15 research outputs found

    Social Media and the Activist Toolkit: User Agreements, Corporate Interests, and the Information Infrastructure of Modern Social Movements

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    Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/91171/1/j.1460-2466.2012.01636.x.pd

    Milky Way Tomography IV: Dissecting Dust

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    We use SDSS photometry of 73 million stars to simultaneously obtain best-fit main-sequence stellar energy distribution (SED) and amount of dust extinction along the line of sight towards each star. Using a subsample of 23 million stars with 2MASS photometry, whose addition enables more robust results, we show that SDSS photometry alone is sufficient to break degeneracies between intrinsic stellar color and dust amount when the shape of extinction curve is fixed. When using both SDSS and 2MASS photometry, the ratio of the total to selective absorption, RVR_V, can be determined with an uncertainty of about 0.1 for most stars in high-extinction regions. These fits enable detailed studies of the dust properties and its spatial distribution, and of the stellar spatial distribution at low Galactic latitudes. Our results are in good agreement with the extinction normalization given by the Schlegel et al. (1998, SFD) dust maps at high northern Galactic latitudes, but indicate that the SFD extinction map appears to be consistently overestimated by about 20% in the southern sky, in agreement with Schlafly et al. (2010). The constraints on the shape of the dust extinction curve across the SDSS and 2MASS bandpasses support the models by Fitzpatrick (1999) and Cardelli et al. (1989). For the latter, we find an RV=3.0±0.1R_V=3.0\pm0.1(random) ±0.1\pm0.1(systematic) over most of the high-latitude sky. At low Galactic latitudes (|b|<5), we demonstrate that the SFD map cannot be reliably used to correct for extinction as most stars are embedded in dust, rather than behind it. We introduce a method for efficient selection of candidate red giant stars in the disk, dubbed "dusty parallax relation", which utilizes a correlation between distance and the extinction along the line of sight. We make these best-fit parameters, as well as all the input SDSS and 2MASS data, publicly available in a user-friendly format.Comment: Submitted to ApJ, 55 pages, 37 figure

    Mutations in sphingosine-1-phosphate lyase cause nephrosis with ichthyosis and adrenal insufficiency

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    Steroid-resistant nephrotic syndrome (SRNS) causes 15% of chronic kidney disease cases. A mutation in 1 of over 40 monogenic genes can be detected in approximately 30% of individuals with SRNS whose symptoms manifest before 25 years of age. However, in many patients, the genetic etiology remains unknown. Here, we have performed whole exome sequencing to identify recessive causes of SRNS. In 7 families with SRNS and facultative ichthyosis, adrenal insufficiency, immunodeficiency, and neurological defects, we identified 9 different recessive mutations in SGPL1, which encodes sphingosine-1-phosphate (S1P) lyase. All mutations resulted in reduced or absent SGPL1 protein and/or enzyme activity. Overexpression of cDNA representing SGPL1 mutations resulted in subcellular mislocalization of SGPL1. Furthermore, expression of WT human SGPL1 rescued growth of SGPL1-deficient dpl1. yeast strains, whereas expression of disease-associated variants did not. Immunofluorescence revealed SGPL1 expression in mouse podocytes and mesangial cells. Knockdown of Sgpl1 in rat mesangial cells inhibited cell migration, which was partially rescued by VPC23109, an S1P receptor antagonist. In Drosophila, Sply mutants, which lack SGPL1, displayed a phenotype reminiscent of nephrotic syndrome in nephrocytes. WT Sply, but not the disease-associated variants, rescued this phenotype. Together, these results indicate that SGPL1 mutations cause a syndromic form of SRNS

    Tools of Resistance

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    DIGIT Is a Conserved Long Noncoding RNA that Regulates GSC Expression to Control Definitive Endoderm Differentiation of Embryonic Stem Cells

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    Long noncoding RNAs (lncRNAs) exhibit diverse functions, including regulation of development. Here, we combine genome-wide mapping of SMAD3 occupancy with expression analysis to identify lncRNAs induced by activin signaling during endoderm differentiation of human embryonic stem cells (hESCs). We find that DIGIT is divergent to Goosecoid (GSC) and expressed during endoderm differentiation. Deletion of the SMAD3-occupied enhancer proximal to DIGIT inhibits DIGIT and GSC expression and definitive endoderm differentiation. Disruption of the gene encoding DIGIT and depletion of the DIGIT transcript reveal that DIGIT is required for definitive endoderm differentiation. In addition, we identify the mouse ortholog of DIGIT and show that it is expressed during development and promotes definitive endoderm differentiation of mouse ESCs. DIGIT regulates GSC in trans, and activation of endogenous GSC expression is sufficient to rescue definitive endoderm differentiation in DIGIT-deficient hESCs. Our study defines DIGIT as a conserved noncoding developmental regulator of definitive endoderm
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