Morphogenesis and growth potentials of organ cultures of the respiratory tract anlage of mice susceptible and resistant to pulmonary blastomogenesis

The morphogenesis and growth potencies have been studied in the long-term organ cultures of different parts of the respiratory tract early rudiment in the mouse strains susceptible (A) and resistant (C57BL) against lung blastomogenesis. Similarities and peculiarities have been shown for the lung rudiment cells developing in vitro and in vivo. The linear differences have been established in morphogenesis and growth potencies of the proximal and distal parts of the respiratory tract rudiment. Possible importance of phenotypic differences in realization of the genetically determined sensitivity of the mouse-lung tissue to spontaneous and induced blastomogenesis is discussed.     

Kinetics and regulatory properties of the disulfide reductase enzyme from mouse liver]

Disulfide reductase (DSR) of mice liver supernatant is kinetically demonstrated as associating-dissociating oligomeric protein with positive homotropic cooperativity for the substrate. Cyclic 3',5'-AMP (10(-11)--10(-5) M) activates DSR and increases V, but does not change either [S]0,5, nor nH and does not shift the plot of specific activity versus the enzyme concentration. ATP, GTP, UTP, CTP, protamine, histone, Mg2+, Ca2+, EDTA (but not adenosine, 5'-AMP, 2'3'-AMP, ADP beef serum albumin) activated DSR. The effects of different modifiers are not summed up. Preincubation is essential for the action of the majority of the activators. Heating for 8 minutes at 55 degrees C desensitized completely DSR to all the modifiers without changing its catalytic activity, [S]0,5 and nH values. Possible mechanisms of activation of DSR, especially the involvement of protein kinase, are discussed.     

Stress CSP310 Protein Uncouples Oxidative Phosphorylation Otherwise than Other Plant Uncoupling Proteins Do

The addition of cold shock CSP310 protein to mitochondria isolated from both monocotyledonous (rye, wheat, and maize) and dicotyledonous (pea) plants uncoupled oxidation from phosphorylation. This uncoupling was caused neither by the damage to mitochondrial membranes nor by the activation of alternative cyanide-resistant oxidase. As distinct from the classical plant uncoupling mitochondrial protein (PUMP), CSP310 uncoupling effect was insensitive to BSA. Therefore, we believe that the mechanism of CSP310 action differs from that of known plant uncoupling proteins.     

Plasmid-determined streptococcal resistance to antibiotics]

The analysis of the genetic organization of the determinant ERLI by means of obtaining and studying the antibiotic sensitive mutants from the strain resistant to erythromycin and lincomycin provided experiment data in favour of the fact that inducable resistance to erythromycin and lincomycin determined by the plasmid might be defined by the same or closely linked genes.     

Morphogenetic characteristics of the aggregates formed in epithelial and mesenchymal recombinations of the lungs from intact and urethane-exposed mouse embryos

A study was made of the morphogenesis of organotypic aggregates obtained by epithelial mesenchymal recombinations from the lungs of embryonic mice, intact and treated with urethane. Normal growth and differentiation of organotypic structures were observed in long-term cultures of aggregates obtained by recombinations of the lung epithelium (E) and mesenchyma (M) from intact (i) embryonic mice (EiMi). Hyperplasia and squamous-cell metaplasia (with or without keratinization) of the epithelium were found in aggregates obtained from E and M of the treated mouse embryos (EtMt) and in aggregates obtained by recombinations of lung E and M from intact and treated embryos (EtMi, EiMt). The data obtained suggest that the alterations in epithelial mesenchymal interactions are of great significance for transplacental lung blastomogenesis and that the mesenchymal lung cells play an important part in mediation of the transplacental carcinogenous effects on epithelial target cells via subsequent epithelial mesenchymal tissue interactions.     

Effect of aflatoxin B1 in vitro and in vivo]

The direct and transplacental action of aflatoxin B1 was studied on organic cultures of the embryonic pulmonary tissue of mice of the A line, BD-IX rats and golden hamsters (Cricetus auratus W.). Its toxic action on the cultures and the absence of any blastomogenic effect was demonstrated. In experiments on mice the transplacental penetration of aflatoxin B1 led to an increase in the incidence of the breast tumours in the progeny.     

Human granulocyte colony stimulating factor (hG-CSF): cloning,overexpression, purification and characterization

Background  

Biopharmaceutical drugs are mainly recombinant proteins produced by biotechnological tools. The patents of many biopharmaceuticals have expired, and biosimilars are thus currently being developed. Human granulocyte colony stimulating factor (hG-CSF) is a hematopoietic cytokine that acts on cells of the neutrophil lineage causing proliferation and differentiation of committed precursor cells and activation of mature neutrophils. Recombinant hG-CSF has been produced in genetically engineered Escherichia coli (Filgrastim) and successfully used to treat cancer patients suffering from chemotherapy-induced neutropenia. Filgrastim is a 175 amino acid protein, containing an extra N-terminal methionine, which is needed for expression in E. coli. Here we describe a simple and low-cost process that is amenable to scaling-up for the production and purification of homogeneous and active recombinant hG-CSF expressed in E. coli cells.     

Increasing the toxic effect of pulmonary carcinogens by destruction of epithelial-mesenchymal interaction in explants of embryonic respiratory tract of mice

The explants from 17-day old embryos of A and C57BL mice were used for long-term organ cultures. The following series of explants were studied: 1) the intact control explants; 2) the explants treated by NMU; 3) the explants treated by BP; 4) the explants isolated from mesenchyma (M); 5) the explants isolated from M and treated by NMU; 6) the explants isolated from M and treated by BP. The survival of explants treated by NMU or BP did not differ from the intact control explants (p less than 0.1). The removal of M decreased the survival only in the explants from the distal RT of A mice (p 0.01). The survival of explants isolated from M and treated by NMU or BP was significantly lower than it was in intact explants (p less than 0.01-0.001). Thus, the destruction of epithelial-mesenchymal interaction induced by removal of M can modulate the toxic effect of pulmonotropic carcinogens.