Lattice QCD with mixed actions

We discuss some of the implications of simulating QCD when the action used for the sea quarks is different from that used for the valence quarks. We present exploratory results for the hadron mass spectrum and pseudoscalar meson decay constants using improved staggered sea quarks and HYP-smeared overlap valence quarks. We propose a method for matching the valence quark mass to the sea quark mass and demonstrate it on UKQCD clover data in the simpler case where the sea and valence actions are the same.Comment: 15 pages, 10 figures some minor modification to text and figures. Accepted for publicatio

The density matrix in the de Broglie-Bohm approach

If the density matrix is treated as an objective description of individual systems, it may become possible to attribute the same objective significance to statistical mechanical properties, such as entropy or temperature, as to properties such as mass or energy. It is shown that the de Broglie-Bohm interpretation of quantum theory can be consistently applied to density matrices as a description of individual systems. The resultant trajectories are examined for the case of the delayed choice interferometer, for which Bell appears to suggest that such an interpretation is not possible. Bell's argument is shown to be based upon a different understanding of the density matrix to that proposed here.Comment: 15 pages, 4 figure

Ginsparg-Wilson Pions Scattering in a Sea of Staggered Quarks

We calculate isospin 2 pion-pion scattering in chiral perturbation theory for a partially quenched, mixed action theory with Ginsparg-Wilson valence quarks and staggered sea quarks. We point out that for some scattering channels, the power-law volume dependence of two pion states in nonunitary theories such as partially quenched or mixed action QCD is identical to that of QCD. Thus one can extract infinite volume scattering parameters from mixed action simulations. We then determine the scattering length for both 2 and 2+1 sea quarks in the isospin limit. The scattering length, when expressed in terms of the pion mass and the decay constant measured on the lattice, has no contributions from mixed valence-sea mesons, thus it does not depend upon the parameter, C_Mix, that appears in the chiral Lagrangian of the mixed theory. In addition, the contributions which nominally arise from operators appearing in the mixed action O(a^2 m_q) Lagrangian exactly cancel when the scattering length is written in this form. This is in contrast to the scattering length expressed in terms of the bare parameters of the chiral Lagrangian, which explicitly exhibits all the sicknesses and lattice spacing dependence allowed by a partially quenched mixed action theory. These results hold for both 2 and 2+1 flavors of sea quarks.Comment: 27 pages, 3 figures. Mistakes corrected in Eqs. (37), (42). Improved discussion in section 4 and related results in Eqs. (33), (37), (40) and (42). Added references. Version to be published in PR

A Simple n-Dimensional Intrinsically Universal Quantum Cellular Automaton

We describe a simple n-dimensional quantum cellular automaton (QCA) capable of simulating all others, in that the initial configuration and the forward evolution of any n-dimensional QCA can be encoded within the initial configuration of the intrinsically universal QCA. Several steps of the intrinsically universal QCA then correspond to one step of the simulated QCA. The simulation preserves the topology in the sense that each cell of the simulated QCA is encoded as a group of adjacent cells in the universal QCA.Comment: 13 pages, 7 figures. In Proceedings of the 4th International Conference on Language and Automata Theory and Applications (LATA 2010), Lecture Notes in Computer Science (LNCS). Journal version: arXiv:0907.382

Light Hadron Masses from Lattice QCD

This article reviews lattice QCD results for the light hadron spectrum. We give an overview of different formulations of lattice QCD, with discussions on the fermion doubling problem and improvement programs. We summarize recent developments in algorithms and analysis techniques, that render calculations with light, dynamical quarks feasible on present day computer resources. Finally, we summarize spectrum results for ground state hadrons and resonances using various actions.Comment: 53 pages, 24 figures, one table; Rev.Mod.Phys. (published version); v2: corrected typ

Quantum decoherence of excitons in a leaky cavity with quasimode

For the excitons in the quantum well placed within a leaky cavity, the quantum decoherence of a mesoscopically superposed states is investigated based on the factorization theory for quantum dissipation. It is found that the coherence of the exciton superposition states will decrease in an oscillating form when the cavity field interacting with the exciton is of the form of quasimode. The effect of the thermal cavity fields on the quantum decoherence of the superposition states of the exciton is studied and it is observed that the higher the temperature of the environment is, the shorter the decoherence characteristic time is.Comment: 1 figure, 7 page

Lorentz Invariance and Origin of Symmetries

In this letter we reconsider the role of Lorentz invariance in the dynamical generation of the observed internal symmetries. We argue that, generally, Lorentz invariance can only be imposed in the sense that all Lorentz non-invariant effects caused by the spontaneous breakdown of Lorentz symmetry are physically unobservable. Remarkably, the application of this principle to the most general relativistically invariant Lagrangian, with arbitrary couplings for all the fields involved, leads by itself to the appearance of a symmetry and, what is more, to the massless vector fields gauging this symmetry in both Abelian and non-Abelian cases. In contrast, purely global symmetries are only generated as accidental consequences of the gauge symmetry.Comment: 10 page LaTeX fil

Ataxia with oculomotor apraxia type 2: clinical, biological and genotype/phenotype correlation study of a cohort of 90 patients

Ataxia with oculomotor apraxia type 2 (AOA2) is an autosomal recessive disease due to mutations in the senataxin gene, causing progressive cerebellar ataxia with peripheral neuropathy, cerebellar atrophy, occasional oculomotor apraxia and elevated alpha-feto-protein (AFP) serum level. We compiled a series of 67 previously reported and 58 novel ataxic patients who underwent senataxin gene sequencing because of suspected AOA2. An AOA2 diagnosis was established for 90 patients, originating from 15 countries worldwide, and 25 new senataxin gene mutations were found. In patients with AOA2, median AFP serum level was 31.0 mu g/l at diagnosis, which was higher than the median AFP level of AOA2 negative patients: 13.8 mu g/l, P = 0.0004; itself higher than the normal level (3.4 mu g/l, range from 0.5 to 17.2 mu g/l) because elevated AFP was one of the possible selection criteria. Polyneuropathy was found in 97.5% of AOA2 patients, cerebellar atrophy in 96%, occasional oculomotor apraxia in 51%, pyramidal signs in 20.5%, head tremor in 14%, dystonia in 13.5%, strabismus in 12.3% and chorea in 9.5%. No patient was lacking both peripheral neuropathy and cerebellar atrophy. The age at onset and presence of occasional oculomotor apraxia were negatively correlated to the progression rate of the disease (P = 0.03 and P = 0.009, respectively), whereas strabismus was positively correlated to the progression rate (P = 0.03). An increased AFP level as well as cerebellar atrophy seem to be stable in the course of the disease and to occur mostly at or before the onset of the disease. One of the two patients with a normal AFP level at diagnosis had high AFP levels 4 years later, while the other had borderline levels. The probability of missing AOA2 diagnosis, in case of sequencing senataxin gene only in non-Friedreich ataxia non-ataxia-telangiectasia ataxic patients with AFP level >= 7 mu g/l, is 0.23% and the probability for a non-Friedreich ataxia non-ataxia-telangiectasia ataxic patient to be affected with AOA2 with AFP levels >= 7 mu g/l is 46%. Therefore, selection of patients with an AFP level above 7 mu g/l for senataxin gene sequencing is a good strategy for AOA2 diagnosis. Pyramidal signs and dystonia were more frequent and disease was less severe with missense mutations in the helicase domain of senataxin gene than with missense mutations out of helicase domain and deletion and nonsense mutations (P = 0.001, P = 0.008 and P = 0.01, respectively). The lack of pyramidal signs in most patients may be explained by masking due to severe motor neuropathy

Spectra of heavy-light and heavy-heavy mesons containing charm quarks, including higher spin states for Nf=2+1N_f=2+ 1

We study the spectra of heavy-light and heavy-heavy mesons containing charm quarks, including higher spin states. We use two sets of $N_f = 2 + 1$ gauge configurations, one set from QCDSF using the SLiNC action, and the other configurations from the Budapest-Marseille-Wuppertal collaboration, using the HEX smeared clover action. To extract information about the excited states, we choose a suitable basis of operators to implement the variational method.Comment: 7 pages, 5 figures, Talk presented at the XXIX International Symposium on Lattice Field Theory, Lattice2011, July 11-16, 2011, The Village at Squaw Valley, California, US

Mutations in SPG11, encoding spatacsin, are a major cause of spastic paraplegia with thin corpus callosum.

Autosomal recessive hereditary spastic paraplegia (ARHSP) with thin corpus callosum (TCC) is a common and clinically distinct form of familial spastic paraplegia that is linked to the SPG11 locus on chromosome 15 in most affected families. We analyzed 12 ARHSP-TCC families, refined the SPG11 candidate interval and identified ten mutations in a previously unidentified gene expressed ubiquitously in the nervous system but most prominently in the cerebellum, cerebral cortex, hippocampus and pineal gland. The mutations were either nonsense or insertions and deletions leading to a frameshift, suggesting a loss-of-function mechanism. The identification of the function of the gene will provide insight into the mechanisms leading to the degeneration of the corticospinal tract and other brain structures in this frequent form of ARHSP