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At least 775 records · Page 43Linked to original sources
PubMed1984

Characterization of a new radiation-sensitive mutant, Escherichia coli K-12 radC102.

A new radiation-sensitive mutant, radC , has been isolated. The radC gene is located at 81.0 min on the Escherichia coli K-12 linkage map. The radC mutation sensitized cells to uv radiation, but unlike most DNA repair mutations, sensitization to X rays was observed only for rich medium-grown cells. For cells grown in rich medium, the radC mutant was normal for gamma-radiation mutagenesis, but showed less uv-radiation mutagenesis than the wild-type strain; it showed normal amounts of X- and uv-radiation-induced DNA degradation, and it was approximately 60% deficient in recombination ability. The radC strain was normal for host cell reactivation of gamma-and uv-irradiated bacteriophage lambda; the radC mutation did not sensitize a recA strain, but did sensitize a radA and a polA strain to X and uv radiation and a uvrA strain to uv radiation. Therefore, we suggest that the radC gene product plays a role in the growth medium-dependent, recA gene-dependent repair of DNA single-strand breaks after X irradiation, and in postreplication repair after uv irradiation.

Cell Survival↗
PubMed1980

Effect of natural background radiation on dermatoglyphic traits.

Long term exposure to natural background radiation could cause gross abnormalities in individuals and at the population level. Studies conducted on the coastal Kerala population which is known to be receiving fifteen times the normal permissible dose of radiation support this. This study aims at understanding the deviations, if any, in the normal human variation as a result of such high natural radiation. A detailed quantitative and qualitative dermatoglyphic study was done on two communities i.e. Hindus and Christians, living separately in the radiation area. The significant differences were observed between control and exposed groups with regard to d-t ridge count, distances c-t and angle atd. The susceptibility of the axial triradius to environmental distrubances is discussed.

Background Radiation↗
PubMed1978

[Quantitative description of the process of cellular radiation inactivation. X. Closing remarks. Ways for further development of the concepts].

The series of communications to check the applicability of one of the most likely models of the loss of reproductive integrity of irradiated eukaryotic cells has been completed by this paper. Many radiobiologists accept the cytogenetic model but no one has analyzed mathematically its applicability. We have succeeded in explaining some significant experimental data and therefore our model is something more than a simple working hypothesis. In this paper the model is considered to prove its significance as the first approach to a more detailed study of the phenomenon.

Cell Survival↗
PubMed1994

Recent advances in cutaneous melanoma oncogenesis research.

The oncogenic transformation of epidermal melanocytes produces primary cutaneous melanoma. In this article, previously published cytogenetic, biochemical, molecular biology, and cell biology studies of cutaneous melanoma oncogenesis are reviewed. A variety of laboratory animal models have been developed for studies of the induction of melanoma, including mice, the laboratory opossum Monodelphis domestica, Sinclair swine, and Xiphophorus fish. Some of the advantages and disadvantages of these animal models are presented for comparison to human melanoma. Cytogenetic and loss of heterozygosity studies over the past decade have demonstrated that human metastatic melanomas contain numerous chromosomal abnormalities, and that normal melanocytes have putative tumor suppressor genes that are presumably deleted or inactivated in transformed melanocytes to yield malignant melanoma cells. The status of research efforts to identify the putative tumor suppressor genes of human chromosomes 1p, 6q, and 9p, implicated in sporadic and familial melanoma, is presented. Furthermore, the roles of ultraviolet radiation, genetic susceptibility, dominant oncogenes, growth factors, the p53 gene, antioxidant enzymes, and DNA tumor viruses in the formation of cutaneous primary melanoma are discussed.

Animals↗