大型反吹风布袋收尘器工艺过程的PLC控制

介绍可编程序控制器 (PLC)在大型反吹风布袋收尘器工艺过程控制的设计 ,以及其收尘、清灰的工作原理与工艺过程中的PLC程序设计编制、系统组成。     

低压脉冲覆膜袋滤收尘器在铅鼓风炉烟气收尘系统中的应用

分析了铅鼓风炉原反吹风布袋收尘器在生产过程中存在的主要问题，介绍了低压脉冲覆膜袋滤收尘器结构特点及应用情况。     

LCPM型袋式除尘器的改进

通过对LCPM型袋式除尘器的故障进行分析,查找产生故障的原因,并重点介绍对布袋结构、过滤材质和反吹风方式的改进,并对改造后的效果进行了讨论。改进后,提高了袋式除尘器的可靠性和收尘效率,检修维护方便,占用空间小。     

3#大布袋收尘器更新改造方案的探讨

通过对3^#大布袋收尘器更新改造方案的对比分析，探讨适合工艺条件的最佳收尘器的选择途径。     

锌挥发窑袋式收尘器清灰技术的研究

株洲冶炼厂锌挥发窑反吹风袋式收尘器清灰失效，研究出停风低压快速脉冲清灰技术，并对２＾＃挥发窑收尘器进行改造试验，结果表明，这种技术是可行的，已具备推广的条件。     

煤粉布袋收尘器控制系统的改进

引言/Preface在中铝山东分公司新建5#煤粉磨工程中,我们最终选用了武汉安环院的专利产品——高浓度煤粉布袋收尘器,该收尘器原配套有先进的PLC控制系统,但由于收尘器只是整个工艺流程中的一个生产设备,而整个流程为DCS控制,且流程中从德国进口的转子秤也配套有PLC控制系统,为避免多种PLC与DCS通讯造成接口和调试困难,经与武汉安环院技术人员协商,决定将布袋收尘器的PLC系统去掉,改为由DCS系统完成。控制要求/Controlrequirement该布袋收尘器共有54个清灰脉冲电磁阀,分两列布置,两列相对应的阀同时喷吹清灰,即每次有两个脉冲阀同时…     

锌挥发窑袋式收尘器清灰技术的研究

株洲冶炼厂锌挥发窑反吹风袋式收尘器清灰失效，研究出停风低压快速脉冲清灰技术，并对２＃挥发窑收尘器进行改造试验．结果表明，这种技术是可行的，已具备推广应用的条件。     

低压脉冲旋转反吹布袋收尘器在有色冶炼行业中的应用

目前有色冶金行业干法收尘主要以布袋收尘器为主。介绍了低压脉冲旋转反吹布袋收尘器在烟尘条件恶劣的精矿干燥、回转窑脱硫干燥收尘中的应用。生产应用对比得出,低压脉冲旋转反吹布袋收尘器具有占地小、运行维护量小、运行成本低、使用寿命长等优点。     

固定式阳极炉烟气收尘系统的优化与实践

介绍了贵冶固定式阳极炉烟气收尘系统的工作原理,分析了系统运行效果不佳的原因;针对阻碍烟气流通的空气冷却器及布袋收尘器等单元进行优化改造,对影响布袋使用寿命的烟气温度进行优化调节,最终收尘系统运行效率提高,环境得到改善。     

阳极炉收尘系统的改造实践

介绍阳极炉原收尘系统的组成及存在的问题,在综合考虑收尘系统余热利用的基础上,通过对几种收尘方式的对比,确定了阳极炉收尘改造的工艺流程,并在阳极炉上应用布袋收尘系统,实现了阳极炉节能减排的目标。     

高浓度防爆型袋收尘器的研制与应用

针对煤粉浓度高及烟煤存在爆炸性的特点,研制出了高浓度、防爆形袋收尘器。高浓度、防爆型袋收尘器在苏钢煤粉制备一级收尘工艺的应用实践表明,该设备是适用于高浓度煤粉一级收尘的理想收尘设备,它不仅收尘效率高,维护管理方便,而且可以降低投资,节约能耗,保护环境。     

自动力除尘器的研制

自动力除尘器是一种新型除尘器，其自身具有引风、净化、排气等功能。本文着重对该除尘器的结构和性能特点进行了分析，并与常用的负式除尘系统作比较。     

Targeted gene disruption shows that knobs enable malaria-infected red cells to cytoadhere under physiological shear stress

Sphingosine, which is on the pathway of sphingomyelin degradation, activates phospholipase C (PLC) delta1 moderately. In the liposome assay effect of sphingosine on PLC delta1 activity depends on KCl concentration. Stimulation of PLC delta1 by sphingosine increased as the KCl concentration is increased from 0 to 100 mM, and then diminished with the increasing KCl. In the liposome assay sphingosine diminishes inhibition of PLC delta1 by sphingomyelin. To determine the domain of PLC delta1 which interacts with sphingosine active proteolytic fragments of PLC delta1 were generated by trypsin digestion of the native enzyme. Sphingosine affects the activity of PLC delta1 fragment which lacked the amino-terminal domain (first 60 amino acids) but not the active fragment that has cleaved the domain spanning the X and Y region of PLC delta1. These observations indicate that for interaction of sphingosine with PLC delta1 intact domain that span regions of conservation, designated as X and Y is necessary. When the activity of PLC delta1 was assayed with PIP2 in the erythrocyte membrane as substrate, sphingosine strongly inhibited PLC delta1. The other homolog of sphingosine 4-hydroxysphinganine (phytosphingosine) inhibited PLC delta1 to much lesser extent. The activity of PLC delta1 was inhibited by 68% and 22% in the presence of 20 microM sphingosine and phytosphingosine, respectively. This inhibition was completely abolished by deoxycholate at a concentration of 1.5 mM. These observations suggest that sphingosine may regulate activity of PLC delta1 in the cell.     

Dependence of the activity of phospholipase C beta on surface pressure and surface composition in phospholipid monolayers and its implications for their regulation

We have examined the influence of surface pressure and phospholipid composition on hydrolysis of phosphatidylinositol (4,5)-bisphosphate (PIP2) by phospholipase C beta 1 (PLC beta 1) and PLC beta 2 in mixed composition phospholipid monolayers. Increasing the monolayer surface pressure from 15 to 36 mN/m reduced the rate at which PIP2 was hydrolyzed by PLC beta 1 and PLC beta 2 by 4-6-fold, although PLC beta 1 was more active than PLC beta 2, even at high surface pressure. Reduced enzyme activity was accompanied by an increase in reaction induction times, suggesting that increasing surface pressure reduced the penetration rate of the enzymes into the monolayer. Quantitation of interfacial enzyme concentration using 35S-labeled PLC beta 1 confirmed that less enzyme was associated with the monolayer at higher pressures. The relationship between PLC activity and substrate concentration was examined at a single surface pressure of 30 mN/m. This relationship was not hyperbolic, and increases in the mole percentage (mol %) of PIP2 in the monolayer resulted in an upwardly-curving increase in PLC activity. Thus, PLC beta 1 activity increased 7-fold and PLC beta 2 activity increased 4-fold when the mol % of PIP2 in the monolayer increased from 17.9% to 29%, increasing further thereafter. Paradoxically, increasing the mol % of PIP2 from 0 to 60% was accompanied by a 3-fold decrease in interfacial enzyme concentrations. Taken together, these data show that the catalytic activity of PLC beta involves some element of penetration of lipid interfaces, and suggest that the organization of the substrate facilitates PLC activity, giving credence to the substrate theory of interfacial activation of phospholipases. We present a hypothesis suggesting that PIP2 molecules coalesce into enriched lateral domains which favor PLC beta activity.     

Mapping a telomere using the translocation eT1(III;V) in Caenorhabditis elegans

TCR engagement activates phospholipase C gamma 1 (PLC gamma 1) via a tyrosine phosphorylation-dependent mechanism. PLC gamma 1 contains a pair of Src homology 2 (SH2) domains whose function is that of promoting protein interactions by binding phosphorylated tyrosine and adjacent amino acids. The role of the PLC gamma 1 SH2 domains in PLC gamma 1 phosphorylation was explored by mutational analysis of an epitope-tagged protein transiently expressed in Jurkat T cells. Mutation of the amino-terminal SH2 domain (SH2(N) domain) resulted in defective tyrosine phosphorylation of PLC gamma 1 in response to TCR/CD3 perturbation. In addition, the PLC gamma 1 SH2(N) domain mutant failed to associate with Grb2 and a 36- to 38-kDa phosphoprotein (p36-38), which has previously been recognized to interact with PLC gamma 1, Grb2, and other molecules involved in TCR signal transduction. Conversely, mutation of the carboxyl-terminal SH2 domain (SH2(C) domain) did not affect TCR-induced tyrosine phosphorylation of PLC gamma 1. Furthermore, binding of p36-38 to PLC gamma 1 was not abrogated by mutations of the SH2(C) domain. In contrast to TCR/CD3 ligation, treatment of cells with pervanadate induced tyrosine phosphorylation of either PLC gamma 1 SH2(N) or SH2(C) domain mutants to a level comparable with that of the wild-type protein, indicating that pervanadate treatment induces an alternate mechanism of PLC gamma 1 phosphorylation. These data indicate that the SH2(N) domain is required for TCR-induced PLC gamma 1 phosphorylation, presumably by participating in the formation of a complex that promotes the association of PLC gamma 1 with a tyrosine kinase.     

PLC的故障诊断及处理方法

在PLC的维修工作中,根据PLC的工作原理,分析造成PLC故障的主要因素,并探讨处理方法。     

Identification of a phospholipase C beta2 region that interacts with Gbeta-gamma

To delineate the phospholipase C (PLC; EC 3.1.4.3) beta2 sequences involved in interactions with the beta-gamma subunits of G proteins, we prepared a number of mammalian expression plasmids encoding a series of PLC beta2 segments that span the region from the beginning of the X box to the end of the Y box. We found the sequence extending from residue Glu-435 to residue Val-641 inhibited Gbeta-gamma-mediated activation of PLC beta2 in transfected COS-7 cells. This PLC beta2 sequence also inhibited ligand-induced activation of PLC in COS-7 cells cotransfected with cDNAs encoding the complement component C5a receptor and PLC beta2 but not in cells transfected with the alpha1B-adrenergic receptor, suggesting that the PLC beta2 residues (Glu-435 to Val-641) inhibit the Gbeta-gamma-mediated but not the Galpha-mediated effect. The inhibitory effect on Gbeta-gamma-mediated activation of PLC beta2 may be the result of the interaction between Gbeta-gamma and the PLC beta2 fragment. This idea was confirmed by the observation that a fusion protein comprising these residues (Glu-435 to Val-641) of PLC beta2 and glutathione S-transferase (GST) bound to Gbeta-gamma in an in vitro binding assay. The Gbeta-gamma-binding region was further narrowed down to 62 amino acids (residues Leu-580 to Val-641) by testing fusion proteins comprising various PLC beta2 sequences and GST in the in vitro binding assay.     

PLC系统在百米重轨吊运中的应用

介绍了用于多台独立吊车合车吊运百米重轨的PLC控制系统。系统采用西门子SIMATIC S7 PLC以及西门子PROFIBUS_DP现场总线控制技术,在多台吊车的PLC之间建立PROFIBUS_DP通讯连接,实现PLC与PLC之间的数据传输,以及PLC与上位机监控站的通信,使多台独立吊车在相互间没有任何物理联合的状态下,通过电气控制系统实现动作同步,实现多台吊车联合吊运百米重轨。     

Activation of phospholipase C gamma by PI 3-kinase-induced PH domain-mediated membrane targeting

Signaling via growth factor receptors frequently results in the concomitant activation of phospholipase C gamma (PLC gamma) and phosphatidylinositol (PI) 3-kinase. While it is well established that tyrosine phosphorylation of PLC gamma is necessary for its activation, we show here that PLC gamma is regulated additionally by the lipid products of PI 3-kinase. We demonstrate that the pleckstrin homology (PH) domain of PLC gamma binds to phosphatidylinositol 3,4,5-trisphosphate [PdtIns(3,4,5)P3], and is targeted to the membrane in response to growth factor stimulation, while a mutated version of this PH domain that does not bind PdtIns(3,4,5)P3 is not membrane targeted. Consistent with these observations, activation of PI 3-kinase causes PLC gamma PH domain-mediated membrane targeting and PLC gamma activation. By contrast, either the inhibition of PI 3-kinase by overexpression of a dominant-negative mutant or the prevention of PLC gamma membrane targeting by overexpression of the PLC gamma PH domain prevents growth factor-induced PLC gamma activation. These experiments reveal a novel mechanism for cross-talk and mutual regulation of activity between two enzymes that participate in the control of phosphoinositide metabolism.