81 research outputs found

    A Spectroscopic Survey of Faint Quasars in the SDSS Deep Stripe: I. Preliminary Results from the Co-added Catalog

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    In this paper we present the first results of a deep spectroscopic survey of faint quasars in the Sloan Digital Sky Survey (SDSS) Southern Survey, a deep survey carried out by repeatedly imaging a 270 deg^2 area. Quasar candidates were selected from the deep data with good completeness over 0<z<5, and 2 to 3 magnitudes fainter than the SDSS main survey. Spectroscopic follow-up was carried out on the 6.5m MMT with Hectospec. The preliminary sample of this SDSS faint quasar survey (hereafter SFQS) covers ~ 3.9 deg^2, contains 414 quasars, and reaches g=22.5. The overall selection efficiency is ~ 66% (~ 80% at g<21.5); the efficiency in the most difficult redshift range (2<z<3) is better than 40%. We use the 1/V_{a} method to derive a binned estimate of the quasar luminosity function (QLF) and model the QLF using maximum likelihood analysis. The best model fits confirm previous results showing that the QLF has steep slopes at the bright end and much flatter slopes (-1.25 at z<2.0 and -1.55 at z>2.0) at the faint end, indicating a break in the QLF slope. Using a luminosity-dependent density evolution model, we find that the quasar density at M_{g}<-22.5 peaks at z~2, which is later in cosmic time than the peak of z~2.5 found from surveys of more luminous objects. The SFQS QLF is consistent with the results of the 2dF QSO Redshift Survey, the SDSS, and the 2dF-SDSS LRG and QSO Survey, but probes fainter quasars. We plan to obtain more quasars from future observations and establish a complete faint quasar sample with more than 1000 objects over 10 deg^2.Comment: 25 pages, 13 figures, accepted for publication in A

    Clinical and molecular genetic features of pulmonary hypertension in patients with hereditary hemorrhagic telangiectasia

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    BACKGROUND: Most patients with familial primary pulmonary hypertension have defects in the gene for bone morphogenetic protein receptor II (BMPR2), a member of the transforming growth factor beta (TGF-beta) superfamily of receptors. Because patients with hereditary hemorrhagic telangiectasia may have lung disease that is indistinguishable from primary pulmonary hypertension, we investigated the genetic basis of lung disease in these patients. METHODS: We evaluated members of five kindreds plus one individual patient with hereditary hemorrhagic telangiectasia and identified 10 cases of pulmonary hypertension. In the two largest families, we used microsatellite markers to test for linkage to genes encoding TGF-beta-receptor proteins, including endoglin and activin-receptor-like kinase 1 (ALK1), and BMPR2. In subjects with hereditary hemorrhagic telangiectasia and pulmonary hypertension, we also scanned ALK1 and BMPR2 for mutations. RESULTS: We identified suggestive linkage of pulmonary hypertension with hereditary hemorrhagic telangiectasia on chromosome 12q13, a region that includes ALK1. We identified amino acid changes in activin-receptor-like kinase 1 that were inherited in subjects who had a disorder with clinical and histologic features indistinguishable from those of primary pulmonary hypertension. Immunohistochemical analysis in four subjects and one control showed pulmonary vascular endothelial expression of activin-receptor-like kinase 1 in normal and diseased pulmonary arteries. CONCLUSIONS: Pulmonary hypertension in association with hereditary hemorrhagic telangiectasia can involve mutations in ALK1. These mutations are associated with diverse effects, including the vascular dilatation characteristic of hereditary hemorrhagic telangiectasia and the occlusion of small pulmonary arteries that is typical of primary pulmonary hypertension
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