我国中厚板生产设备、工艺技术的发展

结合我国近年自主建设的中厚板轧机,介绍了我国在中厚板生产设备、工艺技术方面所进行的研究开发工作和取得的重要进展.中厚板的核心轧制技术,即强力中厚板轧机、轧后控制冷却系统、中厚板轧制的TMCP技术、尺寸精度自动控制、组织性能预测与控制技术、中厚板轧机的计算机控制系统等,已经成功地应用于我国自行开发的中厚板生产线上,表明我国已经具备了具有我国自主知识产权的成套的中厚板生产、设备和自动化技术,我国正在变为中厚板生产强国.     

中厚板控制轧制过程机的设计与应用

结合国内某中厚板轧机改造项目，从控制轧制过程机的设备入手，系统的阐述了控轧过程机的具体功能设计以及数据库设计，并对其中过程机采用的数学模型设定、修正计算和轧件过程跟踪控制作了分析。现场应用结果表明，通过基础自动化的液压AGC控制和过程机模型的自学习，能够获得较高的模型预设定精度和良好的在线修正效果。     

中厚板轧机工况在线监测系统的探讨

分析了中厚板轧机工况在线监测系统的必要性、实用性，同时对中厚板轧机工况在线监测系统的功能、构成、硬件和软件配置及应用前景做了详细的技术阐述。     

结合模型自适应的神经元网络在中厚板轧机轧制力预报中的运用

在中厚板生产过程中,用传统轧制力模型预报中厚板轧机轧制力时存在着较大的误差.为了提高中厚板轧机轧制力的预报精度,采用轧制力模型自适应与人工神经元网络相结合的方法进行中厚板轧制力的在线预报.应用结果表明,采用本方法预报轧制力时精度优于传统的数学模型,相对误差可以控制在±3%以内.     

中厚板轧机工况在线监测系统

介绍了中厚板轧机工况在线监测系统的构成与原理及其在中厚板轧机上的应用情况。     

中厚板平面形状计算机控制系统

基于对中厚板平面形状控制具体特点的分析与研究,提出了中厚板平面形状控制方案。以分布式计算机控制系统作为控制计算机,以三机架冷连轧机第２机架作为模拟同进行了研究,并给出实验结果。     

中厚板轧制过程消除侧弯的两侧辊缝在线调整模型

分析了中厚板轧制过程中两侧辊缝差、轧件入口横向楔形、轧件两侧温度差和轧机两侧刚度差对中厚板两侧厚度偏差的影响。根据实时检测的轧制力、辊缝等数据,利用轧机刚度和轧件塑性系数推导了消除侧弯的两侧辊缝在线自动调整模型。该模型在国内某3 500 mm轧机上进行在线应用,40 mm以下成品钢板两侧厚度偏差控制在0.12 mm以内,消除薄宽规格钢板的刮框事故,轧后钢板的侧弯得到有效控制。     

中厚板轧制过程中的辊缝设定模型及其应用

结合首钢3500mm轧机改造项目，根据中厚板轧制工艺的特点，详细分析了中厚板轧制过程中辊缝设定模型的各种影响因素，并给出了相应的高精度补偿模型，如轧机的自然刚度、油膜厚度变化等。分析了轧件入口厚度偏差对辊缝设定的影响及其在线消除。现场的在线应用结果表明：运用给出的辊缝设定模型，可以大幅提高中厚板轧机的辊缝设定精度，为厚度精度的提高和AGC控制打下了良好的基础。     

中厚板辊式淬火机淬火工艺自动控制系统开发及应用

为满足中厚板热处理线高强度板材产品的淬火工艺开发需要,通过构建基础自动化和过程自动化两级控制系统,自主开发出中厚板辊式淬火机淬火工艺控制系统。基础自动化用于满足淬火机的顺序控制、逻辑控制及设备控制功能,工艺过程控制用于实现淬火工艺参数的模型计算及设定,实现了中厚板辊式淬火机淬火过程的自动控制。将该工艺系统用于中厚板淬火工艺开发及生产,淬火后板材平直度及性能指标达到或优于国外同类进口先进设备的工艺技术水平。     

济钢中厚板厂粗轧机工况在线监测系统的应用实践

表述了中厚板粗轧机工况在线监测的必要性、现实性，对粗轧机工况在线监测系统的原理、组成、功能及其应用实践作了系统的技术阐述。     

Enhancement of postischemic myocardial stunning by calcium overload in hearts of diabetic rats

The effects of Ca2+ concentration on postischemic myocardial stunning were studied in isolated working hearts of rats with streptozotocin-induced diabetes and of age-matched control rats. During reperfusion after 10 min of ischemia, hearts from control rats showed complete recovery of cardiac function of Ca2+ concentrations of 1.25, 1.88, and 2.50 mmol/L, while the recovery of diabetic rats was decreased only at a Ca2+ concentration of 2.50 mmol/L. Although myocardial Na+ and Ca2+ concentrations were comparable between control and diabetic rats, only diabetic rats showed increases in myocardial concentration of Na+ during ischemia and Ca2+ during reperfusion at a Ca2+ concentration of 2.50 mmol/L. Results suggest that diabetic rat hearts are vulnerable to postischemic stunning via an overload of calcium.     

Dietary and physiological studies to investigate the relationship between calcium and magnesium signalling in the mammalian myocardium

This study employs both dietary and physiological studies to investigate the relationship between calcium (Ca2+) and magnesium (Mg2+) signalling in the mammalian myocardium. Rats maintained on a low Mg2+ diet (LMD; 39 mg Kg-1 Mg2+ in food) consumed less food and grew more slowly than control rats fed on a control Mg2+ diet (CMD; 500 mg Kg-1 Mg2+ in food). The Mg2+ contents of the heart and plasma were 85 +/- 3% and 34 +/- 6.5%, respectively relative to the control group. In contrast, Ca2+ contents in the heart and plasma were 177 +/- 5% and 95 +/- 3%. The levels of potassium (K+) was raised in the plasma (129 +/- 16%) and slightly decreased in the heart (88 +/- 6%) compared to CMD. Similarly, sodium (Na+) contents were slightly higher in the heart and lowered in the plasma of low Mg2+ diet rats compared to control Mg2+ diet rat. Perfusion of the isolated Langendorff's rat heart with a physiological salt solution containing low concentrations (0-0.6 mM) of extracellular magnesium [Mg2+]o resulted in a small transient increase in the amplitude of contraction compared to control [Mg2+]o (1.2 mM). In contrast, elevated [Mg2+]o (2-7.2 mM) caused a marked and progressive decrease in contractile force compared to control. In isolated ventricular myocytes the L-type Ca2+ current (ICa,L) was significantly (p < 0.001) attenuated in cells dialysed with 7.1 mM Mg2+ compared to cells dialysed with 2.9 microM Mg2+. The results indicate that hypomagnesemia is associated with decreased levels of Mg2+ and elevated levels of Ca2+ in the heart and moreover, internal Mg2+ is able to modulate the Ca2+ current through the L-type Ca2+ channel which in turn may be involved with the regulation of contractile force in the heart.     

Conditions Favoring Superconditioning of Irrelevant Conditioned Stimuli.

Three appetitive conditioning experiments with rats found partial learning of complex XA+ , XB+ , XAB- (+ stands for reinforced; - stands for unreinforced) negative patterning discriminations with intermixed A+ and B+ trials (Experiment 1). AB+ trials (Experiment 2), and A+ , B+ , and AB+ trials (Experiment 3). In all experiments, differential responding emerged more slowly during the learning of the negative patterning discriminations than during learning of the XA+ , XB+ , XC- control discriminations. Additionally, the negative patterning groups responded more to X than to a separately reinforced Y on unreinforced test trials: thus, X derived superexcitatory properties. This pattern was reversed in the control groups. Results are consistent with theories that allow for different activation patterns when elements are combined. (PsycINFO Database Record (c) 2011 APA, all rights reserved)     

The role of the clinical psychologist in gynecological cancer

To assess the gamma delta TCR T cells in the control of the timing of the mucosal response to enteric parasitic infections, we used C57BL mice, orally infected with 200 viable T. spiralis larvae. The small intestine, spleens and Peyer's patches (PP) were excised on 1, 4, 7, 14, 21 and 29 postinfection days (p.i.) for immunophenotyping and histological studies. Uninfected mice served as control. Characterization of isolated lymphocytes of C57BL control mice, confirmed that T cell immunophenotype differs in spleen, PP and i-IEL. Practically all i-IEL were CD3+ cells (83%). In addition, most of the i-IEL expressed Ly-2 (65%). Among the i-IEL, the level of gamma delta TCR+ cells was significantly higher (29%) than that found in spleen (3%) and PP (3%). The expression was high on CD3+ and Ly-2+ (26 and 21%, respectively) and low on L3T4+ i-IEL (< 1%). During T. spiralis infection alpha beta TCR+ CD3+, gamma delta TCR+ CD3+ and gamma delta TCR+ Ly-2+ i-IEL increased on day 4 and 7. However, infected mice displayed a reduction in i-IEL number from 14 to 29 p.i. day. At the same time the proportion of gamma delta TCR on spleen Ly-2+ and on PP CD3+ and Ly-2+ cells increased on 14 and 21 p.i. day. Adult worms were expelled from the gut by day 14. Thus, the kinetics of gamma delta TCR+ i-IEL, but not spleen and PP gamma delta TCR, corresponded to the kinetics of worm expulsion in C57BL mice. Most murine i-IEL of the gamma delta T cell lineage tend to be cytolytic when activated. We speculated that gamma delta T cells of i-IEL during the early stages of infection recognize and eliminate damaged epithelial cells generated by parasite antigens, simultaneously accelerating the worm expulsion.     

Diltiazem stimulates parathyroid hormone secretion in vivo whereas felodipine does not

The impact of two calcium channel blockers of different structure, diltiazem and felodipine, on PTH secretion was studied under hyper- and hypocalcemic conditions. Six healthy volunteers were investigated before and after treatment with felodipine, then after treatment with diltiazem. Under each of these three conditions, they received first a calcium infusion (0.109 mmol/kg over 130 min). Blood was drawn every 5-10 min for measurements of Ca2+ and intact PTH concentrations, and urine was collected over the infusion periods for measurements of calcium and creatinine. Basal levels of Ca2+ and intact PTH concentrations were similar under the three conditions. During calcium infusion, Ca2+ increased linearly from 1.27 to 1.51 mmol/L during the control period. Based on the whole response curve, Ca2+/time, this rise was less marked (P < 0.002) during each of the calcium channel blocker periods than under control conditions, although the three values of urinary calcium excretion were similar. In addition, PTH secretion was less suppressed on diltiazem than on felodipine therapy or during the control period (P < 0.04). During EDTA infusion, Ca2+ decreased in a linear way from 1.27 to 1.07 mmol/L during the control period. Based on the whole response curve, Ca2+/time, this decrease was more marked during felodipine than during diltiazem treatment or in the control period (P < 0.001). Although Ca2+ concentrations did not differ between the control and diltiazem periods, PTH levels were 1.3-fold higher (P < 0.0001) during diltiazem, but similar in the control and felodipine periods. These data demonstrate that diltiazem, but not felodipine, stimulates PTH secretion in vivo in man, with a maximal effect observed under hypocalcemic conditions.     

高强度特厚板减量化轧制工艺

利用无微合金化Q345D连铸坯料,采用TMCP和RCR+ACC两工艺进行了厚80~85 mm高强度厚板工业试验,对比了两工艺厚板的组织和性能。试验结果表明,经两工艺轧制的钢板均实现了组织和性能的良好匹配。与TMCP工艺相比,采用RCR+ACC工艺的钢板厚度1/4位置和钢板心部组织均匀性、厚度方向上的性能均匀性较好;轧制过程在奥氏体高温区进行,变形抗力低,有利于降低轧机负荷或实现低速大压下轧制,且省去了TMCP工艺中间待温时间,减少了轧制道次,实现了厚板轧制过程的减量化。     

Nedd4 mediates control of an epithelial Na+ channel in salivary duct cells by cytosolic Na+

Epithelial Na+ channels are expressed widely in absorptive epithelia such as the renal collecting duct and the colon and play a critical role in fluid and electrolyte homeostasis. Recent studies have shown that these channels interact via PY motifs in the C terminals of their alpha, beta, and gamma subunits with the WW domains of the ubiquitin-protein ligase Nedd4. Mutation or deletion of these PY motifs (as occurs, for example, in the heritable form of hypertension known as Liddle's syndrome) leads to increased Na+ channel activity. Thus, binding of Nedd4 by the PY motifs would appear to be part of a physiological control system for down-regulation of Na+ channel activity. The nature of this control system is, however, unknown. In the present paper, we show that Nedd4 mediates the ubiquitin-dependent down-regulation of Na+ channel activity in response to increased intracellular Na+. We further show that Nedd4 operates downstream of Go in this feedback pathway. We find, however, that Nedd4 is not involved in the feedback control of Na+ channels by intracellular anions. Finally, we show that Nedd4 has no influence on Na+ channel activity when the Na+ and anion feedback systems are inactive. We conclude that Nedd4 normally mediates feedback control of epithelial Na+ channels by intracellular Na+, and we suggest that the increased Na+ channel activity observed in Liddle's syndrome is attributable to the loss of this regulatory feedback system.     

Cyclosporin A induces a biphasic increase in KCl-induced calcium influx in GH3 pituitary cells

The role of calcineurin in modulation of calcium channel activity was examined in GH3 pituitary cells by using its selective inhibitor cyclosporin A. While cyclosporin A had little effect on basal activity, it induced a biphasic increase in K+-induced 45Ca2+ influx. Cyclosporin A rapidly increased K+-induced 45Ca2+ influx to approximately 140% of control in 1 h and the increment maintained at this magnitude for 1-8 h. Thereafter, K+-induced 45Ca2+ influx gradually increased further to approximately 220% after 24 h exposure to this compound. In the presence of anisomycin, however, the increase occurred at the latter phase was abolished. In addition, the increased calcium influx in cyclosporin A-pretreated cells had a similar sensitivity to KCl and verapamil as in untreated cells. Measurement of intracellular Ca2+ level by Fura-2 analysis indicated that [Ca2+]i increase induced by high K+ or vasoactive intestinal peptide was similarly augmented in cyclosporin A-pretreated cells. Thus the results of this study suggest that calcineurin may play a tonic control on L-type Ca2+ channel, and inhibition of this enzyme may induce a subsequently protein synthesis-dependent higher channel activity.     

骨髓增生异常综合征T淋巴细胞异常与克隆造血

目的 了解T淋巴细胞异常在骨髓增生异常综合征(MDS)克隆造血中的作用.方法 对76例MDS患者的染色体核型、T淋巴细胞亚群及激活状态进行分析.结果 正常核型36例,异常核型40例,异常发生率52.6%.40例异常核型中,三体8(+8)24例,占异常核型的60.0%.与健康对照组比较,MDS患者CD+3 CD-19、CD+3 CD-4 CD+8以及CD+3 HLA-DR+细胞百分率显著升高,CD-3(CD16 CD56)+细胞的百分率明显降低.将MDS患者进行核型分组,异常核型组CD+3(CD16 CD56)+细胞的百分率显著高于正常对照组.将+8核型从MDS异常核型中独立出来进行分析,CD+3 CD+4 CD-8细胞的百分率明显低于正常核型以及其他异常组,CD4/CD8的比值明显低于健康对照组.结论 MDS存在T淋巴细胞异常,异常核型MDS可能恶性克隆增殖更为优势,预后更差.+8核型MDS存在更为严重的免疫监视功能下降,导致恶性克隆过度增殖与残存造血过度受抑.     

Critiquing a research article

NAD+ biosynthesis from tryptophan in the presence of nicotinic acid or vice versa by rat hepatocytes was investigated. In the control hepatocytes, NAD+ synthesis from tryptophan was not affected by nicotinic acid from 0.026 to 0.26 mM. NAD+ synthesis from nicotinic acid was slightly inhibited with varying concentrations of tryptophan from 0.1 to 1.0 mM. In the clofibrate-treated hepatocytes, NAD+ synthesis from tryptophan was greatly increased (234% of the control), while that from nicotinic acid was decreased (71.2% of the control). Both, NAD+ synthesis from tryptophan and that from nicotinic acid were decreased by the coexisting nicotinic acid or tryptophan. Total amount of NAD+ synthesized from tryptophan and nicotinic acid at their physiological concentrations was significantly higher than that in the control hepatocytes as a result of a large increase of NAD+ synthesized from tryptophan. When the metabolic flux of 0.1 or 0.5mM tryptophan was investigated, the glutarate pathway was suppressed in the clofibrate-treated hepatocytes, the quinolinic acid-NAD+ flux being elevated. Similarly to clofibrate, DEHP and CPP revealed an increase in NAD+ synthesis from tryptophan. Mutual relationship of NAD+ biosyntheses from tryptophan and nicotinic acid in rat hepatocytes is discussed and the relevance with peroxisomal proliferation is suggested.