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At least 487 records · Page 27Linked to original sources
PubMed1977

Dosimetric studies in the radiological examination of the hips in young infants with a special fenestration method of gonad protection.

A special lead shield of 1,5 mm Pb, with a fenestration was used for gonad protection during X-Ray of the hips for detection of dysplasia. The window allows the delineation of all parts of the skeleton required to make a correct diagnosis and check the standardized position of the pelvis, while all other parts, especially the gonads are safely shielded. The scattered radiation for the testes was further reduced by a trough-shaped lead shield behind the scrotum. The effectiveness of this gonad protection was measured by direct dosimetric studies on the infant with LiF and CaF2: Dy dosimeters at different adjustments of the X-ray generator and with medium and ultra high speed screen-film combinations.

Female↗
PubMed1982

Estimation of the contribution of ionization and excitation to the lethal effect of ionizing radiation.

A simple theoretical model is proposed for estimating the differential contribution of ionization and excitation to the lethal effect of ionizing radiation. Numerical results were obtained on the basis of published experimental data on the ability of bacterial cells Escherichia coli to undergo photoreactivation of radiation-induced damage. It was shown that inactivation by excitation may be highly significant for UV-hypersensitive cells capable of photoreactivation; inactivation by excitation increased with the energy of ionizing radiation and the volume of irradiated suspensions. The data are in qualitative agreement with the assumption of a possible contribution of the UV-component of Cerenkov radiation to the formation of excitations responsible for the lethal effect and the phenomenon of photoreactivation after ionizing radiation. Some predictions from the model are discussed.

Cell Survival↗
PubMed1975

Study of genetic effects of high energy radiations with different ionizing capacities on extracellular phages.

The inactivating and mutagenic action of high-energy radiations with different ionizing capacities (gamma-rays, protons, alpha-particles and accelerated ions of 12C and 20Ne) was studied by using coliphages lambda11 and SD as subjects. In particular the role of irradiation conditions (broth suspension, pure buffer, dry samples) and of the host functions recA, exrA and polA was investigated. The dose-response curve of induced mutagenesis was studied by measuring the yield of vir mutants in lambda11 and plaque mutants in SD. The following results were obtained. (1) The inactivation kinetics of phages under the action of gamma-rays and protons was first order to a survival of 10(-7). Heavy ions also showed exponential inactivation kinetics to a survival of 10(-4). At higher doses of 20Ne ion bombardment some deviation from one-hit kinetics was observed. For dry samples of phages the dimensions of targets for all types of radiation were approximately proportional to the molecular weights of phage DNA's. For densely ionizing radiation (heavy ions) the inactivating action was 3-5 times weaker than for gamma-rays and protons. (2) Mutagenesis was observed for all types of radiation, but heavy ions were 1-5-2 times less efficient than gamma-rays. For both phages studied the dose-response curve of mutagenesis was non-linear. The dependence on the dose was near to parabolic for lambda11. For SD a plateau or maximum of mutagenesis was observed for the relative number of mutants at a survival of about 10(-4). (3) Host-cell functions recA and exrA were practically indifferent for survival of gamma-irradiated phage lambda11, but indispensable for mutagenesis. Mutation recAI3 abolished induced vir mutations totally and exrA- reduced them significantly. The absence of the function polA had a considerable influence on phage survival, but no effect on vir mutation yield (if compared at the same survival level). (4) In conditions of indirect action of gamma-rays no vir mutations were induced. This is regarded as evidence that the single-strand breaks formed under indirect action conditions cannot serve as pre-mutational damage in DNA.

Alpha Particles↗
PubMed1975

The yield of chromosomal aberrations in rabbit lymphocytes after irradiation in vitro and in vivo.

The culture time of rabbit lymphocytes (41-42h) that provides cells in their first post-stimulation mitosis, was estimated on the basis of the mitotic index, dicentric yield and presence of the cells with these aberrations unaccompanied by acentric fragments, studied as a function of culture duration. The cells obtained in metaphase from cultures terminated at this time displayed no donor-to-donor variation where induction of dicentrics by x-rays was concerned. Rabbit venous blood was irradiated in vitro with a range of X-and gamma-ray doses, and dose-effect curves were obtained by regression analysis. Sixteen rabbits were irradiated in vivo (uniform whole-body irradiation), and blood was sampled 10 min, 6, 24, and 48 h after exposure. The frequency of dicentrics in the lymphocytes cultured did not change significantly over the first 24 h after irradiation. Dose-effect relationships in vivo fell within one standard error confidence limits of the respective curves in vitro. The authors conclude that the latter may be used for estimation of dose in vivo under conditions of homogeneous whole-body irradiation.

Animals↗
PubMed1976

Mutagenicity testing and risk estimation with mammals.

Mammalian test systems are currently used for mutagenicity screening. The necessity and the limitations of standardizing these methods are discussed for dominant-lethal assay. In addition to the refinement of standard methods, the development of new systems in mammals is emphasized. One promising approach is the detection of presumed somatic mutations. Another new development takes advantage of electrophoretic methods for detecting induced structural alterations of gene products. Mammalian experiments will be essential for the assessment of risks from chemical mutagens. The development of standards for the controlled use of chemical mutagens should be guided by the experience accumulated in radiation genetics. Two methods, the measurement of specific-locus mutation rates in mice and the direct determination of the phenotypic damage of dominant genes affecting the skeleton of mice, are recommended for the assessment of the hazard of chemical mutagens.

Animals↗
PubMed1982

Investigations on radiosensitive and radioresistant populations of Drosophila melanogaster. XIV. The genetic factor rar-1: effects in immature oocytes and their inhibition by caffeine.

The genetic factor rar-1 is part of the system of relative radioresistance that has evolved in the irradiated population ROI4 of Drosophila melanogaster. Previous data tentatively indicated an inhibition of rar-1 by caffeine. The present work was devoted to an extension of these caffeine studies to various end-points of genetic radiation damage induced at various exposure levels in immature oocytes of ROI4, of the contemporaneous control population Berlin wild K, and also in those of a substitution stock that carries rar-1 but not the other factors of relative radioresistance in ROI4, namely rar-2 and rar-3. The results show that it is the effect of rar-1 which is inhibited by caffeine. They confirm that rar-1 affects pathways of mutagenesis which produce recessive and dominant lethals but not chromosome losses.

Animals↗
PubMed1984

Differences in DMBA-induced mammary neoplastic responses in two lines of Sprague-Dawley rats.

It has been reported that female Sprague-Dawley rats obtained from a U.S. source and studied in the U.S. gave a larger and more rapid mammary neoplastic response to radiation than did female Sprague-Dawley rats obtained from a Dutch source and studied in The Netherlands. To learn if the different mammary neoplastic responses of the two 'lines' of Sprague-Dawley rats are due to inherent differences between the lines of rats or due to differences in experimental conditions, two groups of rats from the American source and one group from the Dutch source were studied for their response to a chemical carcinogen, dimethylbenzanthracene (DMBA), at the same laboratory. When 10 mg of DMBA per 100 g body wt was given by stomach tube to 28 rats from the Dutch source, 367 days later approximately 25% of these rats had developed mammary carcinomas and approximately 18% had developed mammary fibroadenomas. When the same dose of DMBA was given to rats from the U.S. source, 300 days later 90 and 100% had developed mammary carcinomas and 83 and 95% had developed mammary fibroadenomas. Similar trends were found for the number of neoplasms per rat and the mean time of appearance of the neoplasms. It was concluded that there are inherent differences between Sprague-Dawley rats obtained in the U.S. and Sprague-Dawley rats obtained in The Netherlands in regard to their mammary neoplastic responses to DMBA, as well as in their responses to radiation. Genetic differences between the two lines were confirmed by establishing dissimilarities in the expression of erythrocyte antigens coded for by RT1 (major histocompatibility complex).

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1993

The glutathione cycle is the creative reaction of life and cancer. Cancer causes oncogenes and not vice versa.

Life is definable as a chemical reaction which obeys exponential growth and dies if reversed. Such a reaction must be the commencement of all life so that every evolved form of it inherits these characteristics. As no single reaction known has these two features, life must be a combination of two or more reactions which whilst obeying all the classical laws of physics and chemistry assume an exponential form and effectively act as being irreversible. The reactions of glutathione--oxidation and reduction--when combined in sequence as a cyclical process fulfill these criteria. The cyclic changes of glutathione from reduced to oxidised to reduced forms must therefore be the reaction which creates life and is responsible for cancer's growth. 434 mHz electromagnetic radiation stimulates cancer growth rate by forcing this cycle into activity. Proof of this hypothesis is the long-term control of cancer in 11 patients treated with oxidised glutathione and 434 mHz radiation. Genetic material does not contain any energy system with exponential form, neither is it self-replicating. Genetic material will only reproduce if placed within an immortal cell in which all controls of the glutathione system have been lost, as in a cancer cell. Oncogenes must be the product of cancer and not the reverse.

Adult↗
PubMed1992

The prediction of human tumor radiosensitivity in situ: an approach using chromosome aberrations detected by fluorescence in situ hybridization.

No method of predicting the radiation sensitivity of individual human tumors is presently available, and recently published data show that other factors, in addition to the intrinsic radiosensitivity of the tumor cells, may play a role in the in vivo response of human tumors. Since these factors likely involve the tumor milieu (e.g., cell-cell contact and tumor hypoxia), an in situ assay of radiosensitivity is required. Although an analysis based on chromosome damage is the only suitable assay that would fit the requirements of sensitivity and speed of analysis, conventional examination of chromosome damage is impractical. By allowing the visualization of chromosomes in interphase cells, the technique of premature chromosome condensation (PCC) overcomes the need to culture the tumor cells in vitro, but the technical problem remains of counting a small excess number of breaks over the often large pretreatment chromosome number. We demonstrate here that the combination of fluorescence in situ hybridization (FISH) with PCC enormously simplifies the problem by focusing the analysis on a single chromosome. It also allows exchange aberrations to be scored easily. We demonstrate that the FISH technology may also be used to estimate radiation sensitivity from stable reciprocal translocations in metaphase identified by combining whole chromosome painting with a second color hybridization to the repeat sequences common to the centromeres. Since the frequency of stable translocations should correlate with initial chromosome damage, and since these translocations are not preferentially lost from the irradiated tumor cell population by cell death, an estimate of tumor cell killing following 1-5 dose fractions should be possible. Each of these two methods has its advantages, and a careful study of the two should establish which is superior for routine use to determine tumor radiosensitivity in situ.

Chromosome Aberrations↗