727 research outputs found

    Conception de systèmes polyculture-élevage en Centre Ardenne : défis et enjeux

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    Présentation des essais en polycultures élevage au Centre wallon de Recherches Agronomique

    MoMEMta, a modular toolkit for the Matrix Element Method at the LHC

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    The Matrix Element Method has proven to be a powerful method to optimally exploit the information available in detector data. Its widespread use is nevertheless impeded by its complexity and the associated computing time. MoMEMta, a C++ software package to compute the integrals at the core of the method, provides a versatile implementation of the Matrix Element Method to both the theory and experiment communities. Its modular structure covers the needs of experimental analysis workflows at the LHC without compromising ease of use on simpler and smaller simulated samples used for phenomenological studies. With respect to existing tools, MoMEMta improves on usability and flexibility. In this paper, we present version 1.0 of MoMEMta, together with examples illustrating the wide range of applications at the LHC accessible for the first time with a single tool.Comment: 18 pages, 3 figures; post peer revie

    Expression Analysis of PAC1-R and PACAP Genes in Zebrafish Embryos

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    This study describes the expression of the pituitary adenylate cyclase-activating polypeptide (PACAP1 and PACAP2) and PAC1 receptor genes (PAC1a-R and PAC1b-R) in the brain of zebrafish (Danio rerio) during development. In situ hybridization of the 24- and 48-hpf embryos revealed that PACAP genes were expressed in the telencephalon, the diencephalon, the rhombencephalon, and the neurons in the dorsal part of the spinal cord. PACAP2 mRNA appears to be the most abundant form during brain development. The two PAC1-R subtypes showed a similar expression pattern: mRNAs were detected in the forebrain, the thalamus, and the rhombencephalon. However, in the tectum, only PAC1b-R gene was detected. These results suggest that, in fish, PACAP may play a role in brain development

    An adaptive signaling network in melanoma inflammatory niches confers tolerance to MAPK signaling inhibition

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    Mitogen-activated protein kinase (MAPK) pathway antagonists induce profound clinical responses in advanced cutaneous melanoma, but complete remissions are frustrated by the development of acquired resistance. Before resistance emerges, adaptive responses establish a mutation-independent drug tolerance. Antagonizing these adaptive responses could improve drug effects, thereby thwarting the emergence of acquired resistance. In this study, we reveal that inflammatory niches consisting of tumor-associated macrophages and fibroblasts contribute to treatment tolerance through a cytokine-signaling network that involves macrophage-derived IL-1β and fibroblast-derived CXCR2 ligands. Fibroblasts require IL-1β to produce CXCR2 ligands, and loss of host IL-1R signaling in vivo reduces melanoma growth. In tumors from patients on treatment, signaling from inflammatory niches is amplified in the presence of MAPK inhibitors. Signaling from inflammatory niches counteracts combined BRAF/MEK (MAPK/extracellular signal–regulated kinase kinase) inhibitor treatment, and consequently, inhibiting IL-1R or CXCR2 signaling in vivo enhanced the efficacy of MAPK inhibitors. We conclude that melanoma inflammatory niches adapt to and confer drug tolerance toward BRAF and MEK inhibitors early during treatmen

    Transverse momentum spectra of b jets in pPb collisions at sqrt(s[NN]) = 5.02 TeV

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    We present a measurement of b jet transverse momentum (pt) spectra in proton-lead (pPb) collisions using a dataset corresponding to about 35 inverse nanobarns collected with the CMS detector at the LHC. Jets from b quark fragmentation are found by exploiting the long lifetime of hadrons containing a b quark through tagging methods using distributions of the secondary vertex mass and displacement. Extracted cross sections for b jets are scaled by the effective number of nucleon-nucleon collisions and are compared to a reference obtained from PYTHIA simulations of pp collisions. The PYTHIA-based estimate of the nuclear modification factor is found to be 1.22 +/- 0.15 (stat + syst pPb) +/- 0.27 (syst PYTHIA) averaged over all jets with pt between 55 and 400 GeV/c and with abs(eta[lab]) < 2. We also compare this result to predictions from models using perturbative calculations in quantum chromodynamics

    Gain-of-function human STAT1 mutations impair IL-17 immunity and underlie chronic mucocutaneous candidiasis

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    Chronic mucocutaneous candidiasis disease (CMCD) may be caused by autosomal dominant (AD) IL-17F deficiency or autosomal recessive (AR) IL-17RA deficiency. Here, using whole-exome sequencing, we identified heterozygous germline mutations in STAT1 in 47 patients from 20 kindreds with AD CMCD. Previously described heterozygous STAT1 mutant alleles are loss-of-function and cause AD predisposition to mycobacterial disease caused by impaired STAT1-dependent cellular responses to IFN-γ. Other loss-of-function STAT1 alleles cause AR predisposition to intracellular bacterial and viral diseases, caused by impaired STAT1-dependent responses to IFN-α/β, IFN-γ, IFN-λ, and IL-27. In contrast, the 12 AD CMCD-inducing STAT1 mutant alleles described here are gain-of-function and increase STAT1-dependent cellular responses to these cytokines, and to cytokines that predominantly activate STAT3, such as IL-6 and IL-21. All of these mutations affect the coiled-coil domain and impair the nuclear dephosphorylation of activated STAT1, accounting for their gain-of-function and dominance. Stronger cellular responses to the STAT1-dependent IL-17 inhibitors IFN-α/β, IFN-γ, and IL-27, and stronger STAT1 activation in response to the STAT3-dependent IL-17 inducers IL-6 and IL-21, hinder the development of T cells producing IL-17A, IL-17F, and IL-22. Gain-of-function STAT1 alleles therefore cause AD CMCD by impairing IL-17 immunity

    Measurement of differential cross sections for top quark pair production using the lepton plus jets final state in proton-proton collisions at 13 TeV

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    National Science Foundation (U.S.
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