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- Sun, H., et al.
(författare)
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New Band Structures and an Unpaired Crossing in 78Kr
- 1999
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Ingår i: Physical Review C (Nuclear Physics). - 0556-2813. ; 59:2, s. 655-664
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Tidskriftsartikel (refereegranskat)abstract
- High-spin states in Kr-78 were studied using the Ni-58(Na-23,3p) reaction at 70 MeV and the Ni-58(Si-23,alpha 4p) reaction at 130 MeV. Prompt gamma-gamma coincidences were measured using the Pitt-FSU detector array and the GAMMASPHERE-MICROBALL array. Results from these experiments have led to 26 new excitation levels, some of which have been grouped into 3 new bands. Spins were assigned based on directional correlations of oriented nuclei. Two of the new negative-parity bands appear to form a signature-partner pair based on a two-quasineutron structure, in contrast to the previously known two-quasiproton negative-parity bands. A forking has been observed at the 24(+) state in the yrast band, which calculations suggest may result from an unpaired crossing. The available evidence suggests oblate shapes in the yrast band coexist with prolate shapes in the negative-parity bands. [S0556-2813(99)04602-6].
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| 2. |
- Sun, X F, et al.
(författare)
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A novel p53 germline alteration identified in a late onset breast cancer kindred
- 1996
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Ingår i: Oncogene. - 0950-9232. ; 13:2, s. 11-407
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Tidskriftsartikel (refereegranskat)abstract
- Germline mutations in the p53 tumor suppressor gene are associated with the Li-Fraumeni syndrome, characterized by childhood sarcoma, leukemia and early onset breast cancer and has occasionally been found also in familial breast-ovarian cancer. Most mutations found are of missense type and located in the central region of the gene (exons 5 to 8). In the present study, a germline p53 alteration was identified in a late onset breast cancer family (kindred Lund 5; mean age 58 years) using single stranded conformation polymorphism and sequence analysis. The mutation (a CCG to CTG transition) at codon 82 in exon 4, resulting in a proline to leucine substitution, has not previously been reported and was not present in a control set of 60 healthy individuals. Three of five woman with breast cancer (45, 57 and 65 years) were carriers of the alteration. Loss of heterozygosity at the p53 locus was not seen in the primary tumors of these women, but appeared as a partial loss of the wildtype allele in subsequent recurrent lesions of two gene carriers. The family manifested no linkage to the p53 gene (a two-point LOD-score of -0.41), and has previously also been excluded for linkage to the BRCA1 and BRCA2 loci, as well as being carrier of a BRCA1 germline mutation. Although it seems unlikely that the p53 germline mutation is the major cause of disease predisposition in Lund 5, the data suggest that some p53 alteration may confer a subtle influence on breast cancer development and progression.
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