Data-Gouv-ML/pcri-erc-participations-et-projets-laureats huggingface dataset:
Projet ERC : LOLITA (Horizon 2020, appel 2016, Starting grants)
Domaine scientifique : Physical Sciences and Engineering
Panel : Systems and communication engineering
Entité participante : Carlos III University of Madrid — Pays : Espagne — Rôle : PI
Type d'entité : Enseignement supérieur ou secondaire
Financement ERC de l'entité : 1424000.0 €

The majority of wireless connections in the fifth generation (5G) of wireless systems will most likely be originated by autonomous machines and devices rather than by the human-operated mobile terminals for which traditional broadband services are intended. It is thus expected that enhanced mobile-broadband services will be complemented by new services centered on machine-type communications (MTC). An important emerging area among MTC systems is that of low-latency communications, which targets systems that require reliable real-time communication with stringent requirements on latency and reliability. The design of low-latency wireless communication systems is a great challenge, since it requires a fundamentally different design approach than the one used in current high-rate systems. Indeed, current systems exchange packets of several thousand bits. For such packet lengths, there are error-correcting codes that can correct transmission errors with high probability at rates close to the capacity. Consequently, the design of current systems is supported by the extensive information-theoretical knowledge we have about wireless communications. In contrast, low-latency systems exchange packets of only several hundred bits, so the rate of the error-correcting code must be significantly below the capacity to achieve the desired reliability. Consequently, for such systems, capacity is not a relevant performance measure, and design guidelines that are based on its behavior will be misleading. Currently, we are lacking the theoretical understanding of low-latency wireless communication systems that would be crucial to design them optimally. The presented project addresses this problem by establishing the theoretical framework required to describe the fundamental tradeoffs in low-latency wireless communications. The project's vision is that finite-blocklength information theory will play the same role for low-latency systems as information theory has for current systems.

Mots-clés : information theory,wireless communications
Projet ERC : MUSMICRO (Horizon 2020, appel 2019, Starting grants)
Domaine scientifique : Life Science
Panel : Environmental Biology, Ecology and Evolution
Entité participante : University of Oxford — Pays : Royaume-Uni — Rôle : PI
Type d'entité : Enseignement supérieur ou secondaire
Financement ERC de l'entité : 1771166.0 €

The mammalian gut teems with a particularly dense and diverse microbial community, the composition of which varies widely among hosts. A large body of laboratory work suggests these communities provide important functions for the host – including nutrition, pathogen protection and immune development – but we know very little about what shapes the mammalian gut microbiota, and how it affects the host, in natural populations. A major barrier to progress is a lack of powerful investigative tools for most wild animal species. I will overcome this by studying a natural population of the species that has the best laboratory tools, and knowledge, for the mammalian microbiome: the house mouse. Specifically, I will set up a new wild house mouse system and use it to address three broad questions: 1) what drives natural variation in the gut microbiota? 2) does microbiota variation predict fitness traits in the wild? and, critically, 3) does microbiota variation causally affect fitness-relevant traits? To do this, I will pair detailed, longitudinal studies of wild mice with controlled experiments in the lab, making use of state-of-the-art tools for this species, including: (i) faecal transplant experiments with germ-free animals, to test the phenotypic impact of different wild mouse microbiotas (ii) high resolution genotyping methods and (iii) new radio-frequency identification (RFID) technology we have recently developed for monitoring wild rodent survival and behaviour. By doing so, this project will directly tackle the key unanswered question: does the composition of the mammalian gut microbiota actually matter in nature?

Mots-clés : gut microbiota,adaptation,house mouse,fitness,survival,community
Projet ERC : SMARTHEART (Horizon 2020, appel 2020, Starting grants)
Domaine scientifique : Life Science
Panel : Prevention, Diagnosis and Treatment of Human Diseases
Entité participante : Ghent University — Pays : Belgique — Rôle : PI
Acronyme de l'entité : UGent
Type d'entité : Enseignement supérieur ou secondaire
Financement ERC de l'entité : 1498125.0 €

The management of cardiac arrhythmia remains the largest problem in cardiac electrophysiology. The prevalence of the most frequent arrhythmia, atrial fibrillation (AF), is expected to rise steeply due to the ageing population. In spite of intensive research, the mechanism of atrial fibrillation remains unclear, leading to poor results in its treatment. Ablation of AF often results in complex atrial tachycardia (AT), which are difficult to treat. Also ventricular tachycardias (VT) and fibrillations (VF) are a major cause of sudden cardiac death. Again, eliminating VTs with ablation has achieved only modest success in complex cases. Therefore, there is an urgent need to better understand and localize the sources of arrhythmia in order to improve its treatment. I propose a radical new approach of applying network theory to study the mechanisms of AT, VT and AF. Currently, network theory is known for being the basis for the Google search engine other online social networks, and has myriad applications throughout biology, physics, and social sciences. However, it has never been applied to the heart. In this proposal, based on my invention and preliminary work, I propose to apply network theory to clinical data of cardiac arrhythmia, backed-up by in-silico simulations. A new set of research tools will be created to automatically detect the source of the arrhythmia for complex AT and AF, which will identify possible ablation targets. For VT a substrate analysis is proposed, in order to reveal the structure of the heart to also determine the ablation target. My preliminary results already show that network analysis is able to automatically predict sites of ablation, prior to surgery in AT, largely exceeding the most recent technologies currently used in clinics. Therefore, this translational project will not only provide novel insights into the mechanism of cardiac arrhythmia, but will actually lead to an improved treatment for the patient.

Mots-clés : network theory,cardiac arrhythmia,computer modeling
Projet ERC : CREAM4 (Horizon 2020, appel 2016, Advanced grants)
Domaine scientifique : Physical Sciences and Engineering
Panel : Products and processes engineering
Entité participante : University of Twente — Pays : Pays-Bas — Rôle : PI
Type d'entité : Enseignement supérieur ou secondaire
Financement ERC de l'entité : 2500000.0 €

The management of mesoscale dynamics is the missing link in gaining complete control over chemical processes like heterogeneous catalysis. The ability to accurately position nanoscale active elements in cellular mesoscale (nm to µm-range) structures with high symmetrical order is instrumental in streamlining vital molecular or energetic paths. 3D periodicity in the structure that supports active or adsorption sites minimizes spatial variations in mass transport, whereas mesoscale control of the location of these sites gives a route to tuning activity and functionality. The introduction of mesoscale metamaterials expands the on-going trend in chemistry, of more and more dimensionally refined structured elements, a so to speak "Moore's law in Process Intensification". The roadmap to higher process efficiency dictates a next, disruptive step in mastering manufacturing control at smaller dimensions. The proposed disruptive technology to realize the required mesoscale features is Additive Manufacturing, which is the only method offering the desired freedom in shape, symmetry and composition. More specifically, this project explores electrospinning methods with precise intra-wire control of the position of active sites and accurately tuneable 3D inter-wire distances. This is seen as the ideal technique to reach the mesoscale material target, as the method is scalable to practical device volumes. The main ingredients of the novel technology are microfluidic networks to line up nanoparticles, before electrospinning them with integrated micromachined nozzles, and depositing them accurately in the form of 3D nanowire networks, using integrated circuit collector electrodes. Flow-through, cellular materials which are highly homogeneous in size and composition, or with intentionally embedded gradients, having features designed at the mesoscale, will be investigated for applications in the fields of heterogeneous catalysis and solar energy capture and conversion.

Mots-clés : nanowires,solar to fuel,additive manufacturing
Projet ERC : VISCOMATRIX (Horizon 2020, appel 2019, Starting grants)
Domaine scientifique : Life Science
Panel : Cellular, Developmental and Regenerative Biology
Entité participante : The Francis Crick Institute — Pays : Royaume-Uni — Rôle : Partner
Type d'entité : Recherche
Financement ERC de l'entité : 614212.75 €

The mechanical properties of the extracellular matrix (ECM) regulate processes during development, cancer and wound healing. The vast majority of research efforts in this field have been focused on ECM’s elasticity as a leading determinant of cell and tissue behaviour. However, the ECM is not merely elastic but is instead both viscous and elastic. Due to its viscoelastic nature, the ECM response to mechanical loads is inherently dynamic and evolves with time, independently of matrix degradation or remodelling. Despite the universality of ECM’s viscoelasticity, how viscoelasticity affects tissue function is unknown. Based on our preliminary data, cellular behaviour diverges significantly between viscoelastic and elastic ECMs. We hypothesize that viscoelasticity dominates tissue response. Our objective is to determine the biophysical and molecular mechanisms that regulate viscoelasticity sensing and mechanotransduction in 3D and understand its implications in cell and tissue response. To address, we will use an integrative approach that will combine 3D materials with exquisite control of viscoelastic properties, systematic molecular perturbations, computational modelling and precise quantitative analysis of cellular properties, forces and stresses. While using these tools, we will unravel the molecular mechanisms that regulate viscoelasticity response at single-cell and collective level. We will determine the dynamic role of viscoelasticity in breast homeostasis, malignant transformation and invasion. Finally, we will validate the implications of viscoelasticity by measuring breast ECM’s viscoelastic properties and with in vivo experiments. We expect that this project will unravel novel mechanosensing mechanisms operating at the roots of biological responses. These mechanisms, due to the inherent viscoelastic nature of tissues, will affect many biological fields from morphogenesis to cancer, and applied fields such as tissue engineering and biomaterials design.

Mots-clés : mechanotransduction,mechanosensing,cell mechanics,extracellular matrix,biomaterials,bioengineering
Projet ERC : Neurovulnerability (Horizon 2020, appel 2018, Starting grants)
Domaine scientifique : Life Science
Panel : Neuroscience and Disorders of the Nervous System
Entité participante : German Center for Neurodegenerative Diseases — Pays : Allemagne — Rôle : PI
Acronyme de l'entité : DZNE
Type d'entité : Recherche
Financement ERC de l'entité : 1472667.34 €

The mechanisms behind neuronal death in different motor neuron diseases (MND) remain unknown. These MNDs include the devastating spinal muscular atrophy (SMA) and amyotrophic lateral sclerosis (ALS). A fascinating question in neurodegeneration research is why mutations in ubiquitously expressed genes result in the selective death of a specific neuronal subtype. The ubiquitously expressed and conserved survival of motor neuron (SMN) protein receives its name because its deficit results in MN degeneration. However, SMN known functions -spliceosome assembly and axonal mRNA transport- do not explain the selective MN vulnerability. Accumulation of intracellular aggregates in neurons is a hallmark of most neurodegenerative diseases. The lysosome-autophagy system is the main catabolic pathway for recycling of protein aggregates and damaged organelles, and its role as a quality control system is especially critical in neurons, due to their postmitotic and highly specialized nature. The hypothesis for this proposal is that SMN deficiency leads to a lysosome-autophagy dysfunction which results in a proteostatic failure, underlying MN degeneration. Furthermore, the existing heterogeneity in SMN protein levels across MN populations may determine their probability of survival. To test these hypotheses we will use the CRISPR/Cas9 system to genetically engineer human control, SMA and ALS patient-derived iPSCs to generate isogenic and reporter lines that will allow us to study selective neuronal subtypes at a single-cell level. We will also follow an interdisciplinary approach using a SMA Drosophila model to identify new molecular pathways essential for SMN neuropathology. Altogether, my research proposal aims at untangling the molecular mechanisms underlying selective MN death. Our results will open up new directions of research into the molecular basis of neurodegeneration and will provide clues for the design of therapeutics targeting specific neuronal types or phases of MNDs.

Mots-clés : motor neuron,ipscs,lysosome
Projet ERC : Neurovulnerability (Horizon 2020, appel 2018, Starting grants)
Domaine scientifique : Life Science
Panel : Neuroscience and Disorders of the Nervous System
Entité participante : Spanish National Research Council — Pays : Espagne — Rôle : Partner
Acronyme de l'entité : CSIC
Type d'entité : Recherche
Financement ERC de l'entité : 0.0 €

The mechanisms behind neuronal death in different motor neuron diseases (MND) remain unknown. These MNDs include the devastating spinal muscular atrophy (SMA) and amyotrophic lateral sclerosis (ALS). A fascinating question in neurodegeneration research is why mutations in ubiquitously expressed genes result in the selective death of a specific neuronal subtype. The ubiquitously expressed and conserved survival of motor neuron (SMN) protein receives its name because its deficit results in MN degeneration. However, SMN known functions -spliceosome assembly and axonal mRNA transport- do not explain the selective MN vulnerability. Accumulation of intracellular aggregates in neurons is a hallmark of most neurodegenerative diseases. The lysosome-autophagy system is the main catabolic pathway for recycling of protein aggregates and damaged organelles, and its role as a quality control system is especially critical in neurons, due to their postmitotic and highly specialized nature. The hypothesis for this proposal is that SMN deficiency leads to a lysosome-autophagy dysfunction which results in a proteostatic failure, underlying MN degeneration. Furthermore, the existing heterogeneity in SMN protein levels across MN populations may determine their probability of survival. To test these hypotheses we will use the CRISPR/Cas9 system to genetically engineer human control, SMA and ALS patient-derived iPSCs to generate isogenic and reporter lines that will allow us to study selective neuronal subtypes at a single-cell level. We will also follow an interdisciplinary approach using a SMA Drosophila model to identify new molecular pathways essential for SMN neuropathology. Altogether, my research proposal aims at untangling the molecular mechanisms underlying selective MN death. Our results will open up new directions of research into the molecular basis of neurodegeneration and will provide clues for the design of therapeutics targeting specific neuronal types or phases of MNDs.

Mots-clés : motor neuron,ipscs,lysosome
Projet ERC : IM-ID (Horizon 2020, appel 2018, Starting grants)
Domaine scientifique : Life Science
Panel : Immunity, Infection and Immunotherapy
Entité participante : University of Liège — Pays : Belgique — Rôle : PI
Type d'entité : Enseignement supérieur ou secondaire
Financement ERC de l'entité : 1500000.0 €

The mechanisms underlying lung homeostasis are of fundamental biological importance and have critical implications for the prevention of immune-mediated diseases such as asthma. We have demonstrated that lung Interstitial Macrophages (IM) exhibit a tolerogenic profile and are able to prevent and limit the development of aberrant immune responses against allergens, thus underscoring their role as crucial regulators of lung homeostasis. In addition, we have shown that IM could expand from monocyte precursors upon host exposure to bacterial unmethylated CpG-DNA, resulting in robust protection against allergic asthma. To date, however, IM have only been characterized as a bulk population in functional studies, and little is known about the tissue-instructive signals, specific transcription factors and differentiation programs which contribute to determining their identity (ID) and function, as proposed by the macrophage niche model. We have developed an innovative transgenic tool to selectively target IM which, in combination with high dimensional single cell technologies, will allow us to (1) define the precise ID of IM, i.e. their spatial organization, heterogeneity, molecular signature and the specific TF governing their differentiation and function; (2) investigate how IM ID is imprinted by the local niche to sustain lung homeostasis. Specifically, we aim to identify the epithelial cell-derived chemo-attractive signals controlling IM precursor recruitment and to elucidate the contribution of the lung cholinergic nervous system to IM ID and lung homeostasis. This research will increase our understanding of the basic mechanisms underlying the fine-tuning of tolerogenic IM and will thus provide robust foundations for novel IM-targeted approaches promoting health and preventing airway diseases in which IM (dys)functions have been implicated.

Mots-clés : lung immune homeostasis,macrophage niche,tissue imprinting,master transcription factor,neuroimmune and epithelial cell interactions,selective macrophage targeting,mouse models
Projet ERC : NeuroQure (Horizon 2020, appel 2017, Proof of concept grants)
Entité participante : University of Zurich — Pays : Suisse — Rôle : PI
Acronyme de l'entité : UZH
Type d'entité : Enseignement supérieur ou secondaire
Financement ERC de l'entité : 150000.0 €

The misfolding of the cellular prion protein (PrPC) causes infectious neurodegenerative conditions called prion diseases. In the framework of the ERC-funded study “The Prion Protein in Health and Disease” the team of Adriano Aguzzi has discovered that antibodies against the flexible tail (FT) of PrPC are neuroprotective against prion pathologies. Here we propose to clone and express such antibodies from humans and to develop them as antiprion therapeutics. The principal investigator has founded a company (www.Mabylon.com) which has established a high-yield method for cloning paired heavy and light chains from human memory B cells. The proposed research program will identify rare anti-FT immunoreactive individuals among large populations by high-throughput screening. The clinical information of the selected individuals will help to identify antibodies from persons devoid of pathologies that may be related to anti-PrPC autoimmunity. Therefore, the human antibodies generated within this program will represent fast-track investigational new drug (IND) candidates with safety profiles superior to those of murine or humanized antibodies. Completion of the proposed activities will lead to the development of therapies against prion diseases, which are currently considered untreatable and invariably fatal.

Mots-clés : protein aggregation,prion disease,neurotoxicity,immunotherapy
Projet ERC : COMPLEXITY (Horizon 2020, appel 2015, Starting grants)
Domaine scientifique : Social Sciences and Humanities
Panel : Individuals, Markets and Organisations
Entité participante : University of London — Pays : Royaume-Uni — Rôle : PI
Acronyme de l'entité : U. London
Type d'entité : Enseignement supérieur ou secondaire
Financement ERC de l'entité : 1498947.0 €

The modern financial system has undergone immense transformation in recent years and is far more complex than ever before. In lockstep, financial regulation has also become more complex. This research proposal attempts to improve our understanding of potential drivers of this complexity and the implications of this change on the allocation of resources. Taking a positive rather than a normative approach, I will analyse post-crisis changes at both the micro- and at the macro-levels to create a broader understanding of complexities in the current financial system. In order to do so, I will employ a set of advanced research designs, as well as a uniquely assembled micro-level dataset covering state and privately owned financial institutions in Asia, Africa, South America and Europe. This project will focus on two interconnected areas of research: 1) Organisation of Credit, 2) Financial regulation in a complex environment. The aim of this project is to create a sustainable framework for the study of post-crisis financial systems, and to shape the current debate on the future of post-crisis financial structures and the development of policy in this area. Not only will this research have a considerable impact on our understanding of financial systems, it will also impact fields beyond finance, like Organisational Economics, Industrial Organisation and Development Economics.