Films consisting of TiO2/ZrO2/SiO2 undoped and doped with Au nanoparticles were synthesized by the sol‐gel method. The films were characterized with X‐ray diffraction (XRD), scanning electron microscopy (SEM), spectroscopic ellipsometry (SE) and optical absorption (OA) methods. The XRD study demonstrates the formation of TiO2 anatase nanocrystals and Au nanoparticles. SE and OA measurements of the undoped films showed no significant absorption in the spectral range of 400–1000 nm. Doping with Au nanoparticles resulted in the appearance of a surface plasmon resonance (SPR) absorption band at 600 nm as well as weaker absorption bands in the 300–500 nm region. The observed changes in optical properties agreed with the enhanced photocatalytic activity of Au‐doped TiO2/ZrO2/SiO2 films with gold compared to undoped films. The photocatalytic activity was evaluated by the photodegradation of the organic dye Rhodamine B. Under optimized conditions, the photodecomposition rate of the doped films was several times larger than that of the undoped films. Films of TiO2, TiO2/ZrO2/SiO2 and ternary oxides were investigated.

In acute experiments on anesthetized rats, we studied the effects of modulation of the mitochondrial permeability in medullary cardiovascular neurons (nucl. tractus solitarii, NTS, nucl. ambiguus, AMB, paramedian reticular nucleus, PMn, and lateral reticular nucleus, LRN) on the systemic arterial pressure (SAP). We were the first to show that the mitochondrial permeability is essential for medullary cardiovascular control. An increase in the mitochondrial permeability with injections of an inductor of mitochondrial transition pore opening, phenylarsine oxide (PAO, 0.5 to 504 nmol), into the medullary nuclei resulted in long-lasting decreases in the SAP; at high doses of PAO, these drops could be irreversible and led to the animal's death. Injections of an inhibitor of mitochondrial transition pore opening, melatonin (0.7 to 70.0 nmol), into the medullary nuclei induced dose-dependent increases in the SAP. Melatonin and L-arginine were shown to demonstrate neuroprotective effects due to their ability to attenuate the consequences of increased mitochondrial permeability in medullary cardiovascular neurons.

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