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Träfflista för sökning "WFRF:(Hauke A.) srt2:(2010-2014)"

Sökning: WFRF:(Hauke A.) > (2010-2014)

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1.
  • Schael, S., et al. (författare)
  • Electroweak measurements in electron positron collisions at W-boson-pair energies at LEP
  • 2013
  • Ingår i: Physics Reports. - : Elsevier BV. - 0370-1573 .- 1873-6270. ; 532:4, s. 119-244
  • Forskningsöversikt (refereegranskat)abstract
    • Electroweak measurements performed with data taken at the electron positron collider LEP at CERN from 1995 to 2000 are reported. The combined data set considered in this report corresponds to a total luminosity of about 3 fb(-1) collected by the four LEP experiments ALEPH, DELPHI, 13 and OPAL, at centre-of-mass energies ranging from 130 GeV to 209 GeV. Combining the published results of the four LEP experiments, the measurements include total and differential cross-sections in photon-pair, fermion-pair and four-fermion production, the latter resulting from both double-resonant WW and ZZ production as well as singly resonant production. Total and differential cross-sections are measured precisely, providing a stringent test of the Standard Model at centre-of-mass energies never explored before in electron positron collisions. Final-state interaction effects in four-fermion production, such as those arising from colour reconnection and Bose Einstein correlations between the two W decay systems arising in WW production, are searched for and upper limits on the strength of possible effects are obtained. The data are used to determine fundamental properties of the W boson and the electroweak theory. Among others, the mass and width of the W boson, m(w) and Gamma(w), the branching fraction of W decays to hadrons, B(W -> had), and the trilinear gauge-boson self-couplings g(1)(Z), K-gamma and lambda(gamma), are determined to be: m(w) = 80.376 +/- 0.033 GeV Gamma(w) = 2.195 +/- 0.083 GeV B(W -> had) = 67.41 +/- 0.27% g(1)(Z) = 0.984(-0.020)(+0.018) K-gamma - 0.982 +/- 0.042 lambda(gamma) = 0.022 +/- 0.019. (C) 2013 Elsevier B.V. All rights reserved.
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2.
  • Lill, Christina M., et al. (författare)
  • Closing the case of APOE in multiple sclerosis : no association with disease risk in over 29 000 subjects
  • 2012
  • Ingår i: Journal of Medical Genetics. - : BMJ. - 0022-2593 .- 1468-6244. ; 49:9, s. 558-562
  • Tidskriftsartikel (refereegranskat)abstract
    • Background Single nucleotide polymorphisms (SNPs) rs429358 (ε4) and rs7412 (ε2), both invoking changes in the amino-acid sequence of the apolipoprotein E (APOE) gene, have previously been tested for association with multiple sclerosis (MS) risk. However, none of these studies was sufficiently powered to detect modest effect sizes at acceptable type-I error rates. As both SNPs are only imperfectly captured on commonly used microarray genotyping platforms, their evaluation in the context of genome-wide association studies has been hindered until recently.Methods We genotyped 12 740 subjects hitherto not studied for their APOE status, imputed raw genotype data from 8739 subjects from five independent genome-wide association studies datasets using the most recent high-resolution reference panels, and extracted genotype data for 8265 subjects from previous candidate gene assessments.Results Despite sufficient power to detect associations at genome-wide significance thresholds across a range of ORs, our analyses did not support a role of rs429358 or rs7412 on MS susceptibility. This included meta-analyses of the combined data across 13 913 MS cases and 15 831 controls (OR=0.95, p=0.259, and OR 1.07, p=0.0569, for rs429358 and rs7412, respectively).Conclusion Given the large sample size of our analyses, it is unlikely that the two APOE missense SNPs studied here exert any relevant effects on MS susceptibility.
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3.
  • Birath Scheffel, Christina, et al. (författare)
  • Risky drinking women : contrasting therapeutic approaches
  • 2014
  • Ingår i: Journal of Alcoholism & Drug Dependence. - : OMICS Publishing Group. - 2329-6488. ; 2:3, s. 1000160-
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: The importance of early identification and effective treatment for risky drinking grows with the increasing rate of alcohol use by women. Objectives: This study aims to contrast treatment approaches for two samples of problem drinking women. Methods: The samples consisted of (i) 134 alcohol treatment-seeking Swedish women receiving long-term comprehensive services; and (ii) 152 US women who were not seeking treatment for alcohol but were medical outpatients with one of four conditions exacerbated by excessive alcohol use and received a brief intervention as part of a study. Data consisted of questionnaires assessing alcohol consumption, perceived stress and attitudes towards change. Results: While the treatment-seeking Swedish group drank more alcohol at the start of treatment, all women reduced their consumption of alcohol at the end of treatment/follow-up. Women who reported more stress drank more initially in both samples. Conclusion and Scientific Significance: This report contrasts two “extreme” approaches to treatment: longterm, open-ended, outpatient treatment and, time-limited, structured brief intervention for risky drinking women. Both treatment methods yielded positive results with significantly reduced drinking. Factors associated with successful outcome included the women’s attitudes toward treatment and conviction for the necessity of change in drinking habits.
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4.
  • Migliorini, Gabriele, et al. (författare)
  • Variation at 10p12.2 and 10p14 influences risk of childhood B-cell acute lymphoblastic leukemia and phenotype
  • 2013
  • Ingår i: Blood. - : American Society of Hematology. - 1528-0020 .- 0006-4971. ; 122:19, s. 3298-3307
  • Tidskriftsartikel (refereegranskat)abstract
    • Acute lymphoblastic leukemia (ALL) is the major pediatric cancer diagnosed in economically developed countries with B-cell precursor (BCP)-ALL, accounting for approximately 70% of ALL. Recent genome-wide association studies (GWAS) have provided the first unambiguous evidence for common inherited susceptibility to BCP-ALL, identifying susceptibility loci at 7p12.2, 9p21.3, 10q21.2, and 14q11.2. To identify additional BCP-ALL susceptibility loci, we conducted a GWAS and performed a meta-analysis with a published GWAS totaling 1658 cases and 4723 controls, with validation in 1449 cases and 1488 controls. Combined analysis identified novel loci mapping to 10p12.2 (rs10828317, odds ratio [OR] = 1.23; P = 2.30 x 10(-9)) and 10p14marked by rs3824662(OR = 1.31; P = 8.62 x 10(-12)). The single nucleotide polymorphism rs10828317 is responsible for the N215S polymorphism in exon 7 of PIP4K2A, and rs3824662 localizes to intron 3 of the transcription factor and putative tumor suppressor gene GATA3. The rs10828317 association was shown to be specifically associated with hyperdiploid ALL, whereas the rs3824662-associated risk was confined to nonhyperdiploid non-TEL-AML1 + ALL. The risk allele of rs3824662 was correlated with older age at diagnosis (P < .001) and significantly worse event-free survivorship (P < .0001). These findings provide further insights into the genetic and biological basis of inherited genetic susceptibility to BCP-ALL and the influence of constitutional genotype on disease development.
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5.
  • Riihimäki, Matias, et al. (författare)
  • Metastatic sites and survival in lung cancer.
  • 2014
  • Ingår i: Lung Cancer. - : Elsevier BV. - 1872-8332 .- 0169-5002. ; 86:1, s. 78-84
  • Tidskriftsartikel (refereegranskat)abstract
    • Population-based data on metastatic sites and survival in site-specific metastases are lacking for lung cancer and for any cancer because most cancer registries do not record metastases. This study uses a novel population-based approach to identify metastases from both death certificates and national inpatient data to describe metastatic pathways in lung cancer patients.
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