1,740 research outputs found

    Aligning verb senses in two Italian lexical semantic resources

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    National audienceThis work describes the evaluations of three different approaches, Lexical Match, Sense Similarity based on Personalized Page Rank, and Semantic Match based on Shallow Frame Structures, for word sense alignment of verbs between two Italian lexical-semantic resources, MultiWordNet and the Senso Comune Lexicon. The results obtained are quite satisfying with a final F1 score of 0.47 when merging together Lexical Match and Sense Similarity

    Enriching the "Senso Comune" Platform with Automatically Acquired Data

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    International audienceThis paper reports on research activities on automatic methods for the enrichment of the Senso Comune platform. At this stage of development, we will report on two tasks, namely word sense alignment with MultiWordNet and automatic acquisition of Verb Shallow Frames from sense annotated data in the MultiSemCor corpus. The results obtained are satisfying. We achieved a final F-measure of 0.64 for noun sense alignment and a F-measure of 0.47 for verb sense alignment, and an accuracy of 68% on the acquisition of VerbShallow Frames

    Aligning an Italian WordNet with a lexicographic dictionary: Coping with limited data

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    International audienceThis work describes the evaluations of two approaches, Lexical Matching and Sense Similarity, for word sense alignment between MultiWordNet and a lexicographic dictionary, Senso Comune De Mauro, when having few sense descriptions (MultiWordNet) and no structure over senses (Senso Comune De Mauro). The results obtained from the merging of the two approaches are satisfying, with F1 values of 0.47 for verbs and 0.64 for nouns

    3D migration of cells solving an inverse problem

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    International audienceTraction Force Microscopy (TFM) is an inverse method that allows to obtain the stress field applied by a living cell on the environment on the basis of a pointwise knowledge of the displacement produced by the cell itself during its migration. This biophysical problem, usually addressed in terms of Green functions, can be alternatively tackled in a variational framework. In such a case, a suitable penalty functional has to be minimized. The resulting Euler-Lagrange equations include both the direct problem based on the linear elasticity operator as well as an equation built on its adjoint. Results from a two-dimensional model, i.e. where living cancer cells are migrating on a plane substrate, are briefly presented. While the mathematics is well established also in the three-dimensional case, i.e. where cells are completely embedded in the gel matrix, the experimental data needed are more difficult to obtain than the two-dimensional counterpart. First steps towards the complete three-dimensional traction reconstruction are reported

    Viral proteins targeting mitochondria: controlling cell death

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    AbstractMitochondrial membrane permeabilization (MMP) is a critical step regulating apoptosis. Viruses have evolved multiple strategies to modulate apoptosis for their own benefit. Thus, many viruses code for proteins that act on mitochondria and control apoptosis of infected cells. Viral proapoptotic proteins translocate to mitochondrial membranes and induce MMP, which is often accompanied by mitochondrial swelling and fragmentation. From a structural point of view, all the viral proapoptotic proteins discovered so far contain amphipathic α-helices that are necessary for the proapoptotic effects and seem to have pore-forming properties, as it has been shown for Vpr from human immunodeficiency virus-1 (HIV-1) and HBx from hepatitis B virus (HBV). In contrast, antiapoptotic viral proteins (e.g., M11L from myxoma virus, F1L from vaccinia virus and BHRF1 from Epstein–Barr virus) contain mitochondrial targeting sequences (MTS) in their C-terminus that are homologous to tail-anchoring domains. These domains are similar to those present in many proteins of the Bcl-2 family and are responsible for inserting the protein in the outer mitochondrial membrane leaving the N-terminus of the protein facing the cytosol. The antiapoptotic proteins K7 and K15 from avian encephalomyelitis virus (AEV) and viral mitochondria inhibitor of apoptosis (vMIA) from cytomegalovirus are capable of binding host-specific apoptosis-modulatory proteins such as Bax, Bcl-2, activated caspase 3, CAML, CIDE-B and HAX. In conclusion, viruses modulate apoptosis at the mitochondrial level by multiple different strategies

    Senso Comune as a Knowledge Base of Italian language: The Resource and its Development

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    International audienceSenso Comune is a linguistic knowledge base for the Italian Language, which accommodates the content of a legacy dictionary in a rich formal model. The model is implemented in a platform which allows a community of contributors to enrich the resource. We provide here an overview of the main project features, including the lexical-ontology model, the process of sense classification, and the annotation of meaning definitions (glosses) and lexicographic examples. Also, we will illustrate the latest work of alignment with MultiWordNet, to illustrate the methodologies that have been experimented with, to share some preliminary result, and to highlight some remarkable findings about the semantic coverage of the two resources

    The anti-caspase inhibitor Q-VD-OPH prevents AIDS disease progression in SIV-infected rhesus macaques

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    Apoptosis has been proposed as a key mechanism responsible for CD4+ T cell depletion and immune dysfunction during HIV infection. We demonstrated that Q-VD-OPH, a caspase inhibitor, inhibits spontaneous and activation-induced death of T cells from SIV-infected rhesus macaques (RMs). When administered during the acute phase of infection, Q-VD-OPH was associated with (a) reduced levels of T cell death, (b) preservation of CD4+/CD8+ T cell ratio in lymphoid organs and in the gut, (c) maintenance of memory CD4+ T cells, and (d) increased specific CD4+ T cell response associated with the expression of cytotoxic molecules. Although therapy was limited to the acute phase of infection, Q-VD-OPH-treated RMs showed lower levels of both viral load and cell-associated SIV DNA as compared with control SIV-infected RMs throughout the chronic phase of infection, and prevented the development of AIDS. Overall, our data demonstrate that Q-VD-OPH injection in SIV-infected RMs may represent an adjunctive therapeutic agent to control HIV infection and delaying disease progression to AIDS.This article is dedicated to the memory of Bruno Hurtrel. We also thank Jean-Claude Ameisen for his initial support. We acknowledge Celine Gommet (Institut Pasteur) for her expertise in the follow-up of our primate cohort. We also acknowledge Francois Villinger, who performed TRIM5a polymorphism. ML and JG were supported by fellowships from ANRS. RS thanks Fundacao para a Ciencia e a Tecnologia (FCT) for Investigator FCT Grant IF/00021/2014. This study was supported by research funding from ANRS and CIHR (MOP-133476) to JE. VR is supported by a fellowship from FCT (code SFRH/BD/64064/2009). JE thanks the Canada Research Chair program for financial assistance

    TRPM7 Kinase Controls Calcium Responses in Arterial Thrombosis and Stroke in Mice

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    Objective: TRPM7 (transient receptor potential cation channel, subfamily M, member 7) is a ubiquitously expressed bifunctional protein comprising a transient receptor potential channel segment linked to a cytosolic alpha-type serine/threonine protein kinase domain. TRPM7 forms a constitutively active Mg2+ and Ca2+ permeable channel, which regulates diverse cellular processes in both healthy and diseased conditions, but the physiological role of TRPM7 kinase remains largely unknown. Approach and Results: Here we show that point mutation in TRPM7 kinase domain deleting the kinase activity in mice (Trpm7(R/R)) causes a marked signaling defect in platelets. Trpm7(R/R) platelets showed an impaired PIP2 (phosphatidylinositol-4,5-bisphosphate) metabolism and consequently reduced Ca2+ mobilization in response to stimulation of the major platelet receptors GPVI (glycoprotein VI), CLEC-2 (C-type lectin-like receptor), and PAR (protease-activated receptor). Altered phosphorylation of Syk (spleen tyrosine kinase) and phospholipase C gamma 2 and beta 3 accounted for these global platelet activation defects. In addition, direct activation of STIM1 (stromal interaction molecule 1) with thapsigargin revealed a defective store-operated Ca2+ entry mechanism in the mutant platelets. These defects translated into an impaired platelet aggregate formation under flow and protection of the mice from arterial thrombosis and ischemic stroke in vivo. Conclusions: Our results identify TRPM7 kinase as a key modulator of phospholipase C signaling and store-operated Ca2+ entry in platelets. The protection of Trpm7(R/R) mice from acute ischemic disease without developing intracranial hemorrhage indicates that TRPM7 kinase might be a promising antithrombotic target
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