Data-Gouv-ML/pcri-informations-sur-les-projets-laureats huggingface dataset:
Real Time Imaging with Near Field Focusing Plates (REALTIMEIMAGING)

Framework: FP7 — People
Programme: Marie-Curie Actions
Theme: Marie Skłodowska-Curie
Destination: International Re-integration Grants
Action type: Support for training and career development of researchers (Marie Curie)
Countries involved: Türkiye
Call:  (FP7-PEOPLE-2010-RG, 2010)
Start date: 2010-12-01
End date: 2015-12-01
Duration (months): 48.0
Total project cost (EUR): 100000.0
EU funding (EUR): 100000.0
Participants: 1
Project status: CLOSED

This project describes the four years re-integration program to facilitate a successful and continuous integration of Dr. Ozdal Boyraz’s research in the real time optical detection and imaging field into the EU’s needs, and to support Dr. Ozdal Boyraz’s re-integration to research and educational activities at the Istanbul Sehir University and in EU. Spectroscopy and imaging of biological samples with ultra high resolution are subjects of growing interest. With the advent of nanotechnology, metamaterials, and plasmonic devices the sub wavelength resolution is now a concrete possibility in microscopy. However, the current state of the art imaging tools resort to time averaged analysis to extract high resolution information from a single point at the expense of loosing information on transients and correlated events in the proximity of the focal spot. The proposed research aims to develop a real time system using time-space-wavelength encoded mesh type optical grids to capture the image in a 2-D plane in a single shot. Instead of resorting to imaging with point by point scanning via nano positioning stages, broadband coherent optical sources covering the area of interest are used to capture information from a multiple coordinates by encoding them on a designated color and a time slot to avoid scanning. The design and development of near-field focusing plates is incorporated into the project for subwavelength focusing to mitigate the resolution bottleneck and achieve sub wavelength microscopy in a single shot measurement. Space wavelength mapping has been utilized extensively for arbitrary waveform generation and microwave antenna design. The impact of this technology in bio detection and imaging is yet to be explored in subwavelength domain. Design and fabrications are compatible with conventional CMOS technology and attractive for low cost production.

Keywords: technological sciences,optical signal processing,real time imaging
in toto imaging of embryonic morphogenesis: collective cell movements and symmetry breaking (INTOTOMORPHOGENESIS)

Framework: FP7 — People
Programme: Marie-Curie Actions
Theme: Marie Skłodowska-Curie
Destination: International Re-integration Grants
Action type: Support for training and career development of researchers (Marie Curie)
Countries involved: France
Call:  (FP7-PEOPLE-2010-RG, 2010)
Start date: 2011-09-22
End date: 2015-09-21
Duration (months): 48.0
Total project cost (EUR): 100000.0
EU funding (EUR): 100000.0
Participants: 1
Project status: CLOSED

Successive processes of symmetry breaking are occurring during the sequence of early embryonic morphogenesis. These fascinating events raise fundamental questions that are still under debate and are challenging to investigate. In parallel, recent advances in fluorescent reporters, microscopy and image processing, make possible investigating the dynamics of large cell populations in a developing embryo. It led to the emergence of the in toto imaging concept and provides a unique opportunity to study embryonic development from the scale of the cellular mechanisms to the entire organism. In this context, the purpose of this proposal is to bring novel approaches and techniques of in toto imaging to dissect fundamental processes involved in anterior-posterior symmetry breaking and axis specification in early mammalian embryos. The combination, characterization and development of cutting-edge microscopy, optical manipulation and image processing techniques will enable us to investigate the collective movement of the visceral endoderm in early mouse embryo. This process is the first morphological event that breaks the anterior-posterior symmetry. This study should provide a detailed understanding of the mechanisms involved in the anterior-posterior polarity in mouse embryo. It should also illustrate the crucial role of individual cell behaviors in the emergence of large scale morphogenetic events. This interdisciplinary project will be conducted at Institut Jacques Monod (IJM, Paris). Willy Supatto, the principal investigator, will use his training and experience in optics, biophysics and developmental biology to start a new research activity within Jérôme Collignon’s team at IJM.

Keywords: developmental biology,morphogenesis,symmetry breaking,mouse development,collective cell movements,in toto imaging,multiphoton microscopy,fluorescence light sheet microscopy,image processing
Pathogenetic mechanisms of depression in multiple sclerosis (DEPRESSION IN MS)

Framework: FP7 — People
Programme: Marie-Curie Actions
Theme: Marie Skłodowska-Curie
Destination: International Re-integration Grants
Action type: Support for training and career development of researchers (Marie Curie)
Countries involved: Germany
Call:  (FP7-PEOPLE-2010-RG, 2010)
Start date: 2010-09-01
End date: 2014-08-31
Duration (months): 48.0
Total project cost (EUR): 100000.0
EU funding (EUR): 100000.0
Participants: 1
Project status: CLOSED

Depression is one of the most common symptoms in patients with multiple sclerosis (MS) with a prevalence of up to 50%. Depression is linked to decreased cognitive function, lower quality of life, increases psychosocial and economic burden and is the strongest predictor of suicide. Despite the high clinical relevance, the pathogenetic substrates for depression in MS are poorly understood. Growing evidence suggests that it may be largely biologically mediated by some of the same processes involved in the immunopathogenesis of this neurologic disease. In particular, increases in proinflammatory cytokines, and activation of the hypothalamic-pituitary-adrenal (HPA) axis have independently been shown to be involved in major depressive disorder (MDD) as well as MS. Pregnancy is associated with profound changes in the endocrine and immune system and interestingly, the post partum period is characterized by a higher risk for relapses both in depression and MS. During pregnancy, in contrast, there is an approximately 80% reduction in MS relapse rate, an effect that is stronger than that achieved by any of the currently approved disease-modifying therapies. Thus, pregnancy is a powerful paradigm to study shared mechanisms of disease activity in MS and depression. In the proposed study, we will determine immunological and endocrine correlates of mood changes longitudinally in female relapsing-remitting MS patients during pregnancy and post partum. Clinical interviews and validated questionnaires will be used to examine depression incidence and severity. Blood samples for immune studies, salivary cortisol levels, and measures of depressive symptomatology and cognitive function will be obtained during the 2nd trimester, 3rd trimester, and 3 months post partum. This study will enable us to better understand immune-endocrine mechanisms of depression as well as disease activity in MS. This could have important implications for developing better therapeutic approaches.

Keywords: psychoneuroimmunology,depression,multiple sclerosis,stress hormones,inflammation,cognitive impairment,t cells,glucocorticoid resistance
The role of microRNAs in pancreatic islet dysfunction in type 2 diabetes mellitus (MIRT2DM)

Framework: FP7 — People
Programme: Marie-Curie Actions
Theme: Marie Skłodowska-Curie
Destination: International Re-integration Grants
Action type: Support for training and career development of researchers (Marie Curie)
Countries involved: Netherlands
Call:  (FP7-PEOPLE-2010-RG, 2010)
Start date: 2010-09-01
End date: 2014-08-31
Duration (months): 48.0
Total project cost (EUR): 100000.0
EU funding (EUR): 100000.0
Participants: 1
Project status: CLOSED

Type 2 diabetes mellitus (T2DM) is caused by a relative inability of the endocrine pancreas to meet the increasing metabolic demands of insulin resistance associated with obesity and ageing. Impaired insulin secretion is an early and critical step in the pathogenesis of type 2 diabetes, but the underlying mechanism of ß-cell loss and dysfunction in T2DM are incompletely understood. Recent studies have indicated a role for several microRNAs (miRNAs), a recently discovered class of evolutionarily conserved small noncoding RNAs that regulate gene expression at a posttranscriptional level. Specific expression of miRNAs in β-cells has been reported. However, little is known about the role of miRNAs in the pathogenesis of T2DM. Therefore, the overall objective of this grant proposal is to understand the role of miRNAs in ß-cell function, glucose and lipid metabolism and etiology of T2DM. We aim to determine whether miRNAs are involved in the loss of ß-cell function and ß-cell mass in T2DM and will investigate the potential of miRNAs as a therapeutic target in T2DM. First we will identify miRNAs that are differentially expressed in β-cells of normoglycemic, hyperglycemic and T2DM mice. We will next examine these differentially expressed miRNAs on their potential to dysregulate β-cell physiology in vitro. The impact of the promising miRNAs on β-cell function and β-cell mass will be assessed in C57Bl6 mice by overexpressing or silencing miRNA specifically in β-cells using AAV vectors. To determine the potential of miRNAs that affect β-cell development or function as therapeutic targets for T2DM, we will study these miRNAs in diabetic mice. This work will generate new knowledge about the role of miRNAs in ß-cell function, glucose metabolism and T2DM. This may point to new therapeutic approaches focusing on restoring or silencing of specific miRNAs in pancreatic β-cells.

Keywords: health sciences,diabetology,beta-cells,microrna,type 2 diabetes mellitus
Ultra Low Energy Vertically Integrated Circuits (ULEVIS)

Framework: FP7 — People
Programme: Marie-Curie Actions
Theme: Marie Skłodowska-Curie
Destination: International Re-integration Grants
Action type: Support for training and career development of researchers (Marie Curie)
Countries involved: Türkiye
Call:  (FP7-PEOPLE-2010-RG, 2010)
Start date: 2010-09-15
End date: 2013-09-14
Duration (months): 36.0
Total project cost (EUR): 75000.0
EU funding (EUR): 75000.0
Participants: 1
Project status: CLOSED

The current integrated circuit scaling hits two major roadblocks or walls. One wall is the atomic level feature sizes of the current devices forcing the capabilities of even nano-scale implementations. The other wall is the total power consumed per unit area exceeding the capabilities thermal dissipation techniques limiting the maximum device densities. The solution to the feature size problem is scaling in the orthogonal direction to the conventional device plane - the 3D integration. The solution to the power problem is the use of ultra low power design approaches. However, the 3D integration increases the thermal dissipation problem and ultra low power design can not provide total performance due to low clock speeds unless extremely large number of devices is combined in small areas. We propose a unique combination of ultra low power design approaches and 3D integration to provide an optimal performance to the user. Low power design eliminates the thermal dissipation problem of the 3D integration whereas 3D integration enables dense device integration in small volumes to solve the space-time trade-off in ultra low power design approaches. The result will be a vertically integrated circuit with power efficiencies several hundred times better than current dedicated processors.

Keywords: microsystems,subsystem modules,microengineering,low power,3d integration
Disclosing the molecular bases of electrical signalling in plants (PLANTELEXIGNAL)

Framework: FP7 — People
Programme: Marie-Curie Actions
Theme: Marie Skłodowska-Curie
Destination: International Re-integration Grants
Action type: Support for training and career development of researchers (Marie Curie)
Countries involved: France
Call:  (FP7-PEOPLE-2010-RG, 2010)
Start date: 2010-10-01
End date: 2013-09-30
Duration (months): 36.0
Total project cost (EUR): 75000.0
EU funding (EUR): 75000.0
Participants: 1
Project status: CLOSED

A plant needs to be able to communicate between its various parts so as to enable one part of the plant to inform the rest of any detected stimulus. This allows a co-ordinated physiological response to any external stimuli. Electrical signals such as action potentials (APs) are by far the fastest signalling mechanisms in plants. They are able to broadcast information rapidly throughout a plant, so the whole plant can be almost instantaneously notified of any impending threat or change in circumstance. Thus, APs could be vital in the response of plants to environmental stress. Despite their importance, huge questions remain about the mechanisms behind electrical signalling. Although there is a model for the generation and propagation of plant APs, which involves the cellular influx of calcium and efflux of chloride and potassium through ion channels, little is known about the molecular identify or the regulation of these channels. This is despite the rapidly increasing knowledge about ion transport mechanisms in model plant species such as Arabidopsis thaliana. Focusing on APs in Arabidopsis, this project aims to fill this gap, with the overall aim of “providing a model describing the molecular mechanisms underlying the inception and the propagation of electrical signals in plant tissues”. This project will therefore bring together ion transport mechanisms and electrical signalling in Arabidopsis. The involvement and the regulation of the ion channels involved in mediating ion fluxes during an AP will be intensively investigated, resulting finally in a mathematical model of electrical signalling in plants. The proposal will bring together three groups with expertise in (i) molecular electrophysiology of plant ion channels, (ii) electrophysiology, especially in relation to electrical signalling and (iii) computer-assisted mathematical modelling of plant biological processes, along with a returning European electrophysiologist with expertise in ion transport.

Keywords: plant communication,electrical signalling,action potentials,voltage-gated ion channels,mathematical modelling,potassium,calcium,chloride,symplasm,arabidopsis thaliana
Wnt agonist Dickkopf 3 (DKK3) is a type 2 diabetes susceptibility gene (DKK3 T2DM)

Framework: FP7 — People
Programme: Marie-Curie Actions
Theme: Marie Skłodowska-Curie
Destination: International Re-integration Grants
Action type: Support for training and career development of researchers (Marie Curie)
Countries involved: Sweden
Call:  (FP7-PEOPLE-2010-RG, 2010)
Start date: 2010-09-01
End date: 2013-08-31
Duration (months): 36.0
Total project cost (EUR): 75000.0
EU funding (EUR): 75000.0
Participants: 1
Project status: CLOSED

Type 2 diabetes mellitus (T2DM) is a complex genetic disorder of largely obscure etiology where alleles at numerous loci are thought to interact with environmental and stochastic cues to induce the phenotype. We have recently identified a T2DM susceptibility allele at the DKK3 locus. Using a combination of case/control association and functional studies, we demonstrated that the minor allele of SNP rs11022111 in the DKK3 promoter is significantly associated with T2DM in two Chinese and one Caucasian cohort and results in the disruption of a conserved SP1 binding site, leading to reduced DKK3 expression. We also showed that, in contrast to other members of the DKK family, DKK3 is a likely agonist of Wnt signaling (both canonical and non-canonical), in a Fz- and LRP6-dependent manner and regulates the expression of TCF7L2, another T2DM susceptibility gene. Our preliminary data implicate the regulation of Wnt signaling in the pathogenesis of T2DM. In this proposal, we hypothesize that aberrant Wnt signaling in the adult pancreas can lead to impaired glucose tolerance, insulin secretion and other diabetic phenotypes. To address how Dickkopf 3 influences Wnt signaling in β-cells and pancreatic islets as well as pancreatic islet functions, I propose to identify the subset of Wnt signaling components that are active in MIN6 cells and islets, to characterize the effect of impaired Wnt signaling on islet function and formation, and finally, to investigate the metabolic state of Dkk3-/- mice when challenged with a high fat diet.

Keywords: health sciences,diabetes,signal transduction,wnt,susceptibility genes,candidate gene
Comparative Analysis of Rabbit and Mouse Pluripotency in Embryos and Stem Cells (RABPSTEM)

Framework: FP7 — People
Programme: Marie-Curie Actions
Theme: Marie Skłodowska-Curie
Destination: European Re-integration Grants
Action type: Support for training and career development of researchers (Marie Curie)
Countries involved: Hungary
Call:  (FP7-PEOPLE-2010-RG, 2010)
Start date: 2010-09-01
End date: 2013-08-31
Duration (months): 36.0
Total project cost (EUR): 45000.0
EU funding (EUR): 45000.0
Participants: 1
Project status: CLOSED

The RabPStem proposal is aimed at increasing the fundamental knowledge of basic biological processes of cell pluripotency and differentiation by generating new comparative data on gene expression associated with cell pluripotency. RabPStem links for the first time research activities in a non-rodent (rabbit) and rodent (mouse) mammalian systems and in different cell types, from pluripotent cells in pre-implantation embryos, through embryonic stem cells, to induced pluripotent stem cells. The main scientific aim of RabPStem is to generate novel comparative information on the rabbit pluripotency pathways, which would make the rabbit a true and highly valuable model species for biomedical research. Comparative information on pluripotency regulation and pathways in non-rodent species (including rabbit) is highly valuable for understanding those in humans; a prerequisite for future medical use of human stem cell technology. The proposed basic research would be rapidly translated into practical applications such as the creation of animal models for human diseases and the generation of transgenic rabbits for biotechnology applications. Besides the biotechnology applications, the project is expected to yield novel methods to derive rabbit pluripotent stem cells, such as improved procedures for the derivation, maintenance and differentiation of pluripotent stem cell lines in rabbit. This is important for potential future applications in the fields of regenerative medicine and tissue engineering, and, beyond these areas, in pharmaceutical industry and agriculture.

Keywords: pluripotency,rabbit,embryonic stem cell,mouse,ips
Using gene to phenotype studies to identify type 1 diabetes genes and their functions (GENETICS OF T1D)

Framework: FP7 — People
Programme: Marie-Curie Actions
Theme: Marie Skłodowska-Curie
Destination: International Re-integration Grants
Action type: Support for training and career development of researchers (Marie Curie)
Countries involved: United Kingdom
Call:  (FP7-PEOPLE-2010-RG, 2010)
Start date: 2011-03-01
End date: 2013-02-28
Duration (months): 24.0
Total project cost (EUR): 50000.0
EU funding (EUR): 50000.0
Participants: 1
Project status: CLOSED

Following the recent explosion of GWAS publications, we now have a much better grasp of the common genetic basis of many human complex traits. This dramatic development of genotyping and analytic technologies has allowed to characterize many novel variants associated with human disease. Nevertheless, the identification of these disease-associated loci hasn’t yet translated into a better understanding of the exact nature of the defects causing the pathologic manifestations. In the current research project, we propose to assess the physiological role of the risk variants on relevant phenotypes to identify functional the causal genes associated with type 1 diabetes (T1D) pathogenesis. To address this issue, we will develop highly sensitive and reproducible assays to measure the impact of the different genotypes on the selected phenotypes. By using this quantitative approach, we expect not only to be able to reduce the complexity inherent to the disease phenotype, but also to have the power and sensitivity to detect the important but quantitative physiological effects of common susceptibility alleles of low phenotypic penetrance. In this study we will develop highly sensitive molecular assays, and will take advantage of the core flow cytometry facilities to characterize the cell surface, cytokine production and signaling profile of immune subsets in individuals carrying specific risk alleles. Importantly, we will take advantage of our core genotyping and clinical databases to assess the impact of disease-associated genotypes on these quantitative phenotypes. By integrating the phenotyping data with a high throughput genotyping database in a large sample of individuals, we expect to translate the current knowledge of the genetic risk, into a more physiologically relevant context, in order to narrow down on the actual causal genes contributing to the etiology of human diseases.

Keywords: health sciences,gene-phenotype study,genome-wide association study,genetics of type 1 diabetes
Endosomal sorting of AMPA receptors for synaptic plasticity (ENDOAMPAR)

Framework: FP7 — People
Programme: Marie-Curie Actions
Theme: Marie Skłodowska-Curie
Destination: International Re-integration Grants
Action type: Support for training and career development of researchers (Marie Curie)
Countries involved: Spain
Call:  (FP7-PEOPLE-2010-RG, 2010)
Start date: 2010-10-01
End date: 2014-01-15
Duration (months): 36.0
Total project cost (EUR): 75000.0
EU funding (EUR): 75000.0
Participants: 1
Project status: CLOSED

Synaptic connections in the brain are continuously remodelled in response to neuronal activity. This process, known as synaptic plasticity, is widely seen as the cellular correlate of learning and memory. Hence, it is expected that the elucidation of the mechanism underlying synaptic plasticity will help to understand the pathological alterations that result in cognitive deficits. It is being increasingly appreciated that synaptic transmission can be modulated by postsynaptic membrane trafficking events, which include the insertion and removal of neurotransmitter receptors, such as AMPA-type glutamate receptors, at synapses in response to neuronal activity. These processes are critical for some forms of synaptic plasticity, such as long-term potentiation (LTP) or long-term depression (LTD). However, the mechanisms controlling membrane trafficking at the postsynaptic terminal and its connection to synaptic plasticity are far from clear. The small GTPase Rab5 is a mediator of protein transport from membrane to early endosomes. More specifically, Rab5 removes AMPA receptors from synapses in an activity-dependent manner and this event is necessary and sufficient for LTD. The goal of this project is to study the role of Rab5 effectors APPL1, WDFY2 and EEA1 in the endocytosis of AMPA receptors during synaptic plasticity. Previous work suggest that APPL1 may act as an early sorting station, while phosphoinositides and Rab5 control the divergent trafficking towards EEA1 or WDFY2 endosomes. In this proposal we will evaluate whether these components of the endosomal machinery organize AMPA receptor trafficking in the specialized environment of the postsynaptic terminal during plasticity. To this end we will use a combination of electrophysiology, molecular biology and imaging on brain tissue. We hope that the elucidation of these basic mechanisms of synaptic function will help us to understand the alterations of synaptic plasticity associated to some mental disorders.

Keywords: neurobiology,neurophysiology,brain research,synaptic plasticity,trafficking of receptors,endocytosis