核桃壳还原浸出软锰矿的动力学

探究以核桃壳为还原剂硫酸浸出氧化锰矿过程的动力学。考察了搅拌速度、反应温度、硫酸浓度、反应时间以及核桃壳用量对锰浸出率的影响。结果表明,锰的浸出率随着搅拌速度、硫酸浓度、核桃壳用量的增大和温度的升高而增大。浸出前60 min浸出率的增长速度较快。在反应温度为369 K、硫酸浓度3.5 mol/L、核桃壳加入量40 g/L、反应时间2.5 h、转速200 r/min时,锰浸出率达93.18%。浸出过程属于化学反应控制,对应的活化能为45.5 kJ/mol,硫酸浓度和核桃壳用量的反应级数分别为0.897、0.2。     

废旧锌锰电池中锰和锌在硫酸/草酸溶液中的浸出行为

研究了用硫酸、草酸溶液从废旧锌锰电池材料中浸出锌、锰,考察了浸出时间、草酸浓度、搅拌速度、硫酸浓度和反应温度对锌、锰浸出率的影响。结果表明:硫酸溶液中加入草酸,可有效浸出锌锰电池材料中的锌和锰;在固液质量体积比1/20、硫酸浓度0.5 mol/L、草酸浓度0.25 mol/L、搅拌速度250 r/min、50℃条件下浸出120 min,锌、锰浸出率分别达98.81%和94.91%,浸出效果较好。     

金属锰粉氮化过程动力学研究

为研究金属锰粉的渗氮机理,采用热重分析法分别研究了等温和非等温条件下的氮气中,不同粒度的金属锰粉的氮化反应动力学。研究表明:金属锰粉发生氮化反应的起始温度和氮化锰的分解温度分别为470℃和1 016℃。同一粒度下,随着温度升高,表观速率常数增大,但饱和氮含量反而下降,出现吐氮现象;同一温度下,锰粉粒度越小,氮化速率越快,达到平衡的时间越短。金属锰粉粒度从40目降到100目,氮化反应的表观活化能从189.2 kJ/mol降低到115.2 kJ/mol。不同温度下和不同粒度金属锰粉的氮化过程中界面化学反应是整个过程的控制步骤。     

难选高硅氧化锌矿碱浸出动力学

研究了氢氧化钠处理难选高硅氧化锌矿的浸出动力学,考察了搅拌强度、浸出反应温度、氢氧化钠初始浓度对锌的浸出速率的影响。利用等浸出率法来确定其表观活化能和反应级数,得到表观活化能E=45.7 kJ/mol,属于化学反应控制;其反应级数K=1.4。实验结果表明,提高反应温度可显著提高锌的浸出率,而增大搅拌强度却对锌的浸出率基本无影响。     

四氧化三锰粒度及微观形貌的控制

研究了以硫酸锰为原料,采用空气直接一步氧化法制备四氧化三锰.向反应体系加入不同类型表面活性剂,考察了表面活性剂种类及用量、反应物浓度、搅拌速度、反应温度及氨锰物质的量比等条件对所制备四氧化三锰粒度及形貌的影响.结果表明:表面活性剂对四氧化三锰的粒度和形貌有调控作用,以十二烷基苯磺酸钠(SDBS)为表面活性剂可得到类球形四氧化三锰;在SDBS加入量1.0 g、硫酸锰浓度1.0 mol/L、搅拌速度500 r/min、反应温度70℃、氨锰物质的量比2.6/1条件下,所得四氧化三锰的粒度D50=11.24μm,振实密度达2.47 g/cm3,比表面积为0.87 m2/g,锰质量分数为70.58％,产品质量较好.     

从钒渣中浸出钒的宏观动力学研究

针对攀枝花某企业产出的钒渣,以碳酸氢铵水溶液为浸出剂,研究了从钒渣中浸出钒的宏观动力学,考察了搅拌速度、反应温度、浸出剂质量浓度和颗粒粒度对钒浸出率的影响。结果表明:钒浸出过程遵循"未反应收缩核模型",反应主要受固体产物层扩散控制;钒浸出率随液固体积质量比增大、搅拌速度增大、反应温度升高及浸出剂质量浓度增大、颗粒粒度减小而提高。根据试验数据,建立了宏观动力学模型,求得反应表观活化能E=18.0kJ/mol,指前因子A=0.713,确立了宏观动力学方程。     

石灰在气化脱磷渣中熔解时渣中离子迁移行为研究

针对转炉气化脱磷渣渣系,研究了静态石灰在熔渣中熔解动力学.研究结果表明,在1200～1500℃内,随着温度的升高,石灰熔解速度增大.石灰熔解的表观活化能为Ea=203.1 kJ/mol,拟合反应速率常数与温度关系的直线方程为ln vr=-24.43/T-14.62,其石灰熔解的限制性环节为扩散控制.通过扫描电镜(SEM...     

微波活化铜精矿加压浸出动力学

铜精矿经微波活化后,在初始硫酸浓度1.23 mol/L,液固比（mL/g）30/1,氧分压0.6 MPa,搅拌转速度500 r/min条件下,在408～453 K范围内研究了加压浸出动力学,并与微波活化前浸出动力学进行比较.结果表明,微波活化前后,铜精矿铜、锌浸出行为规律基本一致.在408～438 K范围内,铜精矿微波活化前后,铜浸出速率未见明显变化,而当温度升高至453 K后,铜浸出速率较微波活化前略有增大.当温度低于423 K时,锌浸出速率较微波活化前略有增大;当温度高于438 K时,锌浸出过程反而略有放缓.微波活化铜精矿铜、锌浸出反应的表观活化能分别为56.33、49.77 kJ/mol,铜、锌浸出过程均遵循界面化学反应控制的收缩核模型.与活化前相比,铜精矿经微波活化后铜、锌浸出过程得以促进.     

从电炉烟尘中碱浸锌的动力学研究

用液-固多相反应的未反应核缩芯模型研究了用NaOH溶液从电炉烟尘中浸出锌的动力学。考察了浸出温度、NaOH浓度对锌浸出率的影响。结果表明:温度低于80℃时,锌浸出过程受固膜扩散控制,反应表观活化能为9.581 8kJ/mol;温度高于80℃时,锌浸出过程受界面化学反应控制,反应表观活化能为49.319kJ/mol;浸出反应的表观反应级数为0.983。     

AlH2P3O10·2H2O(I)对水中Ni2+的吸附动力学和热力学研究

采用静态吸附法研究A12O3-P2O5-H2O反应体系产物三聚磷酸二氢铝Ⅰ型二水物[AlH2P3O10·2H2O(I)]吸附水中Ni2+的动力学和热力学.考察了温度、浓度、粒径、pH和搅拌速度对吸附过程的影响,通过不同温度下的吸附等温热力学性能的变化,计算了吸附焓、吸附熵和自由能.结果表明,在试验范围内,AlH2P3O10·2H2O(I)对Ni2+的吸附符合Langmuir吸附等温方程式,过程受颗粒扩散控制,反应级数为1.88,298.15K时的热力学数据为:Ea=11.561 kJ/mol,△H=35.75 kJ/mol,△S=190.58 J/(mol·K),△G=-21.07 kJ/mol,吸附为自发的吸热过程,其吸附动力学总方程为:1-2/3x-(1-x)2/3=0.36r0<'2>C0<'1.88>exp(-11 561/RT).     

11-脱氧甘草次酸-3-O-乙酸酯铈的合成及抑菌性能

以甘草酸为原料,通过酸水解、还原、酯化、络合反应,得到了11-脱氧甘草次酸-3 -O -乙酸酯铈,经核磁共振分析每一步产物,与目标产物一致.将11-脱氧甘草次酸-3 -O -乙酸酯铈配成浓度为0.01 mol/L的溶液进行抑菌实验,对大肠杆菌和放线菌的抑菌圈直径为10.2 mm～ 10.4 mm;对大肠杆菌的最小抑菌浓度为1.25mmo]/L,对放线菌的最小抑菌浓度为2.5 mmol/L.通过电镜照片可以看出,抑菌圈内微生物细胞出现凋溶现象.     

炼钢用Si—Al—Ba—Ca合金替代Si—Al—Fe合金终脱氧实验研究

通过对采用Ｓｉ－Ａｌ－Ｂａ－Ｃａ合金进行脱氧实验研究分析,证实用用此合金脱氧可提高钢的纯净度,改善钢水流动性和提高高线盘条的质量。     

Mn-Fe-C系和Mn-V-C系热力学性质的研究

用碳饱和法研究了1450℃时Mn-Fe-C系和Mn-V-C系有关的热力学性质，得到Mn-Fe-C系：Xc=0.27994-0.10044XFc,lnγc^0=-1.4558,εCC=9.896,εc^Fc=0.359,ρc^Fe=0.064,εc^F3=1.354，C的活度系数表达式为lnγC=-1.4558 9.896Xc 1.354XF3;Mn-V-C系：Xc=0.2771 0.3395Xv,εc^V=-1.225,ρc^V=0.751,εc^V=-4.584，C的活度系数表达式为lnγc=-1.4558 9.896Xc-4.584Xv.     

高铬铸铁抗磨、耐热、耐蚀性能的研究

分析了高铬铸铁具有的抗磨、耐热、耐蚀性机理。通过对化学成分(碳、铬、和锰、钼、铜等合金元素及稀土元素)的含量在此3类铸铁中的影响研究,提出了相关设计参数。     

氧化铟纳米粉的低温制备

本文探讨了一种ITO纳米粉的低温、易于量产的制备方法。将铟锡氢氧化物置于充满氩气的高压釜内,在300℃、2MPa的条件下就可制得ITO的纳米颗粒。用XRD、透射电镜分析ITO纳米颗粒的形貌和粒径以及结晶状况。与其他方法进行对比,本方法反应条件更加柔和,且可以达到量产,有利于推广应用。     

Dual inhibition of human type 4 phosphodiesterase isostates by (R, R)-(+/-)-methyl 3-acetyl-4-[3-(cyclopentyloxy)-4-methoxyphenyl]-3- methyl-1-pyrrolidinecarboxylate

Purified recombinant human type 4 phosphodiesterase B2B (HSPDE4B2B) exists in both a low- and a high-affinity state that bind (R)-rolipram with Kd's of ca. 500 and 1 nM, respectively [Rocque, W. J., Tian, G., Wiseman, J. S., Holmes, W. D., Thompson, I. Z., Willard, D. H., Patel, I. R., Wisely, G. B., Clay, W. C., Kadwell, S. H., Hoffman, C. R., and Luther, M. A. (1997) Biochemistry 36, 14250-14261]. Since the tissue distribution of the two isostates may be significantly different, development of inhibitors that effectively inhibit both forms may be advantageous pharmacologically. In this study, enzyme inhibition and binding of HSPDE4B2B by (R, R)-(+/-)-methyl 3-acetyl-4-[3-(cyclopentyloxy)-4-methoxyphenyl]-3-methyl-1-pyrrolidin ecarboxylate (1), a novel inhibitor of phosphodiesterase 4 (PDE 4), were investigated. Binding experiments demonstrated high-affinity binding of 1 to HSPDE4B2B with a stoichiometry of 1:1. Inhibition of PDE activity showed only a single transition with an observed Ki similar to the apparent Kd determined by the binding experiments. Deletional mutants of HSPDE4B2B, which have been shown to bind (R)-rolipram with low affinity, were shown to interact with 1 with high affinity, indistinguishable from the results obtained with the full-length enzyme. Bound 1 was completely displaced by (R)-rolipram, and the displacement showed a biphasic transition that resembles the biphasic inhibition of HSPDE4B2B by (R)-rolipram. Theoretical analysis of the two transitions exemplified in the interaction of (R)-rolipram with HSPDE4B2B indicated that the two isostates were nonexchangeable. Phosphorylation at serines 487 and 489 on HSPDE4B2B had no effect on the stoichiometry of binding, the affinity for binding, or the inhibition of the enzyme by 1. These data further illustrate the presence of two isostates in PDE 4 as shown previously for (R)-rolipram binding and inhibition. In contrast to (R)-rolipram, where only one of the two isostates of PDE 4 binds with high affinity, 1 is a potent, dual inhibitor of both of the isostates of PDE 4. Kinetic and thermodynamic models describing the interactions between the nonexchangeable isostates of PDE 4 and its ligands are discussed.     

Biliary excretion of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone in the rat

The tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is a potent pancreas carcinogen in rats. The biliary excretion of NNK was therefore studied in anesthetized female Sprague-Dawley rats following i.p. administration of 0.7 mumol/kg [carbonyl-14C]NNK. The concentration of radioactivity peaked within 30 min and decreased thereafter exponentially. Cumulative excretion of radioactivity reached a plateau at 6-9% of the total dose. HPLC analysis revealed the presence of 4-hydroxy-4-(3-pyridyl)butyric acid (hydroxy acid), 4-oxo-4-(3-pyridyl)-butyric acid (keto acid), 4-(methylnitrosamino)-1-(3-pyridyl)-1-butyl beta-D-glucopyranosiduronic acid (NNAL Glu), 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) and NNK. NNAL Glu was the major metabolite contributing 34 +/- 4% of total radioactivity in bile at 30 min and 58 +/- 4% at 5 h. The percentage of acidic metabolites remained constant at approximately 20%. In contrast, the percentage of NNK and NNAL decreased within the first 2 h to < 5% and < 10% respectively. The elimination kinetics of NNK and its metabolites fitted into a one-compartment model with a half-life of 37 min for NNK, 52 min for NNAL and 110 min for NNAL Glu and acidic metabolites. In three rats dosed with 240 mumol/kg NNK i.p., the concentration of radioactivity peaked after 1-2 h and decreased very slowly thereafter. After 5-8 h a total of 12-17% of the dose has been excreted in the bile with no indication of a plateau. At all time points NNAL Glu was the major metabolite contributing up to 95% of total radioactivity in bile. The percentage of acidic metabolites was < 5% throughout the experiment. Whereas NNK contributed one-third of the radioactivity at 30 min and decreased rapidly, the percentage of NNAL in bile remained rather constant at approximately 5-10%. In conclusion, the detection of NNK, NNAL and NNAL Glu gives support to the hypothesis that tobacco-specific carcinogens could reach the pancreas retrograde from the bile, especially at high NNK concentrations.