483 research outputs found

    A Uniformly Selected Sample of Low-mass Black Holes in Seyfert 1 Galaxies

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    We have conducted a systematic search of low-mass black holes (BHs) in active galactic nuclei (AGNs) with broad Halpha emission lines, aiming at building a homogeneous sample that is more complete than previous ones for fainter, less highly accreting sources. For this purpose, we developed a set of elaborate, automated selection procedures and applied it uniformly to the Fourth Data Release of the Sloan Digital Sky Survey. Special attention is given to AGN--galaxy spectral decomposition and emission-line deblending. We define a sample of 309 type 1 AGNs with BH masses in the range 8×1048 \times 10^4--2×1062 \times 10^6 \msun (with a median of 1.2×1061.2 \times 10^6 solar mass), using the virial mass estimator based on the broad Halpha line. About half of our sample of low-mass BHs differs from that of Greene & Ho, with 61 of them discovered here for the first time. Our new sample picks up more AGNs with low accretion rates: the Eddington ratios of the present sample range from < 0.01<~0.01 to ~1, with 30% below 0.1. This suggests that a significant fraction of low-mass BHs in the local Universe are accreting at low rates. The host galaxies of the low-mass BHs have luminosities similar to those of L∗L^* field galaxies, optical colors of Sbc spirals, and stellar spectral features consistent with a continuous star formation history with a mean stellar age of less than 1 Gyr.Comment: Accepted for publication in Ap

    Transcriptional impairment of β-catenin/E-cadherin complex is not associated with β-catenin mutations in colorectal carcinomas

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    We report the absence of β-catenin mutations in 63 sporadic colorectal carcinomas (SCRCs) with demonstrated decreased β-catenin and E-cadherin mRNA expression and E-cadherin protein expression in a subset of carcinomas examined, suggesting that β-catenin mutations are an extremely rare phenomenon in SCRCs and are not responsible for the transcriptional impairment of the β-catenin/E-cadherin adhesion complex observed in these tumours

    Electronic Structure Calculations with LDA+DMFT

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    The LDA+DMFT method is a very powerful tool for gaining insight into the physics of strongly correlated materials. It combines traditional ab-initio density-functional techniques with the dynamical mean-field theory. The core aspects of the method are (i) building material-specific Hubbard-like many-body models and (ii) solving them in the dynamical mean-field approximation. Step (i) requires the construction of a localized one-electron basis, typically a set of Wannier functions. It also involves a number of approximations, such as the choice of the degrees of freedom for which many-body effects are explicitly taken into account, the scheme to account for screening effects, or the form of the double-counting correction. Step (ii) requires the dynamical mean-field solution of multi-orbital generalized Hubbard models. Here central is the quantum-impurity solver, which is also the computationally most demanding part of the full LDA+DMFT approach. In this chapter I will introduce the core aspects of the LDA+DMFT method and present a prototypical application.Comment: 21 pages, 7 figures. Chapter of "Many-Electron Approaches in Physics, Chemistry and Mathematics: A Multidisciplinary View", eds. V. Bach and L. Delle Site, Springer 201

    Adenomatous Polyposis Coli Regulates Axon Arborization and Cytoskeleton Organization via Its N-Terminus

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    Conditional deletion of APC leads to marked disruption of cortical development and to excessive axonal branching of cortical neurons. However, little is known about the cell biological basis of this neuronal morphological regulation. Here we show that APC deficient cortical neuronal growth cones exhibit marked disruption of both microtubule and actin cytoskeleton. Functional analysis of the different APC domains revealed that axonal branches do not result from stabilized β-catenin, and that the C-terminus of APC containing microtubule regulatory domains only partially rescues the branching phenotype. Surprisingly, the N-terminus of APC containing the oligomerization domain and the armadillo repeats completely rescues the branching and cytoskeletal abnormalities. Our data indicate that APC is required for appropriate axon morphological development and that the N-terminus of APC is important for regulation of the neuronal cytoskeleton

    Mutations of the β- and γ-catenin genes are uncommon in human lung, breast, kidney, cervical and ovarian carcinomas

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    β-catenin forms complexes with Tcf and Lef-1 and functions as a transcriptional activator in the Wnt signalling pathway. Although recent investigations have been focused on the role of the adenomatous polyposis coli (APC)/ β-catenin/Tcf pathway in human tumorigenesis, there have been very few reports on mutations of the β-catenin gene in a variety of tumour types. Using PCR and single-strand conformational polymorphism analysis, we examined 93 lung, 9 breast, 6 kidney, 19 cervical and 7 ovarian carcinoma cell lines for mutations in exon 3 of the β-catenin gene. In addition, we tested these same samples for mutations in the NH2-terminal regulatory region of the γ-catenin gene. Mutational analysis for the entire coding region of β-catenin cDNA was also undertaken in 20 lung, 9 breast, 5 kidney and 6 cervical carcinoma cell lines. Deletion of most β-catenin coding exons was confirmed in line NCI-H28 (lung mesothelioma) and a silent mutation at codon 214 in exon 5 was found in HeLa (cervical adenocarcinoma). A missense mutation at codon 19 and a silent mutation at codon 28 in the NH2-terminal regulatory region of the γ-catenin gene were found in H1726 (squamous cell lung carcinoma) and H1048 (small cell lung carcinoma), respectively. Neither deletions nor mutations of these genes were detected in the other cell lines examined. These results suggest that β- and γ-catenins are infrequent mutational targets during development of human lung, breast, kidney, cervical and ovarian carcinomas. © 2001 Cancer Research Campaign http://www.bjcancer.co
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