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We report the first observation of the Xe108→Te104→Sn100 α-decay chain. The α emitters, Xe108 [Eα=4.4(2) MeV, T1/2=58-23+106 μs] and Te104 [Eα=4.9(2) MeV, T1/2<18 ns], decaying into doubly magic Sn100 were produced using a fusion-evaporation reaction Fe54(Ni58,4n)Xe108, and identified with a recoil mass separator and an implantation-decay correlation technique. This is the first time α radioactivity has been observed to a heavy self-conjugate nucleus. A previous benchmark for study of this fundamental decay mode has been the decay of Po212 into doubly magic Pb208. Enhanced proton-neutron interactions in the N=Z parent nuclei may result in superallowed α decays with reduced α-decay widths significantly greater than that for Po212. From the decay chain, we deduce that the α-reduced width for Xe108 or Te104 is more than a factor of 5 larger than that for Po212.
Employing the Argonne Fragment Mass Analyzer and the implantation-decay-decay correlation technique, a weak 0.50(21)% proton decay branch was identified in 108 I for the first time. The 108 I proton-decay width is consistent with a hindered l=2 emission, suggesting a d [Formula presented] origin. Using the extracted 108 I proton-decay Q value of 597(13) keV, and the Q α values of the 108 I and 107 Te isotopes, a proton-decay Q value of 510(20) keV for 104 Sb was deduced. Similarly to the 112,113 Cs proton-emitter pair, the Q p (I108) value is lower than that for the less-exotic neighbor 109 I, possibly due to enhanced proton-neutron interactions in N≈Z nuclei. In contrast, the present Q p (Sb104) is higher than that of 105 Sb, suggesting a weaker interaction energy. For the present Q p (Sb104) value, network calculations with the one-zone X-ray burst model Mazzocchi et al. (2007) [18] predict no significant branching into the Sn-Sb-Te cycle at 103 Sn.
Abstract Background: The rarity of mutations in PALB2, CHEK2 and ATM make it difficult to estimate precisely associated cancer risks. Population-based family studies have provided evidence that at least some of these mutations are associated with breast cancer risk as high as those associated with rare BRCA2 mutations. We aimed to estimate the relative risks associated with specific rare variants in PALB2, CHEK2 and ATM via a multicentre case-control study. Methods: We genotyped 10 rare mutations using the custom iCOGS array: PALB2 c.1592delT, c.2816T>G and c.3113G>A, CHEK2 c.349A>G, c.538C>T, c.715G>A, c.1036C>T, c.1312G>T, and c.1343T>G and ATM c.7271T>G. We assessed associations with breast cancer risk (42 671 cases and 42 164 controls), as well as prostate (22 301 cases and 22 320 controls) and ovarian (14 542 cases and 23 491 controls) cancer risk, for each variant. Results: For European women, strong evidence of association with breast cancer risk was observed for PALB2 c.1592delT OR 3.44 (95% CI 1.39 to 8.52, p = 7.1 × 10−5), PALB2 c.3113G>A OR 4.21 (95% CI 1.84 to 9.60, p = 6.9 × 10−8) and ATM c.7271T>G OR 11.0 (95% CI 1.42 to 85.7, p = 0.0012). We also found evidence of association with breast cancer risk for three variants in CHEK2, c.349A>G OR 2.26 (95% CI 1.29 to 3.95), c.1036C>T OR 5.06 (95% CI 1.09 to 23.5) and c.538C>T OR 1.33 (95% CI 1.05 to 1.67) (p ≤ 0.017). Evidence for prostate cancer risk was observed for CHEK2 c.1343T>G OR 3.03 (95% CI 1.53 to 6.03, p = 0.0006) for African men and CHEK2 c.1312G>T OR 2.21 (95% CI 1.06 to 4.63, p = 0.030) for European men. No evidence of association with ovarian cancer was found for any of these variants. Conclusions: This report adds to accumulating evidence that at least some variants in these genes are associated with an increased risk of breast cancer that is clinically important.