Борьба с биообрастанием природных и сточных вод с использованием энергетических воздействий

Данная работа посвящена анализу методов очистки воды для борьбы с биологическим обрастанием технологического оборудования. Рассмотрены различные способы борьбы с биологическим обрастанием, в том числе: реагентные, безреагентные и электрические. Сформирована концепция применения способа борьбы с биологическим обрастанием технологического оборудования путем электрической обработки теплоносителя. Приведена схема установки, таблица результатов и диаграмма.This work is devoted to the analysis of methods of water purification for fight against biological fouling of processing equipment. Various ways of fight against biological fouling are considered, including: reagent, reagentless and electric. The concept of application of a way of fight against biological fouling of processing equipment by electric processing of the heat carrier is created. The scheme of installation, the table of results and the chart is provided

Mechanical characteristics of the hypereutectic silumin processed by ionelectron-plasma modification

In this paper, the possibility of modifying the surface of a hypereutectic silumin (Al-(18-24) wt.%Si) is shown. Modification of the samples was carried out in two stages. At the first stage, a "film (Zr-5% Ti-5% Cu) / (Al- (18-24) wt.% Si) film system was formed by an ion-plasma method with an arc-sputtering of a Zr-5% Ti-5 cathode % Cu in the "TRIO" installation (IHCE SB RAS). In the second stage, the surface layer of the silumin of the hypereutectic composition was doped by melting the "film-substrate" system with an intense pulsed electron beam at the "SOLO" installation

Evaluation of motor transport drivers professional suitability using road traffic simulator

The article considers a method that allows to determine the degree of development of professionally important qualities of motor vehicle drivers on the basis of the developed hardware-software complex of traffic simulation. The technique of convolution of the test results on the auto-simulator and on the complex of psychological tests "Effecton" is developed. The proposed approach allows to determine the degree of correlation between the results of the developed simulation tests and existing universal psychological tests

Ontogeny of synaptophysin and synaptoporin in the central nervous system

The expression of the synaptic vesicle antigens synaptophysin (SY) and synaptoporin (SO) was studied in the rat striatum, which contains a nearly homogeneous population of GABAergic neurons. In situ hybridization revealed high levels of SY transcripts in the striatal anlage from embryonic day (E) 14 until birth. In contrast. SO hybridization signals were low, and no immunoreactive cell bodies were detected at these stages of development. At E 14, SY-immunoreactivity was restricted to perikarya. In later prenatal stages of development SY-immunoreactivity appeared in puncta (identified as terminals containing immunostained synaptic vesicles), fibers, thick fiber bundles and ‘patches’. In postnatal and adult animals, perikarya of striatal neurons exhibited immunoreaction for SO; ultrastructurally SO antigen was found in the Golgi apparatus and in multivesicular bodies. SO-positive boutons were rare in the striatum. In the neuropil, numerous presynaptic terminals positive for SY were observed. Our data indicate that the expression of synaptic vesicle proteins in GABAergic neurons of the striatum is developmentally regulated. Whereas SY is prevalent during embryonic development, SO is the major synaptic vesicle antigen expressed postnatally by striatal neurons which project to the globus pallidus and the substantia nigra. In contrast synapses of striatal afferents (predominantly from cortex, thalamus and substantia nigra) contain SY

Влияние добавки нановолокон оксида алюминия на стойкость к низкотемпературному разложению керамики на основе диоксида циркония

Cerebral activation in the elderly may depend on general cognitive decline as well as actual retrieval performance. Consequently, activation between subjects with and without Mild Cognitive Impairment (MCI), and between remembered and non-remembered words was compared. Twenty-one MCI and 29 healthy control subjects learned 180 nouns. During retrieval, subjects had to discriminate these and 180 distractor words. fMRI identified response-related activation. Most retrieval-related activation was comparable in both groups. However, MCI subjects showed more activation in the prefrontal cortex than controls during processing of hits and correct rejections. Hits showed increased activation than misses in the precuneus and left lateral parieto-occipital cortex; misses showed more activation than correct rejections in the precuneus to cuneus. Verbal retrieval activated a large common network in the elderly independently of MCI. Increased activation in MCI subjects in prefrontal cortex depends on response category. Activation differences between response categories might reflect success (hits) and effort (misses). Increased retrieval-related activation may be used as early marker in subjects at risk of Alzheimer's disease

Economic vs. juristic thinking in Carl Menger’s principles of economics

Austrian Economic School is increasingly being treated as one of the most significant and ever more influential bodies of ideas affecting the contemporary economic science. It is well known that Carl Menger, the founder of the Austrian School, was a lawyer by education. The paper is devoted to the degree to which his legal education influenced his economic theorizing. After a close examination of the Menger’s conceptual apparatus and the epistemological ramifications of the key notions underlying his thinking, the paper concludes that the juristic background of the far-reaching theoretical contributions contained in Menger’s Principles was truly decisive. That holds true despite the fact that Menger only exceptionally utilized the juristic vocabulary. The key ingredients of his theoretical creation? such as the individual autonomy, the coincidence of the wills in concluding a contract the effective protection of property and making transactions based on the individual motivation to further one’s own interests to the utmost? are clearly inspired and in many ways influenced by private law, particularly the doctrines underlying the Roman Law and the Austrian Civil Code

Dual proteotoxic stress accelerates liver injury via activation of p62-Nrf2

Protein accumulation is the hallmark of various neuronal, muscular, and other human disorders. It is also often seen in the liver as a major protein-secretory organ. For example, aggregation of mutated alpha1-antitrypsin (AAT), referred to as PiZ, is a characteristic feature of AAT deficiency, whereas retention of hepatitis B surface protein (HBs) is found in chronic hepatitis B (CHB) infection. We investigated the interaction of both proteotoxic stresses in humans and mice. Animals overexpressing both PiZ and HBs (HBs-PiZ mice) had greater liver injury, steatosis, and fibrosis. Later they exhibited higher hepatocellular carcinoma load and a more aggressive tumor subtype. Although PiZ and HBs displayed differing solubility properties and distinct distribution patterns, HBs-PiZ animals manifested retention of AAT/HBs in the degradatory pathway and a marked accumulation of the autophagy adaptor p62. Isolation of p62-containing particles revealed retained HBs/AAT and the lipophagy adapter perilipin-2. p62 build-up led to activation of the p62–Nrf2 axis and emergence of reactive oxygen species. Our results demonstrate that the simultaneous presence of two prevalent proteotoxic stresses promotes the development of liver injury due to protein retention and activation of the p62–Nrf2 axis. In humans, the PiZ variant was over-represented in CHB patients with advanced liver fibrosis (unadjusted odds ratio = 9.92 [1.15–85.39]). Current siRNA approaches targeting HBs/AAT should be considered for these individuals. © 2021 The Authors. The Journal of Pathology published by John Wiley & Sons, Ltd. on behalf of The Pathological Society of Great Britain and Ireland

Early onset torsion dystonia (Oppenheim's dystonia)

Early onset torsion dystonia (EOTD) is a rare movement disorder characterized by involuntary, repetitive, sustained muscle contractions or postures involving one or more sites of the body. A US study estimated the prevalence at approximately 1 in 30,000. The estimated prevalence in the general population of Europe seems to be lower, ranging from 1 in 330,000 to 1 in 200,000, although precise numbers are currently not available. The estimated prevalence in the Ashkenazi Jewish population is approximately five to ten times higher, due to a founder mutation. Symptoms of EOTD typically develop first in an arm or leg in middle to late childhood and progress in approximately 30% of patients to other body regions (generalized dystonia) within about five years. Distribution and severity of symptoms vary widely between affected individuals. The majority of cases from various ethnic groups are caused by an autosomal dominantly inherited deletion of 3 bp (GAG) in the DYT1 gene on chromosome 9q34. This gene encodes a protein named torsinA, which is presumed to act as a chaperone protein associated with the endoplasmic reticulum and the nuclear envelope. It may interact with the dopamine transporter and participate in intracellular trafficking, although its precise function within the cell remains to be determined. Molecular genetic diagnostic and genetic counseling is recommended for individuals with age of onset below 26 years, and may also be considered in those with onset after 26 years having a relative with typical early onset dystonia. Treatment options include botulinum toxin injections for focal symptoms, pharmacological therapy such as anticholinergics (most commonly trihexiphenydil) for generalized dystonia and surgical approaches such as deep brain stimulation of the internal globus pallidus or intrathecal baclofen application in severe cases. All patients have normal cognitive function, and despite a high rate of generalization of dystonia, 75% of those patients are able to maintain ambulation and independence, and therefore a comparatively good quality of life, with modern treatment modalities

Investigation of the role of SDHB inactivation in sporadic phaeochromocytoma and neuroblastoma

Germline mutations in the succinate dehydrogenase (SDH) (mitochondrial respiratory chain complex II) subunit B gene, SDHB, cause susceptibility to head and neck paraganglioma and phaeochromocytoma. Previously, we did not identify somatic SDHB mutations in sporadic phaeochromocytoma, but SDHB maps to 1p36, a region of frequent loss of heterozygosity (LOH) in neuroblastoma as well. Hence, to evaluate SDHB as a candidate neuroblastoma tumour suppressor gene (TSG) we performed mutation analysis in 46 primary neuroblastomas by direct sequencing, but did not identify germline or somatic SDHB mutations. As TSGs such as RASSF1A are frequently inactivated by promoter region hypermethylation, we designed a methylation-sensitive PCR-based assay to detect SDHB promoter region methylation. In 21% of primary neuroblastomas and 32% of phaeochromocytomas (32%) methylated (and unmethylated) alleles were detected. Although promoter region methylation was also detected in two neuroblastoma cell lines, this was not associated with silencing of SDHB expression, and treatment with a demethylating agent (5-azacytidine) did not increase SDH activity. These findings suggest that although germline SDHB mutations are an important cause of phaeochromocytoma susceptibility, somatic inactivation of SDHB does not have a major role in sporadic neural crest tumours and SDHB is not the target of 1p36 allele loss in neuroblastoma and phaeochromocytoma

Desmoglein 2 mutant mice develop cardiac fibrosis and dilation

Desmosomes are cell–cell adhesion sites and part of the intercalated discs, which couple adjacent cardiomyocytes. The connection is formed by the extracellular domains of desmosomal cadherins that are also linked to the cytoskeleton on the cytoplasmic side. To examine the contribution of the desmosomal cadherin desmoglein 2 to cardiomyocyte adhesion and cardiac function, mutant mice were prepared lacking a part of the extracellular adhesive domain of desmoglein 2. Most live born mutant mice presented normal overall cardiac morphology at 2 weeks. Some animals, however, displayed extensive fibrotic lesions. Later on, mutants developed ventricular dilation leading to cardiac insufficiency and eventually premature death. Upon histological examination, cardiomyocyte death by calcifying necrosis and replacement by fibrous tissue were observed. Fibrotic lesions were highly proliferative in 2-week-old mutants, whereas the fibrotic lesions of older mutants showed little proliferation indicating the completion of local muscle replacement by scar tissue. Disease progression correlated with increased mRNA expression of c-myc, ANF, BNF, CTGF and GDF15, which are markers for cardiac stress, remodeling and heart failure. Taken together, the desmoglein 2-mutant mice display features of dilative cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy, an inherited human heart disease with pronounced fibrosis and ventricular arrhythmias that has been linked to mutations in desmosomal proteins including desmoglein 2