23 research outputs found

    Functional Integral Construction of the Thirring model: axioms verification and massless limit

    Get PDF
    We construct a QFT for the Thirring model for any value of the mass in a functional integral approach, by proving that a set of Grassmann integrals converges, as the cutoffs are removed and for a proper choice of the bare parameters, to a set of Schwinger functions verifying the Osterwalder-Schrader axioms. The corresponding Ward Identities have anomalies which are not linear in the coupling and which violate the anomaly non-renormalization property. Additional anomalies are present in the closed equation for the interacting propagator, obtained by combining a Schwinger-Dyson equation with Ward Identities.Comment: 55 pages, 9 figure

    Fermions in three-dimensional spinfoam quantum gravity

    Get PDF
    We study the coupling of massive fermions to the quantum mechanical dynamics of spacetime emerging from the spinfoam approach in three dimensions. We first recall the classical theory before constructing a spinfoam model of quantum gravity coupled to spinors. The technique used is based on a finite expansion in inverse fermion masses leading to the computation of the vacuum to vacuum transition amplitude of the theory. The path integral is derived as a sum over closed fermionic loops wrapping around the spinfoam. The effects of quantum torsion are realised as a modification of the intertwining operators assigned to the edges of the two-complex, in accordance with loop quantum gravity. The creation of non-trivial curvature is modelled by a modification of the pure gravity vertex amplitudes. The appendix contains a review of the geometrical and algebraic structures underlying the classical coupling of fermions to three dimensional gravity.Comment: 40 pages, 3 figures, version accepted for publication in GER

    Measurement of cross sections and leptonic forward-backward asymmetries at the Z pole and determination of electroweak parameters

    Get PDF
    We report on the measurement of the leptonic and hadronic cross sections and leptonic forward-backward asymmetries at the Z peak with the L3 detector at LEP. The total luminosity of 40.8 pb −1 collected in the years 1990, 1991 and 1992 corresponds to 1.09·10 6 hadronic and 0.98·10 5 leptonic Z decays observed. These data allow us to determine the electroweak parameters. From the cross sections we derive the properties of the Z boson: assuming lepton universality. We obtain an invisible width of Γ inv =496.5±7.9 MeV which, in the Standard Model, corresponds to a number of light neutrino species of N v =2.981±0.050.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47894/1/10052_2005_Article_BF01574160.pd

    Identification of a gene (lpt-3) required for the addition of phosphoethanolamine to the lipopolysaccharide inner core of Neisseria meningitidis and its role in mediating susceptibility to bactericidal killing and opsonophagocytosis.

    No full text
    We have identified a gene, lpt-3, that is required for the addition of phosphoethanolamine to the 3-position (PEtn-3) on the beta-chain heptose (HepII) of the inner core lipopolysaccharide (LPS) of Neisseria meningitidis (Nm). The presence of this PEtn-3 substituent is characteristic of the LPS of a majority ( approximately 70%) of hypervirulent Nm strains, irrespective of capsular serogroup, and is required for the binding of a previously described monoclonal antibody (mAb B5) to a surface-accessible epitope. All strains of Nm that have PEtn-3 possess the lpt-3 gene. In some lpt-3-containing strains, the 3-position on HepII is preferentially substituted by glucose instead of PEtn, the result of lgtG phase variation mediated by slippage of a homopolymeric tract of cytidines. Inactivation of lpt-3 resulted in loss of PEtn-3, lack of reactivity with mAb B5 and conferred relative resistance to bactericidal killing and opsonophagocytosis by mAb B5 in vitro. Thus, the identification of lpt-3 has facilitated rigorous genetic, structural and immunobiological definition of an immunodominant epitope that is a candidate immunogen for inclusion in an LPS-based vaccine to protect against invasive meningococcal disease

    Assessment of Predictive Genomic Biomarkers for Response to Cisplatin-based Neoadjuvant Chemotherapy in Bladder Cancer

    No full text
    Cisplatin-based neoadjuvant chemotherapy (NAC) followed by radical cystectomy is recommended for patients with muscle-invasive bladder cancer (MIBC). It has been shown that somatic deleterious mutations in ERCC2, gain-of-function mutations in ERBB2, and alterations in ATM, RB1, and FANCC are correlated with pathological response to NAC in MIBC. The objective of this study was to validate these genomic biomarkers in pretreatment transurethral resection material from an independent retrospective cohort of 165 patients with MIBC who subsequently underwent NAC and radical surgery. Patients with ypT0/Tis/Ta/T1N0 disease after surgery were defined as responders. Somatic deleterious mutations in ERCC2 were found in nine of 68 (13%) evaluable responders and two of 95 (2%) evaluable nonresponders (p = 0.009; FDR = 0.03). No correlation was observed between response and alterations in ERBB2 or in ATM, RB1, or FANCC alone or in combination. In an exploratory analysis, no additional genomic alterations discriminated between responders and nonresponders to NAC. No further associations were identified between the aforementioned biomarkers and pathological complete response (ypT0N0) after surgery. In conclusion, we observed a positive association between deleterious mutations in ERCC2 and pathological response to NAC, but not overall survival or recurrence-free survival. Other previously reported genomic biomarkers were not validated. Patient summary: It is currently unknown which patients will respond to chemotherapy before definitive surgery for bladder cancer. Previous studies described several gene mutations in bladder cancer that correlated with chemotherapy response. This study confirmed that patients with bladder cancer with a mutation in the ERCC2 gene often respond to chemotherapy
    corecore