On the existence of a finite-temperature transition in the two-dimensional gauge glass

Results from Monte Carlo simulations of the two-dimensional gauge glass supporting a zero-temperature transition are presented. A finite-size scaling analysis of the correlation length shows that the system does not exhibit spin-glass order at finite temperatures. These results are compared to earlier claims of a finite-temperature transition.Comment: 4 pages, 2 figure

Edge effects in a frustrated Josephson junction array with modulated couplings

A square array of Josephson junctions with modulated strength in a magnetic field with half a flux quantum per plaquette is studied by analytic arguments and dynamical simulations. The modulation is such that alternate columns of junctions are of different strength to the rest. Previous work has shown that this system undergoes an XY followed by an Ising-like vortex lattice disordering transition at a lower temperature. We argue that resistance measurements are a possible probe of the vortex lattice disordering transition as the linear resistance $R_{L}(T)\sim A(T)/L$ with $A(T) \propto (T-T_{cI})$ at intermediate temperatures $T_{cXY}>T>T_{cI}$ due to dissipation at the array edges for a particular geometry and vanishes for other geometries. Extensive dynamical simulations are performed which support the qualitative physical arguments.Comment: 8 pages with figs, RevTeX, to appear in Phys. Rev.

Anomalous dimensions and phase transitions in superconductors

The anomalous scaling in the Ginzburg-Landau model for the superconducting phase transition is studied. It is argued that the negative sign of the $\eta$ exponent is a consequence of a special singular behavior in momentum space. The negative sign of $\eta$ comes from the divergence of the critical correlation function at finite distances. This behavior implies the existence of a Lifshitz point in the phase diagram. The anomalous scaling of the vector potential is also discussed. It is shown that the anomalous dimension of the vector potential $\eta_A=4-d$ has important consequences for the critical dynamics in superconductors. The frequency-dependent conductivity is shown to obey the scaling $\sigma(\omega)\sim\xi^{z-2}$. The prediction $z\approx 3.7$ is obtained from existing Monte Carlo data.Comment: RevTex, 20 pages, no figures; small changes; version accepted in PR

Coherent Compton scattering on light nuclei in the delta resonance region

Coherent Compton scattering on light nuclei in the delta resonance region is studied in the impulse approximation and is shown to be a sensitive probe of the in-medium properties of the delta resonance. The elementary amplitude on a single nucleon is calculated from the unitary K-matrix approach developed previously. Modifications of the properties of the delta resonance due to the nuclear medium are accounted for through the self-energy operator of the delta, calculated from the one-pion loop. The dominant medium effects such as the Pauli blocking, mean-field modification of the nucleon and delta masses, and particle-hole excitations in the pion propagator are consistently included in nuclear matter.Comment: 30 pages, 11 figures, accepted for publication in Phys. Rev.

Differential regulation of β2-adrenoceptor and adenosine A2B receptor signalling by GRK and arrestin proteins in arterial smooth muscle

Generation of cAMP through Gs-coupled G protein-coupled receptor (GPCR) [e.g. β2-adrenoceptor (β2AR), adenosine A2B receptor (A2BR)] activation, induces arterial smooth muscle relaxation, counteracting the actions of vasoconstrictors. Gs-coupled GPCR signalling is regulated by G protein-coupled receptor kinases (GRK) and arrestin proteins, and dysregulation of Gs/GPCR signalling is thought play a role in the development of hypertension, which may be a consequence of enhanced GRK2 and/or arrestin expression. However, despite numerous studies indicating that β2AR and A2BR can be substrates for GRK/arrestin proteins, currently little is known regarding GRK/arrestin regulation of these endogenous receptors in arterial smooth muscle. Here, endogenous GRK isoenzymes and arrestin proteins were selectively depleted using RNA-interference in rat arterial smooth muscle cells (RASM) and the consequences of this for β2AR- and A2BR-mediated adenylyl cyclase (AC) signalling were determined by assessing cAMP accumulation. GRK2 or GRK5 depletion enhanced and prolonged β2AR/AC signalling, while combined deletion of GRK2/5 has an additive effect. Conversely, activation of AC by A2BR was regulated by GRK5, but not GRK2. β2AR desensitization was attenuated following combined GRK2/GRK5 knockdown, but not by depletion of individual GRKs, arrestins, or by inhibiting PKA. Arrestin3 (but not arrestin2) depletion enhanced A2BR-AC signalling and attenuated A2BR desensitization, while β2AR-AC signalling was regulated by both arrestin isoforms. This study provides a first demonstration of how different complements of GRK and arrestin proteins contribute to the regulation of signalling and desensitization of these important receptors mediating vasodilator responses in arterial smooth muscle