Publications by authors named "A N OBROSOV"

In this study, heat-treated and multisurface engineered DIN 1.2367 tool steel was subjected to room and elevated temperature wear tests, and the effect of nitriding on its tribological behavior was investigated. CrN, AlTiN, and CrN/AlTiN coatings with a total thickness of 2 µm were obtained by arc cathodic physical vapor deposition on conventional heat-treated and gas-nitrided steels.

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Objective: Feeding mice a diet containing high fat and high sucrose has been promoted as a good model for type 2 diabetes. This study sought to determine the effect of feeding mice a high fat and high sucrose diet on neuropathy compared to mice fed only a high fat diet and mice fed a high diet and treated with streptozotocin.

Methods: C57Bl/6J mice were divided into five groups and fed the following diets for 20 weeks: Normal (Control); Sucrose enriched (Control + Sucrose), High Fat (Diet-induced obesity (DIO)), High Fat and High Sucrose (DIO + sucrose) and High Fat diet/streptozotocin treated (Diabetic).

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Unlabelled: In this study, we assessed the outcomes after surgical treatment of thoracic post-excision defects in 15 patients, using TiNi knitted surgical meshes and customized artificial TiNi-based ribs.

Methods: Eight patients were diagnosed with advanced non-small cell lung cancer (NSCLC) invading the chest wall, of which five patients were TNM, two were TNM, and one was TNM. Squamous cell carcinoma was identified in three of these patients and adenocarcinoma in five.

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To rigorously explore the role of omega-3 polyunsaturated fatty acids (PUFA) in the treatment of diabetic peripheral neuropathy (DPN), we have created a transgenic mouse utilizing a Cre-lox promoter to control overexpression of human 15-lipoxygenase-1 (15-LOX-1). In this study, we sought to determine the effect of treating type 2 diabetic wild-type mice and transgenic mice ubiquitously overexpressing 15-LOX-1 with menhaden oil on endpoints related to DPN. Wild-type and transgenic mice on a C57Bl/6J background were divided into three groups.

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Previous work by ourselves and others showed that mitoquinone (mitoQ) reduced oxidative damage and prevented hepatic fat accumulation in mice made obese with high-fat (HF) feeding. Here we extended these studies to examine the effect of mitoQ on parameters affecting liver function in rats treated with HF to induce obesity and in rats treated with HF plus streptozotocin (STZ) to model a severe form of type 2 diabetes. In prior reported work, we found that mitoQ significantly improved glycemia based on glucose tolerance data in HF rats but not in the diabetic rats.

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