327 research outputs found

    The e+ e- -> P1 P2 gamma processes close to the Phi peak: toward a model-independent analysis

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    We discuss the general decomposition and possible general parameterizations of the processes e+eγP1P2γe^+ e^- \to \gamma^* \to P_1 P_2 \gamma, where P1P2=π0π0P_1 P_2=\pi^0 \pi^0, π0η\pi^0\eta, or π+π\pi^+\pi^-, for sMΦ\sqrt{s}\approx M_\Phi. Particular attention is devoted to the amplitude where the two pseudoscalar mesons are in a JCP=0++J^{CP}= 0^{++} state, where we propose a general parameterization which should help to shed light on the nature of light scalar mesons.Comment: 12 pages, Late

    Exotic Bound State Production at Hadron Colliders

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    Hadronic production of nonrelativistic boundstates of bb^{\prime} or isosinglet quarks D with suppressed weak decays is investigated for LHC and SSC energies. QCD corrections to production and decay rates are incorporated. Large rates for final states from ηbHZ\eta_{b^{\prime}}\rightarrow HZ are predicted.Comment: 7 pages and 13 figures (figures not includes, can be sent upon request), TTP93-1

    γp\gamma p and γγ\gamma \gamma scattering from pˉp\bar{p}p, pppp forward amplitudes in a QCD eikonal model with a dynamical gluon mass

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    We examine the γp\gamma p photoproduction and the hadronic γγ\gamma \gamma total cross sections by means of a QCD eikonal model with a dynamical infrared mass scale. In this model, where the dynamical gluon mass is the natural regulator for the tree level gluon-gluon scattering, the γp\gamma p and γγ\gamma \gamma total cross sections are derived from the pppp and pˉp\bar{p}p forward scattering amplitudes assuming vector meson dominance and the additive quark model. We show that the validity of the cross section factorization relation σpp/σγp=σγp/σγγ\sigma_{pp}/\sigma_{\gamma p}=\sigma_{\gamma p}/\sigma_{\gamma \gamma} is fulfilled depending on the Monte Carlo model used to unfold the hadronic γγ\gamma \gamma cross section data, and we discuss in detail the case of σ(γγhadrons)\sigma (\gamma \gamma \to hadrons) data with Wγγ>10W_{\gamma \gamma} > 10 GeV unfolded by the Monte Carlo generators PYTHIA and PHOJET. The data seems to favor a mild dependence with the energy of the probability (PhadP_{had}) that the photon interacts as a hadron.Comment: 16 pages, 3 figures; misprints corrected; to appear in Phys. Rev.

    Total photoproduction cross-section at very high energy

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    In this paper we apply to photoproduction total cross-section a model we have proposed for purely hadronic processes and which is based on QCD mini-jets and soft gluon re-summation. We compare the predictions of our model with the HERA data as well as with other models. For cosmic rays, our model predicts substantially higher cross-sections at TeV energies than models based on factorization but lower than models based on mini-jets alone, without soft gluons. We discuss the origin of this difference.Comment: 13 pages, 9 figures. Accepted for publication in EPJC. Changes concern added references, clarifications of the Soft Gluon Resummation method used in the paper, and other changes requested by the Journal referee which do not change the results of the original versio

    Ryanodine receptor 1 (RYR1) mutations in two patients with tubular aggregate myopathy

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    Two likely causative mutations in the RYR1 gene were identified in two patients with myopathy with tubular aggregates, but no evidence of cores or core-like pathology on muscle biopsy. These patients were clinically evaluated and underwent routine laboratory investigations, electrophysiologic tests, muscle biopsy and muscle magnetic resonance imaging (MRI). They reported stiffness of the muscles following sustained activity or cold exposure and had serum creatine kinase elevation. The identified RYR1 mutations (p.Thr2206Met or p.Gly2434Arg, in patient 1 and patient 2, respectively) were previously identified in individuals with malignant hyperthermia susceptibility and are reported as causative according to the European Malignant Hyperthermia Group rules. To our knowledge, these data represent the first identification of causative mutations in the RYR1 gene in patients with tubular aggregate myopathy and extend the spectrum of histological alterations caused by mutation in the RYR1 gene
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