This work describes the wettability and biological performance of Zn- and Cu-containing CaP-based coatings prepared by micro-arc oxidation on pure titanium (Ti) and novel Ti-40Nb alloy. Good hydrophilic properties of all the coatings were demonstrated by the low contact angles with liquids, not exceeding 45°. An increase in the applied voltage led to an increase of the coating roughness and porosity, thereby reducing the contact angles to 6° with water and to 17° with glycerol. The free surface energy of 75 ± 3 mJ/m² for all the coatings were determined. Polar component was calculated as the main component of surface energy, caused by the presence of strong polar PO₄³⁻ and OH⁻ bonds. In vitro studies showed that low Cu and Zn amounts (~0.4 at.%) in the coatings promoted high motility of human adipose-derived multipotent mesenchymal stromal cells (hAMMSC) on the implant/cell interface and subsequent cell ability to differentiate into osteoblasts. In vivo study demonstrated 100% ectopic bone formation only on the surface of the CaP coating on Ti. The Zn- and Cu-containing CaP coatings on both substrates and the CaP coating on the Ti-40Nb alloy slightly decreased the incidence of ectopic osteogenesis down to 67%. The MAO coatings showed antibacterial efficacy against Staphylococcus aureus and can be arranged as follows: Zn-CaP/Ti > Cu-CaP/TiNb, Zn-CaP/TiNb > Cu-CaP/Ti.

This study aims to determine the effectiveness of administering 80 ppm nitric oxide in reducing kidney injury, mitochondrial dysfunction and regulated cell death in kidneys during experimental perfusion. Twenty-four sheep were randomized into four groups: two groups received 80 ppm NO conditioning with 90 min of cardiopulmonary bypass (CPB + NO) or 90 min of CPB and hypothermic circulatory arrest (CPB + CA + NO), while two groups received sham protocols (CPB and CPB + CA). Kidney injury was assessed using laboratory (neutrophil gelatinase-associated lipocalin, an acute kidney injury biomarker) and morphological methods (morphometric histological changes in kidney biopsy specimens). A kidney biopsy was performed 60 min after weaning from mechanical perfusion. NO did not increase the concentrations of inhaled NO₂ and methemoglobin significantly. The NO-conditioning groups showed less severe kidney injury and mitochondrial dysfunction, with statistical significance in the CPB + NO group and reduced tumor necrosis factor-α expression as a trigger of apoptosis and necroptosis in renal tissue in the CPB + CA + NO group compared to the CPB + CA group. The severity of mitochondrial dysfunction in renal tissue was insignificantly lower in the NO-conditioning groups. We conclude that NO administration is safe and effective at reducing kidney injury, mitochondrial dysfunction and regulated cell death in kidneys during experimental CPB.

Aim. To identify early morphological changes in the heart and aorta of rats with experimental metabolic syndrome induced by a high-fat and high-carbohydrate diet (HFHCD).Materials and methods. The study was carried out on male Wistar rats. The animals were divided into two groups: a control group (n = 10) and an experimental group (n = 10). The rats from the control group were fed with a standard laboratory diet. The rats from the experimental group received HFHCD for 12 weeks. Body weight, blood pressure (BP), and individual parameters of carbohydrate and lipid metabolism were assessed in the rats. A histologic examination of the heart and aorta in the animals was performed.Results. Feeding rats with HFHCD led to an increase in body weight, elevation of BP, obesity, hyperglycemia, and triglyceridemia. The histologic examination of the heart in the rats of the experimental group showed signs of vascular disease, lipomatosis, and focal myocardial degeneration. Lipid accumulation in the cells of the media, hyperplasia of adipocytes in the adventitia, and depletion and fragmentation of the elastic lamina were revealed in the aortic wall of the rats receiving HFHCD.Conclusion. The study indicated that HFHCD is an effective way to model metabolic syndrome. Structural disorders in the heart and aorta may be the mainstay for the development of cardiomyopathy and arterial hypertension in diet-induced metabolic syndrome.

Aim. To evaluate the efficiency and safety of nitric oxide delivery for kidney protection in the simulation of cardiopulmonary bypass and circulatory arrest in the experiment.Materials and Methods. We performed an experimental modeling of cardiopulmonary bypass with circulatory arrest in 20 sheep of the Altai breed weighing 30-32 kg. Circulatory arrest was performed at moderate hypothermia (30-32°C) for 15 minutes and was followed by reperfusion and warming up to 37°C. Animals were divided into 2 equal groups: 10 sheep which received nitric oxide (NO) through the inhalations supply and cardiopulmonary bypass machine at a dose of 80 ppm, and 10 control sheep. We further collected biological fluids and tissue specimens for subsequent assessment of the safety of NO use and its nephropro-tective properties.Results. The proposed method of NO therapy during the cardiopulmonary bypass with circulatory arrest was safe and did not lead to an increase in toxic metabolites. In sheep which received NO therapy, the average concentration of NO2 throughout the entire period of the experiment was 1.2 ± 0.19 ppm (with a maximum allowable concentration of 3.0 ppm), and the concentration of methemoglobin (MetHb) was 2.3 ± 0.34% (with a maximum allowable level of 5.0%). Neutrophilic gelatinase-associated lipocalin (NGAL) was significantly lower in sheep which received NO therapy (0.67 ± 0.255 ng/mL versus 2.23 ± 0.881 ng/mL in the control group, p = 0.0001). Acute kidney injury was mitigated in sheep which received NO therapy.Conclusion. Experimental delivery of NO at a dose of 80 ppm during the cardiopulmonary bypass and circulatory arrest is safe and is associated with reduced acute kidney injury.

Закономерности регенерации конъюнктивы и склеры после интраоперационной аппликации раствора циклоспорина А у кроликов со стероидной моделью глаукомы