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Träfflista för sökning "WFRF:(Tong S. P.) srt2:(2006-2009)"

Search: WFRF:(Tong S. P.) > (2006-2009)

  • Result 1-7 of 7
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1.
  • Ablikim, M., et al. (author)
  • Measurements of (XcJ)-> K+K-K+K- decays
  • 2006
  • In: Physics Letters B. - : Elsevier BV. - 0370-2693 .- 1873-2445. ; 642:3, s. 197-202
  • Journal article (peer-reviewed)abstract
    • Using 14M psi(2S) events taken with the BESII detector, chi(cJ) -> 2(K+K-) decays are studied. For the four-kaon final state, the branching fractions are B(chi(c0,1,2) ->.2(K+K-)) = (3.48 +/- 0.23 +/- 0.47) x 10(-3), (0.70 +/- 0.13 +/- 0.10) x 10(-3), and (2.17 +/- 0.20 +/- 0.31) x 10(-3). For the phi K+K- final state, the branching fractions, which are measured for the first time, are B(chi(c0,1,2) -> phi K+K-) = (1.03 +/- 0.22 +/- 0.15) x 10(-3), (0.46 +/- 0.16 +/- 0.06) x 10(-3), and (1.67 +/- 0.26 +/- 0.24) x 10(-4). For the phi phi final state, B(chi(c0,2) -> phi phi) = (0.94 +/- 0.21 +/- 0.13) x 10(-3) and (1.70 +/- 0.30 +/- 0.25) x 10(-3).
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2.
  • Graslund, S, et al. (author)
  • Protein production and purification
  • 2008
  • In: Nature methods. - : Springer Science and Business Media LLC. - 1548-7105 .- 1548-7091. ; 5:2, s. 135-146
  • Journal article (peer-reviewed)
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3.
  • Sodergren, Erica, et al. (author)
  • The genome of the sea urchin Strongylocentrotus purpuratus.
  • 2006
  • In: Science. - : American Association for the Advancement of Science (AAAS). - 1095-9203 .- 0036-8075. ; 314:5801, s. 941-52
  • Journal article (peer-reviewed)abstract
    • We report the sequence and analysis of the 814-megabase genome of the sea urchin Strongylocentrotus purpuratus, a model for developmental and systems biology. The sequencing strategy combined whole-genome shotgun and bacterial artificial chromosome (BAC) sequences. This use of BAC clones, aided by a pooling strategy, overcame difficulties associated with high heterozygosity of the genome. The genome encodes about 23,300 genes, including many previously thought to be vertebrate innovations or known only outside the deuterostomes. This echinoderm genome provides an evolutionary outgroup for the chordates and yields insights into the evolution of deuterostomes.
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4.
  • Smith, A., et al. (author)
  • LunarEX-a proposal to cosmic vision
  • 2009
  • In: Experimental Astronomy. - : Springer Science and Business Media LLC. - 0922-6435 .- 1572-9508. ; 23:3, s. 711-740
  • Journal article (peer-reviewed)
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5.
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6.
  • Demetris, Anthony J, et al. (author)
  • Liver biopsy interpretation for causes of late liver allograft dysfunction.
  • 2006
  • In: Hepatology (Baltimore, Md.). - : Ovid Technologies (Wolters Kluwer Health). - 0270-9139 .- 1527-3350. ; 44:2, s. 489-501
  • Journal article (peer-reviewed)abstract
    • Evaluation of needle biopsies and extensive clinicopathological correlation play an important role in the determination of liver allograft dysfunction occurring more than 1 year after transplantation. Interpretation of these biopsies can be quite difficult because of the high incidence of recurrent diseases that show histopathological, clinical, and serological features that overlap with each other and with rejection. Also, more than one insult can contribute to allograft injury. In an attempt to enable centers to compare and pool results, improve therapy, and better understand pathophysiological disease mechanisms, the Banff Working Group on Liver Allograft Pathology herein proposes a set of consensus criteria for the most common and problematic causes of late liver allograft dysfunction, including late-onset acute and chronic rejection, recurrent and new-onset viral and autoimmune hepatitis, biliary strictures, and recurrent primary biliary cirrhosis and primary sclerosing cholangitis. A discussion of differential diagnosis is also presented.
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7.
  • Prokunina-Olsson, Ludmila, et al. (author)
  • Tissue-specific alternative splicing of TCF7L2
  • 2009
  • In: Human Molecular Genetics. - : Oxford University Press (OUP). - 0964-6906 .- 1460-2083. ; 18:20, s. 3795-3804
  • Journal article (peer-reviewed)abstract
    • Common variants in the transcription factor 7-like 2 (TCF7L2) gene have been identified as the strongest genetic risk factors for type 2 diabetes (T2D). However, the mechanisms by which these non-coding variants increase risk for T2D are not well-established. We used 13 expression assays to survey mRNA expression of multiple TCF7L2 splicing forms in up to 380 samples from eight types of human tissue (pancreas, pancreatic islets, colon, liver, monocytes, skeletal muscle, subcutaneous adipose tissue and lymphoblastoid cell lines) and observed a tissue-specific pattern of alternative splicing. We tested whether the expression of TCF7L2 splicing forms was associated with single nucleotide polymorphisms (SNPs), rs7903146 and rs12255372, located within introns 3 and 4 of the gene and most strongly associated with T2D. Expression of two splicing forms was lower in pancreatic islets with increasing counts of T2D-associated alleles of the SNPs: a ubiquitous splicing form (P = 0.018 for rs7903146 and P = 0.020 for rs12255372) and a splicing form found in pancreatic islets, pancreas and colon but not in other tissues tested here (P = 0.009 for rs12255372 and P = 0.053 for rs7903146). Expression of this form in glucose-stimulated pancreatic islets correlated with expression of proinsulin (r(2) = 0.84-0.90, P < 0.00063). In summary, we identified a tissue-specific pattern of alternative splicing of TCF7L2. After adjustment for multiple tests, no association between expression of TCF7L2 in eight types of human tissue samples and T2D-associated genetic variants remained significant. Alternative splicing of TCF7L2 in pancreatic islets warrants future studies. GenBank Accession Numbers: FJ010164-FJ010174.
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  • Result 1-7 of 7

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