Extreme Ultraviolet Emission in the Fornax Cluster of Galaxies

We present studies of the Extreme Ultraviolet (EUV) emission in the Fornax cluster of galaxies; a relatively nearby well-studied cluster with X-ray emitting cluster gas and a very large radio source. We examine both the large-scale (~size of the X-ray emitting cluster gas), and the small-scale (<arcmin) emission. We find that this cluster has large-scale diffuse EUV emission. However, at the sensitivity level of the existing EUVE data, this emission is due entirely to the low energy tail of the X-ray emitting gas. We have also examined small-scale structures in raw EUVE images of this cluster. We find that small-scale irregularities are present in all raw Deep Survey images as a result of small-scale detector effects. These effects can be removed by appropriate flat-fielding. After flat-fielding, the Fornax cluster still shows a few significant regions of small-scale EUV enhancement. We find that these are emission from stars and galaxies in the field. We find that at existing levels of sensitivity, there is no excess EUV emission in the cluster on either large or small scales.Comment: 6 pages, 3 eps figures, aastex5, Accepted to ApJ

A 1.1 to 1.9 GHz SETI Survey of the Kepler Field: I. A Search for Narrow-band Emission from Select Targets

We present a targeted search for narrow-band (< 5 Hz) drifting sinusoidal radio emission from 86 stars in the Kepler field hosting confirmed or candidate exoplanets. Radio emission less than 5 Hz in spectral extent is currently known to only arise from artificial sources. The stars searched were chosen based on the properties of their putative exoplanets, including stars hosting candidates with 380 K > T_eq > 230 K, stars with 5 or more detected candidates or stars with a super-Earth (R_p 50 day orbit. Baseband voltage data across the entire band between 1.1 and 1.9 GHz were recorded at the Robert C. Byrd Green Bank Telescope between Feb--Apr 2011 and subsequently searched offline. No signals of extraterrestrial origin were found. We estimate that fewer than ~1% of transiting exoplanet systems host technological civilizations that are radio loud in narrow-band emission between 1-2 GHz at an equivalent isotropically radiated power (EIRP) of ~1.5 x 10^21 erg s^-1, approximately eight times the peak EIRP of the Arecibo Planetary Radar, and we limit the the number of 1-2 GHz narrow-band-radio-loud Kardashev type II civilizations in the Milky Way to be < 10^-6 M_solar^-1. Here we describe our observations, data reduction procedures and results.Comment: Accepted to the Astrophysical Journa

A novel Bayesian approach to quantify clinical variables and to determine their spectroscopic counterparts in 1H NMR metabonomic data

<p>Abstract</p> <p>Background</p> <p>A key challenge in metabonomics is to uncover quantitative associations between multidimensional spectroscopic data and biochemical measures used for disease risk assessment and diagnostics. Here we focus on clinically relevant estimation of lipoprotein lipids by ¹H NMR spectroscopy of serum.</p> <p>Results</p> <p>A Bayesian methodology, with a biochemical motivation, is presented for a real ¹H NMR metabonomics data set of 75 serum samples. Lipoprotein lipid concentrations were independently obtained for these samples via ultracentrifugation and specific biochemical assays. The Bayesian models were constructed by Markov chain Monte Carlo (MCMC) and they showed remarkably good quantitative performance, the predictive R-values being 0.985 for the very low density lipoprotein triglycerides (VLDL-TG), 0.787 for the intermediate, 0.943 for the low, and 0.933 for the high density lipoprotein cholesterol (IDL-C, LDL-C and HDL-C, respectively). The modelling produced a kernel-based reformulation of the data, the parameters of which coincided with the well-known biochemical characteristics of the ¹H NMR spectra; particularly for VLDL-TG and HDL-C the Bayesian methodology was able to clearly identify the most characteristic resonances within the heavily overlapping information in the spectra. For IDL-C and LDL-C the resulting model kernels were more complex than those for VLDL-TG and HDL-C, probably reflecting the severe overlap of the IDL and LDL resonances in the ¹H NMR spectra.</p> <p>Conclusion</p> <p>The systematic use of Bayesian MCMC analysis is computationally demanding. Nevertheless, the combination of high-quality quantification and the biochemical rationale of the resulting models is expected to be useful in the field of metabonomics.</p

Current and Nascent SETI Instruments

Here we describe our ongoing efforts to develop high-performance and sensitive instrumentation for use in the search for extra-terrestrial intelligence (SETI). These efforts include our recently deployed Search for Extraterrestrial Emissions from Nearby Developed Intelligent Populations Spectrometer (SERENDIP V.v) and two instruments currently under development; the Heterogeneous Radio SETI Spectrometer (HRSS) for SETI observations in the radio spectrum and the Optical SETI Fast Photometer (OSFP) for SETI observations in the optical band. We will discuss the basic SERENDIP V.v instrument design and initial analysis methodology, along with instrument architectures and observation strategies for OSFP and HRSS. In addition, we will demonstrate how these instruments may be built using low-cost, modular components and programmed and operated by students using common languages, e.g. ANSI C.Comment: 12 pages, 5 figures, Original version appears as Chapter 2 in "The Proceedings of SETI Sessions at the 2010 Astrobiology Science Conference: Communication with Extraterrestrial Intelligence (CETI)," Douglas A. Vakoch, Edito

Adhesive organelles of Gram-negative pathogens assembled with the classical chaperone/usher machinery: structure and function from a clinical standpoint

This review summarizes current knowledge on the structure, function, assembly and biomedical applications of the superfamily of adhesive fimbrial organelles exposed on the surface of Gram-negative pathogens with the classical chaperone/usher machinery. High-resolution three-dimensional (3D) structure studies of the minifibers assembling with the FGL (having a long F1-G1 loop) and FGS (having a short F1-G1 loop) chaperones show that they exploit the same principle of donor-strand complementation for polymerization of subunits. The 3D structure of adhesive subunits bound to host-cell receptors and the final architecture of adhesive fimbrial organelles reveal two functional families of the organelles, respectively, possessing polyadhesive and monoadhesive binding. The FGL and FGS chaperone-assembled polyadhesins are encoded exclusively by the gene clusters of the gamma 3- and kappa-monophyletic groups, respectively, while gene clusters belonging to the gamma 1-, gamma 2-, gamma 4-, and pi-fimbrial clades exclusively encode FGS chaperone-assembled monoadhesins. Novel approaches are suggested for a rational design of antimicrobials inhibiting the organelle assembly or inhibiting their binding to host-cell receptors. Vaccines are currently under development based on the recombinant subunits of adhesins

Evaluating the relationship between circulating lipoprotein lipids and apolipoproteins with risk of coronary heart disease: A multivariable Mendelian randomisation analysis.

BACKGROUND: Circulating lipoprotein lipids cause coronary heart disease (CHD). However, the precise way in which one or more lipoprotein lipid-related entities account for this relationship remains unclear. Using genetic instruments for lipoprotein lipid traits implemented through multivariable Mendelian randomisation (MR), we sought to compare their causal roles in the aetiology of CHD. METHODS AND FINDINGS: We conducted a genome-wide association study (GWAS) of circulating non-fasted lipoprotein lipid traits in the UK Biobank (UKBB) for low-density lipoprotein (LDL) cholesterol, triglycerides, and apolipoprotein B to identify lipid-associated single nucleotide polymorphisms (SNPs). Using data from CARDIoGRAMplusC4D for CHD (consisting of 60,801 cases and 123,504 controls), we performed univariable and multivariable MR analyses. Similar GWAS and MR analyses were conducted for high-density lipoprotein (HDL) cholesterol and apolipoprotein A-I. The GWAS of lipids and apolipoproteins in the UKBB included between 393,193 and 441,016 individuals in whom the mean age was 56.9 y (range 39-73 y) and of whom 54.2% were women. The mean (standard deviation) lipid concentrations were LDL cholesterol 3.57 (0.87) mmol/L and HDL cholesterol 1.45 (0.38) mmol/L, and the median triglycerides was 1.50 (IQR = 1.11) mmol/L. The mean (standard deviation) values for apolipoproteins B and A-I were 1.03 (0.24) g/L and 1.54 (0.27) g/L, respectively. The GWAS identified multiple independent SNPs associated at P < 5 × 10-8 for LDL cholesterol (220), apolipoprotein B (n = 255), triglycerides (440), HDL cholesterol (534), and apolipoprotein A-I (440). Between 56%-93% of SNPs identified for each lipid trait had not been previously reported in large-scale GWASs. Almost half (46%) of these SNPs were associated at P < 5 × 10-8 with more than one lipid-related trait. Assessed individually using MR, LDL cholesterol (odds ratio [OR] 1.66 per 1-standard-deviation-higher trait; 95% CI: 1.49-1.86; P < 0.001), triglycerides (OR 1.34; 95% CI: 1.25-1.44; P < 0.001) and apolipoprotein B (OR 1.73; 95% CI: 1.56-1.91; P < 0.001) had effect estimates consistent with a higher risk of CHD. In multivariable MR, only apolipoprotein B (OR 1.92; 95% CI: 1.31-2.81; P < 0.001) retained a robust effect, with the estimate for LDL cholesterol (OR 0.85; 95% CI: 0.57-1.27; P = 0.44) reversing and that of triglycerides (OR 1.12; 95% CI: 1.02-1.23; P = 0.01) becoming weaker. Individual MR analyses showed a 1-standard-deviation-higher HDL cholesterol (OR 0.80; 95% CI: 0.75-0.86; P < 0.001) and apolipoprotein A-I (OR 0.83; 95% CI: 0.77-0.89; P < 0.001) to lower the risk of CHD, but these effect estimates attenuated substantially to the null on accounting for apolipoprotein B. A limitation is that, owing to the nature of lipoprotein metabolism, measures related to the composition of lipoprotein particles are highly correlated, creating a challenge in making exclusive interpretations on causation of individual components. CONCLUSIONS: These findings suggest that apolipoprotein B is the predominant trait that accounts for the aetiological relationship of lipoprotein lipids with risk of CHD

Hot Gas in the Galactic Thick Disk and Halo Near the Draco Cloud

This paper examines the ultraviolet and X-ray photons generated by hot gas in the Galactic thick disk or halo in the Draco region of the northern hemisphere. Our analysis uses the intensities from four ions, C IV, O VI, O VII, and O VIII, sampling temperatures of ~100,000 to ~3,000,000 K. We measured the O VI, O VII and O VIII intensities from FUSE and XMM-Newton data and subtracted off the local contributions in order to deduce the thick disk/halo contributions. These were supplemented with published C IV intensity and O VI column density measurements. Our estimate of the thermal pressure in the O VI-rich thick disk/halo gas, p_{th}/k = 6500^{+2500}_{-2600} K cm^{-3}, suggests that the thick disk/halo is more highly pressurized than would be expected from theoretical analyses. The ratios of C IV to O VI to O VII to O VIII, intensities were compared with those predicted by theoretical models. Gas which was heated to 3,000,000 K then allowed to cool radiatively cannot produce enough C IV or O VI-generated photons per O VII or O VIII-generated photon. Producing enough C IV and O VI emission requires heating additional gas to 100,000 < T < 1,000,000 K. However, shock heating, which provides heating across this temperature range, overproduces O VI relative to the others. Obtaining the observed mix may require a combination of several processes, including some amount of shock heating, heat conduction, and mixing, as well as radiative cooling of very hot gas.Comment: 10 pages, 2 figures. Accepted for publication in the Astrophysical Journa

Metabolomic Profiling of Statin Use and Genetic Inhibition of HMG-CoA Reductase

Background Statins are first-line therapy for cardiovascular disease prevention, but their systemic effects across lipoprotein subclasses, fatty acids, and circulating metabolites remain incompletely characterized. Objectives This study sought to determine the molecular effects of statin therapy on multiple metabolic pathways. Methods Metabolic profiles based on serum nuclear magnetic resonance metabolomics were quantified at 2 time points in 4 population-based cohorts from the United Kingdom and Finland (N = 5,590; 2.5 to 23.0 years of follow-up). Concentration changes in 80 lipid and metabolite measures during follow-up were compared between 716 individuals who started statin therapy and 4,874 persistent nonusers. To further understand the pharmacological effects of statins, we used Mendelian randomization to assess associations of a genetic variant known to mimic inhibition of HMG-CoA reductase (the intended drug target) with the same lipids and metabolites for 27,914 individuals from 8 population-based cohorts. Results Starting statin therapy was associated with numerous lipoprotein and fatty acid changes, including substantial lowering of remnant cholesterol (80% relative to low-density lipoprotein cholesterol [LDL-C]), but only modest lowering of triglycerides (25% relative to LDL-C). Among fatty acids, omega-6 levels decreased the most (68% relative to LDL-C); other fatty acids were only modestly affected. No robust changes were observed for circulating amino acids, ketones, or glycolysis-related metabolites. The intricate metabolic changes associated with statin use closely matched the association pattern with rs12916 in the HMGCR gene (R2 = 0.94, slope 1.00 ± 0.03). Conclusions Statin use leads to extensive lipid changes beyond LDL-C and appears efficacious for lowering remnant cholesterol. Metabolomic profiling, however, suggested minimal effects on amino acids. The results exemplify how detailed metabolic characterization of genetic proxies for drug targets can inform indications, pleiotropic effects, and pharmacological mechanisms