高强度钢表面裂纹（KIE）的测定

本文对薄板疲劳预制表面裂纹的方法了研究。在此基础上，测定了高强度钢３７ＳｉＭｎＣｒＮｉＭｏＶ，３０Ｃｒ３ＳｉＮｉＭｏＶＡ的表面裂纹韧性值（ＫＩＥ）。结果表明：ＫＩＥ分别为５３ＭＰａ．√ｍ、６０ＭＰａ．√ｍ，为高强度材料的薄壁结构件在工程上应用提供了重要的技术参数。     

材料的成分组织对动态拉伸性能的影响

本文通过分段Ｈｏｐｋｉｎｓｏｎ杆拉伸装置，在１０＾２－１０＾３Ｓ＾－１应变率范围内测试了５８ＳｉＭｎ钢、４５钢、ＰＣｒＮｉ３ＭｏＶＡ钢、Ｄ６０钢、６０３钢、６１７钢和２８ＣｒＭｏＶＡ钢的动态拉伸性能，以研究的应变速率敏感性。     

34CrNi3Mo钢高温变形行为的研究

利用Ｆｏｒｍａｓｔｏｒ－Ｐｒｅｓｓ热模拟试验机，研究了３４ＣｒＮｉ３Ｍｏ合金结构钢在温度８４０～１２００℃变形速度０．１～８０ｓ＾－１的变形条件下的热压缩行为，获得了３４ＣｒＮｉ３Ｍｏ钢在热变形时发生动态再结晶的临界条件（包括临界因子Ｚ１和临界应变ε）及再结晶粒大小Ｄｄｙｎ与Ｚｅｎｅｒ－Ｈｏｌｌｏｍｏｎ因子Ｚ，奥氏体起始晶粒尺寸Ｄ０和应变ε之间的关系，并给出了回归公式。     

30CrNi4MoA高强度高韧性结构钢的研究

本文介绍了高强度、高韧性结构钢３０ＣｒＮｉ４ＭｏＡ的研制，对制成的３０ＣｒＮｉ４ＭｏＡ负的棒材，板材和锻件以及模锻零件进行了全面性能测试，对钢的冶炼、热加工、热处理等工艺制度和钢的组织性能进行了系统而深入的研究。     

34CrNi3Mo钢的高温变形行为

利用Ｆｏｒｍａｓｔｏｒ－Ｐｒｅｓｓ热模拟试验机，研究了３４ＣｒＮｉ３Ｍｏ合金结构钢在温度８４０￣１２００℃，变形速度０．１￣８０ｓ＾－１的变形条件下的热压缩行为。获得了３４ＣｒＮｉ３Ｍｏ钢在热变形时发生动态再结晶的临界条件（包括临界因子Ｚｃ和临界应变εｃ）及再结晶晶粒大小Ｄｄｙｎ与Ｚｅｎｅｒ－Ｈｏｌｌｏｍｏｎ因子Ｚ、奥氏体起始晶粒尺寸Ｄ０和应变ε之间的关系，并给出了回归公式。     

凿岩钎具有合金风的研究

本文叙述了凿岩机用新钢种ＦＦ７１０、１８ＣｒＭｎＮｉ２ＭｏＡ、２７ＳｉＭｎＣｒＮｉ２ＭｏＡ、４０ＭｎＶＡ、４５ＣｒＮｉＭｏＶＡ等的冶炼、加工，热处理工艺等。     

钻杆管端加厚工艺中热脆性问题的分析

用高温拉伸试验方法研究对比了宝钢（ＢＳ）和日本钢管（ＮＫＫ）Ｇ级钻杆的高温力学行为，分析了断裂组织和晶粒，对比了ＢＳ和ＮＫＫ两种钻杆成分设计思想。文中指出：同样在１２００℃左右热成型时Ｃｒ－Ｍｏ钢比Ｍｎ－Ｍｏ钢表面出更大的热脆敏感性。     

非调质抽油杆用钢的研究

以策合金Ｖ、Ｔｉ、Ｍｏ、Ｎｂ等非调质钢代替２０ＣｒＭｏ等调质钢作为Ｄ、Ｈ级抽油杆用钢，减少了石油行业机械厂的设备投资，降低成本，其市场前景广阔。     

汽轮机转子材料的高温时效研究

利用金相显微镜，扫描电子显微镜及Ｘ射线衍射仪对国内外常用的两种汽轮机转子材料３０Ｃｒ２ＭｏＶ和２８ＣｒＮｉＭｏ１Ｖ钢在高温时效过程中的组织与性能变化进行了研究，并对两者进行了比较。     

35CrMoD级空心抽油杆钢的试验研究

本文通过对３５ＣｒＭｏＤ级空心抽油杆钢试制过程的总结和分析，提出了适合承钢生产实际的工艺制度和技术要求。从而，保证了我公司生产的３５ＣｒＭｏ无缝钢管，完全达到石油行业制造Ｄ级空心抽油杆的各种特殊性能和技术要求。     

KD级抽油杆用钢3130的开发生产

KD级抽油杆用钢3130是兼顾强度和耐腐蚀性能的新型抽油杆用钢,根据产品的服役条件和技术协议要求,设计了钢种的化学成分和生产工艺,通过控制S、P、H等杂质元素含量,控制轧制,试验确定合理的热处理工艺,巨能特钢成功开发了KD级抽油杆用3130钢。产品组织均匀,晶粒度5级以上,各类夹杂物≤1.5级,屈服强度≥795 MPa,抗拉强度≥865MPa,伸长率≥15%,冲击功≥60 J,各项性能指标满足用户要求。     

The immunologic effects of IVIG in Kawasaki disease

Kawasaki disease (KD) is an acute febrile illness of early childhood that is associated with the development of coronary artery aneurysms in 15-25% of the cases. The acute phase of KD is characterized by a deficiency of suppressor T cells, marked activation of the immune system and increased secretion of cytokines by immune effector cells. Evidence that this immune activation contributes to the vascular endothelial cell damage in KD is suggested by the observation that patients in the acute phase of KD have circulating antibodies lytic for vascular endothelial cells activated with gamma interferon, IL-1 or tumor necrosis factor. In contrast, sera from these patients do not lyse unstimulated endothelial cells. High dose intravenous gammaglobulin (IVGG) treatment is effective in preventing the occurrence of coronary artery abnormalities in KD. Patients treated with IVGG have a significant increase in T suppressor cells, a decrease in circulating activated T helper cells, and a decrease in spontaneous IgG and IgM synthesis. These observations suggest that IVGG reduces the vasculitis in KD by suppressing the marked immune activation associated with this disease.     

Malignant nonteratoid medulloepithelioma of the ciliary body in an adult

Vascular endothelial growth factor (VEGF) is an angiogenic mitogen that specifically targets vascular endothelial cells. The objective of this study was to evaluate the role of VEGF in Kawasaki disease (KD), the most common cause of systemic vasculitis in childhood. Serum VEGF levels were measured by ELISA in 22 patients with KD, 22 febrile children with infection, and 19 healthy children. Samples from KD patients were divided into three groups: acute stage (n = 20), subacute stage (n = 13), and convalescent stage (n = 15). The results showed that KD patients in the acute and subacute stages had significantly higher levels of VEGF than did patients with infectious diseases and the healthy control subjects. When compared with the VEGF levels of patients with and without coronary artery lesions (CAL), significantly higher levels of VEGF were observed in the subacute stage in patients with CAL and in patients without CAL in the acute stage. Serial examination revealed that the serum VEGF levels in KD patients with CAL increased from a relatively low level in the acute stage to an extremely high level in the subacute stage. In contrast, patients without CAL were found to have extremely high levels of VEGF only in the acute stage of KD. In KD patients, the serum VEGF levels did not correlate with the inflammatory markers and clinical symptoms. Our results raise the possibility that VEGF is involved in the pathogenesis of KD, especially in the development of CAL. Further study is needed to clarify the biologic effect of VEGF on coronary arteries in KD.     

Antihypertensive activity and pharmacokinetics of KD3-671, a nonpeptide AT1-receptor antagonist, in renal hypertensive dogs

The antihypertensive activity and pharmacokinetics of KD3-671 (previously named KT3-671), a nonpeptide AT1-receptor antagonist, were investigated in renal hypertensive dogs with normal or high plasma renin activity (PRA). A single administration of KD3-671 at 3 and 10 mg/kg, p.o., to the hypertensive dogs with high PRA dose-dependently reduced mean blood pressure (MBP), which was not correlated with plasma KD3-671 concentration. Significant increases in PRA and plasma angiotensin (Ang) II occurred 2 h after KD3-671 dosing. Enalapril at 3 mg/kg, p.o., also reduced MBP. Neither KD3-671 nor enalapril affected heart rate. When given orally once a day for 29 days to the hypertensive dogs with normal PRA, KD3-671 at 3 and 10 mg/kg/day dose-dependently reduced MBP, which was smaller than that in the dogs with high PRA. This was the case for enalapril. The hypotension induced by the first dose of KD3-671 or enalapril was consistently observed after doses 8, 15, 22, and 29. After cessation of repeated dosing, no rebound phenomenon in MBP was observed. Pharmacokinetic parameters of KD3-671 were not influenced by repeated dosing. KD3-671 markedly increased both PRA and plasma Ang II concentration at 2 h after dosing. These results suggest that KD3-671 may be useful for the treatment of hypertension.     

KD75型液压泥炮的故障分析与改进

液压泥炮是高炉堵铁口的专用设备,因为泥炮故障造成的高炉慢风、休风现象较多,成为制约高炉生产的瓶颈。文章在介绍安钢450 m3高炉使用的KD75型液压泥炮结构特点及工作原理的基础上,分析液压泥炮在使用过程中出现的打泥机构吊挂系统、液压炮回转机构、打泥机构角度调整系统等故障并提出了改进措施,给出了液压泥炮使用和管理的几点建议。     

Low dialysate [K+] decreases efficiency of hemodialysis and increases urea rebound

In a previous study, it was reported that hemodialysis with dialysate [K+] (KD) of 1.0 or 2.0 mmol/L caused an increase in BP shortly after completion of treatment due to arteriolar constriction. With this background, it was hypothesized that a low KD might decrease dialysis efficiency by a similar mechanism. To evaluate this hypothesis, paired observations of two consecutive 3-h treatments, with KD of 1.0 or 3.0 mmol/L, were performed in 14 stable end-stage renal disease patients. A KD of 1.0 mmol/L resulted in lower values for both urea reduction ratio and Kt/V evaluated at completion of dialysis and 1 h thereafter. Values at equilibrium were urea reduction ratio 42+/-1% versus 47+/-2% (P < 0.02), Kt/V 0.65+/-0.03 versus 0.73+/-0.03 (P < 0.02) for KD 1.0 or 3.0 mmol/L, respectively. The mechanisms responsible for the observed differences in dialysis efficiency were examined using a urea kinetics model that predicts urea sequestration caused by impaired blood flow to urea-rich tissues. For this purpose, urea rebound and its effect on Kt/V (by means of deltaKt/V, calculated as equilibrated minus single pool value) with KD 1.0 and 3.0 mmol/L were assessed. Greater urea rebound, 12.8+/-1.6% versus 8.6+/-1.4% (P < 0.001), and larger deltaKt/V, 0.12+/-0.01 versus 0.10+/-0.02 (P < 0.02), were observed with KD 1.0 mmol/L compared with 3.0 mmol/L. The theoretical model accurately predicted the deltaKt/V observed with KD 1.0 mmol/L. It is concluded that a low KD decreases dialysis efficiency. This effect is likely caused by reduced blood perfusion to nonvisceral organs, largely skeletal muscle. Conversely, hemodialysis with KD 3.0 mmol/L facilitates tissue perfusion, minimizes urea trapping in poorly perfused areas, and improves the efficiency of this treatment modality.     

Predissociation of the 7Li2 2(3)Sigma+g State

Kawasaki disease (KD) is an acute febrile vasculitic syndrome with thrombocytosis occurring in childhood. Transient thrombocytosis of KD is sometimes the cause of complications such as coronary aneurysmal thrombosis and myocardial infarction. We have analysed blood TPO levels in KD and found that 26/31 acute-phase KD patients had detectable blood TPO levels (mean 173 pg/ml; range 89-294 pg/ml), which decreased immediately with the elevation of platelet counts in 5/12 patients studied. Elevated serum level of TPO may have an important role for this ill-defined disease.     

Activation of peripheral blood monocytes and macrophages in Kawasaki disease: ultrastructural and immunocytochemical investigation

Monocytes/macrophages are considered to play an important role in the pathogenesis of Kawasaki disease (KD). However, the morphological and immunocytochemical features of the cells in acute KD have not been investigated. The ultrastructural and immunocytochemical characteristics of peripheral blood CD14+ monocytes/macrophages sorted by a magnetic cell sorter (MACS) during the course of KD were, therefore, studied to evaluate their role in the disease pathogenesis. Electron microscopy showed that CD14+ monocytes/macrophages from patients with acute KD had nuclei with complex shapes, apparent nucleoli and abundant intracytoplasmic granules, some of which were positive for acid phosphatase. The quantity of intracytoplasmic granules was correlated with disease severity, in terms of the duration of fever, maximum level of C-reactive protein and the presence of coronary artery lesions (CAL), suggesting that the monocytes/macrophages were activated and showed increased phagocytosis. Immunocytochemical staining of smears made from cell suspensions of sorted CD14+ monocytes/macrophages was carried out using a monoclonal antibody against tumor necrosis factor (TNF)-alpha. The cytoplasm of monocytes/macrophages from patients with acute KD was strongly positive in comparison to that of cells from control subjects, suggesting that intracytoplasmic granules secrete TNF-alpha.     

Heteromultimeric delayed-rectifier K+ channels in schwann cells: developmental expression and role in cell proliferation

Schwann cells (SCs) are responsible for myelination of nerve fibers in the peripheral nervous system. Voltage-dependent K+ currents, including inactivating A-type (KA), delayed-rectifier (KD), and inward-rectifier (KIR) K+ channels, constitute the main conductances found in SCs. Physiological studies have shown that KD channels may play an important role in SC proliferation and that they are downregulated in the soma as proliferation ceases and myelination proceeds. Recent studies have begun to address the molecular identity of K+ channels in SCs. Here, we show that a large repertoire of K+ channel alpha subunits of the Shaker (Kv1.1, Kv1.2, Kv1.4, and Kv1.5), Shab (Kv2.1), and Shaw (Kv3.1b and Kv3.2) families is expressed in mouse SCs and sciatic nerve. We characterized heteromultimeric channel complexes that consist of either Kv1.5 and Kv1.2 or Kv1.5 and Kv1.4. In postnatal day 4 (P4) sciatic nerve, most of the Kv1.2 channel subunits are involved in heteromultimeric association with Kv1.5. Despite the presence of Kv1. 1 and Kv1.2 alpha subunits, the K+ currents were unaffected by dendrotoxin I (DTX), suggesting that DTX-sensitive channel complexes do not account substantially for SC KD currents. SC proliferation was found to be potently blocked by quinidine or 4-aminopyridine but not by DTX. Consistent with previous physiological studies, our data show that there is a marked downregulation of all KD channel alpha subunits from P1-P4 to P40 in the sciatic nerve. Our results suggest that KD currents are accounted for by a complex combinatorial activity of distinct K+ channel complexes and confirm that KD channels are involved in SC proliferation.     

Consequences of mutations to the phosphorylation site of the alpha-subunit of Na, K-ATPase for ATP binding and E1-E2 conformational equilibrium

Expression of Na, K-ATPase in yeast allowed targeting of alpha beta-units with lethal substitutions at the phosphorylation site alpha 1 (D369N) beta 1 and alpha 1 (D369A) beta 1 at the cell surface at the same concentration of alpha-subunit and [3H] ouabain binding sites as for wild type Na, K-ATPase. Phosphorylation and reaction with vanadate were abolished, and the mutations had no Na, K-ATPase or K-phosphatase activity. Binding of [3H]-ATP at equilibrium revealed an intrinsic high affinity of the D369A mutation for ATP (KD = 2.8 nM) that was 39-fold higher than for wild type Na, K-ATPase (KD = 109 nM). The affinities for ADP were unaffected, indicating that the negative charge at residue 369 determines the contribution of the gamma-phosphate to the free energy of ATP binding. Analysis of the K(+)-ATP antagonism showed that the reduction of charge and hydrophobic substitution at Asp369 of the alpha-subunit caused a large shift in conformational equilibrium toward the E2-form. This was accompanied by a large increase in affinity for [3H] ouabain in Mg2+ medium with KD = 4.9 nM for D369A compared to KD = 51 nM for D369N and KD = 133 nM for wild type, and [3H] ouabain binding (KD = 153 nM) to D369A was detectable even in absence of Mg2+. In addition to its function as receptor of the gamma-phosphate of ATP, Asp369 has important short-range catalytic functions in modulating the affinity for ATP and long-range functions in governing the E1-E2 transitions which are coupled to reorientation of cation sites and changes in affinity for digitalis glycosides.