On cognitive approach to language when studying Russian prefixes expressing relation to the norm

The authors of the report attempt to provide a comprehensive description of some Russian verbal prefixes (including those denoting an action below, equal to or above the norm) based on the cognitive approach to language learning. In addition to theoretical ideas, the report describes an experimental methodology aimed at identifying various semantic features of homonymous verbal prefixes. This methodology has proved effective for teaching Russian as a second language

Дослідження змін потенціалів спинного мозку тварин у залежності від віку

Research of changes of cord dorsum potentials (CDP) of spinal cord (SC) of depending on age in cats. Is shown, that the first negative component of CDP is most stable on amplitude and dynamic characteristic for all age-group. Components of CDP, which were connected to work of polysynaptic neurones and especially with presynaptic inhibition showed large variables and instability at a repeated or long-term stimulation for very young or old animals. We assume, that the specified character of changes of potentials is connected to change of an effective performance of neurones in a brainНа кішках вивчали потенціали дорсальної поверхні (ПДП) спинного мозку (CM) у залежності від віку тварини. З’ясовано, що перший негативний (Nj) комнонент ПДП є найбільш стабільним по амплітуді та динамічних характеристиках для усіх вікових груп. Компоненти, пов’язані з роботою полісинаптичних нейронів, та особливо з пресинаптичним гальмуванням, були більш варіабельні та нестійки при повторних та тривалих подразненнях для дуже молодих або старих тварин. Робиться припущення, що такий характер змін потеніалів пов’язаний зі зменшенням кількості нейронів при старінні та розбудовою синаптичних утворень при дорослішанні. Вірогідно, що по формі ПДП можливо оцінити ступінь старіння мозку або його окремих ланокНа кішках вивчали потенціали дорсальної поверхні (ПДП) спинного мозку (CM) у залежності від віку тварини. З’ясовано, що перший негативний (Nj) комнонент ПДП є найбільш стабільним по амплітуді та динамічних характеристиках для усіх вікових груп. Компоненти, пов’язані з роботою полісинаптичних нейронів, та особливо з пресинаптичним гальмуванням, були більш варіабельні та нестійки при повторних та тривалих подразненнях для дуже молодих або старих тварин. Робиться припущення, що такий характер змін потеніалів пов’язаний зі зменшенням кількості нейронів при старінні та розбудовою синаптичних утворень при дорослішанні. Вірогідно, що по формі ПДП можливо оцінити ступінь старіння мозку або його окремих ланок

Protection of pancreatic INS-1 β-cells from glucose- and fructose-induced cell death by inhibiting mitochondrial permeability transition with cyclosporin A or metformin

Hyperglycemia is detrimental to β-cell viability, playing a major role in the progression of β-cell loss in diabetes mellitus. The permeability transition pore (PTP) is a mitochondrial channel involved in cell death. Recent evidence suggests that PTP inhibitors prevent hyperglycemia-induced cell death in human endothelial cells. In this work, we have examined the involvement of PTP opening in INS-1 cell death induced by high levels of glucose or fructose. PTP regulation was studied by measuring the calcium retention capacity in permeabilized INS-1 cells and by confocal microscopy in intact INS-1 cells. Cell death was analyzed by flow cytometry. We first reported that metformin and cyclosporin A (CsA) prevented Ca2+-induced PTP opening in permeabilized and intact INS-1 cells. We then showed that incubation of INS-1 cells in the presence of 30 mM glucose or 2.5 mM fructose induced PTP opening and led to cell death. As both metformin and CsA prevented glucose- and fructose- induced PTP opening, and hampered glucose- and fructose- induced cell death, we conclude that PTP opening is involved in high glucose- and high fructose- induced INS-1 cell death. We therefore suggest that preventing PTP opening might be a new approach to preserve β-cell viability

Assay for high glucose-mediated islet cell sensitization to apoptosis induced by streptozotocin and cytokines

Pancreatic β-cell apoptosis is known to participate in the β-cell destruction process that occurs in diabetes. It has been described that high glucose level induces a hyperfunctional status which could provoke apoptosis. This phenomenon is known as glucotoxicity and has been proposed that it can play a role in type 1 diabetes mellitus pathogenesis. In this study we develop an experimental design to sensitize pancreatic islet cells by high glucose to streptozotocin (STZ) and proinflammatory cytokines [interleukin (IL)-1β, tumor necrosis factor (TNF)-α and interferon (IFN)-γ]-induced apoptosis. This method is appropriate for subsequent quantification of apoptotic islet cells stained with Tdt-mediated dUTP Nick-End Labeling (TUNEL) and protein expression assays by Western Blotting (WB)

On cognitive approach to language when studying Russian prefixes expressing relation to the norm

The authors of the report attempt to provide a comprehensive description of some Russian verbal prefixes (including those denoting an action below, equal to or above the norm) based on the cognitive approach to language learning. In addition to theoretical ideas, the report describes an experimental methodology aimed at identifying various semantic features of homonymous verbal prefixes. This methodology has proved effective for teaching Russian as a second language

The content of lead in some organs and tissues of Hereford bull-calves

The content of lead in muscles, liver, spleen and testicles is studied in Hereford bulls, aged 18 months. Selectivity of Pb accumulation is identified in organs and tissues. Pb level in organs and tissues may be ranged as follows: liver>spleen>muscles>testicles in the ratio 4.7: 4.4: 1.2: 1. It is shown that the increased concentration of lead in testicles decreases the content of vitamins. Some biological indexes of blood serum are indicators of Pb level in muscles and liver

Effects of Imidazoline Derivative RX871024 on Insulin, Glucagon, and Somatostatin Secretion from Isolated Perfused Rat Pancreas

The effects of the imidazoline compound RX871024 on arginine-induced insulin, glucagon, and somatostatin secretion in the isolated perfused rat pancreas have been investigated. Arginine induced biphasic insulin, glucagon, and somatostatin release when infused for 20 min at 20 mM concentration and 3.3 mM glucose in the medium. RX871024, at 10 μM, did not influence basal hormone secretion but enhanced arginine-stimulated insulin and somatostatin release. In contrast, glucagon secretion was markedly inhibited by 10 μM imidazoline. RX871024 (1 μM) did not significantly affect arginine-induced insulin and somatostatin secretion but had an inhibitory effect on the second phase of glucagon release. In conclusion, RX871024 exerts a complex effect on the endocrine pancreas challenged by arginine, comprising stimulation of insulin and somatostatin release and inhibition of glucagon release. These effects on hormone release probably constitute the main mechanism of the antidiabetogenic action of the imidazolines

Hyperinsulinism induced by targeted suppression of beta cell K(ATP) channels

ATP-sensitive K(+) (K(ATP)) channels couple cell metabolism to electrical activity. To probe the role of K(ATP) in glucose-induced insulin secretion, we have generated transgenic mice expressing a dominant-negative, GFP-tagged K(ATP) channel subunit in which residues 132–134 (Gly-Tyr-Gly) in the selectivity filter were replaced by Ala-Ala-Ala, under control of the insulin promoter. Transgene expression was confirmed by both beta cell-specific green fluorescence and complete suppression of channel activity in those cells (≈70%) that did fluoresce. Transgenic mice developed normally with no increased mortality and displayed normal body weight, blood glucose levels, and islet architecture. However, hyperinsulinism was evident in adult mice as (i) a disproportionately high level of circulating serum insulin for a given glucose concentration (≈2-fold increase in blood insulin), (ii) enhanced glucose-induced insulin release from isolated islets, and (iii) mild yet significant enhancement in glucose tolerance. Enhanced glucose-induced insulin secretion results from both increased glucose sensitivity and increased release at saturating glucose concentration. The results suggest that incomplete suppression of K(ATP) channel activity can give rise to a maintained hyperinsulinism