Open Access

We report on the first steps of an ongoing project to add gauge observables and gauge corrections to the well-studied strong coupling limit of staggered lattice QCD, which has been shown earlier to be amenable to numerical simulations by the worm algorithm in the chiral limit and at finite density. Here we show how to evaluate the expectation value of the Polyakov loop in the framework of the strong coupling limit at finite temperature, allowing to study confinement properties along with those of chiral symmetry breaking. We find the Polyakov loop to rise smoothly, thus signalling deconfinement. The non-analytic nature of the chiral phase transition is reflected in the derivative of the Polyakov loop. We also discuss how to construct an effective theory for non-zero lattice coupling, which is valid to O(b).

It is widely believed that chiral symmetry is spontaneously broken at zero temperature in the strong coupling limit of staggered fermions, for any number of colors and flavors. Using Monte Carlo simulations, we show that this conventional wisdom, based on a mean-field analysis, is wrong. For sufficiently many fundamental flavors, chiral symmetry is restored via a bulk, first-order transition. This chirally symmetric phase appears to be analytically connected with the expected conformal window of manyflavor continuum QCD. We perform simulations in the chirally symmetric phase at zero quark mass for various system sizes L, and measure the torelon mass and the Dirac spectrum. We find that all observables scale with L, which is hence the only infrared length scale. Thus, the strong-coupling chirally restored phase appears as a convenient laboratory to study IR-conformality. Finally, we present a conjecture for the phase diagram of lattice QCD as a function of the bare coupling and the number of quark flavors.

BACKGROUND: In the heart, cytoplasmic actin networks are thought to have important roles in mechanical support, myofibrillogenesis, and ion channel function. However, subcellular localization of cytoplasmic actin isoforms and proteins involved in the modulation of the cytoplasmic actin networks are elusive. Mena and VASP are important regulators of actin dynamics. Due to the lethal phenotype of mice with combined deficiency in Mena and VASP, however, distinct cardiac roles of the proteins remain speculative. In the present study, we analyzed the physiological functions of Mena and VASP in the heart and also investigated the role of the proteins in the organization of cytoplasmic actin networks. RESULTS: We generated a mouse model, which simultaneously lacks Mena and VASP in the heart. Mena/VASP double-deficiency induced dilated cardiomyopathy and conduction abnormalities. In wild-type mice, Mena and VASP specifically interacted with a distinct αII-Spectrin splice variant (SH3i), which is in cardiomyocytes exclusively localized at Z- and intercalated discs. At Z- and intercalated discs, Mena and β-actin localized to the edges of the sarcomeres, where the thin filaments are anchored. In Mena/VASP double-deficient mice, β-actin networks were disrupted and the integrity of Z- and intercalated discs was markedly impaired. CONCLUSIONS: Together, our data suggest that Mena, VASP, and αII-Spectrin assemble cardiac multi-protein complexes, which regulate cytoplasmic actin networks. Conversely, Mena/VASP deficiency results in disrupted β-actin assembly, Z- and intercalated disc malformation, and induces dilated cardiomyopathy and conduction abnormalities.