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University of Santiago de Compostela
Country: Spain
186 Projects, page 1 of 38
  • Funder: EC Project Code: 626212
    Partners: USC
  • Open Access mandate for Publications and Research data
    Funder: EC Project Code: 799037
    Overall Budget: 170,122 EURFunder Contribution: 170,122 EUR
    Partners: USC

    Rheumatoid Arthritis (RA) is an autoimmune chronic disease, characterized by inflammation in multiple joints, ultimately leading to joint deformity, pain and swelling. RA is one of the most frequent inflammatory arthropathies, with a prevalence of 0.3%-1%, striking during the most productive years of adulthood, and is a chronic disabling condition. No therapies exist to prevent RA, and a high percentage of patients do not respond to currently available therapies. Our research aims to integrate expertise on immunology and cutting-edge screening technologies to identify novel immunotherapeutics for RA based on immune modulation mechanisms. The project makes use of an extensive screening effort using a chemical library (60,000 compounds) containing repurposing drugs (drugs already approved for their use for the treatment of other diseases), targeted libraries and lead-like compounds. The aim of the project is to identify novel small molecules capable to modulate the immune response, counterbalancing the altered inflammatory environment that characterizes RA. Elucidation of the mechanism of action of the candidates (cell type, pathway and target) will take place through state-of-the art technologies such as chemoproteomics, RNASeq or CRISPR/Cas9. Ultimately, the most promising candidates will be tested ex vivo in cells from RA patients, providing a proof-of-concept of the therapeutic utility of the identified mechanism. The project is interdisciplinary and will make progress beyond the state of the art, as the identified immunotherapeutics could also be employed to treat other (auto)immune diseases, as well as being potentially translated to immunotherapy of cancer and cardiovascular diseases. The high-quality and originality of this proposal will open up the best career possibilities for the experienced researcher, and will be carried out under the umbrella of a public-private partnership with a pharmaceutical company, boosting European competitiveness.

  • Open Access mandate for Publications and Research data
    Funder: EC Project Code: 101065027
    Funder Contribution: 165,313 EUR
    Partners: USC

    The Pierre Auger Observatory detects extensive air showers that are initiated by protons or nuclei reaching Earth's atmosphere with energies exceeding 10**18 eV (ultra-high energy cosmic rays (UHECR)). The center-of-mass energy of the initial interaction of the CRs in the atmosphere exceeds the energies reached at the LHC by more than an order of magnitude. One of the key results of Auger is the discovery that these interactions of UHECRs do not behave as expected. Compared to simulations the measured air showers contain many more muons. This discrepancy could be simply due to the uncertainty inherent in the extrapolation from the energy scale of the LHC, where we can measure interactions in detail, to UHECR energies. Or it could be new physics! This project proposes to distinguish the two scenarios by the detailed measurement of the shower-to-shower distribution of the muon content as the shape of the distribution is driven by the quantum fluctuations in the first UHE interaction which are sensitive to new physics and the details of hadronic interactions. The measurement will for the first time use hybrid data from the surface and radio detectors of the Pierre Auger Observatory.

  • Project . 2009 - 2012
    Funder: EC Project Code: 239162
    Partners: USC
  • Open Access mandate for Publications
    Funder: EC Project Code: 891721
    Overall Budget: 253,228 EURFunder Contribution: 253,228 EUR
    Partners: USC

    In the last decades, obesity has become a growing health burden hence the importance of understanding its pathophysiology and the need to search for new therapeutic targets. Yanagisawa/Funato Lab (Y/F Lab) has recently discover that a splicing mutation in the Salt-inducible kinase 3 (Sik3) gene is involved in determining sleep need , and as well in a likely defective energy homeostasis since mice mutant for exon 13 of the Sik3 gene present an obese phenotype. The main objective of my proposed action is to identify the role of SIK3 in the central nervous system (CNS) in the regulation of energy balance and study its suitability as a target to develop an anti-obesity therapy. To achieve this, I will use virogenetic approaches in Sik3-ex13 flox mice and a neuron-specific mutant mice line for exon 13 of Sik3 gene will be generated. The molecular characterization of the animal models will be conducted by using several cutting-edge techniques such as RNA-Seq and phosphoproteomics. The identified targets will be functionally analyzed using genetics approaches. In sum, by doing the proposed project I will expect to uncover the influence of a potential new sensor in metabolic homeostasis. Moreover, this work in combination with the one going already on in Y/F Lab in relation to sleep may allow to understand the interrelationship between sleep disorders and obesity.