Neutron-3H and Proton-3He Zero Energy Scattering

The Kohn variational principle and the (correlated) Hyperspherical Harmonics technique are applied to study the n-3H and p-3He scattering at zero energy. Predictions for the singlet and triplet scattering lengths are obtained for non-relativistic nuclear Hamiltonians including two- and three-body potentials. The calculated n-3H total cross section agrees well with the measured value, while some small discrepancy is found for the coherent scattering length. For the p-3He channel, the calculated scattering lengths are in reasonable agreement with the values extrapolated from the measurements made above 1 MeV.Comment: 13 pages, REVTEX, 1 figur

Mdm2-SNP309 polymorphism in prostate cancer: no evidence for association with increased risk or histopathological tumour characteristics

The search for inherited cancer susceptibility factors is a major focus of epidemiologic cancer studies. Analyses of single-nucleotide polymorphisms (SNP) in a variety of genes revealed a correlation between a specific allele variant and cancer predisposition. Human mouse double-minute 2 protein (Mdm2) is a cellular E3 ligase capable of ubiquitination and degradation of p53. Therefore, Mdm2 is a crucial factor of cell cycle control and cell survival. The Mdm2 promoter SNP309 was shown to increase Mdm2 expression and can, thereby, inhibit the p53 pathway. This SNP was found to be associated with increased risk and early onset of various malignancies. For prostate cancer no studies are reported to date. In a case–control study we determined the distribution of the Mdm2 SNP309 in 145 male subjects with prostate cancer and in 124 male controls without any malignancy using RFLP analysis. Cases and controls showed a similar distribution of the SNP (P=0.299). Genotype distribution showed neither an association with histopathological characteristics of the tumours nor with prognosis. Age at disease onset was also not modified by the SNP. This first study of the Mdm2 SNP309 in prostate cancer patients suggests no correlation between a certain allelic variant and an increased cancer risk