[The approaches to planning of medical infrastructure and bed stock in medical organizations in conditions of development and spread of coronavirus infection COVID-19].

The article presents key approaches to methods of assessing and prognosticating the need both for bed stock, considering level of morbidity and epidemiological process in conditions of development and prevalence of coronavirus COVID-19 infection, and as well the regional network of medical organizations of public and municipal health care that should be reoriented to medical care support during pandemic according to 14 evaluation criteria.

[New approaches in the regulation of blood phagocytes and reduction in the formation of oxygen radicals in patients with heart failure].

AIM: The purpose was to study the effect of actovegin on the formation of reactive oxygen species by blood phagocytes of patients with heart failure and on SK-N-SH neuron necrosis. MATERIALS AND METHODS: The generation of superoxide anion (O2-*) were recorded on whole blood samples (50-100 µl). Change lucigenin-dependent hemiluminescence determined on a hemi-luminometer "Biotoks-7". As a stimulator of the phagocyte. phorbol ester (PMA, 1 µm) was used. Necrosis of neurons induced by hydrogen peroxide was determined by fluorescence of propidium iodit. RESULTS: Blood phagocytes of heart failure patients are initially pre-activated (primed). These cells spontaneous generated oxygen radicals. Actovegin dosa-dependent decreased radicals level and radical induced by PMA (1 µm). After PMA maximal inhibitory effect of actovegin observed in doses higher than 2-3 mg/ml. The impact of actovegin on the viability of human SK-N-SH neurons in the presence hydrogen peroxide (100 µm) was studied in vitro. Under these conditions hydrogen peroxide triggered radical-dependent neurons necrosis Actovegin dosa-dependent decreased of neuron death. CONCLUSION: Actovegin inhibits spontaneous and induced formation of reactive oxygen species generated by blood phagocytes of patients with heart failure. Actovegin suppressed necrosis of human SK-N-SH neuroblastoma cells caused by hydrogen peroxide. It is assumed that actovegin protects_cells of arious organs and tissues, including blood cells and neurons that die as a result of ischemia and inflammation by reducing levels of react.ive-oxygenspecies.

[Regulating activity of plasma membranous Ca2+ channels in PC-12 pheochromocytoma cells with chemicals and pharmaceutic agents]. / Reguliatsiia aktivnosti Ca2+-kanalov plazmaticheskikh membran kletok feokhromotsitomy PC-12 s pomoshch'iu khimicheskikh soedinenii i farmakologicheskikh agentov.

The activity of the voltage-operated Ca2+ channels (VOC channels) and store-operated Ca(2+)-channels (SOC channels) was studied on rat pheochromatocytomic cells PC-12 by using the fluorescence calcium dye Fura-2. The VOC channels were transferred in their open state by depolarizing the plasma membranes of the cells through addition of high KCl concentrations (50 mM). The SOC channels were activated by treating the cells with tapsigargine, a special inhibitor of Ca2+ ATPase in the intracellular Ca2+ stores. Verapamil effectively inhibited the activity of the VOC channels (IC50 = 0.6 micron), but failed to affect the SOC channels. Arachidonic acid reduced the level of [Ca2+]-induced TG (200 nM) at a concentration of 3-10 microns). The movement of Ca2+ along the SOC channels was electrogenic. The depolarization of the plasma membrane of PC-12 cells caused no release of Ca(2+) from the intercellular Ca2+ stores. It is concluded that PC-12 cells are a suitable model to study the activity of different Ca2+ channels and search for chemical compounds that affect the potential-dependent and potential-independent Ca2+ channels.