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The article presents an analysis of the potato breeding problems in Russia which are associated with the low phytosanitary state of potato seed material infected with viral and bacterial diseases, as a result, it is necessary to carry out its improvement and the use of Russian varieties. Experiments were conducted in the laboratory of plant microclonal propagation according to the methodological recommendations for improvement and accelerated propagation of seed potatoes. The results of research on refining the technology of seed potato improvement by adding the Oxolin antiviral drug to the standard nutrient medium MS; its optimal concentrations for obtaining the largest number of uninfected plants of the studied varieties were identified. For potato varieties Liga, Hussar, and Real, the optimal concentration was 20 mg/l of Oxolin, while in the varieties Aurora, Real, and Sirenevy tuman, the concentration was 30 mg/l. Therefore, it is necessary to search for antiviral drugs with an alternative mechanism of action which remains very relevant and practically significant. The research results obtained in this work can be applied both to optimize the cultivation regime of potato microclones in vitro and to enhance the productive process of the uninfected microplants.

In the conditions of the North-West zone of Russia, studies of Pikovit vitamin complex preparation were carried out. Since the main way to obtain a healthy seed is clonal micropropagation. Therefore, in the course of the work, the process and method of clonal micropropagation of Russian potato varieties using new preparations were improved, the selection of nutrient media at all stages of cultivation was carried out with the Pikovit preparation at the concentration of 0.5 to 1.5 mg/l. As a result, it was found that use of the Pikovit vitamin complex has a positive effect on the ontogenesis of potato microplants. To obtain well-developed microplants of the early variety Liga, the most optimal concentration is 1.5 mg/l. For other studied varieties of the mid-ripening group Aurora and Gusar, the nutrient medium with the addition of vitamins at the concentration of 1.0 mg/l was optimal.

For effective commercial development of deposits, an increase in the information content of operational exploration is required. In recent years, the range of methods used to obtain complete and reliable information about the structure and properties of the rock mass of a developed field include remote methods of high-frequency electrical prospecting, in particular, the ground penetrating radar (GPR) method. The paper presents a methodological experience in the interpretation of GPR data of sandy river sediments based on the identification of radar facies. In the considered area, four types of radar facies have been identified that characterize the structure of sandy deposits and the morphology of the river bed. The criteria for identifying radar facies were used to analyze wave patterns of loose sediments in a sand and gravel pit and a placer gold deposit. Experimental GPR investigations are presented by data from a sandy-gravel pit (Warsaw, Poland) and from a placer gold deposit (Yakutia, Russia). As an example, a GPR section along the Paplin quarry and its interpretation, with the identification of GPR facies, is presented. A cross-sectional GPR profile of the dredging landfill is considered for the placer gold deposit. The analysis of the wave pattern was carried out, geological boundaries were highlighted. Based on the interpretation results, the characteristics of the rocks were given. It was noted that according to the GPR data, it is possible to identify zones of uplift of bedrock, which can affect the course of the dredge. As a result of using GPR in a swampy area where drilling was impossible, a deep three-layer section was obtained. The presented results of the successful use of GPR investigations and methodological approaches in the interpretation of data, show the promise of using the GPR method in assessing mining and geological conditions, in particular, placer deposits. At the same time, the efficiency of obtaining data can further contribute to the optimization of technology and increase the efficiency of field development.

The cardiotonic steroid marinobufagenin (MBG) has been implicated in the pathogenesis of experimental uremic cardiomyopathy, which is characterized by progressive cardiac fibrosis. We examined whether the transcription factor Friend leukemia integration-1 (Fli-1) might be involved in this process. Fli-1-knockdown mice demonstrated greater cardiac collagen-1 expression and fibrosis compared with wild-type mice; both developed increased cardiac collagen expression and fibrosis after 5/6 nephrectomy. There was a strong inverse relationship between the expressions of Fli-1 and procollagen in primary culture of rat cardiac and human dermal fibroblasts as well as a cell line derived from renal fibroblasts and MBG-induced decreases in nuclear Fli-1 as well as increases in procollagen-1 expression in these cells. Transfection of a Fli-1 expression vector prevented increased procollagen- 1 expression from MBG. MBG exposure induced a rapid translocation of the [delta]-isoform of protein kinase C (PKC[delta]) to the nucleus. This translocation was prevented by pharmacological inhibition of phospholipase C, and MBG-induced increases in procollagen-1 expression were prevented with a PKC[delta]- but not a PKC[alpha]-specific inhibitor. Finally, immunoprecipitation studies strongly suggest that MBG induced phosphorylation of Fli-1. We feel these data support a causal relationship with MBG-induced translocation of PKC[delta], which results in phosphorylation of as well as decreases in nuclear Fli-1 expression, which, in turn, leads to increases in collagen production. Should these findings be confirmed, we speculate that this pathway may represent a therapeutic target for uremic cardiomyopathy as well as other conditions associated with excessive fibrosis. renal failure; cardiotonic steroids; fibrosis

We recently demonstrated that the cardiotonic steroid marinobufagenin (MBG) induced fibrosis in rat hearts through direct stimulation of collagen I secretion by cardiac fibroblasts. This stimulation was also responsible for the cardiac fibrosis seen in experimental renal failure. In this study, the effect of MBG on the development of renal fibrosis in rats was investigated. Four weeks of MBG infusion triggered mild periglomerular and peritubular fibrosis in the cortex and the appearance of fibrotic scars in the corticomedullary junction of the kidney. MBG also significantly increased the protein levels and nuclear localization of the transcription factor Snail in the tubular epithelia. It is known that activation of Snail is associated with epithelial-to-mesenchymal transition (EMT) during renal fibrosis. To examine whether MBG alone can trigger EMT, we used the porcine proximal tubular cell line LLC-PK1. MBG (100 nM) caused LLC-PK1 cells grown to confluence to acquire a fibroblast-like shape and have an invasive motility. The expressions of the mesenchymal proteins collagen I, fibronectin, and vimentin were increased twofold. However, the total level of E-cadherin remained unchanged. These alterations in LLC-PK1 cells in the presence of MBG were accompanied by elevated expression and nuclear translocation of Snail. During the time course of EMT, MBG did not have measurable inhibitory effects on the ion pumping activity of its natural ligand, [Na.sup.+]-[K.sup.+]-ATPase. Our data suggest that the MBG may be an important factor in inducing EMT and, through this mechanism, elevated levels of MBG in chronic renal failure may play a role in the progressive fibrosis. cardiotonic steroid hormone; ouabain; [Na.sup.+]-[K.sup.+]-ATPase; transcription factor Snail

Abstract Background Placental malfunction in preeclampsia is believed to be a consequence of aberrant differentiation of trophoblast lineages and changes in utero-placental oxygenation. The transcription factor Snail, a master regulator molecule of epithelial-mesenchymal transition in embryonic development and in cancer, is shown to be involved in trophoblast differentiation as well. Moreover, Snail can be controlled by oxidative stress and hypoxia. Therefore, we examined the expression of Snail and its downstream target, e-cadherin, in human normal term, preterm and preeclamptic placentas, and in pregnant rats that developed preeclampsia-like symptoms in the response to a 20-fold increase in sodium intake. Methods Western blotting analysis was used for comparative expression of Snail and e- cadherin in total protein extracts. Placental cells expressing Snail and e-cadherin were identified by immunohistochemical double-labeling technique. Results The levels of Snail protein were decreased in human preeclamptic placentas by 30% (p < 0.01) compared to normal term, and in the rat model by 40% (p < 0.001) compared to control placentas. In preterm placentas, the levels of Snail expression varied, yet there was a strong trend toward statistical significance between preterm and preeclamptic placentas. In humans, e-cadherin protein level was 30% higher in preeclamptic (p < 0.05) placentas and similarly, but not significantly (p = 0.1), high in the preterm placentas compared to normal term. In the rat model of preeclampsia, e-cadherin was increased by 60% (p < 0.01). Immunohistochemical examination of human placentas demonstrated Snail-positive staining in the nuclei of the villous trophoblasts and mesenchymal cells and in the invasive trophoblasts of the decidua. In the rat placenta, the majority of Snail positive cells were spongiotrophoblasts of the junctional zone, while in the labyrinth, Snail-positive sinusoidal giant trophoblasts cells were found in some focal areas located close to the junctional zone. Conclusion We demonstrated that human preeclampsia and the salt-induced rat model of preeclampsia are associated with the reduced levels of Snail protein in placenta. Down-regulation of the transcription factor Snail in placental progenitor cell lineages, either by intrinsic defects and/or by extrinsic and maternal factors, may affect normal placenta development and function and thus contribute to the pathology of preeclampsia.