Smooth Random Surfaces from Tight Immersions?

We investigate actions for dynamically triangulated random surfaces that consist of a gaussian or area term plus the {\it modulus} of the gaussian curvature and compare their behavior with both gaussian plus extrinsic curvature and ``Steiner'' actions.Comment: 7 page

Cluster variation - Pade` approximants method for the simple cubic Ising model

The cluster variation - Pade` approximant method is a recently proposed tool, based on the extrapolation of low/high temperature results obtained with the cluster variation method, for the determination of critical parameters in Ising-like models. Here the method is applied to the three-dimensional simple cubic Ising model, and new results, obtained with an 18-site basic cluster, are reported. Other techniques for extracting non-classical critical exponents are also applied and their results compared with those by the cluster variation - Pade` approximant method.Comment: 8 RevTeX pages, 3 PostScript figure

Reciprocal regulation of PKA and rac signaling

Activated G protein-coupled receptors (GPCRs) and receptor tyrosine kinases relay extracellular signals through spatial and temporal controlled kinase and GTPase entities. These enzymes are coordinated by multifunctional scaffolding proteins for precise intracellular signal processing. The cAMP-dependent protein kinase A (PKA) is the prime example for compartmentalized signal transmission downstream of distinct GPCRs. A-kinase anchoring proteins tether PKA to specific intracellular sites to ensure precision and directionality of PKA phosphorylation events. Here, we show that the Rho-GTPase Rac contains A-kinase anchoring protein properties and forms a dynamic cellular protein complex with PKA. The formation of this transient core complex depends on binary interactions with PKA subunits, cAMP levels and cellular GTP-loading accounting for bidirectional consequences on PKA and Rac downstream signaling. We show that GTP-Rac stabilizes the inactive PKA holoenzyme. However, β-adrenergic receptor-mediated activation of GTP-Rac–bound PKA routes signals to the Raf-Mek-Erk cascade, which is critically implicated in cell proliferation. We describe a further mechanism of how cAMP enhances nuclear Erk1/2 signaling: It emanates from transphosphorylation of p21-activated kinases in their evolutionary conserved kinase-activation loop through GTP-Rac compartmentalized PKA activities. Sole transphosphorylation of p21-activated kinases is not sufficient to activate Erk1/2. It requires complex formation of both kinases with GTP-Rac1 to unleash cAMP-PKA–boosted activation of Raf-Mek-Erk. Consequently GTP-Rac functions as a dual kinase-tuning scaffold that favors the PKA holoenzyme and contributes to potentiate Erk1/2 signaling. Our findings offer additional mechanistic insights how β-adrenergic receptor-controlled PKA activities enhance GTP-Rac–mediated activation of nuclear Erk1/2 signaling

Compartmentalized PDE4A5 signaling impairs hippocampal synaptic plasticity and long-term memory

Alterations in cAMP signaling are thought to contribute to neurocognitive and neuropsychiatric disorders. Members of the cAMP-specific phosphodiesterase 4 (PDE4) family, which contains >25 different isoforms, play a key role in determining spatial cAMP degradation so as to orchestrate compartmentalized cAMP signaling in cells. Each isoform binds to a different set of protein complexes through its unique N-terminal domain, thereby leading to targeted degradation of cAMP in specific intracellular compartments. However, the functional role of specific compartmentalized PDE4 isoforms has not been examined in vivo. Here, we show that increasing protein levels of the PDE4A5 isoform in mouse hippocampal excitatory neurons impairs a long-lasting form of hippocampal synaptic plasticity and attenuates hippocampus-dependent long-term memories without affecting anxiety. In contrast, viral expression of a truncated version of PDE4A5, which lacks the unique N-terminal targeting domain, does not affect long-term memory. Further, overexpression of the PDE4A1 isoform, which targets a different subset of signalosomes, leaves memory undisturbed. Fluorescence resonance energy transfer sensor-based cAMP measurements reveal that the full-length PDE4A5, in contrast to the truncated form, hampers forskolin-mediated increases in neuronal cAMP levels. Our study indicates that the unique N-terminal localization domain of PDE4A5 is essential for the targeting of specific cAMP-dependent signaling underlying synaptic plasticity and memory. The development of compounds to disrupt the compartmentalization of individual PDE4 isoforms by targeting their unique N-terminal domains may provide a fruitful approach to prevent cognitive deficits in neuropsychiatric and neurocognitive disorders that are associated with alterations in cAMP signaling

A study of the etapipi channel produced in central pp interactions at 450 GeV/c

The reaction pp -> pf (eta pi pi) ps has been studied at 450 GeV/c. There is clear evidence for an a2(1320)pi decay mode of the eta2(1645) and eta2(1870). In addition, there is evidence for an a0(980)pi$ decay mode of both resonances and an f2(1270)eta decay mode of the eta2(1870). No evidence is found for a JPC = 2++ a2(1320)pi wave.Comment: 15 pages, Latex, 4 Figures Branching ratio a2pi /f2 eta correcte

A Potts/Ising Correspondence on Thin Graphs

We note that it is possible to construct a bond vertex model that displays q-state Potts criticality on an ensemble of phi3 random graphs of arbitrary topology, which we denote as ``thin'' random graphs in contrast to the fat graphs of the planar diagram expansion. Since the four vertex model in question also serves to describe the critical behaviour of the Ising model in field, the formulation reveals an isomorphism between the Potts and Ising models on thin random graphs. On planar graphs a similar correspondence is present only for q=1, the value associated with percolation.Comment: 6 pages, 5 figure

Dynamic Critical Behavior of the Swendsen-Wang Algorithm: The Two-Dimensional 3-State Potts Model Revisited

We have performed a high-precision Monte Carlo study of the dynamic critical behavior of the Swendsen-Wang algorithm for the two-dimensional 3-state Potts model. We find that the Li-Sokal bound ($\tau_{int,E} \geq const \times C_H$) is almost but not quite sharp. The ratio $\tau_{int,E} / C_H$ seems to diverge either as a small power ($\approx 0.08$) or as a logarithm.Comment: 35 pages including 3 figures. Self-unpacking file containing the LaTeX file, the needed macros (epsf.sty, indent.sty, subeqnarray.sty, and eqsection.sty) and the 3 Postscript figures. Revised version fixes a normalization error in \xi (with many thanks to Wolfhard Janke for finding the error!). To be published in J. Stat. Phys. 87, no. 1/2 (April 1997