铝电解槽早期破损原因分析及应对措施

根据铝电解槽早期破损现象。进行了破损原因分析。认为铝液渗漏、阴极块的破损、化学反应腐蚀等是导致铝电解槽的早期破损的主要原因。并据此提出了延长槽寿命的措施。     

500kA铝电解槽阴极破损分析及对策

某电解铝厂500 kA铝电解槽由于电磁场、热平衡设计不合理，工艺运行参数不匹配，电解槽早期破损严重，给电解槽长寿命、高效率运行带来巨大的风险。本文通过对电解槽进行解剖，深入分析电解槽阴极炭块破损机理，可知电解槽早期破损主要分为槽壳变形、阴极炭块破损、侧部破损等几大类。为了解决阴极破损问题，在不改变阴极母线结构的前提下对电解槽内衬、工艺技术参数等方面进行深度优化，最终有效解决了电解槽早期破损的问题，实现了延长电解槽寿命的目的。     

200kA铝电解槽破损分析及中修实践

通过对早期破损槽的炉底分析,阐述了早期破损槽的破损原因,并对破损槽进行了中修实践,延长了槽龄,取得了满意的效果。     

大型预焙电解槽早期阴极内衬破损机理及控制措施

文章通过对350 kA系列大修槽启动投产后发现有早期破损现象,认真分析阴极内衬早期破损的机理,结合现场实际状况从筑炉质量、焙烧启动、后期管理的方面加以探讨并提出减少电解槽早期阴极内衬破损概率的控制措施.     

200 kA铝电解槽破损分析及中修实践

通过对早期破损槽的炉底分析,阐述了早期破损槽的破损原因,并对破损槽进行了中修实践,延长了槽龄,取得了满意的效果。      

240kA预焙槽早期内衬破损的原因及对策

针对240kA预焙槽早期内衬破损的实际状况,对引起内衬破损的原因进行了分析归纳,并指出完好的焙烧启动过程、合理的启动后期管理及早期规整的高分子炉帮是避免预焙槽早期内衬破损的有效措施。     

预焙铝电解槽破损特征及原因

分析了铝电解槽早期破损的机理、原因,阐述了防止铝电解槽早期破损的一些思路.     

铝电解槽早期破损与焙烧启动

通过对电解槽内衬早期破损的过程、表现形式及反应机理的分析，从理论上分析了槽内衬早期破损与焙烧启动方式的关系，阐明了其中的制约因素，并通过对铝液焙烧与焦粒焙烧的技术特征对比，论述了采用焦粒焙烧对减少电解槽内衬早期破损的有益之处。     

80kA小型预焙槽早期破损原因初探

针对80kA小型预焙槽早期破损多、槽寿命短的问题，采用干刨试验槽的方法，通过对破损槽的槽壳、槽内衬侧部碳块、伸腿、底部碳块、耐火层等部位消耗破损状况的分析，认为造成电解槽早期破损的主要原因是摇篮架抗剪切强度差、铝液焙烧工艺存在缺陷以及电解行程的波动。采取增加补强筋板加强摇篮架抗剪切强度，采用焦粒焙烧启动工艺，优化平稳生产行程等措施，解决了电解槽早期破损问题，延长了电解槽寿命。     

铝电解槽早期破损原因及预防

本文分析了铝电解槽发生早期破损的原因,指出设计缺陷,施工质量差,炭素材料不合格,焙烧启动制度不完善和停限电是造成铝电解槽产生早期破损的原因,并指出了防止电解槽早期破损的措施。     

大型铝电解槽生产初期工艺控制优化

文章介绍了大型预焙铝电解槽生产初期的特点,根据在某铝厂进行成功试验的结果提出了在大型预焙电解槽生产启动初期的工艺参数的设置,以达到电解槽高效、节能、低耗、环保、高槽寿命的目的.     

Glucose may induce cell death through a free radical-mediated mechanism

It has been reported that glucose may autooxidize generating free radicals which have been hypothesized to induce important cellular abnormalities. To investigate the cell damage induced by glucose-dependent oxidative stress, the FRTL5 cell strain was incubated in 10 or 20 mM glucose, either alone or in the presence of buthionine-sulfoximine, a transition state inhibitor that blocks glutathione synthesis. We found indeed that buthionine-sulfoximine greatly inhibited glutathione production and increased malondialdehyde (a marker of oxidative cell damage) levels, especially in 20mM glucose. We also found that, when glutathione production was inhibited, 10mM glucose induced apoptosis and 20 mM glucose induced necrosis. These data show that the glucose-dependent cell damage is a function of glutathione production. They also show that such glucose-dependent free radical production may be critical for determining cell damage, even for small variations as the ones we tested (from 10 to 20 mM glucose).     

500kA铝电解槽早期破损剖析

电解槽是铝电解生产的主体设备,电解槽的寿命长短直接影响到吨铝生产成本,进而影响企业经济效益。电解槽达不到设计寿命,甚至出现早期破损,会增加吨铝均摊成本,电解槽长寿是铝行业研究的长期课题。通过对某电解铝企业500kA电解槽破损后进行刨炉研究,认为其早期破损的原因主要是所用筑炉防渗料质量存在缺陷、焙烧升温速度过快、技术条件匹配不合理、系列电流强度波动较大等,并在此基础上提出了预防电解槽早期破损的措施,为电解槽提高槽寿命提供借鉴和参考。     

DNA double-strand break repair functions defend against parvovirus infection

We measured parvovirus replication and sensitivity to X-ray damage in nine CHO cell lines representing a variety of DNA repair deficiencies. We found that parvovirus replication efficiency increases with radiosensitivity. Parvovirus replication is disrupted at an early stage of infection in DNA repair-proficient cells, before conversion of the single-stranded viral DNA genome into the double-stranded replicative form. Thus, status of the DNA repair machinery inversely correlates with parvovirus replication and is proportional to the host's ability to repair X-ray-induced damage.     

Role of nitric oxide in rat nephrotoxic nephritis: comparison between inducible and constitutive nitric oxide synthase

Nitric oxide (NO), generated by inducible NO synthase (iNOS) in migrating macrophages, is increased in glomerulonephritis. This study investigates the effect of NO inhibition on rat nephrotoxic nephritis (NTN) to clarify the role of NO production in glomerular damage. NTN was induced in Sprague Dawley rats by an injection of an anti-glomerular basement membrane (GBM) antibody. Urinary nitrite excretion and nitrite release from kidney slices (5.47 +/- 1.19 versus 2.15 +/- 0.73 nmol/mg protein, NTN versus Control, P < 0.05) were increased in NTN on day 2. Glomerular macrophage infiltration and intercellular adhesion molecule (ICAM)-1 expression increased from day 2. iNOS expression was increased in interstitial macrophages. Glomerular endothelial cell NOS (ecNOS) expression evaluated by counting immunogold particles along GBM was suppressed (0.06 +/- 0.02 versus 0.35 +/- 0.04 gold/micron GBM, P < 0.0001). Glomerular damage developed progressively. NG-nitro-L-arginine methyl ester (L-NAME), which inhibits both iNOS and ecNOS and aminoguanidine (AG), a relatively selective inhibitor for iNOS, equally suppressed nitrite in urine and renal tissue. Glomerular ICAM-1 expression and macrophage infiltration were reduced by L-NAME, but not by AG. Expression of ecNOS was significantly increased by L-NAME (0.91 +/- 0.08, P < 0.0001 versus NTN), but slightly by AG (0.18 +/- 0.04). AG significantly and L-NAME slightly attenuated the glomerular damage at day 4. In conclusion, suppression of iNOS prevents glomerular damage in the early stage of NTN. Treatment by L-NAME reduces macrophage infiltration by suppression of ICAM-1 expression, which may be explained by an increase in ecNOS expression.     

基于内聚力模型的金属粉末压坯拉伸裂纹扩展模拟

压坯裂纹损伤预测分析对于生产高质量粉末冶金零件具有重要的指导作用。本文将修正的Drucker–Prager Cap模型与内聚力损伤模型相结合,并利用Python语言在损伤断裂区域内批量插入内聚力单元,模拟金属粉末压坯在外载荷作用下裂纹扩展过程。同时,采用不同类型的内聚力模型对巴西圆盘实验过程进行模拟,通过实验验证对比分析可知,采用指数内聚力模型模拟压坯拉伸裂纹扩展的结果与实验结果更为吻合,并且与实验后期压坯边缘出现剪切带的现象也较为一致。     

高温花岗岩热冲击后力学特性及损伤演化规律研究

在干热型地热资源开发过程中,高温岩石面临遇水冷却引起的热冲击损伤问题。为了研究高温花岗岩在热冲击作用后的力学特性和损伤演化规律,开展了25～600 ℃范围内不同温度热冲击作用下花岗岩试件的单轴压缩试验,获得了热冲击花岗岩试件的应力?应变关系;提出了一种考虑初始热冲击损伤与加载期间试件微元破裂损伤相结合的热?力耦合损伤本构模型,并对统计损伤本构模型的相关参数进行了理论求解;考虑热冲击损伤引起的孔隙结构劣化效应,引入压密系数对热冲击花岗岩的本构关系进行了修正;通过试验应力?应变曲线对模型的有效性进行了对比和验证,讨论了温度水平对热冲击花岗岩单轴压缩损伤演化规律的影响。研究结果表明,随着热冲击温度的升高,花岗岩试件的初始热损伤不断增大,应力?应变曲线具有明显的非线性压密阶段;引入压密系数修正的统计损伤本构模型能够更加准确地表征热冲击花岗岩在初始加载阶段的非线性压密特征;在热冲击温度较低时,损伤变量演化曲线上升较为陡峭,随着热冲击温度的升高,曲线上升速率逐渐变缓并由非线性向线性转变。