1,291 research outputs found

    Violences sexuelles en milieu universitaire au QuĂ©bec : rapport de recherche de l’enquĂȘte ESSIMU

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    Cette recherche, intitulĂ©e « EnquĂȘte SexualitĂ©, SĂ©curitĂ© et Interactions en Milieu Universitaire(ESSIMU) : Ce qu’en disent Ă©tudiant.es, enseignant.es et employĂ©.es », a permis d’établir un portrait des violences sexuelles se dĂ©roulant en contexte universitaire au QuĂ©bec. Cette enquĂȘte d’envergure provinciale regroupe 12 chercheures provenant des 6 universitĂ©s suivantes : UniversitĂ© du QuĂ©bec Ă  MontrĂ©al, UniversitĂ© de MontrĂ©al, UniversitĂ© Laval, UniversitĂ© de Sherbrooke, UniversitĂ© du QuĂ©bec en Outaouais et UniversitĂ© du QuĂ©bec Ă  Chicoutimi. L’équipe interdisciplinaire et interuniversitaire compte Ă©galement le Regroupement quĂ©bĂ©cois des centres d’aide et de lutte contre les agressions Ă  caractĂšre sexuel et le Service aux collectivitĂ©s de l’UQAM. Afin de documenter les situations de violence sexuelle vĂ©cues en milieu universitaire (VSMU), l’équipe ESSIMU a rĂ©alisĂ© en 2016 une vaste Ă©tude auprĂšs de 9 284 rĂ©pondant.es dans 6 universitĂ©s quĂ©bĂ©coises francophones. Le questionnaire, administrĂ© en ligne, a permis de rendre compte d’un large Ă©ventail de manifestations de violence sexuelle vĂ©cues par l’ensemble de la communautĂ© universitaire (Ă©tudiant ou travaillant Ă  l’universitĂ©). La mesure de victimisation distinguait le harcĂšlement sexuel (comportements verbaux et non verbaux qui traduisent des attitudes insultantes, hostiles et dĂ©gradantes), les comportements sexuels non dĂ©sirĂ©s (comportements verbaux et non verbaux Ă  caractĂšre sexuel, offensants, non dĂ©sirĂ©s ou non rĂ©ciproques, incluant la tentative de viol et l’agression sexuelle) et la coercition sexuelle (chantage en retour de rĂ©compenses)

    Cellular Senescence Is Immunogenic and Promotes Antitumor Immunity

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    Senescencia celular; Inmunidad antitumoralSenescĂšncia cel·lular; Immunitat antitumoralCellular senescence; Antitumor immunityCellular senescence is a stress response that activates innate immune cells, but little is known about its interplay with the adaptive immune system. Here, we show that senescent cells combine several features that render them highly efficient in activating dendritic cells (DC) and antigen-specific CD8 T cells. This includes the release of alarmins, activation of IFN signaling, enhanced MHC class I machinery, and presentation of senescence-associated self-peptides that can activate CD8 T cells. In the context of cancer, immunization with senescent cancer cells elicits strong antitumor protection mediated by DCs and CD8 T cells. Interestingly, this protection is superior to immunization with cancer cells undergoing immunogenic cell death. Finally, the induction of senescence in human primary cancer cells also augments their ability to activate autologous antigen-specific tumor-infiltrating CD8 lymphocytes. Our study indicates that senescent cancer cells can be exploited to develop efficient and protective CD8-dependent antitumor immune responses. Significance: Our study shows that senescent cells are endowed with a high immunogenic potential—superior to the gold standard of immunogenic cell death. We harness these properties of senescent cells to trigger efficient and protective CD8-dependent antitumor immune responses.We are grateful to Maria Isabel Muñoz for assistance with the animal protocols; to Kevin Kovalchik for help with data sharing; to Francesca Castoldi for help in total RNA extraction for B16F10 and IMR-90 cells; to Fredrik Fagerstrom-Billai, Susann FĂ€lt, Anastasios Damdimopoulos, and David Brodin at Bioinformatics and Expression Analysis Core Facility, Karolinska Institute (KI), for assistance in RNA-seq and analysis; to the IRB core facilities (Functional Genomics, Biostatistics/Bioinformatics and Histopathology); and to the PCB (Animal House) for general research support. I. Marin was the recipient of an FPI fellowship from the Spanish Ministry of Science (PRE2018-083381). O. Boix was the recipient of an FPI-AGAUR fellowship from the Generalitat de Catalunya. A. Garcia-Garijo was supported by a PERIS grant (SLT017/20/000131) from the Generalitat de Catalunya. J.A. LĂłpez-DomĂ­nguez and M. Kovatcheva were supported by a fellowship from the Spanish Association Against Cancer (AECC). Work in the laboratory of E. Caron was funded by the Fonds de recherche du QuĂ©bec – SantĂ© (FRQS), the Cole Foundation, CHU Sainte-Justine, the Charles-Bruneau Foundation, the Canada Foundation for Innovation, the National Sciences and Engineering Research Council (#RGPIN-2020-05232), and the Canadian Institutes of Health Research (#174924). E. Garralda received funding from the Comprehensive Program of Cancer Immunotherapy and Immunology II (CAIMI-II) supported by the BBVA Foundation (grant 53/2021). The M. Abad lab received funding from the Spanish Ministry of Science and Innovation (RTI2018-102046-B-I00A and RTC-2017-6123-1) and the AECC (PRYCO211023SERR). M. Abad was the recipient of a RamĂłn y Cajal contract from the Spanish Ministry of Science and Innovation (RYC-2013-14747). A. Gros received funding from the Spanish Ministry of Science cofunded by the European Regional Development Fund (ERDF; RTC-2017-6123-1), from the Instituto de Salud Carlos III (MS15/00058), and from CAIMI-II (grant 53/2021) supported by the BBVA Foundation. The work in the laboratory of F. Pietrocola is supported by a KI Starting Grant, a Starting Grant from the Swedish Research Council (2019_02050_3), and grants from the Harald Jeanssons Foundation, the Loo and Hans Osterman Foundation, and Cancerfonden (21 1637 Pj). Work in the laboratory of M. Serrano was funded by the IRB and La Caixa Foundation, and by grants from the Spanish Ministry of Science cofunded by the European Regional Development Fund (SAF-2017-82613-R, RTC-2017-6123-1), the European Research Council (ERC-2014-AdG/669622), Secretaria d'Universitats i Recerca del Departament d'Empresa i Coneixement of Catalonia (Grup de Recerca consolidat 2017 SGR 282), and the AECC (PRYCO211023SERR). The publication costs of this article were defrayed in part by the payment of publication fees. Therefore, and solely to indicate this fact, this article is hereby marked “advertisement” in accordance with 18 USC section 1734

    Cellular senescence is immunogenic and promotes anti-tumor immunity

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    Cellular senescence is a stress response that activates innate immune cells, but little is known about its interplay with the adaptive immune system. Here, we show that senescent cells combine several features that render them highly efficient in activating dendritic cells (DCs) and antigen-specific CD8 T cells. This includes the release of alarmins, activation of interferon signaling, enhanced MHC class I machinery, and presentation of senescence-specific self-peptides that can activate CD8 T cells. In the context of cancer, immunization with senescent cancer cells elicits strong anti-tumor protection mediated by DCs and CD8 T cells. Interestingly, this protection is superior to immunization with cancer cells undergoing immunogenic cell death. Finally, the induction of senescence in human primary cancer cells also augments their ability to activate autologous antigen-specific tumor-infiltrating CD8 lymphocytes. Our study indicates that senescent cancer cells can be exploited to develop efficient and protective CD8-dependent anti-tumor immune responses

    Search for heavy resonances decaying to two Higgs bosons in final states containing four b quarks

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    A search is presented for narrow heavy resonances X decaying into pairs of Higgs bosons (H) in proton-proton collisions collected by the CMS experiment at the LHC at root s = 8 TeV. The data correspond to an integrated luminosity of 19.7 fb(-1). The search considers HH resonances with masses between 1 and 3 TeV, having final states of two b quark pairs. Each Higgs boson is produced with large momentum, and the hadronization products of the pair of b quarks can usually be reconstructed as single large jets. The background from multijet and t (t) over bar events is significantly reduced by applying requirements related to the flavor of the jet, its mass, and its substructure. The signal would be identified as a peak on top of the dijet invariant mass spectrum of the remaining background events. No evidence is observed for such a signal. Upper limits obtained at 95 confidence level for the product of the production cross section and branching fraction sigma(gg -> X) B(X -> HH -> b (b) over barb (b) over bar) range from 10 to 1.5 fb for the mass of X from 1.15 to 2.0 TeV, significantly extending previous searches. For a warped extra dimension theory with amass scale Lambda(R) = 1 TeV, the data exclude radion scalar masses between 1.15 and 1.55 TeV

    Measurement of the top quark mass using charged particles in pp collisions at root s=8 TeV

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    Peer reviewe

    Measurement of t(t)over-bar normalised multi-differential cross sections in pp collisions at root s=13 TeV, and simultaneous determination of the strong coupling strength, top quark pole mass, and parton distribution functions

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