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Sökning: WFRF:(Klug R)

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  • 2017
  • swepub:Mat__t
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  • de Angelis, G., et al. (författare)
  • Coherent proton-neutron contribution to octupole correlations in the neutron-deficient Xe-114 nucleus
  • 2002
  • Ingår i: Physics Letters B. - 0370-2693 .- 1873-2445. ; 535:04-jan, s. 93-102
  • Tidskriftsartikel (refereegranskat)abstract
    • Gamma ray linear polarization and picosecond lifetimes have been measured for levels in the neutron deficient nucleus Xe-114 using the EUROBALL IV spectrometer and the Cologne plunger device. The EUCLIDES Si-ball was used to improve the reaction channel selectivity. The linear polarization results have, for the first time, unambiguously determined the electromagnetic character of the dipole transitions de-exciting the negative parity level sequence, providing clear evidence for enhanced octupole collectivity. The discovery of two E3 transitions and the measurement of the lifetimes of the states depopulated by these transitions have allowed a quantitative determination of the octupole collectivity in the A approximate to 112 mass region. The large measured B(E3) values, close to approximate to 70 W.u., are among the strongest observed hitherto and indicate a coherent proton-neutron contribution to the octupole moment.
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  • Klug, Stefanie J, et al. (författare)
  • TP53 codon 72 polymorphism and cervical cancer : a pooled analysis of individual data from 49 studies
  • 2009
  • Ingår i: The Lancet Oncology. - 1470-2045 .- 1474-5488. ; 10:8, s. 772-784
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Cervical cancer is caused primarily by human papillomaviruses (HPV). The polymorphism rs1042522 at codon 72 of the TP53 tumour-suppressor gene has been investigated as a genetic cofactor. More than 80 studies were done between 1998 and 2006, after it was initially reported that women who are homozygous for the arginine allele had a risk for cervical cancer seven times higher than women who were heterozygous for the allele. However, results have been inconsistent. Here we analyse pooled data from 49 studies to determine whether there is an association between TP53 codon 72 polymorphism and cervical cancer. METHODS: Individual data on 7946 cases and 7888 controls from 49 different studies worldwide were reanalysed. Odds ratios (OR) were estimated using logistic regression, stratifying by study and ethnic origin. Subgroup analyses were done for infection with HPV, ethnic origin, Hardy-Weinberg equilibrium, study quality, and the material used to determine TP53 genotype. FINDINGS: The pooled estimates (OR) for invasive cervical cancer were 1.22 (95% CI 1.08-1.39) for arginine homozygotes compared with heterozygotes, and 1.13 (0.94-1.35) for arginine homozygotes versus proline homozygotes. Subgroup analyses showed significant excess risks only in studies where controls were not in Hardy-Weinberg equilibrium (1.71 [1.21-2.42] for arginine homozygotes compared with heterozygotes), in non-epidemiological studies (1.35 [1.15-1.58] for arginine homozygotes compared with heterozygotes), and in studies where TP53 genotype was determined from tumour tissue (1.39 [1.13-1.73] for arginine homozygotes compared with heterozygotes). Null results were noted in studies with sound epidemiological design and conduct (1.06 [0.87-1.29] for arginine homozygotes compared with heterozygotes), and studies in which TP53 genotype was determined from white blood cells (1.06 [0.87-1.29] for arginine homozygotes compared with heterozygotes). INTERPRETATION: Subgroup analyses indicated that excess risks were most likely not due to clinical or biological factors, but to errors in study methods. No association was found between cervical cancer and TP53 codon 72 polymorphism when the analysis was restricted to methodologically sound studies.
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