Cytotoxic action of the chemical substances found as admixtures in medical immunobiological preparations

The cytotoxic action (CTA) of chemical substances contained as admixtures in medical immunobiological preparations on human diploid cells has been studied. Such chemical substances as rivanol and merthiolate in admissible concentrations show the highest degree of CTA. The results obtained in this investigation indicate that different concentrations of chemical substances may produce equal CTA; thus, thiolate in toxic in a dose of 0.8 microgram/ml; the same CTA is produced by aluminium sulfate in a concentration of 500 micrograms/ml. Small doses of chemical substances, producing no explicit manifestations of the cytotoxic effect, may have latent CTA determined by additional methods of investigation. CTA may be manifested as lethal, sublethal and latent cell lesions. In working out regulations on the test for CTA it is expedient to indicate admissible residual amounts of chemical substances contained in finished medical immunobiological preparations, considering that these amounts must be incapable of producing CTA in cell cultures. The conclusion has been made on the expediency of denoting small amounts of chemical substances capable of producing latent CTA as tentatively tolerable doses.     

Uracil metabolism in golden hamster after irradiation.

The catabolism of uracil and the total balance of excreted radioactivity were studied in golden hamsters after a peroral application of 14C-uracil. Twenty-four hours after administration most of the radioactivity taken up appeared in expired carbon dioxide. The percent proportion of radioactivity in carbon dioxide was independent of the amount of uracil administered. On the other hand, the percentage of radioactivity excreted in urine depended on the amount of uracil taken up, high doses of the compound causing up to eight-fold increase in urine-excreted radioactivity. Most of the exogenously-administered uracil was catabolized within the first 5 hours. Irradiation had no substantial effect on the dynamics of uracil catabolism. Analysis of urine revealed that most urine-excreted radioactivity is in the form of uracil. On peroral application of high doses of uracil to irradiated hamsters, their urine was found to contain barbituric acid which originated from uracil.     

Chromosome imbalance and cellular proliferation potential in vitro

The effect of chromosome unbalance on the cell proliferative potential (cloning efficiency) was studied. The proliferative potential of the cells obtained from spontaneous abortions with chromosome unbalance appeared drastically reduced as compared with the proliferative potential of the cells from medical abortions. Chromosome unbalance in postnatal cells did not lead to diminution of the proliferative potential as compared with control.     

Endocrine-metabolic relations in rats with genetic arterial hypertension

Levels of triiodothyronine, thyroxine, insulin, glucose and free fatty acids in the blood; contents of adrenaline, noradrenaline in adrenals and glycogen in the liver; activity of phenylethanolamine-N-methyltransferase in adrenals, hexokinase and glucose-6-phosphatase in the liver were studied in male Wistar rats and rats with inherited stress-induced arterial hypertension /ISIAH/. It was found that genetically caused rise of hypophyseal-thyroid systems activity in ISIAH-rats leads to a decrease of insulin blood level, activation of lipolysis and breach of glucose tolerance.     

Spatiotemporal patterns of macrophage migration inhibitory factor (Mif) expression in the mouse placenta

Background  

Macrophage migration inhibitory factor (MIF) has special pro-inflammatory roles, affecting the functions of macrophages and lymphocytes and counter-regulating the effects of glucocorticoids on the immune response. The conspicuous expression of MIF during human implantation and early embryonic development also suggests this factor acts in reproductive functions. The overall goal of this study was to evaluate Mif expression by trophoblast and embryo placental cells during mouse pregnancy.     

Targeting of the Enhanced Green Fluorescent Protein Reporter to Adrenergic Cells in Mice

Adrenaline and noradrenaline are important neurotransmitter hormones that mediate physiological stress responses in adult mammals, and are essential for cardiovascular function during a critical period of embryonic/fetal development. In this study, we describe a novel mouse model system for identifying and characterizing adrenergic cells. Specifically, we generated a reporter mouse strain in which a nuclear-localized enhanced green fluorescent protein gene (nEGFP) was inserted into exon 1 of the gene encoding Phenylethanolamine n-methyltransferase (Pnmt), the enzyme responsible for production of adrenaline from noradrenaline. Our analysis demonstrates that this knock-in mutation effectively marks adrenergic cells in embryonic and adult mice. We see expression of nEGFP in Pnmt-expressing cells of the adrenal medulla in adult animals. We also note that nEGFP expression recapitulates the restricted expression of Pnmt in the embryonic heart. Finally, we show that nEGFP and Pnmt expressions are each induced in parallel during the in vitro differentiation of pluripotent mouse embryonic stem cells into beating cardiomyocytes. Thus, this new mouse genetic model should be useful for the identification and functional characterization of adrenergic cells in vitro and in vivo.     

In vitro movement of human embryonic fibroblasts with normal and anomalous sets of chromosomes

Migration of diploid postnatal and embryonic diploid and aneuploid cells was studied using a modified method of investigation of leukocyte migration under agarose. The method permits to study migration of fibroblasts and other proliferating cells. Embryonic fibroblasts were shown to move faster, than postnatal fibroblasts. Cells with trisomy 7, 9 and C, and triploid cells were found to move slower than diploid cells. Locomotor disturbances are supposed to be the basis of impairment of morphogenesis in chromosomal anomalies in man.