高炉炉缸活性的分析探讨

高炉安全长寿、降低高炉能源消耗成为现代高炉技术发展的主要方向,而其关键在于提高高炉炉缸活性.在介绍高炉炉缸活性变差特征的基础上,从高炉上部调剂、下部调剂、渣铁物性、高炉原燃料性能等方面,就如何提高高炉炉缸活性进行了分析和探讨.     

我国高炉工艺设计的技术进步

对我国高炉工艺设计的技术进步进行了阐述,认为在高炉大型化、高富氧高风温大喷煤、高效长寿高炉技术、高风温热风炉、高炉煤气干式布袋除尘、高炉煤气压力能回收、高炉设备和耐火材料国产化等方面取得了长足的发展,并指出了我国高炉生产面临的问题.     

关于高炉炉缸长寿的关键问题解析

 高炉长寿化是大型高炉发展的必然趋势,实现高炉长寿的关键在于弄清高炉侵蚀的根本原因。从高炉炉缸侵蚀机理、高炉炉缸象脚型侵蚀原因、高炉炉缸圆周方向侵蚀不均匀性、高炉冷却强度与冷却效率以及高炉炉缸维护技术等5个方面探讨了高炉长寿存在的共性问题,指出高炉炉缸炭砖损毁的本质是碳不饱和铁水对炭砖的溶蚀。具体结果表明,首先,高炉炉缸象脚型侵蚀最严重部位位于高炉炉缸死料柱的根部位置;其次,阐明了直接导致高炉存在不均匀侵蚀的主要原因在于冷却系统的冷却水量和送风系统的风量在高炉周向方向分配不均匀;然后,阐明了冷却系统的作用本质是降低耐火材料热面温度,并提出了高炉冷却强度指数及高炉冷却效率指数;最后,分析了采用无钛矿护炉和钛矿护炉两种模式的高炉炉缸维护技术。     

炼铁厂高炉供水及水质稳定的探讨

介绍了唐钢炼铁厂高炉安全供水、高炉水冷却、高炉水水质稳定工艺,重点阐述了高炉正常供水和事故供水系统的改造,改造后满足了高炉生产要求。     

高炉装备长周期稳定生产实践

联合特钢通过高炉关键装备的技术改进,延长了高炉装备的使用寿命,高炉设备的检修周期由60～90 d延长至180～270 d;建立高炉长周期低休风率管控技术,高炉休风率降低至0.5%,实现了高炉的长周期低休风率运行;建立完善的设备运行管理制度,落实高炉全设备一体化管控制度,提高了高炉系统的稳定性,实现了高炉生产的低耗、多产、高效、长寿的目标。     

汉钢1号高炉技术改进

汉钢1号高炉2020年4月份进行了中修,主要更换了高炉冷却壁,处理热风炉拱顶,对高炉的水系统、检测系统进行了升级改造,高炉送风后采取了一系列操作技术方法,经过实践,在技术指标提升、高炉安全运行方面总结出适合1号高炉的操作管理办法,实现了高炉的安全、稳定、低耗、高效生产。     

武钢高炉燃料比波动的影响因素

针对武钢高炉在同一段时期内不同高炉燃料比差异很大的情况,重点从焦炭质量、烧结矿质量、高炉炉身热效率、碱金属及锌危害、铁钢不平衡等方面,探讨了造成高炉燃料比波动的原因。认为,焦炭水分的大幅上升期间,能造成高炉燃料比增加10～15kg/t。另外,与8号高炉相比,4、5号高炉燃料比明显偏高,其原因一是4、5号高炉的炉身热效率明显要低于8号高炉,二是4、5号高炉原料中的碱金属偏高,尤其锌负荷长期在0.4kg/t以上。     

高炉系统氯元素研究进展及未来展望

 为明晰高炉中的氯元素对干法除尘高炉冶炼过程的影响,综述了高炉入炉料中氯元素的赋存状态、行为以及所带来的危害。进一步采用离子色谱法研究了国丰1号1 780 m3干法除尘高炉氯元素的来源, 焦炭和喷吹煤粉带入高炉中氯所占入炉料带入高炉中氯总量的比例分别为45.4 %和29.48 %, 而宝钢、唐钢和迁钢的3座干法除尘高炉中氯的来源主要是烧结矿,其比例分别为47.12 %、43.59%和44.89%,这主要与高炉入炉料种类、用量以及氯元素质量分数的不同有关,所以在对待高炉氯元素来源问题上应该具体高炉具体分析。通过热力学分析得出高炉入炉料中的氯化物在高炉内主要生成HCl,基于对高炉系统氯元素的研究,提出了高炉的降氯措施,并展望了高炉系统氯元素的未来研究方向。     

炼铁厂高炉供水问题及改造探讨

阐述了唐钢炼铁厂高炉安全供水、高炉水冷却、高炉水水质稳定问题,重点介绍了高炉正常供水和事故供水补水系统的改造,改造后满足了高炉生产。     

首钢长钢8号高炉长寿生产实践

高炉长寿是一项系统工程,仅靠任何单一技术无法实现高炉长寿目标,必须统筹考虑高炉设计、砌筑、维护及操作等各个环节。首钢长钢8号高炉第二代炉龄在加强高炉长寿方面通过建立完善的监控设施、推行高炉长寿体检管控模式、建立数据化研判机制、推行护炉措施、控制边缘气流、在线更换冷却壁、炉衬喷补以及精细化高炉操作等措施,实现了高炉稳定顺行,单位炉容产铁量10 640 t/m³,达到长寿高炉标准。     

The S1(1A1)-S0(1A1) Electronic Transition of Jet-Cooled o-Difluorobenzene

Retinal pigment epithelium transplantation has been proposed as adjunctive treatment for age-related macular degeneration following surgical excision of choroidal neovascular membranes. The goal of this study was to develop a model to evaluate retinal pigment epithelium transplantation onto human Bruch's membrane in vitro. We investigated the ability of cultured fetal human retinal pigment epithelium to colonize human cadaver Bruch's membrane, determined the incubation time needed to form a monolayer and to exhibit apical microvilli and tight junctions, and assessed the production of basement membrane. Freshly enucleated (less than 48 hours old) human eyes were cut through the pars plana, and the anterior segment, vitreous, and retina were removed. The native retinal pigment epithelium was debrided with a surgical sponge. Bruch's membrane and choroid at the macula were trephined with a 7.0 mm diameter trephine and then incubated with 1/2 ml of Dulbecco's modified Eagle's medium +15% fetal calf serum+basic fibroblast growth factor (1 ng ml-1), and fetal human retinal pigment epithelium at a concentration of 242,000 cells ml-1. Specimens were incubated for 1, 4, 6, 8, 12, or 24 hours. The specimens were fixed in half strength Karnovsky's fixative, processed, and analysed with scanning and transmission electron microscopy. The retinal pigment epithelium covered the debrided macular specimens to different degrees at different incubation times. After 1 hour, the cells started to attach and flatten (median percent coverage: 78%). The extent of Bruch's membrane coverage by fetal retinal pigment epithelium varied greatly between specimens. After 4-6 hours, the cells covered the entire debrided surface in a monolayer (median percent coverage: 97.2% at 4 hours, 99.8% at 6 hours). Tight junctions were observed, and the cells had few apical microvilli. The lateral cell borders were obliquely oriented with respect to Bruch's membrane, and the nuclei were elongated, exhibited prominent nucleoli, and were oriented parallel to Bruch's membrane. After 6-8 hours, cells started to become hexagonal (median percent coverage at 8 hours: 99.97%). Cells attached to the inner collagenous layer tended to be flatter than cells attached to residual native basement membrane. At 12 and 24 hours, expression of hexagonal shape, tight junctions, and apical microvilli were observed more frequently (median percent coverage: 99.87% at 12 and 100% at 24 hours). No newly formed basement membrane was observed at these time points. In separate experiments comparing attachment in the presence and absence of native RPE basement membrane, the presence of native retinal pigment epithelial basement membrane promoted the early attachment of the cells and more rapid expression of normal morphology. This in vitro system provides a reproducible way to study the adherence of retinal pigment epithelium to normal and diseased human Bruch's membrane.     

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NF1 (neurofibromatosis type 1)

Several distinct Ras GTPase activating proteins (GAPs) from mammals, including Ras GAP of 120 kDa (GAP1) and NF1, stimulate the intrinsic GTPase activity of normal Ras, but not oncogenic Ras mutants (Trahey and McCormick, 1987). That is the reason why normal Ras remains predominantly in the inactive GDP-bound form (D-Ras), whereas oncogenic Ras remains constitutively in the active GTP-bound form (T-Ras). NF1 is a tumor suppressor of 2818 amino acids whose disruption or deletion causes brain tumors called neurofibromatosis type 1 by elevating the T-Ras level. T-Ras activates several distinct oncogenic effectors, including Ser/Thr kinase Raf, GAP1, P1-3 kinase, PKC-zeta and Ra1 GDS. Interestingly, the binding of T-Ras to either GAPs or these oncogenic effectors requires the same effector domain I (residues 32-40) of T-Ras molecule. In other words, these GAPs and effectors compete for binding to T-Ras. Using a series of N- and C-terminal deletion mutants of NF1, we identified a 78 amino acid fragment (NF78, residues 1441-1518) as the minimum GAP domain, and a 56 amino acid fragment (NF 56, residues 1441-1496) as the minimum Ras-binding domain. Furthermore, we identified the Raf fragment of 81 amino acids (Raf81, residues, 51-131) as the minimum Ras-binding domain with a high affinity. We found that (i) these NF1 fragments and Raf81 compete for binding to T-Ras, and that (ii) over-expression of these NF1 or Raf fragments strongly suppresses the malignant transformation caused by oncogenic Ras mutants. Thus, these agents offer a unique opportunity to control the proliferation of T-Ras-associated tumors that represent more than 30% of all human carcinomas including neurofibromatosis type 1.     

Modulation of JunD.AP-1 DNA binding activity by AP-1-associated factor 1 (AF-1)

AP-1-associated factor 1 (AF-1), is a novel protein complex that dramatically enhances the assembly of JunD-containing dimers onto AP-1 consensus sites. We describe the partial purification of AF-1 from nuclear extracts of the T-cell line MLA 144 by ionic, hydrophobic and gel filtration chromatography. AF-1 is a DNA-binding protein composed of low molecular mass polypeptides of 7-17 kDa that exists in solution as a 34-kDa complex. JunD interactions with DNA are accelerated in the presence of AF-1 through the formation of a true tri-molecular complex with JunD dimers and DNA that assembles much more rapidly on DNA than JunD alone. DNA binding analysis of AF-1 interaction with JunD.AP-1 and DNA shows that AF-1 increases the DNA binding affinity of JunD for AP-1 sites over 100-fold. DNA cleavage footprint analysis of isolated AF-1.JunD DNA complexes shows that the ternary complex makes nearly twice as many contacts with DNA than JunD dimers alone. AF-1 interacts readily, but differentially with Jun homodimers and Jun.Fos heterodimers. These findings distinguish AF-1 as a significant protein-specific modulator of AP-1.JunD in T-cells.