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

Distribution and inter-regional relationship of amyloid-beta plaque deposition in a 5xFAD mouse model of Alzheimer’s disease

Alzheimer’s disease (AD) is the most common form of dementia. Although previous studies have selectively investigated the localization of amyloid-beta (Aβ) deposition in certain brain regions, a comprehensive characterization of the rostro-caudal distribution of Aβ plaques in the brain and their inter-regional correlation remain unexplored. Our results demonstrated remarkable working and spatial memory deficits in 9-month-old 5xFAD mice compared to wildtype mice. High Aβ plaque load was detected in the somatosensory cortex, piriform cortex, thalamus, and dorsal/ventral hippocampus; moderate levels of Aβ plaques were observed in the motor cortex, orbital cortex, visual cortex, and retrosplenial dysgranular cortex; and low levels of Aβ plaques were located in the amygdala, and the cerebellum; but no Aβ plaques were found in the hypothalamus, raphe nuclei, vestibular nucleus, and cuneate nucleus. Interestingly, the deposition of Aβ plaques was positively associated with brain inter-regions including the prefrontal cortex, somatosensory cortex, medial amygdala, thalamus, and the hippocampus. In conclusion, this study provides a comprehensive morphological profile of Aβ deposition in the brain and its inter-regional correlation. This suggests an association between Aβ plaque deposition and specific brain regions in AD pathogenesis

Neuro-Cells therapy improves motor outcomes and suppresses inflammation during experimental syndrome of amyotrophic lateral sclerosis in mice

Aims: Mutations in DNA/RNA-binding factor (fused-in-sarcoma) FUS and superoxide dismutase-1 (SOD-1) cause amyotrophic lateral sclerosis (ALS). They were reproduced in SOD-1-G93A (SOD-1) and new FUS[1-359]-transgenic (FUS-tg) mice, where inflammation contributes to disease progression. The effects of standard disease therapy and anti-inflammatory treatments were investigated using these mutants. Methods: FUS-tg mice or controls received either vehicle, or standard ALS treatment riluzole (8 mg/kg/day), or anti-inflammatory drug a selective blocker of cyclooxygenase-2 celecoxib (30 mg/kg/day) for six weeks, or a single intracerebroventricular (i.c.v.) infusion of Neuro-Cells (a preparation of 1.39 × 106 mesenchymal and hemopoietic human stem cells, containing 5 × 105 of CD34+ cells), which showed anti-inflammatory properties. SOD-1 mice received i.c.v.-administration of Neuro-Cells or vehicle. Results: All FUS-tg-treated animals displayed less marked reductions in weight gain, food/water intake, and motor deficits than FUS-tg-vehicle-treated mice. Neuro-Cell-treated mutants had reduced muscle atrophy and lumbar motor neuron degeneration. This group but not celecoxib-FUS-tg-treated mice had ameliorated motor performance and lumbar expression of microglial activation marker, ionized calcium-binding adapter molecule-1 (Iba-1), and glycogen-synthase-kinase-3ß (GSK-3ß). The Neuro-Cells-treated-SOD-1 mice showed better motor functions than vehicle-treated-SOD-1 group. Conclusion: The neuropathology in FUS-tg mice is sensitive to standard ALS treatments and Neuro-Cells infusion. The latter improves motor outcomes in two ALS models possibly by suppressing microglial activation. © 2019 The Authors. CNS Neuroscience & Therapeutics published by John Wiley & Sons LtdWe thank ?5-100? Russian Excellence Program, Prof. Daniel C. Anthony, Diana Babayevskaya, and Arina Kosakova for their highly valuable contribution. ?Neuro-Cells? preparation was provided by Neuroplast BV, Maastricht, Netherlands

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

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

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

Altered Behaviour, Dopamine and Norepinephrine Regulation in Stressed Mice Heterozygous in TPH2 Gene

Gene-environment interaction (GxE) determines the vulnerability of an individual to a spectrum of stress-related neuropsychiatric disorders. Increased impulsivity, excessive aggression, and other behavioural characteristics are associated with variants within the tryptophan hydroxylase-2 (Tph2) gene, a key enzyme in brain serotonin synthesis. This phenotype is recapitulated in naïve mice with complete, but not with partial Tph2 inactivation. Tph2 haploinsufficiency in animals reflects allelic variation of Tph2 facilitating the elucidation of respective GxE mechanisms. Recently, we showed excessive aggression and altered serotonin brain metabolism in heterozygous Tph2-deficient male mice (Tph2+/−) after predator stress exposure. Here, we sought to extend these studies by investigating aggressive and anxiety-like behaviours, sociability, and the brain metabolism of dopamine and noradrenaline. Separately, Tph2+/− mice were examined for exploration activity in a novel environment and for the potentiation of helplessness in the modified swim test (ModFST). Predation stress procedure increased measures of aggression, dominancy, and suppressed sociability in Tph2+/− mice, which was the opposite of that observed in control mice. Anxiety-like behaviour was unaltered in the mutants and elevated in controls. Tph2+/− mice exposed to environmental novelty or to the ModFST exhibited increased novelty exploration and no increase in floating behaviour compared to controls, which is suggestive of resilience to stress and despair. High-performance liquid chromatography (HPLC) revealed significant genotype-dependent differences in the metabolism of dopamine, and norepinephrine within the brain tissue. In conclusion, environmentally challenged Tph2+/− mice exhibit behaviours that resemble the behaviour of non-stressed null mutants, which reveals how GxE interaction studies can unmask latent genetically determined predispositions. © 2020 The Authors.The authors' work reported here was supported by Deutsche Forschungsgemeinschaft (DFG:CRC TRR58A1/A5), DAAD (to ES), 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) and the President's program of PhD Exchange of RF-2017 (to TS and DA). We appreciate the valuable technical help of Natalia Bazhenova, Drs. Alexander Trofimov and Natalia Markova with this project

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