112 research outputs found

    Dark matter halo properties from galaxy-galaxy lensing

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    We present results for a galaxy-galaxy lensing study based on imaging data from the Canada-France-Hawaii Telescope Legacy Survey Wide. From a 12 million object multi-colour catalogue for 124 deg^2 of photometric data in the u*g'r'i'z' filters we compute photometric redshifts (with a scatter of \sigma_{\Delta z/(1+z)} = 0.033 and an outlier rate of \eta=2.0 per cent for i'<=22.5) and extract galaxy shapes down to i'=24.0. We select a sample of lenses and sources with 0.05 < z_d <= 1 and 0.05 < z_s <= 2. We fit three different galaxy halo profiles to the lensing signal, a singular isothermal sphere (SIS), a truncated isothermal sphere (BBS) and a universal density profile (NFW). We derive velocity dispersions by fitting an SIS out to 100 h^{-1} kpc to the excess surface mass density \Delta\Sigma and perform maximum likelihood analyses out to a maximum scale of 2 h^{-1} Mpc to obtain halo parameters and scaling relations. We find luminosity scaling relations of \sigma_{red} ~ L^{0.24+-0.03} for the red lens sample, \sigma_{blue} ~ L^{0.23+-0.03} for blue lenses and \sigma ~ L^{0.29+-0.02} for the combined lens sample with zeropoints of \sigma*_{red}=162+-2 km/s, \sigma*_{blue}=115+-3 km/s and \sigma*=135+-2 km/s at a chosen reference luminosity L*_{r'} = 1.6 \times 10^10 h^{-2} L_{r',sun}. The steeper slope for the combined sample is due to the different zeropoints of the blue and red lenses and the fact that blue lenses dominate at low luminosities and red lenses at high luminosities. The mean effective redshifts for the lens samples are =0.28 for red lenses, =0.35 for blue lenses and =0.34 for the combined lens sample.Comment: 62 pages, 55 figures, accepted for publication in MNRAS, abridged abstract, includes corrections from final proof. Our created catalogues (photometry, photometric redshifts and shears) are publicly available at http://www.usm.uni-muenchen.de/people/stella/GGL

    Activation of apoptotic pathways in experimental acute afterload-induced right ventricular failure

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    Objective: The pathobiology of persistent right ventricular failure observed after an acute increase in right ventricular afterload remains incompletely understood. We hypothesized that persistent right ventricular dysfunction might be related to activation of apoptotic pathways. Design: Prospective, randomized, controlled animal study. Setting: University research laboratory. Subjects: Mongrel dogs. Interventions: Fourteen anesthetized dogs were randomized to a transient 90-min pulmonary artery constriction operation to induce persistent right ventricular failure or to a sham operation followed 30 mins later by hemodynamic measurements and sampling of cardiac tissue. Measurements and main results: We evaluated effective arterial elastance to estimate right ventricular afterload and end-systolic elastance to estimate right ventricular contractility. Transient increase in pulmonary artery pressure persistently increased effective arterial elastance from 0.75 ± 0.08 to 1.37 ± 0.18 mm Hg/mL and decreased end-systolic elastance from 1.06 ± 0.09 to 0.49 ± 0.09 mm Hg/mL, end-systolic elastance/effective arterial elastance from 1.44 ± 0.06 to 0.34 ± 0.03, and cardiac output from 3.78 ± 0.16 to 1.46 ± 0.10 L/min, indicating right ventricular failure. At the pathobiologic level, we assessed apoptosis by real-time quantitative polymerase chain reaction, Western blotting, enzyme-linked immunosorbent assay, and immunohistochemistry. As compared with the sham-operated group, and with the left ventricle in animals with persistent right ventricular failure, there were decreased right ventricular and septal expressions of Bcl-2 with no changes in expressions of Bax, resulting in an increased Bax/Bcl-2 ratio. Right ventricular and septal Bcl-XL, and right ventricular Bcl-w gene expressions were decreased as compared with the sham-operated group, whereas Bak gene expression did not change. There were activations of right ventricular caspases-8 and-9 and of right ventricular and septal caspase-3. Diffuse right ventricular and septal apoptosis was confirmed by terminal deoxynucleotidyl transferase dUTP nick-end labeling staining. There were also increased right ventricular and septal protein expressions of tumor necrosis factor-alpha. Conclusions: Acute afterload-induced persistent right ventricular failure appears to be related to an early activation of apoptotic pathways and to a local overexpression of tumor necrosis factor-alpha, a proinflammatory cytokine. Copyright © 2010 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

    X-Ray Groups of Galaxies in the Aegis Deep and Wide Fields

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    We present the results of a search for extended X-ray sources and their corresponding galaxy groups from 800-ks Chandra coverage of the All-wavelength Extended Groth Strip International Survey (AEGIS). This yields one of the largest X-ray selected galaxy group catalogs from a blind survey to date. The red-sequence technique and spectroscopic redshifts allow us to identify 100% of reliable sources, leading to a catalog of 52 galaxy groups. The groups span the redshift range z0.0661.544z\sim0.066-1.544 and virial mass range M2001.34×10131.33×1014MM_{200}\sim1.34\times 10^{13}-1.33\times 10^{14}M_\odot. For the 49 extended sources which lie within DEEP2 and DEEP3 Galaxy Redshift Survey coverage, we identify spectroscopic counterparts and determine velocity dispersions. We select member galaxies by applying different cuts along the line of sight or in projected spatial coordinates. A constant cut along the line of sight can cause a large scatter in scaling relations in low-mass or high-mass systems depending on the size of cut. A velocity dispersion based virial radius can more overestimate velocity dispersion in comparison to X-ray based virial radius for low mass systems. There is no significant difference between these two radial cuts for more massive systems. Independent of radial cut, overestimation of velocity dispersion can be created in case of existence of significant substructure and also compactness in X-ray emission which mostly occur in low mass systems. We also present a comparison between X-ray galaxy groups and optical galaxy groups detected using the Voronoi-Delaunay method (VDM) for DEEP2 data in this field.Comment: Accepted for publication in AP

    A Multiband Study of the Galaxy Populations of the First Four Sunyaev--Zeldovich Effect selected Galaxy Clusters

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    We present first results of an examination of the optical properties of the galaxy populations in SZE selected galaxy clusters. Using clusters selected by the South Pole Telescope survey and deep multiband optical data from the Blanco Cosmology Survey, we measure the radial profile, the luminosity function, the blue fraction and the halo occupation number of the galaxy populations of these four clusters with redshifts ranging from 0.3 to 1. Our goal is to understand whether there are differences among the galaxy populations of these SZE selected clusters and previously studied clusters selected in the optical and the X-ray. The radial distributions of galaxies in the four systems are consistent with NFW profiles with a galaxy concentration of 3 to 6. We show that the characteristic luminosities in grizgriz bands are consistent with passively evolving populations emerging from a single burst at redshift z=3z=3. The faint end power law slope of the luminosity function is found to be on average α1.2\alpha \approx -1.2 in griz. Halo occupation numbers (to m+2m^*+2) for these systems appear to be consistent with those based on X-ray selected clusters. The blue fraction estimated to 0.36L0.36L^*, for the three lower redshift systems, suggests an increase with redshift, although with the current sample the uncertainties are still large. Overall, this pilot study of the first four clusters provides no evidence that the galaxy populations in these systems differ significantly from those in previously studied cluster populations selected in the X-ray or the optical.Comment: 12 pages, 12 figures and 3 tables. Accepted for publication in Ap

    Proportional Relations Between Systolic, Diastolic and Mean Pulmonary Artery Pressure are Explained by Vascular Properties

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    Recently, it was shown that proportional relationships exist between systolic, diastolic and mean pulmonary artery pressure (Psys, Pdia and Pmean) and that they are maintained under various conditions in both health and disease. An arterial-ventricular interaction model was used to study the contribution of model parameters to the ratios Psys/Pmean, and Pdia/Pmean. The heart was modeled by a time-varying elastance function, and the arterial system by a three-element windkessel model consisting of peripheral resistance, Rp, arterial compliance Ca, and pulmonary artery characteristic impedance Z0. Baseline model parameters were estimated in control subjects and compared to values estimated in patients with pulmonary hypertension. Results indicate that experimentally derived ratios Psys/Pmean and Pdia/Pmean could be accurately reproduced using our model (1.59 and 0.61 vs. 1.55 and 0.64, respectively). Sensitivity analysis showed that the (empirical) constancy of Psys/Pmean and Pdia/Pmean was primarily based on the inverse hyperbolic relation between total vascular resistance (RT; calculated as Rp + Z0) and Ca, (i.e. constant RTCa product). Of the cardiac parameters, only heart rate affected the pressure ratios, but the contribution was small. Therefore, we conclude that proportional relations between systolic, diastolic and mean pulmonary artery pressure result from the constancy of RTCa thus from pulmonary arterial properties, with only little influence of heart rate

    Hypoxia, not pulmonary vascular pressure induces blood flow through intrapulmonary arteriovenous anastomoses

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    Blood flow through intrapulmonary arteriovenous anastomoses (IPAVA) is increased with exposure to acute hypoxia and has been associated with pulmonary artery systolic pressure (PASP). We aimed to determine the direct relationship between blood flow through IPAVA and PASP in 10 participants with no detectable intracardiac shunt by comparing: (1) isocapnic hypoxia (control); (2) isocapnic hypoxia with oral administration of acetazolamide (AZ; 250 mg, three times-a-day for 48 h) to prevent increases in PASP, and (3) isocapnic hypoxia with AZ and 8.4% NaHCO3 infusion (AZ+HCO3-) to control for AZ-induced acidosis. Isocapnic hypoxia (20 min) was maintained by end-tidal forcing, blood flow through IPAVA was determined by agitated saline contrast echocardiography and PASP was estimated by Doppler ultrasound. Arterial blood samples were collected at rest before each isocapnic-hypoxia condition to determine pH, [HCO3-], and PaCO2. AZ decreased pH (-0.08 ± 0.01), [HCO3-] (-7.1 ± 0.7 mmol/l), and PaCO2 (-4.5 ± 1.4 mmHg; p<0.01), while intravenous NaHCO3 restored arterial blood gas parameters to control levels. Although PASP increased from baseline in all three hypoxic conditions (p<0.05), a main effect of condition expressed an 11 ± 2% reduction in PASP from control (p<0.001) following AZ administration while intravenous NaHCO3 partially restored the PASP response to isocapnic hypoxia. Blood flow through IPAVA increased during exposure to isocapnic hypoxia (p<0.01) and was unrelated to PASP, cardiac output and pulmonary vascular resistance for all conditions. In conclusion, isocapnic hypoxia induces blood flow through IPAVA independent of changes in PASP and the influence of AZ on the PASP response to isocapnic hypoxia is dependent upon the H+ concentration or PaCO2. Abbreviations list: AZ, acetazolamide; FEV1, forced expiratory volume in 1 second; FIO2, fraction of inspired oxygen; FVC, forced vital capacity; Hb, total haemoglobin; HPV, hypoxic pulmonary vasoconstriction; HR, heart rate; IPAVA, intrapulmonary arteriovenous anastomoses; MAP, mean arterial pressure; PASP, pulmonary artery systolic pressure; PETCO2, end-tidal partial pressure of carbon dioxide; PETO2, end-tidal partial pressure of oxygen; PFO, patent foramen ovale; PVR, pulmonary vascular resistance; Q̇c, cardiac output; RVOT, right ventricular outflow tract; SpO2, oxyhaemoglobin saturation; SV, stroke volume; TRV, tricuspid regurgitant velocity; V̇E, minute ventilation; VTI, velocity-time integra

    Mutation of von Hippel–Lindau Tumour Suppressor and Human Cardiopulmonary Physiology

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    BACKGROUND: The von Hippel–Lindau tumour suppressor protein–hypoxia-inducible factor (VHL–HIF) pathway has attracted widespread medical interest as a transcriptional system controlling cellular responses to hypoxia, yet insights into its role in systemic human physiology remain limited. Chuvash polycythaemia has recently been defined as a new form of VHL-associated disease, distinct from the classical VHL-associated inherited cancer syndrome, in which germline homozygosity for a hypomorphic VHL allele causes a generalised abnormality in VHL–HIF signalling. Affected individuals thus provide a unique opportunity to explore the integrative physiology of this signalling pathway. This study investigated patients with Chuvash polycythaemia in order to analyse the role of the VHL–HIF pathway in systemic human cardiopulmonary physiology. METHODS AND FINDINGS: Twelve participants, three with Chuvash polycythaemia and nine controls, were studied at baseline and during hypoxia. Participants breathed through a mouthpiece, and pulmonary ventilation was measured while pulmonary vascular tone was assessed echocardiographically. Individuals with Chuvash polycythaemia were found to have striking abnormalities in respiratory and pulmonary vascular regulation. Basal ventilation and pulmonary vascular tone were elevated, and ventilatory, pulmonary vasoconstrictive, and heart rate responses to acute hypoxia were greatly increased. CONCLUSIONS: The features observed in this small group of patients with Chuvash polycythaemia are highly characteristic of those associated with acclimatisation to the hypoxia of high altitude. More generally, the phenotype associated with Chuvash polycythaemia demonstrates that VHL plays a major role in the underlying calibration and homeostasis of the respiratory and cardiovascular systems, most likely through its central role in the regulation of HIF
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