron transfer. The best electroactive biofilms will be grown in MFCs. We expect to increase 10-fold the electrical power output and to make MFCs applicable to a wider range of electrical and electronic systems. Lastly, we will develop the first amperometric biosensor for environmental monitoring of acetate based on electroactive biofilms. The proposed project will produce innovative research in two strategic European areas of applied biotechnology, namely renewable energy sources and industrial biosensors. During the four years of research, we will collaborate with engineers, microbiologists, and electrochemists from research institutions across Europe and the USA. In the last part of the project we expect to patent our innovative biosensor technology and find industrial partners interested to its realization.

Keywords: biofilms,bioelectrochemistry,extracellular electron transfer,geobacter,microbial fuel cells,biosensors,bioremediation control
“Linking dendritic mRNA metabolism to neuronal functions and disorders” (DENDRITIC MRNAS)

Framework: FP7 — People
Programme: Marie-Curie Actions
Theme: Marie Skłodowska-Curie
Destination: International Re-integration Grants
Action type: Support for training and career development of researchers (Marie Curie)
Countries involved: Italy
Call:  (FP7-PEOPLE-IRG-2008, 2008)
Start date: 2009-02-01
End date: 2013-01-31
Duration (months): 48.0
Total project cost (EUR): 100000.0
EU funding (EUR): 100000.0
Participants: 1
Project status: CLOSED

Synaptogenesis and synaptic plasticity rely on protein synthesis, in particular on localized translation within dendrites. The aim of my project will focus on investigating the multiple and overlapping molecular mechanisms that contribute to fine-tuning the expression of dendritic mRNA at synapses. In my previous work, I have identified a novel regulatory pathway that involves splicing and modulates the stability and expression of a subset of neuronal and dendritic mRNAs. Prominent amongst the mRNAs analyzed in my studies is Arc, encoding a protein essential for memory consolidation and maintenance of LTP. Several approaches will be undertaken to elucidate the molecular elements controlling Arc mRNA expression: 1) In vivo biochemical isolation and characterization of the ribonucleoprotein particle associated with Arc mRNA 3’UTR region. The procedure will be designed in order to identify trans-acting factors whose binding is connected to: i) synaptic activity ii) dendritic transport iii) splicing of the mRNA. 2) To unveil the role of the identified factors, assays will be carried out in vivo and in cultured neurons, and will include: silencing via lentiviral expression of siRNAs, microscopy, electrophysiology and expression of reporter Arc genes carrying specific modifications. 3) Involvement of miRNAs and of cis-acting elements in controlling synaptic Arc protein expression will also be tested. miRNAs-dependent regulation will be verified in cultured neurons and potential coupling with other pathways of translational and mRNA stability regulation will be tested. Overall, the in vivo biochemical and functional characterization of both cis- and trans-acting factors controlling the expression of Arc mRNA, will allow a better understanding of the mechanisms underlying its modulation, and likely shed light on the pathways controlling dendritic mRNA localized expression and synaptic plasticity.

Keywords: molecular biology,molecular genetics,neurobiology,gene expression in neurons.
The molecular mechanism of the reversible switch between cell proliferation and migration. The regulatory function of the ERK pathway and ERK pathway scaffold RACK1 (PROMOTE)

Framework: FP7 — People
Programme: Marie-Curie Actions
Theme: Marie Skłodowska-Curie
Destination: International Re-integration Grants
Action type: Support for training and career development of researchers (Marie Curie)
Countries involved: Czechia
Call:  (FP7-PEOPLE-IRG-2008, 2008)
Start date: 2009-03-01
End date: 2013-02-28
Duration (months): 48.0
Total project cost (EUR): 100000.0
EU funding (EUR): 100000.0
Participants: 1
Project status: CLOSED

Recent studies suggest that the microenvironment surrounding primary tumor cells can temporarily change tumor cell gene expression, resulting in suppressed cell proliferation and increased cell motility. This genetic program allows tumor cells to invade the surrounding tissue, metastasize to distant parts of the body and suppress apoptosis induced by changes in the environment. Once cells reach a favorable milieu, they suppress migration, reactivate the proliferation program and expand in the target organ. Although many components involved in this switch between proliferative and migratory phenotypes have been identified, the precise molecular mechanism remains unknown. One of the protein shown to be specifically overexpresed in migratory but not in proliferating cells is adaptor/scaffold protein RACK1. We recently identified RACK1 as a scaffold-like protein in the ERK pathway which controls ERK activation and targets active ERK to specific intracellular compartments. My preliminary evidence indicates that the expression level of RACK1 correlates with the cell's ability to either migrate or proliferate. Thus, RACK1 may serve as a key molecular “switch” that controls whether ERK signaling regulates the proliferative or the migratory program. The goal of this research proposal is to understand how RACK1 and the ERK pathway regulate the switch between proliferative and migratory phenotypes and the contribution this “migratory switch” has on the development and progression of colorectal cancer.

Keywords: protein kinase,erk,scaffold,signal transduction,migration,proliferation
Human Capital, Public Policies, and Income Inequality Within and Across Countries (HUMAN CAPITAL)

Framework: FP7 — People
Programme: Marie-Curie Actions
Theme: Marie Skłodowska-Curie
Destination: International Re-integration Grants
Action type: Support for training and career development of researchers (Marie Curie)
Countries involved: Spain
Call:  (FP7-PEOPLE-IRG-2008, 2008)
Start date: 2009-05-01
End date: 2013-04-30
Duration (months): 48.0
Total project cost (EUR): 100000.0
EU funding (EUR): 100000.0
Participants: 1
Project status: CLOSED

One of the most important challenges in economic sciences is to explain the observed large differences in the wealth of nations. Although, total factor productivity is at the core of income inequality across countries. One of the main difficulties is that there are no measures of quality of education and productivity across countries. To assess the sources of cross-country income inequality, economists need to assume away cross-country differences in the quality of schooling and to measure productivity as a residual. It would be unfeasible to do a standard variance decomposition analysis as economic theory implies that quality of education and total factor productivity are likely to be jointly determined. Moreover, without a tight measurement of human capital and its effects on the economy, no sound analyses can be carried out of the impact of public educational policies. The proposal aims too, to develop a structural model of human capital investments decisions and use this model for two socio-economic studies: 1. International quantitative assessment of total factor productivity and human capital in accounting for the per capita income inequalities observed; 2. Quantitative cross-country investigation of public policies on the distribution of education and income, and intergenerational mobility The project proposes to use the new theoretical framework to evaluate the aggregate and distributive effects of some recent proposals for reforming taxation and education institutions in O.E.C.D. countries. The research will make easier to understand the poverty of the nations and provide European policy makers with valuable insights for reducing the extent of poverty. This proposal will help the researcher, Andrés Erosa, to reintegrate among the European academics and will provide a clear input to the European research area. Andres Erosa is eager to be one of the leading researchers of the IMDEA Social Sciences and to become a reference among European academics.

Keywords: macroeconomics,human capital,heterogeneous agents economies,income distribution,taxation and pubic policy
NMDA receptor processing in an animal model for schizophrenia (NMRPAMS)

Framework: FP7 — People
Programme: Marie-Curie Actions
Theme: Marie Skłodowska-Curie
Destination: International Re-integration Grants
Action type: Support for training and career development of researchers (Marie Curie)
Countries involved: Denmark
Call:  (FP7-PEOPLE-IRG-2008, 2008)
Start date: 2008-09-01
End date: 2012-08-31
Duration (months): 48.0
Total project cost (EUR): 100000.0
EU funding (EUR): 100000.0
Participants: 1
Project status: CLOSED

The pathophysiological mechanisms causing schizophrenia are not well known. Schizophrenia is characterized by symptoms such as hallucinations, emotional isolation and cognitive deficits. Altered neurotransmission through the glutamate transmitter system has been linked to this devastating psychiatric illness. In particular, observations that functional antagonism of the N-methyl-D-apartate (NMDA) glutamate receptor by phencyclidine (PCP) worsens all symptoms in patients and induces a schizophrenia-like psychosis in healthy volunteers have implicated this receptor in schizophrenia. The NMDA receptor, which is principally expressed in postsynaptic spines, is a multimeric protein assembly consisting of the obligatory NR1 subunit in different constellations with NR2A or NR2B subunits. Through alternative splicing of NR1, several regulatory domains are introduced in the receptor, which significantly influence early processing including assembly and forward trafficking. Based on functional divergence, receptors assembled from NR2A and NR2B proteins similarly contribute with functional specialization of the receptor. Studies in postmortem brain indicate that mechanisms associated with early NMDA receptor processing might be altered in schizophrenia. This includes evidence for altered NR1 splicing and compromised trafficking of NR2B-type NMDA receptors. Based on a hypothesis of altered NMDA receptor processing, in this project we will use an animal model to study, in a translational manner, changes in alternative splicing, assembly and trafficking of new NR2A and NR2B receptors in schizophrenia. Furthermore, we will analyze if NMDA receptor processing is modulated by peptides known to enhance cognition. Due to the specialized roles NR2A and NR2B receptors play during complex functions such as cognition, improved understanding of how this receptor system is altered in schizophrenia might lead to improved treatment of symptoms not well treated today.

Keywords: neurobiology,alternative splicing,glutamate,neurotransmission,protein synthesis,receptor assembly,cognition,protein interaction,postsynaptic density
Validation of the disease model and therapy for retinitis pigmentosa 11 (RP11MOUSE)

Framework: FP7 — People
Programme: Marie-Curie Actions
Theme: Marie Skłodowska-Curie
Destination: European Re-integration Grants
Action type: Support for training and career development of researchers (Marie Curie)
Countries involved: France
Call:  (FP7-PEOPLE-ERG-2008, 2008)
Start date: 2009-05-18
End date: 2012-05-17
Duration (months): 36.0
Total project cost (EUR): 45000.0
EU funding (EUR): 45000.0
Participants: 1
Project status: CLOSED

With a prevalence of 1 in 3500 retinitis pigmentosa (RP) is a significant cause of blindness in the Western world. RP is a group of hereditary retinal disorders, for which there is no effective treatment. It is mostly caused by mutations in genes related to the biochemistry of photoreceptors. PRPF31, however was the first ubiquitously expressed gene implicated in this disorder. Mutations in this gene are responsible for one of the commoner forms of autosomal dominant RP (RP11) with implications for a significant proportion of patients. Overall it has been noted that patients who manifest the disease present a severe form of retinal degeneration, often losing vision completely by the third decade. With the cloning of PRPF31, a novel class of genes, i.e. splicing factor genes, causing RP was revealed (PRPF3, PRPF8, PAP-1). These four genes are associated with a common splicing complex, U4/U6.U5 snRNP, and they are likely to share the molecular mechanism of the pathology. It has been noted that in families affected by PRPF31 mutations, manifestation of the disease is also dependent on the expression level of the wild-type PRPF31 allele. Thus, high levels of wild-type PRPF31 protein, can override the effect of mutant copy of the PRPF31 gene. This is known as partial penetrance and can be viewed as nature’s way of curing the disease. Learning from the clinical data, I would like to establish an RP11 animal model to validate the therapeutic effect of increasing PRPF31 expression. At first instance, Prpf31 levels in mouse will be reduced with RNA interference (RNAi) technology and the course of the disease progression will be assessed. The RNAi will be administered by subretinal injections. Subsequently, the rescue of the retinal phenotype will be brought about with delivery of the wild-type copy of the Prpf31 gene in AAV2/5 vector.

Keywords: retinitis pigmentosa,blindness,retina,molecular genetics,gene therapy,mouse model,rnai
Phenogenomics of sirtuin corepressor family (SIRTUINS)

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: Switzerland
Call:  (ERC-2008-AdG, 2008)
Start date: 2009-02-01
End date: 2014-01-31
Duration (months): 60.0
Total project cost (EUR): 2485000.0
EU funding (EUR): 2485000.0
Participants: 1
Project status: CLOSED

By modulating the activity of transcription factors, cofactors influence cellular and organismal metabolic pathways. Recently the role of the sirtuin cofactor gene family received a lot of attention in this context, as their beneficial impact on longevity was linked to effects on metabolic control. Most sirtuins catalyze deacetylation reactions that are tightly linked to cellular energy (NAD+) levels. To ascertain the tissue-specific contributions of sirtuins in metabolism, we propose here to: 1) identify novel deacetylation targets for the sirtuins; 2) generate and characterize genetically engineered mouse models (GEMMs) with somatic mutations in the 7 sirtuin genes in liver, muscle and adipose tissue, key metabolic tissues; 3) study mouse models with natural genetic variation in sirtuin expression, such as found in genetic reference populations (GRPs), like the BxD recombinant inbred mouse lines; and 4) validate the relevance of sirtuin signaling for human metabolism through clinical genetic studies. As the goal is to progress towards the treatment and prevention of metabolic diseases in humans, GEMMs are optimized to study the actions of isolated genetic loci and are thus insufficient to characterize polygenic networks and genetic interactions. Moreover environmental factors can impact on the manifestations of the genotype or phenocopy the genetically produced phenotype. Thus, to dissect complex genetic traits, experimental models, like GRPs, that imitate the genetic structure of human populations provide complimentary information to that obtained from GEMMs. As we will combine data generated using directional genetic strategies in GEMMs with a high-throughput phenogenomic analysis of GRPs, our approach merges the benefits of clear-cut results of single gene perturbations in a given tissue with subtle alterations that result from natural innumerable allelic variants. This will ultimately favor the definition of the role of the sirtuins in metabolic homeostasis.

Keywords: transcription,sirtuins,longevity,energy expenditure
Strategic Cooperation between Ukraine, Belarus and EU in Information and Communication Technologies (SCUBE-ICT)

Framework: FP7 — Cooperation
Programme: Information and Communication Technologies
Destination: Horizontal support actions
Action type: Coordination and support actions
Countries involved: Greece,Spain,Belarus,Ukraine,United Kingdom
Call:  (FP7-ICT-2007-3, 2007)
Start date: 2009-01-01
End date: 2010-12-31
Duration (months): 24.0
Total project cost (EUR): 777002.0
EU funding (EUR): 620000.0
Participants: 11
Project status: CLOSED

EU, Belarus and Ukraine face common ICT R&D opportunities and challenges that create a favourable environment for strategic collaboration. The main aim of SCUBE-ICT is to increase co-operation between ICT researchers from the three regions. The project will achieve its overall aim via a range of activities: 1. Assessing the ICT collaboration potential for the three regions. This involves production of a "White Paper on ICT R&D in Belarus and Ukraine"; mapping the Belarusian and Ukrainian ICT actors; reporting on opportunities for Bel/Ukr ICT actors in the EU; and reporting on opportunities for EU ICT actors in Bel/Ukr; 2. Organising awareness-raising and training events about the EC’s ICT R&D programmes for Bel/Ukr ICT actors. Also, organising networking/partnership events with motivated EU and Bel/Ukr ICT actors to initiate research collaborations between them; 3. Providing advanced support services to competent Bel/Ukr ICT actors to build long-term relationships with key EU counterparts. Central to this will be implementation of Joint Action Plans, which are mini roadmaps describing in detail how to reach research collaboration goals; 4. Enhancing ICT R&D policy dialogue between policy makers and stakeholders from EU and Bel/Ukr ICT communities. ICT R&D Policy Working Groups will be established in Bel/Ukr that meet to discuss co-operation in areas of mutual interest and develop a Road Map towards a Joint Strategy in ICT R&D. The SCUBE-ICT project’s measurable results will include: a. Website and online database with information about 100-150 ICT actors in Bel/Ukr; b. 4 awareness raising/training events in Bel/Ukr concerning FP7 ICT; c. 6 ICT networking events; d. Support to at least 15 Bel/Ukr ICT actors to establish Joint Action Plans with EU actors; e. Support to at least 10 Bel/Ukr ICT actors to make FP7 proposals; f. ICT R&D Policy Working Groups involving EU and Bel/Ukr; and g. Roadmap towards a Joint Strategy in ICT R&D.

Keywords: ict,cooperation,belarus,ukraine