Structure of 10Be from the 12C 12C,14O 10Be reaction

The 12C 12C,14O two proton pick up reaction has been measured at 211.4 MeV incident energy to study the structure of states of 10Be up to excitation energies of 12 MeV. The measured partial angular distributions show pronounced oscillatory shapes, which were described by coupled reaction channels calculations. Spin parity assignments could be derived from these characteristic shapes and two definite assignments have been made. The state at 11.8 MeV has been identified as the 4 member of the ground state band, and the state at 10.55 MeV is assigned J pi 3 . At 5.96 MeV only the 1 1 member of the known 2 2 1 1 doublet is populated. The angular distribution of the peak at 9.50 MeV, which consists of several unresolved states, has been unfolded using contributions from known states at 9.56 MeV, 2 , and 9.27 MeV, 4 . The inclusion of a state at 9.4 MeV reported by Daito it et al. from the 10B t,3He 10Be reaction and tentatively assigned 3 improved the fit considerably. A K 2 band is formed with the 2 2 state as the band head and the 3 state as the second member. The structures of the K pi 0 1, 2 2, and 1 1 bands are discusse

Disentangling unclear nuclear breakup channels of beryllium-9 using the three-axis Dalitz plot

The three-axis Dalitz plot has been applied to the breakup of a nucleus into unequal mass fragments for the first time. The Dalitz plot allows clear identification of the various breakup channels of 9Be → 2α + n process. The method has allowed the branching ratio for the 6.38 MeV level in9Be to be provisionally calculated when examining the 9Be(4He, α)ααn reaction. The effects of non-uniform angular distributions on the Dalitz plot must still be properly investigated along with the effects of contaminant reaction channels. It is proposed that this method could be used to determine the breakup branching ratio of a newly-measured level in this nucleus

Stochastic modelling of tumorigenesis in p53 deficient mice.

Stochastic models of tumorigenesis have been developed to investigate the implications of experimental data on tumour induction in wild-type and p53-deficient mice for tumorigenesis mechanisms. Conventional multistage models in which inactivation of each p53 allele represents a distinct stage predict excessively large numbers of tumours in p53-deficient genotypes, allowing this category of model to be rejected. Multistage multipath models, in which a p53-mediated pathway co-exists with one or more p53-independent pathways, are consistent with the data, although these models require unknown pathways and do not enable age-specific curves of tumour appearance to be computed. An alternative model that fits the data is the 'multigate' model in which tumorigenesis results from a small number of gate-pass (enabling) events independently of p53 status. The role of p53 inactivation is as a rate modifier that accelerates the gate-pass events. This model implies that wild-type p53 acts as a 'caretaker' to maintain genetic uniformity in cell populations, and that p53 inactivation increases the probability of occurrence of a viable cellular mutant by a factor of about ten. The multigate model predicts a relationship between the time pattern of tumour occurrence and tumour genotype that should be experimentally testable. Stochastic modelling may help to distinguish 'gatekeeper' and 'caretaker' genes in other tumorigenic pathays