EDTA-CoⅢ光度法测定高含量钴

关于微量钴的分析已有报道[1～3] ,常见的亚硝基 β萘酚和亚硝基R盐光度法[4] 仅适用于低含量钴的测定 ,对于高含量钴 ,本文采用EDTA -Co 光度法 ,方法选择性高 ,灵敏度低 ,用于测定高含量钴 ,准确度较为理想。1　实验部分1 1　主要仪器和试剂72 1型分光光度计。钴标准溶液 :1mg/L ;EDTA溶液 :0 1mol/L ;过氧化氢 :ρ约 1 1 1 g/mL ;H2 SO4溶液 :1 + 1 ;氨水溶液 :1 + 1。1 2　实验方法移取适量Co 标准溶液于 1 0 0mL烧杯中 ,加入 5mLEDTA溶液 ,摇匀 ,再加入 5滴过氧化氢溶液 ,摇匀 ,置于电热板上加热微沸至溶液变为紫色并…     

印度的铝工业

印度的铝工业始于 1 886年 ,当时采用Ｈａｌｌ-Ｈｅｒ ａｕｌｔ工艺技术炼铝 ,1 943年铝锭产量 1 2 92ｔ。目前 ,氧化铝产量已达 1 80万ｔ,铝金属产量达 70万ｔ。近年来 ,特别是 1 988～ 1 989年间 ,由于进口限制 ,较低的生产能力利用率和电力资源缺乏 ,加之政府对铝价格的控制 ,对分配的控制 ,印度可提供的铝锭受到了限制。1 991～ 1 992年间情况发生了变化 ,印度两大铝业公司Ｎａｌｃｏ和Ｈｉｎｄａｌｃｏ稳定地增加产量使印度铝锭产量达到 51 .4万ｔ/ａ,1 989年政府解除了对铝的控制也刺激了铝的消费。1　印度铝工业的潜力1 .1　铝矾土资…     

碳酸盐共沉淀法合成LiNi1/3Co1/3Mn1/3O2及其电化学性能

以碳酸盐共沉淀法合成了Ni1/3Co1/3Mn1/3CO3前驱体,然后以Ni1/3Co1/3Mn1/3CO3和LiOH·H2O为原料,合成出了层状锂离子电池正极材料Li Ni1/3Co1/3Mn1/3O2.通过XRD,SEM和电化学测试对Li Ni1/3Co1/3Mn1/3O2材料的结构、形貌及电化学性能进行了测试和表征.结果表明,800℃烧结12 h所合成的样品粒度大小分布比较均匀,以0.2 C充放电,其首次放电容量为153 mAh·g-1,循环30次后容量为140 mAh·g-1.     

700MPa微合金高强钢奥氏体高温变形行为研究

研究了一种700 MPa微合金高强钢。在热力模拟试验机上进行了试验钢的单道次压缩试验,通过其各种变形参数的研究,建立了试验钢的变形抗力数学模型和动态再结晶模型。试验结果显示:试验钢在变形温度为950℃,应变速率为0.1 s-1;变形温度为1 000℃,应变速率为0.1 s-1;变形温度为1 050℃,应变速率为0.1s-1或1 s-1;变形温度为1 100℃,应变速率为0.1 s-1、1 s-1或5 s-1这几种条件下会发生动态再结晶。     

2Cr12NiMo1W1V超临界汽轮机叶片用耐热钢的热变形行为

 为了解决2Cr12NiMo1W1V耐热钢在锻造过程中晶粒粗大和组织不均匀的问题，利用Gleeble-3800热模拟试验机，在变形温度为1 000～1 200 ℃、应变速率为0.01～10 s－1、变形量为70%的条件下，研究和分析了2Cr12NiMo1W1V耐热钢的高温塑性变形和动态再结晶行为。结果表明，该耐热钢的真应力-应变曲线具有动态再结晶特征。再结晶晶粒尺寸随着变形温度的增加或应变速率的降低呈增加趋势，在变形温度为1 150～1 200 ℃，应变速率为0.01 s－1时，晶粒尺寸急剧增加。在真应力-应变曲线的基础上，建立了材料热变形本构方程，其热激活能为453.74 kJ/mol。根据峰值应力绘制了合金的热加工图并获得在各加工条件下的效率值，合金的最佳热加工区间为变形温度为1 000～1 150 ℃、应变速率为0.1～1 s－1以及变形温度为1 060～1 125 ℃、应变速率为0.1～10 s－1。     

TiN纳米颗粒在ZGMn13中存在形式及对基体微观形貌的影响

 利用吹氩加入法制备了含微量纳米TiN的ZGMn13钢,研究了外加TiN颗粒在高锰钢中的存在形式以及对奥氏体组织形态的影响。运用扫描电镜及其附带的能谱仪、透射电镜等手段,分析了TiN和ZGMn13钢的微观组织形貌、化学成分以及相结构。结果表明,TiN纳米粒子部分团聚长大,另一部分仍以纳米形态存在于奥氏体中,且与奥氏体具有较好的界面匹配关系;奥氏体与TiN具有[[1]11]γ//[[1]11 ]N、(202)γ//(202)N,[[1]11]γ//[[1]11 ]N、(220)γ//(220)N,[[1]11]γ//[[1]11 ]N、(422)γ//(422)N以及[[1]12]γ//[0[1]1]N、(220)γ//(022)N,[[1]12]γ//[0[1]1]N、(1[1]1)γ(200)N的晶体学位向关系,并且(1[1]1)γ晶面与TiN的(200)N晶面呈现共格现象;此外,基体奥氏体中存在着高密度相互缠结的位错,局部区域出现与奥氏体具有(1100)ε // (1[1]3)γ、[0001]ε// [1[5]2]γ的晶体学位向关系的相互平行的针状ε-马氏体,且两相界面共格。     

“牛”人“微”语

一根筷子能折断，十双筷子难折断。幼世纪是英雄退位、团队进位的年代，拥有人群和市场为王。1＋1=2叫数学；1＋1=11叫经济学；．1,1＋1=1叫领导学；如果你能做到1＋1=111，让自己呈几何级数裂变，你就铁定能成为行业老大。     

Nd2(Mn1-x,Alx)17化合物的结构性质

对电弧炉熔炼的Nd2 (Mn1 -x,Alx) 1 7(x =1～ 10 )化合物进行了X射线衍射研究。结果表明 ,Nd2 (Mn1 -x,Alx) 1 7(x =1～ 10 )化合物具有Th2 Zn1 7型结构 ,随着Al替代量的增加 ,Nd2 (Mn1 -x,Alx) 1 7(x =1～ 10 )化合物的晶格常数a ,c及单胞体积V都增加。对样品的时效研究表明 ,Nd2 (Mn1 -x,Alx) 1 7(x =1～ 10 )化合物在自然环境中十分稳定 ,这表明Al比C更能使富锰的 2∶17相 (Th2 Zn1 7)稳定。     

Zwint-1及其变异体Zwint-1v在HeLa细胞不同细胞周期中的亚定位

目的:探讨Zw10结合因子-1(zeste white 10 interactor-1,Zwint-1)及其变异体(Zwint-1v)在HeLa细胞不同细胞周期中的亚定位.方法:采用胸腺嘧啶核苷双阻断法将HeLa细胞同步化,通过瞬时转染及间接免疫荧光检测,观察Zwint-1及Zwint-1v在HeLa细胞不同细胞周期中的亚定位.结果:在HeLa细胞间期,Zwint-1野生型定位于细胞质,而Zwint-1v定位于细胞核;在分裂期,Zwint-1野生型及Zwint-1v定位于纺锤体与着丝粒上.Zwint-1v定位较野生型更趋近于细胞核.结论:Zwint-1及Zwint-1v在HeLa细胞不同细胞周期的亚定位存在差异.     

GH625合金焊管的再结晶退火

研究了退火工艺对 GH62 5无缝焊管的形变再结晶行为 .通过对形变量为 4 0 % ,分别在1 0 0 0℃、 1 0 2 0℃、 1 0 80℃、 1 1 2 0℃和 1 1 60℃下退火 1 5min的无缝焊管的金相分析 ,确定了其再结晶温度 .合适的工艺条件下 ,可以有效细化 GH62 5冷轧后的混晶组织     

冷轧压下率对无抑制剂取向硅钢初次再结晶退火的影响

对无抑制剂取向硅钢不同压下率下初次再结晶退火后的显微组织、宏观织构和微观织构进行了研究.结果表明,冷轧板织构主要为α取向线{001}＜110＞、{112}＜110＞和{111}＜110＞织构以及γ取向线{111}＜110＞织构.初次再结晶退火后,α取向线织构减弱,织构主要为γ取向线{111}＜112＞织构.随冷轧压下率的增加,冷轧和初次再结晶织构强度增加.当压下率为88％时,初次再结晶退火后 Goss 织构和{111}＜112＞织构强度最高,最有利于发生二次再结晶.EBSD 分析显示,Goss 取向晶粒大多与{111}＜112＞取向晶粒相邻.提高冷轧压下率,Goss取向晶粒和{111}＜112＞取向晶粒都增加,Goss 取向晶粒偏离理想取向角度减少.     

氢醌容量法测定金时滴定温度及其相关问题的讨论

氢醌与金的氧化还原速度较慢，容易产生滴定误差，主要是第二步岐化反应比较慢。不少工作者往往以提高滴定温度来加快反应速度，但容易出现灰色，结果会偏低。作者经过实验，发现只要注意控制滴定温度，就可以避免出现灰色，测定结果准确可靠。     

Genotype-specific transcriptional regulation of PAI-1 gene by insulin, hypertriglyceridemic VLDL, and Lp(a) in transfected, cultured human endothelial cells

Plasminogen activator inhibitor-1 (PAI-1) has been shown to be an independent risk factor for coronary artery disease. Variations in plasma PAI-1 levels have been attributed to variations in the PAI-1 gene, and associations between PAI-1 levels and PAI-1 genotypes suggest that PAI-1 expression may be regulated in a genotype-specific manner by insulin, hypertriglyceridemic (HTG) very low density lipoprotein (VLDL), or lipoprotein(a) [Lp(a)]. Polymerase chain reaction-amplified 1106-bp fragments of the promoter of the 1/1 and 2/2 PAI-1 genotypes were sequenced and showed 5 regions of small nucleotide differences in the 1/1 versus 2/2 PAI-1 promoters that consistently occurred with high frequency. These fragments were ligated into the luciferase reporter gene, and 1/1 and 2/2 PAI-1 genotype human umbilical vein endothelial cell (HUVEC) cultures were transiently transfected with their respective p1PAI110/luc and p2PAI110/luc constructs and vice versa. Insulin induced an approximately 12- to 16-fold increase in luciferase activity in both the 1/1 and 2/2 PAI-1 genotype HUVEC cultures transfected with the p1PAI110/luc construct. HTG-VLDL and Lp(a) induced luciferase activity by approximately 14- to 16- and approximately 8- to 11-fold, respectively, in both the 1/1 and 2/2 PAI-1 genotype HUVEC cultures transfected with the p2PAI110/luc construct. The positive control interleukin-1 showed an approximately 7- to 12-fold response in the 1/1 and 2/2 PAI-1 genotype HUVEC cultures transfected with either of the constructs. These cross-over results demonstrate that regulation of either the 1/1 or 2/2 PAI-1 genotype by its respective inducer is due to the promoter itself and not to some factor(s) expressed differently in the 1/1 or 2/2 PAI-1 genotype HUVEC cultures.     

Stimulation of phospholipase C-beta 2 by recombinant guanine-nucleotide-binding protein beta gamma dimers produced in a baculovirus/insect cell expression system. Requirement of gamma-subunit isoprenylation for stimulation of phospholipase C

Recombinant wild-type beta 1 gamma 1 dimers of signal-transducing guanine nucleotide-binding proteins (G proteins) and beta 1 gamma 1 dimers carrying a mutation known to block gamma-subunit isoprenylation (beta 1 gamma 1 C71S) were expressed in baculovirus-infected insect cells. Both wild-type and mutant beta 1 gamma 1 dimers were found in soluble fractions of infected cells upon subcellular fractionation. Anion exchange chromatographic and metabolic-radiolabeling studies revealed that the soluble beta 1 gamma 1 preparation contained approximately equal amounts of non-isoprenylated and isoprenylated beta 1 gamma 1 dimers. Soluble wild-type and mutant beta 1 gamma 1 dimers and native beta 1 gamma 1 dimers purified from bovine retina were reconstituted with recombinant phospholipase C-beta 2. Only isoprenylated beta 1 gamma 1 dimers were capable of stimulating phospholipase C-beta 2. The results show that gamma-subunit isoprenylation and/or additional post-translational processing of the protein are required for beta gamma subunit stimulation of phospholipase C.     

Tolerance to osmotic shocks in rats kidney cortex and medulla

BACKGROUND: Cytokines and cytokine antagonists modulate human immunodeficiency virus (HIV) replication in vitro and may be involved in HIV disease pathogenesis. An understanding of these cytokine networks may suggest novel treatment strategies for HIV-seropositive persons. MATERIALS AND METHODS: U1 cells, a chronically infected promonocytic cell line, were stimulated with interleukin 1 alpha (IL-1 alpha), IL-1 beta or tumor necrosis factor (TNF) for 24 hr. The effects of these cytokines, and of anti-IL-1 receptor type 1 and type 2 (IL-1RI and II) antibody, IL-1 receptor antagonist (IL-1Ra), and recombinant human TNF binding protein type 1 (rhTBP-1, a form of TNF receptor p55), on HIV-1 replication, as measured by ELISA for HIV-1 p24 antigen, were determined. The effects of IL-1 and IL-1Ra on nuclear factor-kappa B (NF-kappa B) DNA binding activity, as measured by electrophoretic mobility shift assays, were also determined. RESULTS: IL-1 alpha and IL-1 beta increased p24 antigen production in a concentration-dependent manner. IL-1Ra completely, and rhTBP-1 partially, suppressed IL-1-induced p24 antigen production. IL-1 increased NF-kappa B DNA binding activity and IL-1Ra blocked this effect. Since IL-1Ra blocks IL-1 from binding to both the IL-1RI and Il-1RII, monoclonal antibodies directed against each receptor were used to ascertain which IL-1R mediates IL-1-induced HIV-1 expression. Antibody to the IL-1RI reduced IL-1-induced p24 antigen production. Although anti-IL-1RII antibody blocked the binding of 125IL-1-1 alpha to U1 cells by 99%, this antibody did not affect IL-1-induced p24 antigen production. IL-1 beta enhanced TNF alpha-induced HIV expression when added before or simultaneously with TNF alpha. CONCLUSIONS: IL-1 induces HIV-1 expression (via the IL-1RI) and NF-kappa B activity in U1 cells. These effects are blocked by IL-1Ra and partially mediated by TNF. IL-1 enhances TNF alpha-induced HIV replication in U1 cells.     

Sp1 and egr-1 have opposing effects on the regulation of the rat Pgp2/mdr1b gene

The promoter of the rat pgp2/mdr1b gene has a GC-rich region (pgp2GC) that is highly conserved in mdr genes and contains an consensus Sp1 site. Sp1's role in transactivation of the pgp2/mdr1b promoter was tested in Drosophila Schneider cells. The pgp2/mdr1b promoter was strongly activated by co-transfected wild type Sp1 but not mutant Sp1 and mutation of the Sp1 site abrogated Sp1-dependent transactivation. In gel shift assays, the same mutations abolished Sp1-DNA complex formation. Moreover, basal activity of the pgp2/mdr1b Sp1 mutant promoter was dramatically lower. Enforced ectopic overexpression of Sp1 in H35 rat hepatoma cells revealed that cell lines overexpressing Sp1 had increased endogenous pgp2/mdr1b mRNA, demonstrating that Sp1 activates the endogenous pgp2/mdr1b gene. Pgp2GC oligonucleotide also bound Egr-1 in gel shift assays and Egr-1 competitively displaced bound Sp1. In transient transfections of H35 cells (and human LS180 and HepG2 cells) Egr-1 potently and specifically suppressed pgp2/mdr1b promoter activity and mutations in the Egr-1 site decreased Egr-1 binding and correlated with pgp2/mdr1b up-regulation. Ectopic overexpression of Egr-1 in H35 cells decreased Pgp expression and selectively increased vinblastine sensitivity. In conclusion, Sp1 positively regulates while Egr-1 negatively regulates the rat pgp2/mdr1b gene. Moreover, competitive interactions between Sp1 and Egr-1 in all likelihood determine the constitutive expression of the pgp2/mdr1b gene in H35 cells.