Data-Gouv-ML/pcri-informations-sur-les-projets-laureats huggingface dataset:
EU and North African Migrants: Health and Health Systems (EUNAM)

Framework: FP7 — Cooperation
Programme: Health
Destination: Optimising the delivery of healthcare to European citizens
Action type: Coordination and support actions
Countries involved: Germany,Sweden,Italy,France,Tunisia,Egypt,Morocco,Algeria
Call:  (FP7-HEALTH-2010-single-stage, 2010)
Start date: 2011-04-01
End date: 2015-03-31
Duration (months): 48.0
Total project cost (EUR): 2405314.0
EU funding (EUR): 1998430.0
Participants: 8
Project status: CLOSED

The coordinates of human health are complex even in a single population but they are even more complex in migrants whose life situation is always influenced by the host country and the country of origin. Some migrants may experience several host countries and some return to the country of origin. Thus it is important to survey well being, health status, disease panorama and use of health services of immigrants compared to the native population; such analyses would be incomplete without casting a view on the same indicators and parameters in the country of origin. Thus for this project we have collected a team of experts to cover health aspects of the full cycle of migration, viewing the health situation in Egypt, Tunisia and Algeria as representatives of the Mediterranean North African (NA) partner countries, the origins of vast numbers of immigrants in EU. The EU partner countries from France, Italy, Germany (subcontracting Slovenia) and Sweden are not only receivers of the NA immigrants but they also have larger numbers of immigrants from others areas, allowing comparisons between immigrant groups. The team has experience on a variety of health and disease measures and it has an access to a variety of survey and register material relating to population health, disease patterns and function of health care systems. Many of the surveys and diseases registers have been carried out/constructed by the present partners who thus possess unique sources of data. The team will be in the position to respond to the expectations of the call by reviewing health effects of migration from the country of origin to the host country and coming up with scientifically valid state-of-the-art evaluations and appropriate recommendations for scientific and health policy measures in improving the conditions for the EU immigrants.

Keywords: well being,cardiovascular disease,cancer,incidence difference
The impact of endosymbionts on the evolution of host sex determination mechanisms (ENDOSEXDET)

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: France
Call:  (ERC-2010-StG_20091118, 2010)
Start date: 2011-01-01
End date: 2015-12-31
Duration (months): 60.0
Total project cost (EUR): 1403285.0
EU funding (EUR): 1403285.0
Participants: 1
Project status: CLOSED

Appreciation of endosymbiosis, a type of symbiosis in which a microbial partner lives within its host cells, as an important source of evolutionary novelty has developed relatively recently. In this proposal, we investigate a fundamental evolutionary process influenced by bacterial endosymbionts: the mechanisms of sex determination of their eukaryotic hosts. In animals, the most common system of sex determination is genetic. It can also be affected by inherited bacterial endosymbionts. However, very few systems have been analyzed and there is no extensive empirical evidence of how endosymbionts can shape host sex-determining systems. In the isopod crustacean Armadillidium vulgare, genetic sex determination follows female heterogamety. However, many A. vulgare populations harbour Wolbachia bacterial endosymbionts which can invert genetic males into phenotypic functional females. Other sex-determining factors have been identified in A. vulgare: a feminizing f element which may be a Wolbachia genome fragment carrying feminization information inserted into the host nuclear genome, and a masculinizing gene which can restore the male sex in the presence of the f element, as a result of a genetic conflict. Thus, sex determination mechanisms in A. vulgare seem to be largely driven by Wolbachia endosymbionts. However, the molecular genetic basis and evolutionary history of all these sex-determining factors is unknown. The A. vulgare/Wolbachia model provides a unique opportunity for directly investigating the impact of endosymbionts on the evolution of host sex determination mechanisms at the molecular genetic level. We will address this issue using the latest developments of molecular genetics technologies, such as next-generation DNA sequencing and high throughput genotyping.

Keywords: feminizing endosymbionts host sex determination genetic conflict next generation sequencing
TARGETING TUMOUR ASSOCIATED MACROPHAGES IN CANCER (TMAC)

Framework: FP7 — Ideas
Programme: European Research Council
Theme: European research council
Destination: Starting grants
Action type: Support for frontier research (ERC)
Panel: Physiology, Pathophysiology and Endocrinology
Countries involved: France
Call:  (ERC-2010-StG_20091118, 2010)
Start date: 2010-12-01
End date: 2015-11-30
Duration (months): 60.0
Total project cost (EUR): 1499222.0
EU funding (EUR): 1499222.0
Participants: 1
Project status: CLOSED

There is increasing evidence that the body s ability to mount an immune response to cancer cells may dictate which patients are cured of cancer by conventional therapy. Macrophages have a central role in both innate and adaptive immunity; both human and experimental cancers become infiltrated by macrophages, however tumour-associated macrophages (TAM) are corrupted by the tumour microenvironment to promote survival, invasion and metastasis of cancer cells. TAM also contribute to immune-suppression in cancer and evasion of anti-tumour immunity. It is not clear what factors promote the pro-tumour TAM phenotype or the signalling pathways involved. The intrinsic anti-tumour potential of macrophages as innate immune cells and their abundance in solid tumours makes them an attractive therapeutic target. The challenge is to block the cancer-promoting function of these cells and restore their anti-tumour effects. We have previously shown that NF-ºB inhibits the classical activation of macrophages in the context of inflammation and cancer and our preliminary data show that NF-ºB activation in TAM inhibits anti-tumour immunity in transplantable models of cancer. Further studies have shown a subset of IKK²-regulated genes in macrophages are dependent on p38 MAP Kinase (MAPK14) and targeting p38 activity in macrophages also blocks the TAM phenotype. These data suggest IKK²-p38 signalling maintains the pro-tumour phenotype of TAM and inhibits anti-tumour immunity.In this project we will extend our preliminary observations in transplantable tumour models to clinically relevant genetic models of spontaneous cancer in mice. We will also map IKK² and p38 target genes in TAM and investigate IKK²/p38 dependent mechanisms of gene regulation.

Keywords: macrophages
A European Platform for Translational Cancer Research (EUROCANPLATFORM)

Framework: FP7 — Cooperation
Programme: Health
Destination: Translating research for human health
Action type: Network of Excellence
Countries involved: Sweden,France,Denmark,Norway,Spain,Italy,Germany,France,France,United Kingdom,United Kingdom,Hungary,Netherlands,Netherlands,United Kingdom,Belgium,Germany,Spain,Spain,Belgium,Switzerland,Netherlands
Call:  (FP7-HEALTH-2010-single-stage, 2010)
Start date: 2011-01-01
End date: 2016-12-31
Duration (months): 72.0
Total project cost (EUR): 15561005.72
EU funding (EUR): 11998454.0
Participants: 28
Project status: CLOSED

Europe has a number of advantages as regards developing translational cancer research, yet there is no clear European strategy to meet the increasing burden posed by cancer. The FP6 Eurocan+Plus project analysed the barriers underlying the increasing fragmentation of cancer research and stressed the need to improve collaboration between basic/preclinical and comprehensive cancer centres (CCCs), institutions in which care and prevention is integrated with research and education. Furthermore, it proposed the creation of a platform of interlinked cancer centres with shared infrastructures and collaborative projects to facilitate rapid advances in knowledge, and their translation into better cancer care. In response to these challenges and in line with the call, EurocanPlatform will work towards the goal of decreasing cancer mortality by dealing with three main areas of strategic research: prevention, early detection and improved treatments. It will build the necessary resources and know-how for the entire research continuum: basic research, early and late translational research, clinical research, epidemiological research, implementation in care and population based outcome research. There will be a strong focus on discovery-driven translational cancer research in five selected tumours: breast, head-neck, lung, malignant melanoma and pancreatic cancer. Joint structures and programmes for early detection will contribute to optimal treatment, and novel prevention research programmes will integrate prevention activities in clinical cancer centres as well as public prevention. Collaborations will also include molecular pathway-driven clinical research supported by joint structures for omics, biobanking and biomarker validation to support clinical trials aimed at enhancing patient benefits by individualised treatments. EurocanPlatform is unique in its nature and represents a commitment from cancer centres to join forces and resources in order to fight cancer.

Keywords: translational research,biomarkers,prevention,early detection,personalized cancer medicine
Functional and regulatory protein networks of chromatin modifying enzymes (CHROMATINMODWEB)

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: Cyprus
Call:  (ERC-2010-StG_20091118, 2010)
Start date: 2011-01-01
End date: 2016-06-30
Duration (months): 66.0
Total project cost (EUR): 1498278.8
EU funding (EUR): 1498278.8
Participants: 1
Project status: CLOSED

Proper and controlled expression of genes is essential for normal cell growth. Chromatin modifying enzymes play a fundamental role in the control of gene expression and their deregulation is often linked to cancer. In recent years chromatin modifiers have been considered key targets for cancer therapy and this demands a full understanding of their biological functions. Previous biochemical and structural studies have focused on the identification of chromatin modifying enzymes and characterization of their substrate specificities and catalytic mechanisms. However, a comprehensive view of the biological processes, signaling pathways and regulatory circuits in which these enzymes participate is missing. Protein arginine methyltransferases (PRMTs), which methylate histones and are evolutionarily conserved from yeast to human, constitute an example of chromatin modifying enzymes whose functional and regulatory networks remain unexplored. I propose to use complementary state-of-the-art genomic and proteomic approaches in order to identify the protein networks and cellular pathways that are linked to PRMTs. In parallel, I will identify novel regulatory circuits and define the molecular mechanisms that control methylation of specific histone arginine residues. I will utilize the yeast S. cerevisiae as a model organism because it allows genetic, biochemical and genomic approaches to be combined. Most importantly, many of the pathways and mechanisms in yeast are highly conserved and therefore, the findings from this study will be pertinent to human and other eukaryotic organisms. Establishing a global cellular wiring diagram of PRMTs will serve as a paradigm for other chromatin modifiers and is imperative for assessing the efficacy of these enzymes as therapeutic targets.

Keywords: arginine methylation,saccharomyces cerevisiae,genetic interactions,histone modifications
System-wide analysis of regulatory processes that mediate at the boarder of metabolome and proteome (METABOLICREGULATORS)

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: United Kingdom
Call:  (ERC-2010-StG_20091118, 2010)
Start date: 2011-06-01
End date: 2016-05-31
Duration (months): 60.0
Total project cost (EUR): 1499996.0
EU funding (EUR): 1499996.0
Participants: 1
Project status: CLOSED

The metabolic network has a modular architecture, is robust to perturbations, and responds to biological stimuli. The balance of the network, and the passageway of network substructures to operate at different activity, requires intensive interactions between the metabolic network, the transcriptome and the proteome. However, the biochemical mechanisms monitoring the metabolic network are only barely understood. Changes in network activity are often mediated through so called reporter metabolites: general -network interconnecting cofactors and reaction substrates - and specific pathway intermediates. These metabolites bridge the gap between the small molecule and macromolecular universe of the cell. Here we propose combining systematic yeast genetics with targeted metabolomics and proteomics to understand mechanisms of metabolic regulation on a genome-scale level. In principle, we will elaborate multiple reaction monitoring (MRM) assays that facilitate quantification of enzymes and intermediates of selected metabolic pathways via liquid chromatography tandem mass spectrometry. The analysis will be performed on metabolic processes that influence aging; those will be analyzed and the results validated by chemical-genetic profiling and competitive lifespan experiments. The anticipated results will yield in a system-wide picture of interactions between the metabolome and regulatory components of the cell. Furthermore, it will identify novel genetic and biochemical interactions of the aging process. Understanding these mechanisms will stimulate new research directions in Systems Biology and support the development of therapeutic strategies against diseases of aging.

Keywords: metabolic network,reporter metabolite,chemical-genetic interactions,systematic yeast genetics,robustness
Dynamic Interplay between Eukaryotic Chromosomes: Impact on Genome Stability (DICIG)

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: France
Call:  (ERC-2010-StG_20091118, 2010)
Start date: 2011-06-01
End date: 2017-05-31
Duration (months): 72.0
Total project cost (EUR): 1497000.0
EU funding (EUR): 1497000.0
Participants: 1
Project status: CLOSED

The structure and role of the DNA molecule raise fascinating questions regarding its dynamics, i.e. not only the tri-dimensional reorganisation associated with functional events at short time-scale, but also the structural changes, i.e. rearrangements, that occur in the chromosome over generations. It is increasingly obvious that the physical properties of both the chromosomes and their environment the nucleoplasm, the nuclear periphery, cytoskeleton, etc. are playing important roles in the dynamic changes observed. For instance, we recently showed that chromosome movements during mid-prophase of meiosis in budding yeast result from a trans-acting force generated at the level of the global cytoskeleton network, suggesting that extranuclear mechanical trans-acting signals could also regulate chromosomal metabolism in other ways. Our objectives are to make important contributions to the understanding of the mechanical and functional interplay between the cytoskeleton, the nuclear periphery, and chromosomes through in vitro and in vivo interdisciplinary approaches. We will investigate three questions of fundamental importance: i) the potential transmission and function of mechanical forces from the cytoskeleton to chromatin during interphase, ii) the physical principles that govern chromosome reorganization under mechanical force in vitro, and iii) the global chromatin dynamics during the fundamental S phase and its impact on genome stability. We will use a combination of high-resolution imaging, micromanipulation, and high-throughput molecular techniques (chromosome conformation capture and ChIP-Seq) to reach our goals. Most of these studies will be performed in budding yeast, but will have repercussions in our understanding of higher eukaryotes metabolism.

Keywords: microfluidic,replication,chromosome dynamics,chromatin organization
Protein Friction of Molecular Machines: Nanomechanics with Optical Tweezers (NANOMECH)

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: Germany,Germany
Call:  (ERC-2010-StG_20091118, 2010)
Start date: 2010-12-01
End date: 2015-11-30
Duration (months): 60.0
Total project cost (EUR): 1500000.0
EU funding (EUR): 1500000.0
Participants: 2
Project status: CLOSED

Molecular machines---assemblies of macromolecules, often fueled by nucleotide hydrolysis---are fascinating devices and crucial for driving self-organization in cells. While protein components of many biological machines have been identified, and in many cases their structures have been solved, the mechanical principles that govern the operation of biological machines are poorly understood. For example, how much force can they generate; and what limits their speed and efficiency? These questions have been difficult to answer because the tools needed to study nanometer-sized machines that generate minute forces on the order of piconewtons have not been available until recently. Friction arises between proteins when they interact by making and breaking weak intermolecular bonds. When a bond breaks, the energy stored in its deformation is dissipated. Protein friction is a useful concept because it provides mechanical insight and allows for quantitative theoretical understanding of the dynamics and energy balance of mechanical cellular processes. In cells, many motor proteins often cooperate to drive motility. I will ask how friction and force-generation arise and scale with the number of motors to elucidate how collective behavior and self-organization emerge. The goals of this interdisciplinary project address the role that protein friction plays in limiting the dynamics and efficiency of microtubule-based motor proteins using a novel, combined optical tweezers and single-molecule fluorescence apparatus. In the long term, I hope that our avant-garde nanotechnological tools will be applicable to other molecular machines and that the studies on microtubule-based motors will shed light on the way that cells use energy to create pattern and order.

Keywords: single molecule biophysics,biological nanomachines,molecular motors,optical tweezers,friction
Post-infectious immune reprogramming and its association with persistence and chronicity of respiratory allergic diseases (PREDICTA)

Framework: FP7 — Cooperation
Programme: Health
Destination: Translating research for human health
Action type: Collaborative project
Countries involved: Greece,United Kingdom,Austria,Switzerland,Poland,Belgium,Germany,Finland,Germany,France
Call:  (FP7-HEALTH-2010-single-stage, 2010)
Start date: 2010-10-01
End date: 2016-03-31
Duration (months): 66.0
Total project cost (EUR): 7862161.8
EU funding (EUR): 5991600.0
Participants: 13
Project status: CLOSED

Chronic inflammatory diseases associated with allergy, including asthma and rhinitis, constitute a major and continuously growing public health concern for Europe. However, the causative factors and mechanisms converting a physiological inflammatory reaction to a chronic response triggering allergic disease remain elusive. Viral infections, particularly those caused by human rhinoviruses (RV) are the most frequent triggers of acute asthma exacerbations. RV infections have more recently been associated with asthma initiation; there is evidence suggesting that such infections may also contribute to respiratory allergy persistence. The strategic aims of PreDicta are to evaluate the hypothesis that repeated infections reprogram the immune system towards a persistent inflammatory pattern leading to respiratory allergies by (i) dissecting the molecular and cellular mechanisms involved in the lack of resolution of inflammation in the context of a human disease, (ii) identifying specific infectious agents and underlying altered host-pathogen interactions, and develop relevant prognostic and therapeutic strategies. PreDicta follows three interconnected workflows: models, mechanisms and translational output. Models include a longitudinal cohort in children, mouse models of repeated virus infection, primary epithelial cultures from patients, viral-bacterial interaction models, and models of epithelial-T-cell-dendritic cell interactions. These will be used to look into disease persistence, inflammation patterns, dysbiosis, immune regulation and resolution of inflammation. Translational outputs include prognostic use of subtype-specific antiviral antibodies, DNAZymes for therapeutic use and delivery technologies targeted to the bronchial epithelium. This interdisciplinary Consortium with strong track record, unique resources and strong translational focus, aims to produce new knowledge and technologies that can rapidly and effectively reach clinical care.

Keywords: allergy,asthma,immune regulation,inflammation,resolution,rhinitis,rhinovirus,viral infections