2300XP电铲电控系统的国产化数字化改造

本文针对2300XP电铲电控系统原设计中存在的问题进行分析,阐述了德兴铜矿电铲国产化数字化电控系统成功改造的实例及引发的思考。     

关于延长2300XP电铲履带架寿命的探讨

从结构、受力入手,分析了2300XP电铲履带架容易损坏的原因,提出了改进方案。     

2300XP电铲勺杆的矫正

2300XP电铲是德兴铜矿采矿重要设备,因服役年限很长等多方面原因,所有电铲勺杆均出现不同程度的变形,制约了电铲的效率。针对2300XP电铲勺杆实际变形情况,结合勺杆的材质,采用合理的工艺对变形的勺杆进行修复,将能直接影响修复后的勺杆实际使用寿命。通过反复实践,我们采用火焰矫正工艺,对弯曲的勺杆空腹梁进行变形矫正并取得了成功,对类视焊接结构件的修理有一定的借鉴作用。     

WK-35电铲AFE柜检查及常见启动故障分析

随着德兴铜矿采矿日生产量13万t扩能,2010年首次购买了WK-35型电铲,与以往的2300XPA/C电铲相比,最大的区别就是其控制系统采用了更先进的交流变频调速系统。简要介绍了变频调速系统的组成及工作原理。在生产实践中积累了大量的维修经验,详细阐述了AFE柜的上电检查内容及常见启动故障解决措施。     

分流线路在2300XPC电铲的应用探讨

电铲的运行好坏将直接影响着矿山的生产能力,然而电铲在恶劣的环境下作业,电铲的分流保护线路容易失效,阐述了分流线路的工作原理及在2300xpc电铲上的应用,探讨分析了分流线路的可靠性及存在的主要问题,并对分流线路的故障及处理提出了合理的解决办法及建议,使电铲更安全、可靠地运行,为企业节约了成本。     

2300XPC电铲无功功率补偿断路器的改进

2300XPC电铲电气采用国外先进的直流调速系统,无功功率补偿柜提供整流器所需要的无功功率补偿,同时在挖掘机正常运行期间过滤电气系统所产生的主要谐波,因此我们采用的是进口无功功率补偿断路器。无功功率补偿断路器的工作原理是RPC柜内的电抗器和电容发生短路而起到一种保护作用从而防止其他电气柜发生更严重的损坏。无功功率补偿断路器在南方野外下雨环境下,易出现无功功率补偿断路器600V电压会串入低压辅助触点信号线,导致RPC远程站柜内元件大部分烧坏严重,影响电铲的稳定性。经过几个月不断改进,减少了电铲无功补偿断路器的故障时间,大大提高了电铲的可开动率。     

电气自动化控制设备故障预防与检修技术探析

随着近些年来电气自动化的快速发展,电气自动化技术以及自动化质量被电气行业越来越关注,并且在电气自动化技术中控制设备起到非常重要的作用,但是控制设备也是电气自动化中最容易出现问题的一环,当控制设备出现故障的时候往往会影响到整个控制设备的运行,基于此,我们在对电气自动化控制设备的运行以及自动化设备的故障预防和检修技术方面应该更加大力的发展.文章就将对电气控制设备的故障进行分析,并且对故障的预防进行更加深入的探讨,为了电气行业的自动化生产可以正常使用技术提供了一定的参考.     

电铲除尘通风装置的改造

电铲上使用现有除尘通风装置系统已难以满足日益提高的矿山作业现场安全生产环保要求.以2300XPA型电铲除尘通风装置为例,对电铲除尘通风装置原设计中存在的问题进行分析,提出电铲除尘通风装置改造的可行性方案,并组织实施,取得良好的效果.该方案对其他型号电铲除尘装置的改造具有一定的借鉴和指导意义.     

行车电气故障分析与处理

<正>1前言2011年炼铁A区煤棚行车故障222起,其中行车电气故障占总故障的78%。统计电气故障种类主要有:电缆故障,占电气故障的30%;电气元件损坏,占70%。说明电气元件的损坏是造成行车故障主要原因。2分析与处理2.1原因分析A区煤棚行车提升、开闭电机的调速电阻同档位的切换设计采用同一接触器来完成,在抓煤的时候,若开闭主令控制器已打到第三档,开闭电机的调速电阻切完,此时若马上操作提     

电铲备件国产化获突破

江铜德兴铜矿现有12台电铲,其中5台2300XP电铲使用年限均已达到15年。由于使用年限长,其结构件和总成件老化严重,不但维修成本高,而且严重影响设备的使用效率。为了保证电铲的正常运行,急需购买一套履带架部件。但电铲主机厂美国P＆H公司两个月后回复是,一套履带架部件报价高达154万多美元,即使采用由P＆H公司监制、国内合作制造的方式,价格也高达70万美元／套,为此,实施国产化成为唯一的出路。公司相关单位积极寻求与国内大中型国有企业合作,     

基于S7-300的挖掘机无功补偿系统

2300XP型矿用挖掘机,其无功补偿控制系统采用2组副边就地补偿方式,控制电路由集成运放组成其温漂大,精度差,故障率高。为此将其改造成基于S7-300型PLC为主的数字控制,给出了具体的硬件构成,软件程序。从根本上杜绝了故障源,完全适应挖掘机现场作业,经实测功率因数在0.9以上,控制精确,投资少,效果显著。     

Development of a new easy complementation assay for DNA repair deficient human syndromes using cloned repair genes

Nucleotide excision repair (NER)-deficient human cells have been assigned so far to a genetic complementation group by a somatic cell fusion assay and, more recently, by microinjection of cloned DNA repair genes. We describe a new technique, based on the host cell reactivation assay, for the rapid determination of the complementation group of NER-deficient xeroderma pigmentosum (XP), Cockayne's syndrome (CS) and photosensitive trichothiodystrophy (TTD) human cells by cotransfection of a UV-irradiated reporter plasmid with a second vector containing a cloned repair gene. Expression of the reporter gene, either chloramphenicol acetyltransferase (CAT) or luciferase, reflects the DNA repair ability restored by the introduction of the appropriate repair gene. All genetically characterized XP, CS and TTD/XP-D cells tested failed to express the UV-irradiated reporter gene, this reflecting their NER deficiency whereas cotransfection with the repair plasmid expressing a gene specific for the given complementation group increased the enzyme activity to the level reached by normal cells. Selective recovery of both reporter enzyme activities was observed after cotransfection with the XPC gene for the XP17VI cells and with the XPA gene for both XP18VI and XP19VI cells. Using this method, we assigned three new NER-deficient human cells obtained from patients presenting clinical symptoms described as classical XP to either XP group A (XP18VI and XP19VI) and XP group C (XP17VI). Therefore, this technique increases the range of methods now available to determine the complementation group of new NER deficient patients with the advantage, unlike the somatic cell fusion assay or the microinjection procedure, of being simple, rapid, and inexpensive.     

Xeroderma pigmentosum complementation group G associated with Cockayne syndrome

Xeroderma pigmentosum (XP) and Cockayne syndrome (CS) are two rare inherited disorders with a clinical and cellular hypersensitivity to the UV component of the sunlight spectrum. Although the two traits are generally considered as clinically and genetically distinct entities, on the biochemical level a defect in the nucleotide excision-repair (NER) pathway is involved in both. Classical CS patients are primarily deficient in the preferential repair of DNA damage in actively transcribed genes, whereas in most XP patients the genetic defect affects both "preferential" and "overall" NER modalities. Here we report a genetic study of two unrelated, severely affected patients with the clinical characteristics of CS but with a biochemical defect typical of XP. By complementation analysis, using somatic cell fusion and nuclear microinjection of cloned repair genes, we assign these two patients to XP complementation group G, which previously was not associated with CS. This observation extends the earlier identification of two patients with a rare combined XP/CS phenotype within XP complementation groups B and D, respectively. It indicates that some mutations in at least three of the seven genes known to be involved in XP also can result in a picture of partial or even full-blown CS. We conclude that the syndromes XP and CS are biochemically closely related and may be part of a broader clinical disease spectrum. We suggest, as a possible molecular mechanism underlying this relation, that the XPGC repair gene has an additional vital function, as shown for some other NER genes.     

Relationship of the xeroderma pigmentosum group E DNA repair defect to the chromatin and DNA binding proteins UV-DDB and replication protein A

Cells from complementation groups A through G of the heritable sun-sensitive disorder xeroderma pigmentosum (XP) show defects in nucleotide excision repair of damaged DNA. Proteins representing groups A, B, C, D, F, and G are subunits of the core recognition and incision machinery of repair. XP group E (XP-E) is the mildest form of the disorder, and cells generally show about 50% of the normal repair level. We investigated two protein factors previously implicated in the XP-E defect, UV-damaged DNA binding protein (UV-DDB) and replication protein A (RPA). Three newly identified XP-E cell lines (XP23PV, XP25PV, and a line formerly classified as an XP variant) were defective in UV-DDB binding activity but had levels of RPA in the normal range. The XP-E cell extracts did not display a significant nucleotide excision repair defect in vitro, with either UV-irradiated DNA or a uniquely placed cisplatin lesion used as a substrate. Purified UV-DDB protein did not stimulate repair of naked DNA by DDB- XP-E cell extracts, but microinjection of the protein into DDB- XP-E cells could partially correct the repair defect. RPA stimulated repair in normal, XP-E, or complemented extracts from other XP groups, and so the effect of RPA was not specific for XP-E cell extracts. These data strengthen the connection between XP-E and UV-DDB. Coupled with previous results, the findings suggest that UV-DDB has a role in the repair of DNA in chromatin.     

Descriptive features of gastric ulcers: do endoscopists agree on what they see?

The alkaline single cell gel test (SCG test or comet assay) was used to study the contribution of excision repair activity to the observed DNA effect after mutagen treatment. The cytotoxicity and genotoxicity of UV-irradiation and the chemical mutagens 4-nitroquinoline-1-oxide (4NQO), benzo[a]pyrene (BP) and 7,12-dimethyl-benz[a]anthracene (DMBA) were compared in a normal human cell line (MRC5CV1) and an excision-deficient xeroderma pigmentosum (XP) cell line (XP12ROSV). The XP cells showed increased cell killing after treatment with all mutagens tested, but did not show a clear increase in DNA migration in the comet assay. DNA effects in MRC5 cells were strongly enhanced by the repair inhibitor aphidicolin (APC), while under the same experimental conditions, APC had no effect on the XP cell line. The enhancing effect of APC on DNA migration in MRC5 cells and the lack of effects in XP cells indicate that the induced DNA effects of 4NQO, BP and DMBA in the comet assay mainly represent the activity of an excision repair process.     

Proteins that participate in nucleotide excision repair of DNA in mammalian cells

The most versatile strategy for repair of damage to DNA, and the main process for repair of UV-induced damage, is nucleotide excision repair. In mammalian cells, the complete mechanism involves more than 20 polypeptides, and defects in many of these are associated with various forms of inherited disorders in humans. The syndrome xeroderma pigmentosum (XP) is associated with mutagen hypersensitivity and increased cancer frequency, and studies of the nucleotide excision repair defect in this disease have been particularly informative. Many of the XP proteins are now being characterized. XPA binds to DNA, with a preference for damaged base pairs. XPC activity is part of a protein complex with single-stranded DNA binding activity. The XPG protein is a nuclease.