RESUMEN
In this paper we study the critical behavior of the fully connected p-color Potts spin glass at the dynamical transition. In the framework of mode coupling theory (MCT), the time autocorrelation function displays a two-step relaxation, with two exponents governing the approach to the plateau and the exit from it. Exploiting a relation between static and equilibrium dynamics which has been recently introduced, we are able to compute the critical slowing down exponents at the dynamical transition with arbitrary precision and for any value of the number of colors p. When available, we compare our exact results with numerical simulations. In addition, we present a detailed study of the dynamical transition in the large p limit, showing that the system is not equivalent to a random energy model.
RESUMEN
A method is provided to compute the exponent parameter λ yielding the dynamic exponents of critical slowing down in mode coupling theory. It is independent from the dynamic approach and based on the formulation of an effective static field theory. Expressions of λ in terms of third order coefficients of the action expansion or, equivalently, in terms of six point cumulants are provided. Applications are reported to a number of mean-field models: with hard and soft variables and both fully connected and dilute interactions. Comparisons with existing results for the Potts glass model, the random orthogonal model, hard and soft-spin Sherrington-Kirkpatrick, and p-spin models are presented.
RESUMEN
Possible mechanisms involved in inhaled sodium metabisulfite (MBS)-induced bronchoconstriction include cholinergic reflex and release of tachykinins from sensory nerve endings. Tachykinins are potent bronchoconstrictors cleaved and inactivated by neutral endopeptidase (NEP) in the airways. To investigate the role of tachykinins in airway response to MBS, we assessed the effect of NEP-inhibitor thiorphan on airway response to MBS in nine nonatopic, nonasthmatic subjects. Two inhalational challenges with doubling doses of MBS (0.03 to 16 mumol) were performed 3 d apart. Ten minutes before MBS challenge, subjects randomly inhaled either thiorphan (1.25 mg) or placebo according to a double-blind cross-over design. Airflow at 30% of vital capacity (V30p) from partial expiratory flow-volume curves was measured at baseline, 10 min after thiorphan or placebo, and 2 min after each MBS dose. The dose of MBS causing 40% fall in V30p (PD40V30p) was calculated. Neither thiorphan nor placebo affected baseline airway caliber. Thiorphan caused a leftward shift of the dose-response curve to MBS. After placebo a measurable PD40V30p was obtained in four of nine subjects. In these subjects PD40V30p fell significantly after thiorphan inhalation. Four of five subjects who did not exhibit PD40V30p after placebo showed measurable PD40V30p after thiorphan. Percent fall in V30p caused by highest dose of MBS was significantly greater after thiorphan compared with placebo (55.9 +/- 4.6% versus 30.8 +/- 5.6%; mean +/- SE; p < 0.001). Results of this study demonstrate that the NEP-inhibitor thiorphan increases MBS-induced bronchoconstriction in normal subjects, suggesting that tachykinins are involved in airway responses to inhaled MBS.