The Chandra Source Catalog

The Chandra Source Catalog (CSC) is a general purpose virtual X-ray astrophysics facility that provides access to a carefully selected set of generally useful quantities for individual X-ray sources, and is designed to satisfy the needs of a broad-based group of scientists, including those who may be less familiar with astronomical data analysis in the X-ray regime. The first release of the CSC includes information about 94,676 distinct X-ray sources detected in a subset of public ACIS imaging observations from roughly the first eight years of the Chandra mission. This release of the catalog includes point and compact sources with observed spatial extents <~ 30''. The catalog (1) provides access to the best estimates of the X-ray source properties for detected sources, with good scientific fidelity, and directly supports scientific analysis using the individual source data; (2) facilitates analysis of a wide range of statistical properties for classes of X-ray sources; and (3) provides efficient access to calibrated observational data and ancillary data products for individual X-ray sources, so that users can perform detailed further analysis using existing tools. The catalog includes real X-ray sources detected with flux estimates that are at least 3 times their estimated 1 sigma uncertainties in at least one energy band, while maintaining the number of spurious sources at a level of <~ 1 false source per field for a 100 ks observation. For each detected source, the CSC provides commonly tabulated quantities, including source position, extent, multi-band fluxes, hardness ratios, and variability statistics, derived from the observations in which the source is detected. In addition to these traditional catalog elements, for each X-ray source the CSC includes an extensive set of file-based data products that can be manipulated interactively.Comment: To appear in The Astrophysical Journal Supplement Series, 53 pages, 27 figure

Statistical Characterization of the Chandra Source Catalog

The first release of the Chandra Source Catalog (CSC) contains ~95,000 X-ray sources in a total area of ~0.75% of the entire sky, using data from ~3,900 separate ACIS observations of a multitude of different types of X-ray sources. In order to maximize the scientific benefit of such a large, heterogeneous data-set, careful characterization of the statistical properties of the catalog, i.e., completeness, sensitivity, false source rate, and accuracy of source properties, is required. Characterization efforts of other, large Chandra catalogs, such as the ChaMP Point Source Catalog (Kim et al. 2007) or the 2 Mega-second Deep Field Surveys (Alexander et al. 2003), while informative, cannot serve this purpose, since the CSC analysis procedures are significantly different and the range of allowable data is much less restrictive. We describe here the characterization process for the CSC. This process includes both a comparison of real CSC results with those of other, deeper Chandra catalogs of the same targets and extensive simulations of blank-sky and point source populations.Comment: To be published in the Astrophysical Journal Supplement Series (Fig. 52 replaced with a version which astro-ph can convert to PDF without issues.

Attaching and effacing (A/E) lesion formation by enteropathogenic E. coli on human intestinal mucosa is dependent on non-LEE effectors

Enteropathogenic E. coli (EPEC) is a human pathogen that causes acute and chronic pediatric diarrhea. The hallmark of EPEC infection is the formation of attaching and effacing (A/E) lesions in the intestinal epithelium. Formation of A/E lesions is mediated by genes located on the pathogenicity island locus of enterocyte effacement (LEE), which encode the adhesin intimin, a type III secretion system (T3SS) and six effectors, including the essential translocated intimin receptor (Tir). Seventeen additional effectors are encoded by genes located outside the LEE, in insertion elements and prophages. Here, using a stepwise approach, we generated an EPEC mutant lacking the entire effector genes (EPEC0) and intermediate mutants. We show that EPEC0 contains a functional T3SS. An EPEC mutant expressing intimin but lacking all the LEE effectors but Tir (EPEC1) was able to trigger robust actin polymerization in HeLa cells and mucin-producing intestinal LS174T cells. However, EPEC1 was unable to form A/E lesions on human intestinal in vitro organ cultures (IVOC). Screening the intermediate mutants for genes involved in A/E lesion formation on IVOC revealed that strains lacking non-LEE effector/s have a marginal ability to form A/E lesions. Furthermore, we found that Efa1/LifA proteins are important for A/E lesion formation efficiency in EPEC strains lacking multiple effectors. Taken together, these results demonstrate the intricate relationships between T3SS effectors and the essential role non-LEE effectors play in A/E lesion formation on mucosal surfaces

Modulation of host cell processes by T3SS effectors

Two of the enteric Escherichia coli pathotypes-enteropathogenic E. coli (EPEC) and enterohaemorrhagic E. coli (EHEC)-have a conserved type 3 secretion system which is essential for virulence. The T3SS is used to translocate between 25 and 50 bacterial proteins directly into the host cytosol where they manipulate a variety of host cell processes to establish a successful infection. In this chapter, we discuss effectors from EPEC/EHEC in the context of the host proteins and processes that they target-the actin cytoskeleton, small guanosine triphosphatases and innate immune signalling pathways that regulate inflammation and cell death. Many of these translocated proteins have been extensively characterised, which has helped obtain insights into the mechanisms of pathogenesis of these bacteria and also understand the host pathways they target in more detail. With increasing knowledge of the positive and negative regulation of host signalling pathways by different effectors, a future challenge is to investigate how the specific effector repertoire of each strain cooperates over the course of an infection

Climate change impacts on human health over Europe through its effect on air quality

Abstract This review examines the current literature on the effects of future emissions and climate change on particulate matter (PM) and O3 air quality and on the consequent health impacts, with a focus on Europe. There is considerable literature on the effects of climate change on O3 but fewer studies on the effects of climate change on PM concentrations. Under the latest Intergovernmental Panel on Climate Change (IPCC) 5th assessment report (AR5) Representative Concentration Pathways (RCPs), background O3 entering Europe is expected to decrease under most scenarios due to higher water vapour concentrations in a warmer climate. However, under the extreme pathway RCP8.5 higher (more than double) methane (CH4) abundances lead to increases in background O3 that offset the O3 decrease due to climate change especially for the 2100 period. Regionally, in polluted areas with high levels of nitrogen oxides (NOx), elevated surface temperatures and humidities yield increases in surface O3 – termed the O3 climate penalty – especially in southern Europe. The O3 response is larger for metrics that represent the higher end of the O3 distribution, such as daily maximum O3. Future changes in PM concentrations due to climate change are much less certain, although several recent studies also suggest a PM climate penalty due to high temperatures and humidity and reduced precipitation in northern mid-latitude land regions in 2100. A larger number of studies have examined both future climate and emissions changes under the RCP scenarios. Under these pathways the impact of emission changes on air quality out to the 2050s will be larger than that due to climate change, because of large reductions in emissions of O3 and PM pollutant precursor emissions and the more limited climate change response itself. Climate change will also affect climate extreme events such as heatwaves. Air pollution episodes are associated with stagnation events and sometimes heat waves. Air quality during the 2003 heatwave over Europe has been examined in numerous studies and mechanisms for enhancing O3 have been identified. There are few studies on health effects associated with climate change impacts alone on air quality, but these report higher O3-related health burdens in polluted populated regions and greater PM2.5 health burdens in these emission regions. Studies that examine the combined impacts of climate change and anthropogenic emissions change under the RCP scenarios report reductions in global and European premature O3-respiratory related and PM mortalities arising from the large decreases in precursor emissions. Under RCP 8.5 the large increase in CH4 leads to global and European excess O3-respiratory related mortalities in 2100. For future health effects, besides uncertainty in future O3 and particularly PM concentrations, there is also uncertainty in risk estimates such as effect modification by temperature on pollutant-response relationships and potential future adaptation that would alter exposure risk