Разработка системы управления сепаратора факельной системы установки комплексной подготовки газа

Объектом исследования является блок подготовки газа (сепаратор факельной системы) установки комплексной подготовки газа. Цель работы – разработка системы управления сепаратора факельной системы установки комплексной подготовки газа с использованием ПЛК, на основе выбранной SCADA-системы.The object of the study is the gas treatment unit (flare system separator) of the complex gas treatment unit. The aim of the work is the development of a control system for the flare system separator of the complex gas treatment unit using PLCs, based on the selected SCADA system

12 Years of GENEX Framework: What did Practice Learn from Science in Terms of Web-Based Ideation?

In Open Innovation, companies open up their innovation activities to external stakeholders. Using web-based ideation platforms (WBIP), companies crowdsource ideas for innovations from their customers. Ideation can be considered as a create process. Therefore, in this research we analyze how current web-based ideation platforms run by firms support Shneiderman’s GENEX framework that aims at supporting creativity in information systems. By doing so, we were able to identify the state-of-the-art in practice as well as further research areas. We analyzed 16 web-based ideation platforms in total. Results indicate that current WBIP use creativity tasks different intensive and that some GENEX tasks are already well implemented, while others require further research. Results are discussed and theoretical and practical contributions, limitations and identified research questions provided

Selenium-binding protein 1 (SELENBP1) is a copper-dependent thiol oxidase

Selenium-binding protein 1 (SELENBP1) was reported to act as a methanethiol oxidase (MTO) in humans, catalyzing the conversion of methanethiol to hydrogen peroxide, hydrogen sulfide and formaldehyde. Here, we identify copper ions as essential to this novel MTO activity. Site-directed mutagenesis of putative copper-binding sites in human SELENBP1 produced as recombinant protein in E. coli resulted in loss of its enzymatic function. On the other hand, the eponymous binding of selenium (as selenite) was no requirement for MTO activity and only moderately increased SELENBP1-catalyzed oxidation of methanethiol. Furthermore, SEMO-1, the SELENBP1 ortholog recently identified in the nematode C. elegans, also requires copper ions, and MTO activity was enhanced or abrogated, respectively, if worms were grown in the presence of cupric chloride or of a Cu chelator. In addition to methanethiol, we identified novel substrates of SELENBP1 from the group of volatile sulfur compounds, ranging from ethanethiol to 1-pentanethiol as well as 2-propene-1-thiol. Gut microbiome-derived methanethiol as well as food-derived volatile sulfur compounds (VSCs) account for malodors that may contribute to extraoral halitosis in humans, if not metabolized properly. As SELENBP1 is particularly abundant in tissues exposed to VSCs, such as colon, liver, and lung, it appears to contribute to copper-dependent VSC degradation

Laquinimod ameliorates secondary brain inflammation

Accumulating evidence suggests that a degenerative processes within the brain can trigger the formation of new, focal inflammatory lesions in Multiple Sclerosis (MS). Here, we used a novel pre-clinical MS animal model to test whether the amelioration of degenerative brain events reduces the secondary recruitment of peripheral immune cells and, in consequence, inflammatory lesion development. Neural degeneration was induced by a 3 weeks cuprizone intoxication period. To mitigate the cuprizone-induced pathology, animals were treated with Laquinimod (25 mg/kg) during the cuprizone-intoxication period. At the beginning of week 6, encephalitogenic T cell development in peripheral lymphoid organs was induced by the immunization with myelin oligodendrocyte glycoprotein 35-55 peptide (i.e., Cup/EAE). Demyelination, axonal injury and reactive gliosis were determined by immunohistochemistry. Positron emission tomography (PET) imaging was performed to analyze glia activation in vivo. Vehicle-treated cuprizone mice displayed extensive callosal demyelination, glia activation and enhanced TSPO-ligand binding. This cuprizone-induced pathology was profoundly ameliorated in mice treated with Laquinimod. In vehicle-treated Cup/EAE mice, the cuprizone-induced pathology triggered massive peripheral immune cell recruitment into the forebrain, evidenced by multifocal perivascular inflammation, glia activation and neuro-axonal injury. While anti myelin oligodendrocyte glycoprotein 35-55 peptide immune responses were comparable in vehicle- and Laquinimod-treated Cup/EAE mice, the cuprizone-triggered immune cell recruitment was ameliorated by the Laquinimod treatment. This study clearly illustrates that amelioration of a primary brain-intrinsic degenerative process secondary halts peripheral immune cell recruitment and, in consequence, inflammatory lesion development. These findings have important consequences for the interpretation of the results of clinical studies