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At least 793 records · Page 44Linked to original sources
PubMed1994

[Health effects of atomic bomb radiation].

The health effects of atomic bomb radiation have been studied by the Atomic Bomb Casualty Commission (ABCC) and its successor, the Radiation Effects Research Foundation (RERF) based on a fixed population of atomic bomb survivors in Hiroshima and Nagasaki which had been established in 1950. The results obtained to the present can be classified into the following three categories: (1) The effects for which a strong association with atomic bomb radiation has been found include malignant neoplasms, cataracts, chromosomal aberrations, small head size and mental retardation among the in utero exposed. (2) A weak association has been found in the several sites of cancers, some non-cancer mortalities and immunological abnormalities. (3) No association has been observed in some types of leukemia, osteosarcoma, accelerated aging, sterility and hereditary effects.

Follow-Up Studies↗
PubMed1993

Experimental and theoretical cross sections for Escherichia coli mutants B, B/r, and Bs-1 after heavy-ion irradiation.

Data for the inactivation of three Escherichia coli mutants by energetic heavy ions are fitted by the track theory of a one-hit detector in an extended target mode. The respective E0's are 46, 36.5, and 12.6 Gy for E. coli B, B/r, and Bs-1 and a0, the assumed target radius, is 0.5 microns for all three. The parameter E0, the D37 with gamma rays, is measured directly, while a0 is fitted to the data. It is significant that neither a point target model nor calculations with a0 = 0.2 and 1.0 micron fit the data. Our fitted target radius, a0, approximates the size of the bacterium. These results raise questions as to why the E. coli mutants are one-hit detectors, and concerning the differences in the E0's in relation to a mechanistic interpretation of cell killing.

Acceleration↗
PubMed1993

In vitro split-dose recovery of glioblastoma multiforme.

Glioblastoma multiforme is among the most clinically resistant tumors to radiation. This resistance may be due to several different factors, such as a low intrinsic radiation sensitivity, a high recovery capacity, an increased number of clonogens, and a high hypoxic fraction. Previously, we have demonstrated a very wide range of intrinsic radiation sensitivities of cells of glioblastoma multiforme cell lines in vitro after single-dose irradiation. That is, the cells of some glioblastoma multiforme cell lines were quite sensitive, while for others the sensitivity of glioblastoma multiforme was among the lower range of sensitivities reported in the literature. This finding indicates that inherent cellular radiation sensitivity is not the sole determinant of the in vivo response of glioblastoma multiforme tumors. In this report, we evaluate the role of split-dose recovery determined in vitro in relation to the poor clinical outcome of glioblastoma multiforme. Cells of seven early-passage glioblastoma multiforme cell lines and six cell lines derived from tumors of a type frequently treated successfully (two squamous cell carcinomas of head and neck, three breast cancers, and one low-grade astrocytoma cell line) were studied. The in vitro split-dose recovery has been measured using colony formation as an end point. The cells were maintained at 37 degrees C for a period of 6 h between the doses of radiation. Results are presented in terms of a recovery ratio: the ratio of the mean inactivation dose of split-dose radiation to that of single-dose radiation. The data show significantly higher recovery ratios for glioblastoma multiforme than for the other types of histology; however, glioblastoma multiforme showed a wide range of recovery ratios, varying from 1.12 to 2.02. This indicates that cells of some glioblastoma multiforme cell lines exhibit minimal split-dose recovery. No correlation was found between the recovery ratio and the intrinsic radiation sensitivity of the cell lines studied. From these data, we conclude that the recovery capacity may not be the major determinant of the clinical radiation resistance of some glioblastoma multiforme.

Cell Survival↗
PubMedDate not supplied

[The methodological aspects of experimental modelling and of assessing the hereditary sequelae of the irradiation of one and both parents].

The paper summarises some methodological approaches which may be used in experimental modelling and study of hereditary radiation effects in mammals. These approaches are aimed to the elucidation of the possible specific character (aggravation) of radiation damage in the offspring determined by the participation of two exposed parents in conception. The main attention is drawn to the dependence of hereditary radiation effects yield on the stages of the cell cycle of the parent germ cells at the moment of exposure and to criteria of evaluation of radiation damage in the offspring during the ontogenetic development.

Animals↗
PubMed1976

[Radiotherapy of inflammatory diseases -- indicated still today? (author's transl)].

The good response of inflammatory diseases to a low dose radiotherapy is well known. Mainly, this fact is based on experiences made in the time before antibacterial chemotherapy area. In this study our results are presented which were obtained by treating 90 patients with radiotherapy in the last years, exlusively. With respect to the end of the treatment a success rate of more than 90% was achieved. This result was compared with literature and with own findings from radiotherapy of patients with degenerative joint diseases. From the viewpoint of radio-protection the radiotherapy should be initiated as early as possible because in these cases better results could be attained at low doses. Especially, the radiotherapy of the following diseases seems to be favourable: parotitis, mastitis, abscess, furuncle, paronychia and panaritium. Besides the complications and risks of the chemotherapy the somatic and genetic radiation injuries are discussed. When radiation therapy is applied skilfully the side effects of a locally and regionally limited therapy may be neglected. It is recommended to extend the indication for radiotherapy of inflammatory diseases.

Abscess↗
PubMedDate not supplied

Biological effects of diagnostic irradiation.

Medical radiation continues to be an area of concern to the patient. However, the technologist can reassure him that trained operators apply the radiation and that there are many built-in and accessory safety factors. Beyond that, however, the technologist can reassure himself that he is not responsible for unnecessary radiation by making full use of all safety measures, whether they are part of or accessory to the equipment, or are part of his judgment as to technique. To do this, he needs a sound knowledge of how damage occurs and a continual updating on research and equipment that will make his reassuring words to the patient honest ones.

Female↗
PubMed1965

Genetic Factors in Radiation Resistance of Bacillus subtilis.

Zamenhof, Stephen (University of California, Los Angeles), Hela Bursztyn, T. K. Ramachandra Reddy, and Patrice J. Zamenhof. Genetic factors in radiation resistance of Bacillus subtilis. J. Bacteriol. 90:108-115. 1965.-A study of several wild cross-transformable strains of Bacillus subtilis revealed differences in the resistance of their spores to X rays. Closer study of two such strains revealed differences of the same type when vegetative cells were exposed to X rays or to ultraviolet light (UV). Cell cultures repeatedly exposed to sublethal doses of UV (with cultivation between exposures) became more resistant to UV, presumably by enrichment in a more UV-resistant mutant. A sulfanilamide-resistant mutant of one strain (vegetative cells and spores) was less resistant to ionizing radiation; this sensitivity was transferable by transformation. No difference in radiation-induced mutability could be demonstrated in any of the strains studied. It is concluded that, at least in the cases studied, (i) the differences in radiation resistance of spores of different strains are not just a result of a superimposition of a common spore resistance mechanism(s) but rather are an amplification of genetically determined resistance differences in vegetative cells of these strains; (ii) sulfanilamide-resistance locus (p-aminobenzoic acid overproduction locus) is one of the loci of radiation sensitivity; (iii) no evidence was obtained that the differences in radiation resistance of cells or spores can be ascribed to differences in radiation resistance of their deoxyribonucleic acid.

Journal Article↗
PubMed1999

Characterization of genetic instability in radiation- and benzene-induced murine acute leukemia.

This study, using the CBA/Ca mouse as a model, compares genetic lesions associated with radiation- and benzene-induced acute leukemias. Specific types of leukemia included in the analyses are radiation-induced acute myeloid leukemia (ML), and benzene-induced lymphoblastic leukemias, lymphomas, or mix-lineage leukemias. These leukemias have histopathological characteristics similar to those seen in human acute leukemias. G-band cytogenetic analysis showed that specific deletions involving regions D-E of one copy of mouse chromosome 2 [del(2)(D-E)] were frequently associated in both radiation- and benzene-induced acute leukemias. In addition, translocations of chr2(D-E) were also observed in some cases. These results suggest an important role of chr2 (D-E) deletions and translocations in the development of radiation- and benzene-induced murine acute leukemias. Fluorescence in situ hybridization with DNA probes specific for 2(D-E), constructed in our laboratory by means of chromosomal microdissection and PCR amplification, also demonstrate 2(D-E) deletions and/or translocations in these leukemic cells. Aneuploidy of chromosomes 3, 15, 16, and Y were also frequently detected in benzene-induced leukemic cells with or without lesions on chr2. These cytogenetic findings support the previous observations that metabolites of benzene lead to spindle-fiber disruption or abnormal cytokinesis in exposed animals. In summary, genetic instabilities observed in leukemic cells isolated from mice that had developed leukemia after exposure to radiation or benzene are syntenic with those frequently detected in patients with myelodysplastic syndrome, acute ML, and acute lymphoblastic leukemia. Thus, the CBA/Ca mouse has several characteristics that make it an excellent model for the study of radiation or benzene leukemogenesis in humans.

Animals↗
PubMed1997

[Genetic predisposition and radiation sensitivity of tumors].

BACKGROUND: Studies on normal tissue radiation sensitivity have demonstrated profound differences of individual sensitivities. A number of genetic syndromes associated with abnormal radiation sensitivity have been described. Significant differences have also been detected in persons without known genetic disorders. The question arises as to whether tumors originating from normal tissues with abnormal radiation sensitivity share this abnormal sensitivity and as to whether a general correlation between normal tissue sensitivity and tumor tissue sensitivity can be substantiated. METHODS: Experimental and clinical data derived from own investigations and an extensive review of the literature was used to answer the question. RESULTS: Experimental studies on normal and tumor tissues of SCID-and C3H-mice demonstrated that the 2.7-fold enhanced radiation sensitivity of SCID normal tissues is also found in SCID tumors. Clinical investigations on cervical carcinoma and breast cancer patients revealed higher local control rates in patients with more pronounced acute side effects. A weak trend towards the same relationship was found in head and neck cancer patients. Case reports on unusually severe acute radiation side effects or unexpected tumor remissions as well as few reports on radiotherapy in ataxia telangiectasia (AT) patients suggest a correlation between normal- and tumor-tissue radiation sensitivity. Studies on fibroblasts and tumor cells from the same patient support this hypothesis in soft tissue sarcoma patients, but do not so for head and neck cancer patients. Tumor cells exhibit a considerably higher variation of radiation sensitivities than normal tissue cells. CONCLUSIONS: Experimental and clinical data are compatible with the hypothesis that normal tissue radiation sensitivity predicts for tumor tissue sensitivity. However, in view of the larger heterogeneity of tumor cell radiation sensitivity as compared to normal tissue radiation sensitivity, the development of a clinically useful predictive test for tumor sensitivity based on normal cell sensitivity appears to be unrealistic.

Animals↗