PREPARATION MAGNESIUM DIBORIDE BY MAGNIATHERMAL BORON OXIDE BASED ON SUPERCONDUCTING PROPERTIES

Results of receiving a diborid of magnesium are given in work by magniathermal oxidation of boron composite compounds at different argon pressures and temperatures. The relevance of a research is proved by superconducting properties of magnesium diboride. Synthesis of magnesium diboride itself accelerates, due to wall burning and thermal explosion of exothermic mixture of the reaction products of magniathermal. It is shown that the use of SHS method at high argon pressure and temperature allows to obtain magnesium diboride of high purity

FabSim3: An automation toolkit for verified simulations using high performance computing

A common feature of computational modelling and simulation research is the need to perform many tasks in complex sequences to achieve a usable result. This will typically involve tasks such as preparing input data, pre-processing, running simulations on a local or remote machine, post-processing, and performing coupling communications, validations and/or optimisations. Tasks like these can involve manual steps which are time and effort intensive, especially when it involves the management of large ensemble runs. Additionally, human errors become more likely and numerous as the research work becomes more complex, increasing the risk of damaging the credibility of simulation results. Automation tools can help ensure the credibility of simulation results by reducing the manual time and effort required to perform these research tasks, by making more rigorous procedures tractable, and by reducing the probability of human error due to a reduced number of manual actions. In addition, efficiency gained through automation can help researchers to perform more research within the budget and effort constraints imposed by their projects. This paper presents the main software release of FabSim3, and explains how our automation toolkit can improve and simplify a range of tasks for researchers and application developers. FabSim3 helps to prepare, submit, execute, retrieve, and analyze simulation workflows. By providing a suitable level of abstraction, FabSim3 reduces the complexity of setting up and managing a large-scale simulation scenario, while still providing transparent access to the underlying layers for effective debugging. The tool also facilitates job submission and management (including staging and curation of files and environments) for a range of different supercomputing environments. Although FabSim3 itself is application-agnostic, it supports a provably extensible plugin system where users automate simulation and analysis workflows for their own application domains. To highlight this, we briefly describe a selection of these plugins and we demonstrate the efficiency of the toolkit in handling large ensemble workflows.EPSRC under grant agreement EP/W007711/1, as well as by the VECMA and HiDALGO projects, which have received funding from the European Union Horizon 2020 research and innovation programme under grant agreement nos 800925 and 824115. In addition, FabFlee was supported by the ITFLOWS project and FabCovid19 by the STAMINA project, both of which have received funding from the European Union’s Horizon 2020 research and innovation programme under grant agreement No 882986 and No 883441 respectivel

Thermodynamic Simulation of Simultaneous Extraction of Metals During Waste Processing Industry

The depletion of ores, a rise in the cost of their extraction, enrichment and processing led in the last 10‒15 years to a sharp rise in prices for tungsten products. Therefore, the processing began to involve technogenic waste ‒ dumps of enrichment factories and metallurgical industries, which previously did not represent the commercial interest on this case, we present the information on the results of the thermodynamic modeling of tungsten and bismuth chloride distillation in the processing of industrial waste using NaCl as a chlorinating agent. To calculate thermodynamic models for the associated extraction of tungsten and bismuth from industrial wastes, the ASTRA-4 software complex was used which created on basis of the maximum entropy of all possible reactions occurring during the retrieval of refractory metals from waste. Thus, the calculations carried out and experimental studies of the main provisions of thermodynamic calculation have shown the possibility of using NaCl salts for bismuth chlorination. At the same time, the maximum degree of sublimation of bismuth not be lower than 98% and can be achieved even at a temperature of 1200 K and a pressure of 0.01–0.1 MPa. At the same time, NaCl is not an effective chlorinating agent for retrieving of tungsten during high-temperature processing of industrial wastes

BCL-XL ACTIVITY INFLUENCES OUTCOME OF THE MITOTIC ARREST

Microtubule-targeting (MT) drugs taxanes and vinca alkaloids are widely used as chemotherapeutic agents against different tumors for more than 30 years because of their ability to block mitotic progression by disrupting the mitotic spindle and activating the spindle assembly checkpoint (SAC) for a prolonged period of time. However, responses to mitotic arrest are different—some cells die during mitotic arrest, whereas others undergo mitotic slippage and survive becoming able for proliferation. Using normal fibroblasts and several cancer cell types we determined two critical doses, T1 and T2, of mitotic inhibitors (nocodazole, Taxol, and vinorelbine). T1 is the maximal dose cells can tolerate undergoing normal division, and T2 is the minimal mitostatic dose, wherein > 90% of mitotic cells are arrested in mitosis. In all studied cell lines after treatment with mitotic inhibitors in a dose above T2 cells had entered mitosis either die or undergo mitotic slippage. We show that for all three drugs used cell death during mitotic arrest and after slippage proceeded via mitochondriadependent apoptosis. We determined two types of cancer cells: sensitive to mitotic arrest, that is, undergoing death in mitosis (DiM) frequently, and resistant to mitotic arrest, that is, undergoing mitotic slippage followed by prolonged survival. We then determined that inhibition of Bcl-xL, but not other antiapoptotic proteins of the Bcl-2 group that regulate MOMP, make resistant cells susceptible to DiM induced by mitotic inhibitors. Combined treatment with MT drugs and highly specific Bcl-xL inhibitors A-1155643 or A-1331852 allows achieving 100% DiM in a time significantly shorter than maximal duration of mitotic arrest in all types of cultured cells tested. We further examined efficacy of sequential treatment of cultured cells using mitotic inhibitors followed by inhibitors of Bcl-xL anti-apoptotic protein and for the first time show that sensitivity to Bcl-xL inhibitors rapidly declines after mitotic slippage. Thus sequential use of mitotic inhibitors and inhibitors of Bcl-xL anti-apoptotic protein will be efficient only if the Bcl-xL inhibitor will be added before mitotic slippage occurs or soon afterward. The combined treatment proposed might be an efficient approach to anti-cancer therapy

FACS-CHARM: A Hybrid Agent-Based and Discrete-Event Simulation Approach for Covid-19 Management at Regional Level

10.13039/100010661-EU H2020 STAMINA (Grant Number: 883441

FabSim3: An automation toolkit for verified simulations using high performance computing

A common feature of computational modelling and simulation research is the need to perform many tasks in complex sequences to achieve a usable result. This will typically involve tasks such as preparing input data, pre-processing, running simulations on a local or remote machine, post-processing, and performing coupling communications, validations and/or optimisations. Tasks like these can involve manual steps which are time and effort intensive, especially when it involves the management of large ensemble runs. Additionally, human errors become more likely and numerous as the research work becomes more complex, increasing the risk of damaging the credibility of simulation results. Automation tools can help ensure the credibility of simulation results by reducing the manual time and effort required to perform these research tasks, by making more rigorous procedures tractable, and by reducing the probability of human error due to a reduced number of manual actions. In addition, efficiency gained through automation can help researchers to perform more research within the budget and effort constraints imposed by their projects. This paper presents the main software release of FabSim3, and explains how our automation toolkit can improve and simplify a range of tasks for researchers and application developers. FabSim3 helps to prepare, submit, execute, retrieve, and analyze simulation workflows. By providing a suitable level of abstraction, FabSim3 reduces the complexity of setting up and managing a large-scale simulation scenario, while still providing transparent access to the underlying layers for effective debugging. The tool also facilitates job submission and management (including staging and curation of files and environments) for a range of different supercomputing environments. Although FabSim3 itself is application-agnostic, it supports a provably extensible plugin system where users automate simulation and analysis workflows for their own application domains. To highlight this, we briefly describe a selection of these plugins and we demonstrate the efficiency of the toolkit in handling large ensemble workflows

Image1_Bcl-xL activity influences outcome of the mitotic arrest.jpg

Microtubule-targeting (MT) drugs taxanes and vinca alkaloids are widely used as chemotherapeutic agents against different tumors for more than 30 years because of their ability to block mitotic progression by disrupting the mitotic spindle and activating the spindle assembly checkpoint (SAC) for a prolonged period of time. However, responses to mitotic arrest are different—some cells die during mitotic arrest, whereas others undergo mitotic slippage and survive becoming able for proliferation. Using normal fibroblasts and several cancer cell types we determined two critical doses, T1 and T2, of mitotic inhibitors (nocodazole, Taxol, and vinorelbine). T1 is the maximal dose cells can tolerate undergoing normal division, and T2 is the minimal mitostatic dose, wherein > 90% of mitotic cells are arrested in mitosis. In all studied cell lines after treatment with mitotic inhibitors in a dose above T2 cells had entered mitosis either die or undergo mitotic slippage. We show that for all three drugs used cell death during mitotic arrest and after slippage proceeded via mitochondria-dependent apoptosis. We determined two types of cancer cells: sensitive to mitotic arrest, that is, undergoing death in mitosis (DiM) frequently, and resistant to mitotic arrest, that is, undergoing mitotic slippage followed by prolonged survival. We then determined that inhibition of Bcl-xL, but not other anti-apoptotic proteins of the Bcl-2 group that regulate MOMP, make resistant cells susceptible to DiM induced by mitotic inhibitors. Combined treatment with MT drugs and highly specific Bcl-xL inhibitors A-1155643 or A-1331852 allows achieving 100% DiM in a time significantly shorter than maximal duration of mitotic arrest in all types of cultured cells tested. We further examined efficacy of sequential treatment of cultured cells using mitotic inhibitors followed by inhibitors of Bcl-xL anti-apoptotic protein and for the first time show that sensitivity to Bcl-xL inhibitors rapidly declines after mitotic slippage. Thus sequential use of mitotic inhibitors and inhibitors of Bcl-xL anti-apoptotic protein will be efficient only if the Bcl-xL inhibitor will be added before mitotic slippage occurs or soon afterward. The combined treatment proposed might be an efficient approach to anti-cancer therapy.</p

DataSheet1_Bcl-xL activity influences outcome of the mitotic arrest.pdf

Microtubule-targeting (MT) drugs taxanes and vinca alkaloids are widely used as chemotherapeutic agents against different tumors for more than 30 years because of their ability to block mitotic progression by disrupting the mitotic spindle and activating the spindle assembly checkpoint (SAC) for a prolonged period of time. However, responses to mitotic arrest are different—some cells die during mitotic arrest, whereas others undergo mitotic slippage and survive becoming able for proliferation. Using normal fibroblasts and several cancer cell types we determined two critical doses, T1 and T2, of mitotic inhibitors (nocodazole, Taxol, and vinorelbine). T1 is the maximal dose cells can tolerate undergoing normal division, and T2 is the minimal mitostatic dose, wherein > 90% of mitotic cells are arrested in mitosis. In all studied cell lines after treatment with mitotic inhibitors in a dose above T2 cells had entered mitosis either die or undergo mitotic slippage. We show that for all three drugs used cell death during mitotic arrest and after slippage proceeded via mitochondria-dependent apoptosis. We determined two types of cancer cells: sensitive to mitotic arrest, that is, undergoing death in mitosis (DiM) frequently, and resistant to mitotic arrest, that is, undergoing mitotic slippage followed by prolonged survival. We then determined that inhibition of Bcl-xL, but not other anti-apoptotic proteins of the Bcl-2 group that regulate MOMP, make resistant cells susceptible to DiM induced by mitotic inhibitors. Combined treatment with MT drugs and highly specific Bcl-xL inhibitors A-1155643 or A-1331852 allows achieving 100% DiM in a time significantly shorter than maximal duration of mitotic arrest in all types of cultured cells tested. We further examined efficacy of sequential treatment of cultured cells using mitotic inhibitors followed by inhibitors of Bcl-xL anti-apoptotic protein and for the first time show that sensitivity to Bcl-xL inhibitors rapidly declines after mitotic slippage. Thus sequential use of mitotic inhibitors and inhibitors of Bcl-xL anti-apoptotic protein will be efficient only if the Bcl-xL inhibitor will be added before mitotic slippage occurs or soon afterward. The combined treatment proposed might be an efficient approach to anti-cancer therapy.</p