190 research outputs found

    Observational estimates of the initial power spectrum at small scale from Lyman-α\alpha absorbers

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    We present a new method of measuring the power spectrum of initial perturbations to an unprecedently small scale of \sim 10h1h^{-1} kpc. We apply this method to a sample of 4500 Ly-α\alpha absorbers and recover the cold dark matter (CDM) like power spectrum at scales 300h1\geq 300h^{-1}kpc with a precision of \sim 10%. However at scales 10300h1\sim 10 - 300 h^{-1}kpc the measured and CDM--like spectra are noticeable different. This result suggests a complex inflation with generation of excess power at small scales. The magnitude and reliability of these deviations depend also upon the possible incompleteness of our sample and poorly understood process of formation of weak absorbers. Confirmation of the CDM--like shape of the initial power spectrum or detection of its distortions at small scales are equally important for widely discussed problems of physics of the early Universe, galaxy formation, and reheating of the Universe. Our method links the observed mass function of absorbers with the correlation function of the initial velocity field and therefore it avoids the Nyquist restrictions limiting the investigations based on the smoothed flux or density fields. The physical model of absorbers adopted here asserts that they are formed in the course of both linear and nonlinear adiabatic or shock compression of dark matter (DM) and gaseous matter. At scales 1h1\geq 1h^{-1}Mpc all characteristics of the DM component and, in particular, their redshift distribution are found to be consistent with theoretical expectations for Gaussian initial perturbations with a CDM--like power spectrum.Comment: 22 pages, 10 figure

    Galaxy Clusters in the Line of Sight to Background Quasars: II. Environmental effects on the sizes of baryonic halo sizes

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    Based on recent results on the frequency of MgII absorption line systems in the "QSO behind RCS clusters" survey (QbC), we analyse the effects of the cluster environment on the sizes of baryonic haloes around galaxies. We use two independent models, i) an empirical halo occupation model which fits current measurements of the clustering and luminosity function of galaxies at low and high redshifts, and ii) the GALFORM semi-analytic model of galaxy formation, which follows the evolution of the galaxy population from first principles, adjusted to match the statistics of low and high redshift galaxies. In both models we constrain the MgII halo sizes of field and cluster galaxies using observational results on the observed MgII statistics. Our results for the field are in good agreement with previous works, indicating a typical \mgii\ halo size of $r_MgII ~ 50h_71^-1kpc in the semi-analytic model, and slightly lower in the halo occupation number approach. For the cluster environment, we find that both models require a median MgII halo size of r_MgII< 10h_71^-1kpc in order to reproduce the observed statistics on absorption line systems in clusters of galaxies. Based on the Chen & Tinker (2008) result that stronger systems occur closer to the MgII halo centre, we find that strong absorption systems in clusters of galaxies occur at roughly a fixed fraction of the cold-warm halo size out to 1h_71^-1Mpc from the cluster centres. In contrast, weaker absorption systems appear to occur at progressively shorter relative fractions of this halo as the distance to the cluster centre decreases.Comment: 12 pages, 8 figures, accepted for publication in MNRA

    Propensity score estimation in the presence of length‐biased sampling: a non‐parametric adjustment approach

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    The pervasive use of prevalent cohort studies on disease duration increasingly calls for an appropriate methodology to account for the biases that invariably accompany samples formed by such data. It is well known, for example, that subjects with shorter lifetime are less likely to be present in such studies. Moreover, certain covariate values could be preferentially selected into the sample, being linked to the long‐term survivors. The existing methodology for estimating the propensity score using data collected on prevalent cases requires the correct conditional survival/hazard function given the treatment and covariates. This requirement can be alleviated if the disease under study has stationary incidence, the so‐called stationarity assumption. We propose a non‐parametric adjustment technique based on a weighted estimating equation for estimating the propensity score, which does not require modeling the conditional survival/hazard function when the stationarity assumption holds. The estimator's large‐sample properties are established, and its small‐sample behavior is studied via simulation. The estimated propensity score is utilized to estimate the survival curves. Copyright © 2014 John Wiley & Sons, Ltd.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/106732/1/sta446.pd

    Multivariate proteomic profiling identifies novel accessory proteins of coated vesicles.

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    Despite recent advances in mass spectrometry, proteomic characterization of transport vesicles remains challenging. Here, we describe a multivariate proteomics approach to analyzing clathrin-coated vesicles (CCVs) from HeLa cells. siRNA knockdown of coat components and different fractionation protocols were used to obtain modified coated vesicle-enriched fractions, which were compared by stable isotope labeling of amino acids in cell culture (SILAC)-based quantitative mass spectrometry. 10 datasets were combined through principal component analysis into a "profiling" cluster analysis. Overall, 136 CCV-associated proteins were predicted, including 36 new proteins. The method identified >93% of established CCV coat proteins and assigned >91% correctly to intracellular or endocytic CCVs. Furthermore, the profiling analysis extends to less well characterized types of coated vesicles, and we identify and characterize the first AP-4 accessory protein, which we have named tepsin. Finally, our data explain how sequestration of TACC3 in cytosolic clathrin cages causes the severe mitotic defects observed in auxilin-depleted cells. The profiling approach can be adapted to address related cell and systems biological questions

    CCR2 and CXCR3 agonistic chemokines are differently expressed and regulated in human alveolar epithelial cells type II

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    The attraction of leukocytes from circulation to inflamed lungs depends on the activation of both the leukocytes and the resident cells within the lung. In this study we determined gene expression and secretion patterns for monocyte chemoattractant protein-1 (MCP-1/CCL2) and T-cell specific CXCR3 agonistic chemokines (Mig/CXCL9, IP-10/CXCL10, and I-TAC/CXCL11) in TNF-α-, IFN-γ-, and IL-1β-stimulated human alveolar epithelial cells type II (AEC-II). AEC-II constitutively expressed high level of CCL2 mRNA in vitro and in situ , and released CCL2 protein in vitro . Treatment of AEC-II with proinflammatory cytokines up-regulated both CCL2 mRNA expression and release of immunoreactive CCL2, whereas IFN-γ had no effect on CCL2 release. In contrast, CXCR3 agonistic chemokines were not detected in freshly isolated AEC-II or in non-stimulated epithelial like cell line A549. IFN-γ, alone or in combination with IL-1β and TNF-α resulted in an increase in CXCL10, CXCL11, and CXCL9 mRNA expression and generation of CXCL10 protein by AEC-II or A549 cells. CXCL10 gene expression and secretion were induced in dose-dependent manner after cytokine-stimulation of AEC-II with an order of potency IFN-γ>>IL-1β ≥ TNF-α. Additionally, we localized the CCL2 and CXCL10 mRNAs in human lung tissue explants by in situ hybridization, and demonstrated the selective effects of cytokines and dexamethasone on CCL2 and CXCL10 expression. These data suggest that the regulation of the CCL2 and CXCL10 expression exhibit significant differences in their mechanisms, and also demonstrate that the alveolar epithelium contributes to the cytokine milieu of the lung, with the ability to respond to locally generated cytokines and to produce potent mediators of the local inflammatory response
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