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Sökning: WFRF:(Tak Paul P) > (2014)

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1.
  • Chen, Jo-Hsin, et al. (författare)
  • HERSCHEL HIFI OBSERVATIONS OF O-2 TOWARD ORION: SPECIAL CONDITIONS FOR SHOCK ENHANCED EMISSION
  • 2014
  • Ingår i: Astrophysical Journal. - 1538-4357 .- 0004-637X. ; 793:2, s. Article nr. 111 -
  • Tidskriftsartikel (refereegranskat)abstract
    • We report observations of molecular oxygen (O-2) rotational transitions at 487 GHz, 774 GHz, and 1121 GHz toward Orion Peak A. The O-2 lines at 487 GHz and 774 GHz are detected at velocities of 10-12 km s(-1) with line widths similar to 3 km s(-1); however, the transition at 1121 GHz is not detected. The observed line characteristics, combined with the results of earlier observations, suggest that the region responsible for the O-2 emission is similar or equal to 9" (6 x 10(16) cm) in size, and is located close to the H-2 Peak 1 position (where vibrationally excited H-2 emission peaks), and not at Peak A, 23" away. The peak O-2 column density is similar to 1.1 x 10(18) cm(-2). The line velocity is close to that of the 621 GHz water maser emission found in this portion of the Orion Molecular Cloud, and having a shock with velocity vector lying nearly in the plane of the sky is consistent with producing maximum maser gain along the line of sight. The enhanced O-2 abundance compared to that generally found in dense interstellar clouds can be explained by passage of a low-velocity C shock through a clump with preshock density 2 x 10(4) cm(-3), if a reasonable flux of UV radiation is present. The postshock O-2 can explain the emission from the source if its line-of-sight dimension is similar or equal to 10 times larger than its size on the plane of the sky. The special geometry and conditions required may explain why O-2 emission has not been detected in the cores of other massive star-forming molecular clouds.
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2.
  • Okada, Yukinori, et al. (författare)
  • Genetics of rheumatoid arthritis contributes to biology and drug discovery
  • 2014
  • Ingår i: Nature. - : Nature Publishing Group. - 0028-0836 .- 1476-4687. ; 506:7488, s. 376-381
  • Tidskriftsartikel (refereegranskat)abstract
    • A major challenge in human genetics is to devise a systematic strategy to integrate disease-associated variants with diverse genomic and biological data sets to provide insight into disease pathogenesis and guide drug discovery for complex traits such as rheumatoid arthritis (RA)(1). Here we performed a genome-wide association study meta-analysis in a total of >100,000 subjects of European and Asian ancestries (29,880 RA cases and 73,758 controls), by evaluating similar to 10 million single-nucleotide polymorphisms. We discovered 42 novel RA risk loci at a genome-wide level of significance, bringing the total to 101 (refs 2-4). We devised an in silico pipeline using established bioinformatics methods based on functional annotation(5), cis-acting expression quantitative trait loci(6) and pathway analyses(7-9)-as well as novel methods based on genetic overlap with human primary immunodeficiency, haematological cancer somatic mutations and knockout mouse phenotypes-to identify 98 biological candidate genes at these 101 risk loci. We demonstrate that these genes are the targets of approved therapies for RA, and further suggest that drugs approved for other indications may be repurposed for the treatment of RA. Together, this comprehensive genetic study sheds light on fundamental genes, pathways and cell types that contribute to RA pathogenesis, and provides empirical evidence that the genetics of RA can provide important information for drug discovery.
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