520,395 research outputs found
Measurement of the ratio of prompt χ c to J / ψ production in pp collisions at √s = 7 TeV
No full textThe prompt production of charmonium χ c and J / ψ states is studied in proton-proton collisions at a centre-of-mass energy of √s = 7 TeV at the Large Hadron Collider. The χ c and J / ψ mesons are identified through their decays χ c → J / ψ γ and J / ψ → μ + μ - using 36 pb - 1 of data collected by the LHCb detector in 2010. The ratio of the prompt production cross-sections for χ c and J / ψ, σ (χ c → J / ψ γ) / σ (J / ψ), is determined as a function of the J / ψ transverse momentum in the range 2 < p T J / ψ < 15 GeV / c. The results are in excellent agreement with next-to-leading order non-relativistic expectations and show a significant discrepancy compared with the colour singlet model prediction at leading order, especially in the low p T J / ψ region
Letter from Carl T. Hayden to C. H. Gensler, Havasupai Reservation
No full textLetter from Carl T. Hayden to C. H. Gensler, Havasupai Indian Reservation, regarding Hualapai and Cataract Canyons geography
Participation of c-FLIP in NLRP3 and AIM2 inflammasome activation
No full textCellular FLICE-inhibitory protein (c-FLIP) is an inhibitor of caspase-8 and is required for macrophage survival. Recent studies have revealed a selective role of caspase-8 in noncanonical IL-1 beta production that is independent of caspase-1 or inflammasome. Here we demonstrated that c-FLIPL is an unexpected contributor to canonical inflammasome activation for the generation of caspase-1 and active IL-1 beta. Hemizygotic deletion of c-FLIP impaired ATP-and monosodium uric acid (MSU)-induced IL-1 beta production in macrophages primed through Toll-like receptors (TLRs). Decreased IL-1 beta expression was attributed to a reduced activation of caspase-1 in c-FLIP hemizygotic cells. In contrast, the production of TNF-alpha was not affected by downregulation in c-FLIP. c-FLIPL interacted with NLRP3 or procaspase-1. c-FLIP is required for the full NLRP3 inflammasome assembly and NLRP3 mitochondrial localization, and c-FLIP is associated with NLRP3 inflammasome. c-FLIP downregulation also reduced AIM2 inflammasome activation. In contrast, c-FLIP inhibited SMAC mimetic-, FasL-, or Dectin-1-induced IL-1 beta generation that is caspase-8-mediated. Our results demonstrate a prominent role of c-FLIPL in the optimal activation of the NLRP3 and AIM2 inflammasomes, and suggest that c-FLIP could be a valid target for treatment of inflammatory diseases caused by over-activation of inflammasomes
Correlation of group C meningococcal conjugate vaccine response with B- and T-lymphocyte activity.
No full textDespite the success of conjugate vaccination against meningococcal group C (MenC) disease, post-vaccination, some individuals still exhibit rapid waning of initially protective bactericidal antibody levels. The mechanism of this relative loss of humoral protection remains undetermined. In this report we have investigated the relationship between T- and B-cell activation and co-stimulation and the loss of protective antibody titers. We have found that healthy volunteers who lose protective MenC antibody levels one year after receipt of glycoconjugate vaccine exhibit no detectable cellular defect in polyclonal B- or T-cell activation, proliferation or the B-memory pool. This suggests that the processes underlying the more rapid loss of antibody levels are independent of defects in either initial T- or B-cell activation
Self-archiving practice and the influence of publisher policies in the social sciences
No full textAuthors in different disciplines exhibit very different behaviours on the so-called ‘green’ road to open access, i.e. self-archiving. This study looks at the self-archiving behaviour of authors publishing in leading journals in six social science disciplines. It tests the hypothesis that authors are self-archiving according to the norms of their respective disciplines rather than following self-archiving policies of publishers, and that, as a result, they are self-archiving significant numbers of publisher PDF versions. It finds significant levels of
self-archiving, as well as significant self-archiving of
the publisher PDF version, in all the disciplines
investigated. Publishers’ self-archiving policies have
no influence on author self-archiving practice
A possible mechanism of superconductivity in high-T-c cuprates
No full textThis paper derives a generic T-c formula by using the long-range phase coherence condition in quantum phase fluctuation of the order parameter. Taking the two-local-spin-mediated interaction (TLSMI) proposed by Liu and Chen [Phys. Rev. B 58 (1998) 8812] as a Cooper pair potential, and the T-c formula, this paper explains five basic experimental facts in high-T-c cuprates. The aim of this paper is to show that TLSMI is a possible pairing mechanism of superconductivity in high-T-c cuprates. (C) 2000 Elsevier Science B.V. All rights reserved.Physics, AppliedSCI(E)EI0ARTICLE4276-28434
Memorandum from A. E. Demaray to E. C. Finney
No full textFour letters of correspondence about the purchase of Bright Angel Trail between A. E. Demaray, Acting Director of the Grand Canyon National Park; E. C. Finney, Department of the Interior First Assistant Secretary; Carl T. Hayden, Representative (AZ); and Stephen T. Mather, Director of the National Park Service
DNA fusion gene vaccination mobilizes effective anti-leukemic cytotoxic T lymphocytes from a tolerized repertoire
No full textThe majority of known human tumor-associated antigens derive from non-mutated self proteins. T cell tolerance, essential to prevent autoimmunity, must therefore be cautiously circumvented to generate cytotoxic T cell responses against these targets. Our strategy uses DNA fusion vaccines to activate high levels of peptide-specific CTL. Key foreign sequences from tetanus toxin activate tolerance-breaking CD4+ T cell help. Candidate MHC class Ibinding tumor peptide sequences are fused to the C terminus for optimal processing and presentation. To model performance against a leukemia-associated antigen in a tolerized setting, we constructed a fusion vaccine encoding an immunodominant CTL epitopederived from Friend murine leukemia virus gag protein (FMuLVgag) and vaccinated tolerant FMuLVgag-transgenic (gag-Tg) mice. Vaccination with the construct induced epitopespecificIFN-c-producing CD8+ T cells in normal and gag-Tg mice. The frequency and avidity of activated cells were reduced in gag-Tg mice, and no autoimmune injury resulted. However, these CD8+ T cells did exhibit gag-specific cytotoxicity in vitro and in vivo. Also, epitope-specific CTL killed FBL-3 leukemia cells expressing endogenous FMuLVgag antigen and protected against leukemia challenge in vivo. These results demonstrate a simple strategy to engage anti-microbial T cell help to activate epitope-specific polyclonal CD8+ T cell responses from a residual tolerized repertoire
Elevated CD4+/CD25+ T cell frequency and function during acute hepatitis C presage chronic evolution.
No full textHepatitis C virus (HCV) determines an acute hepatitis evolving to persistent infection in 50–80% of patients. Different mechanisms have been proposed to explain disease evolution, including viral escape, failure of the T helper immune network, and host genetic factors. Among CD4+ T cell subsets, lymphocytes expressing constitutively CD25 (interleukin 2 receptor alpha chain), namely T regulatory cells (Treg), appear to play a critical role in controlling chronic evolution of HCV mediated liver diseases. Here we investigate the frequency and functional activity of CD3+/CD4+/CD25+ Tregs in acute HCV infection in relation to its evolution over time
Heterogeneous and tissue-specific regulation of effector T cell responses by IFN-gamma during Plasmodium berghei ANKA infection.
No full textIFN-γ and T cells are both required for the development of experimental cerebral malaria during Plasmodium berghei ANKA infection. Surprisingly, however, the role of IFN-γ in shaping the effector CD4(+) and CD8(+) T cell response during this infection has not been examined in detail. To address this, we have compared the effector T cell responses in wild-type and IFN-γ(-/-) mice during P. berghei ANKA infection. The expansion of splenic CD4(+) and CD8(+) T cells during P. berghei ANKA infection was unaffected by the absence of IFN-γ, but the contraction phase of the T cell response was significantly attenuated. Splenic T cell activation and effector function were essentially normal in IFN-γ(-/-) mice; however, the migration to, and accumulation of, effector CD4(+) and CD8(+) T cells in the lung, liver, and brain was altered in IFN-γ(-/-) mice. Interestingly, activation and accumulation of T cells in various nonlymphoid organs was differently affected by lack of IFN-γ, suggesting that IFN-γ influences T cell effector function to varying levels in different anatomical locations. Importantly, control of splenic T cell numbers during P. berghei ANKA infection depended on active IFN-γ-dependent environmental signals--leading to T cell apoptosis--rather than upon intrinsic alterations in T cell programming. To our knowledge, this is the first study to fully investigate the role of IFN-γ in modulating T cell function during P. berghei ANKA infection and reveals that IFN-γ is required for efficient contraction of the pool of activated T cells
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