ПОВЫШЕНИЕ ЭФФЕКТИВНОСТИ РАСКРЫТИЯ МИНЕРАЛЬНЫХ АССОЦИАЦИЙ РЕДКОЗЕМЕЛЬНЫХ РУД ПО КОМБИНИРОВАННЫМ ТЕХНОЛОГИЯМ

In terms of rare-earth ores of the Tatarsky and Tomtorsky deposits (Krasnoyarsky Territory), the possibility of increasing the extent of investigated sample breaking down by means of discharge-impulse intensification of the grinding process is considered. The use of the combined scheme of ore dressing called «grinding for 20 minutes – discharge-impulse processing with specific energy of 9,2 kJ/dm3» allows increasing the extent of lanthanum and yttrium recovery into the acid solution by 3,8 and 2,8 % respectively during sintering of processed samples with soda.На примере редкоземельных руд Татарского и Томторского месторождений (Красноярский кр.) рассмотрена возможность повышения степени раскрытия исследуемых проб за счет разрядно-импульсной интенсификации процесса измельчения. Применение комбинированной схемы рудоподготовки «измельчение 20 мин – разрядно-импульсная обработка с удельной энергией 9,2 кДж/дм3» позволит повысить степень извлечения лантана и иттрия в кислый раствор на 3,8 и 2,8 % соответственно при спекании подготовленных проб с содой

On the origin of 140 GHz emission from the 4 July 2012 solar flare

The sub-THz event observed on the 4 July 2012 with the Bauman Moscow State Technical University Radio Telescope RT-7.5 at 93 and 140~GHz as well as Kislovodsk and Mets\"ahovi radio telescopes, Radio Solar Telescope Network (RSTN), GOES, RHESSI, and SDO orbital stations is analyzed. The spectral flux between 93 and 140 GHz has been observed increasing with frequency. On the basis of the SDO/AIA data the differential emission measure has been calculated. It is shown that the thermal coronal plasma with the temperature above 0.5~MK cannot be responsible for the observed sub-THz flare emission. The non-thermal gyrosynchrotron mechanism can be responsible for the microwave emission near $10$~GHz but the observed millimeter spectral characteristics are likely to be produced by the thermal bremsstrahlung emission from plasma with a temperature of about 0.1~MK.Comment: 18 pages, 6 figure

Understanding How Stress Responses and Stress-Related Behaviors Have Evolved in Zebrafish and Mammals

Stress response is essential for the organism to quickly restore physiological homeostasis disturbed by various environmental insults. In addition to well-established physiological cascades, stress also evokes various brain and behavioral responses. Aquatic animal models, including the zebrafish (Danio rerio), have been extensively used to probe pathobiological mechanisms of stress and stress-related brain disorders. Here, we critically discuss the use of zebrafish models for studying mechanisms of stress and modeling its disorders experimentally, with a particular cross-taxon focus on the potential evolution of stress responses from zebrafish to rodents and humans, as well as its translational implications. © 2021 The AuthorsAVK is supported by the Zebrafish Platform Construction Fund from the Southwest University (Chongqing, China). The collaboration was supported by the Russian Science Foundation (RSF) grant 19-15-00053. KAD is supported by the President of Russia Graduate Fellowship, and the Special Rector's Fellowship for SPSU students. ACVVG is supported by the FAPERGS research fellowship 19/2551-0001-669-7. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript

A Ni(III) complex stabilized by silica nanoparticles as an efficient nanoheterogeneous catalyst for oxidative C-H fluoroalkylation

© The Royal Society of Chemistry 2016.We have developed NiIII-doped silica nanoparticles ([(bpy)xNiIII]@SiO2) as a recyclable, low-leaching, and efficient oxidative functionalization nanocatalyst for aromatic C-H bonds. The catalyst is obtained by doping the complex [(bpy)3NiII] on silica nanoparticles along with its subsequent electrooxidation to [(bpy)xNiIII] without an additional oxidant. The coupling reaction of arenes with perfluoroheptanoic acid occurs with 100% conversion of reactants in a single step at room temperature under nanoheterogeneous conditions. The catalyst content is only 1% with respect to the substrates under electrochemical regeneration conditions. The catalyst can be easily separated from the reaction mixture and reused a minimum of five times. The results emphasize immobilization on the silica support and the electrochemical regeneration of NiIII complexes as a facile route for developing an efficient nanocatalyst for oxidative functionalization

The neuronal insulin sensitizer dicholine succinate reduces stress-induced depressive traits and memory deficit: possible role of insulin-like growth factor 2.

BACKGROUND: A number of epidemiological studies have established a link between insulin resistance and the prevalence of depression. The occurrence of depression was found to precede the onset of diabetes and was hypothesized to be associated with inherited inter-related insufficiency of the peripheral and central insulin receptors. Recently, dicholine succinate, a sensitizer of the neuronal insulin receptor, was shown to stimulate insulin-dependent H2O2 production of the mitochondrial respiratory chain leading to an enhancement of insulin receptor autophosphorylation in neurons. As such, this mechanism can be a novel target for the elevation of insulin signaling. RESULTS: Administration of DS (25 mg/kg/day, intraperitoneal) in CD1 mice for 7 days prior to the onset of stress procedure, diminished manifestations of anhedonia defined in a sucrose test and behavioral despair in the forced swim test. Treatment with dicholine succinate reduced the anxiety scores of stressed mice in the dark/light box paradigm, precluded stress-induced decreases of long-term contextual memory in the step-down avoidance test and hippocampal gene expression of IGF2. CONCLUSIONS: Our data suggest that dicholine succinate has an antidepressant-like effect, which might be mediated via the up-regulation of hippocampal expression of IGF2, and implicate the neuronal insulin receptor in the pathogenesis of stress-induced depressive syndrome.journal articleresearch support, non-u.s. gov't2012 Sep 182012 09 18importe

Stress-induced aggression in heterozygous TPH2 mutant mice is associated with alterations in serotonin turnover and expression of 5-HT6 and AMPA subunit 2A receptors

Background: The contribution of gene-environment interactions that lead to excessive aggression is poorly understood. Environmental stressors and mutations of the gene encoding tryptophan hydroxylase-2 (TPH2) are known to influence aggression. For example, TPH2 null mutant mice (Tph2−/−) are naturally highly aggressive, while heterozygous mice (Tph2+/−) lack a behavioral phenotype and are considered endophenotypically normal. Here we sought to discover whether an environmental stressor would affect the phenotype of the genetically ‘susceptible’ heterozygous mice (Tph2+/−). Methods: Tph2+/− male mice or Tph2+/+ controls were subjected to a five-day long rat exposure stress paradigm. Brain serotonin metabolism and the expression of selected genes encoding serotonin receptors, AMPA receptors, and stress markers were studied. Results: Stressed Tph2+/− mice displayed increased levels of aggression and social dominance, whereas Tph2+/+ animals became less aggressive and less dominant. Brain tissue concentrations of serotonin, its precursor hydroxytryptophan and its metabolite 5-hydroxyindoleacetic acid were significantly altered in all groups in the prefrontal cortex, striatum, amygdala, hippocampus and dorsal raphe after stress. Compared to non-stressed animals, the concentration of 5-hydroxytryptophan was elevated in the amygdala though decreased in the other brain structures. The overexpression of the AMPA receptor subunit, GluA2, and downregulation of 5-HT6 receptor, as well as overexpression of c-fos and glycogen-synthase-kinase-3β (GSK3-β), were found in most structures of the stressed Tph2+/− mice. Limitations: Rescue experiments would help to verify causal relationships of reported changes. Conclusions: The interaction of a partial TPH2 gene deficit with stress results in pathological aggression and molecular changes, and suggests that the presence of genetic susceptibility can augment aggression in seemingly resistant phenotypes. © 2020 The Authors602805Seventh Framework Programme, FP7Deutsche Forschungsgemeinschaft, DFG: CRC TRR 58 A1/A5Horizon 2020 Framework Programme, H2020: 728018Russian Foundation for Basic Research, RFBR: 15-04-03602Deutsche Forschungsgemeinschaft, DFGRussian Foundation for Basic Research, RFBRThe authors’ work reported here was supported Deutsche Forschungsgemeinschaft (DFG: CRC TRR 58 A1/A5), the European Union's Seventh Framework Programme (FP7/2007–2013) under Grant No. 602805 (Aggressotype) and the Horizon 2020 Research and Innovation Programme under Grant No. 728018 (Eat2beNICE) (to KPL and TS), the “5-100” Russian Academic Excellence Project (to KPL and TS) and the Russian Foundation of Basic Research (RFBR Grant No. 15-04-03602 to TS). We appreciate the valuable technical help of Dr. Joao Costa-Nunes and Dolores Bonopartos with this project

Towards Modeling Anhedonia and Its Treatment in Zebrafish

Mood disorders, especially depression, are a major cause of human disability. The loss of pleasure (anhedonia) is a common, severely debilitating symptom of clinical depression. Experimental animal models are widely used to better understand depression pathogenesis and to develop novel antidepressant therapies. In rodents, various experimental models of anhedonia have already been developed and extensively validated. Complementing rodent studies, the zebrafish (Danio rerio) is emerging as a powerful model organism to assess pathobiological mechanisms of affective disorders, including depression. Here, we critically discuss the potential of zebrafish for modeling anhedonia and studying its molecular mechanisms and translational implications. © 2021 The Author(s). Published by Oxford University Press on behalf of CINP

Modulation of Behavioral and Neurochemical Responses of Adult Zebrafish by Fluoxetine, Eicosapentaenoic Acid and Lipopolysaccharide in the Prolonged Chronic Unpredictable Stress Model

Long-term recurrent stress is a common cause of neuropsychiatric disorders. Animal models are widely used to study the pathogenesis of stress-related psychiatric disorders. The zebrafish (Danio rerio) is emerging as a powerful tool to study chronic stress and its mechanisms. Here, we developed a prolonged 11-week chronic unpredictable stress (PCUS) model in zebrafish to more fully mimic chronic stress in human populations. We also examined behavioral and neurochemical alterations in zebrafish, and attempted to modulate these states by 3-week treatment with an antidepressant fluoxetine, a neuroprotective omega-3 polyunsaturated fatty acid eicosapentaenoic acid (EPA), a pro-inflammatory endotoxin lipopolysaccharide (LPS), and their combinations. Overall, PCUS induced severe anxiety and elevated norepinephrine levels, whereas fluoxetine (alone or combined with other agents) corrected most of these behavioral deficits. While EPA and LPS alone had little effects on the zebrafish PCUS-induced anxiety behavior, both fluoxetine (alone or in combination) and EPA restored norepinephrine levels, whereas LPS + EPA increased dopamine levels. As these data support the validity of PCUS as an effective tool to study stress-related pathologies in zebrafish, further research is needed into the ability of various conventional and novel treatments to modulate behavioral and neurochemical biomarkers of chronic stress in this model organism. © 2021, The Author(s).This research was supported solely by the Russian Science Foundation (RSF) grant 19‐15‐00053. K.A.D. is supported by the Special Rector’s Productivity Fellowship for SPSU PhD Students, and the lab is supported by St. Petersburg State University state budgetary funds (project ID 73026081). A.V.K. is the Chair of the International Zebrafish Neuroscience Research Consortium (ZNRC) and President of the International Stress and Behavior Society (ISBS, www.stress-and-behavior.com) that coordinated this collaborative multi-laboratory project. The consortium provided a collaborative idea exchange platform for this study, it is not considered as affiliation and did not fund the study. A.V.K. lab is supported by the Southwest University (SWU) Zebrafish Platform Construction Fund (Chongqing, China). The authors thank Professor Raul R. Gainetdinov (Institute of Translational Biomedicine, St. Petersburg State University, St. Petersburg, Russia) for his generous assistance with the HPLC studies in his laboratory. The funders had no role in the design, analyses, and interpretation of the submitted study, or decision to publish

Animal models of major depressive disorder and the implications for drug discovery and development

Introduction: Depression is a highly debilitating psychiatric disorder that affects the global population and causes severe disabilities and suicide. Depression pathogenesis remains poorly understood, and the disorder is often treatment-resistant and recurrent, necessitating the development of novel therapies, models and concepts in this field. Areas covered: Animal models are indispensable for translational biological psychiatry, and markedly advance the study of depression. Novel approaches continuously emerge that may help untangle the disorder heterogeneity and unclear categories of disease classification systems. Some of these approaches include widening the spectrum of model species used for translational research, using a broader range of test paradigms, exploring new pathogenic pathways and biomarkers, and focusing more closely on processes beyond neural cells (e.g. glial, inflammatory and metabolic deficits). Expert opinion: Dividing the core symptoms into easily translatable, evolutionarily conserved phenotypes is an effective way to reevaluate current depression modeling. Conceptually novel approaches based on the endophenotype paradigm, cross-species trait genetics and ‘domain interplay concept’, as well as using a wider spectrum of model organisms and target systems will enhance experimental modeling of depression and antidepressant drug discovery. © 2019, © 2019 Informa UK Limited, trading as Taylor & Francis Group

Predation Stress Causes Excessive Aggression in Female Mice with Partial Genetic Inactivation of Tryptophan Hydroxylase-2: Evidence for Altered Myelination-Related Processes

The interaction between brain serotonin (5-HT) deficiency and environmental adversity may predispose females to excessive aggression. Specifically, complete inactivation of the gene encoding tryptophan hydroxylase-2 (Tph2) results in the absence of neuronal 5-HT synthesis and excessive aggressiveness in both male and female null mutant (Tph2−/−) mice. In heterozygous male mice (Tph2+/−), there is a moderate reduction in brain 5-HT levels, and when they are exposed to stress, they exhibit increased aggression. Here, we exposed female Tph2+/− mice to a five-day rat predation stress paradigm and assessed their emotionality and social interaction/aggression-like behaviors. Tph2+/− females exhibited excessive aggression and increased dominant behavior. Stressed mutants displayed altered gene expression of the 5-HT receptors Htr1a and Htr2a, glycogen synthase kinase-3 β (GSK-3β), and c-fos as well as myelination-related transcripts in the prefrontal cortex: myelin basic protein (Mbp), proteolipid protein 1 (Plp1), myelin-associated glycoprotein (Mag), and myelin oligodendrocyte glycoprotein (Mog). The expression of the plasticity markers synaptophysin (Syp) and cAMP response element binding protein (Creb), but not AMPA receptor subunit A2 (GluA2), were affected by genotype. Moreover, in a separate experiment, naïve female Tph2+/− mice showed signs of enhanced stress resilience in the modified swim test with repeated swimming sessions. Taken together, the combination of a moderate reduction in brain 5-HT with environmental challenges results in behavioral changes in female mice that resemble the aggression-related behavior and resilience seen in stressed male mutants; additionally, the combination is comparable to the phenotype of null mutants lacking neuronal 5-HT. Changes in myelination-associated processes are suspected to underpin the molecular mechanisms leading to aggressive behavior. © 2022 by the authors. Licensee MDPI, Basel, Switzerland.Seventh Framework Programme, FP7: 602805; Deutsche Forschungsgemeinschaft, DFG: CRC TRR58A1/A5; Russian Academy of Sciences, РАН: N0520-2019-0031; Horizon 2020: 101007642, 728018Funding: The authors’ animal work reported here was supported by Deutsche Forschungsgemein-schaft (DFG:CRC TRR58A1/A5), the European Union’s Seventh Framework Programme (FP7/2007– 2013) under Grant No. 602805 (Aggressotype), the Horizon 2020 Research and Innovation Programme under Grant No. 728018 (Eat2beNice) (to K.P.L. and T.S.) and Grant No. 101007642 (PhytoAPP) (to D.A. and T.S.), and Swiss-Russian Cooperation grant RPG Russia 2020 (to S.W. and K.P.L.). Molecular data analysis was supported by RAS N0520-2019-0031 (to E.S. and T.S.). The sponsors had no role in study design, in the collection, analysis, and interpretation of data; in the writing of the report, and in the decision to submit the article for publication