Hard X-ray emission from the Galactic ridge

We present results of a study of the Galactic ridge X-ray emission (GRXE) in hard X-rays performed with the IBIS telescope aboard INTEGRAL. The imaging capabilities of this coding aperture telescope make it possible to account for the flux from bright Galactic point sources whereas the wide field of view permits to collect large flux from the underlying GRXE. Extensive study of the IBIS/ISGRI detector background allowed us to construct a model that predicts the detector count rate with $\sim1-2$% accuracy in the energy band 17-60 keV. The derived longitude and latitude profiles of the ridge emission are in good agreement with the Galactic distribution of stars obtained from infrared observations. This, along with the measured hard X-ray spectrum of the Galactic ridge emission strongly indicates its stellar origin. The derived unit stellar mass emissivity of the ridge in the energy band 17-60 keV, $(0.9 - 1.2)\times 10^{27}$\lummass (assuming a bulge mass of $1-1.3 \times 10^{10} M_\odot$) agrees with that of local (in the Solar neigborhood) accreting magnetic white dwarf binaries - dominant contributors to the GRXE at these energies. In addition, the shape of the obtained GRXE spectrum can be used to determine the average mass of white dwarfs in such systems in the Galaxy as \sim0.5 M_{\sun}. The total hard X-ray luminosity of the GRXE is $L_{\rm 17-60 keV} =(3.7\pm0.2)\times10^{37}$\lum in the 17--60 keV band. At energies 70--200 keV no additional contribution to the total emission of the Galaxy apart from the detected point sources is seen.Comment: 13 pages, 19 figures, submitted to Astronomy and Astrophysic

Are we losing the battle against cardiometabolic disease? The case for a paradigm shift in primary prevention

Kraushaar LE, Krämer A. Are we losing the battle against cardiometabolic disease? The case for a paradigm shift in primary prevention. BMC Public Health. 2009;9(1):64.Background: Cardiovascular and diabetic disease are the leading and preventable causes of death worldwide. The currently prognosticated dramatic increase in disease burden over the next two decades, however, bespeaks a low confidence in our prevention ability. This conflicts with the almost enthusiastic reporting of study results, which demonstrate substantial risk reductions secondary to simple lifestyle changes. Discussion: There is a case to be made for a disregard of the difference between statistical significance and clinical relevance of the reported data. Nevertheless, lifestyle change remains the main weapon in our battle against the epidemic of cardiometabolic disease. But along the way from risk screening to intervention to maintenance the compound inefficiencies of current primary preventive strategies marginalize their impact. Summary: Unless we dramatically change the ways in which we deploy preventive interventions we will inevitably lose the battle. In this paper we will argue for three provocative strategy changes, namely (a) the disbanding of screening in favor of population-wide enrollment into preventive interventions, (b) the substitution of the current cost utility analysis for a return-on-investment centered appraisal of interventions, and (c) the replacement of standardized programs modeled around acute care by individualized and perpetual interventions

Vascular robustness: The missing parameter in cardiovascular risk prediction

Undetected high risk for premature death of cardiovascular disease (CVD) among individuals with low-to-moderate risk factor scores is an acknowledged obstacle to CVD prevention. The vasculature's functional robustness against risk factor derailment may serve as a novel discriminator of mortality risk under similar risk factor loads. To test this assumption, we hypothesized that the expected inverse robustness-mortality association is verifiable as a significant trend along the age spectrum of risk factor-challenged cohorts.This is a retrospective cohort study of 372 adults (mean age 56.1 years, range 21–92; 45% female) with a variety of CV risk factors.An arterial model (VascAssist 2, iSYMED GmbH, Germany) was used to derive global parameters of arterial function from non-invasively acquired pulse pressure waves. Participants were stratified by health status: apparently healthy (AH; n = 221); with hypertension and/or hypercholesterolemia (CC; n = 61); with history of CV event(s) (CVE; n = 90). Multivariate linear regression was used to derive a robustness score which was calibrated against the CVD mortality hazard rate of a sub-cohort of the LURIC study (n = 1369; mean age 59.1 years, range 20–75; 37% female).Robustness correlated linearly with calendar age in CC (F(1, 59) = 10.42; p < 0.01) and CVE (F(1, 88) = 40.34; p < 0.0001) but not in the AH strata, supporting the hypothesis of preferential elimination of less robust individuals along the aging trajectory under risk factor challenges.Vascular robustness may serve as a biomarker of vulnerability to CVD risk factor challenges, prognosticating otherwise undetectable elevated risk for premature CVD mortality. Keywords: Cardiovascular diseases, Risk factors, Robustness, Preventio