One of the most important pathological consequences of renal ischemia/reperfusion (I/R) is kidney malfunctioning. I/R leads to oxidative stress, which affects not only nephron cells but also cells of the vascular wall, especially endothelium, resulting in its damage. Assessment of endothelial damage, its role in pathological changes in organ functioning, and approaches to normalization of endothelial and renal functions are vital problems that need to be resolved. The goal of this study was to examine functional and morphological impairments occurring in the endothelium of renal vessels after I/R and to explore the possibility of alleviation of the severity of these changes using mitochondria-targeted antioxidant 10-(6'-plastoquinonyl)decylrhodamine 19 (SkQR1). Here we demonstrate that 40-min ischemia with 10-min reperfusion results in a profound change in the structure of endothelial cells mitochondria, accompanied by vasoconstriction of renal blood vessels, reduced renal blood flow, and increased number of endothelial cells circulating in the blood. Permeability of the kidney vascular wall increased 48 h after I/R. Injection of SkQR1 improves recovery of renal blood flow and reduces vascular resistance of the kidney in the first minutes of reperfusion; it also reduces the severity of renal insufficiency and normalizes permeability of renal endothelium 48 h after I/R. In in vitro experiments, SkQR1 provided protection of endothelial cells from death provoked by oxygen-glucose deprivation. On the other hand, an inhibitor of NO-synthases, L-nitroarginine, abolished the positive effects of SkQR1 on hemodynamics and protection from renal failure. Thus, dysfunction and death of endothelial cells play an important role in the development of reperfusion injury of renal tissues. Our results indicate that the major pathogenic factors in the endothelial damage are oxidative stress and mitochondrial damage within endothelial cells, while mitochondria-targeted antioxidants could be an effective tool for the protection of tissue from negative effects of ischemia.

Sodium is a key element in a living organism. The increase of its concentration is an indicator of many pathological conditions. 23 Na MRI is a quantitative method that allows to determine the sodium content in tissues and organs in vivo. This method has not yet entered clinical practice widely, but it has already been used as a clinical research tool to investigate diseases such as brain tumors, breast cancer, stroke, multiple sclerosis, hypertension, diabetes, ischemic heart disease, osteoarthritis. The active development of the 23 Na MRI is promoted by the growth of available magnetic fields, the expansion of hardware capabilities, and the development of pulse sequences with ultra-short echo time.

Remote ischemic preconditioning of hind limbs (RIPC) is an effective method for preventing brain injury resulting from ischemia. However, in numerous studies RIPC has been used on the background of administered anesthetics, which also could exhibit neuroprotective properties. Therefore, investigation of the signaling pathways triggered by RIPC and the effect of anesthetics is important. In this study, we explored the effect of anesthetics (chloral hydrate and Zoletil) on the ability of RIPC to protect the brain from injury caused by ischemia and reperfusion. We found that RIPC without anesthesia resulted in statistically significant decrease in neurological deficit 24 h after ischemia, but did not affect the volume of brain injury. Administration of chloral hydrate or Zoletil one day prior to brain ischemia produced a preconditioning effect by their own, decreasing the degree of neurological deficit and lowering the volume of infarct with the use of Zoletil. The protective effects observed after RIPC with chloral hydrate or Zoletil were similar to those observed when only the respective anesthetic was used. RIPC was accompanied by significant increase in the level of brain proteins associated with the induction of ischemic tolerance such as pGSK-3β, BDNF, and HSP70. However, Zoletil did not affect the level of these proteins 24 h after injection, and chloral hydrate caused increase of only pGSK-3β. We conclude that RIPC, chloral hydrate, and Zoletil produce a significant neuroprotective effect, but the simultaneous use of anesthetics with RIPC does not enhance the degree of neuroprotection.

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Corundum-carbon refractories and ramming bodies are being used for lining cupola furnaces and mixer-type cast iron handling ladles [1][2][3][4][5]. Corundum-carbon refractories possess high slag resistance, but their apparent density and strength abruptly decrease with increasing carbon content. Furthermore, their low oxidation resistance forms one of the significant shortcomings.Additions of 5-15% silicon carbide and a mixture of silicon and aluminum powders have been suggested [5][6][7][8] for strengthening corundum-carbon refractories and decreasing the degree of oxidation of carbon.This paper deals with a study of the optimum content of the graphite and silicon carbide additives in a mullite-corundum body produced incorporating a binder based on orthophosphoric acid; for this purpose, the simplex-grid method of experimental planning was used. The content of AI=O3 in the original body amounted to not less than 88% * and the P202 content was 2.5-3.0%. We used crystalline graphite (GOST 5279-74) containing approximately 98% particles having a minus 0.09-n~n size and the No. 12/6 grade silicon carbide (GOST 3647-80). We introduced 5-15% graphite and silicon carbide additives into the ramming body.Cubic specimens having an edge of 40 mm were compacted from the experimental systems at a pressure of 30 N/mm 2. After drying, the specimens were placed in a Kryptol charge and were fired at 1580~for 6 h using a reverberatory furnace. The ultimate compressive strength of the fired specimens was determined.The crucible method was used to determine the resistance of the bodies to the action of slag and molten cast iron. The chemical composition of the slag was as follows, %: SiO2 42.98; AI203 10.24; CaO 39.75; MgO 2.71; MnO 2.26; FeO 3.02; K20 0.28; and Na20 0.Ii. The carbon content in the cast iron sample (chip) was found to be 4.47%. Along with slag pellets and cast iron chips, the specimens were placed in a Kryptol charge and were fired at 1500~ for a period of 2 h. After cooling, the area attacked by molten cast iron or slag was determined on the transverse section of the specimens.The degree of oxidation was determined from the changes occurring in the weight of the experimental systems during the process of heat treating at 800~ for 4 h in air. The heattreatment temperature (800~ was chosen based on the published data [7] indicating that the oxidation rate of graphite abruptly increases in the 650-800~ range and that it remains almost constant at a temperature exceeding 800~Heat treatment of the samples (weighing 30 g) was carried out in corundum crucibles.The following factors were chosen as variables: X I -content of the mullite-corundum body based on a phosphate 5inder with a 70-90% region of determination (range of variation); X 2 -content of the graphite additive with a 5-15% region of determination; and X 3 -silicon carbide content with a 5-15% region of determination.The investigated functions included the ultimate compressive strength of the specimens fired at 1580~ (Ocm, N/mm2); the area attacked (corroded) ...

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