腐蚀管道剩余寿命的性能衰减模型研究

管道在长期的运行过程中，由于介质和土壤的腐蚀性，管材的微塑性变形、结构转变和渗氢等。不仅会使管道出现各种腐蚀损伤，而且还存在着老化效应和氢化作用，导致管材的脆变并改变材料的塑性，使机械性质参数发生衰退，从管材性能衰减和腐蚀损伤角度研究了管道的剩余寿命，提出了根据结构承载能力的极限值确定塑性变形时工作寿命的方法，为了确定剩余使用寿命，对剪切损伤率和屈服性能比等概念进行定义，在掌握管材金属剪切损害率和屈服性能比的时间特性基础上，建立了剩余寿命计算模型。并给出了算例。     

钢筋混凝土结构锈蚀损伤定位

对钢筋混凝土结构锈蚀损伤定位进行了研究,以频率变化平方比作为锈蚀损伤参数,从理论上证明该参数是锈蚀损伤位置的函数。锈蚀钢筋混凝土结构试验结果表明预测的损伤位置和实际的损伤位置较一致,模态参数用于检测混凝土结构构件中的损伤,为大型结构的鉴定和评估提供了新的途径。     

水平连续铸钢凝固过程数值模拟

本文在分析水平连铸传热特征的基础上，给出了一维情况下，计算结晶器出口处铸坯凝固层厚度的解析式，建立了计及轴向传热的连续坯凝固模拟模型。进行了连续坯二维传热的凝固数值模拟，其模拟结果与实验结果吻合较好，具有普遍应用价值。     

胸神经后皮支及其营养血管的解剖学研究

目的：为临床设计背部皮神经营养血管皮瓣提供解剖学基础。方法：在l7例34侧成人躯干标本上，用显微解剖法观测第l—l2胸神经后皮支及其营养血管的来源．走行及分布规律。结果：第l—l2胸神经后皮支的伴行动脉为肋间后动脉的背侧皮支。皮神经及其伴行动脉于脊柱两旁相应肋间穿出深筋膜，呈节段性、重叠性分布于背部皮肤，皮神经营养血管相互间形成丰富的吻合。结论：可设计以第l—12胸神经后皮支及其营养血管为蒂的皮神经营养血管皮瓣。     

Structure,function and signal transduction of vascular endothelial growth factor receptor-2

Angiogenesis, or the formation of new blood vessels out of pre-existing capillaries, is very important in many physiologic and pathologic processes, such as embryonic development, cancer, retinopathies, etc. Vascular endothelial growth factor receptor-2 (VEGFR-2) plays a key role in angiogenesis. In this review, we discussed the structure, function and signal transduction of vascular endothelial growth factor receptor-2. Understanding these should provide important insights into how new strategies can be devised to interfere in the physiologic and pathologic processes involved in angiogensis.     

保温油罐抗风圈腐蚀穿孔的修复及改造

保温油罐抗风圈及罐底板外根部因酸雨聚积形成电化学腐蚀。由于沿海地区空气温度大，盐分重及罐内的温度高，加快了设备的腐蚀。通过对1000立方米燃料油罐的腐蚀原因分析，提出了改造与预防措施。改造后的抗风圈结构能有效地排出进入保温层内的雨水，从而避免了的电化学腐蚀。     

Colonization and histopathology of susceptible and resistant carnation cultivars infected with Fusarium oxysporum f. sp. dianthi

Stems of the susceptible Early Sam and resistant Novada carnations were inoculated with a conidial suspension ofFusarium oxysporum f. sp.dianthi. Stem segments of either cultivar were sampled regularly and used for determination of fungal growth and for microscopical investigation.Early Sam showed typicalFusarium wilt symptoms and its stems were colonized intensively. The observed vascular browning appeared to be caused by discolouration of primary walls of infected vessels and surrounding cells. Vessels were rarely occluded with gel. Cell wall degradation led to the formation of stem cavities. Hyperplasia of xylem parenchyma was not seen.In Novada, fungal colonization remained low throughout the experiment. Macroscopic symptoms were absent except for longitudinal bursts in the stem, which appeared to be caused by hyperplasia of xylem parenchyma bordering infection. Vascular gelation occurred in the infected tissues, causing some vascular browning also. Xylem vessel regeneration was observed in the hyperplastic layer. Cavities were not formed, and wall discolouration was rare. Vascular gelation is considered part of theFusarium wilt resistance mechanism. It is followed by xylem vessel regeneration, which expresses a general plant response to vascular dysfunction rather than being part of the resistance mechanism.Although of different origin, vascular browning as such occurs in both susceptible and resistant interactions. In breeding for resistance, care should hence be taken with the current use of browning as an indication of disease.Samenvatting Anjers van de vatbare cultivar Early Sam en de resistente cultivar Novada werden geïnoculeerd met een conidiënsuspensie vanFusarium oxysporum f. sp.dianthi. Van beide cultivars werden regelmatig stengeldelen geoogst om deze microscopisch te onderzoeken en om de schimmelgroei te bepalen.Early Sam vertoonde de voor deze verwelkingsziekte kenmerkende symptomen en werd intensief gekoloniseerd. Aan het vaatweefsel waargenomen bruinkleuring bleek veroorzaakt te worden door verkleuring van de primaire wanden van geïnfecteerde vaten en de hen omringende cellen. Zelden trad er in de vaten gomvorming op. Celwandafbraak veroorzaakte de vorming van holten in de stengel. Hyperplasie van het houtparenchym werd niet waargenomen.In Novada bleef de schimmelgroei gedurende het hele experiment beperkt. Macroscopisch waren er enkel lengtescheuren in de stengel te zien, die veroorzaakt bleken te worden door hyperplasie van aan de infectie grenzend houtparenchym. In het geïnfecteerde vaatweefsel optredende gomvorming veroorzaakte ook enige bruinkleuring. In het hyperplastische weefsel werd regeneratie van houtvaten waargenomen. In de stengel werden geen holten gevormd, en verkleuring van de celwanden kwam weinig voor. De vorming van gommen in de houtvaten maakt waarschijnlijk deel uit van het resistentiemechanisme. De daarop volgende houtvatregeneratie is eerder een algemene reactie van de plant op vaatverstopping dan een deel van het resistentiemechanisme.Vaatverbruining, zij het van verschillende oorsprong, komt voor in zowel vatbare als resistente interacties. Om die reden moet men in de resistentieveredeling bij de anjer voorzichtig zijn met het gebruik van bruinkleuring als ziekteïndicatie.     

Movement of Xanthomonas campestris pv. vitians in the stems of lettuce and seed contamination

Xanthomonas campestris pv. vitians , the causal agent of bacterial leaf spot of lettuce (BLS), can be seedborne, but the mechanism by which the bacteria contaminates and/or infects lettuce seed is not known. In this study, the capacity of X. campestris pv. vitians to enter and translocate within the vascular system of lettuce plants was examined. The stems of 8- to 11-week-old lettuce plants were stab-inoculated, and movement of X. campestris pv. vitians was monitored at various intervals. At 4, 8, 12 and 16 h post-inoculation (hpi), X. campestris pv. vitians was recovered from 2 to 10 cm above (depending on stem length) and 2 cm below the inoculation site. Xanthomonas campestris pv. vitians was also recovered from surface-disinfested stem sections of spray-inoculated plants. Together, these results are consistent with X. campestris pv. vitians invading and moving systemically within the vascular system of lettuce plants. To investigate the mechanism of seed contamination, lettuce plants at the vegetative stage of growth were spray-inoculated with X. campestris pv. vitians and allowed to develop BLS. Seed collected from these plants had a 2% incidence of X. campestris pv. vitians external colonization, but no bacteria were recovered from within the seed.     

Metallothionein inhibits homocysteine-induced proliferation of rat vascular smooth muscle cells

AIM:To investigate the effect of metallothionein(MT) on proliferation of rat vascular smooth muscle cells (VSMCs) stimulated by homocysteine and its mechanism. METHODS:VSMCs proliferation was measured by [³-H]-TdR incorporation, mitogen-activated protein kinase(MAPK)activity were determined by immunoprecipitation method, the intracellular contents of MT and malondialdehyde (MDA)were assayed by -hemoglobin saturation method and TBA reaction, respectively, and lactate dehydrogenase (LDH) leakage was measured by NADH oxidation. RESULTS:Hcy(10^-6-10^-4 mmol/L) stimulated [³-H]-TdR incorporation by the VSMCs in a concentration-dependent manner. Compared with control, [³-H]-TdR incorporation in VSMCs treated with 0.1 mmol/L Hcy was increased by 4.2 fold (P＜0.01). Meanwhile, Hcy enhanced MAPK activity, MDA formation and LDH release (P＜0.01)in a concentration-dependent manner. Treatment of VSMCs with MT alone did not change above parameters, compared with control. However, MT (10^-6-10^-4 mol/L)attenuated significantly Hcy-stimulated proliferation of VSMCs (P＜0.01)in a concentration-dependent manner. And MT inhibited obviously Hcy-induced activation of MAPK activity, MDA formation and LDH release. Preincubation of VSMCs with 0.5 mmol/L ZnCl₂ for 6 h induced an increase cellular MT content by 5.7-fold (P＜0.01). The MT-overexpressed VSMCs resisted Hcy-stimulating action on MAPK activity, MDA formation and LDH leakage (P＜0.01). CONCLUSION:These results show that MT has an inhibitory effect on Hcy-induced VSMCs proliferation, and that MT could inhibit Hcy-stimulated MAPK activity and lipid peroxidation.