Lattice QCD as a video game

The speed, bandwidth and cost characteristics of today's PC graphics cards make them an attractive target as general purpose computational platforms. High performance can be achieved also for lattice simulations but the actual implementation can be cumbersome. This paper outlines the architecture and programming model of modern graphics cards for the lattice practitioner with the goal of exploiting these chips for Monte Carlo simulations. Sample code is also given. (c) 2007 Elsevier B.V. All rights reserved

The QCD equation of state at finite T and mu

We calculate the pressure (p), the energy density (epsilon) and the baryon density (n(B)) of QCD at finite temperatures (T) and chemical potentials (mu). The recently proposed overlap improving multi-parameter reweighting technique is used to determine observables at nonvanishing chemical potentials. Our results are obtained by studying n(f) =2+1 dynamical staggered quarks with semi-realistic masses on N-t = 4 lattices

The QCD phase diagram for external magnetic fields

The effect of an external (electro)magnetic field on the finite temperature transition of QCD is studied. We generate configurations at various values of the quantized magnetic flux with $N_f=2+1$ flavors of stout smeared staggered quarks, with physical masses. Thermodynamic observables including the chiral condensate and susceptibility, and the strange quark number susceptibility are measured as functions of the field strength. We perform the renormalization of the studied observables and extrapolate the results to the continuum limit using $N_t=6,8$ and 10 lattices. We also check for finite volume effects using various lattice volumes. We find from all of our observables that the transition temperature $T_c$ significantly decreases with increasing magnetic field. This is in conflict with various model calculations that predict an increasing $T_c(B)$. From a finite volume scaling analysis we find that the analytic crossover that is present at B=0 persists up to our largest magnetic fields $eB \approx 1 \textmd{GeV}^2$, and that the transition strength increases mildly up to this $eB\approx1 \textmd{GeV}^2$.Comment: 22 pages, 13 figure

SU(2) chiral perturbation theory low-energy constants from staggered 2+1 flavor simulations

We extract the NLO low-energy constants \bar\ell_3 and \bar\ell_4 of SU(2) chiral perturbation theory, based on precise lattice data for the pion mass and decay constant on ensembles generated by the Wuppertal-Budapest collaboration for QCD thermodynamics. These ensembles feature 2+1 flavors of 2-fold stout-smeared dynamical staggered fermions combined with Symanzik glue, with pion masses varying from 135 MeV to 435 MeV, lattice scales between 0.7 GeV and 2.0 GeV, while m_s is kept fixed at its physical value. Moderate taste splittings and the scale being set through the pion decay constant allow us to restrict ourselves to the taste pseudoscalar state and to use formulae from continuum ChPT. Finally, by dropping the data points near 135 MeV from the fits, we can explore the range of pion masses that is needed in SU(2) ChPT to reliably extrapolate to the physical point

Lattice QCD at the physical point: light quark masses

Ordinary matter is described by six fundamental parameters: three couplings (gravitational, electromagnetic and strong) and three masses: the electron's (m_e) and those of the up (m_u) and down (m_d) quarks. An additional mass enters through quantum fluctuations: the strange quark mass (m_s). The three couplings and m_e are known with an accuracy of better than a few per mil. Despite their importance, $m_u$, $m_d$ (their average m_{ud}) and m_s are relatively poorly known: e.g. the Particle Data Group quotes them with conservative errors close to 25%. Here we determine these quantities with a precision below 2% by performing ab initio lattice quantum chromodynamics (QCD) calculations, in which all systematics are controlled. We use pion and quark masses down to (and even below) their physical values, lattice sizes of up to 6 fm, and five lattice spacings to extrapolate to continuum spacetime. All necessary renormalizations are performed nonperturbatively.Comment: 9 pages, 2 figures, 1 table. v2: published version, one reference adde

Rho decay width from the lattice

The XXVIII International Symposium on Lattice Field Theory, June 14-19, 2010, Villasimius, Sardinia ItalyInternational audienceWhile the masses of light hadrons have been extensively studied in lattice QCD simulations, there exist only a few exploratory calculations of the strong decay widths of hadronic resonances. We will present preliminary results of a computation of the rho meson width obtained using $N_f=2+1$ flavor simulations. The work is based on L\"uscher's formalism and its extension to moving frames

Identification of a novel truncating PALB2 mutation and analysis of its contribution to early-onset breast cancer in French-Canadian women

Abstract Background PALB2 has recently been identified as a breast cancer susceptibility gene. PALB2 mutations are rare causes of hereditary breast cancer but may be important in countries such as Finland where a founder mutation is present. We sought to estimate the contribution of PALB2 mutations to the burden of breast cancer in French Canadians from Quebec. Methods We screened all coding exons of PALB2 in a sample of 50 French-Canadian women diagnosed with either early-onset breast cancer or familial breast cancer at a single Montreal hospital. The genetic variants identified in this sample were then studied in 356 additional women with breast cancer diagnosed before age 50 and in 6,448 newborn controls. Results We identified a single protein-truncating mutation in PALB2 (c.2323 C>T, resulting in Q775X) in 1 of the 50 high-risk women. This variant was present in 2 of 356 breast cancer cases and in none of 6,440 newborn French-Canadian controls (P = 0.003). We also identified two novel new non-synonymous single nucleotide polymorphisms in exon 4 of PALB2 (c.5038 A>G [I76V] and c.5156 G>T [G115V]). G115V was found in 1 of 356 cases and in 15 of 6,442 controls (P = 0.6). The I76V variant was not identified in either the extended case series or the controls. Conclusion We have identified a novel truncating mutation in PALB2. The mutation was found in approximately 0.5% of unselected French-Canadian women with early-onset breast cancer and appears to have a single origin. Although mutations are infrequent, PALB2 can be added to the list of breast cancer susceptibility genes for which founder mutations have been identified in the French-Canadian population

Molecular and cellular mechanisms underlying the evolution of form and function in the amniote jaw.

The amniote jaw complex is a remarkable amalgamation of derivatives from distinct embryonic cell lineages. During development, the cells in these lineages experience concerted movements, migrations, and signaling interactions that take them from their initial origins to their final destinations and imbue their derivatives with aspects of form including their axial orientation, anatomical identity, size, and shape. Perturbations along the way can produce defects and disease, but also generate the variation necessary for jaw evolution and adaptation. We focus on molecular and cellular mechanisms that regulate form in the amniote jaw complex, and that enable structural and functional integration. Special emphasis is placed on the role of cranial neural crest mesenchyme (NCM) during the species-specific patterning of bone, cartilage, tendon, muscle, and other jaw tissues. We also address the effects of biomechanical forces during jaw development and discuss ways in which certain molecular and cellular responses add adaptive and evolutionary plasticity to jaw morphology. Overall, we highlight how variation in molecular and cellular programs can promote the phenomenal diversity and functional morphology achieved during amniote jaw evolution or lead to the range of jaw defects and disease that affect the human condition

Tryptophan and Non-Tryptophan Fluorescence of the Eye Lens Proteins Provides Diagnostics of Cataract at the Molecular Level

The chemical nature of the non-tryptophan (non-Trp) fluorescence of porcine and human eye lens proteins was identified by Mass Spectrometry (MS) and Fluorescence Steady-State and Lifetime spectroscopy as post-translational modifications (PTM) of Trp and Arg amino acid residues. Fluorescence intensity profiles measured along the optical axis of human eye lenses with age-related nuclear cataract showed increasing concentration of fluorescent PTM towards the lens centre in accord with the increased optical density in the lens nucleolus. Significant differences between fluorescence lifetimes of “free” Trp derivatives hydroxytryptophan (OH-Trp), N-formylkynurenine (NFK), kynurenine (Kyn), hydroxykynurenine (OH-Kyn) and their residues were observed. Notably, the lifetime constants of these residues in a model peptide were considerably greater than those of their “free” counterparts. Fluorescence of Trp, its derivatives and argpyrimidine (ArgP) can be excited at the red edge of the Trp absorption band which allows normalisation of the emission spectra of these PTMs to the fluorescence intensity of Trp, to determine semi-quantitatively their concentration. We show that the cumulative fraction of OH-Trp, NFK and ArgP emission dominates the total fluorescence spectrum in both emulsified post-surgical human cataract protein samples, as well as in whole lenses and that this correlates strongly with cataract grade and age

Regulation of Anthrax Toxin-Specific Antibody Titers by Natural Killer T Cell-Derived IL-4 and IFNγ

Activation of Natural Killer-like T cells (NKT) with the CD1d ligand α-GC leads to enhanced production of anthrax toxin protective Ag (PA)-neutralizing Abs, yet the underlying mechanism for this adjuvant effect is not known. In the current study we examined the role of Th1 and Th2 type responses in NKT-mediated enhancement of antibody responses to PA. First, the contribution of IL-4 and IFNγ to the production of PA-specific toxin-neutralizing Abs was examined. By immunizing C57Bl/6 controls IL-4−/− mice and IFNγ−/− mice and performing passive serum transfer experiments, it was observed that sera containing PA-specific IgG1, IgG2b and IgG2c neutralized toxin in vitro and conferred protection in vivo. Sera containing IgG2b and IgG2c neutralized toxin in vitro but were not sufficient for protection in vivo. Sera containing IgG1 and IgG2b neutralized toxin in vitro and conferred protection in vivo. IgG1 therefore emerged as a good correlate of protection. Next, C57Bl/6 mice were immunized with PA alone or PA plus a Th2-skewing α-GC derivative known as OCH. Neutralizing PA-specific IgG1 responses were modestly enhanced by OCH in C57Bl/6 mice. Conversely, IgG2b and IgG2c were considerably enhanced in PA/OCH-immunized IL-4−/− mice but did not confer protection. Finally, bone marrow chimeras were generated such that NKT cells were unable to express IL-4 or IFNγ. NKT-derived IL-4 was required for OCH-enhanced primary IgG1 responses but not recall responses. NKT-derived IL-4 and IFNγ also influenced primary and recall IgG2b and IgG2c titers. These data suggest targeted skewing of the Th2 response by α-GC derivatives can be exploited to optimize anthrax vaccination