小松铰卡分动箱拆装新工艺

城门山铜矿目前拥有10台小松HM400-2铰卡,自2017年设备进入大修期后,分动箱开始出现漏油及内部磨损故障,需要对分动箱进行拆卸检修。而按小松铰卡装配手册拆卸步骤,需要将变速箱和分动箱一起拆卸吊出后,才能对分动箱进行拆装及检修,需耗费大量人工。针对分动箱拆装困难的难题,我们对其安装方式及结构进行分析,研究发明一种分动箱拆装新工艺,节省了大量人工成本及检修时间,此方法亦对其他设备总成件拆装具有借鉴意义。     

桥式起重机卷扬筒装配结构改进

卷扬筒是起重机起升机构的重要部件。在日常的检修中,如更换起升机构中的易损件,势必涉及到卷扬筒的拆装,由于目前桥式起重机卷扬简装配结构设计的特点,使卷扬筒的安装和拆卸十分困难,我厂起重机检修工人在长期的经验积累中发现,只要在安装结构上稍加改进,增设一个轴承挡圈,便会使卷扬筒的拆装变得十分简便,拆装时间可从原来4小时缩短到1时左右。     

强制循环蒸发器中混流泵的应用与维护

通过对强制循环泵结构研究,针对拆卸叶轮困难,安全隐患大,进出口管道割除焊接难度大,时间长等影响混流泵检修工期的现状。找到检修过程的难点并对检修过程进行分析,找到将叶轮首先固定,再拆装轴承体总成,彻底改变混流泵检修的次序从而优化整个检修过程的全新检修模式,极大的减少检修步骤,减轻检修工作量,缩短检修工期。     

阳极炉圆盘浇铸机中心回转支撑检修的流程优化

以往对圆盘浇铸机中心回转支撑实施常规检修,需要在拆卸圆盘辐射梁、横梁及中心筒的情况下进行,检修耗时长,劳动强度大,生活效率低。通过制作专用工装,采用一步到位更换圆盘浇铸机中心回转支撑的整体拆装检修方案及配套措施,不仅可以大幅缩短检修时间,而且可以降低检修劳动强度和节省检修费用,具有较大的行业推广应用价值。     

用8t汽车起重机拆装36m^2带冷机头轮

３６ｍ＾２带冷机头轮的拆装，由于起吊高度的要求，传统上往往选用４０ｔ汽车起重机，介绍一种简便易行的方法，可用８ｔ汽车起重机替代４０ｔ汽车起重机拆装，大大节省了检修的直接和间接费用。     

中冶宝钢技术创新双边剪前板拆装新工艺

承担宝钢分公司宽厚板厂剪切线设备维检的中冶宝钢技术第二检修分公司厚板检修队自发组织研究、经工艺设计论证,研制创新双边剪前板拆装新工艺,实现安全优质、节约成本、提高工效的良好效益。     

用8t汽车起重机拆装36m^2带冷机头轮

３６ｍ＾２事实同头的拆装，由于起吊高度的要求，传统上往往用４０ｔ汽车起重机。本文介绍一各简便、易行的方法，可用８ｔ汽车起重机替代４０ｔ汽车起同拆装头轮，大大节省检修费用。     

50吨炼铜转炉风眼装置的改造

一、前言我厂50吨炼铜转炉是吹炼冰铜的主要设备。全厂共有三台转炉,每台转炉安装有20个风眼,其中使用18个。由于转炉吹炼炉龄短,炉衬检修频繁,每次检修都要拆装风管,     

TYH140F-3555型减速机检修技术

随着机械设备的结构呈现多样化和复杂化,对检修技术提出更高的要求。通过对TYH140F-3555型减速机检修技术的介绍,阐述在烧结机主传动装置拆装工艺过程中应注意的几个环节,锁紧套、扭力杆和大齿轮等主要零部件安装技术要领,从而全面掌握TYH140F-3555型减速机检修技术要点。     

宝钢宽厚板厂双边剪前板拆装新工艺研制成功

中冶宝钢技术第二检修分公司经过工艺设计论证,自主研制创新宝钢分公司宽厚板厂剪切线设备双边剪前板拆装新工艺获得成功,取得了安全优质、节约成本、提高工效的良好效益。     

转炉倾动装置的改进设计

对传统型全悬挂转炉倾动装置进行了改进设计,联轴器采用了径向弹性柱销联轴器,承载能力高,制动器与电机分装于一次减速机的前后两侧,联轴器和制动器拆装方便,有利于提高了转炉设备的运行可靠性,检修维护也更加方便。     

The penile disassembly technique in hypospadias repair

OBJECTIVE: To report experience and results with penile disassembly in hypospadias repair. PATIENTS AND METHODS: From November 1995 to May 1997 penile disassembly was used in 92 patients aged from 9 months to 32 years. The indications for operation were hypospadias with severe penile curvature (especially with curvature in the distal third of the corpora cavernosa), chordee without hypospadias, and small penis with hypospadias. The technique involves separating the penis into its component parts, i.e. the glans cap with neurovascular bundle dorsally, together with the undivided or divided urethra and urethral plate ventrally, and the corpora cavernosa. The manoeuvre allows any curvature to be corrected, especially when in the distal third of the corporal bodies, glans tilt to be rectified, and the penis to be enlarged, particularly elongated, which is a significant gain in small penises with hypospadias. RESULTS: The patients were followed for 3-20 months (mean 14); the penis was straightened in all cases, with no recurrence of curvature. In 37 patients (40%) penile disassembly combined with extensive urethral mobilization resolved the hypospadiac meatus with no need to form a neourethra; the penis was larger after surgery. Complications were related to urethroplasty and included four urethral stenoses, two fistulae and three diverticula. There was no injury to the neurovascular bundle and urethra; sensitivity and erection were preserved in all patients. CONCLUSION: The penile disassembly technique is most effective for hypospadias with severe curvature, especially for glans tilt and curvature located distally. Penile augmentation is possible using this technique.     

Evidence that a viral replicase protein is involved in the disassembly of tobacco mosaic virus particles in vivo

Tobacco mosaic virus (TMV) particles have been shown to undergo bidirectional disassembly when they are introduced into host cells. Approximately three-quarters of the genomic RNA (i.e., the 126-kDa and 183-kDa protein ORFs) is first uncoated in the 5'-to-3' direction and the process is then completed by removal of coat protein molecules in the 3'-to-5' direction. An effort was made to determine whether the 126-kDa protein or the 183-kDa protein, both of which are involved in replication of the viral RNA, is required for the second part of the disassembly reaction. It was shown that progeny negative-strand viral RNA begins to be produced in inoculated cells at about the same time that 3'-to-5' disassembly is initiated thus suggesting that the two processes may be coupled. Particles containing mutant forms of the viral RNA in which large sections of the 126-kDa and 183-kDa protein ORFs were missing were not disassembled in the 3'-to-5' direction when they were introduced into cells. However, they were disassembled when the inoculum contained purified TMV RNA from which, presumably, the two functional proteins could be translated Particles containing mutants of the RNA from which a few codons had been deleted in or near conserved regions in the 126-kDa protein ORF also did not undergo 3'-to-5' disassembly unless mixed with wild type viral RNA prior to inoculation. These results suggest that the 126-kDa and/or 183-kDa protein plays a role in the completion of disassembly of TMV particles at the onset of the infection process.     

Rho and Rab small G proteins coordinately reorganize stress fibers and focal adhesions in MDCK cells

The Rho subfamily of the Rho small G protein family (Rho) regulates formation of stress fibers and focal adhesions in many types of cultured cells. In moving cells, dynamic and coordinate disassembly and reassembly of stress fibers and focal adhesions are observed, but the precise mechanisms in the regulation of these processes are poorly understood. We previously showed that 12-O-tetradecanoylphorbol-13-acetate (TPA) first induced disassembly of stress fibers and focal adhesions followed by their reassembly in MDCK cells. The reassembled stress fibers showed radial-like morphology that was apparently different from the original. We analyzed here the mechanisms of these TPA-induced processes. Rho inactivation and activation were necessary for the TPA-induced disassembly and reassembly, respectively, of stress fibers and focal adhesions. Both inactivation and activation of the Rac subfamily of the Rho family (Rac) inhibited the TPA-induced reassembly of stress fibers and focal adhesions but not their TPA-induced disassembly. Moreover, microinjection or transient expression of Rab GDI, a regulator of all the Rab small G protein family members, inhibited the TPA-induced reassembly of stress fibers and focal adhesions but not their TPA-induced disassembly, indicating that, furthermore, activation of some Rab family members is necessary for their TPA-induced reassembly. Of the Rab family members, at least Rab5 activation was necessary for the TPA-induced reassembly of stress fibers and focal adhesions. The TPA-induced, small G protein-mediated reorganization of stress fibers and focal adhesions was closely related to the TPA-induced cell motility. These results indicate that the Rho and Rab family members coordinately regulate the TPA-induced reorganization of stress fibers and focal adhesions that may cause cell motility.     

APC-mediated proteolysis of Ase1 and the morphogenesis of the mitotic spindle

The molecular mechanisms that link cell-cycle controls to the mitotic apparatus are poorly understood. A component of the Saccharomyces cerevisiae spindle, Ase1, was observed to undergo cell cycle-specific degradation mediated by the cyclosome, or anaphase promoting complex (APC). Ase1 was degraded when cells exited from mitosis and entered G1. Inappropriate expression of stable Ase1 during G1 produced a spindle defect that is sensed by the spindle assembly checkpoint. In addition, loss of ASE1 function destabilized telophase spindles, and expression of a nondegradable Ase1 mutant delayed spindle disassembly. APC-mediated proteolysis therefore appears to regulate both spindle assembly and disassembly.     

大中型齿式联轴器的保护性拆卸

通过一台轧机主传动齿轮座输入轴齿式联轴器外齿圈的成功拆卸的例子,阐述了现场采用传统方法对大中型齿式联轴器进行保护性拆除的理论计算方法与工艺要点。     

Histamine-evoked chromaffin cell scinderin redistribution, F-actin disassembly, and secretion: in the absence of cortical F-actin disassembly, an increase in intracellular Ca2+ fails to trigger exocytosis

Histamine is a known chromaffin cell secretagogue that induces Ca(2+) -dependent release of catecholamines. However, conflicting evidence exists as to the source of Ca2+ utilized in histamine-evoked secretion. Here we report that histamine-H1 receptor activation induces redistribution of scinderin, a Ca(2+)-dependent F-actin severing protein, cortical F-actin disassembly, and catecholamine release. Histamine evoked similar patterns of distribution of scinderin and filamentous actin. The rapid responses to histamine occurred in the absence of extracellular Ca2+ and were triggered by release of Ca2+ from intracellular stores. The trigger for the release of Ca2+ was inositol 1,4,5-trisphosphate because U-73122, a phospholipase C inhibitor, but not its inactive isomer (U-73343), inhibited the increases in IP3 and intracellular Ca2+ levels, scinderin redistribution, cortical F-actin disassembly, and catecholamine release in response to histamine. Thapsigargin, an agent known to mobilize intracellular Ca2+, blocked the rise in intracellular Ca2+ concentration, scinderin redistribution, F-actin disassembly, and catecholamine secretion in response to histamine. Calphostin C and chelerythrine, two inhibitors of protein kinase C, blocked all responses to histamine with the exception of the release of Ca2+ from intracellular stores. This suggests that protein kinase C is involved in histamine-induced responses. The results also show that in the absence of F-actin disassembly, rises in intracellular Ca2+ concentration are not by themselves capable of triggering catecholamine release.     

Actin disassembles reversibly during electrically induced recycling of synaptic vesicles in cultured neurons

We have studied depolarization-induced regulation of actin assembly in exocytotically active areas of dissociated chick sympathetic neurons. Active areas were identified with the fluorescent dye FM1-43 which labels synaptic vesicles that recycle in these regions. Exocytosis (electrically stimulated) was monitored in real time through depletion of FM1-43 fluorescence. To study depolarization-induced disassembly of actin in the FM1-43-stained regions, the cells were fixed after different periods of depolarization and stained with rhodamine phalloidin, which binds preferentially to the filamentous form of actin. In active regions, actin disassembles and reassembles during continuous 2 min depolarization. Actin disassembly that occurs after the first 25 s of depolarization was detected by a reduction in rhodamine phalloidin staining and confirmed by correlative electron microscopy. Immunogold staining revealed that actin is abundant throughout resting terminals. In some experiments, actin filaments were stabilized by loading cells with unlabelled phalloidin before stimulating secretion. Stabilizing the filaments does not alter the initial release but strongly reduces the release rate at later stages. These data are consistent with a model in which partial disassembly of actin filaments is necessary for facilitating the transport of vesicles within the terminal and reassembly is necessary for limiting that movement.     

Olfactory function in monozygotic twins discordant for schizophrenia

Microtubule disassembly is commonly believed to be a process of endwise tubulin dimer release. The present study demonstrates by video interference contrast microscopy that Escherichia coli lipopolysaccharide (LPS) caused microtubule disassembly in vitro by both endwise shortening and fragmentation. In contrast, the microtubules were only shortened from their ends in the presence of DNA, used as another example of a macromolecular microtubule effector. LPS-caused microtubule fragmentation was confirmed by transmission electron microscopy. Because of its ability to induce both fragmentation and endwise shortening, LPS, which is involved in sepsis pathogenesis, has to be regarded as a highly active microtubule-destabilizing agent.