Agency: European Commission | Branch: H2020 | Program: MSCA-ITN-ETN | Phase: MSCA-ITN-2015-ETN | Award Amount: 3.89M | Year: 2016
Environmental microbial surveys have revealed a remarkable diversity of microeukaryotic life in most ecosystems, the majority of which had previously escaped detection. From an ecological point of view this work highlighted our ignorance of critical microbial players in natural environmental processes, including primary production, biogeochemical cycling and trophic interactions such as parasitism and grazing. Consequently, our understanding of community function is partial, limiting our ability to study environmental change. While, from an evolutionary perspective, we are missing major components of the Tree of Life giving rise to a fragmented understanding of how major cellular functions have evolved. Single cell genomics (SCG), including single cell transcriptomics, is an emerging technology that has the potential to retrieve genomic information from individual uncultured microbes recovered directly from natural environments and promises to provide new tools to investigate microeukaryotes in unparalleled detail. The aim of this ITN is therefore to train a new generation of scientists with the highest expertise, in SCG, from the initial stages of cell sorting to genome sequencing and gene annotation, to the full exploitation of the data obtained. Such progress will allow the European research community for the first time to address critical ecological and evolutionary questions. SINGEK will drive training through research by both local and network-wide activities, secondments, and workshops, and by establishing an environment that extends far beyond each partner team. This training environment will also provide the transferable skills essential for successful career development. This network of well connected and highly qualified scientists with expertise in eukaryotic SCG will be ready to implement this technology beyond ecology and evolution to other fields such as biomedicine or biotechnology driving innovation across the EU.
Agency: European Commission | Branch: H2020 | Program: CSA | Phase: INFRADEV-02-2016 | Award Amount: 4.00M | Year: 2017
Sustainable food security and increasing availability of plant biomass for human nutrition and bioindustries is the key challenge for the coming decades. The analysis of crop performance with respect to structure, function, quality and interaction with the environment (phenotyping) remains the bottleneck for the exploitation of crop genetic diversity required for the enhancement of plant productivity and progress in plant breeding. This requires substantial and concerted action to develop and to increase the availability of phenotyping infrastructures. The European Strategic Forum for Research Infrastructure (ESFRI) has identified Plant Phenotyping as a priority for the European research area and EMPHASIS has been listed on the ESFRI ROADMAP as an infrastructure project to develop and implement a pan-European plant phenotyping infrastructure. The project EMPHASIS-PREP will provide the basis for the establishment the legal framework, the business plan and preparation of an information system for a sustainable and innovative pan-European infrastructure for plant phenotyping within the framework of EMPHASIS. EMPHASIS-PREP will establish a transparent, open and inclusive process, the project partners will foster efficient work in the project in close cooperation with the European plant phenotyping community and all stakeholders. EMPHASIS-PREP includes four major steps: i) mapping (infrastructure, funders, access procedure and models, stakeholder community, e-infrastructure, imaging approaches, legal and governance scenarios); ii) gapping - analysing the gaps and limitations based on the mapping activities; iii) developing strategies to address the gaps; iv) combining the strategies in a business plan for future operation of EPMPHASIS within a corresponding legal framework.
Agency: European Commission | Branch: H2020 | Program: RIA | Phase: INFRADEV-3-2015 | Award Amount: 19.05M | Year: 2015
The life sciences are undergoing a transformation. Modern experimental tools study the molecules, reactions, and organisation of life in unprecedented detail. The precipitous drop in costs for high-throughput biology has enabled European research laboratories to produce an ever-increasing amount of data. Life scientists are rapidly generating the most complex and heterogeneous datasets that science can currently imagine, with unprecedented volumes of biological data to manage. Data will only generate long-term value if it is Findable, Accessible, Interoperable and Re-usable (FAIR). This requires a scalable infrastructure that connects local, national and European efforts and provides standards, tools and training for data stewardship. Formally established as a legal entity in January 2014, ELIXIR - the European life science Infrastructure for Biological Information - is a distributed organisation comprising national bioinformatics research infrastructures and the European Bioinformatics Institute (EMBL-EBI). This coordinated infrastructure includes data standards, exchange, interoperability, storage, security and training. Recognising the importance of a data foundation for European life sciences, the ESFRI and European Council named ELIXIR as one of Europes priority Research Infrastructures. In response ELIXIR have developed ELIXIR-EXCELERATE. The project will fast-track ELIXIRs early implementation phase by i) coordinate and enhance existing resources into a world-leading data service for academia and industry, ii) grow bioinformatics capacity and competence across Europe, and iii) complete the management processes needed for a large distributed infrastructure. ELIXIR-EXCELERATE will deliver a step-change in the life sciences. It will enable cost-effective and sustainable management and re-use of data for millions of users across the globe and improve the competitiveness of European life science industries through accessible data and robust standards and tools.
Lamkanfi M.,VIB |
Lamkanfi M.,Ghent University |
Cell | Year: 2014
Recent studies have offered a glimpse into the sophisticated mechanisms by which inflammasomes respond to danger and promote secretion of interleukin (IL)-1β and IL-18. Activation of caspases 1 and 11 in canonical and noncanonical inflammasomes, respectively, also protects against infection by triggering pyroptosis, a proinflammatory and lytic mode of cell death. The therapeutic potential of inhibiting these proinflammatory caspases in infectious and autoimmune diseases is raised by the successful deployment of anti-IL-1 therapies to control autoinflammatory diseases associated with aberrant inflammasome signaling. This Review summarizes recent insights into inflammasome biology and discusses the questions that remain in the field. © 2014 Elsevier Inc.
Agency: European Commission | Branch: H2020 | Program: RIA | Phase: SC1-PM-01-2016 | Award Amount: 16.02M | Year: 2017
The SYSCID consortium aims to develop a systems medicine approach for disease prediction in CID. We will focus on three major CID indications with distinct characteristics, yet a large overlap of their molecular risk map: inflammatory bowel disease, systemic lupus erythematodes and rheumatoid arthritis. We have joined 15 partners from major cohorts and initiatives in Europe (e.g.IHEC, ICGC, TwinsUK and Meta-HIT) to investigate human data sets on three major levels of resolution: whole blood signatures, signatures from purified immune cell types (with a focus on CD14 and CD4/CD8) and selected single cell level analyses. Principle data layers will comprise SNP variome, methylome, transcriptome and gut microbiome. SYSCID employs a dedicated data management infrastructure, strong algorithmic development groups (including an SME for exploitation of innovative software tools for data deconvolution) and will validate results in independent retrospective and prospective clinical cohorts. Using this setup we will focus on three fundamental aims : (i) the identification of shared and unique core disease signatures which are associated with the disease state and independent of temporal variation, (ii) the generation of predictive models of disease outcome- builds on previous work that pathways/biomarkers for disease outcome are distinct from initial disease risk and may be shared across diseases to guide therapy decisions on an individual patient basis, (iii) reprogramming disease - will identify and target temporally stable epigenetic alterations in macrophages and lymphocytes in epigenome editing approaches as biological validation and potential novel therapeutic tool. Thus, SYSCID will foster the development of solid biomarkers and models as stratification in future long-term systems medicine clinical trials but also investigate new causative therapies by editing the epigenome code in specific immune cells, e.g. to alleviate macrophage polarization defects.
Agency: European Commission | Branch: H2020 | Program: RIA | Phase: NMBP-10-2016 | Award Amount: 6.00M | Year: 2017
The overall objective of B-SMART is: 1. to design modular nanoparticles, 2. to manufacture them via a quality-by-design protocol, 3. to achieve delivery of therapeutic RNAs to the brain and treat neurodegenerative diseases. I. To design modular nanoparticles consisting of o an active RNA payload o established (lipid-based), emerging (trigger-responsive polymer-based) or exploratory (extracellular vesicle-based) nanoparticles o a targeting ligand consisting of the variable domain of heavy chain only antibodies (also known as VHHs or nanobodies), which are coupled to the carrier platform II. To manufacture the modular nanoparticles using a microfluidic assembly system that will ensure quality-by-design: uniform nanoparticles across research sites and excellent control over the physico-chemical parameters. III. To test pre-clinical activity of formulations with promising in vitro activity with good cell/blood compatibility and to select the best RNA-formulation for clinical translation to treat neurodegenerative diseases. Pre-clinical efficacy is tested after o local injection o nasal administration o systemic administration The neurodegenerative diseases carry a high burden for patients since they are without exception progressive. But they also carry a substantial socio-economic burden with estimated costs of 130 billion euro. per year (2008). IV. The technical work in B-SMART will be supported by project management. It ensures that the project is coordinated in a clear, unambiguous and mutually acceptable manner and that the project achieves its objectives, within the given financial and time constraints. in B-SMART we expect to arrive at a scale-able nanoparticle formulation with uniform characteristics that shows strong pre-clinical evidence of therapeutic efficacy and is ready for clinical translation.
Agency: European Commission | Branch: H2020 | Program: CSA | Phase: INFRADEV-03-2016-2017 | Award Amount: 3.95M | Year: 2017
Instruct-Ultra aims to advance the scope and efficiency of implementation of Instruct and consolidate the foundations for long-term sustainability. This will be achieved through specific objectives: expand Instruct membership to new Member States and increase global links; engage new user communities; improve efficiencies in service delivery; improve data capture and management; adjust the scale and reliability of the infrastructure. Instruct-Ultra will deliver these alongside the transition to ERIC legal status and rapid developments in, and increased demand for, integrated structural biology infrastructure. These advances in the scale and speed of delivery will earn further trust within the life science community. One focus will to expand membership to Eastern European states and EFTA countries, integrating their structural biology communities into Instruct and providing new opportunities to support research excellence and raise standards. Opportunities for engaging with industrialised and developing countries outside the ERA will build on existing cooperative work between Instruct and Asian, African and South American countries to establish strong bilateral programmes of benefit to both parties, giving Instruct better engagement in emerging global challenges and positioning Instruct as a trusted global resource for high quality structural biology services. Starting from baseline operations four years ago Instruct has now identified key areas of service which should be expanded, new potential user groups, and opportunities for more reliable, efficient and sometimes remotely used workflows. Instruct-Ultra will therefore test new modes of access and pilot new service methods in high demand areas to accelerate access for more users. Instruct-Ultra will reinforce Instruct operations by updating and expanding the business plan and structural biology roadmap, whilst improving the interface with academia and industry as a strategy to sustainability.
Agency: European Commission | Branch: H2020 | Program: IA | Phase: ICT-24-2016 | Award Amount: 1.55M | Year: 2017
Creating effective ways for citizen science is immensely important. Scientists in all fields increasingly rely on active public participation for experiments and analyses of complex and/or massive data, and the outreach and education possibilities of citizen science are enormous. Yet there are three key issues for any citizen science project: (i) reach out to a sufficiently large audience, (ii) lower the threshold to participation as much as possible, and (iii) provide incentives to continue participant engagement. We created Massively Multiplayer Online Science to connect scientific research and video games as a seamless gaming experience. Research tasks completely integrated with game mechanics, narrative and visuals can open up a new channel between the gamer and the scientific community. Converting a small fraction of the billions of hours spent with playing video games will bring an enormous contribution to scientific research, and in the meantime will change how video games expertise is perceived. The goal of GAPARS project is to develop and validate the reference platform enabling the injection of scientific tasks into on-line communities, such as gamers. To do so, we gathered a unique team of prestigious participants and one major game editor, all with a track-record of excellence in management and in their respective domain of expertise. This project will put Europe on the map with a new genre of serious games.
Agency: European Commission | Branch: H2020 | Program: RIA | Phase: NMP-12-2015 | Award Amount: 7.69M | Year: 2016
Alzheimers disease (AD) is the leading cause of dementia in the Western world and to date no cure nor any preventive strategy are available for this neurodegenerative disorder. Bacterial 16S rRNA sequencing from fecal samples revealed a remarkable shift in the gut microbiota of conventionally-raised AD mice compared to healthy, wild-type mice. Based on these findings, we generated germ-free Alzheimer (GF-AD) mouse model and discovered a drastic reduction of cerebral A amyloid pathology when compared to control AD mice with natural intestinal microbiota. In contrast, fecal transplantation of GF-AD with harvested microbiota from conventionally-raised AD mice dramatically increased cerebral A pathology. Altogether, these results strongly support a microbial involvement in the development of AD and show how gut microbiome modulation can slow down or halt its onset. This paves the road to new indirect diagnostic and therapeutic approaches for AD prevention, based on gut microbiota modulation through probiotic cocktails. Based on these findings, the present proposal aims at designing and optimizing an efficient encapsulation strategy to guarantee the survival and the delivery of probiotic strains in the gut as opposed to standard strategies targeting directly the brain. A successful accomplishment of this goal will also allow to derive AD risk factors and to establish an objective baseline setting for AD diagnosis. Ultimately, the present project will open new horizons in biomedical diagnostics and personalized medicine through the marketing of these technologies and therapeutic concepts.
Agency: European Commission | Branch: H2020 | Program: ERC-COG | Phase: ERC-CoG-2015 | Award Amount: 2.00M | Year: 2017
Programmed cell death is essential for homeostasis, and its deregulation contributes to human disease. Inflammasome-induced pyroptosis of infected macrophages contributes to host defense against infections, but the concomitant release of inflammatory danger signals and leaderless cytokines is detrimental in chronic inflammatory diseases. The central hypothesis of the PyroPop ERC Consolidator project is that inflammasomes are cytosolic platforms that couple pathogen sensing to multiple programmed cell death modes. This is based on our preliminary data showing that inflammasomes can be triggered to switch from inflammatory pyroptosis to programmed necrosis and non-inflammatory apoptosis. This suggests that the (patho)physiological outcomes of inflammasome activation may be modulated for therapeutic purposes. However, the molecular machinery and effector mechanisms of pyroptosis, inflammasome-induced apoptosis and programmed necrosis are virtually unknown. My objectives are (i) to explore the cleavage events and subcellular dynamics of pyroptosis by proteomics and high-resolution time-lapse microscopy; (ii) to clarify the molecular mechanisms of pyroptosis and inflammasome-controlled cell death switching; and (iii) to address how inflammasome-associated cell death modes impact on anti-bacterial host defense and chronic inflammatory pathology in vivo through the identification of pyroptosis-selective biomarkers and clinical analysis of pyroptosis-deficient mouse models. The central hypothesis in this regard is that inflammasome-mediated secretion of leaderless cytokines (such as IL-1 and IL-18) and danger signals may be mechanistically coupled to pyroptosis, but not apoptosis induction. By clarifying the mechanisms of inflammasome-controlled programmed cell death, this project may set the path for the development of an entirely novel class of inflammation-modulating therapies that are based on converting inflammatory pyroptosis into non-inflammatory apoptosis.