Data-Gouv-ML/pcri-informations-sur-les-projets-laureats huggingface dataset:
The effect of a sedentary lifestyle on type 2 diabetes and its complications (SEDIAB)

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-2011-CIG, 2011)
Start date: 2011-12-01
End date: 2015-11-30
Duration (months): 48.0
Total project cost (EUR): 100000.0
EU funding (EUR): 100000.0
Participants: 1
Project status: CLOSED

Low physical activity is a well-known risk factor of many healthy problems. It is, however, not clear whether the increased health risks are due to lack of moderate to vigorous activity or due to a more sedentary lifestyle. Sedentary behaviour cannot simply be defined as the lack of moderate to vigorous activity but is defined as engaging in activities which marginally increase energy expenditure above resting level such as sitting, using the computer, and watching television. Understanding the health consequences of sedentary behaviour independently and jointly associated with physical activity is essential in order to promote healthy behaviours and more effective guidelines. In the present proposal we aim to disentangle the relation between objectively measured sedentary behaviour and physical activity in relation to type 2 diabetes and diabetic complications in the Maastricht Study in the Netherlands. The Maastricht Study is a large newly established cohort study focusing on the determinants and consequences of type 2 diabetes. Using the innovative activPAL™ accelerometer we will be able to examine daily activity across the full range of activity intensities. The objectives of the current proposal are: 1) to describe and compare patterns of daily activity among people with diabetes, prediabetes and those without type 2 diabetes; 2) to examine the association between sedentary behaviour and prevalent and incident (pre)diabetes and to understand whether this is independent of physical activity; and 3) to examine the relation between sedentary behaviour and prevalent and incident diabetic complications and to understand whether this is independent of physical activity. This research will both advance the physical activity research field and the diabetes field. The discoveries of the project are expected to have important public health impact and can affect both physical activity guidelines and guidelines to prevent/delay type 2 diabetes and its complications.

Keywords: health sciences,chronic diseases,accelerometry,diabetes,epidemiology,physical activity,sedentariness
Principles of Chromatin Organization (CHROMATINPRINCIPLES)

Framework: FP7 — Ideas
Programme: European Research Council
Theme: European research council
Destination: Advanced grants
Action type: Support for frontier research (ERC)
Panel: Genetics, Genomics, Bioinformatics and Systems Biology
Countries involved: Netherlands
Call:  (ERC-2011-ADG_20110310, 2011)
Start date: 2012-03-01
End date: 2017-02-28
Duration (months): 60.0
Total project cost (EUR): 2495080.0
EU funding (EUR): 2495080.0
Participants: 1
Project status: CLOSED

Chromatin is the ensemble of genomic DNA and hundreds of structural and regulatory proteins. Together these proteins govern the gene expression program of a cell. While biochemical and genetic approaches have tought us much about interactions between individual chromatin proteins, we still lack a “big picture” of chromatin: how is the entire interaction network of chromatin proteins organized? My lab discovered that chromatin in Drosophila consists of a limited number of principal types that partition the genome into domains with distinct regulatory properties. Among these is BLACK chromatin, a novel repressive type of chromatin that covers nearly half of the fly genome. It is still largely unclear how these different chromatin types are formed, how they are targeted to specific genomic regions, and how they interact with each other. Here, I propose a combination of systematic approaches aimed to gain insight into the basic mechanisms that drive the partioning of the genome into distinct chromatin types. New genomics techniques, developed in my laboratory, will be used to construct an integrated view of the interplay of more than one hundred representative chromatin proteins with each other and with sequence elements in the genome. Specifically, we will: (1) Study the genome-wide dynamic repositioning of chromatin domains during development in relation to gene regulation; (2) Use a novel and versatile parallel genome-wide reporter assay to dissect the interplay among DNA sequences and chromatin types; (3) Combine computational modeling with a high-throughput genome-wide assay to uncover the network of interactions responsible for the formation of the principal chromatin types; (4) Dissect the molecular architecture of BLACK chromatin and its role in gene repression. The results will provide understanding of the basic principles that govern the structure and composition of chromatin, and reveal how the principal chromatin types together direct gene expression.

Keywords: chromatin,genome-wide,interaction network,high-throughput assays,bioinformatics
Strategic Energy Technology Plan 2011 conference, Warsaw, Poland (SET-POLAND)

Framework: FP7 — Cooperation
Programme: Energy
Destination: Energy
Action type: Coordination and support actions
Countries involved: Poland
Call:  (FP7-Adhoc-2007-13, 2007)
Start date: 2011-07-01
End date: 2012-06-30
Duration (months): 12.0
Total project cost (EUR): 253820.0
EU funding (EUR): 118226.0
Participants: 1
Project status: CLOSED

The Strategic Energy Technology Plan is the technology pillar of the EU's energy and climate policy. The SET-Plan describes concrete actions to build a coherent energy research landscape in Europe and to better organize research efforts across Europe, selecting technologies with the greatest potential and planning together how money should be invested. The SET-Plan 2011 conference during the Polish Presidency of the EU Council will be jointly organized by IPPT and European Commission. In general, the conference is the communication on the progress of the implementation of all SET-Plan action lines. The main focus of the conference will be to bring a strong political resolution on financing of technologies, which are under the Strategic Energy Technology Plan, for the next financial framework (2013-2020). The second main goal during the SET-Plan 2011 conference is to commit stakeholders to develop holistic solutions to urban energy and transport problems in some selected 'model smart cities'. Additionally the progress and the achievements of the European Industrial Initiatives and the EERA Joint Programmes will be presented and the relations of the SET-Plan with the EU 2020 Strategy as well as continuation of FP7 will be discussed.

Keywords: set-plan strategic energy technology research industrial initiatives eera nuclear sustainable
HEPATITIS C VIRUS AND HOST LIPOPROTEIN METABOLISM (LIPOHCV)

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-2011-CIG, 2011)
Start date: 2011-09-01
End date: 2015-08-31
Duration (months): 48.0
Total project cost (EUR): 100000.0
EU funding (EUR): 100000.0
Participants: 1
Project status: CLOSED

Over 3% of the world population is chronically infected by the hepatitis C virus (HCV). Chronic infection is associated with liver disease that leads to fibrosis and cirrhosis and ultimately to hepatocellular carcinoma (HCC). There is no vaccine for HCV and the current treatment is only partially effective and toxic. Consequently, HCV infection is one of the leading causes of liver transplantation worldwide. HCV depends heavily on cellular lipid and lipoprotein metabolism to replicate and produce infectious particles. This dependence coincides with the fact that chronic HCV infection is associated with alterations of the liver lipid metabolism. These alterations are manifested by abnormal accumulation of lipids in hepatocytes (steatosis) in a significant proportion of the patients. In patients responding to interferon treatment, steatosis subsides as the viral titers decrease, suggesting that HCV replication and viral protein expression are a major determinant for these alterations. However, little is known about the molecular mechanisms underlying the interference of HCV infection with lipid metabolism. Understanding how HCV exploits the cellular lipid and lipoprotein biosynthetic machinery might contribute to understanding important aspects of the pathogenesis of chronic HCV infection. In this application, we propose to use a cell culture HCV infection model that we recently developed to study the intersection of cellular lipid and lipoprotein metabolism with basic aspects of HCV infection.

Keywords: hepatitis c virus,lipoprotein,virion assembly,ppar
Quantitative Molecular Map of the Neuronal Surface (MOLECMAP)

Framework: FP7 — Ideas
Programme: European Research Council
Theme: European research council
Destination: Advanced grants
Action type: Support for frontier research (ERC)
Panel: Neurosciences and neural disorders
Countries involved: Hungary
Call:  (ERC-2011-ADG_20110310, 2011)
Start date: 2012-02-01
End date: 2017-01-31
Duration (months): 60.0
Total project cost (EUR): 2494446.0
EU funding (EUR): 2494446.0
Participants: 1
Project status: CLOSED

The most fundamental roles of nerve cells are the detection of chemical neurotransmitters to generate synaptic potentials; the summation of these potentials to create their output signals; and the consequent release of their own neurotransmitter molecules. All of these functions require the orchestrated work of hundreds of molecules targeted to specialized regions of the cells. In nerve cells, more than in any other cell type, a single molecule could fulfill very different functional roles depending on its subcellular location. For example, dendritic voltage-gated Ca2+ channels play a role in the integration and plasticity of synaptic inputs, whereas the same channels when concentrated in presynaptic active zones are essential for neurotransmitter release. Thus, the function of a protein in nerve cells cannot be understood from its expression or lack of it, but its precise subcellular location, density and molecular environment needs to be determined. The major aim of the present proposal is to create a quantitative molecular map of the surface of hippocampal pyramidal cells (PCs). We will start by examining voltage-gated ion channels due to their pivotal roles in input summation, output generation and neurotransmitter release. We will apply high resolution quantitative molecular neuroanatomical techniques to reveal their densities in 19 different axo-somato-dendritic plasma membrane compartments of CA1 PCs. Functional predictions will be generated using detailed, morphologically realistic multicompartmental PC models with experimentally determined ion channel distributions and densities. Such predictions will be tested by combining in vitro patch-clamp electrophysiology and imaging techniques with correlated light- and electron microscopy. Our results will provide the first quantitative molecular map of the neuronal surface and will reveal new mechanisms that increase the computational power and the functional diversity of nerve cells.

Keywords: immunohistochemistry patch-clamp electrophysiology ion channels neurotransmission hippocampus
Investigating new therapeutic approaches to Friedreich's Ataxia (FAST)

Framework: FP7 — Ideas
Programme: European Research Council
Theme: European research council
Destination: Advanced grants
Action type: Support for frontier research (ERC)
Panel: Diagnostic tools, therapies and public health
Countries involved: Italy
Call:  (ERC-2011-ADG_20110310, 2011)
Start date: 2012-03-01
End date: 2015-02-28
Duration (months): 36.0
Total project cost (EUR): 1496200.0
EU funding (EUR): 1496200.0
Participants: 1
Project status: CLOSED

Friedreich’s Ataxia (FRDA) is a devastating degenerative disease with no specific therapy. It is passed by autosomal recessive inheritance and affects 1:30,000 individuals in Caucasian populations. Symptoms appear in the first decade of life and include progressive and unremitting lack of movement coordination, leading to complete inability, and dilated cardiomyopathy leading to congestive heart failure, the most common cause of premature death. FRDA is due to the insufficient transcription of the gene coding for the mitochondrial protein frataxin. Reduced cellular levels of frataxin cause impaired mitochondrial function and increased sensitivity to oxidative stress, leading to accelerated cell death in critical tissues. Severity of the disease critically depends on residual frataxin levels. Therapeutic efforts are mostly focused on increasing cellular frataxin . We found that frataxin is normally degraded by the ubiquitin-proteasome system. We identified the lysine responsible for the ubiquitination of frataxin and, by computational screening followed by experimental validation, we identified and validated a series of small molecules, called ubiquitin-competing molecules (UCM), that prevent frataxin ubiquitination and induce frataxin accumulation in cells derived from FRDA patients. Moreover, treatment with UCM partially rescues aconitase and ATP production defects in cells derived from FRDA patients. Our goal is two fold: 1) submit a set of leads we already identified, as well as their new and more complex derivatives, to preclinical testing in FRDA mice 2) identify the E3 ligase that is responsible for frataxin ubiquitination, and investigate the possibility to use it as a druggable target for small molecules to prevent frataxin degradation.

Keywords: friedreich's ataxia,ubiquitin,e3 ligase,frataxin
Capacity and dynamics of agribusiness innovation systems (CABIS)

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: Denmark
Call:  (FP7-PEOPLE-2011-CIG, 2011)
Start date: 2011-12-01
End date: 2013-11-30
Duration (months): 24.0
Total project cost (EUR): 50000.0
EU funding (EUR): 50000.0
Participants: 1
Project status: CLOSED

Recently, many developing countries have experienced a significant growth in their agribusiness sector. Agribusiness is recognized for its potential for creating growth and eradicating poverty and there is an increasing need for dynamic innovation processes due to increased globalization, integration in global value chains, and radical changes in institutions and knowledge structures. The concept of ‘Innovation Systems’ (IS) can be applied to analyse how institutions, knowledge generation and diffusion, and commercial activities interact in today’s diversification of innovation. In practice, such agribusiness innovation systems (ABIS) in developing countries have often shown limited innovation capacity which threatens the sector’s competitive position and future development. This Post Doc project aims to enhance our understanding of factors limiting the increasingly dynamic IS. The project will develop a conceptual framework and analytical methods to identify limitations and intervention recommendations for strengthening innovation capacity in ABIS in the comparative case study involving Vietnam and Tanzania. During the last 20 years, these countries have had a similar political and economic development in terms of a transition from socialism to market-oriented economy, but in spite of this, the two countries have experienced significant differences in their development trajectories, hence providing a rich background for theory building and conceptualization.

Keywords: social sciences
Large-scale identification of Coxiella burnetii virulence factors (Q-SCREEN)

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-2011-CIG, 2011)
Start date: 2011-04-01
End date: 2014-03-31
Duration (months): 36.0
Total project cost (EUR): 75000.0
EU funding (EUR): 75000.0
Participants: 1
Project status: CLOSED

Coxiella burnetii is an obligate intracellular gram-negative bacterium responsible of the zoonosis Q fever, a disease that manifests as an acute flu-like illness. Due to its high infectivity it has been classified as a class B biothreat. In natural infections Coxiella mainly targets macrophages whereas in vitro is capable of infecting a wide variety of cell types. As several other pathogens Coxiella replicates in a large phagosomal vacuole, but differently from any other known pathogen, Coxiella has the capacity of thriving in a parasitophorous vacuole which is biochemically indistinguishable from lysosomes. Despite the interest that Coxiella infections raise, its obligate intracellular nature has hampered the research activity due to the impossibility of genetic manipulation and growth in broth. The mechanisms of subversion of host functions remain therefore obscure and the number of Coxiella virulence factors identified is limited to the bacterial LPS. The recent characterization of a specific growth medium that allows axenic growth of Coxiella opens the way to genetic engineering of the bacterium. The aim of this project is the large-scale identification of Coxiella virulence factors by generating a bank of mutants by transposon mutagenesis. This will be coupled to the set up of robust high throughput screens to identify phenotypes that will allow the characterization of virulence factors.

Keywords: infections,bacteriology,cell biology,molecular genetics
Reactive Oxygen Species and Hypothalamic Glucose Sensitive Neurons: a new mechanism in glucose homeostasis (NEUROSENS)

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-2011-CIG, 2011)
Start date: 2011-08-01
End date: 2014-07-31
Duration (months): 36.0
Total project cost (EUR): 75000.0
EU funding (EUR): 75000.0
Participants: 1
Project status: CLOSED

Development of obesity and diabetes is the consequence of impaired glucose homeostasis regulation. The hypothalamic area of the brain and more precisely the arcuate nucleus (ARC) plays a critical role in this regulation. The ARC detects changes in blood glucose level and triggers appropriate physiological responses. For instance, increased brain glucose level increases insulin secretion and decreases food intake. Different populations of glucose sensitive neurons have been characterize in the ARC. Glucose excited (GE) neurons increase their electrical activity when extracellular glucose level rises from 2.5 to 5 mM, 2.5 mM being the physiological basal brain glucose level. By analogy, high-glucose excited (HGE) neurons increase their activity as glucose levels rises above 5 mM. Despite being studied by many groups, the molecular mechanisms and physiological roles of GE and HGE neurons are not fully understood. Preliminary work suggests that ARC mitochondrial reactive oxygen species (mROS) production is involved in glucose homeostasis. We showed that inhibition of ARC mROS production impairs increased brain glucose level-induced insulin secretion and food intake inhibition. We hypothesize that mROS production is involved in GE and/or HGE neurons glucose sensitivity. Four specific aims will test our hypothesis. Specific Aim 1 will determine whether ARC GE and/or HGE neurons produce mROS in response to increased glucose level and. Specific Aim 2 and 3 will determine whether whether mROS are involved in ARC GE and HGE neurons glucose sensitivity. Finally, Specific Aim 4 will determine whether ARC HGE neurons are involved in glucose homeostasis. This project is highly original and innovative in regards of the hypothesis proposed and technical strategies used. Understanding molecular mechanisms and physiological roles of ARC GE and HGE neurons will significantly improve the knowledge in glucose homeostasis against development of diabetes and obesity.

Keywords: health sciences,neurophysiology,brain research,diabetology
Identification and characterisation of novel cell-fate influencing genes in pre-implantation mouse development (IDNOVCELFAT2011)

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: Czechia
Call:  (FP7-PEOPLE-2011-CIG, 2011)
Start date: 2011-11-01
End date: 2015-10-31
Duration (months): 48.0
Total project cost (EUR): 100000.0
EU funding (EUR): 100000.0
Participants: 1
Project status: CLOSED

Just prior to uterus implantation mammalian blastocyst stage embryos have already started the process of generating and segregating different cell types required for continued development. Exactly how this remarkable transformation from a single fertilised egg to a highly ordered multi-cellular blastocyst occurs, within just a few days, remains a fascinating and enduring question. During this time embryonic cells either start to adopt specialised functions (differentiate) or they can remain in a so-called ‘pluripotent’ state, only differentiating later in development. Understanding the mechanisms behind such in vivo ‘cell-fate decisions’ is fundamentally important but can also provide insight into the proposed future application of stem cell based regenerative therapies. Research on mouse embryos has begun to address these cell-fate related issues and has highlighted the importance of tight temporal control of specific gene expression and the impact of relative cell position (i.e. on the outside of, or encapsulated within the embryo) to blastocyst formation. Herein, we propose to identify, verify and thoroughly characterise novel early mouse embryo cell-fate influencing genes. Candidate genes have already been identified by integrating our unpublished experimental data aimed at uncovering genes differentially expressed in outer and inner cells with pre-existing datasets describing gene expression throughout the whole of early development. Accordingly, we plan to disrupt the expression of these candidate genes within discreet cell populations of the developing mouse embryo and to observe whether this will affect their ultimate cell-fate. If so, we will determine how this impacts upon already known cell-fate related genes and mechanisms of cell segregation. We will also investigate the consequences of disrupting our validated/ novel cell-fate genes by assessing global effects on gene expression and in turn will yield additional candidate genes for future research.

Keywords: developmental biology,animal embryology,laboratory animal science,pre-implantation,mouse,cell-fate