Data-Gouv-ML/pcri-informations-sur-les-projets-laureats huggingface dataset:
ON THE COSTS OF KNOWLEDGE PRIVATIZATION (SOFTPAT)

Framework: FP7 — People
Programme: Marie-Curie Actions
Theme: Marie Skłodowska-Curie
Destination: Life-long training and career development
Action type: Support for training and career development of researchers (Marie Curie)
Countries involved: Luxembourg
Call:  (FP7-PEOPLE-2013-CIG, 2013)
Start date: 2014-05-01
End date: 2018-04-30
Duration (months): 48.0
Total project cost (EUR): 100000.0
EU funding (EUR): 100000.0
Participants: 1
Project status: CLOSED

Patent systems are supposed to spur incentives to innovate 1) by granting inventors temporary monopoly rights that allow them to recoup their research and development (R&D) investment and 2) by facilitating follow-up inventions by making information about technical inventions available to the public. In other words, patents make technical information available to society at the cost of “privatization” of this knowledge. Knowledge freely available to the public, as for instance through scientific publications, has been shown to be essential for corporate innovation and productivity growth. The privatization of knowledge can, hence, hamper innovation and technological progress. This project makes use of a natural experiment to investigate the effects of knowledge privatization. It is in general hard to examine the effects of patent systems because virtually all industrialized economies have patent systems in place so that a counterfactual situation, i.e. how an economy would look like without patents, is missing as a required benchmark for policy evaluation. This project will make use of the introduction of software patents in the U.S. in the mid-1990s as an event that allows identifying effects of the establishment of patent rights. This project will, first, investigate the extent to which the introduction of software patents led to a privatization of knowledge. In other word, the switch from publications in academic journals and proceedings to patents by individual software engineers will be scrutinized. In the next steps, implications of knowledge privatization for corporate productivity and industry concentration of R&D will be investigated. Since the introduction of U.S. software patents coincided with the internet revolution control samples from Europe will be used. Europe did not experience an introduction of software patents in the 1990s so that the comparison allows to separate patent regulation induced effects from macroeconomic shocks.

Keywords: knowledge privatization,patents,innovation,productivity,industry concentration,software patents
Measuring and modeling how misregulation in gene regulatory networks causes intellectual disability (MISREGULATID)

Framework: FP7 — People
Programme: Marie-Curie Actions
Theme: Marie Skłodowska-Curie
Destination: Life-long training and career development
Action type: Support for training and career development of researchers (Marie Curie)
Countries involved: Netherlands
Call:  (FP7-PEOPLE-2013-CIG, 2013)
Start date: 2014-03-01
End date: 2018-02-28
Duration (months): 48.0
Total project cost (EUR): 100000.0
EU funding (EUR): 100000.0
Participants: 1
Project status: CLOSED

Intellectual disability (ID) is a neurodevelopmental disorder with a strong genetic component. For many patients the genetic cause is yet unknown as no protein-damaging mutations can be identified. To accurately predict the risk for ID from a person’s complete DNA sequence, it is essential to know how and when genetic perturbation of a gene regulatory element causes abnormal neurodevelopment. The knowledge and statistical methodology to do so are currently lacking. Recently, the ENCODE and Roadmap Epigenomics projects identified millions of gene regulatory elements across a wide range of tissues. These regulatory elements are small DNA regions where cooperative binding of specific transcription factors (TFs) strongly influences the level of expression of one or more genes, often in a highly tissue-specific manner. However, since only static characterizations are available, it is very difficult to predict how the transcriptional network defined by the regulatory elements responds to genetic perturbations. I will therefore perturb gene regulatory elements underlying ID by knocking-down the expression of established ID transcription factors in neurons. Previous efforts relied on partial or noisy measurements of TF binding. Instead, I will use TF-footprinting to obtain a complete view of how the knock-down perturbs TF-binding in gene regulatory elements. Combining this with gene expression and epigenetic profiling, I will model of how perturbation of cooperative binding in regulatory elements causes misregulation of ID and neurodevelopmental genes. To predict how perturbation of the transcriptional network disrupts biological pathways, I will integrate in my Bayesian network model existing data sets of neuronal morphology, structural brain imaging GWAS, and behavioural studies in model organisms. My research will provide much-needed understanding and methodology to predict the functional consequences of genetic perturbation of gene regulatory elements for ID.

Keywords: genomics,gene regulation,gene regulatory networks,transcriptional networks,intellectual disability
Innate immune recognition of intracellular DNA as 'stranger' and 'danger' signal (IFNDNA)

Framework: FP7 — People
Programme: Marie-Curie Actions
Theme: Marie Skłodowska-Curie
Destination: Life-long training and career development
Action type: Support for training and career development of researchers (Marie Curie)
Countries involved: United Kingdom
Call:  (FP7-PEOPLE-2013-CIG, 2013)
Start date: 2015-01-01
End date: 2018-12-31
Duration (months): 48.0
Total project cost (EUR): 100000.0
EU funding (EUR): 100000.0
Participants: 2
Project status: CLOSED

The innate immune system provides an immediate response to infection and injury. It relies on the detection of pathogen-associated molecular patterns (PAMPs), molecular hallmarks of infection which are shared amongst different pathogens but are absent from healthy host cells. The detection of intracellular DNA as PAMP has emerged a key event in the innate immune response to DNA viruses, retroviruses and intracellular bacteria. In some circumstances the body’s own DNA can also be also detected as a danger-associated molecular pattern (DAMP), e.g. when DNA from dying cells is not cleared effectively, and this can play a role in the development of autoimmune conditions such as systemic lupus erythematosus. One of the responses to foreign DNA is the secretion of interferons and pro-inflammatory cytokines, which then help to establish an antiviral state in the infected cell and its neighbours, and alert more specialised immune cells to the danger. Several proteins have been proposed to act as interferon-inducing DNA receptors, including most recently the enzyme cyclic GMP-AMP synthase, which provides a particularly elegant signalling pathway through production of cyclic GMP-AMP as second messenger. However, it is no yet know whether other receptor proteins also utilise this signalling pathway, how signalling is regulated, and how foreign DNA is distinguished from the cell's own genome. The objectives of this project are: 1.) To test the involvement of DNA receptors in the recognition of DNA as 'stranger' and 'danger' signal in human cells 2.) To examine the interplay between DNA receptor candidates 3.) To identify novel regulators of the DNA-induced signalling pathway 4.) To define the nature of the DNA ligand that is recognised by innate immune receptors By elucidating the molecular mechanisms of DNA sensing by the innate immune system, this project has great scientific and medical relevance for the fields of infection, vaccination and autoimmunity.

Keywords: innate immunity,interferon,dna sensing.
Are Heat Shock Protein 90 (Hsp90) Co-Chaperones Virulence Factors in the Human Fungal Pathogen Candida albicans? (HSP90COCHAPERONES)

Framework: FP7 — People
Programme: Marie-Curie Actions
Theme: Marie Skłodowska-Curie
Destination: Life-long training and career development
Action type: Support for training and career development of researchers (Marie Curie)
Countries involved: United Kingdom
Call:  (FP7-PEOPLE-2013-CIG, 2013)
Start date: 2014-11-01
End date: 2019-07-03
Duration (months): 48.0
Total project cost (EUR): 100000.0
EU funding (EUR): 100000.0
Participants: 1
Project status: CLOSED

Most women will suffer at least one Candida albicans infection in their life. While the majority of infections are not life-threatening, 50% of systemic infections in immunocompromised patients are lethal. Treating C. albicans is challenging due to the close association with its human host, paucity of drug targets and drug resistances. The conserved essential heat shock protein 90 (Hsp90) governs virulence, morphogenesis and drug resistance in C. albicans. Yet, Hsp90 inhibition during mouse candidemia caused host toxicity. Hsp90 does not operate alone. In C. albicans it associates with ten co-chaperones. In C. albicans but not its non-pathogenic relative Saccharomyces cerevisiae, co-chaperone genes are close to telomeres, which is reminiscent of virulence genes in other pathogens. By targeting virulence genes, instead of essential genes, C. albicans virulence could be decreased without reducing its fitness, which would alleviate selective pressure favoring drug resistance mutations. Thus, are C. albicans co-chaperones virulence factors that could be exploited as drug targets? Hsp90 co-chaperones will be investigated in three objectives: (1) Quantify the impact of Hsp90 co-chaperones on fungal virulence. Gene deletion mutants will be tested in four virulence assays. (2) Determine the causes and consequences of the telomere proximal localization. Loss-of-heterozygosity (LOH) and transcriptional silencing will be measured in wild type as well as LOH and silencing mutants to determine cause of proximal telomere location and consequences on virulences. (3) Elucidate the transcriptional regulation of Hsp90 co-chaperone genes. Co-chaperones will be screened for transcription factor (TF) binding sites and ChIP-seq conducted on TFs controlling co-chaperone expression. Understanding the virulence potential and transcriptional landscape of Hsp90 co-chaperones will yield insights into fungal virulence strategies and further their development as drug targets.

Keywords: candida albicans,saccharomyces cerevisiae,hsp90,cdc37,co-chaperones,telomeres,chip-seq,biofilms,iron,virulence,loh,transcriptional silencing,darwinian medicine
Identification of alternative splicing networks defining embryonic stem cell identity (SPLICE-STEM)

Framework: FP7 — People
Programme: Marie-Curie Actions
Theme: Marie Skłodowska-Curie
Destination: Life-long training and career development
Action type: Support for training and career development of researchers (Marie Curie)
Countries involved: France
Call:  (FP7-PEOPLE-2013-CIG, 2013)
Start date: 2014-03-01
End date: 2018-02-28
Duration (months): 48.0
Total project cost (EUR): 100000.0
EU funding (EUR): 100000.0
Participants: 1
Project status: CLOSED

Adult, embryonic stem cells (ESC) and induced pluripotent stem cells (iPSC) possess the fundamental properties to self-renew while remaining pluripotent. These unique capacities are regulated by gene networks which expression is tightly controlled at the epigenetic, transcriptional and post-transcriptional levels to insure proper stem cell fate decisions in response to developmental or environmental cues. Alterations of these networks in cancer stem cells (CSC) support their tumorigenic activity. Therefore, defining the molecular pathways that control the maintenance of self-renewal and pluripotency is not only important to understand normal development but could also improve the clinical potential of adult stem cells, ESCs and iPSCs, and reveal novel strategies to target CSCs. Our objective is to identify novel mechanisms controlling the genetic programs that define the fate of ESCs. Along this line, we recently revealed a central role for alternative splicing (AS) in the regulation of the core ESC pluripotency regulatory circuitry. AS affects over 95% of multi-exon human genes and regulates gene expression by promoting transcriptome and proteome diversity. Although ESCs display a high degree of transcriptome complexity and express a large number of isoforms of unknown function, the extent and significance of AS contribution to this functional diversity remain largely unclear. We propose to characterize molecular pathways that modulate AS programs and reshape the landscape of gene regulation which controls the pluripotency and self-renewal capacities of stem cells. More precisely, we will: 1- Identify splicing factors that control conserved AS events in mouse ESCs and support the maintenance self-renewal and pluripotency; 2- Characterize AS and gene networks coordinated by these essential factors to reshape the transcriptome of mouse ESCs; 3- Define the regulatory code underlying the in vivo regulation of ESC-specific AS networks by these splicing factors.

Keywords: embryonic stem cells,pluripotency and self-renewal maintenance,transcriptome diversity,alternative splicing regulation,novel splicing factors,splicing networks,prediction of splicing outcome
Quantitative Banking (BANKING)

Framework: FP7 — People
Programme: Marie-Curie Actions
Theme: Marie Skłodowska-Curie
Destination: Life-long training and career development
Action type: Support for training and career development of researchers (Marie Curie)
Countries involved: United Kingdom
Call:  (FP7-PEOPLE-2013-CIG, 2013)
Start date: 2014-04-01
End date: 2018-03-31
Duration (months): 48.0
Total project cost (EUR): 100000.0
EU funding (EUR): 100000.0
Participants: 1
Project status: CLOSED

This is a quantitative study of banking behaviour in both partial and general equilibrium settings with incomplete markets. Despite the importance of banks and the possibility of banking defaults in a crisis, there exists little work studying bank behaviour in a quantitative setting. Using micro data from banks’ balance sheets, we establish stylized facts about individual bank behaviour. At the cross sectional level, more leveraged banks are more likely to default, larger banks (by asset size) are more leveraged, have lower equity as a share of deposits and rely more heavily on the federal funds market to finance new loans. At the time series (aggregate) level, problem loans rise in a recession and are negatively correlated with new loan growth, the aggregate default rate is strongly countercyclical, while banks face substantial idiosyncratic (background) risk in the form of liquidity shocks through deposit changes and problem loans. We propose to build different quantitative models to understand these facts. The bank faces realistic aggregate and idiosyncratic risks in the form of problem loan processes and deposit growth. At the same time the bank faces realistic regulatory constraints like a leverage constraint. The bank chooses whether to default or not. If the bank does not default, then the bank chooses the amount of new loans to make, the amount of liquid securities to hold and the amount of borrowing on the interbank market. The model is calibrated, solved and simulated to generate predictions close to its empirical counterparts. Interesting counterfactuals given this setup include increasing core tier-I capital ratios from 8% to 9%. Another interesting counterfactual involves new loans funding when the interbank market freezes. The modelling perspective opens up a substantial number of issues that can be addressed in a quantitative setting: comparing different recapitalization methods, optimal regulatory responses and optimal central bank policy

Keywords: banking behaviour,quantitative models,bank balance sheets,liquidity shocks,default,regulatory constraints,interbank market,capital ratios,optimal central bank policy
Next generation ultrafast continuously running imaging system for biomedical applications (NULTIS)

Framework: FP7 — People
Programme: Marie-Curie Actions
Theme: Marie Skłodowska-Curie
Destination: Life-long training and career development
Action type: Support for training and career development of researchers (Marie Curie)
Countries involved: United Kingdom
Call:  (FP7-PEOPLE-2013-CIG, 2013)
Start date: 2014-07-01
End date: 2018-06-30
Duration (months): 48.0
Total project cost (EUR): 100000.0
EU funding (EUR): 100000.0
Participants: 1
Project status: CLOSED

Ultrafast continuously running cameras are a vital tool in capturing and visualizing ultrafast non-repetitive events, such as chemical dynamics, microfluidics, and laser nuclear fusion. Following active involvement in the successful development of the world’s fastest continuously running camera over the last two years, the applicant proposes to develop the next generation ultrafast imaging systems and to apply the developed systems in interdisciplinary scientific research. This research has two main objectives: 1. To develop the next generation ultrafast (~100 Mfps) imaging systems with new capabilities, such as phase-contrast imaging, Raman scattering detection, on-chip integration and with significantly enhanced spatial resolution. 2. To apply the developed instruments in biomedical research. The proposed research builds on the applicant's extensive expertise in photonics and electronics with a good track record of collaboration with researchers from different disciplines. To develop the next generation ultrafast imaging system, original and innovative techniques will be utilized. For instance, by incorporating a Michelson interferometer into the imaging optics, phase-contrast imaging capability will be created. Real-time Raman-spectroscopy-based imaging will be achieved by mirroring the Raman spectrum to a temporal waveform and applying distributed Raman amplification. Photonic integrated circuits (PIC) technology will be used to develop an integrated on-chip imaging system. Physical implementation of the system in shorter wavelength region and applying a compressive sampling algorithm will greatly improve spatial resolution. Furthermore, combining with microfluidic chips, next generation flow microscope system will be developed for high-throughput screening of rare cancer cells in blood. The technique developed will provide an indispensable tool for significant advancements in interdisciplinary research where high-throughput imaging instruments are essential.

Keywords: photonics,optical imaging,microwave photonics,biophotonics,ultrafast optics,microscopy,chromatic dispersion,mode-locked laser,fiber bragg grating,cancer.
Unravelling the Nascent Code: Signals sensed and transmitted by the nascent chain to acquire its functional state or reprogram gene expression (THE NASCENT CODE)

Framework: FP7 — People
Programme: Marie-Curie Actions
Theme: Marie Skłodowska-Curie
Destination: Life-long training and career development
Action type: Support for training and career development of researchers (Marie Curie)
Countries involved: Spain
Call:  (FP7-PEOPLE-2013-CIG, 2013)
Start date: 2014-07-14
End date: 2018-07-13
Duration (months): 48.0
Total project cost (EUR): 100000.0
EU funding (EUR): 100000.0
Participants: 1
Project status: CLOSED

Emerging biochemical and biophysical data strongly suggest that the transformation of the potential set of proteins, encrypted in the genome, into its actual vital functional set, is a manifestation not just of the genetic code, but of an additional layer of information encoded within the newly synthesized polypeptide nascent chain. To date, we know that immediately upon the first steps of protein synthesis, a variety of signals are formed within the evolving nascent chain (NC). These signals, by acting directly on the ribosome or by recruiting additional cellular machines, have the ability to direct new steps in the transformation of the NC and guide it towards the acquisition of its final functional state and cellular location. Due to its distinct nature, I will refer this ensemble of signals as THE NASCENT CODE. Despite our knowledge of its existence, we know very little about its mechanism of action. The goal of this research is to unravel the molecular determinants of the nascent code and to decipher how the signals, embedded in the primary sequence of the NC, orchestrate the concerted action of the ribosome and its ancillary factors (i,e, SecA, TF). The approach entails the reconstructing of the process describing the birth of a protein and following its progress over time. The techniques used in the analysis of this process, namely fluorescence spectroscopy, Cryo electron microscopy, solid state NMR-DNP, solution state NMR and X-ray crystallography, will illuminate macroscopic to atomic level details of the dynamics, structure and interactions of the key players involved. The realization of this research project will allow us to understand an essential process in the cell, for which very little structural information is currently available, and provide the structural foundation to intervene and control this process for biotechnological or therapeutic reasons.

Keywords: co-translational protein folding and sorting,x-ray crystallography,nmr,cryo-em
Commercialization of a nanomechanical flow cytometer for cell pre-screening (ONCOMECHANICS)

Framework: FP7 — Ideas
Programme: European Research Council
Theme: European research council
Destination: Proof of concept grants
Action type: Support for frontier research (ERC)
Countries involved: Spain
Call:  (ERC-2013-PoC, 2013)
Start date: 2014-06-01
End date: 2015-05-31
Duration (months): 12.0
Total project cost (EUR): 149993.0
EU funding (EUR): 149993.0
Participants: 1
Project status: CLOSED

As a result of the research undertaken in the NANOFORCELLS project (ERC-StG-2011-278860), we have successfully developed instrumentation for the investigation of cell mechanics to discriminate cancer cells from healthy cells by novel physical biomarkers, placing a particular emphasis in the elasticity and viscoelasticity of the cells. In order to accelerate the market entry of the results, the present project will focus on conducting a market feasibility study of the nanomechanical flow cytometer developed, as well as clarifying the IP position strategy and making an initial approach to potential partners and investors. The nanomechanical device to be taken to proof-of-concept, provides label-free classification of cells attending to their volume, mass, density and viscoelasticity. The device is capable of enabling parallel measurements of physical properties of hundreds of individual cells per minute, opening the route for portable tests that would enable determining the health status of cells from blood samples (f.e. leukaemia) based on their mechanical properties. This device will become an ideal tool for the study of drug effects on the physical properties of the cell with research and prognostic value, once made commercially available. The expected outcomes of the PoC project will be an increased understanding of the target markets and the definition of a commercialization roadmap to exploit the device. We envision that research groups within this biomedical field would be a first target market for the product use. The work undertaken so far requires further investment in order to bring the laboratory device to a marketable device and turn the outputs of the NANOFORCELLS project into a commercial proposition.

Keywords: 278860