Galaxy-galaxy weak-lensing measurement from SDSS: II. host halo properties of galaxy groups

As the second paper of a series on studying galaxy-galaxy lensing signals using the Sloan Digital Sky Survey Data Release 7 (SDSS DR7), we present our measurement and modelling of the lensing signals around groups of galaxies. We divide the groups into four halo mass bins, and measure the signals around four different halo-center tracers: brightest central galaxy (BCG), luminosity-weighted center, number-weighted center and X-ray peak position. For X-ray and SDSS DR7 cross identified groups, we further split the groups into low and high X-ray emission subsamples, both of which are assigned with two halo-center tracers, BCGs and X-ray peak positions. The galaxy-galaxy lensing signals show that BCGs, among the four candidates, are the best halo-center tracers. We model the lensing signals using a combination of four contributions: off-centered NFW host halo profile, sub-halo contribution, stellar contribution, and projected 2-halo term. We sample the posterior of 5 parameters i.e., halo mass, concentration, off-centering distance, sub halo mass, and fraction of subhalos via a MCMC package using the galaxy-galaxy lensing signals. After taking into account the sampling effects (e.g. Eddington bias), we found the best fit halo masses obtained from lensing signals are quite consistent with those obtained in the group catalog based on an abundance matching method, except in the lowest mass bin. Subject headings: (cosmology:) gravitational lensing, galaxies: clusters: generalComment: 12 pages, 7 figures, submitted to Ap

Sub-wavelength terahertz beam profiling of a THz source via an all-optical knife-edge technique

Terahertz technologies recently emerged as outstanding candidates for a variety of applications in such sectors as security, biomedical, pharmaceutical, aero spatial, etc. Imaging the terahertz field, however, still remains a challenge, particularly when sub-wavelength resolutions are involved. Here we demonstrate an all-optical technique for the terahertz near-field imaging directly at the source plane. A thin layer (<100 nm-thickness) of photo carriers is induced on the surface of the terahertz generation crystal, which acts as an all-optical, virtual blade for terahertz near-field imaging via a knife-edge technique. Remarkably, and in spite of the fact that the proposed approach does not require any mechanical probe, such as tips or apertures, we are able to demonstrate the imaging of a terahertz source with deeply sub-wavelength features (<30 μm) directly in its emission plane

Interactions between p-Akt and Smad3 in injured muscles initiate myogenesis or fibrogenesis

In catabolic conditions such as aging and diabetes, IGF signaling is impaired and fibrosis develops in skeletal muscles. To examine whether impaired IGF signaling initiates muscle fibrosis, we generated IGF-IR+/- heterozygous mice by crossing loxP-floxed IGF-IR (exon 3) mice with MyoD-cre mice. IGF-IR+/- mice were studied because we were unable to obtain homozygous IGF-IR-KO mice. in IGF-IR+/- mice, both growth and expression of myogenic genes (MyoD and myogenin; markers of satellite cell proliferation and differentiation, respectively) were depressed. Likewise, in injured muscles of IGF-IR+/- mice, there was impaired regeneration, depressed expression of MyoD and myogenin, and increased expression of TGF-beta 1, alpha-SMA, collagen I, and fibrosis. To uncover mechanisms stimulating fibrosis, we isolated satellite cells from muscles of IGF-IR+/- mice and found reduced proliferation and differentiation plus increased TGF-beta 1 production. in C2C12 myoblasts (a model of satellite cells), IGF-I treatment inhibited TGF-beta 1-stimulated Smad3 phosphorylation, its nuclear translocation, and expression of fibronectin. Using immunoprecipitation assay, we found an interaction between p-Akt or Akt with Smad3 in wild-type mouse muscles and in C2C12 myoblasts; importantly, IGF-I increased p-Akt and Smad3 interaction, whereas TGF-beta 1 decreased it. Therefore, in muscles of IGF-IR+/- mice, the reduction in IGF-IR reduces p-Akt, allowing for dissociation and nuclear translocation of Smad3 to enhance the TGF-beta 1 signaling pathway, leading to fibrosis. Thus, strategies to improve IGF signaling could prevent fibrosis in catabolic conditions with impaired IGF signaling.Satellite HealthAmerican Diabetes AssociationNational Institute of Diabetes and Digestive and Kidney DiseasesBaylor Coll Med, Div Nephrol, Dept Med, Houston, TX 77030 USAEmory Univ, Dept Med, Div Renal, Atlanta, GA 30322 USACapital Med Univ, Beijing An Zhen Hosp, Beijing Inst Heart Lung & Blood Vessel Dis, Beijing, Peoples R ChinaUniversidade Federal de São Paulo, Div Nephrol, Dept Med, São Paulo, BrazilUniversidade Federal de São Paulo, Div Nephrol, Dept Med, São Paulo, BrazilAmerican Diabetes Association: 1-11-BS-194National Institute of Diabetes and Digestive and Kidney Diseases: R37-DK-37175National Institute of Diabetes and Digestive and Kidney Diseases: T32-DK-62706Web of Scienc

Subunit organization of the membrane-bound HIV-1 envelope glycoprotein trimer

The trimeric human immunodeficiency virus type 1 (HIV-1) envelope glycoprotein (Env) spike is a molecular machine that mediates virus entry into host cells and is the sole target for virus-neutralizing antibodies. The mature Env spike results from cleavage of a trimeric gp160 precursor into three gp120 and three gp41 subunits. Here we describe an ~11-Å cryo-EM structure of the trimeric HIV-1 Env precursor in its unliganded state. The three gp120 and three gp41 subunits form a cage-like structure with an interior void surrounding the trimer axis. Interprotomer contacts are limited to the gp41 transmembrane region, the torus-like gp41 ectodomain, and a gp120 trimer association domain composed of the V1/V2 and V3 variable regions. The cage-like architecture, which is unique among characterized viral envelope proteins, restricts antibody access, reflecting requirements imposed by HIV-1 persistence in the host

An Actor-Based Model of Social Network Influence on Adolescent Body Size, Screen Time, and Playing Sports

Recent studies suggest that obesity may be “contagious” between individuals in social networks. Social contagion (influence), however, may not be identifiable using traditional statistical approaches because they cannot distinguish contagion from homophily (the propensity for individuals to select friends who are similar to themselves) or from shared environmental influences. In this paper, we apply the stochastic actor-based model (SABM) framework developed by Snijders and colleagues to data on adolescent body mass index (BMI), screen time, and playing active sports. Our primary hypothesis was that social influences on adolescent body size and related behaviors are independent of friend selection. Employing the SABM, we simultaneously modeled network dynamics (friendship selection based on homophily and structural characteristics of the network) and social influence. We focused on the 2 largest schools in the National Longitudinal Study of Adolescent Health (Add Health) and held the school environment constant by examining the 2 school networks separately (N = 624 and 1151). Results show support in both schools for homophily on BMI, but also for social influence on BMI. There was no evidence of homophily on screen time in either school, while only one of the schools showed homophily on playing active sports. There was, however, evidence of social influence on screen time in one of the schools, and playing active sports in both schools. These results suggest that both homophily and social influence are important in understanding patterns of adolescent obesity. Intervention efforts should take into consideration peers’ influence on one another, rather than treating “high risk” adolescents in isolation

O-mannosyl phosphorylation of alpha-dystroglycan is required for laminin binding.

Alpha-dystroglycan (alpha-DG) is a cell-surface glycoprotein that acts as a receptor for both extracellular matrix proteins containing laminin-G domains and certain arenaviruses. Receptor binding is thought to be mediated by a posttranslational modification, and defective binding with laminin underlies a subclass of congenital muscular dystrophy. Using mass spectrometry- and nuclear magnetic resonance (NMR)-based structural analyses, we identified a phosphorylated O-mannosyl glycan on the mucin-like domain of recombinant alpha-DG, which was required for laminin binding. We demonstrated that patients with muscle-eye-brain disease and Fukuyama congenital muscular dystrophy, as well as mice with myodystrophy, commonly have defects in a postphosphoryl modification of this phosphorylated O-linked mannose, and that this modification is mediated by the like-acetylglucosaminyltransferase (LARGE) protein. These findings expand our understanding of the mechanisms that underlie congenital muscular dystrophy

A herpesvirus encoded Qa-1 mimic inhibits natural killer cell cytotoxicity through CD94/NKG2A receptor engagement

A recurrent theme in viral immune evasion is the sabotage of MHC-I antigen presentation, which brings virus the concomitant issue of \u27missing-self\u27 recognition by NK cells that use inhibitory receptors to detect surface MHC-I proteins. Here, we report that rodent herpesvirus Peru (RHVP) encodes a Qa-1 like protein (pQa-1) via RNA splicing to counteract NK activation. While pQa-1 surface expression is stabilized by the same canonical peptides presented by murine Qa-1, pQa-1 is GPI-anchored and resistant to the activity of RHVP pK3, a ubiquitin ligase that targets MHC-I for degradation. pQa-1 tetramer staining indicates that it recognizes CD94/NKG2A receptors. Consistently, pQa-1 selectively inhibits NKG2