A Dichotomy in Satellite Quenching Around L* Galaxies

We examine the star formation properties of bright (~0.1 L*) satellites around isolated ~L* hosts in the local Universe using spectroscopically confirmed systems in the Sloan Digital Sky Survey DR7. Our selection method is carefully designed with the aid of N-body simulations to avoid groups and clusters. We find that satellites are significantly more likely to be quenched than a stellar mass-matched sample of isolated galaxies. Remarkably, this quenching occurs only for satellites of hosts that are themselves quenched: while star formation is unaffected in the satellites of star-forming hosts, satellites around quiescent hosts are more than twice as likely to be quenched than stellar-mass matched field samples. One implication of this is that whatever shuts down star formation in isolated, passive L* galaxies also plays at least an indirect role in quenching star formation in their bright satellites. The previously-reported tendency for "galactic conformity" in color/morphology may be a by-product of this host-specific quenching dichotomy. The S\'ersic indices of quenched satellites are statistically identical to those of field galaxies with the same specific star formation rates, suggesting that environmental and secular quenching give rise to the same morphological structure. By studying the distribution of pairwise velocities between the hosts and satellites, we find dynamical evidence that passive host galaxies reside in dark matter halos that are ~45% more massive than those of star-forming host galaxies of the same stellar mass. We emphasize that even around passive hosts, the mere fact that galaxies become satellites does not typically result in star formation quenching: we find that only ~30% of ~0.1 L* galaxies that fall in from the field are quenched around passive hosts, compared with ~0% around star forming hosts.Comment: 14 pages, 9 figure

Judgement and supply chain dynamics

Forecasting demand at the individual stock-keeping-unit (SKU) level often necessitates the use of statistical methods, such as exponential smoothing. In some organizations, however, statistical forecasts will be subject to judgemental adjustments by managers. Although a number of empirical and ‘laboratory’ studies have been performed in this area, no formal OR modelling has been conducted to offer insights into the impact such adjustments may have on supply chain performance and the potential development of mitigation mechanisms. This is because of the associated dynamic complexity and the situation-specific nature of the problem at hand. In conjunction with appropriate stock control rules, demand forecasts help decide how much to order. It is a common practice that replenishment orders may also be subject to judgemental intervention, adding further to the dynamic system complexity and interdependence. The system dynamics (SD) modelling method can help advance knowledge in this area, where mathematical modelling cannot accommodate the associated complexity. This study, which constitutes part of a UK government funded (EPSRC) project, uses SD models to evaluate the effects of forecasting and ordering adjustments for a wide set of scenarios involving: three different inventory policies; seven different (combinations of) points of intervention; and four different (combinations of) types of judgmental intervention (optimistic and pessimistic). The results enable insights to be gained into the performance of the entire supply chain. An agenda for further research concludes the paper

Site-Specific Effects of PECAM-1 on Atherosclerosis in LDL Receptor-Deficient Mice

Objective—Atherosclerosis is a vascular disease that involves lesion formation at sites of disturbed flow under the influence of genetic and environmental factors. Endothelial expression of adhesion molecules that enable infiltration of immune cells is important for lesion development. Platelet/endothelial cell adhesion molecule-1 (PECAM-1; CD31) is an adhesion and signaling receptor expressed by many cells involved in atherosclerotic lesion development. PECAM-1 transduces signals required for proinflammatory adhesion molecule expression at atherosusceptible sites; thus, it is predicted to be proatherosclerotic. PECAM-1 also inhibits inflammatory responses, on which basis it is predicted to be atheroprotective. Methods and Results—We evaluated herein the effect of PECAM-1 deficiency on development of atherosclerosis in LDL receptor– deficient mice. We found that PECAM-1 has both proatherosclerotic and atheroprotective effects, but that the former dominate in the inner curvature of the aortic arch whereas the latter dominate in the aortic sinus, branching arteries, and descending aorta. Endothelial cell expression of PECAM-1 was sufficient for its atheroprotective effects in the aortic sinus but not in the descending aorta, where the atheroprotective effects of PECAM-1 also required its expression on bone marrow–derived cells. Conclusion—We conclude that PECAM-1 influences initiation and progression of atherosclerosis both positively and negatively, and that it does so in a site-specific manner. (Arterioscler Thromb Vasc Biol. 2008;28:1996-2002

Crocidolite asbestos induces apoptosis of pleural mesothelial cells: role of reactive oxygen species and poly(ADP-ribosyl) polymerase.

Mesothelial cells, the progenitor cells of the asbestos-induced tumor mesothelioma, are particularly sensitive to the toxic effects of asbestos, although the molecular mechanisms by which asbestos induces injury in mesothelial cells are not known. We asked whether asbestos induced apoptosis in mesothelial cells and whether reactive oxygen species were important. Rabbit pleural mesothelial cells were exposed to crocidolite asbestos or control particles (1-10 micrograms/cm2) over 24 hr and evaluated for oligonucleosomal DNA fragmentation, loss of membrane phospholipid asymmetry, and nuclear condensation. Asbestos fibers, not control particles, induced apoptosis in mesothelial cells by all assays. Induction of apoptosis was dose dependent; crocidolite (5 micrograms/cm2) induced apoptosis (15.0 +/- 1.1%, mean +/- SE; n = 12) versus control particles (< 4%), as measured by appearance of nuclear condensation. Apoptosis induced by asbestos, but not by actinomycin D, was inhibited by extracellular catalase, superoxide dismutase in the presence of catalase, hypoxia (8% oxygen), deferoxamine, and 3-aminobenzamide (an inhibitor of the nuclear enzyme, poly(adenosine diphosphate-ribosyl) polymerase). We conclude that asbestos induces apoptosis in mesothelial cells via reactive oxygen species. We speculate that escape from this pathway could allow the abnormal survival of mesothelial cells with asbestos-induced mutations

Nitrosative damage to free and zinc-bound cysteine thiols underlies nitric oxide toxicity in wild-type Borrelia burgdorferi

Borrelia burgdorferi encounters potentially harmful reactive nitrogen species (RNS) throughout its infective cycle. In this study, diethylamine NONOate (DEA/NO) was used to characterize the lethal effects of RNS on B. burgdorferi. RNS produce a variety of DNA lesions in a broad spectrum of microbial pathogens; however, levels of the DNA deamination product, deoxyinosine, and the numbers of apurinic/apyrimidinic (AP) sites were identical in DNA isolated from untreated and DEA/NO-treated B. burgdorferi cells. Strains with mutations in the nucleotide excision repair (NER) pathway genes uvrC or uvrB treated with DEA/NO had significantly higher spontaneous mutation frequencies, increased numbers of AP sites in DNA and reduced survival compared with wild-type controls. Polyunsaturated fatty acids in B. burgdorferi cell membranes, which are susceptible to peroxidation by reactive oxygen species (ROS), were not sensitive to RNS-mediated lipid peroxidation. However, treatment of B. burgdorferi cells with DEA/NO resulted in nitrosative damage to several proteins, including the zinc-dependent glycolytic enzyme fructose-1,6-bisphosphate aldolase (BB0445), the Borrelia oxidative stress regulator (BosR) and neutrophil-activating protein (NapA). Collectively, these data suggested that nitrosative damage to proteins harbouring free or zinc-bound cysteine thiols, rather than DNA or membrane lipids underlies RNS toxicity in wild-type B. burgdorferi

A fitting formula for the merger timescale of galaxies in hierarchical clustering

We study galaxy mergers using a high-resolution cosmological hydro/N-body simulation with star formation, and compare the measured merger timescales with theoretical predictions based on the Chandrasekhar formula. In contrast to Navarro et al., our numerical results indicate, that the commonly used equation for the merger timescale given by Lacey and Cole, systematically underestimates the merger timescales for minor mergers and overestimates those for major mergers. This behavior is partly explained by the poor performance of their expression for the Coulomb logarithm, \ln (m_pri/m_sat). The two alternative forms \ln (1+m_pri/m_sat) and 1/2\ln [1+(m_pri/m_sat)^2] for the Coulomb logarithm can account for the mass dependence of merger timescale successfully, but both of them underestimate the merger time scale by a factor 2. Since \ln (1+m_pri/m_sat) represents the mass dependence slightly better we adopt this expression for the Coulomb logarithm. Furthermore, we find that the dependence of the merger timescale on the circularity parameter \epsilon is much weaker than the widely adopted power-law \epsilon^{0.78}, whereas 0.94*{\epsilon}^{0.60}+0.60 provides a good match to the data. Based on these findings, we present an accurate and convenient fitting formula for the merger timescale of galaxies in cold dark matter models.Comment: 16 pages, 14 figures, accepted for publication in ApJ, minor changes in the last few sentences of the discussio