Data-Gouv-ML/pcri-informations-sur-les-projets-laureats huggingface dataset:
Open Mashup Enterprise service platform for LinkEd data in The TElco domain (OMELETTE)

Framework: FP7 — Cooperation
Programme: Information and Communication Technologies
Destination: Pervasive and Trustworthy network and service infrastructures
Action type: Collaborative project
Countries involved: China,Germany,Germany,Netherlands,Italy,Spain,United Kingdom,Germany
Call:  (FP7-ICT-2009-5, 2009)
Start date: 2010-10-01
End date: 2013-06-30
Duration (months): 33.0
Total project cost (EUR): 5963457.0
EU funding (EUR): 3823392.0
Participants: 9
Project status: CLOSED

The convergence of Telecom, IT and content services drives new emerging service markets based on an open Internet of Services. Mashups have gained big success in the so-called Web 2.0. The success of the Web 2.0 services has encouraged Telcos to expose their assets as Telco services in order to provide third parties with facilities to build their business. Moreover, the exposure of network infrastructure as services is facilitating the entry of new API-driven telco agents that bring traditional telco services (telephony, messaging, IP location, etc.) to the Web. Yet, the technologies underlying each of the different mashup types are heterogeneous, which makes integration challenging. Also, mashups do not offer a universal composition model either, since mashup development is not vendor independent. In this landscape, OMELETTE aims at researching on the development, management, governance, execution and conception of converged services with a specific focus on the telco domain. OMELETTE will create a sound model of mashups that follows the REST architectural style (also supported by standard widget technology), as well as a standard specification of a mashup-containing platform that may guarantee portability and interoperability among different vendors and versions. These concepts will be based on a solid theoretical model of mashup foundations and the specific requirements gained from the telco domain. OMELETTE will aim at breaking the barriers between the web, telecommunication and hybrid services, taking into account the convergence of IT/telecom/content systems. OMELETTE will foster as well the reuse of existing components and mashups, thanks to its automated service discovery functionalities. Project OMELETTE aims at developing an open platform for building convergent mashups for the telco domain to be used within several industry-driven use cases.

Keywords: mashup,widget,interoperability,platform,recommendation,telco library,assisted development,automated discovery,telco mashups,speech mashups,streaming mashups,web mashup
Education in Cultural Understanding, Technologically-Enhanced (ECUTE)

Framework: FP7 — Cooperation
Programme: Information and Communication Technologies
Destination: Digital libraries and content
Action type: Collaborative project
Countries involved: United Kingdom,Portugal,Germany,Netherlands,Germany,United Kingdom,Japan
Call:  (FP7-ICT-2009-5, 2009)
Start date: 2010-09-01
End date: 2013-12-31
Duration (months): 40.0
Total project cost (EUR): 3297014.0
EU funding (EUR): 2400000.0
Participants: 8
Project status: CLOSED

In 21stC Europe, many cultural, ethnic and religious groups must live and work together. This is not always a smooth process; cultural differences can lead to social stresses and sometimes outright conflict. Thus education in cultural awareness and understanding has a very significant role. This is an educational domain in which attitudes and behaviours count much more than knowledge alone, and where developing empathy is a key pedagogical mechanism. Experiential approaches using role-play and case-studies have been shown to be highly effective, but can be difficult and expensive to organise. eCUTE will develop innovative technologically-enhanced learning approaches in cultural awareness and understanding that will help with these problems, based on virtual world simulations with intelligent interactive graphical characters embodying models of culturally-specific behaviour and interaction in scenarios developed via a user-centred design process. It will target two contrasting learner types-late primary-age children (9-11) and young adults (18-25) . We will: a) Develop pedagogical approaches to education in cultural understanding grounded in psychological and educational theory; b) Create believable cultural learning scenarios based on theoretical approaches that connect with the experiences of the target learner groups c) Establish an operational parameterisation of theoretically derived cultural behaviour and use it to create synthetic cultures and characters that behave as if they live within such cultures; d) Develop expressive behaviour for synthetic characters that is culturally appropriate; e)Create two cultural Virtual Learning Environments (VLEs), one for late-primary children and the other for young adults based on virtual dramas using synthetic characters with culturally-specific interaction behaviour; f)Evaluate the created systems with stakeholder, teacher and learner groups, demonstrating their learning efficacy.

Keywords: education in cultural awareness and understanding,intelligent virtual actors,narrative and affective engagement
Microbial translocation across host barriers (MICROTRANS)

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: France
Call:  (ERC-2010-StG_20091118, 2010)
Start date: 2010-11-01
End date: 2016-10-31
Duration (months): 72.0
Total project cost (EUR): 1499710.0
EU funding (EUR): 1499710.0
Participants: 1
Project status: CLOSED

Infections remain the primary cause of mortality in humans. New infections are emerging, and resistance to antimicrobial drugs is widespread and expanding. There is thus an urgent need to develop novel therapeutic strategies based on rationally-designed drugs blocking the pathogenic effects of microbes on the host. A prerequisite for this is a complete understanding of the pathophysiology of infectious diseases. Systemic infections result from the invasion of hosts by a microbial pathogens, and a critical pathogenic determinant is thus microbial translocation from the external environment into the host and dissemination to protected tissues such as the central nervous system and the fetus. Our project is focused on understanding the molecular mechanisms underlying the ability of certain microbes to cross the intestinal barrier, the blood-brain barrier and/or the placental barrier. Specifically, we will pursue the following objectives: (i) understand how invasive pathogens adhere to host barriers, (ii) understand how invasive pathogens cross cell monolayer barriers, (iii) determine microbial fate and dynamics within the host, and (iv) determine how host responses influence barrier vulnerability to invasive pathogens. Because we will address these biological questions in a tissue and whole-host context, this project will integrate in vitro, ex vivo, and in vivo approaches. It will allow us to address questions in a novel dimension, defining a transition from cellular microbiology to tissular microbiology. Completion of our objectives will provide critical information on key pathophysiological steps critical for the understanding of microbial pathogenesis, and will also improve our basic knowledge of host barriers biology during homeostasis and upon microbial aggression.

Keywords: infection,barrier,pathophysiology,bacteria,epithelial,endothelial,cell,tissue,in vivo,imaging
Single-Molecule BioAssays at Elevated Concentrations (SIMBA)

Framework: FP7 — Ideas
Programme: European Research Council
Theme: European research council
Destination: Starting grants
Action type: Support for frontier research (ERC)
Panel: Applied life sciences and biotechnology
Countries involved: Germany
Call:  (ERC-2010-StG_20091118, 2010)
Start date: 2010-11-01
End date: 2016-10-31
Duration (months): 72.0
Total project cost (EUR): 1456374.0
EU funding (EUR): 1456374.0
Participants: 1
Project status: CLOSED

In order to advance single-molecule fluorescence spectroscopy to the next level, handling and analysis of single molecules has to become broadly available. A further quantum leap is required to proceed to commercially successful applications such as drug screening and medical diagnostics. In this project, I suggest a strategy to overcome the fundamental gap between the nanomolar concentration regime of current optical single-molecule spectroscopy and the nano- to millimolar dissociation constants of typical biomolecular interactions. I will use nano-apertures, which confine the detection to sub-attoliter volumes and allow single-molecule studies at elevated concentrations. To overcome unspecific binding and deteriorated fluorescence signals in the nano-apertures, I will use tailor-made DNA nanostructures produced by DNA origami. These nanostructures will match the nano-apertures like a plug in a socket. Inserting molecules at programmed positions in the nanostructures will open up a new realm of applications by the ability to immobilize exactly one molecule per nano-aperture and by obtaining comparable signals from every nano-aperture. I will spectroscopically characterize the nano-apertures creating a fluorescence map of their inside. I will exemplarily use the new abilities for previously impossible applications such as several folds improvement of single-molecule DNA sequencing, direct single-molecule RNA sequencing by reverse transcriptase for cancer screening, for paralleled drug screening of HIV protease inhibitors and for studying the chemomechanical coupling of single helicases. In summary, I envision a broadly applicable platform that has the potential to become a golden standard by enabling both ground breaking fundamental research and commercial applications.

Keywords: single molecule spectroscopy,dna nanotechnology,molecular motors enzymes,biomolecular assays,drug screening,medical diagnostic
Revealing the mechanism of host membrane rupture by invasive pathogens and its role in triggering the immune response (RUPTEFFECTS)

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: France
Call:  (ERC-2010-StG_20091118, 2010)
Start date: 2011-03-01
End date: 2016-08-31
Duration (months): 66.0
Total project cost (EUR): 1488512.0
EU funding (EUR): 1488512.0
Participants: 1
Project status: CLOSED

Pathogens have been evolving with their hosts for millions of years adopting tailored strategies to propagate within the host body and evading the host immune response. It is crucial to understand the underlying strategies employed by pathogens on the cellular and molecular level in order to develop novel weapons against them. On the cellular level, host-pathogen interactions are generally very dynamic and tightly regulated. Therefore, it has been difficult to establish methodologies that can capture this cross-talk. To overcome these hurdles, we have been developing novel approaches to monitor the dynamic host-pathogen interactions. Our laboratory is taking advantage of fluorescent reporter molecules, which we use and/or develop to obtain information on molecular processes in single living cells. The key question of host cell invasion to be addressed will be (i) how do entero-pathogenic bacteria invade cells and (ii) how do the latter sense the incoming pathogens. First, we will use a novel assay to understand how an individual invading bacterium, such as Shigella hijacks host cellular machineries and ruptures the vacuolar membranes upon cellular uptake to escape into the host cytoplasm. Secondly, we will reveal how the change of intracellular localization of invasive pathogens impacts on the induced host immune response. Concerning this, we have established an assay to track the host gene expression response quantitatively (from any promoter of interest) during pathogen invasion in single cells with a timely resolution of seconds to minutes. Together, this will allow us to precisely understand the molecular mechanisms how invasive bacteria interfere with eukaryotic cellular trafficking and signal transduction pathways to alter host immune responses. Thus, beyond providing novel targets for antimicrobial therapy, our study will pave the way to understand fundamental cellular processes.

Keywords: functionalized microscopy
Cell and gene therapy based strategies to correct the bleeding phenotype in Hemophilia A (CGT HEMOPHILIA A)

Framework: FP7 — Ideas
Programme: European Research Council
Theme: European research council
Destination: Starting grants
Action type: Support for frontier research (ERC)
Panel: Diagnostic tools, therapies and public health
Countries involved: Italy
Call:  (ERC-2010-StG_20091118, 2010)
Start date: 2011-05-01
End date: 2017-04-30
Duration (months): 72.0
Total project cost (EUR): 1123000.0
EU funding (EUR): 1123000.0
Participants: 1
Project status: CLOSED

Currently, haemophilia A cannot be cured. To prevent major bleeding episodes in haemophilia, human Factor VIII (FVIII) protein must be frequently administered as prophylaxis or on demand. This treatment is complicated by its high cost and development of antibodies that neutralize FVIII activity in 20 to 30% of the patients. Therefore, permanent solutions in the form of cell and gene therapy are very attractive for haemophilia A. Recently, we demonstrated in a murine model that liver sinusoidal endothelial cells (LSEC) produce and secrete FVIII, although not exclusively. We have also found that these mice can be treated by reconstitution with wild-type bone marrow, indicating that bone marrow-derived cells, of hematopoietic, mesenchymal or even endothelial origin, can produce and secrete FVIII. Based on these findings in mice, I propose that human LSEC, umbilical cord blood cells, and bone marrow cells might be suitable sources of FVIII to be used for cell replacement therapy for haemophilia A. To advance opportunities for cell and gene therapies in haemophilia A and for identifying additional cell sources of FVIII, I intend to explore whether replacement of liver endothelium and bone marrow in immnocompromised Haemophilia A mice with healthy human cells will provide therapeutic correction. Recently, the possibility of reprogramming mature somatic cells to generate induced pluripotent stem (iPS) cells has enabled the derivation of disease-specific pluripotent cells, thus providing unprecedented experimental platforms to treat human diseases. Therefore, I intend to study whether the generation of patient-specific iPS cells may be applied to cell and gene therapy of coagulation disorders and in particular for the treatment of Haemophilia A. Studies with these novel target cells may impact significantly the future course of Haemophilia A by providing proof-of feasibility of a novel therapy strategies.

Keywords: hemophilia
THE ENZYMATIC MACHINERY OF HUMAN MITOCHONDRIAL DNA MAINTENANCE (REPMIT)

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: Sweden
Call:  (ERC-2010-StG_20091118, 2010)
Start date: 2011-04-01
End date: 2016-03-31
Duration (months): 60.0
Total project cost (EUR): 1492684.0
EU funding (EUR): 1492684.0
Participants: 1
Project status: CLOSED

SUMMARY Mitochondria are required to convert food into usable energy forms and every cell contains thousands of them. Unlike most other cellular compartments, mitochondria have their own genomes (mtDNA) that encode for 13 of the about 90 proteins present in the respiratory chain. All proteins necessary for mtDNA replication, as well as transcription and translation of mtDNA-encoded genes, are encoded in the nucleus. Mutations in nuclear-encoded proteins required for mtDNA maintenance is an important cause of neurodegeneration and muscle diseases. The common result of these defects is either mtDNA depletion or accumulation of multiple deletions of mtDNA in postmitotic tissues. Research in my laboratory will elucidate the molecular mechanisms and regulation of mitochondrial DNA replication in human cells. We will establish how mtDNA is packaged into nucleoprotein complexes, a.k.a. nucleoids and establish how these nucleoids are selected for mtDNA replication. We will elucidate the molecular mechanisms by which specific mutations in the mtDNA replication machinery affect mtDNA maintenance and cause human disease. Mitochondrial dysfunction is not limited to rare, genetic disorders, but also associated with age-associated common diseases as well as with the normal aging process. I will use my biochemical insights in combination with mouse genetics to address the hypothesis that increased mtDNA mutation load may be an important cause of normal aging. My specific aims will be: Aim 1. To define how initiation of mtDNA replication at OriH is regulated. Aim 2. To identify and characterize regulators of mtDNA replication. Aim 3. To characterize the structure and function of the mtDNA nucleoid in DNA replication. Aim 4. To address the mitochondrial theory of ageing

Keywords: mitochondrion,dna replication
Network Principles of Neuroendocrine Control: Tuberoinfundibular Dopamine (TIDA) Oscillations and the Regulation of Lactation (ENDOSWITCH)

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-2010-StG_20091118, 2010)
Start date: 2011-01-01
End date: 2015-12-31
Duration (months): 60.0
Total project cost (EUR): 1493958.0
EU funding (EUR): 1493958.0
Participants: 1
Project status: CLOSED

The hypothalamus is essential for our survival and orchestrates every vital function of the body, from defence against predators and energy metabolism to reproduction. Yet, the network mechanisms underlying these actions remain largely hidden in a black box . Here, we will focus on the hypothalamic neuroendocrine system, where we have identified a novel robust network oscillation in the tuberoinfundibular dopamine (TIDA) neurons that control prolactin release. This oscillation is synchronized between neurons via gap junctions, and phasic firing is transformed into tonic discharge by compounds that functionally oppose neuroendocrine dopamine actions. Using this novel preparation, we will investigate the 1) the cellular (conductance) and network (connectivity) mechanisms underlying TIDA rhythmicity; 2) how TIDA activity is affected by hormones and transmitters that affect lactation; 3) the functional significance of phasic vs. tonic discharge in the regulation of dopamine release and lactation; and 4) the generality of TIDA cellular and network properties to other parvocellular neuron populations. These questions will be addressed through several in vitro and in vivo electrophysiological techniques, including slice whole-cell recording, extracellular in vivo recording, voltammetry and optical recording. These experiments will provide novel insight into the link between network interactions and behaviour, and have important clinical implications for e.g. endocrine and reproductive disorders.

Keywords: dopamine,electrophysiology,hypothalamus,network,oscillation,lactation,neuroendocrine,peptide
HIF and hepcidin : missing links between infection, iron metabolism and cancer ? (HIFHEPC)

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: 2011-06-01
End date: 2016-05-31
Duration (months): 60.0
Total project cost (EUR): 1500000.0
EU funding (EUR): 1500000.0
Participants: 1
Project status: CLOSED

HIF transcription factors, central mediators of cellular adaptation to critically low oxygen levels (=hypoxia), have been largely studied for their crucial role during cancer development. Our recent findings have unveiled two new major roles of HIF. First, in innate immunity and infection, we demonstrated the key contributions of HIFs in regulating important immune effectors molecules. Second, we highlighted the role of HIFs in iron metabolism as critical regulators of iron absorption in the intestine and in systemic iron homeostasis by regulating the liver synthesis of the iron regulatory hormone, hepcidin. These results open new research areas and our research program, based on unique mouse models of conditional HIFs and hepcidin knockout, will be developed around three main axes. 1) define the physiological roles of HIF and hepcidin in different key organs involved in maintaining body iron homeostasis. A detailed understanding of the regulation of iron-related proteins is a prerequisite in the development of therapeutics for iron diseases, which pose a major problem worldwide. 2) study the role of hepcidin during bacterial infection and tumorigenesis, two pathological conditions where iron is critically required for the proliferation of the pathogens and for cancer cells to feed their high metabolic activity. 3) determine the contribution of HIFs in the initiation of tumor development in response to infection. Indeed, our findings that HIF is stabilized by bacteria, even under normal levels of oxygen, and is an essential component of the inflammation response, let us to speculate that HIFs may be a missing link between infection and cancer by triggering a high chronic inflammatory response. For that, we will use the model of the gastric cancer, whose the initiating event is an infection by Helicobacter Pylori.

Keywords: iron,hif,hepcidin,infection,cancer