We compare the mortality in the years 1946-85 in a cohort of 31, 159 children born to parents one or both of whom were exposed to the atomic bombing of Hiroshima and Nagasaki (a parental gonadal dose ≥ 0.01 Sv) with that in a control group of 41, 069 children. The average gonadal dose for the exposed parents was 0.435 Sv. The mean age of the cohorts was 28.8 years.
In the ≥0.01 Sv dose group 1, 253 deaths were observed in the subset of children both of whose parents have been assigned DS86 doses. 3.2% were attributed to cancers, 72.9% to all diseases except neoplasms. These proportions in the 0 Sv dose group were about the same.
Based on a linear relative risk model, no statistically significant increase in the mortality attributable to diseases other than neoplasms is noted following parental exposure, the excess relative risk being 0.030 (± 0.046) per sievert based on the DS86 doses (RBE of neutrons= 20). For fatal cancer, no statistically significant effect of parental radiation dose was also observed. An analysis based on the full sample, using not only the DS86 dose group but also ad hoc dose group, yields essentially the same results as the analysis restricted to the DS86 dose group.

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After UV-irradiation of G1 phase cells, most gene conversion and crossing-over took place in cells of incisionproficient strains without post-irradiation incubation. In contrast, incision-deficient cells markedly induced both of these recombinational events only after irradiated cells were incubated for several hours in liquid growth medium before selection. These results indicate that when G1 cells are irradiated with UV recombinational events are initiated during that G1 phase in incision-proficient strains; whereas, they are not initiated in irradiated incisiondeficient strains before the cells reach the S/G2 phase. Experimental γ-ray results also suggest that post-irradiation incubation is not required for incision-proficient and -deficient strains to initiate mitotic recombinational events. Taken together, these results show that the formation of incision nicks and of post-replication gaps in DNA appears to be necessary for the initiation of recombinational events after UV treatment; whereas, it is not required after γ-irradiation.

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After the photoaddition of mono and bifunctional furocoumarins to G1 phase cells, most gene conversion and crossing-over occurred without post-irradiation incubation of these cells in incision-proficient strains. In contrast, incision-deficient cells showed marked induction of both recombinational events only after treated cells had been incubated for several hours before selection. These results indicate that when furocoumarins are photoadded to G1 cells, initiation of recombinational events occurs during the same G1 phase in the incisionproficient cells; whereas, it occurs only after post-irradiation DNA replication in incision-deficient cells. The action of the PSO2 gene product specific for the repair of DNA crosslinks in recombination induction is discussed and compared to the actions of the excision repair genes RAD1 and RAD2.

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To determine what the role of RAS oncogene is in radiation-induced leukemia, we investigated the frequency of mutations and the sites of the base substitution of activated N and K-RAS oncogenes in 25 leukemic patients who had been exposed to the atomic bomb and compared the results with those for 47 non-exposed leukemic patients. To detect the presence of mutated RAS oncogene, we used the PCR method to analyze DNAs from leukemic cells and from nude mouse tumors formed by in vivo selection assay.
Eight of the 25 exposed leukemic patients (32010) and 13 of the 47 non-exposed leukemic patients (27.6010) had RAS oncogene mutations. No significant differences were found between the exposed and non-exposed groups in frequency of mutation and the sites of base substitution on the RAS oncogene sequence. This study should prove valuable for understanding the role of RAS oncogene mutation in the genesis of radiation-induced leukemias.
List of Abbreviations:
DMBA: dimethylbenz anthracene, MNU: methylnitrosourea, CML: chronic myelocytic leukemia, AML: acute myelocytic leukemia, ALL: acute lymphocytic leukemia, ANLL: acute non-lymphocytic leukemia, RAEB: refractory anemia with excess blasts, PCR: polymerase chain reaction

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Inoue and Iwakura recently reported that the specific activity ratio of organically-bound ³H to free water ³H in polished rice samples collected in Japan and China was lower than unity. Their paper was the first to report the systematic apparent elimination of ³H for incorporation to organically-bound form in samples collected from the general environment. To confirm their result, seven unpolished rice samples obtained just after harvesting were analyzed for ³H. The mean specific activity ratio of organically-bound ³H to free water ³H was found to be 0.57, somewhat lower than the data by Inoue and Iwakura. This small difference may be caused by the different sampling years and/or the possible replacement of free water by atmospheric water vapor after harvesting.

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The effects of irradiation on the growth regulatory function of marrow stromal cells (MSC), and on the committed granulocyte-macrophage progenitor cells (GM-CFC), were investigated using a liquid culture system. CSF activity in the supernatant of irradiated MSC (0-900 rads) increased markedly with the increase of MSC irradiation dose. CSF-inhibitory activity in the supernatant of irradiated MSC (0-900 rads) also increased with the increase of MSC irradiation dose. Furthermore, the activity of exogenous CSF added to the supernatant of 900 rad-irradiated MSC was lost more slowly than that of non-irradiated MSC. These data suggest that irradiation affected CSF production, inhibitor production and consumption of CSF by MSC.

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A device to irradiate a monolayer of cultured cells with α-particles using an Am-241 α-source (33.4 MBq) was designed to investigate RBEs of α-particles in cell killing, induction of chromosome aberration, mutagenic changes and transformation. This device can be used conveniently in a common laboratory by a small number of researchers without any limitation of machine time. The device performs as follows: (1) The energy of α-particles at the entrance of the cell layer is 3.20 MeV with a standard deviation of 0.25 MeV, (2) the incident angle to the cell layer is 82.8 degrees with a standard deviation of 3.2 degrees, (3) the fluence rate is 4.7 × 10⁵ cm^-2, min^-1, (4) the average LET∞, for a cell layer 5μm thick is 138 keV/μm, (5) the average dose rate for a cell layer 5 μm thick is 0.10 Gy/min., (6) a temperature and CO₂ concentration conducive to cell cultivation are maintained during irradiation.

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Metallothionein functions as a radical scavenger protecting cells from the indirect effect of radiations. We investigated the effect of bismuth nitrate, an efficient inducer of metallothionein, on acute and late effects of radiation in mice. Metallothionein contents were examined in several organs after the administration of bismuth nitrate. The content in bone marrow increased 2-fold in the treated as compared to the control mice. This treatment protected irradiated mice from bone marrow death and increased the number of endogenous spleen colonies. The metallothionein content in the ileum did not change after treatment with bismuth nitrate. Mice were not protected by bismuth nitrate when exposed to 9 Gy of X-rays. This suggests that this agent does not protect from gastrointestinal death. The incidence of X-ray-induced thymic lymphomas was lowered by the administration of bismuth nitrate in mice exposed to four fractionated doses of 1.3 Gy of X-rays. These results indicate that bismuth nitrate effectively modified both acute and late effects of X-rays by inducing metallothionein in the target tissues.

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