Numerical modelling of low-temperature non-equilibrium plasma of pulsing corona and breakdown

The method of determining an existence region of the non-equilibrium plasma of the pulsating negative corona and breakdown is developed. The low-temperature non-equilibrium pulsing plasma of the point-to-plane negative corona and a transition form to the breakdown in nitrogen-oxygen mixture are numerically simulated. It is shown that plasma parameters are pulsing in time as well as in space. In the phase of corona pulse peak, its position adjoins the cathode surface, no further than 0.01 cm. In the initial phase of breakdown, it extends far beyond the surface, within the distance of 0.03 cm. At the same time, the electron temperature changes in almost full anti-phase to the current: from 9100 K to 19000 K during the corona pulse peak and from 6000 K to 20000 K in initial phases of the breakdown. The average plasma density changes in the range 7 × 10¹¹ − 8 × 10¹² cm⁻³ in the first case and 1 × 10¹³ − 5 × 10¹³ cm⁻³ in the case of breakdown.Запропоновано метод визначення областi iснування нерiвноважної плазми корони i газового пробиття. Низькотемпературна нерiвноважна пульсуюча плазма негативної корони мiж вiстрям i площиною та перехiдної форми до пробиття чисельно змодельована у сумiшi азоту i кисню. Показано, що параметри плазми пульсують, як у часi, так i в просторi розряду. Вона розмiщується безпосередньо бiля поверхнi катода, не далi, нiж 0.01 см у фазi пiку iмпульсу корони i високочастотного iмпульсу пробиття, i розширюється у межах 0.03 см вiд поверхнi до дрейфової областi у початковiй фазi пробиття. Температура електронiв змiнюється у майже повнiй антифазi до струму: вiд 9100 до 19000 К протягом пiку iмпульсу корони i вiд 6000 до 20000 К у початкових фазах пробиття. Усереднена густина плазми приймає значення 7 × 10¹¹ − 8 × 10¹² cm⁻³ у першому випадку i 1 × 10¹³ − 5 × 10¹³ cm⁻³ у випадку пробиття

SOME PECULIARITIES OF BENTONITE REGENERATION BY MEANS OF USING HIGH-FREQUENCY EMANATION (ON THE EXAMPLE OF BIOGENIC IONS)

Розглянуто питання оптимізації процесів очищення природних і стічних вод. Основну увагу звернуто на розроблення нових методів і методик підвищення ефективності регенерації природного сорбенту бентоніту. Зокрема, запропоновано новий метод стимуляції та регенерації цього сорбенту – дія на нього надвисокочастотного електромагнітного випромінювання (НВЧ ЕМВ) у поєднанні з промиванням водою. Побудовано графіки зміни параметрів адсорбції біогенних іонів (амонію, нітритів, нітратів та фосфатів) залежно від способу оброблення сорбенту. За рівняннями ізотерм Ленгмюра розраховано відповідні константи адсорбційних процесів.Рассмотрены вопросы оптимизации процессов очистки природных и сточных вод. Главное внимание уделено разработке новых методов и методик повышения эффективности регенерации природного сорбента бентонита. В частности, предложен новый метод стимуляции и регенерации этого сорбента – воздействие на него сверхвысокочастотным электромагнитным излучением (СВЧ ЭМИ) совместно с промывкой водой. Построены графики изменения параметров адсорбции биогенных ионов (аммония, нитритов, нитратов и фосфатов) в зависимости от способа обработки сорбента. По уравнениям изотерм Ленгмюра рассчитаны соответствующие константы адсорбционных процессов.Several equations of optimization processes of purification natural and waste water are reviewed. The main attention is paid to the development of new methods and techniques for improving the efficiency of regeneration of natural sorbent bentonite. The new method of stimulation and regeneration of the sorbent – the effect on it of microwave electromagnetic radiation (EMR UHF) in combination with flushing water is proposed in particular. Graphs of parameters adsorption of biogenic ions (ammonia, nitrites, nitrates and phosphates) depending on the method of processing the sorbent are designed. Corresponding constants of adsorption processes are calculated according to Langmuir isotherms equations

Проблеми рейтингового позиціювання як фактору впливу на конкурентоспроможність закладів вищої освіти в умовах міжнародних економічних відносин (Rating positions as an influence factor on competitiveness of higher education institutions in the conditions of international economic relations)

Досліджено комплексні критерії, індикатори та відповідні вагові коефіцієнти впливу на інтегровані рейтингові бали закладів вищої освіти України у світових та вітчизняних рейтингах. Акцентовано увагу на їх недосконалості. Обґрунтовано припущення, що інтелектуальні та матеріальні витрати на участь у різноманітних рейтингуваннях є доцільними та економічно обґрунтованими лише у випадку відповідності між рейтинговою позицією та рівнем котирування ЗВО серед абітурієнтів. Сформульовано принцип підпорядкування стратегії розвитку ЗВО ключовій меті. Запропоновано в якості пріоритетного критерію застосовувати рівень підготовки абітурієнтів (середній бал ЗНО) під час зарахування на контракт. (The positions of higher education institutions (HEI) of Ukraine in the world and national ratings are considered. The complex criteria, indicators and their respective weighting factors for the integrated rating point are investigated. The imperfections of the principles of formation of existing world and national ratings are revealed. Reasons for low positions of Ukrainian HEI in world rankings are detected. The components of complex criteria are analyzed, among which the main focus is on a group of economic indicators. It is proved that key indices are directly related to the level of the country’s economy as a whole, the volume of private and state orders for scientific and technical developments, and the level of integration of scientific and pedagogical workers in world scientific processes. On the basis of the analysis of indices and complex criteria of domestic ratings TOP 200 Ukraine and the Consolidated Rating, a conclusion has been drawn that there is a discrepancy between the HEI positions in domestic ratings and their competitiveness. The authors make an assumption that the intellectual and material costs involved in various rating activities are feasible and economically justified only if there is a match between the rating position and the level of quotation of the HEI among the entrants. The principle of subordination the strategy for the HEI development as a key objective, which must be significantly different from achieving the highest possible position in existing ratings, is formulated. The selection of an increase in the number of high-level entrants who are ready to receive education in a certain institution of education for the funds of individuals or legal entities is proposed as a priority objective. The choice in favor of a particular institution of education of the most talented and best trained youth should be the main strategic goal of the educational institution. In order to influence the rating positions of the HEI competitiveness in the formation of integrated rating criteria, it is proposed to include the number of indices: the index of the level of comfort of the educational process, namely: the level of provision with hostels, libraries and high-quality auditor, the index of quality of distance information support of the educational process, the index of quality of communication processes «teacher- student», the index of the assessment of employers and graduates of the level of training specialists. It is proposed to apply the theory of fuzzy sets and fuzzy logic in the basis of the methodology taking into account these qualitative indicators.

Alcohol Rehabilitation Within 30 Days of Hospital Discharge Is Associated With Reduced Readmission, Relapse, and Death in Patients With Alcoholic Hepatitis

Background & Aims Patients admitted to the hospital for alcoholic hepatitis (AH) are at increased risk of readmission and death. We aimed to identify factors associated with readmission, alcohol relapse, and mortality. Methods We performed a retrospective analysis of consecutive patients admitted with AH to a tertiary care hospital from 1999 through 2016 (test cohort, n = 135). We validated our findings in a prospective analysis of patients in a multi-center AH research consortium from 2013 through 2017 (validation cohort, n = 159). Alcohol relapse was defined as any amount of alcohol consumption within 30 days after hospital discharge. Early alcohol rehabilitation was defined as residential or outpatient addiction treatment or mutual support group participation within 30 days after hospital discharge. Results Thirty-day readmission rates were 30% in both cohorts. Alcohol relapse rates were 37% in the test and 34% in the validation cohort. Following hospital discharge, 27 patients (20%) in the test cohort and 19 patients (16%) in the validation cohort attended early alcohol rehabilitation. There were 53 deaths (39%) in a median follow-up time of 2.8 years and 42 deaths (26%) in a median follow-up time of 1.3 years, respectively. In the test cohort, early alcohol rehabilitation reduced odds for 30-day readmission (adjusted odds ratios [AOR] 0.16; 95% CI, 0.04–0.65; P = .01), 30-day alcohol relapse (AOR, 0.11; 95% CI, 0.02–0.53; P < .001), and death (adjusted hazard ratio [AHR], 0.20; 95% CI, 0.05–0.56; P = .001). In the validation cohort early alcohol rehabilitation reduced odds for 30-day readmission (AOR, 0.30; 95% CI, 0.09–0.98; P = .04), 30-day alcohol relapse (AOR 0.09; 95% CI, 0.01–0.73; P = .02), and death (AHR, 0.20; 95% CI, 0.01–0.94; P = .04). A model combining alcohol rehabilitation and bilirubin identified patients with readmission to the hospital within 30 days with an area under the receiver operating characteristic curve of 0.73. Conclusions In an analysis from two cohorts of patients admitted with AH, early alcohol rehabilitation can reduce risk of hospital readmission, alcohol relapse, and death and should be considered as a quality indicator in AH hospitalization treatment

Molecular Mechanism of Capacitative Calcium Entry Deficits in Familial Alzheimer’s Disease

Poster PresentationPresenilin (PS) is the catalytic subunit of the gamma-secretase which is responsible for the cleavage of amyloid precursor protein to form beta amyloid (Aβ). Mutations in PS associated with familial Alzheimer’s disease (FAD) increase the Aβ plaques formation in the brain and cause neurodegeneration. Apart from this, FAD-linked PS mutations have been demonstrated to disrupt intracellular calcium (Ca2+) regulation. Accumulating evidence suggests that Ca2+ disruption may play a proximal role in the AD pathogenesis. Mutant PS exaggerated Ca2+ release from the endoplasmic reticulum (ER). It also attenuated Ca2+ entry through the capacitative Ca2+ entry (CCE) pathway, yet, the mechanism is not fully understood. Using a human neuroblast cell line SH-SY5Y and Ca2+ imaging technique, we observed CCE deficits in FAD-linked PS1-M146L retroviral infected cell. The attenuation of CCE in PS1 mutant cells was not mediated by the down-regulation of STIM1 and Orai1 expression, the known essential molecular players in the CCE pathway. Instead, we identified a molecular interaction between PS and STIM1 proteins by immunoprecipitation. On the other hand, immunofluorescence staining showed a significant reduction in puncta formation after ER Ca2+ depleted by thapsigargin in cells infected with PS1-M146L as compared to the wild type PS1 infected cells. Taken together, our results suggest a molecular mechanism for the CCE deficits in FAD associated with PS1 mutations. The interaction of mutant PS1 with STIM1 exerts a negative impact on its oligomerization and/or its interaction with Orai1. Our results may suggest molecular targets for the development of therapeutic agents that help to treat the disease.published_or_final_versio

Functional Role of the Polymorphic 647 T/C Variant of ENT1 (SLC29A1) and Its Association with Alcohol Withdrawal Seizures

Adenosine is involved in several neurological and behavioral disorders including alcoholism. In cultured cell and animal studies, type 1 equilibrative nucleoside transporter (ENT1, slc29a1), which regulates adenosine levels, is known to regulate ethanol sensitivity and preference. Interestingly, in humans, the ENT1 (SLC29A1) gene contains a non-synonymous single nucleotide polymorphism (647 T/C; rs45573936) that might be involved in the functional change of ENT1. Our functional analysis showed that prolonged ethanol exposure increased adenosine uptake activity of mutant cells (ENT1-216Thr) compared to wild-type (ENT1-216Ile) transfected cells, which might result in reduced extracellular adenosine levels. We found that mice lacking ENT1 displayed increased propensity to ethanol withdrawal seizures compared to wild-type littermates. We further investigated a possible association of the 647C variant with alcoholism and the history of alcohol withdrawal seizures in subjects of European ancestry recruited from two independent sites. Analyses of the combined data set showed an association of the 647C variant and alcohol dependence with withdrawal seizures at the nominally significant level. Together with the functional data, our findings suggest a potential contribution of a genetic variant of ENT1 to the development of alcoholism with increased risk of alcohol withdrawal-induced seizures in humans

Effects of antidepressant treatment on heart rate variability in major depression: A quantitative review

<p>Abstract</p> <p>Background</p> <p>The literature measuring effects of antidepressant and electroconvulsive therapy (ECT) for major depression on heart rate variability (HRV) in medically well individuals was reviewed.</p> <p>Methods</p> <p>Fourteen studies evaluating HRV were included. Twenty three pre-post or within group comparisons were available. Treatment impact on measures of HRV was pooled over studies. We examined different classes of antidepressants, and for short and long electrocardiogram (ECG) recordings separately.</p> <p>Results</p> <p>Tricyclic antidepressants (TCAs) were associated with declines in most measures of HRV and significant increase in heart rate (HR) in studies with short recording intervals. No significant changes were found for longer recording times.</p> <p>Treatment effects with selective serotonin reuptake inhibitors (SSRIs) were more variable. Short-recording studies revealed a significant decrease in HR and an increase in one HRV measure. In two 24-hour recording studies no significant changes were observed. No relationship between ECT and HRV has been established in the literature. The effects of other drugs are reported.</p> <p>Limitations</p> <p>Few studies measure the effects of treatment of depression on HRV. Existing studies have generally used very small samples, employing a variety of measurements and methodologies.</p> <p>Conclusion</p> <p>We confirm that TCAs are associated with a large decrease in HRV and increase HR. However, data for SSRIs is not clear. Although the effect of SSRIs on HRV is weaker than for TCAs, evidence shows that SSRIs are associated with a small decrease in HR, and an increase in one measure of HRV. The use of TCAs in depression leads to changes in HRV that are associated with increased risk of mortality.</p

Ethanol-Associated Changes in Glutamate Reward Neurocircuitry: A Minireview of Clinical and Preclinical Genetic Findings

Herein, we have reviewed the role of glutamate, the major excitatory neurotransmitter in the brain, in a number of neurochemical, -physiological, and -behavioral processes mediating the development of alcohol dependence. The findings discussed include results from both preclinical as well as neuroimaging and postmortem clinical studies. Expression levels for a number of glutamate-associated genes and/or proteins are modulated by alcohol abuse and dependence. These changes in expression include metabotropic receptors and ionotropic receptor subunits as well as different glutamate transporters. Moreover, these changes in gene expression parallel the pharmacologic manipulation of these same receptors and transporters. Some of these gene expression changes may have predated alcohol abuse and dependence because a number of glutamate-associated polymorphisms are related to a genetic predisposition to develop alcohol dependence. Other glutamate-associated polymorphisms are linked to age at the onset of alcohol-dependence and initial level of response/sensitivity to alcohol. Finally, findings of innate and/or ethanol-induced glutamate-associated gene expression differences/changes observed in a genetic animal model of alcoholism, the P rat, are summarized. Overall, the existing literature indicates that changes in glutamate receptors, transporters, enzymes, and scaffolding proteins are crucial for the development of alcohol dependence and there is a substantial genetic component to these effects. This indicates that continued research into the genetic underpinnings of these glutamate-associated effects will provide important novel molecular targets for treating alcohol abuse and dependence

A large-scale genome-wide association study meta-analysis of cannabis use disorder

Summary Background Variation in liability to cannabis use disorder has a strong genetic component (estimated twin and family heritability about 50–70%) and is associated with negative outcomes, including increased risk of psychopathology. The aim of the study was to conduct a large genome-wide association study (GWAS) to identify novel genetic variants associated with cannabis use disorder. Methods To conduct this GWAS meta-analysis of cannabis use disorder and identify associations with genetic loci, we used samples from the Psychiatric Genomics Consortium Substance Use Disorders working group, iPSYCH, and deCODE (20 916 case samples, 363 116 control samples in total), contrasting cannabis use disorder cases with controls. To examine the genetic overlap between cannabis use disorder and 22 traits of interest (chosen because of previously published phenotypic correlations [eg, psychiatric disorders] or hypothesised associations [eg, chronotype] with cannabis use disorder), we used linkage disequilibrium score regression to calculate genetic correlations. Findings We identified two genome-wide significant loci: a novel chromosome 7 locus (FOXP2, lead single-nucleotide polymorphism [SNP] rs7783012; odds ratio [OR] 1·11, 95% CI 1·07–1·15, p=1·84 × 10−9) and the previously identified chromosome 8 locus (near CHRNA2 and EPHX2, lead SNP rs4732724; OR 0·89, 95% CI 0·86–0·93, p=6·46 × 10−9). Cannabis use disorder and cannabis use were genetically correlated (rg 0·50, p=1·50 × 10−21), but they showed significantly different genetic correlations with 12 of the 22 traits we tested, suggesting at least partially different genetic underpinnings of cannabis use and cannabis use disorder. Cannabis use disorder was positively genetically correlated with other psychopathology, including ADHD, major depression, and schizophrenia. Interpretation These findings support the theory that cannabis use disorder has shared genetic liability with other psychopathology, and there is a distinction between genetic liability to cannabis use and cannabis use disorder. Funding National Institute of Mental Health; National Institute on Alcohol Abuse and Alcoholism; National Institute on Drug Abuse; Center for Genomics and Personalized Medicine and the Centre for Integrative Sequencing; The European Commission, Horizon 2020; National Institute of Child Health and Human Development; Health Research Council of New Zealand; National Institute on Aging; Wellcome Trust Case Control Consortium; UK Research and Innovation Medical Research Council (UKRI MRC); The Brain & Behavior Research Foundation; National Institute on Deafness and Other Communication Disorders; Substance Abuse and Mental Health Services Administration (SAMHSA); National Institute of Biomedical Imaging and Bioengineering; National Health and Medical Research Council (NHMRC) Australia; Tobacco-Related Disease Research Program of the University of California; Families for Borderline Personality Disorder Research (Beth and Rob Elliott) 2018 NARSAD Young Investigator Grant; The National Child Health Research Foundation (Cure Kids); The Canterbury Medical Research Foundation; The New Zealand Lottery Grants Board; The University of Otago; The Carney Centre for Pharmacogenomics; The James Hume Bequest Fund; National Institutes of Health: Genes, Environment and Health Initiative; National Institutes of Health; National Cancer Institute; The William T Grant Foundation; Australian Research Council; The Virginia Tobacco Settlement Foundation; The VISN 1 and VISN 4 Mental Illness Research, Education, and Clinical Centers of the US Department of Veterans Affairs; The 5th Framework Programme (FP-5) GenomEUtwin Project; The Lundbeck Foundation; NIH-funded Shared Instrumentation Grant S10RR025141; Clinical Translational Sciences Award grants; National Institute of Neurological Disorders and Stroke; National Heart, Lung, and Blood Institute; National Institute of General Medical Sciences.Peer reviewe

Evidence of causal effect of major depression on alcohol dependence: findings from the psychiatric genomics consortium

BACKGROUND Despite established clinical associations among major depression (MD), alcohol dependence (AD), and alcohol consumption (AC), the nature of the causal relationship between them is not completely understood. We leveraged genome-wide data from the Psychiatric Genomics Consortium (PGC) and UK Biobank to test for the presence of shared genetic mechanisms and causal relationships among MD, AD, and AC. METHODS Linkage disequilibrium score regression and Mendelian randomization (MR) were performed using genome-wide data from the PGC (MD: 135 458 cases and 344 901 controls; AD: 10 206 cases and 28 480 controls) and UK Biobank (AC-frequency: 438 308 individuals; AC-quantity: 307 098 individuals). RESULTS Positive genetic correlation was observed between MD and AD (rgMD−AD = + 0.47, P = 6.6 × 10−10). AC-quantity showed positive genetic correlation with both AD (rgAD−AC quantity = + 0.75, P = 1.8 × 10−14) and MD (rgMD−AC quantity = + 0.14, P = 2.9 × 10−7), while there was negative correlation of AC-frequency with MD (rgMD−AC frequency = −0.17, P = 1.5 × 10−10) and a non-significant result with AD. MR analyses confirmed the presence of pleiotropy among these four traits. However, the MD-AD results reflect a mediated-pleiotropy mechanism (i.e. causal relationship) with an effect of MD on AD (beta = 0.28, P = 1.29 × 10−6). There was no evidence for reverse causation. CONCLUSION This study supports a causal role for genetic liability of MD on AD based on genetic datasets including thousands of individuals. Understanding mechanisms underlying MD-AD comorbidity addresses important public health concerns and has the potential to facilitate prevention and intervention efforts