Method for assessing unevenness of cellulose insulation layers aging of power transformers winding

Introduction. Improving the methods of estimating the insulation aging of the oil-immersed power transformer windings is an urgent task for transformer condition monitoring systems. The scientific novelty of the work is to take into account the uneven distribution of temperature and humidity along the vertical axis of the winding in modeling the aging of insulation and to develop methods for determining the conditions under which the aging rate of insulation in the intermediate layer will exceed aging rate in the hottest layer. The purpose of the work is to evaluate the wear unevenness of cellulose insulation based on modeling the distribution of temperature and humidity along the vertical axis of the power transformer winding. Methods. The transformer winding is mentally divided into horizontal layers of equal height, the reduction of service life is calculated in parallel for all horizontal layers. Layer with the maximum degree of aging for the entire period of operation and storage of the transformer is recognized as determining the reduction in the service life of the insulation of the transformer as a whole. A model of the interaction of winding layers is developed, with determination of temperatures, humidity, relative rate of aging of each layer due to temperature and humidity as a function of traditional design parameters such as load, cooling temperature, heat capacity and thermal resistance of transformer. The index of exceeding the aging rate by the layered method in comparison with this rate for the hottest layer is offered. The method of genetic algorithms determines the conditions for obtaining the maximum value of this index. Results. A computer model has been developed to predict the aging of the cellulose insulation of transformer windings. According to the proposed method, a layer with significantly shorter insulation aging time (in the example, time reduced by 39.18 %) than for the upper layer was determined, which confirms the feasibility of layer-by-layer monitoring and modeling of insulation aging processes of power oil-immersed transformer windings.Вступ. Вдосконалення методик оцінки старіння целюлозної ізоляції обмоток силового маслонаповненого трансформатора є актуальним завданням для систем моніторингу стану трансформаторів. Наукова новизна роботи полягає в урахуванні нерівномірності розподілів температури та вологості вздовж вертикальної осі обмотки при моделюванні процесів старіння ізоляції та у розробці методики визначення умов, за яких швидкість зносу ізоляції у проміжному шарі буде максимально перевищувати швидкість у найбільш нагрітому шарі обмотки. Метою роботи є оцінка нерівномірності зносу целюлозної ізоляції на основі моделювання розподілу температури та вологості вздовж вертикальної осі обмотки силових трансформаторів. Методи. Обмотка трансформатора подумки розділена на горизонтальні шари рівної висоти, підрахунок скорочення строку служби виконується паралельно за усіма горизонтальними шарами, а шар, що має максимальний ступінь старіння за весь період експлуатації та зберігання трансформатору визнається найбільш ресурс витратним шаром, який визначає скорочення строку служби ізоляції трансформатора в цілому. Розроблена модель взаємодії шарів обмотки, з визначенням температур, вологості, відносної швидкості старіння кожного шару внаслідок дії температури та вологи як функції традиційних розрахункових параметрів, таких як навантаження, температура охолодного середовища, теплоємність та тепловий опір трансформатора. Запропонований показник перевищення швидкості скорочення строку служби пошаровим методом у порівнянні з цієї швидкістю для найбільш нагрітого шару. Методом генетичних алгоритмів визначені умови для отримання максимального значення цього показника. Результати. Розроблена комп’ютерна модель для прогнозування старіння целюлозної ізоляції обмоток. За запропонованою методикою визначено найбільш ресурс витратний шар зі значно меншим часом старіння ізоляції (у прикладі час зменшено на 39,18 %), ніж для верхнього шару, що підтверджує доцільність пошарового моніторингу та моделювання процесів старіння ізоляції обмоток силового маслонаповненого трансформатора

Use of algorithm of the prevention complex of inflammatory processes in the oral cavity in metabolic syndrome

The aim of the work was to evaluate in the experiment the effectiveness of the developed treatment-and-prophylactic complex for the prevention of periodontal tissue disorders under metabolic syndrome simulation. Materials and methods. The study of biochemical and immunological changes in the blood serum, liver and gingival tissue was performed during simulation on the metabolic syndrome of alimentary genesis on Wistar rats, all animals were divided into 5 groups: 1) intact; 2) with simulated metabolic syndrome; 3) in a week after the start of MS simulation 5 times a week in the morning perorally administered a “Capillaroprotect” aqueous solution (bioflavonoid, antioxidant) produced by “Ekosvit Oil” (Ukraine) at a rate of 135 mg/kg; 4) under similar conditions receiving the preparation based on the dihydroquercetin were locally applied on gums a new dental elixir based on bee products and adaptogens of plant origin by 0,5 ml/rat with a tampon, which has held for 5–7 minutes; 5) during MS simulation from the second week were used the preparation based on the dihydroquercetin, the dental elixir topically on gums and physiotherapy. Results. Under conditions of experimental MS simulation with a diet rich in saturated fats and carbohydrate there are systemic disorders in the body: reduced nonspecific antimicrobial protection, increased microbial contamination, intensification of lipid peroxidation, the development of inflammation and hepatotoxicity. Prophylactic administration of the proposed dihydroquercetin preparation to animals in the process of simulation of MS significantly inhibits the established disorders, positively affecting the biochemical parameters of the blood serum, liver tissue, periodontium, reducing triglycerides, total cholesterol, glucose level, restoring the state of non-specific resistance, lipid metabolism, preventing inflammation and hepatosis, as well as contamination with pathogenic microflora. Conclusion. The proposed treatment-and-prophylactic complex, which includes the dihydroquercetin preparation, used per os in combination with local therapy of periodontal tissues with a tooth elixir based on propolis and biologically active substances of plant origin adaptogens with ultraphonophoresis under induced metabolic syndrome significantly removed the negative effects of its most important component

Thermodynamic aspects of materials' hardness: prediction of novel superhard high-pressure phases

In the present work we have proposed the method that allows one to easily estimate hardness and bulk modulus of known or hypothetical solid phases from the data on Gibbs energy of atomization of the elements and corresponding covalent radii. It has been shown that hardness and bulk moduli of compounds strongly correlate with their thermodynamic and structural properties. The proposed method may be used for a large number of compounds with various types of chemical bonding and structures; moreover, the temperature dependence of hardness may be calculated, that has been performed for diamond and cubic boron nitride. The correctness of this approach has been shown for the recently synthesized superhard diamond-like BC5. It has been predicted that the hypothetical forms of B2O3, diamond-like boron, BCx and COx, which could be synthesized at high pressures and temperatures, should have extreme hardness

Применение экзомного секвенирования для диагностики наследственных моторно-сенсорных нейропатий

Introduction. Hereditary motor and sensory neuropathies, a highly genetic heterogeneous group of disorders, have a phenotype caused by peripheral nerve damage.Purpose of the study – to assess the extent of genetic heterogeneity of hereditary motor and sensory neuropathies in Russian patients and to evaluate the diagnostic effectiveness of using full-exome research methods to find the genetic cause of hereditary motor and sensory neuropathies.Materials and methods. The material for the study was DNA samples from 51 patients and their family members referred for whole exome sequencing to the DNA-diagnostics laboratory of Research Centre for Medical Genetics in 2017–2019. Methods: whole exome sequencing, Sanger sequencing, restriction fragment length polymorphism.Results. Whole exome sequencing in combination with segregation analysis of the pathogenic variants in families allowed to determine the cause of the disease in 41 % of cases. In another 16 % of cases, candidate genetic variants as a possible cause of the disease were revealed, but additional studies are needed to confirm it. The most frequently mutated gene was MFN2 caused neuropathy in 6 unrelated families. MPZ gene mutations were detected in two families, AARS gene mutations were revealed in another two families, and mutations in GJB1, HINT1, INF2, LRSAM1, LITAF, MME, NEFL, WWOX were detected once. Among the causal variants, mutations in B4GALNT1 caused spastic paraplegia, in COL6A1 led to Bethlem’s congenital muscular dystrophy, and in SYT2 caused congenital myasthenic syndrome indicating difficulties in differential diagnosis of inherited neuromuscular disorders. A PMP22 duplication was detected in 2 families prior to whole exome sequencing.Conclusion. Whole exome sequencing is very important for finding the molecular cause of hereditary motor and sensory neuropathies. In most cases, additional methods should be used to clarify the pathogenicity of variants detected by whole exome sequencing. However, it is necessary to remember that the most common cause of the disease is a large duplication of the region 17p11.2.Введение. Наследственные моторно-сенсорные нейропатии – обширная генетически-гетерогенная группа наследственных болезней, при которых клинический фенотип обусловлен тем или иным поражением периферических нервов.Цель исследования – оценить размах генетической гетерогенности наследственных моторно-сенсорных нейропатий у российских больных и диагностическую эффективность использования полноэкзомных методов исследования для поиска генетической причины наследственных моторно-сенсорных нейропатий.Материалы и методы. Материалом для исследования послужили образцы ДНК 51 больного и членов их семей, обратившихся за экзомным секвенированием в лабораторию ДНК-диагностики ФГБНУ «Медико-генетический научный центр им. академика Н. П. Бочкова» в 2017–2019 гг. Методы: полноэкзомное секвенирование, секвенирование по Сенгеру, метод анализа полиморфизма длин амплификационных фрагментов.Результаты. Используя экзомное секвенирование в сочетании с анализом сегрегации патогенных вариантов, удалось установить причину болезни в семьях у 41 % пациентов. Еще у 16 % выявлены кандидатные генетические варианты, являющиеся возможной причиной заболевания, однако для подтверждения этого необходимы дополнительные исследования, которые по решению семей не были проведены. Наиболее часто (в 6 неродственных семьях) выявлены мутации гена MFN2, в 2 семьях – гена MPZ, в 2 – AARS, по 1 случаю – GJB1, HINT1, INF2, LRSAM1, LITAF, MME, NEFL, WWOX. Среди причинных вариантов были выявлены мутации генов, отвечающих за спастическую параплегию (B4GALNT1), врожденную мышечную дистрофию Бетлема (COL6A1), миастению (SYT2), что свидетельствует о трудностях дифференциальной диагностики наследственных нервно-мышечных заболеваний. В 2 семьях до проведения полноэкзомного секвенирования (WES) была детектирована дупликация на хромосоме 17.Выводы. Экзомные методы исследования очень важны для поиска молекулярной причины наследственной моторно-сенсорной нейропатии. Для уточнения патогенности вариантов, выявленных при экзомном секвенировании, в большинстве случаев необходимо использовать дополнительные методы. Однако, несмотря на их высокую информативность, следует помнить, что наиболее частой причиной болезни является крупная дупликация региона 17p11.2

Dark sectors 2016 Workshop: community report

This report, based on the Dark Sectors workshop at SLAC in April 2016, summarizes the scientific importance of searches for dark sector dark matter and forces at masses beneath the weak-scale, the status of this broad international field, the important milestones motivating future exploration, and promising experimental opportunities to reach these milestones over the next 5-10 years

Spike Timing and Reliability in Cortical Pyramidal Neurons: Effects of EPSC Kinetics, Input Synchronization and Background Noise on Spike Timing

In vivo studies have shown that neurons in the neocortex can generate action potentials at high temporal precision. The mechanisms controlling timing and reliability of action potential generation in neocortical neurons, however, are still poorly understood. Here we investigated the temporal precision and reliability of spike firing in cortical layer V pyramidal cells at near-threshold membrane potentials. Timing and reliability of spike responses were a function of EPSC kinetics, temporal jitter of population excitatory inputs, and of background synaptic noise. We used somatic current injection to mimic population synaptic input events and measured spike probability and spike time precision (STP), the latter defined as the time window (Δt) holding 80% of response spikes. EPSC rise and decay times were varied over the known physiological spectrum. At spike threshold level, EPSC decay time had a stronger influence on STP than rise time. Generally, STP was highest (≤2.45 ms) in response to synchronous compounds of EPSCs with fast rise and decay kinetics. Compounds with slow EPSC kinetics (decay time constants>6 ms) triggered spikes at lower temporal precision (≥6.58 ms). We found an overall linear relationship between STP and spike delay. The difference in STP between fast and slow compound EPSCs could be reduced by incrementing the amplitude of slow compound EPSCs. The introduction of a temporal jitter to compound EPSCs had a comparatively small effect on STP, with a tenfold increase in jitter resulting in only a five fold decrease in STP. In the presence of simulated synaptic background activity, precisely timed spikes could still be induced by fast EPSCs, but not by slow EPSCs

Ephrin-A5 Suppresses Neurotrophin Evoked Neuronal Motility, ERK Activation and Gene Expression

During brain development, growth cones respond to attractive and repulsive axon guidance cues. How growth cones integrate guidance instructions is poorly understood. Here, we demonstrate a link between BDNF (brain derived neurotrophic factor), promoting axonal branching and ephrin-A5, mediating axonal repulsion via Eph receptor tyrosine kinase activation. BDNF enhanced growth cone filopodial dynamics and neurite branching of primary neurons. We show that ephrin-A5 antagonized this BDNF-evoked neuronal motility. BDNF increased ERK phosphorylation (P-ERK) and nuclear ERK entry. Ephrin-A5 suppressed BDNF-induced ERK activity and might sequester P-ERK in the cytoplasm. Neurotrophins are well established stimulators of a neuronal immediate early gene (IEG) response. This is confirmed in this study by e.g. c-fos, Egr1 and Arc upregulation upon BDNF application. This BDNF-evoked IEG response required the transcription factor SRF (serum response factor). Notably, ephrin-A5 suppressed a BDNF-evoked neuronal IEG response, suggesting a role of Eph receptors in modulating gene expression. In opposite to IEGs, long-term ephrin-A5 application induced cytoskeletal gene expression of tropomyosin and actinin. To uncover specific Eph receptors mediating ephrin-As impact on neurotrophin signaling, EphA7 deficient mice were analyzed. In EphA7 deficient neurons alterations in growth cone morphology were observed. However, ephrin-A5 still counteracted neurotrophin signaling suggesting that EphA7 is not required for ephrin and BDNF crosstalk. In sum, our data suggest an interaction of ephrin-As and neurotrophin signaling pathways converging at ERK signaling and nuclear gene activity. As ephrins are involved in development and function of many organs, such modulation of receptor tyrosine kinase signaling and gene expression by Ephs might not be limited to the nervous system