[en] BNL experiment 859 is a single arm magnetic spectrometer with a second level trigger based on particle identification. During the 1991 and 1992 running periods the apparatus was triggered by events with at least one kaon in the spectrometer for collisions of a 14.6 A GeV/c Si beam with both Al and Au targets, resulting in a great increase in the kaon data set for the Si + Al and Si + Au systems. The cascade code ARC has shown promise in reproducing the published E802 results. Kaon p perpendicular spectra, dn/dy distributions and comparisons to ARC results for these systems will be presented

[en] In May 1958 the NRU reactor hall was badly contaminated by a damaged fuel rod that broke apart during its removal from the reactor. Radioactive fission products were spread around the reactor hall and into adjacent areas when a piece of the fuel rod fell into the maintenance pit and burned. AECL staff and others completed the decontamination in 2 1/2 months. This paper reports the results of a follow-up study of the AECL participants. No statistically significant increases in deaths from cancer or other diseases were found in this group

[en] Data on the follow-up of CRNL employees who died during employment or after retirement have been updated to 1982 December 31. Updated tables on mortality for AECL participants in the 1953 NRX clean-up and in the 1958 NRU decontamination are also included in this report. Preliminary mortality data on two other groups are presented here for (a) female employees of CRNL, 1966-1982 and (b) male employees of CRNL who have accumulated lifetime occupational doses of 0.2 Sv (20 rem) or more. Data on types of fatal cancer recorded for long-term male CRNL employees over the period 1966-1982 are also given. No statistically significant increases in cancer deaths were found in any of the groups analyzed

[en] Data available to date on the mortality of continuing and retired employees of the Chalk River Nuclear Laboratories are consistent with the Σhealthy workerΣ effect that has been observed in similar studies at other nuclear facilities. Because of an accident at the NRX research reactor in December 1952, the reactor was largely dismantled and rebuilt in 1953-54. These operations involved appreciable radiation exposures to a number of employees. The follow-up of the 850 on-site AECL staff involved in the clean-up has indicated that there were no unusual patterns in the mortality of this group when compared with those of the general population of Ontario

[en] Mice heterozygous for Trp53 are radiation-sensitive and cancer-prone, spontaneously developing a variety of cancer types. Osteosarcomas in the spine lead to paralysis, while lymphomas lead rapidly to death, distinct events that provide objective measures of latency. The effects of a single low-dose (10 or 100 mGy), low-dose-rate (0.5 mGy/min) ⁶⁰Co γ irradiation on lymphoma or spinal osteosarcoma frequency and latency, defined as time of death or of onset of paralysis, respectively, were examined. Compared to spontaneous lymphomas or to spinal osteosarcomas leading to paralysis in unexposed mice, an exposure of 7-8-week-old Trp53^+/- mice to 10 or 100 mGy had no significant effect on tumor frequency, indicating no effect on tumor initiation. All tumors are therefore assumed to be of spontaneous origin. However, a 10-mGy exposure reduced the risk of both lymphomas and spinal osteosarcomas by significantly increasing tumor latency, indicating that the main in vivo effect of a low-dose exposure is a reduction in the rate at which spontaneously initiated cells progress to malignancy. The effect of this adaptive response persisted for the entire life span of all the animals that developed these tumors. Exposure to 100 mGy delayed lymphoma latency longer than the 10-mGy exposure. However, the 100-mGy dose increased spinal osteosarcoma risk by decreasing overall latency compared to unexposed control mice. That result suggested that this higher dose was in a transition zone between reduced and increased risk, but that the dose at which the transition occurs varies with the tumor type. (author)

[en] AGS experiment E859 is a follow-on to experiment E802 that uses a second-level trigger based on particle identification to enhance the collection of rare species. We now have high statistics spectra over a broad range in rapidity and transverse momentum for both positive and negative kaons, allowing a detailed comparison of these particles for the first time in AGS heavy-ion experiments. The K^- are seen to have a narrower rapidity distribution than the K⁺, a difference which may be due to the way in which resonances contribute to the yield of K^- and K⁺. (orig.)

[en] It was shown previously that a heat shock induces a transient increase in the resistance of wild-type Saccharomyces cerevisiae to the lethal effects of ionizing radiation. This increase was similar to the increase in resistance to thermal killing induced by the same heat shock, but appeared at a slightly earlier time after the temperature increase. This type showed that while excision-defective mutants respond like the wild type, recombination-deficient mutants do not display this heat-shock induction of radiation resistance, but still show induction of thermal resistance. Radiation survival curves of wild-type cells exposed to the elevated temperature were able to resolve two populations of cells on the basis of their sensitivity to ionizing radiation. Following a heat shock, the proportion of resitant cells increased temporarily in parallel with the increase in radiation resistance. We conclude that heat-shock induction of radiation resistance in wild-type diploid yeast results from at least two changes, an increase in recombinational repair capacity, possibly associated with G1 cells, and a shift in population distribution to a higher fraction of resistant cells. We further conclude that heat-shock induction of thermal resistance proceeds by an independent mechanism

[en] Radiation resistance and thermal resistance vary as a function of culture temperature in logarithmically growing Saccharomyces cerevisiae and are related to the optimum temperature for growth. Radiation resistance and thermal resistance were also induced when cells grown at low temperatures were subjected to a heat shock at or above the optimum growth temperature. Exposure to ionizing radiation followed by a short incubation at low temperature also induced resistance to killing by heat. Heat-shocked cells are induced to a level of thermal and radioresistance much greater than the characteristic resistance level of cells grown continuously at the shock temperature. This high level of resistance, which resembles that of stationary-phase cells, decays to the characteristic log-phase level within one doubling of cell number after the heat shock. Both induction of resistance and decay of that induction require protein synthesis. It is postulated that induction of resistance by heat shock or ionizing radiation is a response of the cells to stress and represents a preparation to enter stationary phase

[en] Yeast, as well as higher eukaryotes, are induced to increase thermal resistnace (thermotolerance) by prior exposure to a heat stress. Prior exposure to an acute dose of either ⁶⁰Co γ or 254-nm ultraviolet radiation, at sublethal or fractionally lethal doses, is shown to cause a marked increase in the resistance of Saccharomyces cerevisiae to killing by heat. Partial induction by radiation followed by maximum induction by heat did not produce an additive response when compared to a maximum induction by heat alone, suggesting that the same process was induced by both heat and radiation. Irradiation with 254-nm uv light followed by an immediate, partial photoreversal of pyrimidine dimers with long-wavelength uv light resulted in a reduced level of resistance compared to cells not exposed to the photoreversal light, indicating that the cells specifically recognized pyrimidine dimers as a signal to increase their thermal resistance. Exposure to 254-nm uv or ionizing radiation induced thermal resistance in mutants defective in either excision repair (rad3, uv-sensitive) or recombinational repair (rad52, γ-sensitive), suggesting that recognition and repair of DNA damage by these systems are not a part of the signal which initiates an increase in resistance to heat. These data indicate that types of DNA damage as diverse as those produced by ionizing radiation and by ultraviolet light are recognized as a signal by the yeast cell to increase its thermal resistance

[en] Human genotypes are known that confer both increased susceptibility or resistance to DNA damage and increased cancer risk after exposure to carcinogenic agents, including ionizing radiation (NAS 1980). The existence of sensitive subgroups at elevated risk, if they are of appreciable size, could have significant impact on the actual distribution of risk. The radiosensitive disorder ataxia-telangiectasia (A-T) serves as a good example: the significant at risk group, A-T heterozygotes, is estimated to comprise between 0.5% and 5% of the total population, and has a twofold elevated lifetime risk of fatal neoplasia. Other genetic syndromes that manifest abnormal radiosensitivity are also known, but no estimates are available for the population frequency of all such phenotypes, or for their overall degree of increased risk. As the first part of a program addressing these questions, we have developed a rapid and inexpensive assay for screening members of the general population for abnormal radiosensitivity; such persons would be regarded as at presumptive elevated risk of radiogenic cancer. Our method utilizes lymphoblastoid cell lines and chronic as opposed to acute gamma-ray exposure to amplify the difference between normal and somewhat sensitive strains. A simple grow-back assay assesses the survival response. Information on the extent of natural variation in inherited susceptibility to radiogenic cancers could be most useful for radiation protection in the future