B -> D* l nu and B -> D l nu form factors in staggered chiral perturbation theory

We calculate the B -> D and B -> D* form factors at zero recoil in Staggered Chiral Perturbation Theory. We consider heavy-light mesons in which only the light (u, d, or s) quark is staggered; current lattice simulations generally use a highly improved action such as the Fermilab or NRQCD action for the heavy (b or c) quark. We work to lowest nontrivial order in the heavy quark expansion and to one-loop in the chiral expansion. We present results for a partially quenched theory with three sea quarks in which there are no mass degeneracies (the "1+1+1" theory) and for a partially quenched theory in which the u and d sea quark masses are equal (the "2+1" theory). We also present results for full (2+1) QCD, along with a numerical estimate of the size of staggered discretization errors. Finally, we calculate the finite volume corrections to the form factors and estimate their numerical size in current lattice simulations.Comment: 19 pages, 6 figures, references added, expanded discussion in Section I

Association of a MET genetic variant with autism-associated maternal autoantibodies to fetal brain proteins and cytokine expression.

The contribution of peripheral immunity to autism spectrum disorders (ASDs) risk is debated and poorly understood. Some mothers of children with ASD have autoantibodies that react to fetal brain proteins, raising the possibility that a subset of ASD cases may be associated with a maternal antibody response during gestation. The mechanism by which the maternal immune system breaks tolerance has not been addressed. We hypothesized that the mechanism may involve decreased expression of the MET receptor tyrosine kinase, an ASD risk gene that also serves as a key negative regulator of immune responsiveness. In a sample of 365 mothers, including 202 mothers of children with ASD, the functional MET promoter variant rs1858830 C allele was strongly associated with the presence of an ASD-specific 37+73-kDa band pattern of maternal autoantibodies to fetal brain proteins (P=0.003). To determine the mechanism of this genetic association, we measured MET protein and cytokine production in freshly prepared peripheral blood mononuclear cells from 76 mothers of ASD and typically developing children. The MET rs1858830 C allele was significantly associated with MET protein expression (P=0.025). Moreover, decreased expression of the regulatory cytokine IL-10 was associated with both the MET gene C allele (P=0.001) and reduced MET protein levels (P=0.002). These results indicate genetic distinction among mothers who produce ASD-associated antibodies to fetal brain proteins, and suggest a potential mechanism for how a genetically determined decrease in MET protein production may lead to a reduction in immune regulation

Taste violations in the scalar correlator in mixed action simulations

We study the behavior of the isovector scalar correlator, which is particularly sensitive to lattice artifacts, using domain-wall valence quarks on a staggered sea (generated by the MILC collaboration). We analyze this according to the prediction from chiral perturbation theory determined by Prelovsek, which indicates that the leading unitarity violations come from taste breaking effects. We show that our data behaves in the way predicted by Prelovsek, thus verifying that the largest contribution to the violations of unitarity which arise at finite lattice spacing can be described by the mixed-action chiral perturbation theory

The hadronic vacuum polarization contribution to aμa_{\mu} from full lattice QCD

We determine the contribution to the anomalous magnetic moment of the muon from the $\alpha^2_{\mathrm{QED}}$ hadronic vacuum polarization diagram using full lattice QCD and including $u/d$ quarks with physical masses for the first time. We use gluon field configurations that include $u$, $d$, $s$ and $c$ quarks in the sea at multiple values of the lattice spacing, multiple $u/d$ masses and multiple volumes that allow us to include an analysis of finite-volume effects. We obtain a result for $a_{\mu}^{\mathrm{HVP,LO}}$ of $667(6)(12)$, where the first error is from the lattice calculation and the second includes systematic errors from missing QED and isospin-breaking effects and from quark-line disconnected diagrams. Our result implies a discrepancy between the experimental determination of $a_{\mu}$ and the Standard Model of 3$\sigma$.Comment: 14 pages, 10 figures. Discussion of method extended with additional tests and figures added. Typographical errors correcte

Maternal antibodies from mothers of children with autism alter brain growth and social behavior development in the rhesus monkey.

Antibodies directed against fetal brain proteins of 37 and 73 kDa molecular weight are found in approximately 12% of mothers who have children with autism spectrum disorder (ASD), but not in mothers of typically developing children. This finding has raised the possibility that these immunoglobulin G (IgG) class antibodies cross the placenta during pregnancy and impact brain development, leading to one form of ASD. We evaluated the pathogenic potential of these antibodies by using a nonhuman primate model. IgG was isolated from mothers of children with ASD (IgG-ASD) and of typically developing children (IgG-CON). The purified IgG was administered to two groups of female rhesus monkeys (IgG-ASD; n=8 and IgG-CON; n=8) during the first and second trimesters of pregnancy. Another control group of pregnant monkeys (n=8) was untreated. Brain and behavioral development of the offspring were assessed for 2 years. Behavioral differences were first detected when the macaque mothers responded to their IgG-ASD offspring with heightened protectiveness during early development. As they matured, IgG-ASD offspring consistently deviated from species-typical social norms by more frequently approaching familiar peers. The increased approach was not reciprocated and did not lead to sustained social interactions. Even more striking, IgG-ASD offspring displayed inappropriate approach behavior to unfamiliar peers, clearly deviating from normal macaque social behavior. Longitudinal magnetic resonance imaging analyses revealed that male IgG-ASD offspring had enlarged brain volume compared with controls. White matter volume increases appeared to be driving the brain differences in the IgG-ASD offspring and these differences were most pronounced in the frontal lobes

The Kaon B-parameter in Mixed Action Chiral Perturbation Theory

We calculate the kaon B-parameter, B_K, in chiral perturbation theory for a partially quenched, mixed action theory with Ginsparg-Wilson valence quarks and staggered sea quarks. We find that the resulting expression is similar to that in the continuum, and in fact has only two additional unknown parameters. At one-loop order, taste-symmetry violations in the staggered sea sector only contribute to flavor-disconnected diagrams by generating an O(a^2) shift to the masses of taste-singlet sea-sea mesons. Lattice discretization errors also give rise to an analytic term which shifts the tree-level value of B_K by an amount of O(a^2). This term, however, is not strictly due to taste-breaking, and is therefore also present in the expression for B_K for pure G-W lattice fermions. We also present a numerical study of the mixed B_K expression in order to demonstrate that both discretization errors and finite volume effects are small and under control on the MILC improved staggered lattices.Comment: 29 pages, 4 figures; Expanded spurion discussion, other discussions clarified, version to appear in PR