Метод расчета теплопереноса излучением в засыпках сферических частиц

A new technique for implementing external (particle-to-wall) and particle-to-particle radiative heat transfer in discrete elements method (DEM) simulations is proposed. It is based on the idea that an expected view factor value depends on relevant local bed parameters (distance between particles, particle radius ratio, and local bed porosity). Calculation of average view factors via the formula requires considerably less computational effort than direct in situ integration, when this happens a reasonable average value and an overall accuracy comparable to direct calculation are provided. Both mono- and polydisperse mixtures of spherical opaque particles were considered. It was shown that using nondimensional parameters, a simple general dependence for an external radiative heat flux may be introduced. Exponential and linear fits were proposed for estimating the particle-particle radiative heat flux. The generalization of the obtained formulas for various bed porosities is proposed. The distribution of cumulative transferred heat flux across the particles up to a certain distance was found, and the recommendations regarding the choice of that parameter to achieve a desired accuracy were formulated. Also, the method to account for the particle emissivity was proposed on the basis of the empirical dependence between emissivity and radiative heat flux in porous materials. The proposed method satisfies all the requirements to become a standard implementation of radiative heat transfer calculation in DEM.Предложена новая методика, позволяющая проводить расчет теплопереноса излучением между частицами, а также между частицами и границей, в подходе метода дискретных элементов (discrete elements method, DEM). В ее основе лежит идея о том, что математическое ожидание угловых коэффициентов между частицами можно выразить как функцию набора значимых локальных параметров засыпки, таких как расстояние между частицами, отношение их радиусов и локальное значение пористости слоя частиц. Расчет значения углового коэффициента по формуле требует существенно меньше вычислительных ресурсов, чем прямое их вычисление двойным интегрированием, при этом обеспечивается реалистичное среднее значение величины и сопоставимая с методами прямого вычисления общая точность расчета. Рассмотрены монодисперсные и полидисперсные засыпки сферических непрозрачных частиц. Показано, что использование безразмерных параметров позволяет сформулировать зависимости для угловых коэффициентов в общем виде. В частности, для углового коэффициента между частицами засыпки была предложена экспоненциальная и линейная аппроксимации. Также в работе получено обобщение зависимостей для различных значений пористости слоя. Было найдено распределение суммарной передаваемой мощности излучения в зависимости от дальности до учитываемых частиц-соседей, даны рекомендации по выбору этого параметра в зависимости от требуемой точности расчета. Помимо этого, на основании эмпирических наблюдений эффективной теплопроводности засыпок предложен способ учета влияния коэффициента черноты материала частиц на величину теплообмена излучением между частицами. Предложенный метод обладает всем необходимым для того, чтобы стать стандартной реализацией механизма переноса тепла излучением в методе дискретных элементов

УСТОЙЧИВОСТЬ ПЛОСКОГО ФРОНТА ФИЛЬТРАЦИОННОГО ГОРЕНИЯ ТВЕРДОГО ТОПЛИВА

Analysis of thermal-hydrodynamic instability of plane filtration combustion front of solid fuel is performed. The boundaries of stable region for co-flow combustion wave are determined by numerical modeling. Possible scenarios of plane combustion front evolution o new steady-state or oscillating structures are investigated. The results are expressed in terms of dimensionless parameters.Проведен анализ тепло-гидродинамической неустойчивости плоского фронта фильтрационного горения твердого топлива. С использованием численного моделирования определены границы области устойчивых режимов для спутных волн горения. Исследованы возможные сценарии перестройки плоского фронта горения в новые стационарные или колебательные структуры. Результаты сформулированы в терминах безразмерных параметров

An ER source for H2O2

The endoplasmic reticulum (ER)-localized peroxiredoxin 4 (PRDX4) supports disulfide bond formation in eukaryotic cells lacking endoplasmic reticulum oxidase 1 (ERO1). The source of peroxide that fuels PRDX4-mediated disulfide bond formation has remained a mystery, because ERO1 is believed to be a major producer of hydrogen peroxide (H2O2) in the ER lumen. We report on a simple kinetic technique to track H2O2 equilibration between cellular compartments, suggesting that the ER is relatively isolated from cytosolic or mitochondrial H2O2 pools. Furthermore, expression of an ER-adapted catalase to degrade lumenal H2O2 attenuated PRDX4-mediated disulfide bond formation in cells lacking ERO1, whereas depletion of H2O2 in the cytosol or mitochondria had no similar effect. ER catalase did not effect the slow residual disulfide bond formation in cells lacking both ERO1 and PRDX4. These observations point to exploitation of a hitherto unrecognized lumenal source of H2O2 by PRDX4 and a parallel slow H2O2-independent pathway for disulfide formation.Supported by grants from the Wellcome Trust (Wellcome 084812) the European Commission (EU FP7 Beta-Bat No: 277713) and Fundação para a Ciência e Tecnologia, Portugal (PTDC/QUI-BIQ/119677/2010) and, a Wellcome Trust Strategic Award for core facilities to the Cambridge Institute for Medical Research (Wellcome 100140). DR is a Wellcome Trust Principal Research Fellow. TK was supported by Strategic Young Researcher Overseas Visits Program for Accelerating Brain Circulation, Japan Society for the Promotion of Science (JSPS)This is the author accepted manuscript. The final version is available from Rockefeller University Press via http://dx.doi.org/10.1083/jcb.20150612

Roles of the 15-kDa Selenoprotein (Sep15) in Redox Homeostasis and Cataract Development Revealed by the Analysis of Sep 15 Knockout Mice

The 15-kDa selenoprotein (Sep15) is a thioredoxin-like, endoplasmic reticulum-resident protein involved in the quality control of glycoprotein folding through its interaction with UDP-glucose:glycoprotein glucosyltransferase. Expression of Sep15 is regulated by dietary selenium and the unfolded protein response, but its specific function is not known. In this study, we developed and characterized Sep15 KO mice by targeted removal of exon 2 of the Sep15 gene coding for the cysteinerich UDP-glucose:glycoprotein glucosyltransferase-binding domain. These KO mice synthesized a mutant mRNA, but the shortened protein product could be detected neither in tissues nor in Sep15 KO embryonic fibroblasts. Sep15 KO mice were viable and fertile, showed normal brain morphology, and did not activate endoplasmic reticulum stress pathways. However, parameters of oxidative stress were elevated in the livers of these mice. We found that Sep15 mRNA was enriched during lens development. Further phenotypic characterization of Sep15KO mice revealed a prominent nuclear cataract that developed at an early age. These cataracts did not appear to be associated with severe oxidative stress or glucose dysregulation.Wesuggest that the cataracts resulted from an improper folding status of lens proteins caused by Sep15 deficiency

Roles of the 15-kDa Selenoprotein (Sep15) in Redox Homeostasis and Cataract Development Revealed by the Analysis of Sep 15 Knockout Mice

The 15-kDa selenoprotein (Sep15) is a thioredoxin-like, endoplasmic reticulum-resident protein involved in the quality control of glycoprotein folding through its interaction with UDP-glucose:glycoprotein glucosyltransferase. Expression of Sep15 is regulated by dietary selenium and the unfolded protein response, but its specific function is not known. In this study, we developed and characterized Sep15 KO mice by targeted removal of exon 2 of the Sep15 gene coding for the cysteinerich UDP-glucose:glycoprotein glucosyltransferase-binding domain. These KO mice synthesized a mutant mRNA, but the shortened protein product could be detected neither in tissues nor in Sep15 KO embryonic fibroblasts. Sep15 KO mice were viable and fertile, showed normal brain morphology, and did not activate endoplasmic reticulum stress pathways. However, parameters of oxidative stress were elevated in the livers of these mice. We found that Sep15 mRNA was enriched during lens development. Further phenotypic characterization of Sep15KO mice revealed a prominent nuclear cataract that developed at an early age. These cataracts did not appear to be associated with severe oxidative stress or glucose dysregulation.Wesuggest that the cataracts resulted from an improper folding status of lens proteins caused by Sep15 deficiency

Effect of Oxidative Stress on Homer Scaffolding Proteins

Homer proteins are a family of multifaceted scaffolding proteins that participate in the organization of signaling complexes at the post-synaptic density and in a variety of tissues including striated muscle. Homer isoforms form multimers via their C-terminal coiled coil domains, which allows for the formation of a polymeric network in combination with other scaffolding proteins. We hypothesized that the ability of Homer isoforms to serve as scaffolds would be influenced by oxidative stress. We have found by standard SDS-PAGE of lysates from adult mouse skeletal muscle exposed to air oxidation that Homer migrates as both a dimer and monomer in the absence of reducing agents and solely as a monomer in the presence of a reducing agent, suggesting that Homer dimers exposed to oxidation could be modified by the presence of an inter-molecular disulfide bond. Analysis of the peptide sequence of Homer 1b revealed the presence of only two cysteine residues located adjacent to the C-terminal coiled-coil domain. HEK 293 cells were transfected with wild-type and cysteine mutant forms of Homer 1b and exposed to oxidative stress by addition of menadione, which resulted in the formation of disulfide bonds except in the double mutant (C246G, C365G). Exposure of myofibers from adult mice to oxidative stress resulted in decreased solubility of endogenous Homer isoforms. This change in solubility was dependent on disulfide bond formation. In vitro binding assays revealed that cross-linking of Homer dimers enhanced the ability of Homer 1b to bind Drebrin, a known interacting partner. Our results show that oxidative stress results in disulfide cross-linking of Homer isoforms and loss of solubility of Homer scaffolds. This suggests that disulfide cross-linking of a Homer polymeric network may contribute to the pathophysiology seen in neurodegenerative diseases and myopathies characterized by oxidative stress

Potentiating antibacterial activity by predictably enhancing endogenous microbial ROS production

The ever-increasing incidence of antibiotic-resistant infections combined with a weak pipeline of new antibiotics has created a global public health crisis1. Accordingly, novel strategies for enhancing our antibiotic arsenal are needed. As antibiotics kill bacteria in part by inducing reactive oxygen species (ROS)2–4, we reasoned that targeting microbial ROS production might potentiate antibiotic activity. Here we show that ROS production can be predictably enhanced in Escherichia coli, increasing the bacteria’s susceptibility to oxidative attack. We developed an ensemble, genome-scale metabolic modeling approach capable of predicting ROS production in E. coli. The metabolic network was systematically perturbed and its flux distribution analyzed to identify targets predicted to increase ROS production. In silico–predicted targets were experimentally validated and shown to confer increased susceptibility to oxidants. Validated targets also increased susceptibility to killing by antibiotics. This work establishes a systems-based method to tune ROS production in bacteria and demonstrates that increased microbial ROS production can potentiate killing by oxidants and antibiotics

Plant ionomics: from elemental profiling to environmental adaptation

Ionomics is a high-throughput elemental profiling approach to study the molecular mechanistic basis underlying mineral nutrient and trace element composition (also known as the ionome) of living organisms. Since the concept of ionomics was first introduced more than 10 years ago, significant progress has been made in the identification of genes and gene networks that control the ionome. In this update, we summarize the progress made in using the ionomics approach over the last decade, including the identification of genes by forward genetics and the study of natural ionomic variation. We further discuss the potential application of ionomics to the investigation of the ecological functions of ionomic alleles in adaptation to the environment

Reduced Utilization of Selenium by Naked Mole Rats Due to a Specific Defect in GPx1 Expression

Naked mole rat (MR) Heterocephalus glaber is a rodent model of delayed aging because of its unusually long life span (\u3e28 years). It is also not known to develop cancer. In the current work, tissue imaging by x-ray fluorescence microscopy and direct analyses of trace elements revealed low levels of selenium in the MR liver and kidney, whereas MR and mouse brains had similar selenium levels. This effect was not explained by uniform selenium deficiency because methionine sulfoxide reductase activities were similar in mice and MR. However, glutathione peroxidase activity was an order of magnitude lower inMRliver and kidney than in mouse tissues. In addition, metabolic labeling of MR cells with 75Se revealed a loss of the abundant glutathione peroxidase 1 (GPx1) band, whereas other selenoproteins were preserved. To characterize theMRselenoproteome, we sequenced its liver transcriptome. Gene reconstruction revealed standard selenoprotein sequences except for GPx1, which had an early stop codon, and SelP, which had low selenocysteine content. When expressed inHEK293cells,MRGPx1waspresent in low levels,and its expression could be rescued neither by removing the early stop codon nor by replacing its SECIS element. In addition, GPx1 mRNAwas present in lower levels inMRliver than in mouse liver. To determine if GPx1 deficiency could account for the reduced selenium content, we analyzed GPx1 knock-out mice and found reduced selenium levels in their livers and kidneys. Thus, MR is characterized by the reduced utilization of selenium due to a specific defect in GPx1 expression

Photosynthesis-dependent H₂O₂ transfer from chloroplasts to nuclei provides a high-light signalling mechanism

Chloroplasts communicate information by signalling to nuclei during acclimation to fluctuating light. Several potential operating signals originating from chloroplasts have been proposed, but none have been shown to move to nuclei to modulate gene expression. One proposed signal is hydrogen peroxide (H2O2) produced by chloroplasts in a light-dependent manner. Using HyPer2, a genetically encoded fluorescent H2O2 sensor, we show that in photosynthetic Nicotiana benthamiana epidermal cells, exposure to high light increases H2O2 production in chloroplast stroma, cytosol and nuclei. Critically, over-expression of stromal ascorbate peroxidase (H2O2 scavenger) or treatment with DCMU (photosynthesis inhibitor) attenuates nuclear H2O2 accumulation and high light-responsive gene expression. Cytosolic ascorbate peroxidase over-expression has little effect on nuclear H2O2 accumulation and high light-responsive gene expression. This is because the H2O2 derives from a sub-population of chloroplasts closely associated with nuclei. Therefore, direct H2O2 transfer from chloroplasts to nuclei, avoiding the cytosol, enables photosynthetic control over gene expression