Non-perturbative volume-reduction of large-N QCD with adjoint fermions

We use nonperturbative lattice techniques to study the volume-reduced "Eguchi-Kawai" version of four-dimensional large-N QCD with a single adjoint Dirac fermion. We explore the phase diagram of this single-site theory in the space of quark mass and gauge coupling using Wilson fermions for a number of colors in the range 8 <= N <= 15. Our evidence suggests that these values of N are large enough to determine the nature of the phase diagram for N-->oo. We identify the region in the parameter space where the (Z_N)^4 center-symmetry is intact. According to previous theoretical work using the orbifolding paradigm, and assuming that translation invariance is not spontaneously broken in the infinite-volume theory, in this region volume reduction holds: the single-site and infinite-volume theories become equivalent when N-->oo. We find strong evidence that this region includes both light and heavy quarks (with masses that are at the cutoff scale), and our results are consistent with this region extending towards the continuum limit. We also compare the action density and the eigenvalue density of the overlap Dirac operator in the fundamental representation with those obtained in large-N pure-gauge theory.Comment: 49 pages, 23 figures. v2: Clarified connection of ZN symmetry realization and the validity of reduction in the abstract, quantified what we mean by "heavy quarks" in abstract, updated discussion on Refs [12,14,15], added a discussion on the kappa dependence of the physical mass, extended discussion on what might happen in the continuum and at N=oo, updated ref'

In search of a Hagedorn transition in SU(N) lattice gauge theories at large-N

We investigate on the lattice the metastable confined phase above Tc in SU(N) gauge theories, for N=8,10, and 12. In particular we focus on the decrease with the temperature of the mass of the lightest state that couples to Polyakov loops. We find that at T=Tc the corresponding effective string tension \sigma_{eff}(T) is approximately half its value at T=0, and that as we increase T beyond Tc, while remaining in the confined phase, \sigma_{eff}(T) continues to decrease. We extrapolate \sigma_{eff}(T) to even higher temperatures, and interpret the temperature where it vanishes as the Hagedorn temperature T_H. For SU(12) we find that T_H/Tc=1.116(9), when we use the exponent of the three-dimensional XY model for the extrapolation, which seems to be slightly preferred over a mean-field exponent by our data.Comment: 20 pages, 12 figures. New version includes: a more extensive error analysis, a discussion on the behavior of masses near T_H, and additional acknowledgements and references. Results and conclusions do not chang

Spatially resolved electrochemistry in ionic liquids : surface structure effects on triiodide reduction at platinum electrodes

Understanding the relationship between electrochemical activity and electrode structure is vital for improving the efficiency of dye-sensitized solar cells. Here, the reduction of triiodide to iodide in 1-butyl-3-methylimidazolium tetrafluoroborate ([BMIm][BF4]) room temperature ionic liquid (RTIL) is investigated on polycrystalline platinum using scanning electrochemical cell microscopy (SECCM) and correlated to the crystallographic orientation from electron backscatter diffraction (EBSD). Although the rate determining step in all grains was the first electron transfer, significant grain-dependent variations in activity were revealed, with grains with a dominant (110) crystallographic character exhibiting higher catalytic activity compared to those with a major (100) orientation. The SECCM technique is demonstrated to resolve heterogeneity in activity, highlighting that methods incorporating polycrystalline electrodes miss vital details for understanding and optimizing electrocatalysts. An additional advantage of the SECCM over single-crystal techniques is its ability to probe high index facets

Breakdown of large-N quenched reduction in SU(N) lattice gauge theories

We study the validity of the large-N equivalence between four-dimensional SU(N) lattice gauge theory and its momentum quenched version--the Quenched Eguchi-Kawai (QEK) model. We find that the assumptions needed for the proofs of equivalence do not automatically follow from the quenching prescription. We use weak-coupling arguments to show that large-N equivalence is in fact likely to break down in the QEK model, and that this is due to dynamically generated correlations between different Euclidean components of the gauge fields. We then use Monte-Carlo simulations at intermediate couplings with 20 <= N <= 200 to provide strong evidence for the presence of these correlations and for the consequent breakdown of reduction. This evidence includes a large discrepancy between the transition coupling of the "bulk" transition in lattice gauge theories and the coupling at which the QEK model goes through a strongly first-order transition. To accurately measure this discrepancy we adapt the recently introduced Wang-Landau algorithm to gauge theories.Comment: 51 pages, 16 figures, Published verion. Historical inaccuracies in the review of the quenched Eguchi-Kawai model are corrected, discussion on reduction at strong-coupling added, references updated, typos corrected. No changes to results or conclusion

ER Stress-Induced eIF2-alpha Phosphorylation Underlies Sensitivity of Striatal Neurons to Pathogenic Huntingtin

A hallmark of Huntington's disease is the pronounced sensitivity of striatal neurons to polyglutamine-expanded huntingtin expression. Here we show that cultured striatal cells and murine brain striatum have remarkably low levels of phosphorylation of translation initiation factor eIF2 alpha, a stress-induced process that interferes with general protein synthesis and also induces differential translation of pro-apoptotic factors. EIF2 alpha phosphorylation was elevated in a striatal cell line stably expressing pathogenic huntingtin, as well as in brain sections of Huntington's disease model mice. Pathogenic huntingtin caused endoplasmic reticulum (ER) stress and increased eIF2 alpha phosphorylation by increasing the activity of PKR-like ER-localized eIF2 alpha kinase (PERK). Importantly, striatal neurons exhibited special sensitivity to ER stress-inducing agents, which was potentiated by pathogenic huntingtin. We could strongly reduce huntingtin toxicity by inhibiting PERK. Therefore, alteration of protein homeostasis and eIF2 alpha phosphorylation status by pathogenic huntingtin appears to be an important cause of striatal cell death. A dephosphorylated state of eIF2 alpha has been linked to cognition, which suggests that the effect of pathogenic huntingtin might also be a source of the early cognitive impairment seen in patients