1. |
- Abbasi, R, et al.
(author)
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Determination of the atmospheric neutrino flux and searches for new physics with AMANDA-II
- 2009
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In: Physical Review D. - 1550-7998 .- 1550-2368. ; 79, s. 102005-
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Journal article (peer-reviewed)abstract
- The AMANDA-II detector, operating since 2000 in the deep ice at the geographic South Pole, has accumulated a large sample of atmospheric muon neutrinos in the 100 GeV to 10 TeV energy range. The zenith angle and energy distribution of these events can be used to search for various phenomenological signatures of quantum gravity in the neutrino sector, such as violation of Lorentz invariance or quantum decoherence. Analyzing a set of 5511 candidate neutrino events collected during 1387 days of livetime from 2000 to 2006, we find no evidence for such effects and set upper limits on violation of Lorentz invariance and quantum decoherence parameters using a maximum likelihood method. Given the absence of evidence for new flavor-changing physics, we use the same methodology to determine the conventional atmospheric muon neutrino flux above 100 GeV.
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2. |
- Abbasi, R, et al.
(author)
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FIRST NEUTRINO POINT-SOURCE RESULTS FROM THE 22 STRING ICECUBE DETECTOR
- 2009
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In: Astrophysical Journal Letters. - 2041-8205. ; 701, s. L47-L51
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Journal article (peer-reviewed)abstract
- We present new results of searches for neutrino point sources in the northern sky, using data recorded in 2007-2008 with 22 strings of the IceCube detector (approximately one-fourth of the planned total) and 275.7 days of live time. The final sample of 5114 neutrino candidate events agrees well with the expected background of atmospheric muon neutrinos and a small component of atmospheric muons. No evidence of a point source is found, with the most significant excess of events in the sky at 2.2 sigma after accounting for all trials. The average upper limit over the northern sky for point sources of muon-neutrinos with E-2 spectrum is E-2 Phi(v mu) < 1.4 x 10(-11) TeV cm(-2) s(-1), in the energy range from 3 TeV to 3 PeV, improving the previous best average upper limit by the AMANDA-II detector by a factor of 2.
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3. |
- Sodergren, Erica, et al.
(author)
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The genome of the sea urchin Strongylocentrotus purpuratus.
- 2006
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In: Science. - : American Association for the Advancement of Science (AAAS). - 1095-9203 .- 0036-8075. ; 314:5801, s. 941-52
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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. |
- Aad, G., et al.
(author)
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The ATLAS Experiment at the CERN Large Hadron Collider
- 2008
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In: Journal of Instrumentation. - 1748-0221. ; 3:S08003
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Research review (peer-reviewed)abstract
- The ATLAS detector as installed in its experimental cavern at point 1 at CERN is described in this paper. A brief overview of the expected performance of the detector when the Large Hadron Collider begins operation is also presented.
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5. |
- Pace, Rishika A., et al.
(author)
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Collagen VI glycine mutations: Perturbed assembly and a spectrum of clinical severity
- 2008
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In: Annals of Neurology. - : Wiley. - 1531-8249 .- 0364-5134. ; 64:3, s. 294-303
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Journal article (peer-reviewed)abstract
- Objective: The collagen VI muscular dystrophies, Bethlem myopathy and Ullrich congenital muscular dystrophy, form a continuum of clinical phenotypes. Glycine mutations in the triple helix have been identified in both Bethlem and Ullrich congenital muscular dystrophy, but it is not known why they cause these different phenotypes. Methods: We studied eight new patients who presented with a spectrum of clinical severity, screened the three collagen VI messenger RNA for mutations, and examined collagen VI biosynthesis and the assembly pathway. Results: All eight patients had heterozygous glycine mutations toward the N-terminal end of the triple helix. The mutations produced two assembly phenotypes. In the first patient group, collagen VI dimers accumulated in the cell but not the medium, microfibril formation in the medium was moderately reduced, and the amount of collagen VI in the extracellular matrix was not significantly altered. The second group had more severe assembly defects: some secreted collagen VI tetramers were not disulfide bonded, microfibril formation in the medium was severely compromised, and collagen VI in the extracellular matrix was reduced. Interpretation: These data indicate that collagen VI glycine mutations impair the assembly pathway in different ways and disease severity correlates with the assembly abnormality. In mildly affected patients, normal amounts of collagen VI were deposited in the fibroblast matrix, whereas in patients with moderate-to-severe disability, assembly defects led to a reduced collagen VI fibroblast matrix. This study thus provides an explanation for how different glycine mutations produce a spectrum of clinical severity.
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6. |
- Sun, Jielin, et al.
(author)
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Evidence for two independent prostate cancer risk-associated loci in the HNF1B gene at 17q12
- 2008
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In: Nature Genetics. - London : Nature Publishing Group. - 1061-4036 .- 1546-1718. ; 40:10, s. 1153-1155
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Journal article (other academic/artistic)abstract
- We carried out a fine-mapping study in the HNF1B gene at 17q12 in two study populations and identified a second locus associated with prostate cancer risk, 26 kb centromeric to the first known locus (rs4430796); these loci are separated by a recombination hot spot. We confirmed the association with a SNP in the second locus (rs11649743) in five additional populations, with P = 1.7 10-9 for an allelic test of the seven studies combined. The association at each SNP remained significant after adjustment for the other SNP.
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7. |
- Zheng, S. Lilly, et al.
(author)
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Genetic variants and family history predict prostate cancer similar to prostate-specific antigen
- 2009
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In: Clinical Cancer Research. - 1078-0432 .- 1557-3265. ; 15:3, s. 1105-1111
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Journal article (peer-reviewed)abstract
- PURPOSE: Although prostate-specific antigen (PSA) is the best biomarker for predicting prostate cancer, its predictive performance needs to be improved. Results from the Prostate Cancer Prevention Trial revealed the overall performance measured by the areas under curve of the receiver operating characteristic at 0.68. The goal of the present study is to assess the ability of genetic variants as a PSA-independent method to predict prostate cancer risk. EXPERIMENTAL DESIGN: We systematically evaluated all prostate cancer risk variants that were identified from genome-wide association studies during the past year in a large population-based prostate cancer case-control study population in Sweden, including 2,893 prostate cancer patients and 1,781 men without prostate cancer. RESULTS: Twelve single nucleotide polymorphisms were independently associated with prostate cancer risk in this Swedish study population. Using a cutoff of any 11 risk alleles or family history, the sensitivity and specificity for predicting prostate cancer were 0.25 and 0.86, respectively. The overall predictive performance of prostate cancer using genetic variants, family history, and age, measured by areas under curve was 0.65 (95% confidence interval, 0.63-0.66), significantly improved over that of family history and age (0.61%; 95% confidence interval, 0.59-0.62; P = 2.3 x 10(-10)). CONCLUSION: The predictive performance for prostate cancer using genetic variants and family history is similar to that of PSA. The utility of genetic testing, alone and in combination with PSA levels, should be evaluated in large studies such as the European Randomized Study for Prostate Cancer trial and Prostate Cancer Prevention Trial.
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