233 research outputs found

    A Consistent Comparison of Bias Models using Observational Data

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    We investigate five different models for the dark matter halo bias, ie., the ratio of the fluctuations of mass tracers to those of the underlying mass, by comparing their cosmological evolution using optical QSO and galaxy bias data at different redshifts, consistently scaled to the WMAP7 cosmology. Under the assumption that each halo hosts one extragalactic mass tracer, we use a χ2\chi^2 minimization procedure to determine the free parameters of the bias models as well as to statistically quantify their ability to represent the observational data. Using the Akaike information criterion we find that the model that represents best the observational data is the Basilakos & Plionis (2001; 2003) model with the tracer merger extension of Basilakos, Plionis & Ragone-Figueroa (2008) model. The only other statistically equivalent model, as indicated by the same criterion, is the Tinker et al. (2010) model. Finally, we find an average, over the different models, dark matter halo mass that hosts optical QSOs of: Mh2.7(±0.6)×1012h1MM_h\simeq 2.7 (\pm 0.6) \times 10^{12} h^{-1} M_{\odot}, while the corresponding value for optical galaxies is: Mh6.3(±2.1)×1011h1MM_h\simeq 6.3 (\pm 2.1) \times 10^{11} h^{-1} M_{\odot}.Comment: MNRAS in press, 12 pages, 6 color figures, 4 table

    The Halo Mass-Bias Redshift Evolution in the Λ\LambdaCDM Cosmology

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    We derive an analytic model for the redshift evolution of linear-bias, allowing for interactions and merging of the mass-tracers, by solving a second order differential equation based on linear perturbation theory and the Friedmann-Lemaitre solutions of the cosmological field equations. We then study the halo-mass dependence of the bias evolution, using the dark matter halo distribution in a Λ\LambdaCDM simulation in order to calibrate the free parameters of the model. Finally, we compare our theoretical predictions with available observational data and find a good agreement. In particular, we find that the bias of optical QSO's evolve differently than those selected in X-rays and that their corresponding typical dark matter halo mass is 1013h1M\sim 10^{13} h^{-1} M_{\odot} and \magcir 5 \times 10^{13} h^{-1} M_{\odot}, respectively.Comment: 8 pages, 5 figures, accepted for publication in Ap

    Modelling the shapes of the largest gravitationally bound objects

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    We combine the physics of the ellipsoidal collapse model with the excursion set theory to study the shapes of dark matter halos. In particular, we develop an analytic approximation to the nonlinear evolution that is more accurate than the Zeldovich approximation; we introduce a planar representation of halo axis ratios, which allows a concise and intuitive description of the dynamics of collapsing regions and allows one to relate the final shape of a halo to its initial shape; we provide simple physical explanations for some empirical fitting formulae obtained from numerical studies. Comparison with simulations is challenging, as there is no agreement about how to define a non-spherical gravitationally bound object. Nevertheless, we find that our model matches the conditional minor-to-intermediate axis ratio distribution rather well, although it disagrees with the numerical results in reproducing the minor-to-major axis ratio distribution. In particular, the mass dependence of the minor-to-major axis distribution appears to be the opposite to what is found in many previous numerical studies, where low-mass halos are preferentially more spherical than high-mass halos. In our model, the high-mass halos are predicted to be more spherical, consistent with results based on a more recent and elaborate halo finding algorithm, and with observations of the mass dependence of the shapes of early-type galaxies. We suggest that some of the disagreement with some previous numerical studies may be alleviated if we consider only isolated halos.Comment: 15 pages, 8 figures. New appendix added, extended discussion. Matches version accepted by MNRA

    Multimodality of rich clusters from the SDSS DR8 within the supercluster-void network

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    We study the relations between the multimodality of galaxy clusters drawn from the SDSS DR8 and the environment where they reside. As cluster environment we consider the global luminosity density field, supercluster membership, and supercluster morphology. We use 3D normal mixture modelling, the Dressler-Shectman test, and the peculiar velocity of cluster main galaxies as signatures of multimodality of clusters. We calculate the luminosity density field to study the environmental densities around clusters, and to find superclusters where clusters reside. We determine the morphology of superclusters with the Minkowski functionals and compare the properties of clusters in superclusters of different morphology. We apply principal component analysis to study the relations between the multimodality parametres of clusters and their environment simultaneously. We find that multimodal clusters reside in higher density environment than unimodal clusters. Clusters in superclusters have higher probability to have substructure than isolated clusters. The superclusters can be divided into two main morphological types, spiders and filaments. Clusters in superclusters of spider morphology have higher probabilities to have substructure and larger peculiar velocities of their main galaxies than clusters in superclusters of filament morphology. The most luminous clusters are located in the high-density cores of rich superclusters. Five of seven most luminous clusters, and five of seven most multimodal clusters reside in spider-type superclusters; four of seven most unimodal clusters reside in filament-type superclusters. Our study shows the importance of the role of superclusters as high density environment which affects the properties of galaxy systems in them.Comment: 16 pages, 12 figures, 2 online tables, accepted for publication in Astronomy and Astrophysic

    High-resolution genome-wide cytosine methylation profiling with simultaneous copy number analysis and optimization for limited cell numbers

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    Many genome-wide assays involve the generation of a subset (or representation) of the genome following restriction enzyme digestion. The use of enzymes sensitive to cytosine methylation allows high-throughput analysis of this epigenetic regulatory process. We show that the use of a dual-adapter approach allows us to generate genomic representations that includes fragments of <200 bp in size, previously not possible when using the standard approach of using a single adapter. By expanding the representation to smaller fragments using HpaII or MspI, we increase the representation by these isoschizomers to more than 1.32 million loci in the human genome, representing 98.5% of CpG islands and 91.1% of refSeq promoters. This advance allows the development of a new, high-resolution version of our HpaII-tiny fragment Enrichment by Ligation-mediated PCR (HELP) assay to study cytosine methylation. We also show that the MspI representation generates information about copy-number variation, that the assay can be used on as little as 10 ng of DNA and that massively parallel sequencing can be used as an alternative to microarrays to read the output of the assay, making this a powerful discovery platform for studies of genomic and epigenomic abnormalities

    Widespread Hypomethylation Occurs Early and Synergizes with Gene Amplification during Esophageal Carcinogenesis

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    Although a combination of genomic and epigenetic alterations are implicated in the multistep transformation of normal squamous esophageal epithelium to Barrett esophagus, dysplasia, and adenocarcinoma, the combinatorial effect of these changes is unknown. By integrating genome-wide DNA methylation, copy number, and transcriptomic datasets obtained from endoscopic biopsies of neoplastic progression within the same individual, we are uniquely able to define the molecular events associated progression of Barrett esophagus. We find that the previously reported global hypomethylation phenomenon in cancer has its origins at the earliest stages of epithelial carcinogenesis. Promoter hypomethylation synergizes with gene amplification and leads to significant upregulation of a chr4q21 chemokine cluster and other transcripts during Barrett neoplasia. In contrast, gene-specific hypermethylation is observed at a restricted number of loci and, in combination with hemi-allelic deletions, leads to downregulatation of selected transcripts during multistep progression. We also observe that epigenetic regulation during epithelial carcinogenesis is not restricted to traditionally defined “CpG islands,” but may also occur through a mechanism of differential methylation outside of these regions. Finally, validation of novel upregulated targets (CXCL1 and 3, GATA6, and DMBT1) in a larger independent panel of samples confirms the utility of integrative analysis in cancer biomarker discovery

    Fouling mechanisms of ultrafiltration membranes fouled with whey model solutions

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    In this work, three ultrafiltration (UF) membranes with different molecular weight cut-offs (MWCOs) and made of different materials were fouled with several whey model solutions that consisted of bovine serum albumin (BSA) (1% w/w), BSA (1% w/w) and CaCl2 (0.06% w/w in calcium) and whey protein concentrate (WPC) with a total protein content of 45% w/w at three different concentrations (22.2, 33.3 and 44.4 g·L− 1). The influence of MWCO and membrane material on the fouling mechanism dominating the UF process was investigated. Experiments were performed using two flat-sheet organic membranes and a ceramic monotubular membrane whose MWCOs were 5, 30 and 15 kDa, respectively. Hermia's models adapted to crossflow UF, a combined model based on complete blocking and cake formation equations and a resistance-in-series model were fitted to permeate flux decline curves. The results demonstrated that permeate flux decline was accurately predicted by all the models studied. However, the models that fitted the best to permeate flux decline experimental data were the combined model and the resistance-in-series model. Therefore, complete blocking and cake formation were the predominant mechanisms for all the membranes and feed solutions tested.The authors of this work wish to gratefully acknowledge the financial support of the Spanish Ministry of Science and Innovation through the project CTM2010-20186.Corbatón Báguena, MJ.; Alvarez Blanco, S.; Vincent Vela, MC. (2015). Fouling mechanisms of ultrafiltration membranes fouled with whey model solutions. Desalination. 360:87-96. https://doi.org/10.1016/j.desal.2015.01.019S879636

    Solar Radiation and Tidal Exposure as Environmental Drivers of Enhalus acoroides Dominated Seagrass Meadows

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    There is strong evidence of a global long-term decline in seagrass meadows that is widely attributed to anthropogenic activity. Yet in many regions, attributing these changes to actual activities is difficult, as there exists limited understanding of the natural processes that can influence these valuable ecosystem service providers. Being able to separate natural from anthropogenic causes of seagrass change is important for developing strategies that effectively mitigate and manage anthropogenic impacts on seagrass, and promote coastal ecosystems resilient to future environmental change. The present study investigated the influence of environmental and climate related factors on seagrass biomass in a large ≈250 ha meadow in tropical north east Australia. Annual monitoring of the intertidal Enhalus acoroides (L.f.) Royle seagrass meadow over eleven years revealed a declining trend in above-ground biomass (54% significant overall reduction from 2000 to 2010). Partial Least Squares Regression found this reduction to be significantly and negatively correlated with tidal exposure, and significantly and negatively correlated with the amount of solar radiation. This study documents how natural long-term tidal variability can influence long-term seagrass dynamics. Exposure to desiccation, high UV, and daytime temperature regimes are discussed as the likely mechanisms for the action of these factors in causing this decline. The results emphasise the importance of understanding and assessing natural environmentally-driven change when interpreting the results of seagrass monitoring programs

    Enhanced Astrocytic Nitric Oxide Production and Neuronal Modifications in the Neocortex of a NOS2 Mutant Mouse

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    BACKGROUND: It has been well accepted that glial cells in the central nervous system (CNS) produce nitric oxide (NO) through the induction of a nitric oxide synthase isoform (NOS2) only in response to various insults. Recently we described rapid astroglial, NOS2-dependent, NO production in the neocortex of healthy mice on a time scale relevant to neuronal activity. To explore a possible role for astroglial NOS2 in normal brain function we investigated a NOS2 knockout mouse (B6;129P2-Nos2(tm1Lau)/J, Jackson Laboratory). Previous studies of this mouse strain revealed mainly altered immune responses, but no compensatory pathways and no CNS abnormalities have been reported. METHODOLOGY/PRINCIPAL FINDINGS: To our surprise, using NO imaging in brain slices in combination with biochemical methods we uncovered robust NO production by neocortical astrocytes of the NOS2 mutant. These findings indicate the existence of an alternative pathway that increases basal NOS activity. In addition, the astroglial mutation instigated modifications of neuronal attributes, shown by changes in the membrane properties of pyramidal neurons, and revealed in distinct behavioral abnormalities characterized by an increase in stress-related parameters. CONCLUSIONS/SIGNIFICANCE: The results strongly indicate the involvement of astrocytic-derived NO in modifying the activity of neuronal networks. In addition, the findings corroborate data linking NO signaling with stress-related behavior, and highlight the potential use of this genetic model for studies of stress-susceptibility. Lastly, our results beg re-examination of previous studies that used this mouse strain to examine the pathophysiology of brain insults, assuming lack of astrocytic nitrosative reaction
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