Data-Gouv-ML/pcri-informations-sur-les-projets-laureats huggingface dataset:
The Role of Visual Experience in Spatial Cognition (RVESC)

Framework: FP7 — People
Programme: Marie-Curie Actions
Theme: Marie Skłodowska-Curie
Destination: Intra-European Fellowships
Action type: Support for training and career development of researchers (Marie Curie)
Countries involved: United Kingdom
Call:  (FP7-PEOPLE-2010-IEF, 2010)
Start date: 2011-03-01
End date: 2013-02-28
Duration (months): 24.0
Total project cost (EUR): 203049.6
EU funding (EUR): 203049.6
Participants: 1
Project status: CLOSED

Thanks to the neural plasticity the remaining modalities can reorganise the human brain to compensate the effects of blindness. Yet, studies investigating the performance of visually impaired people in spatial tasks reported mixed results. This suggests that vision might be crucial for spatial tasks. Other studies reported that visual experience is necessary to establish an allocentric (external) reference frame to integrate multisensory inputs occurring within the peripersonal space. However, it is still unclear whether visual experience affects also the spatial representation of extra-personal environment where people perform their daily activities. Mou and McNamara (2002), surprisingly, found that memory of regularly disposed visually-learned room-sized sets of objects was better when the task required using an allocentric rather than an egocentric reference frame. Our sets will be learned through proprioception and audition, and by using the sensory substitution device called ‘vOICe’. Congenitally and late visually impaired and blindfolded sighted participants will be tested. If visual experience is necessary for allocentric spatial representation then, participants will perform better in the spatial task requiring the use of their ‘preferential’ spatial reference frame; allocentric for participants with visual experience and egocentric for those without visual experience. The use of vOICe for spatial learning will assess whether, by mimicking visual input, it can trigger the use of an allocentric reference frame by people without visual experience. This issue will be investigated also by using a tactile reference frame (similar to the ‘bumps’ on floor of public buildings) that will surround the set to trigger a ‘global’ spatial representation. Thus, these studies will improve our understanding of the development of human spatial cognition and, moreover, will find results with potential concrete application in the development of aids for visually impaired people

Keywords: experimental psychology,spatial memory,multisensory integration,blindness,vision,haptics,audition,sensory substitution,rehabilitation
Gastrointestinal and neuropeptides regulating food intake in fish in response to dietary lipid composition (GASTRONEUROPEP)

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: Spain
Call:  (FP7-PEOPLE-2010-RG, 2010)
Start date: 2011-10-01
End date: 2014-09-30
Duration (months): 36.0
Total project cost (EUR): 45000.0
EU funding (EUR): 45000.0
Participants: 1
Project status: CLOSED

There is an urgent need to replace fish oil (FO) and meal (FM) from wild stocks in aquaculture diets with more sustainable alternatives, being vegetable oils (VO) the primary candidates. However, these oils are devoid of essential n-3 long-chain PUFA (LC-PUFA) and can be particularly rich in n-6 PUFA, leading to imbalances in the n-6/n-3 ratio. This situation is similar to what is presently observed in other animal production sectors as well as in human nutrition. It is relatively well established how these changes in dietary lipid composition might affect lipid metabolism but potential effects on the regulation of appetite and food intake mediated by gastrointestinal and neuropeptides are possible and have been hardly investigated. This will be the objective of the present project, which will employ an interdisciplinary approach combining traditional nutritional and physiological studies with molecular analyses to evaluate potential impacts of more sustainable feed formulations on the regulation of food intake, while also uncovering the mechanisms behind it. The knowledge gained from this project is of high scientific and socio-economical importance to the future development and expansion of the European aquaculture industry. In addition, if physiological mechanisms of regulation of appetite and satiety in fish are similar to those in mammals, as has been suggested, knowledge gained might be applicable to other animal production sectors and even human nutrition, including studies of nutritional disorders (e.g. obesity). Finally, the effects of FO replacement by VO in aquaculture diets on lipid metabolism have been the research focus of the candidate in the past 3 years. The present project would thus enable the transfer of knowledge and competence from a northern European to a Mediterranean aquaculture context, while allowing the reintegration within an Institution with high opportunities for professional development and stabilization.

Keywords: animal nutrition,aquaculture,fish lipid nutrition,n-6/n-3 polyunsaturated fatty acids,metabolism,control of food intake,sustainable diets for aquaculture
Molecular mechanisms leading to genome-wide DNA demethylation during epigenetic reprogramming. (REPROGRAMMING)

Framework: FP7 — People
Programme: Marie-Curie Actions
Theme: Marie Skłodowska-Curie
Destination: Intra-European Fellowships
Action type: Support for training and career development of researchers (Marie Curie)
Countries involved: United Kingdom
Call:  (FP7-PEOPLE-2010-IEF, 2010)
Start date: 2011-04-01
End date: 2013-03-31
Duration (months): 24.0
Total project cost (EUR): 199549.6
EU funding (EUR): 199549.6
Participants: 1
Project status: CLOSED

Epigenetic reprogramming is a developmental process involving both genome-wide DNA demethylation and chromatin remodelling. Under physiological conditions it occurs at distinct stages of normal embryonic development. However, under in vitro conditions induction of this process can restore pluripotency in somatic cells, and in aberrant situations a similar dedifferentiation process can initiate carcinogenesis. While the kinetics of the reprogramming that occurs in the course of normal development has been well documented, initial steps inducing this process and how DNA methylation marks are removed in vivo remain elusive. The involvement of DNA repair mechanisms in DNA demethylation during epigenetic reprogramming has been recently suggested. The presented project proposes to investigate the upstream events initiating epigenetic reprogramming by using both in vivo and in vitro approaches. We will focus on recently discovered candidates involved in 5-methylcytosine hydroxylation and will investigate a possible involvement of this modification of 5-methylcytosine in the epigenetic reprogramming during mouse development. We will also examine the potential repair enzymes able to remove this epigenetic mark in order to highlight other protein partners involved in this process. Data obtained on this pathway will not only enrich our understanding towards developmental reprogramming, but also enhance our ability to manipulate cell fate in vitro.

Keywords: dna demethylation,epigenetic reprogramming,base excision repair pathway,developmental biology.
The genomic basis of emerging fungal pathogenicity (FUNGI-PATHNCODE)

Framework: FP7 — People
Programme: Marie-Curie Actions
Theme: Marie Skłodowska-Curie
Destination: Intra-European Fellowships
Action type: Support for training and career development of researchers (Marie Curie)
Countries involved: Spain
Call:  (FP7-PEOPLE-2010-IEF, 2010)
Start date: 2012-01-01
End date: 2013-12-31
Duration (months): 24.0
Total project cost (EUR): 230480.0
EU funding (EUR): 230480.0
Participants: 1
Project status: CLOSED

In the study of human pathogens most of the attention has been given to viral and bacterial species, and fungi have been largely neglected. To date there is no broad, large-scale census of the genomic elements shared by fungal pathogenic species. Also, no large-scale scan for selective pressure variability has been undertaken, even though all the elements are in place to do so. There has neither been a multi-species search for conserved noncoding elements that may be key to explaining the regulation of crucially important functional elements and networks. The overall goal of this study is to gain insight on the evolution of the genomic elements involved in fungal human pathogenicity through the analysis of the selective constraints acting on coding and noncoding sequences. For this purpose we will combine genome sequencing, transcriptomics (RNA-seq), comparative genomics and evolutionary analyses. This project will throw light on fundamental questions about the key genes, regulatory elements and phenotypic traits that are involved in infection or how emergent, opportunistic pathogens originate relatively rapidly from non-pathogenic ancestors. Finally, the list of identified relevant genes and regulatory elements can provide much needed targets for developing pharmaceutical and therapeutic strategies.

Keywords: natural sciences,emergent fungal pathogens,new plant and animal diseases,comparative genomics,phylogenomics,selective pressure,regulatory changes,noncoding rna,networks,bioinformatics
The interplay of learning and motivational systems in addictive behaviour (ILMA)

Framework: FP7 — People
Programme: Marie-Curie Actions
Theme: Marie Skłodowska-Curie
Destination: International Incoming Fellowships
Action type: Support for training and career development of researchers (Marie Curie)
Countries involved: United Kingdom
Call:  (FP7-PEOPLE-2010-IIF, 2010)
Start date: 2012-04-01
End date: 2014-03-31
Duration (months): 24.0
Total project cost (EUR): 210092.8
EU funding (EUR): 210092.8
Participants: 1
Project status: CLOSED

An ability to predict the consequences of one’s actions is the hallmark of adaptive intelligence. Learning involves the updating of predictions based on past experience, a process thought to be driven by dopaminergic neurons. Dopaminergic systems can also impart motivational control over learned behaviour. Drug-induced dopamine release can subvert these adaptive systems and link desire for addictive drugs with particular behaviours, environmental cues and motivational states. A fly learning to associate an odour with impending punishment requires synaptic input from the PPL1 cluster of dopaminergic neurons to mushroom body neurons, where olfactory memories are stored. A subset of PPL1 neurons is also responsible for satiety-dependent appetitive memory retrieval. The PPL1 cluster of dopaminergic neurons therefore represents a potential site where learning and motivational circuits intersect. I will use optogenetic and genetic methods to address three specific aims directed at understanding the learning algorithm and its subversion by addictive drugs. 1) I will establish transgenic lines providing genetic access to subsets of PPL1 neurons. 2) I will use an optogenetic reporter to monitor the activity of the PPL1 neurons in vivo, in order to test the hypothesis that PPL1 neurons encode the prediction errors used to update valuations during learning. The effect of drugs of abuse on this process will be determined. 3) I will use a single-fly behavioural assay to establish which cells are necessary, and which sufficient, to drive learning and to test the effects drugs of abuse on learning. A new learning based behavioural assay of addiction will also be developed for gaining access to the motivational component of addiction in Drosophila.

Keywords: learning,addiction,dopamine drosophila,2-photon microscopy
Regulation of AMPA type of glutamate receptor surface diffusion by Protein Kinase ζ (AMPAZETA)

Framework: FP7 — People
Programme: Marie-Curie Actions
Theme: Marie Skłodowska-Curie
Destination: International Incoming Fellowships
Action type: Support for training and career development of researchers (Marie Curie)
Countries involved: France
Call:  (FP7-PEOPLE-2010-IIF, 2010)
Start date: 2011-09-17
End date: 2013-09-16
Duration (months): 24.0
Total project cost (EUR): 195064.0
EU funding (EUR): 195064.0
Participants: 1
Project status: CLOSED

In recent years significant progress has been made into deciphering the initial triggering mechanisms responsible for the induction of synaptic strengthening. Contrarily, very few studies address the question as to which cellular processes are responsible for the maintenance of LTP. Recently, the protein kinase M zeta (PKMζ, an atypical protein kinase C) has taken center stage in the field of synaptic plasticity due to its unique role in the maintenance of LTP. Among some of the most crucial observations are: 1) the increased in PKMζ mRNA level following LTP5, 2) Its protein product is constitutively active, 3) postsynaptic perfusion of PKMζ alone increases synaptic strength, 4) it is necessary and sufficient for the maintenance of LTP. Furthermore, its inhibition reverses pre-established LTP and most importantly erases memories. Therefore this protein merits a primary role in the maintenance of memory traces. Although PKMζ activity is crucial for the persistence of LTP however little is known about its precise cellular and molecular mechanisms of action. Recent evidence point to its role in the rapid redistribution of preexisting surface receptors on the plasma membrane. For example, pharmacologically blocking postsynaptic exocytosis with Botulinum toxin B fails to disrupt PKMζ-induced synaptic potentiation. Meanwhile the same manipulation leads to rapid and persistent rundown of synaptic transmission. Provided that blocking exocytosis is not involved in the PKMζ-mediated effects on synaptic transmission leads me to hypothesize that PKMζ must regulates surface diffusion of AMPARs either by trapping at the postsynaptic density or reshuffling of AMPARs from extrasynaptic to synaptic sites. In this proposal I will test this using a combination of high resolution imaging techniques, molecular biology and electrophysiology.

Keywords: ?-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate receptor,lateral diffusion,mobility synaptic plasticity,short term plasticity,organotypic slices,culture neuronsural sciences,neurophysiology
Application of Electromagnetic Fields for Enhancement of Structural Metal Performance (EMFFORMET)

Framework: FP7 — People
Programme: Marie-Curie Actions
Theme: Marie Skłodowska-Curie
Destination: International Incoming Fellowships
Action type: Support for training and career development of researchers (Marie Curie)
Countries involved: United Kingdom
Call:  (FP7-PEOPLE-2010-IIF, 2010)
Start date: 2011-07-01
End date: 2013-06-30
Duration (months): 24.0
Total project cost (EUR): 278680.0
EU funding (EUR): 278680.0
Participants: 1
Project status: CLOSED

The external parameters generally used in the traditional processing of structural metals are temperature, pressure and time. External electromagnetic fields (EMF) have significant potential for use in materials processing. Experimental data reasonably indicate that EMF can influence the microstructure and mechanical properties of materials. They suggest that application of EMF may be an effective, inexpensive and an easy-to-perform technique for performance control of parts and structural elements. The mechanisms of EMF influence are not well-understood and as a result the technique is underexploited. Two kinds of treatments will be explored in the Project: direct passage of pulsed electric current (PEC) through the metal and application of pulsed magnetic field (PMF) or altering magnetic field (AMF) to the metal. The Project will focus on the investigation and promotion of the EMF treatment-induced effects of the refinement of A356 aluminium casting alloy and enhancement of the corrosion and wear resistance of titanium alloys and steel. The Project aims to understand the mechanisms by which EMF affects materials properties. The objectives are: (1) to transfer knowledge of EMF treatment to the Host institution via creation of an experimental facility for the treatment of metals in molten and solid states and providing training courses (2) to fulfil a series of comprehensive tests for the experimental evidence of the benefits of the treatment for refinement of castings and enhancement of the corrosion and wear resistance of metals (3) to understand the mechanisms by which metals performance is achieved (4) to undertake interaction with industrial companies to introduce the treatment. The Project is at the junction of Mechanical, Materials and Electrotechnical Engineering, Physics (metallophysics, electromagnetism) and Computing (multiphysics numerical simulation) and aims to generate new knowledge and technological possibilities.

Keywords: mechanical and thermal properties,electromagnetism,biomaterial engineering,materials engineering,electromechanical engineering,metallurgy engineering,metal technology,mechanical engineering
The role of rhythmic synaptic plasticity in regulating sleep and behavioral performance (SLEEP PLASTICITY)

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-2010-RG, 2010)
Start date: 2011-04-01
End date: 2015-03-31
Duration (months): 48.0
Total project cost (EUR): 100000.0
EU funding (EUR): 100000.0
Participants: 1
Project status: CLOSED

Alterations in endogenous circadian rhythm and debilitating sleep disorders represent an unsolved medical problem. The circadian clock regulates the sleep/wake cycle and is complemented by homeostatic sleep pressure factors. Surprisingly, why we sleep and how the clock synchronizes rhythmic behavior, remain a mystery. Intriguing hypotheses suggest that the role of sleep is to maintain synaptic homeostasis or to reactivate specific circuits that are important to memory and learning. Also, it is postulated that clock-controlled genes affect behavior through the remodelling of synapses throughout the day and night. Therefore, it is important to isolate and characterize specific circuits that demonstrate rhythmic synaptic plasticity and to understand how they affect behavior in a live vertebrate. In this proposal, the transparent and diurnal zebrafish model will be used to examine patterns of synaptic plasticity and behavior during the day and night. The zebrafish is ideally suited to study sleep and circadian rhythms, and the neuronal networks are largely conserved with mammals. We recently showed, for the first time, circadian and homeostatic sleep control of rhythmic structural synaptic plasticity in zebrafish. The goal of this proposal is to identify and characterize new functional circuits involved in circadian, sleep, and memory regulation. We will use in-vivo imaging techniques to visualize rhythmic synapses during the day and night, and after sleep deprivation in multiple neuronal circuits. Loss- and gain-of-function approaches will be used to understand how specific circuits regulate synaptic plasticity and behavioral performance. These data should provide important evidence for the role of the circadian clock and sleep in regulating synaptic plasticity and behavior. This study is expected to provide a critical framework to understand the function of sleep, and may help in the treatment of sleep disorders.

Keywords: sleep,circadian,synapse,zebrafish,memory
To what extent can design principles for complex networks be derived from the study of error propagation phenomenon in smart and bio-inspired network structures? (EPP)

Framework: FP7 — People
Programme: Marie-Curie Actions
Theme: Marie Skłodowska-Curie
Destination: Intra-European Fellowships
Action type: Support for training and career development of researchers (Marie Curie)
Countries involved: United Kingdom
Call:  (FP7-PEOPLE-2010-IEF, 2010)
Start date: 2012-08-20
End date: 2014-08-19
Duration (months): 24.0
Total project cost (EUR): 272980.0
EU funding (EUR): 272980.0
Participants: 1
Project status: CLOSED

The main subject of the proposed project is concerned with the question of whether and to what extent design principles for complex networks can be derived from the study of error propagation phenomenon (short EPP) in modern network structures found in biological, transportation and communication systems. In this project, we generalize propagation model to explicitly consider failure propagation. First of all, different classes of failures should be identified, that might affect the scenario under the examination: explosion, flood, short-circuit, fire, disease, PC-virus, etc. Then, for each one, it should be identified how it spreads with appropriate taxonomy and the graph associated with the specific class of failures. By using the global and local efficiency the effects of errors and attacks both on the global and the local properties of the network can be investigated. The crucial point is that the global organization and local modularity efficiency are extremely sensitive to the following types of errors: omission, commission, contamination and crash, which play the main role in maintaining networks’ connectivity. Five key objectives of the project are: (a) to develop a semantic network and a simulation tool for error propagation using real-time agents and example networks; (b) to perform empirical studies of example networks that enable to examine the robustness; (c) to analyse the effect of real and generated errors not only on the global properties, but also on the local properties of the network; (d) to develop and test new structures for complex systems less sensitive to errors and attacks than known structures and to measure its effects on network performance; (e) to combine results from simulations and empirical observations in order to investigate how system can be best (re)modelled to be less sensitive to errors and attacks.

Keywords: error propagation,systems analysis and models development,autonomic computing,intelligent agents,software development,modelling networks,knowledge engineering,agent technology