| 1. |
- Toshito, T., et al.
(författare)
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Measurements of projectile-like Be-8 and B-9 production in 200-400 MeV/nucleon C-12 on water
- 2008
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Ingår i: Physical Review C - Nuclear Physics. - 2469-9985 .- 2469-9993. ; 78:6, s. 4-
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Tidskriftsartikel (refereegranskat)abstract
- We have studied the production of the projectile-like fragments Be-8 and B-9 produced in interactions of 200 to 400 MeV/nucleon carbon ions with water, using emulsion detectors. In this Brief Report we present the first published production cross section of the projectile-like fragment B-9 in the energy region above 100 MeV/nucleon. The measured production cross sections of these nuclides were compared to calculations using a semiempirical model. We found that the measured cross sections deviate from the calculated values by a factor up to about six. This information is of importance for benchmarking and improving heavy ion nuclear reaction models.
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| 2. |
- Toshito, T., et al.
(författare)
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Measurements of total and partial charge-changing cross sections for 200-to 400-MeV/nucleon C-12 on water and polycarbonate
- 2007
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Ingår i: Physical Review C - Nuclear Physics. - 2469-9985 .- 2469-9993. ; 75:5, s. 8-
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Tidskriftsartikel (refereegranskat)abstract
- We have studied charged nuclear fragments produced by 200- to 400-MeV/nucleon carbon ions, interacting with water and polycarbonate, using a newly developed emulsion detector. Total and partial charge-changing cross sections for the production of B, Be, and Li fragments were measured and compared with both previously published measurements and model predictions. This study is of importance for validating and improving carbon-ion therapy treatment planning systems and for estimating the radiological risks for personnel on space missions, because carbon is a significant component of galactic cosmic rays.
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| 3. |
- Klug, Stefanie J, et al.
(författare)
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TP53 codon 72 polymorphism and cervical cancer : a pooled analysis of individual data from 49 studies
- 2009
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Ingår i: The Lancet Oncology. - 1470-2045 .- 1474-5488. ; 10:8, s. 772-784
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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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