New perspectives on strong z=0.5 MgII absorbers: are halo-mass and equivalent width anti-correlated?

We measure the mean halo-mass of z=0.5 MgII absorbers using the cross-correlation (over co-moving scales 0.05-13h^{-1}Mpc) between 1806 MgII quasar absorption systems and ~250,000 Luminous Red Galaxies (LRGs), both selected from the SDSS DR3. The MgII systems have rest-frame equivalent widths W_r(2796)>=0.3A. From the ratio of the MgII-LRG cross-correlation to the LRG-LRG auto-correlation, we find that the bias ratio between MgII absorbers and LRGs is 0.65+/-0.08, which implies that the absorber host-galaxies have a mean halo-mass 20-40 times smaller than that of the LRGs; the MgII absorbers have halos of mean mass =11.94+/-0.31(stat)+/-0.25(sys). We demonstrate that this statistical technique, which does not require any spectroscopic follow-up, does not suffer from contaminants such as stars or foreground and background galaxies. Finally, we find that the absorber halo-mass is anti-correlated with the equivalent width. If MgII absorbers were virialized in galaxy halos a positive M_h-W_r correlation would have been observed since W_r(2796) is a direct measure of the velocity spread of the MgII sub-components. Thus, our results demonstrate that the individual clouds of a MgII system are not virialized in the gaseous halos of the host-galaxies. We review past results in the literature on the statistics of MgII absorbers and find that they too require an M_h-W_r anti-correlation. When combined with measurements of the equivalent width distribution, the M_h-W_r anti-correlation naturally explains why absorbers with W_r(2796)>=2A are not seen at large impact parameters. We interpret the M_h-W_r anti-correlation within the starburst scenario where strong MgII absorbers are produced by supernovae-driven winds.Comment: 18 pages, 12 EPS figures, Accepted by MNRAS. Full table of MgII absorbers available at http://www.ast.cam.ac.uk/~mim/pub.html, minor changes to match the published tex

Quasar-Galaxy and Galaxy-Galaxy Cross-Correlations: Model Predictions with Realistic Galaxies

Several measurements of QSO-galaxy correlations have reported signals much larger than predictions of magnification by large-scale structure. We find that the expected signal depends stronly on the properties of the foreground galaxy population. On arcminute scales it can be either larger or smaller by a factor of two for different galaxy types in comparison with a linearly biased version of the mass distribution. Thus the resolution of some of the excess measurements may lie in examining the halo occupation properties of the galaxy population sampled by a given survey; this is also the primary information such measurements will provide. We use the halo model of clustering and simulations to predict the magnification induced cross-correlations and errors for forthcoming surveys. With the full Sloan Digital Sky Survey the statistical errors will be below 1 percent for the galaxy-galaxy correlations and significantly larger for QSO-galaxy correlations. Thus accurate constraints on parameters of the galaxy halo occupation distribution can be obtained from small scale measurements and on the bias parameter from large scales. Since the lensing induced cross-correlation measures the first moment of the halo occupation number of galaxies, these measurements can provide the basis for interpreting galaxy clustering measurements which measure the second and higher order moments.Comment: 11 pages, 4 figures, matches version in MNRA

Ancestral bias in the Hras1 gene and distal Chromosome 7 among inbred mice

Inbred strains of mice vary in their frequency of liver tumors initiated by a mutation in the Hras1 (H-ras) proto-oncogene. We sequenced 4.5 kb of the Hras1 gene on distal Chr 7 in a diverse set of 12 commonly used laboratory inbred strains of mice and detected no sequence variation to account for strain-specific differences in Hras1 mutation prevalence. Furthermore, the Hras1 sequence is essentially monoallelic for an ancestral gene derived from the M. m. domesticus species. To determine if the monoallelism and associated low rate of polymorphism are unique to Hras1 or representative of the general chromosomal locale, we extended the sequence analysis to 12 genes in the final 8 Mb of distal Chr 7. A region of at least 2.5 Mb that encompasses several genes, including Hras1 and the H19/Igf2 loci, demonstrates virtually no sequence variation. The 12 inbred strains share one dominant haplotype derived from the M. m. domesticus allele. Chromosomal regions flanking the monoallelic segment exhibit a significantly higher rate of variation and multiple haplotypes, a majority of which are attributed to M. m. domesticus or M. m. musculus ancestry

Predominant modifier of extreme liver cancer susceptibility in C57BR/cdJ female mice localized to 6 Mb on chromosome 17

Sex hormones influence the susceptibility of inbred mice to liver cancer. C57BR/cdJ (BR) females are extremely susceptible to spontaneous and chemically induced liver tumors, in part due to a lack of protection against hepatocarcinogenesis normally offered by ovarian hormones. BR males are also moderately susceptible, and the susceptibility of both sexes of BR mice to liver tumors induced with N,N-diethylnitrosamine relative to the resistant C57BL/6J (B6) strain is caused by two loci designated Hcf1 and Hcf2 (hepatocarcinogenesis in females) located on chromosomes 17 and 1, respectively. The Hcf1 locus on chromosome 17 is the predominant modifier of liver cancer in BR mice. To validate the existence of this locus and investigate its potential interaction with Hcf2, congenic mice for each region were generated. Homozygosity for the B6.BR(D17Mit164-D17Mit2) region resulted in a 4-fold increase in liver tumor multiplicity in females and a 4.5-fold increase in males compared with B6 controls. A series of 16 recombinants covering the entire congenic region was developed to further narrow the area containing Hcf1. Susceptible heterozygous recombinants demonstrated a 3- to 7-fold effect in females and a 1.5- to 2-fold effect in males compared with B6 siblings. The effect in susceptible lines completely recapitulated the susceptibility of heterozygous full-length chromosome 17 congenics and furthermore narrowed the location of the Hcf1 locus to a single region of the chromosome from 30.05 to 35.83 Mb

The PPCD1 Mouse: Characterization of a Mouse Model for Posterior Polymorphous Corneal Dystrophy and Identification of a Candidate Gene

The PPCD1 mouse, a spontaneous mutant that arose in our mouse colony, is characterized by an enlarged anterior chamber resulting from metaplasia of the corneal endothelium and blockage of the iridocorneal angle by epithelialized corneal endothelial cells. The presence of stratified multilayered corneal endothelial cells with abnormal patterns of cytokeratin expression are remarkably similar to those observed in human posterior polymorphous corneal dystrophy (PPCD) and the sporadic condition, iridocorneal endothelial syndrome. Affected eyes exhibit epithelialized corneal endothelial cells, with inappropriate cytokeratin expression and proliferation over the iridocorneal angle and posterior cornea. We have termed this the “mouse PPCD1” phenotype and mapped the mouse locus for this phenotype, designated “Ppcd1”, to a 6.1 Mbp interval on Chromosome 2, which is syntenic to the human Chromosome 20 PPCD1 interval. Inheritance of the mouse PPCD1 phenotype is autosomal dominant, with complete penetrance on the sensitive DBA/2J background and decreased penetrance on the C57BL/6J background. Comparative genome hybridization has identified a hemizygous 78 Kbp duplication in the mapped interval. The endpoints of the duplication are located in positions that disrupt the genes Csrp2bp and 6330439K17Rik and lead to duplication of the pseudogene LOC100043552. Quantitative reverse transcriptase-PCR indicates that expression levels of Csrp2bp and 6330439K17Rik are decreased in eyes of PPCD1 mice. Based on the observations of decreased gene expression levels, association with ZEB1-related pathways, and the report of corneal opacities in Csrp2bptm1a(KOMP)Wtsi heterozygotes and embryonic lethality in nulls, we postulate that duplication of the 78 Kbp segment leading to haploinsufficiency of Csrp2bp is responsible for the mouse PPCD1 phenotype. Similarly, CSRP2BP haploinsufficiency may lead to human PPCD

A review of elliptical and disc galaxy structure, and modern scaling laws

A century ago, in 1911 and 1913, Plummer and then Reynolds introduced their models to describe the radial distribution of stars in `nebulae'. This article reviews the progress since then, providing both an historical perspective and a contemporary review of the stellar structure of bulges, discs and elliptical galaxies. The quantification of galaxy nuclei, such as central mass deficits and excess nuclear light, plus the structure of dark matter halos and cD galaxy envelopes, are discussed. Issues pertaining to spiral galaxies including dust, bulge-to-disc ratios, bulgeless galaxies, bars and the identification of pseudobulges are also reviewed. An array of modern scaling relations involving sizes, luminosities, surface brightnesses and stellar concentrations are presented, many of which are shown to be curved. These 'redshift zero' relations not only quantify the behavior and nature of galaxies in the Universe today, but are the modern benchmark for evolutionary studies of galaxies, whether based on observations, N-body-simulations or semi-analytical modelling. For example, it is shown that some of the recently discovered compact elliptical galaxies at 1.5 < z < 2.5 may be the bulges of modern disc galaxies.Comment: Condensed version (due to Contract) of an invited review article to appear in "Planets, Stars and Stellar Systems"(www.springer.com/astronomy/book/978-90-481-8818-5). 500+ references incl. many somewhat forgotten, pioneer papers. Original submission to Springer: 07-June-201