厚板拉伸异常断口分析

针对厚板进行拉伸测试时出现断口分层,断后伸长率低的问题,采用金相、扫描电镜等检验手段对问题钢种的拉伸断口进行断口形貌、非金属夹杂物、组织分布等一系列分析。研究表明,断口分层的实质为氢脆,是由于氢的存在以及钢板中非金属夹杂物、带状组织和中心偏析共同作用的结果,提出相应措施减缓氢脆断裂的发生,改善断后伸长率。     

厚规格船板钢拉伸断口分层的原因分析

针对莱钢厚规格船板钢DH36拉伸试样表面出现麻点、裂纹,拉伸断口分层,断后伸长率低的问题,利用低倍、金相及扫描电镜等分析手段,对问题试样的显微组织及断口情况进行分析。结果表明,钢板中心部位碳和合金元素偏析及夹杂物在晶界处析出导致的带状组织、魏氏组织及微裂纹是断口分层的主要原因。制定合适的加热温度,减小成分偏析,抑制心部魏氏组织,可减缓这种分层现象。     

退火工艺对鞋内包头用6061铝合金板材组织和性能的影响

通过显微组织观察、力学性能测试、杯突试验等手段研究了退火工艺参数对劳保鞋内包头用6061铝合金板材显微组织、力学性能和成形性能的影响.结果表明:随着退火温度的升高和保温时间的延长,合金由纤维状组织向再结晶组织转变,合金强度降低,伸长率和杯突值增大;而随着退火温度进一步升高,合金固溶强化效果加强,合金强度增大,伸长率和杯...     

Q460C中厚钢板伸长率不合格的原因分析

针对热轧Q460C中厚钢板在拉伸试验中出现伸长率不合格的问题,通过对拉伸试样断口形貌、断口区域的金相组织以及低倍硫印检验分析,认为钢板中夹杂物含量较高、中心偏析、中间裂纹和板材带状组织是导致伸长率不合格的主要原因,并提出相应解决措施。     

Q460C中厚钢板正火前后性能不合格原因分析

在Q460C低合金高强度中厚钢板开发过程中,通过采取微合金化和TMCP相结合的工艺措施,对轧制态伸长率不合格钢板进行正火处理,并对比分析轧制态和正火态钢板的组织、性能.结果 表明:轧制态钢板产生严重珠光体带状组织、中心局部区域M+B组织以及混晶组织,是钢板伸长率不合格的主要原因;而正火后钢板组织晶粒比正火前粗大,是屈服...     

预拉伸对6082铝合金时效组织与性能的影响

实验采用固溶淬火、预拉伸、人工时效的顺序处理合金材料,然后通过力学性能测试、金相观察等手段,分析不同预拉伸量对6082合金组织和性能的影响.结果表明,预拉伸量为0.0％～2.0％,材料的屈服强度与抗拉强度随着预拉伸量的增加而升高,伸长率下降;当预拉伸量为2.0％～6.5％时,强度值和伸长率呈缓慢下降并趋于平稳.随着预拉...     

调质型容器钢板探伤不合机理研究

调质型容器钢板生产过程中出现大批量探伤不合,通过运用金相检验、扫描电镜等手段,对探伤不合钢板的组织进行观察,发现夹杂物、中心裂纹、偏析等缺陷,分析认为中心裂纹是导致探伤不合的主要原因,并对钢板中心裂纹产生的机理进行了研究。     

压力容器用钢板Q345R延伸率不合格原因分析

针对Q345R锅炉与压力容器用钢板断后伸长率不合格的问题,利用直读光谱仪、金相显微镜、扫描电镜等设备对Q345R断后伸长率不合格试样进行了化学成分、金相组织、断口形貌等方面的检测分析。分析结果表明,钢中的硫化锰夹杂物、贝氏体组织和带状组织是造成Q345R钢板断后伸长率不合格的主要原因。通过提高铸坯炼钢冶金质量、降低锰和硫元素含量、减轻成分偏析、采用合理的控轧控冷工艺、减少异常组织产生等措施,使得Q345R钢板的断后伸长率明显提高。     

TMCP工艺对Si—Mn系贝氏体钢组织与性能的影响

研究了轧后中温缓慢冷却与中温等温两种不同的热机械控制工艺(thermomechanical control process,TMCP)对硅锰系贝氏体钢的组织与性能的影响.通过拉伸试验机测试试验钢的力学性能,利用扫描电子显微镜、电子背散射衍射等分析手段对试验钢进行显微组织结构分析,并利用X射线衍射测定残余奥氏体含量.结果表明:随着轧后连续缓慢冷却开始温度的升高,贝氏体钢的抗拉强度、硬度及拉伸应变硬化指数n值有所提高,伸长率和冲击韧性降低,屈强比先降低后升高.随着轧后等温时间的延长,贝氏体钢的抗拉强度与屈强比先降低后升高,伸长率及冲击韧性先升高后降低.相对于等温制度,连续缓慢冷却可得到更好的综合力学性能,强塑积明显高于前者,伸长率比前者高20%以上.     

退火温度对钨铼合金组织和性能的影响

采用粉末冶金工艺制备了钨铼合金,通过拉伸性能测试、硬度测试、光学显微观察等手段,研究了退火温度对钨铼合金组织和性能的影响。研究表明：锻造后的钨铼合金室温抗拉强度为1620 MPa,断后伸长率为20%,维氏硬度为HV₃₀ 540。钨铼合金在1500℃时开始发生局部再结晶,1700℃时发生晶粒长大。钨铼合金的室温抗拉强度、维氏硬度随着退火温度的提高而降低,断后伸长率随着退火温度的升高先增大后减小。     

Learning to achieve perfect timesharing: Architectural implications of Hazeltine, Teague, and Ivry (2002).

E. Hazeltine, D. Teague, and R. B. Ivry (see record 2002-02997-003) have presented data that have been interpreted as evidence against a central bottleneck. This article describes simulations of their Experiments 1 and 4 in the ACT-R cognitive architecture, which does possess a central bottleneck in production execution. The simulation model is capable of accounting for the emergence of near-perfect timesharing in Experiment 1 and the detailed data on the distribution of response times from Experiment 4. With practice, the central bottleneck in ACT-R will be reduced to a maximum of 50 ms (1 production cycle) and can often be much less, depending on timing of stages and variability in their times. The authors also show, with a mathematical analysis of E. Hazeltine et al.'s Experiment 2, that the expected dual costs for these kinds of highly practiced tasks will be small in many circumstances, often under 10 ms. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

论当量品位理论优化矿区中心孤岛境界

本文通过介绍当量品位理论在德兴铜矿铜厂矿区中心孤岛境界优化设计中的实践应用,提出开采多金属矿床的矿山企业应从境界设计上、生产控制上综合考虑多金属元素的综合回收,从而可提高资源的利用程度, 又可保证企业经济利润最大化。     

General pharmacology of loracarbef in animals

Loracarbef ((6R, 7S)-7-[(R)-2-amino-2-phenyl-acetamido]-3-chloro-8-oxo-1- azabicyclo [4.2.0]oct-2-ene-2-carboxylic acid, monohydrate, LY 163892, CAS 121961-22-6) is a carbacephem antibiotic targeted for use in the treatment of infectious disease. The potential pharmacological effects of this agent were examined on cardiovascular, respiratory, gastrointestinal, central nervous and autonomic nervous systems. Also examined were local anesthetic activity, effects on platelet aggregation, circulating blood glucose, primary antibody production, renal function, blood coagulation, ocular irritation, and the acute inflammatory response. Doses of 100, 1000, and 2000 mg/kg given by the oral route were selected for most in vivo studies. Concentrations up to 3 x 10(-3) mol/l were used in vitro. Loracarbef was essentially inactive in the tests of central and autonomic nervous system function, platelet aggregation, renal function, blood hemolysis, primary antibody production, blood coagulation, and ocular irritation. It had no local anesthetic activity. At high oral or intravenous doses, representing significant multiples of the therapeutic dose, loracarbef caused changes in gastrointestinal (decrease in gastric acid production and gastric fluid volume; increased biliary output), cardiovascular (increased mean pressure, cardiac output, heart rate, and femoral flow), blood glucose (increased glucose levels), and anti-inflammatory tests (suppressed acute inflammatory response). In summary, loracarbef exhibited minimal activity in these pharmacodynamic studies. These results indicate loracarbef has a low potential to produce adverse effects at therapeutic doses.     

D6A大型锻材白点缺陷探讨及工艺改进

根据D6A钢种探伤合格率低,试制初期探伤合格率仅有30%左右,探伤缺陷主要表现为棒材中心部位密集型缺陷等特点,制定了新的生产工艺及热处理工艺,通过新工艺改进,该钢的探伤合格率已达到80%以上,基本解决了探伤合格率低的问题。     

Effects of ginkgolides on interleukin-1, tumor necrosis factor-alpha and nitric oxide production by rat microglia stimulated with lipopolysaccharides in vitro

The effects of ginkgolide A (CAS 15291-75-5, BN52020, GA) and B (CAS 15291-77-7, BN52021, GB) on interleukin (IL)-1, tumor necrosis factor-alpha (TNF-alpha) and nitric oxide (NO) production in resting and lipopolysaccharide (LPS)-stimulated neonatal rat microglia were studied. Apafant (CAS 105219-56-5), a platelet activating factor (PAF) antagonist of triazolobenzodiazepine type was used as control. The biological activities of IL-1 and TNF-alpha were tested by mouse thymocyte proliferation and L929 cytotoxicity assay, respectively. NO concentration was represented by nitrite and determined by Griess reaction. GA 1 nmol/1-10 mumol/l inhibited IL-1 production, and 100 nmol/l-10 mumol/l decreased TNF-alpha and NO production in dose-dependent manner. GB inhibited IL-1, TNF-alpha and NO production at the concentrations 10 nmol/l-10 mumol/l, 100 nmol/l-10 mumol/l and 10 nmol/l-10 mumol/l, respectively. Apafant inhibited IL-1, but not TNF-alpha and NO production. GB plus apafant (50 mumol/l) showed IL-1 and NO inhibitory effects, but not on TNF-alpha. The manner was different from that of GB or apafant alone. The results suggested that GA and GB inhibited proinflammatory cytokines and NO production from LPS-stimulated rat microglia, however, apafant inhibited IL-1 production only. The effects of GA and GB on proinflammatory cytokines and NO production from rat microglia do not seem to be based on PAF receptor antagonism. In addition, GA and GB are regarded as promising agents for the treatment of some neurodegenerative diseases in the central nervous system.     

Design and Application of CSC-Roll for Heavy Reduction of the Bloom Continuous Casting Process

Metallurgical and Materials Transactions B - Center quality control is a key issue affecting large-section bloom production and product quality. The central convex roll could avoid the bloom side...     

Isolation and characterization of the human prosaposin promoter

Male C57BL/6N mice were chosen to determine Fos production during acquisition of context-dependent fear and after re-exposure to the conditioning context. Fear-conditioning was induced by a single exposure of mice to a context followed by an electric shock. Control groups consisted of mice exposed to context only (Context group) or to an immediate electric shock. When contextual retention was measured 24 h after conditioning (retention test 1), significant contextual generalization was observed. However, when animals were exposed to a different context from days 2-5 after conditioning and then tested for retention on day 6 (retention test 2), generalization was markedly reduced. After the training, the fear-conditioned mice produced higher Fos levels than mice exposed to an immediate shock in the hippocampus, medial amygdaloid nucleus and parietal somatosensory cortex. Both shock groups produced significantly more Fos than the Context group in the central nucleus of the amygdala. After retention test 1, fear-conditioned mice generated more Fos in the hippocampus and central amygdaloid nucleus than the two control groups. However, all groups exhibited similarly low Fos production after retention test 2. The results demonstrated that simultaneous Fos production in the hippocampus, central and medial nuclei of amygdala and somatosensory parietal cortex closely paralleled the ability of mice to acquire conditioned fear. In contrast, Fos production after the retention tests did not correlate with the expression of conditioned fear.     

Induction of antigen-specific tolerance for the treatment of ongoing, relapsing autoimmune encephalomyelitis: a comparison between oral and peripheral tolerance

Experimental autoimmune encephalomyelitis (EAE) is a T cell-mediated autoimmune demyelinating disease of the central nervous system that serves as an animal model for multiple sclerosis. Various forms of Ag-specific tolerance have been used prophylactically to prevent development of acute EAE. Here we compare the induction of Ag-specific tolerance using two regimens, proteolipid protein 139-151 (PLP139-151) peptide-coupled splenocytes and oral administration of PLP139-151, for efficacy in the reduction of established, chronic clinical EAE. PLP139-151-coupled splenocytes and not oral administration of PLP139-151 was able to down-regulate established EAE, including subsequent relapses. PLP139-151 peptide-coupled splenocytes were effective at reducing Ag-specific T cell proliferation and IL-2 and IFN-gamma production, while concomitantly increasing IL-4 production. Oral administration of PLP139-151 did not reduce IL-2 or IFN-gamma production and appeared to increase Ag-specific T cell proliferation. Neither multiple high nor low doses of PLP139-151 were effective at decreasing ongoing clinical EAE or PLP139-151-specific IL-2 and IFN-gamma production. These results suggest that PLP139-151 peptide-induced tolerance is an efficacious treatment for ongoing, R-EAE when the peptide is coupled to chemically fixed splenocytes and not when given orally.     

2Cr12NiMo1WlV不锈钢Φ180mm棒材低倍中心黑色区缺陷分析和退火工艺改进

2Cr12NiMo1W1V钢Φ180mm棒材的生产工艺流程为80t BOF-VD-LF-ESR 6t锭-锻造-900℃退火。2Cr12NiMo1W1V不锈钢棒材成品低倍组织中出现GB/T1979-2001《结构钢低倍组织缺陷评级图》中无对应类型的中心黑色腐蚀区域缺陷,分析得出,该钢退火后的正常组织为铁素体基体+碳化物,而中心区域为板条马氏体+托氏体,托氏体耐腐蚀性差,形成黑色区域。将原先的退火工艺优化为900℃-700℃等温退火工艺,可保证全截面组织的均匀转变。该工艺可消除和避免2Cr12NiMo1W1V钢棒材中心黑色区域。     

Expression and release of tumor necrosis factor-alpha by explants of mouse cornea

PURPOSE: To elucidate a possible target of immunosuppressive agents widely used in the treatment of corneal disorders, the authors determined whether corneal cells are capable of expressing and releasing tumor necrosis factor-alpha (TNF alpha) on lipopolysaccharide (LPS) stimulation, and they investigated whether TNF alpha production can be modulated by pharmacologic agents. METHODS: Trephined central corneas from C57BL/6 mice were kept in culture for 3 days. Release of TNF alpha after a 24-hour stimulation with LPS (1 microgram/ml) into the culture medium was determined both by bioassay and by enzyme-linked immunosorbent assay. Expression of TNF alpha mRNA after 6-hour stimulation was examined by polymerase chain reaction. Immunofluorescent staining on cryostat sections of cultured corneas was performed to localize TNF alpha in the tissue. Corneal explants were pretreated with immunosuppressive agents (prednisolone, budesonide, cyclosporin A) for 48 hours, followed by 6-or 24-hour stimulation with LPS in the continuous presence of the agents. RESULTS: Lipopolysaccharide stimulated TNF alpha release into the culture medium. The addition of budesonide (10(-7) M) or prednisolone (10(-6) M) significantly inhibited LPS-induced TNF alpha release, whereas cyclosporin A (10(-7) - 10(-5) M) had no marked effect. Levels of TNF alpha mRNA in corneal explants increased fivefold after stimulation with LPS. Immunohistochemical staining revealed that TNF alpha was expressed in the epithelial cells. Budesonide markedly decreased mRNA expression and abolished immunostaining of TNF alpha stimulated by LPS. CONCLUSIONS: TNF alpha is produced and released by the epithelial cells of mouse central cornea in response to LPS. Contrary to cyclosporin A, corticosteroids such as prednisolone and budesonide potently inhibit TNF alpha production.