Immunoreactive systems in the healing of aseptic and infected wounds in an experiment

Main parameters of systemic immune reactivity were studied in 240 mature Wistar male rats with simulated aseptic and infected surface wounds before surgical intervention, and 1-10, 12 and 15 days after it. It was stated that aseptic wounds were responsible for nonspecific systemic response to the stress, whereas the presence of bacterial flora in the wound inhibited the development of humoral immune response in the presence of T-cell activation thus causing the dysfunction of the immune system and therefore affecting the course of wound progress. The consideration of all factors mentioned permits averting wound purulent complications in postsurgical period.     

Radiation-induced instability of yeast chimeric chromosomes

Instability of the I chimeric chromosome of the yeast Saccharomyces induced by gamma-irradiation has been studied. The chimeric chromosome analysed contained an integrated pYF91 plasmid. Cells of the integrant were irradiated and then mated with non-irradiated cells of the proper tester strain marked by ade1 mutation (red colour of colonies). We isolated 10 hybrids with pink colonies on selective medium. They displayed high degree of mitotic instability during growth on nonselective medium, segregating red colonies (15 to 90% of the total). Tetrad analysis showed that some of the unstable chromosomes exhibited lethal effect in haploids, while others were viable and could pass through meiosis retaining their instability.     

Genetic control of mitotic crossing over in yeasts. IV. The induction of mitotic crossing over by chemical mutagens with different mechanisms of action

The genetic effects of methyl methanesulphonate (MMS) and bifunctional quinacrine mustard (QM) have been studied in three diploid strains of the yeast Saccharomyces cerevisiae: T1, with normal radiosensitivity, T2 - the excision-deficient mutant (rad2 rad2) and T3 - the mutant defective in recombinational repair (rad54 rad54). The strain T3 was much more sensitive to the lethal action of MMS than T1, but T2 did not differ from T1. The strain T2 was more sensitive to QM than T1 and T3. Both mutagens induce mitotic crossing over in T2 at a higher frequency than T1. MMS is not able to induce mitotic crossing over in T3 and QM demonstrates a very low induction. Treatment of the strains T1 and T2 with MMS and T1 with QM induces mitotic crossing over during the first cell division more often than during the second one. In most cases, QM induces mitotic crossing over in cells of the strain T2 during the second division. We suppose that the damages of DNA induced by QM in the wild type cells can be excised, but in the rad2 cells the gaps in DNA appeared after replication. In both cases, single-strand breaks of DNA are the main reason for mitotic crossing over.