大型预焙电解槽效应控制分析

本文讨论了中铝青海分公司200 kA大型预焙电解槽阳极效应控制情况,分析了阳极效应发生的机理和控制思路。以铝电解智能控制系统为核心,结合电解技术条件和标准化的人工作业,进一步降低阳极效应系数,减少吨铝电耗,最后给出了控制效果。     

开槽阳极在铝电解槽上的应用与研究

本文通过对开槽阳极在大型预焙铝电解上的应用,证明了使用开槽阳极可以有效的降低阳极过电压,减少阳极效应发生,提高电流效率,从而起到节省电能的作用。     

浅析铝电解生产的阳极效应

本文通过对铝电解生产中的阳极效应发生的机理、危害性以及对阳极效应发生的条件进行分析,提出了控制阳极效应的途径。     

浅谈大型预焙铝电解槽阳极效应管理

阐述了铝电解槽阳极效应发生的机理和对电解生产的影响,介绍了阳极效应管理的重点工作和某厂350kA铝电解系列降低阳极效应系数的生产实践及取得的效益。     

阳极效应及其对电解铝生产的影响

阳极效应是铝电解生产中不可避免的一种现象,在生产实践中,应合理选择阳极效应系数,减少阳极效应对生产产生的不良影响,从而降低能耗,降低成本,提高产品质量,提高企业经济效益。     

阳极效应是电解工艺的重要标志

在分析论述阳极效应发生的机理和特征基础上 ,阐明了阳极效应在铝电解中的重要意义 ,并结合我公司对阳极效应的管理 ,摸清单槽的运行情况 ,进行微机跟踪记录     

200kA预焙槽效应预报控制分析

阳极效应(AE)是铝电解过程中发生在阳极上的一种特殊现象,对铝电解生产过程的稳定性破坏很大。所以,现代铝电解工艺希望尽可能地减少AE发生及降低AE系数。当今普遍采用的AE预报的基本做法是对依据槽电压和系列电流的同步采样值所计算出的槽电阻序列进行滤波(或平滑)处理,并求其斜率然后将滤波电阻值及其斜率值分别与限定值比较,作出判断。下面就中铝青海分公司第三电解厂200 kA预焙电解槽阳极效应及其预报进行分析。(1)效应机理。阳极效应的发生是电解质中氧化铝浓度较低所致。不合适的浓度和温度的共同作用使电解过程中电流通路受到直…     

铝电解阳极开槽技术研究

本文通过深入分析铝电解工艺中阳极压降、阳极效应及阳极在电解质中排渣过程,从阳极外形、理化指标入手,优化阳极炭块结构。开槽阳极的使用,使阳极压降降低了60mV以上,吨铝节能180kwh/t.Al左右;开槽阳极使电解过程中阳极效应从0.20个/槽·日降低到0.05个/槽·日。降低了阳极压降、减少了阳极效应,原铝直流电耗进一步降低,产生更多经济效益和社会效益。     

铜电积中铅钙锡阳极钝化层的管理

现代铜电解槽中最常用的阳极为铅钙锡合金阳极,在铜电积过程中,PbO_2(过氧化铅)层在阳极表面形成。这层PbO_2的重要性在于保护金属铅阳极不被酸腐蚀,以使析氧反应有一个合理的交换电流密度。然而,在非正常状况或者断电条件下,PbO_2的电化学行为会导致阳极退化,并且导致铜阴极含铅量过高,以及为清除槽底累积的阳极泥而频繁停工。当发生停电或电解槽需要清理而断电时,便会出现非正常状况。某些电解槽为上述情况配置了有限容量的备用整流器。本文描述了PbO_2层形成和损坏的机理,并且确定了维持阳极表面PbO_2层致密性所需要提供的最小电流密度。     

阳极效应对铝电解生产的影响

分析了阳极效应对铝电解生产的影响,重点对阳极效应发生时的一些现象进行深入浅出的讨论,并对如何优化控制一定的阳极效应、实现高产低耗作了探讨。     

Neuregulins and erbB receptors at neuromuscular junctions and at agrin-induced postsynaptic-like apparatus in skeletal muscle

This study has characterized the repertoire of the anion exchanger (AE) family members expressed within the guinea pig organ of Corti, the auditory neuroepithelia. Both AE2 and AE3 cDNAs were present, but AE1 cDNA was not detected. The more abundant AE2 was sequenced and its expression characterized in the cochlea. The 3888 base pairs (bp) AE2 sequence, compiled from multiple clones, includes 150 bp of upstream non-coding sequence and 3717 bp of open reading frame encoding a protein of 1238 amino acids. Immunoblot of cochlear homogenate revealed a single AE2-immunoreactive band of Mr 180 kDa. In situ hybridization and immunohistochemical analysis localized AE2 expression to several tissues and cell types within the guinea pig inner ear, including superior half of the spiral ligament and within the interdental cells lining the spiral limbus. However, AE2 was not clearly detected in the outer hair cells (OHC) of the organ of Corti by either immunohistochemistry or in situ hybridization. The results of these studies imply a physiologic role of AE2 in the cochlear homeostasis, but do not support its role as a potential 'motor protein' in mediating the in vitro-observed voltage-gated, ATP-independent OHC motility.     

Geographical distribution of dengue and socioeconomic factors in an urban locality in southeastern Brazil]

The hydrochloric acid secreting parietal cells of the human stomach mucosa have been shown to express anion exchanger 2 (AE2). AE2 is restricted to the basolateral membrane domain and is responsible for the basolateral uptake of Cl- and release of HCO3-. It is unknown which mechanism is responsible for the basolateral positioning of AE2 in parietal cells. We raised the question whether AE2 might be immobilized at the cell surface by linkage via ankyrin to the spectrin/actin-based membrane cytoskeleton. In the present study we communicate two observations that support this hypothesis, namely that in parietal cells ankyrin is localized with AE2 along the basolateral cell surface and, secondly, that purified erythrocyte ankyrin binds to the in vitro-translated cytoplasmic domain of AE2. We conclude from these observations that AE2 in parietal cells might be linked via ankyrin to the basolateral membrane cytoskeleton and that this type of linkage might play a role in immobilizing AE2 in a non-random fashion along the basolateral membrane domain.     

Novel AE1 mutations in recessive distal renal tubular acidosis. Loss-of-function is rescued by glycophorin A

The AE1 gene encodes band 3 Cl-/HCO3- exchangers that are expressed both in the erythrocyte and in the acid-secreting, type A intercalated cells of the kidney. Kidney AE1 contributes to urinary acidification by providing the major exit route for HCO3- across the basolateral membrane. Several AE1 mutations cosegregate with dominantly transmitted nonsyndromic renal tubular acidosis (dRTA). However, the modest degree of in vitro hypofunction exhibited by these dRTA-associated mutations fails to explain the disease phenotype in light of the normal urinary acidification associated with the complete loss-of-function exhibited by AE1 mutations linked to dominant spherocytosis. We report here novel AE1 mutations linked to a recessive syndrome of dRTA and hemolytic anemia in which red cell anion transport is normal. Both affected individuals were triply homozygous for two benign mutations M31T and K56E and for the loss-of-function mutation, G701D. AE1 G701D loss-of-function was accompanied by impaired trafficking to the Xenopus oocyte surface. Coexpression with AE1 G701D of the erythroid AE1 chaperonin, glycophorin A, rescued both AE1-mediated Cl- transport and AE1 surface expression in oocytes. The genetic and functional data both suggest that the homozygous AE1 G701D mutation causes recessively transmitted dRTA in this kindred with apparently normal erythroid anion transport.     

The trouble with cognitive subtraction

The mechanism(s) by which zinc is transported into cells has not been identified. Since zinc uptake is inhibited by reducing the temperature, zinc uptake may depend on the movement of plasma membrane micoenvironments, such as endocytosis or potocytosis. We investigated the potential role of potocytosis in cellular zinc uptake by incubating normal and acrodermatitis enteropathica fibroblasts with nystatin, a sterol-binding drug previously shown to inhibit potocytosis. Zinc uptake was determined during initial rates of uptake (10 min) following incubation of the fibroblasts in 50 micrograms nystatin/mL or 0.1% dimethylsulfoxide for 10 min at 37 degrees C. The cells were then incubated with 1 to 30 microM 65zinc. Michaelis-Menten kinetics were observed for zinc uptake. Nystatin inhibited zinc uptake in both the normal and AE fibroblasts. Reduced cellular uptake of zinc was associated with its internalization, not its external binding. In normal fibroblasts, nystatin significantly reduced the K(m) 56% and the Vmax 69%. In the AE fibroblasts, nystatin treatment significantly reduced the Vmax 59%, but did not significantly affect the K(m). The AE mutation alone affected the Vmax for cellular zinc uptake. The control AE fibroblasts exhibited a 40% reduction in Vmax compared to control normal fibroblasts. We conclude that nystatin exerts its effect on zinc uptake by reducing the velocity at which zinc traverses the cell membrane, possibly through potocytosis. Furthermore, the AE mutation also affects zinc transport by reducing zinc transport.     

Purification and characterization of herpes simplex virus type 1 alkaline exonuclease expressed in Escherichia coli

The alkaline exonuclease (AE) encoded by the herpes simplex virus type 1 (HSV-1) UL12 open reading frame was inducibly expressed in Escherichia coli and purified without the use of chromatographic separation. This recombinant AE was found to exhibit the same biochemical properties as the virus-encoded protein and was used to confirm the existence of a weak endonucleolytic activity in the enzyme. Antisera raised against the recombinant protein recognized several forms of the AE in HSV-1-infected cells. This expression and purification strategy will provide an economical and easily accessible alternative source of HSV-1 AE for future in vitro studies.     

Regulation of Cl-/ HCO3- exchange by cystic fibrosis transmembrane conductance regulator expressed in NIH 3T3 and HEK 293 cells

A central function of cystic fibrosis transmembrane conductance regulator (CFTR)-expressing tissues is the secretion of fluid containing 100-140 mM HCO3-. High levels of HCO3- maintain secreted proteins such as mucins (all tissues) and digestive enzymes (pancreas) in a soluble and/or inactive state. HCO3- secretion is impaired in CF in all CFTR-expressing, HCO3--secreting tissues examined. The mechanism responsible for this critical problem in CF is unknown. Since a major component of HCO3- secretion in CFTR-expressing cells is mediated by the action of a Cl-/HCO3- exchanger (AE), in the present work we examined the regulation of AE activity by CFTR. In NIH 3T3 cells stably transfected with wild type CFTR and in HEK 293 cells expressing WT and several mutant CFTR, activation of CFTR by cAMP stimulated AE activity. Pharmacological and mutagenesis studies indicated that expression of CFTR in the plasma membrane, but not the Cl- conductive function of CFTR was required for activation of AE. Furthermore, mutations in NBD2 altered regulation of AE activity by CFTR independent of their effect on Cl- channel activity. At very high expression levels CFTR modified the sensitivity of AE to 4,4'-diisothiocyanatostilbene-2, 2'-disulfonate. The novel finding of regulation of Cl-/HCO3- exchange by CFTR reported here may have important physiological implications and explain, at least in part, the impaired HCO3- secretion in CF.     

The structure and organization of the human erythroid anion exchanger (AE1) gene

The AE1 (anion exchanger, band 3) protein is expressed in erythrocytes and in the A-type intercalated cells of the kidney distal collecting tubule. In both cell types it mediates the electroneutral transport of chloride and bicarbonate ions across the lipid bilayer, and, in erythrocytes, it also serves as the critical attachment site of the peripheral membrane skeleton. We have characterized the human AE1 gene using overlapping clones isolated from a phage library of human genomic DNA. The gene spans approximately 20 kb and consists of 20 exons separated by 19 introns. The structure of the human AE1 gene corresponds closely with that of the previously characterized mouse AE1 gene, with a high degree of conservation of exon/intron junctions, as well as exon and intron nucleotide sequences. The putative upstream and internal promoter sequences of the human AE1 gene used in erythroid and kidney cells, respectively, are described. We also report the nucleotide sequence of the entire 3' noncoding region of exon 20, which was lacking in the published cDNA sequences. In addition, we have characterized 9 Alu repeat elements found within the body of the human AE1 gene that are members of 4 related subfamilies that appear to have entered the genome at different times during primate evolution.     

Inhibin A is a sensitive and specific marker for testicular sex cord-stromal tumors

We compared the expression of inhibin A, chromogranin, synaptophysin, S-100 protein, cytokeratins AE1/AE3, 7, and 20, and estrogen and progesterone receptors in testicular sex cord-stromal tumors: 11 Sertoli cell tumors, 3 Sertoli cell adenomas (nodules), 26 benign Leydig cell tumors, 7 malignant Leydig cell tumors (defined clinically by metastatic behavior), and a variety of germ cell tumors. Inhibin was the most sensitive marker, expressed in 91% of the Sertoli cell tumors and 100% of the Sertoli cell adenomas and Leydig cell tumors. The non-neoplastic Sertoli and Leydig cells invariably stained for inhibin. Conversely, no germ cell tumors were immunoreactive. One testicular tumor of the adrenogenital syndrome was immunoreactive. Neuroendocrine marker immunoreactivity was variable. Chromogranin was expressed in the non-neoplastic Sertoli and Leydig cells, 82% of the Sertoli cell tumors, 92% of the benign Leydig cell tumors, and 43% of the malignant Leydig cell tumors. Synaptophysin was expressed in the non-neoplastic Sertoli and Leydig cells, 45% of the Sertoll cell tumors, and 70% of the Leydig cell tumors, in approximately similar proportions between the benign and malignant Leydig cell tumors. S-100 protein was expressed in 64% of the Sertoli cell tumors, 8% of the benign Leydig cell tumors, and none of the malignant Leydig cell tumors. Cytokeratins AE1/AE3 were expressed in 64% of the Sertoli cell tumors and 42% of the Leydig cell tumors, with similar proportions in the benign and malignant cases. Estrogen and progesterone receptor expression were identified in 24 and 39% of benign and malignant Leydig cell tumors, respectively. We conclude that inhibin is a characteristic marker for Sertoli and Leydig cells and that it serves to differentiate testicular sex cord-stromal tumors from germ cell tumors.     

Immunohistochemical study of epithelioid hemangioendothelioma in the leg: a case report

Epithelioid hemangioendothelioma is a relatively rare lesion. Although its histogenesis has been well described, its immunohistochemical characteristics remain controversial. A case of epithelioid hemangioendothelioma of the soft tissue of the right leg in a 67-year-old Chinese woman is reported. Histologic findings of intracytoplasmic lumina in the tumor cells and positive immunostaining for vimentin, factor VIII-related antigen. CD34 and Ulex europaeus agglutinin 1 (UEA-1) were obtained, demonstrating differentiation of the tumor cells to endothelial cells, although staining for antibodies to cytokeratins AE1/AE3 and CAM5.2 was weak. CD34 as well as Factor VIII-related antigen is a useful marker of endothelial differentiation in this tumor. A review of the literature is also presented.