Rhapsody. II. Subhalo Properties and the Impact of Tidal Stripping From a Statistical Sample of Cluster-Size Halos

We discuss the properties of subhalos in cluster-size halos, using a high-resolution statistical sample: the Rhapsody simulations introduced in Wu et al. (2012). We demonstrate that the criteria applied to select subhalos have significant impact on the inferred properties of the sample, including the scatter in the number of subhalos, the correlation between the subhalo number and formation time, and the shape of subhalos' spatial distribution and velocity structure. We find that the number of subhalos, when selected using the peak maximum circular velocity in their histories (a property expected to be closely related to the galaxy luminosity), is uncorrelated with the formation time of the main halo. This is in contrast to the previously reported correlation from studies where subhalos are selected by the current maximum circular velocity; we show that this difference is a result of the tidal stripping of the subhalos. We also find that the dominance of the main halo and the subhalo mass fraction are strongly correlated with halo concentration and formation history. These correlations are important to take into account when interpreting results from cluster samples selected with different criteria. Our sample also includes a fossil cluster, which is presented separately and placed in the context of the rest of the sample.Comment: 15 pages, 10 figures; Paper I: arXiv:1209.3309; replaced to match published versio

Report of the 2005 Snowmass Top/QCD Working Group

This report discusses several topics in both top quark physics and QCD at an International Linear Collider (ILC). Issues such as measurements at the $t\bar{t}$ threshold, including both theoretical and machine requirements, and the determination of electroweak top quark couplings, are reviewed. New results concerning the potential of a 500 GeV $e^+e^-$ collider for measuring $Wtb$ couplings and the top quark Yukawa coupling are presented. The status of higher order QCD corrections to jet production cross sections, heavy quark form factors, and longitudinal gauge boson scattering, needed for percent-level studies at the ILC, are reviewed. A new study of the measurement of the hadronic structure of the photon at a $\gamma\gamma$ collider is presented. The effects on top quark properties from several models of new physics, including composite models, Little Higgs theories, and CPT violation, are studied.Comment: 39 pages, many figs; typos fixed and refs added. Contributed to the 2005 International Linear Collider Physics and Detector Workshop and 2nd ILC Accelerator Workshop, Snowmass, Colorado, 14-27 Aug 200

Inaugural Address at the Inauguration of Dr. C. Dorr Demaray by Dr. S. C. Eastvold

Inaugural Address at the Inauguration of Dr. C. Dorr Demaray by Dr. S. C. Eastvold, Seattle Pacific College, Tuesday, March 1, [1960,] at 2:30 p.m.https://digitalcommons.spu.edu/inauguration_demaray_1960/1004/thumbnail.jp

The role of hybrid ubiquitin chains in the MyD88 and other innate immune signalling pathways

The adaptor protein MyD88 is required for signal transmission by Toll-like Receptors (TLRs) and receptors of the interleukin 1 (IL-1) family of cytokines. MyD88 signalling triggers the formation of Lys63-linked and Met1-linked ubiquitin (K63-Ub, M1-Ub) chains within minutes. The K63-Ub chains, which are formed by the E3 ubiquitin ligases TRAF6, Pellino1 and Pellino2, activate TAK1, the master kinase that switches on mitogen-activated protein (MAP) kinase cascades and initiates activation of the canonical IκB kinase (IKK) complex. The M1-Ub chains, which are formed by the Linear Ubiquitin chain Assembly Complex (LUBAC), bind to the NEMO component of the IKK complex and are required for TAK1 to activate IKKs, but not MAP kinases. An essential E3 ligase-independent role of TRAF6 is to recruit LUBAC into the MyD88 signalling complex, where it recognises preformed K63-Ub chains attached to protein components of these complexes, such as IRAK1, producing ubiquitin chains containing both types of linkage, termed K63/M1-Ub hybrids. The formation of K63/M1-Ub hybrids, which is a feature of several innate immune signalling pathways, permits the co-recruitment of proteins that interact with either K63-Ub or M1-Ub chains. Two likely roles for K63/M1- Ub hybrids are to facilitate the TAK1-dependent activation of the IKK complex and to prevent the hyper-activation of these kinases by recruiting A20 and A20-binding inhibitor of NF-κB1 (ABIN1). These proteins restrict activation of the TAK1 and IKK complexes, probably by competing with them for binding to K63/M1-Ub hybrids. The formation of K63/M1-Ub hybrids may also regulate the rate at which the ubiquitin linkages in these chains are hydrolysed. The IKK-catalysed phosphorylation of some of its substrates permits their recognition by the E3 ligase SCFβ TRCP, leading to their Lys48-linked ubiquitylation and proteasomal degradation. Innate immune signalling is therefore controlled by the formation and destruction of three different types of ubiquitin linkage