Data-Gouv-ML/pcri-informations-sur-les-projets-laureats huggingface dataset:
Fourth generation photocatalysts: nano-engineered composites for water decontamination in low-cost paintable photoreactors (4G-PHOTOCAT)

Framework: FP7 — Cooperation
Programme: Nanosciences, Nanotechnologies, Materials and new Production Technologies - NMP
Destination: Materials
Action type: Collaborative project
Countries involved: Germany,United Kingdom,Czechia,Poland,Finland,Malaysia,Viet Nam,Czechia
Call:  (FP7-NMP-2012-SMALL-6, 2012)
Start date: 2013-01-01
End date: 2015-12-31
Duration (months): 36.0
Total project cost (EUR): 4884982.8
EU funding (EUR): 3727767.0
Participants: 10
Project status: CLOSED

The project 4G-PHOTOCAT allies the expertise of 7 academic and 3 industrial partners from 5 EU countries (Germany, United Kingdom, Czech Republic, Poland, and Finland) and 2 ASEAN countries (Malaysia and Vietnam) for the development of a novel generation of low-cost nano-engineered photocatalysts for sunlight-driven water depollution. Through rational design of composites in which the solar light-absorbing semiconductors are coupled to nanostructured redox co-catalysts based on abundant elements, the recombination of photogenerated charges will be suppressed and the rate of photocatalytic reactions will be maximized. In order to achieve fabrication of optimal architectures, advanced chemical deposition techniques with a high degree of control over composition and morphology will be employed and further developed. Furthermore, novel protocols will be developed for the implementation of the photocatalysts into a liquid paint, allowing for the deposition of robust photoactive layers onto flat surfaces, without compromising the photoactivity of immobilized photocatalysts. Such paintable photoreactors are envisaged particularly as low-cost devices for detoxification of water from highly toxic persistent organic pollutants which represent a serious health issue in many remote rural areas of Vietnam and other countries. The 4G-PHOTOCAT project will provide novel scientific insights into the correlation between compositional/structural properties and photocatalytic reaction rates under sunlight irradiation, as well as improved fabrication methods and enhanced product portfolio for the industrial partners. Finally, 4G-PHOTOCAT will lead to intensified collaboration between scientists working at the cutting edge of synthetic chemistry, materials science, heterogeneous photocatalysis, theoretical modelling, and environmental analytics, as well as to unique reinforcement of cooperation between scientists and industry partners from EU and ASEAN countries.

Keywords: photocatalysis,water remediation,nano-engineering,co-catalysts,atomic layer deposition,paintable photoreactor,persistent organic pollutants,herbicides,vietnam
Complex Synthetic Mimics of the Cell Membrane (COSMIC)

Framework: FP7 — Ideas
Programme: European Research Council
Theme: European research council
Destination: Starting grants
Action type: Support for frontier research (ERC)
Panel: Molecular and Structural Biology and Biochemistry
Countries involved: United Kingdom
Call:  (ERC-2012-StG_20111109, 2012)
Start date: 2013-02-01
End date: 2018-10-31
Duration (months): 69.0
Total project cost (EUR): 1498523.0
EU funding (EUR): 1498523.0
Participants: 2
Project status: CLOSED

I propose to bridge the gap between simple in vitro measurements of biological processes, and the complexities of the cellular environment. This requires reduced in vitro systems that are sufficiently complex to reproduce the subtleties of the in vivo biological phenomenon, but sufficiently controllable to test how quantitative changes in a particular property affects function. The challenge is to step beyond the most simple and straightforward in vitro mimics of the cell membrane, and create model systems that more closely reproduce the conditions in vivo. I propose to tackle two specific, but interrelated membrane phenomena, that are currently not captured in artificial bilayers and create new complex mimics of the cell membrane capable of tackling these systems; namely (1) protein crowding and the cytoskeleton, and (2) lateral forces and membrane curvature. Testing our synthetic mimics with models that we understand in vivo is vital. This benchmarking will ensure that the mimics we create are relevant and will help ensure the more ambitious later goals of the this proposal are successful.We will then take these tools to go on and aim to create a synthetic mimic of the bacterial membrane. However we are not limited to creating purely natural duplicates, and we can exploit a much wider range of building material than nature. In addition to creating complex mimics, we will also create totally new synthetic systems inspired by the properties of the cell membrane, but possessing unique properties.

Keywords: synthetic biology membrane biophysics single-molecule imaging
Predictive toxicology of engineered nanoparticles (PRENANOTOX)

Framework: FP7 — Cooperation
Programme: Nanosciences, Nanotechnologies, Materials and new Production Technologies - NMP
Destination: Nanosciences and Nanotechnologies
Action type: Collaborative project
Countries involved: Israel,Italy,Germany
Call:  (FP7-NMP-2012-SMALL-6, 2012)
Start date: 2013-01-01
End date: 2015-12-31
Duration (months): 36.0
Total project cost (EUR): 1289902.67
EU funding (EUR): 997734.0
Participants: 3
Project status: CLOSED

The production of many consumer products based on manufactured NanoParticles (NPs) has led to a growing public and regulatory concern about the safety of nanomaterials. Since experimental toxicological testing of NPs, especially in vivo animal studies is costly and time-consuming, it is necessary to develop a novel research field and associated methods and tools to reach the goal of predictive nanotoxicology. The PreNanoTox consortium addresses three currently missing critical elements needed to develop a platform for predictive nanotoxicology and our suggested approach of providing them: (1) There is a current lack of unified large database – We suggest to form this database by applying cutting edge information extraction tools on large repository of scientific articles; (2) There is a need for better understanding the underlying mechanisms of the primary interaction of NP with the cell membrane – We suggest to apply appropriate theory and simulation assuming that the surface chemistry of a NP (affecting NP’s surface reactivity, hydrophobicity, or surface electrostatics) as well as its other physical properties (e.g. size and shape) determine the strength of the non-specific adsorption of NPs to a cell surface, leading beyond a certain adhesion-strength threshold, to efficient uptake of the NPs; (3) There is a need to extend the traditional QSAR paradigm to the field of nanotoxicology – This will be carried out by linking appropriate NP descriptors, with emphasis on those which determine the strength of adsorption of NPs to cells, with biological responses. The PreNanoTox consortium is made up of four research groups (from three scientific organizations), which lead in information technology, soft matter modeling, computational chemistry and in-vitro toxicology, yielding a synergetic output. This project will assist in safe designing of new engineered NPs as well as reducing tha extent needed for empirical testing of toxicity.

Keywords: nanoparticles,toxicology,modelling,interaction with membrane
Evolutionary mechanisms of epigenomic and chromosomal aberrations in cancer (EVOEPIC)

Framework: FP7 — Ideas
Programme: European Research Council
Theme: European research council
Destination: Starting grants
Action type: Support for frontier research (ERC)
Panel: Genetics,Genomics,Bioinformatics and Systems Biology
Countries involved: Israel
Call:  (ERC-2012-StG_20111109, 2012)
Start date: 2012-12-01
End date: 2017-11-30
Duration (months): 60.0
Total project cost (EUR): 1499998.0
EU funding (EUR): 1499998.0
Participants: 1
Project status: CLOSED

Our working hypothesis is that tumorigenesis is an evolutionary process that fundamentally couples few major driving events (point mutations, rearrangements) with a complex flux of minor aberrations, many of which are epigenetic. We believe that these minor events are critical factors in the emergence of the cancer phenotype, and that understanding them is essential to the characterization of the disease. In particular, we hypothesize that a quantitative and principled evolutionary model for carcinogenesis is imperative for understanding the heterogeneity within tumor cell populations and predicting the effects of cancer therapies. We will therefore develop an interdisciplinary scheme that combines theoretical models of cancer evolution with in vitro evolutionary experiments and new methods for assaying the population heterogeneity of epigenomic organization. By developing techniques to interrogate DNA methylation and its interaction with other key epigenetic marks at the single-cell level, we will allow quantitative theoretical predictions to be scrutinized and refined. By combining models describing epigenetic aberrations with direct measurements of chromatin organization using Hi-C and 4C-seq, we shall revisit fundamental questions on the causative nature of epigenetic changes during carcinogenesis. Ultimately, we will apply both theoretical and experimental methodologies to assay and characterize the evolutionary histories of tumor cell populations from multiple mouse models and clinical patient samples.

Keywords: cancer evolution,dna methylation,carcinogenesis,hi-c,single cell epigenomics
IN VIVO REPROGRAMMING: A NOVEL ROUTE TO BRAIN REPAIR (IN-BRAIN)

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: Sweden
Call:  (ERC-2012-StG_20111109, 2012)
Start date: 2013-03-01
End date: 2018-02-28
Duration (months): 60.0
Total project cost (EUR): 1500000.0
EU funding (EUR): 1500000.0
Participants: 1
Project status: CLOSED

Recent progress on direct re-programming into functional neurons provides a new approach towards cell-based therapy for neurodegenerative disorders. The induced neurons (iNs) are a novel type of cell resulting from rapid and remarkable conversion of somatic cells into subtype-specific functional neurons. Importantly they are non-proliferating which make them interesting alternatives to induced pluripotent (iPS) cells as sources of patient specific neurons for exogenous cell replacement therapy and disease modeling. Another major advantage with direct conversion over iPS cells is that the reprogramming could be performed in vivo. While direct conversion has been successful in organs such as the pancreas, where exocrine cells can be directly converted into insulin producing cells by viral injections in vivo (Zhou et al., Nature, 2008), the method is yet to be explored in the brain. Once direct conversion of non-neuronal cells into subtype specific neurons directly in the brain is established, it provides a new strategy for cell based brain repair that do not depend on exogenous cells. The overall goal of this project is to provide proof-of-principle that induced neurogenesis is achievable in the adult brain through guided transcription factor reprogramming of non-neuronal cells, to determine which cells are best suited as cellular substrate for in vivo neural conversion, and to compare this approach with transplantation of converted fibroblasts. The ability to directly reprogram cell fate using defined combinations of transcription factors have already turned basic studies of stem cell differentiation and cell therapy into a new direction. Establishing this technique in vivo would be another paradigm-shifting finding that opens up for novel strategies for brain repair

Keywords: direct neural conversion induced neurons in vivo induced nurogenesis
Photoreception in Drosophila larvae: Information coding in a simple neuronal circuit (PHOTONAVINET)

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
Call:  (ERC-2012-StG_20111109, 2012)
Start date: 2013-01-01
End date: 2017-12-31
Duration (months): 60.0
Total project cost (EUR): 1491873.0
EU funding (EUR): 1491873.0
Participants: 1
Project status: CLOSED

How does the neuronal network of the brain mediate its function? This fundamental question in biology is still a puzzle, despite decades of intensive work. A seemingly unsolvable obstacle when studying the brain is its enormous complexity. A powerful approach to understand our brain uses “simple” brains of animal models, in which one can genetically identify and manipulate neurons. The brain of the fruit fly Drosophila melanogaster is widely used as an impacting model system to study how the brain functions with the advantage that the fly brain is much simpler compared to the mammalian brain. Even another one order of magnitude simpler is the brain of the Drosophila larva consisting of an estimated 10’000 neurons. We use the Drosophila larva as an excellent model to genetically dissect a comparably simple visual system. The eye of the larva consists only of two types of photoreceptor neurons: four blue-sensitive cells expressing Rhodopsin5 (Rh5) and eight green-sensitive cells expressing Rhodpsin6 (Rh6). The photoreceptors transmit the information to a small set of target neurons in the larval optic neuropil (LON). We found that only 12-15 brain interneurons connect to the LON, which can be classified in four different groups, according to location and neurotransmitter they use. The goal of this project is to dissect neuronal circuits of visual information processing: from mapping synaptic connections in the circuit to the behavioural impact of neurons. Preliminary results of my laboratory and a “step-by-step strategy” support the feasibility to reach these ambitious goals (Sprecher et al., 2011; Von Essen et al., 2011, Keene et al., 2011).

Keywords: visual system,behavioral neuroscience
Dosage sensitive genes in evolution and disease (DOSE)

Framework: FP7 — Ideas
Programme: European Research Council
Theme: European research council
Destination: Starting grants
Action type: Support for frontier research (ERC)
Panel: Evolutionary, population and environmental biology
Countries involved: Ireland
Call:  (ERC-2012-StG_20111109, 2012)
Start date: 2013-01-01
End date: 2018-12-31
Duration (months): 72.0
Total project cost (EUR): 1358534.0
EU funding (EUR): 1358534.0
Participants: 1
Project status: CLOSED

Evolutionary change of gene copy number through gene duplication is a relatively pervasive phenomenon in eukaryotic genomes. However, for a subset of genes such changes are deleterious because they result in imbalances in the cell. Such dosage-sensitive genes have been increasingly implicated in disease, particularly through the association of copy number variants (CNVs) with pathogenicity. In my lab we have previously discovered that many genes in the human genome which were retained after whole genome duplication (WGD) are refractory to gene duplication both over evolutionary timescales and within populations. These are expected characteristics of dosage-balanced genes. Many of these genes are implicated in human disease. I now propose to take a computational (dry-lab) approach to examine the evolution of dosage-balanced genes further and to develop a sophisticated model of evolutionary constraint of copy number. These models will enable the identification of dosage-balanced genes and their consideration as novel candidate disease loci. Recognising and interpreting patterns of constraint is the cornerstone of molecular evolution. Through careful analysis of genome sequences with respect to gene duplication over evolutionary times and within populations, we will develop a formal and generalised model of copy-number evolution and constraint. We will use these models to identify candidate disease loci within pathogenic CNVs. We will also study the characteristics of known disease genes in order to identify novel candidate loci for dosage-dependent disease. This is an ambitious and high impact project that has the potential to yield major insights into gene copy-number constraint and its relationship to complex disease.

Keywords: gene duplication,evolutionary constraint,dosage-balanced genes,genome duplication,disease genes,copy number variation.
Neurobiological basis of collective decision making in the human brain (NEUROCODEC)

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: United Kingdom
Call:  (ERC-2012-StG_20111109, 2012)
Start date: 2013-01-01
End date: 2017-12-31
Duration (months): 60.0
Total project cost (EUR): 1486197.0
EU funding (EUR): 1486197.0
Participants: 1
Project status: CLOSED

We continually interact with each other & share information to make decisions together as friends, families, committees, juries, interest groups and institutions. The question of how collective decisions are made dates back many centuries and has been vigorously studied in social psychology and political economics, but the biological basis of collective decision making in human brain is almost entirely unknown. This question is arguably at the heart of human society’s urgent need to communicate effectively & find better ways of arriving at global collective decisions. My research has provided new and potentially important computational models of collective decision-making based on empirical data from visual psychophysics. I propose to characterize the neurobiological basis of joint decisions by combining recent advances in economics and social cognitive neuroscience in a novel interdisciplinary research program that will ask 4 questions: (1)How do we learn to make better collective decisions? (2)What are the brain mechanisms underlying the different psychological components of collective decision making? (3)What makes some people better & some others worse at joint decisions? (4)What is the role of the neuro-modulatory hormones oxytocin & testosterone in collective decisions? I plan to develop a formal theoretical model of collective decision-making (Q1) & use converging evidence from complementary methodologies e.g. behavioural experiments & fMRI (Q2), structural brain imaging (Q3) and neuro-pharmacology (Q4) to test & advance the model. My findings could help understand what physiological events underlie our ability to learn from experience to contribute effectively to group efforts and also disclose the biological basis that makes some of us better and some worse at working in groups . The results may provide a clearer picture of how hormonal interactions in the brain strike a balance between trusting ourselves vs accepting the opinion of others.

Keywords: collective decision-making,cooperative behavior,feedback,learning,fmri,mri,oxytocin,communication,psychophysics
Solving an evolutionary jigsaw puzzle: A next-generation genomics approach to trace the origins of the eukaryotic cell (PUZZLE_CELL)

Framework: FP7 — Ideas
Programme: European Research Council
Theme: European research council
Destination: Starting grants
Action type: Support for frontier research (ERC)
Panel: Evolutionary, population and environmental biology
Countries involved: Sweden
Call:  (ERC-2012-StG_20111109, 2012)
Start date: 2012-11-01
End date: 2017-10-31
Duration (months): 60.0
Total project cost (EUR): 1721440.0
EU funding (EUR): 1721440.0
Participants: 1
Project status: CLOSED

The origin of the eukaryotic cell represents an enigmatic yet dramatically incomplete evolutionary puzzle. The few pieces of this puzzle that we have managed to identify thus far indicate that the eukaryotic cell most probably emerged via a fusion of an archaeal and an alphaproteobacterial cell. Yet, beyond this, scientific debate is mainly engulfed by speculation, which, to a large extent, is fed by our poor understanding of the identity of these bacterial and archaeal fusion partners. In the current research proposal, I aim to identify contemporary relatives of the bacterial and archaeal lineages that once founded the eukaryotic cell using novel single-cell genomics and phylogenomics approaches. Till this end, environmental samples that are enriched for the target microbial lineages will be collected and analyzed at the single cell level. A novel microdroplet-based single-cell analysis platform will be implemented that allows for the analysis of millions of individual cells. After target cells have been identified, their genomic material will be amplified, and subjected to next-generation sequencing analysis. Subsequent state-of-the-art phylogenomic analyses will elucidate the taxonomic affiliation of these target cells in relation to other archaeal and bacterial lineages, as well as to eukaryotes. The proposed strategy will identify hundreds of novel prokaryotic lineages, some of which representing close contemporary relatives of the ‘parental’ lineages that founded the eukaryotic cell. The genomic exploration of these lineages will add the taxonomic resolution that is needed to start solving the evolutionary puzzle of the emergence of the eukaryotic cell.

Keywords: archaea,alphaproteobacteria,origin of eukaryotes,phylogenomics,eukaryogenesis,endosymbiosis,evolution,single-cell genomics,archaeal parent,next-generation sequencing,mitochondria
The mechanisms that underlie the development of a tendon-bone attachment unit (TENDONTOBONE)

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: Israel
Call:  (ERC-2012-StG_20111109, 2012)
Start date: 2013-01-01
End date: 2017-12-31
Duration (months): 60.0
Total project cost (EUR): 1499999.0
EU funding (EUR): 1499999.0
Participants: 1
Project status: CLOSED

We walk, run and jump using the complex and ingenious musculoskeletal system. It is therefore puzzling that although each of its components has been extensively studied, research of the musculoskeleton as an integrated system and, in particular, of its assembly has been scarce. In recent years, studies conducted in my lab have demonstrated the centrality of cross regulation between musculoskeletal tissues in skeletogenesis. These works have provided me with the inspiration for a revolutionary hypothesis on the way tendons connect to bones, along with sufficient preliminary data on which to base it. The critical component in the assembly of the musculoskeleton is the formation of an attachment unit, where a tendon is inserted into a bone. Instead of two tissues that attach to each other, my novel hypothesis suggests that the entire attachment unit originates from a single pool of progenitor cells, which following differentiation diverges to form a tendon attached to cartilage. With the support of the ERC scheme, I will uncover the previously uncharacterized cellular origin of the attachment unit and the genetic program underlying its development. The attachment unit is a compound tissue, as it is composed of chondrocytes at one end and of tenocytes at the other end. We will investigate the mechanisms that facilitate in situ differentiation of mesenchymal progenitor cells into two distinct cell fates, under one defined niche. In addition, I will identify the contribution of both mechanical stimuli and molecular signals to the development of the attachment unit. The ultimate goal of this program is to provide a complete picture of attachment unit development, in order to promote understanding of musculoskeletal assembly. The acquired knowledge may provide the basis for new therapies for enthesopathies, through tissue engineering or repair.

Keywords: musculoskeleton,bone,tendon,enthesis,attachment site,bone eminence,cartilage,chondrocyte,tenocyte,progenitor cell,cell fate determination,differentiation,mechanotransduction