Gluon Radiation in ttˉt\bar t Production and Decay at the LHC

Understanding the pattern of gluon radiation in $t \bar t$ production and decay processes is important for making an accurate determination of the top mass from the momenta of its decay products. The larger energy of the LHC $pp$ collider boosts the top cross section by a factor of 100 compared to that at the Tevatron, but it also increases the amount of additional gluon radiation. We calculate the cross section for gluon radiation in top production and decay at the LHC. The distributions of this radiation are presented and the exact matrix-element results are compared with results from the HERWIG parton-shower Monte Carlo.Comment: 16 pages including 7 figures, plain LaTeX; minor corrections to text; results unchange

Structural and electrical transport properties of superconducting Au{0.7}In{0.3} films: A random array of superconductor-normal metal-superconductor (SNS) Josephson junctions

The structural and superconducting properties of Au{0.7}In{0.3} films, grown by interdiffusion of alternating Au and In layers, have been studied. The films were found to consist of a uniform solid solution of Au{0.9}In{0.1}, with excess In precipitated in the form of In-rich grains of various Au-In phases (with distinct atomic compositions), including intermetallic compounds. As the temperature was lowered, these individual grains became superconducting at a particular transition temperature (Tc), determined primarily by the atomic composition of the grain, before a fully superconducting state of zero resistance was established. From the observed onset Tc, it was inferred that up to three different superconducting phases could have formed in these Au{0.7}In{0.3} films, all of which were embedded in a uniform Au{0.9}In{0.1} matrix. Among these phases, the Tc of a particular one, 0.8 K, is higher than any previously reported for the Au-In system. The electrical transport properties were studied down to low temperatures. The transport results were found to be well correlated with those of the structural studies. The present work suggests that Au{0.7}In{0.3} can be modeled as a random array of superconductor-normal metal-superconductor (SNS) Josephson junctions. The effect of disorder and the nature of the superconducting transition in these Au{0.7}In{0.3} films are discussed.Comment: 8 text pages, 10 figures in one separate PDF file, submitted to PR

Loss of α-Synuclein Does Not Affect Mitochondrial Bioenergetics in Rodent Neurons.

Increased α-synuclein (αsyn) and mitochondrial dysfunction play central roles in the pathogenesis of Parkinson's disease (PD), and lowering αsyn is under intensive investigation as a therapeutic strategy for PD. Increased αsyn levels disrupt mitochondria and impair respiration, while reduced αsyn protects against mitochondrial toxins, suggesting that interactions between αsyn and mitochondria influences the pathologic and physiologic functions of αsyn. However, we do not know if αsyn affects normal mitochondrial function or if lowering αsyn levels impacts bioenergetic function, especially at the nerve terminal where αsyn is enriched. To determine if αsyn is required for normal mitochondrial function in neurons, we comprehensively evaluated how lowering αsyn affects mitochondrial function. We found that αsyn knockout (KO) does not affect the respiration of cultured hippocampal neurons or cortical and dopaminergic synaptosomes, and that neither loss of αsyn nor all three (α, β and γ) syn isoforms decreased mitochondria-derived ATP levels at the synapse. Similarly, neither αsyn KO nor knockdown altered the capacity of synaptic mitochondria to meet the energy requirements of synaptic vesicle cycling or influenced the localization of mitochondria to dopamine (DA) synapses in vivo. Finally, αsyn KO did not affect overall energy metabolism in mice assessed with a Comprehensive Lab Animal Monitoring System. These studies suggest either that αsyn has little or no significant physiological effect on mitochondrial bioenergetic function, or that any such functions are fully compensated for when lost. These results implicate that αsyn levels can be reduced in neurons without impairing (or improving) mitochondrial bioenergetics or distribution

The failure of stellar feedback, magnetic fields, conduction, and morphological quenching in maintaining red galaxies

The quenching "maintenance'" and related "cooling flow" problems are important in galaxies from Milky Way mass through clusters. We investigate this in halos with masses $\sim 10^{12}-10^{14}\,{\rm M}_{\odot}$, using non-cosmological high-resolution hydrodynamic simulations with the FIRE-2 (Feedback In Realistic Environments) stellar feedback model. We specifically focus on physics present without AGN, and show that various proposed "non-AGN" solution mechanisms in the literature, including Type Ia supernovae, shocked AGB winds, other forms of stellar feedback (e.g. cosmic rays), magnetic fields, Spitzer-Braginskii conduction, or "morphological quenching" do not halt or substantially reduce cooling flows nor maintain "quenched" galaxies in this mass range. We show that stellar feedback (including cosmic rays from SNe) alters the balance of cold/warm gas and the rate at which the cooled gas within the galaxy turns into stars, but not the net baryonic inflow. If anything, outflowing metals and dense gas promote additional cooling. Conduction is important only in the most massive halos, as expected, but even at $\sim 10^{14}\,{\rm M}_{\odot}$ reduces inflow only by a factor $\sim 2$ (owing to saturation effects and anisotropic suppression). Changing the morphology of the galaxies only slightly alters their Toomre-$Q$ parameter, and has no effect on cooling (as expected), so has essentially no effect on cooling flows or maintaining quenching. This all supports the idea that additional physics, e.g., AGN feedback, must be important in massive galaxies.Comment: 16 pages, 12 figure

Direct Measurement of the Top Quark Charge at Hadron Colliders

We consider photon radiation in tbar-t events at the upgraded Fermilab Tevatron and the CERN Large Hadron Collider (LHC) as a tool to measure the electric charge of the top quark. We analyze the contributions of tbar-t-gamma production and radiative top quark decays to p-p, pbar-p -> gamma l^+/- nu bbar-b jj, assuming that both b-quarks are tagged. With 20~fb^{-1} at the Tevatron, the possibility that the ``top quark'' discovered in Run I is actually an exotic charge -4/3 quark can be ruled out at the 95% confidence level. At the LHC, it will be possible to determine the charge of the top quark with an accuracy of about 10%.Comment: Revtex, 24 pages, 2 tables, 9 figure

Inhibition of MHC Class I Is a Virulence Factor in Herpes Simplex Virus Infection of Mice

Herpes simplex virus (HSV) has a number of genes devoted to immune evasion. One such gene, ICP47, binds to the transporter associated with antigen presentation (TAP) 1/2 thereby preventing transport of viral peptides into the endoplasmic reticulum, loading of peptides onto nascent major histocompatibility complex (MHC) class I molecules, and presentation of peptides to CD8 T cells. However, ICP47 binds poorly to murine TAP1/2 and so inhibits antigen presentation by MHC class I in mice much less efficiently than in humans, limiting the utility of murine models to address the importance of MHC class I inhibition in HSV immunopathogenesis. To address this limitation, we generated recombinant HSVs that efficiently inhibit antigen presentation by murine MHC class I. These recombinant viruses prevented cytotoxic T lymphocyte killing of infected cells in vitro, replicated to higher titers in the central nervous system, and induced paralysis more frequently than control HSV. This increase in virulence was due to inhibition of antigen presentation to CD8 T cells, since these differences were not evident in MHC class I-deficient mice or in mice in which CD8 T cells were depleted. Inhibition of MHC class I by the recombinant viruses did not impair the induction of the HSV-specific CD8 T-cell response, indicating that cross-presentation is the principal mechanism by which HSV-specific CD8 T cells are induced. This inhibition in turn facilitates greater viral entry, replication, and/or survival in the central nervous system, leading to an increased incidence of paralysis