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

Measuring Active-Sterile Neutrino Oscillations with a Stopped Pion Neutrino Source

The question of the existence of light sterile neutrinos is of great interest in many areas of particle physics, astrophysics, and cosmology. Furthermore, should the MiniBooNE experiment at Fermilab confirm the LSND oscillation signal, then new measurements are required to identify the mechanism responsible for these oscillations. Possibilities include sterile neutrinos, CP or CPT violation, variable mass neutrinos, Lorentz violation, and extra dimensions. In this paper, we consider an experiment at a stopped pion neutrino source to determine if active-sterile neutrino oscillations with delta-m greater than 0.1 eV2 can account for the signal. By exploiting stopped pi+ decay to produce a monoenergetic nu_mu source, and measuring the rate of the neutral current reaction nu_x + 12C -> nu_x +12C* as a function of distance from the source, we show that a convincing test for active-sterile neutrino oscillations can be performed.Comment: 10 pages, 9 figure

Elucidation of copper environment in a Cu-Cr-Fe oxide catalyst through in situ high-resolution XANES investigation

Copper containing materials are widely used in a range of catalytic applications. Here, we report the use of Cu K-edge high resolution XANES to determine the local site symmetry of copper ions during the thermal treatment of a Cu-Cr-Fe oxide catalyst. We exploited the Cu K-edge XANES spectral features, in particular the correlation between area under the pre-edge peak and its position to determine the local environment of Cu2+ ions. The information gained from this investigation rules out the presence of Cu2+ ions in a tetrahedral or square planar geometry, a mixture of these sites, or in a reduced oxidation state. Evidence is presented that the Cu2+ ions in the Cu-Cr-Fe oxide system are present in a distorted octahedral environment

Inclusion and Analysis of Older Adults in RCTs

Surgical oncolog

Higher-order hadronic-vacuum-polarization contribution to the muon g-2 from lattice QCD

We introduce a new method for calculating the ${\rm O}(\alpha^3)$ hadronic-vacuum-polarization contribution to the muon anomalous magnetic moment from ${ab-initio}$ lattice QCD. We first derive expressions suitable for computing the higher-order contributions either from the renormalized vacuum polarization function $\hat\Pi(q^2)$, or directly from the lattice vector-current correlator in Euclidean space. We then demonstrate the approach using previously-published results for the Taylor coefficients of $\hat\Pi(q^2)$ that were obtained on four-flavor QCD gauge-field configurations with physical light-quark masses. We obtain $10^{10} a_\mu^{\rm HVP,HO} = -9.3(1.3)$, in agreement with, but with a larger uncertainty than, determinations from $e^+e^- \to {\rm hadrons}$ data plus dispersion relations.Comment: Expanded and clarified discussion and revised Figure 4. Results unchanged. 11 pages, 5 tables, 5 figures. Version accepted to Physical Review

Activation of the Nrf2 response by intrinsic hepatotoxic drugs correlates with suppression of NF-κB activation and sensitizes toward TNFα-induced cytotoxicity

Drug-induced liver injury (DILI) is an important problem both in the clinic and in the development of new safer medicines. Two pivotal adaptation and survival responses to adverse drug reactions are oxidative stress and cytokine signaling based on the activation of the transcription factors Nrf2 and NF-κB, respectively. Here, we systematically investigated Nrf2 and NF-κB signaling upon DILI-related drug exposure. Transcriptomics analyses of 90 DILI compounds in primary human hepatocytes revealed that a strong Nrf2 activation is associated with a suppression of endogenous NF-κB activity. These responses were translated into quantitative high-content live-cell imaging of induction of a selective Nrf2 target, GFP-tagged Srxn1, and the altered nuclear translocation dynamics of a subunit of NF-κB, GFP-tagged p65, upon TNFR signaling induced by TNFα using HepG2 cells. Strong activation of GFP-Srxn1 expression by DILI compounds typically correlated with suppression of NF-κB nuclear translocation, yet reversely, activation of NF-κB by TNFα did not affect the Nrf2 response. DILI compounds that provided strong Nrf2 activation, including diclofenac, carbamazepine and ketoconazole, sensitized toward TNFα-mediated cytotoxicity. This was related to an adaptive primary protective response of Nrf2, since loss of Nrf2 enhanced this cytotoxic synergy with TNFα, while KEAP1 downregulation was cytoprotective. These data indicate that both Nrf2 and NF-κB signaling may be pivotal in the regulation of DILI. We propose that the NF-κB-inhibiting effects that coincide with a strong Nrf2 stress response likely sensitize liver cells to pro-apoptotic signaling cascades induced by intrinsic cytotoxic pro-inflammatory cytokines

No Excess Mortality in Patients Aged 50 Years and Older Who Received Treatment for Ductal Carcinoma In Situ of the Breast

Background. The incidence of ductal carcinoma in situ (DCIS) has increased at a fast rate.The aim of this study was to assess the incidence and treatment in the Netherlands and estimate the excess mortality risk of DCIS. Methods. From the Netherlands Cancer Registry, adult female patients (diagnosed 1997–2005) with DCIS were selected. Treatment was described according to age. Relative mortality at 10 years of follow-up was calculated by dividing observed mortality over expected mortality. Expected mortality was calculated using the matched Dutch general population. Results. Overall, 8421 patients were included in this study. For patients aged 50–64, and 65–74 an increase in breast-conserving surgery was observed over time (P < 0.001). For patients over 75 years of age, 8.0% did not undergo surgery; this percentage remained stable over time (P = 0.07). Overall, treated patients aged >50 years experienced no excess mortality regardless of treatment (relative mortality 1.0). Conclusion. The present population-based study of almost 8500 patients showed no excess mortality in surgically treated women over 50 years with DCIS

Turbulence anisotropy and the SO(3) description

We study strongly turbulent windtunnel flows with controlled anisotropy. Using a recent formalism based on angular momentum and the irreducible representations of the SO(3) rotation group, we attempt to extract this anisotropy from the angular dependence of second-order structure functions. Our instrumentation allows a measurement of both the separation and the angle dependence of the structure function. In axisymmetric turbulence which has a weak anisotropy, this more extended information produces ambiguous results. In more strongly anisotropic shear turbulence, the SO(3) description enables one to find the anisotropy scaling exponent. The key quality of the SO(3) description is that structure functions are a mixture of algebraic functions of the scale with exponents ordered such that the contribution of anisotropies diminishes at small scales. However, we find that in third-order structure functions of homogeneous shear turbulence the anisotropic contribution is always large and of the same order of magnitude as the isotropic part. Our results concern the minimum instrumentation needed to determine the parameters of the SO(3) description, and raise several questions about its ability to describe the angle dependence of high-order structure functions

Further characterization of autoantibodies to GABAergic neurons in the central nervous system produced by a subset of children with autism

<p>Abstract</p> <p>Background</p> <p>Autism is a neurodevelopmental disorder characterized by impairments in social interaction and deficits in verbal and nonverbal communication, together with the presence of repetitive behaviors or a limited repertoire of activities and interests. The causes of autism are currently unclear. In a previous study, we determined that 21% of children with autism have plasma autoantibodies that are immunoreactive with a population of neurons in the cerebellum that appear to be Golgi cells, which are GABAergic interneurons.</p> <p>Methods</p> <p>We have extended this analysis by examining plasma immunoreactivity in the remainder of the brain. To determine cell specificity, double-labeling studies that included one of the calcium-binding proteins that are commonly colocalized in GABAergic neurons (calbindin, parvalbumin or calretinin) were also carried out to determine which GABAergic neurons are immunoreactive. Coronal sections through the rostrocaudal extent of the macaque monkey brain were reacted with plasma from each of seven individuals with autism who had previously demonstrated positive Golgi cell staining, as well as six negative controls. In addition, brain sections from adult male mice were similarly examined.</p> <p>Results</p> <p>In each case, specific staining was observed for neurons that had the morphological appearance of interneurons. By double-labeling sections with plasma and with antibodies directed against γ-aminobutyric acid (GABA), we determined that all autoantibody-positive neurons were GABAergic. However, not all GABAergic neurons were autoantibody-positive. Calbindin was colabeled in several of the autoantibody-labeled cells, while parvalbumin colabeling was less frequently observed. Autoantibody-positive cells rarely expressed calretinin. Sections from the mouse brain processed similarly to the primate sections also demonstrated immunoreactivity to interneurons distributed throughout the neocortex and many subcortical regions. Some cell populations stained in the primate (such as the Golgi neurons in the cerebellum) were not as robustly immunoreactive in the mouse brain.</p> <p>Conclusions</p> <p>These results suggest that the earlier report of autoantibody immunoreactivity to specific cells in the cerebellum extend to other regions of the brain. Further, these findings confirm the autoantibody-targeted cells to be a subpopulation of GABAergic interneurons. The potential impact of these autoantibodies on GABAergic disruption with respect to the etiology of autism is discussed herein.</p