碳酸钡法去除有色金属冶炼厂综合废水中Ca~(2+)和SO_4~(2-)的试验研究

有色金属冶炼厂产生大量含重金属的酸性废水。目前,重金属废水处理大都采用石灰中和法,但经处理后的出水中Ca2+和SO2-4浓度偏高,不适合作工艺循环冷却水系统的补充水。因此,提出用BaCO3去除Ca2+和SO2-4。分析了BaCO3去除水中Ca2+和SO42-机理,通过动态试验,研究了不同投加剂量、反应温度、反应时间以及沉淀时间对BaCO3去除水中Ca2+和SO2-4的影响。     

SO_4~(2-)在锂盐生产过程中的行为与消除方法

采用锂去母—石灰石焙烧法生产锂盐,SO_4~(2-)是影响产品质量的主要因素之一。本文从生产实践出发,对SO_4~(2-)引入工艺过程中的行为进行了分析,并对消除SO_4~(2-)影响的方法进行了分析与讨论。     

电解锰废水中Cr~(6+)、Mn~(2+)的去除方法研究

通过实验研究了还原沉淀-晶种曝气组合工艺去除电解锰废水中Cr6+和Mn2+,并探索了最佳工艺条件.首先以Na2SO3做还原剂将Cr6+转化为Cr3+后再通过化学沉淀法除去,然后采用加入MnO2做晶种曝气氧化去除废水中的Mn2+.结果表明:当Na2SO3投加量为0.5 g/L,还原反应pH值为4,还原反应时间6 min,Cr6+可完全转化为Cr3+.Cr3+在pH值为8时沉淀最完全,出水总铬浓度可从100 mg/L降到0.5 mg/L以下.除铬后,当MnO2投加量为25 g/L,废水pH值为9,曝气10 min,出水Mn2+浓度可从1 000 mg/L降到0.4 mg/L以下.通过以上处理出水总铬和总锰均达到我国《污水综合排放标准(GB8978-1996)》一级要求.     

Ca~(2+)-CO_3~(2-)-Glu~(2-)-H_2O体系热力学分析

根据碳酸钙在谷氨酸盐体系(Glu~(2-)-H_2O体系)中的溶解热力学平衡方程建立了其溶解热力学模型,分别分析了298K时体系中钙离子总浓度、游离钙浓度、游离谷氨酸根离子浓度、游离碳酸根离子浓度、钙物种分布以及谷氨酸根物种分布热力学结果。结果表明,在酸性谷氨酸盐体系中(pH7),碳酸钙溶解以酸浸作用为主,碳酸钙可以大量溶于酸性谷氨酸盐体系中;在碱性谷氨酸盐体系中(7pH14),碳酸钙溶解以谷氨酸根离子与钙离子配合作用为主,由于谷氨酸根离子与钙离子配合能力较弱,碳酸钙不可能溶于碱性谷氨酸盐体系中。     

铜冶炼酸性废水中铼的回收新工艺研究

研究了铜冶炼酸性废水中回收铼的一种新工艺,确定了硫化沉淀-选择性浸出-萃取-蒸发-结晶的工艺流程和各工序的关键工艺参数,重点分析了砷、锑、铋、锌等杂质的走向和脱除方法。研究表明,采用其他系统产生的含硫废水作沉淀剂,可优先选择沉淀铼,铼的沉淀率达到90%以上,过程中无硫化氢产生;从铼沉淀渣到铼酸铵产品,铼的回收率大于80%,产出铼酸铵产品符合YS/T894—2013标准,其中铼酸铵质量分数大于99%,铼质量分数大于68%。整个工艺处理过程成本较低,易于实现工程化。     

Ca~(2+)-CO_3~(2-)-Ida~(2-)-H_2O体系热力学分析

根据碳酸钙在亚氨基二乙酸盐体系(Ida~(2-)-H_2O体系)中的溶解热力学平衡方程建立其溶解热力学模型,分析了298K条件下体系中总钙浓度、游离钙浓度、游离亚氨基二乙酸根离子浓度、游离碳酸根离子浓度、钙物种及亚氨基二乙酸根物种的分布。结果表明:在酸性亚氨基二乙酸盐体系中,碳酸钙的溶解以酸溶作用为主,碳酸钙可以大量溶于酸性亚氨基二乙酸盐体系中;在碱性亚氨基二乙酸盐体系中,碳酸钙的溶解以亚氨基二乙酸根离子与钙离子配合作用为主,由于二者配合能力较弱,所以碳酸钙不会溶解。     

改性膨润土吸附冶炼废水中Cu~(2+)和Ni~(2+)的动力学

研究了实验室制备的6种改性膨润土对冶炼废水中Cu2+和Ni 2+的吸附动力学。结果表明,改性膨润土对Cu2+、Ni 2+的吸附在40min内基本达到平衡,在30℃时,吸附符合准二级动力学模型,其反应速率与反应物浓度的二次方成正比。     

三段生物制剂-石灰法深度处理酸性重金属废水

采用生物制剂与石灰三段法深度处理株洲冶炼集团股份有限公司酸性重金属废水,工业试验运行过程中对总废水及处理后出水中各重金属浓度进行监测,并对渣样进行分析。结果表明：重金属浓度分别由锌84.63-583.39 mg/L,铅1.11-20.43 mg/L,镉2.38-19.18 mg/L,铜0.35-6.51 mg/L,砷0.71-1.19 mg/L,汞0.001 2-0.063 mg/L脱除至锌0.12-0.83 mg/L,铅0.18-0.46 mg/L,镉0.008-0.046 mg/L,铜0.12-0.19 mg/L,砷0.005-0.009 mg/L,汞0.000 12-0.002 2 mg/L,处理后出水各重金属含量均远低于《铅、锌工业污染物排放标准GB 25466-2010》。整套工艺只需控制一段水解pH值为9.0,无需硫酸、NaOH再次调节二段及三段水解pH值。配合渣中锌的质量分数达到了29.5%,可以作为锌冶炼企业的原料回收其中的重金属。     

高浓度H_2SO_4体系中Cl~-和SO_4~(2-)对N235萃取钒的影响

采用加盐萃取法从高酸浸出液中直接分离富集钒,考察了酸度、N235浓度、氯化钠浓度、硫酸钠浓度对N235萃取分离高浓度硫酸溶液中钒的影响,并确定了萃合物的结构。结果表明,Cl~-和SO_4~(2-)对硫酸体系钒的萃取均有一定提高,但Cl~-的作用效果更显著。在不加盐的条件下,采用20%N235为萃取剂,磺化煤油为稀释剂,硫酸浓度1mol/L,萃取时间10min,相比A/O=1∶1,经单级萃取,硫酸体系中钒萃取率仅为30%左右;加入一定量的NaCl、Na_2SO_4后,钒萃取率分别达到80%、47%。Cl-作用于硫酸体系时,与钒以离子缔和形式形成萃合物(R_3N)_x·(VO_2~+·Cl~-)_y;SO_4~(2-)的加入可促进VO_2SO_4~-的形成,使萃取率提高。     

碳羟磷灰石(CHAP)吸附废水中锰离子的动力学研究

主要研究了碳羟磷灰石(CHAP)对二价锰离子的吸附性能。从pH、吸附时间及初始Mn2+浓度3方面对吸附能力的影响进行吸附试验。试验结果表明:在常温常压,CHAP吸附Mn2+的最佳pH值为6,最佳吸附时间为60 min,吸附量达到22.44mg/g。CHAP对Mn2+的吸附过程符合准二级反应动力学模型。CHAP吸附Mn2+的能力随着废水中Mn2+浓度增加而增加,最大的吸附量达24.29mg/g,CHAP对Mn2+的吸附符合Langmuir吸附等温式。     

去除稀土工业废水中Ca2+、Mg2+的研究

反渗透法作为稀土工业废水处理领域的一种高新技术应用日益广泛,如何防止稀土废水中的钙、镁污染和堵塞膜元件,是当前反渗透技术应用中的一个难点.本文研究用碳酸钠和氢氧化钠沉淀废水中的钙、镁离子,取得了一定的效果,并研究了絮凝剂的加入对沉淀快速沉降的影响.     

Saltatory propagation of Ca2+ waves by Ca2+ sparks

Punctate releases of Ca2+, called Ca2+ sparks, originate at the regular array of t-tubules in cardiac myocytes and skeletal muscle. During Ca2+ overload sparks serve as sites for the initiation and propagation of Ca2+ waves in myocytes. Computer simulations of spark-mediated waves are performed with model release sites that reproduce the adaptive Ca2+ release observed for the ryanodine receptor. The speed of these waves is proportional to the diffusion constant of Ca2+, D, rather than D, as is true for reaction-diffusion equations in a continuous excitable medium. A simplified "fire-diffuse-fire" model that mimics the properties of Ca2+-induced Ca2+ release (CICR) from isolated sites is used to explain this saltatory mode of wave propagation. Saltatory and continuous wave propagation can be differentiated by the temperature and Ca2+ buffer dependence of wave speed.     

稀碱洗涤法去除混合碳酸稀土中SO42-和Al杂质

用稀的氢氧化钠溶液对混合碳酸稀土进行洗涤,有效地除去大部分杂质SO42-和Al,分别讨论了碱的用量对SO42-和Al去除率的影响,得到了SO42-和Al去除率分别为大于99%和70%.     

Ca2+ pool emptying stimulates Ca2+ entry activated by S-nitrosylation

The entry of Ca2+ following Ca2+ pool release is a major component of Ca2+ signals; yet despite intense study, how "store-operated" entry channels are activated is unresolved. Because S-nitrosylation has become recognized as an important regulatory modification of several key channel proteins, its role in Ca2+ entry was investigated. A novel class of lipophilic NO donors activated Ca2+ entry independent of the well defined NO target, guanylate cyclase. Strikingly similar entry of Ca2+ induced by cell permeant alkylators indicated that this Ca2+ entry process was activated through thiol modification. Significantly, Ca2+ entry activated by either NO donors or alkylators was highly stimulated by Ca2+ pool depletion, which increased both the rate of Ca2+ release and the sensitivity to thiol modifiers. The results indicate that S-nitrosylation underlies activation of an important store-operated Ca2+ entry mechanism.     

The Ca2+ transport mechanisms of mitochondria and Ca2+ uptake from physiological-type Ca2+ transients

Mitochondria contain a sophisticated system for transporting Ca2+. The existence of a uniporter and of both Na+-dependent and -independent efflux mechanisms has been known for years. Recently, a new mechanism, called the RaM, which seems adapted for sequestering Ca2+ from physiological transients or pulses has been discovered. The RaM shows a conductivity at the beginning of a Ca2+ pulse that is much higher than the conductivity of the uniporter. This conductivity decreases very rapidly following the increase in [Ca2+] outside the mitochondria. This decrease in the Ca2+ conductivity of the RaM is associated with binding of Ca2+ to an external regulatory site. When liver mitochondria are exposed to a sequence of pulses, uptake of labeled Ca2+ via the RaM appears additive between pulses. Ruthenium red inhibits the RaM in liver mitochondria but much larger amounts are required than for inhibition of the mitochondrial Ca2+ uniporter. Spermine, ATP and GTP increase Ca2+ uptake via the RaM. Maximum uptake via the RaM from a single Ca2+ pulse in the physiological range has been observed to be approximately 7 nmole/mg protein, suggesting that Ca2+ uptake via the RaM and uniporter from physiological pulses may be sufficient to activate the Ca2+-sensitive metabolic reactions in the mitochondrial matrix which increase the rate of ATP production. RaM-mediated Ca2+ uptake has also been observed in heart mitochondria. Evidence for Ca2+ uptake into the mitochondria in a variety of tissues described in the literature is reviewed for evidence of participation of the RaM in this uptake. Possible ways in which the differences in transport via the RaM and the uniporter may be used to differentiate between metabolic and apoptotic signaling are discussed.     

Selective activation of Ca2+-activated K+ channels by co-localized Ca2+ channels in hippocampal neurons

Calcium entry through voltage-gated calcium channels can activate either large- (BK) or small- (SK) conductance calcium-activated potassium channels. In hippocampal neurons, activation of BK channels underlies the falling phase of an action potential and generation of the fast afterhyperpolarization (AHP). In contrast, SK channel activation underlies generation of the slow AHP after a burst of action potentials. The source of calcium for BK channel activation is unknown, but the slow AHP is blocked by dihydropyridine antagonists, indicating that L-type calcium channels provide the calcium for activation of SK channels. It is not understood how this specialized coupling between calcium and potassium channels is achieved. Here we study channel activity in cell-attached patches from hippocampal neurons and report a unique specificity of coupling. L-type channels activate SK channels only, without activating BK channels present in the same patch. The delay between the opening of L-type channels and SK channels indicates that these channels are 50-150 nm apart. In contrast, N-type calcium channels activate BK channels only, with opening of the two channel types being nearly coincident. This temporal association indicates that N and BK channels are very close. Finally, P/Q-type calcium channels do not couple to either SK or BK channels. These data indicate an absolute segregation of coupling between channels, and illustrate the functional importance of submembrane calcium microdomains.     

Zinc inhibits Ca2+ transport by rat brain NA+/Ca2+ exchanger

Calcium transport by the Na+/Ca2+ exchanger was measured in plasma membranes vesicles purified from rat brain and in primary rat cortical cell culture. Sodium-loaded vesicles rapidly accumulate Ca2+ via Na+/Ca2+ exchange (Na+(i)-dependent Ca2+ uptake). Extravesicular zinc inhibited Na+/Ca2+ exchange as evidenced by a reduction of the initial velocity of Ca2+ uptake. Significant inhibition of Ca2+ uptake was seen at concentrations of zinc as low as 3 microM. Lineweaver-Burk analysis of the data was consistent with noncompetitive inhibition with respect to extravesicular Ca2+ concentration. The Ki for zinc inhibition of Ca2+ uptake determined from a Dixon plot was 14.5 microM. This is within the range of zinc concentrations thought to be obtained extracellularly after excitation. When vesicles were preloaded with Ca2+, extravesicular zinc also inhibited reversal of Na+/Ca2+ exchange (Na+(i)-dependent Ca2+ release) although its potency was much less: concentrations of > or = 30 microM zinc were required. Zinc inhibition of Ca2+ release was not Na+ dependent. Na+(i)-dependent calcium uptake by rat cortical cells in primary culture also was inhibited by zinc. The extent of inhibition was similar to that seen for inhibition of Na+(i)-dependent Ca2+ uptake in membrane vesicles, but the potency was less. The results suggest that Ca2+ transport by the Na+/Ca2+ exchanger is inhibited by concentrations of zinc thought to be attained extracellularly after excitation.     

Correlated effluxes of adenine nucleotides, Mg2+ and Ca2+ induced in rat-liver mitochondria by external Ca2+ and phosphate

The presence of inorganic phosphate and Ca2+ in the external medium induces a closely parallel efflux of both endogenous adenine nucleotides and Mg2+ from rat liver mitochondria. These effluxes are (a) pH-dependent and inhibited by uncouplers, respiration inhibitors and external Mg2+; (b) completely prevented by bongkrekate, but stimulated by atractylate. ATP, ADP or AMP each inhibit the release of Mg2+ promoted by Ca2+ and phosphate; however, in the presence of oligomycin and P1,P5-di(adenosine-5')-pentaphosphate (an inhibitor of adenylate kinase) only ADP is effective. Also the release of accumulated Ca2+ observed when approximately 50% Mg2+ is discharged is retarded by bongkrekate and added Mg2+ whereas it is accelerated by atractylate. All adenine nucleotides have a significant effect in retarding the efflux of accumulated Ca2+ but, in the presence of oligomycin and P1,P5-di(adenosine-5')-pentaphosphate, only ADP is active. From these results we conclude that effluxes of Mg2+, Ca2+ and adenine nucleotide from rat liver mitochondria induced by external phosphate are interconnected and regulated by external ADP and Mg2+ levels.