Comparison of endogenous lectins and glycosidases in wheat grains.
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Biomedical subjects
Publications and source records attributed to R C Miller.
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Two recombinant DNA plasmids coding for Drosophila tRNAVal3b hybridize to two different loci on the drosophila genome. Plasmid pDt41R hydridizines at the 90BC site, and pDt78R hybridizes at the 84D site. Heteroduplexes of the two plasmids were examined by electron microscopy. The study shows that the Drosophila segments have significant homology only over the length of the tRNAVal3b genes.
Depending on its time of addition to Syrian hamster embryo or mouse C3H 10T1/2 cells the protease inhibitor antipain (AP) can enhance, or reduce, radiation induced-oncogenic transformations. These opposing influences are not paralleled by changes in sister chromatid exchanges in either cell system. A 24 h treatment with 10 microM AP prior to, and during irradiation, with removal 10 min after irradiation results in greater than a two-fold increase in transformants. Conversely, a 24 h treatment beginning 10 min after irradiation results in about a two-fold decrease in transformants. The utility of AP as an agent for the reduction of tumorigenesis is brought into question, since quite short temporal differences in application can result in near five-fold differences in the frequencies of oncogenic transformations.
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Modification of sister chromatid exchanges and radiation-induced transformation in mouse C3H/10T 1/2 and Syrian hamster embryo cells by the tumor promoter 12-O-tetradecanoylphorbol-13-acetate and two retinoids, the trimethylmethoxyphenyl analog of N-ethyl retinamide and beta-all-trans-retinoic acid, has been studied. 12-O-tetradecanoylphorbol-13-acetate alone enhances, and retinoids alone reduce radiation-induced transformation. When both compounds were present, the retinoids not only reduced the oncogenic effects of radiation but completely eliminated the promoting effects of 12-O-tetradecanoylphorbol-13-acetate. These results were not paralleled by changes in sister chromatid exchange frequencies, indicating that, while sister chromatid exchanges may be useful as indicators of primary carcinogen mutagens, they may have little utility when secondary agents after the response of cells to a primary initiator.
In a patient with a 13qXp translocation and retinoblastoma the band associated with retinoblastoma (13q14) was clearly translocated intact to the X chromosome rather than being the breakpoint of the translocation. Genetic inactivation of the derivative X chromosome shown by late labeling and cell hybridization techniques in the predominance of cells indicated a functional monosomy for this segment as the most likely predisposing factor in producing retinoblastoma.
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The potential of hyperthermia for producing oncogenic transformation in vitro was assessed using C3H/10T 1/2 mouse embryo cells. Temperatures in the range of 40 degrees to 45 degrees C caused no transformations, whether or not the heat treatment was associated with significant cell killing. In addition modest hyperthermia appreciably reduced the transformation frequencies associated with X-ray doses. The findings suggest an additional benefit in combining ionizing radiations with hyperthermia.
The C3H/10T 1/2 cell line, cultured in vitro, was used to study the induction of oncogenic transformations produced by electron affinic compounds which function as hypoxic cell radiosensitizers. The relationship between the incidence of oncogenic transformations and drug concentration was obtained for 3-day exposures to misonidazole. At a concentration of 1 mM, a comparison was made of the carcinogenic potential of misonidazole, desmethylmisonidazole, Ro-07-0741, and SR 2508. Misonidazole and desmethylmisonidazole induced similar frequencies of transformation, while the frequency was doubled for Ro-07-0741 and increased by a factor of 5 for SR 2508. The relative carcinogenicity of the various alternatives to misonidazole is clearly a factor in choosing the next compound to be tested in the clinic.
An interstitial deletion of chromosome 13 with breakpoints at 13q22 and 13q32 is presented. The clinical findings associated with this deletion are discussed in relation to the correlations of specific chromosomal bands with constellations of congenital defects as described by Niebuhr and Ottosen (1973), Niebuhr (1977). Lewandowski and Yunis (1975), and Noel et al. (1976).
Recombinant plasmids carrying Drosophila melanogaster tRNA genes were constructed by ligation of HindIII-cleaved Drosophila DNA to HindIII cut pBR322 DNA. 90 clones were isolated that contained genes for one or more of eleven tRNAs. 43 of the plasmids were characterized by a number of methods: restriction nuclease digestion; agarose gel electrophoresis; hybridization with individual, purified, 125I-labelled Drosophila tRNA molecules and in situ hybridization to Drosophila chromosomes. The results show that several different tRNA genes have been isolated which code for single, specific isoacceptors. The DNAs from 8 plasmids each hybridize to single sites on Drosophila polytene chromosomes. In addition, the data show examples of two different plasmids hybridizing to different loci coding for the same tRNA; this means that we have isolated representatives of tRNA genes which map at widely separated points on the Drosophila genome.
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An established line of mouse fibroblasts, C3H/10T1/2 cells, was used for the assessment in vitro of oncogenic transformations caused by single and split doses of x-rays. The shape of the dose-response relationship was determined over the range from 0.1 to 10 Gy. It was found that splitting the x-ray dose into two equal fractions, separated by 5 hr, led to a reduction in transformation frequency at doses above 1.5-2 Gy but to an enhancement of transformation at lower doses. The observations reported cast doubt on the assessment of human cancer risk at lo dose levels by a linear extrapolation from available high-dose data from the Japanese atomic bomb survivors or from persons exposed for medical purposes.