TiO_2-聚乙烯复合膜的制备及红外光谱对其膜层结构的表征

开发了以Ｔｉ４＋为桥联剂制备无机－有机复合膜的新方法以自制的硅藻土多孔陶瓷为基膜（支撑体），使用浸涂法－热致相转化法相结合制备了ＴｉＯ２－聚乙烯复合膜，并用红外光谱表征了复合膜层与层之间的结合方式和强度，支撑体中的ＳｉＯ２通过Ｔｉ４＋与聚乙烯的分子之间形成了新的化合物型膜层     

Transient Current Behaviour for Iron in 3.5%NaCl and 3.5%NaCl+ 1%NaNO_2 Solutions during Corrosion Fatigue

The transient current behaviour for Iron in 3.5%NaCl and 3.5%NaCl +1%NaNO2 solutions during corrosion fatigue (CF) process has been investigated at different given strain amplitudes and strain rates. The results show that elastic strain has little contribution to material dissolution. The elastic tension strain results in the decrease in the transient current, while the elastic compression strain increases the transient current. Compared to the elastic deformation, plastic deformation affects material dissolution evidently For iron in 3.5%NaCl solution, the strain amplitude plays a dominant role in the dissolution process accelerated by the plastic strain, while in 3.5%NaCl+1%NaNO2 solution, both the strain amplitude and strain rate play an important role in this process. In this paper, the effect of the elastic deformation on the material dissolution and the relation between the tension and compression current peak values under the plastic cycle deformation are discussed     

噻二唑二聚物/丁氧基三乙二醇复合物的合成

合成了噻二唑二聚物/丁氧基三乙二醇复合物。反应物的摩尔比及反应温度影响产物作为添加剂加入到润滑脂中的抗烧结性能。在最佳反应条件下,即n(噻二唑二聚物)∶n(丁氧基三乙二醇)=0.5∶1.0,反应温度125℃时,产率为85%。通过分子模拟、红外光谱、13C核磁共振及N、S元素的含量测定,探讨了产物的结构及反应机理。结果表明,噻二唑二聚物与丁氧基三乙二醇的摩尔比越大,在金属表面形成配位的噻二唑环的个数就越多,就会表现出更强的吸附特性,从而表现出更高的抗烧结性能。     

灵活运用数据库设计理论

简介了关系模型、键、完整性规则、E-R模型、函数依赖、模式分解和关系模式的范式等数据库技术基础和规范化设计理论，从键和完整性规则的实现、数据冗余的特殊情况和字典设计等方面论述了在实际设计工作中如何灵活运用关系数据库设计理论。     

Successful weight loss in a self-taught, self-administered program

There is little evidence concerning the effectiveness of self-help materials for weight control. The purpose of this research was to evaluate a self-help weight-loss program. Obese (body fat > or = 25.0%, range = 25.0-48.6%, mean +/- SEM = 36.5 +/- 1.3%) men (n = 14) and women (n = 21) were given a workbook detailing a behavior modification approach to weight loss that emphasizes self-monitoring of diet and exercise behaviors, and then sent home for 6 months to learn how to lose weight on their own. A group of 9 controls (CONT) who did not get a workbook were used for comparison. ANOVA showed that the experimental group (EXP) lost 8.1 +/- 0.9 (mean +/- SEM) kg body weight, 6.4 +/- 0.8 kg fat, and 3.9 +/- 0.6% body fat; all significant over time (p < 0.001) and different from the CONT (p < 0.0001) who showed no change in these variables. The EXP also reduced their fat intake (% of joules) from 36.1 +/- 1.0% to 27.9 +/- 1.3% (p < 0.0001), increased their carbohydrate intake from 45.7 +/- 1.2% to 50.0 +/- 1.7% (p < 0.007) and their protein intake from 16.3 +/- 0.05% to 20.7 +/- 0.7% (0 < 0.03), all of which were significantly different (p < 0.03) than the CONT who did not change. Dietary fiber increased in the EXP from 19.8 +/- 1.4 to 27.3 +/- 2.2 g/d (p < 0.001) even with a significant reduction in energy intake (11.3 +/- 0.6 vs. 8.9 +/- 0.5 Mj/d; p < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Cytoskeletal changes during neurogenesis in cultures of avain neural crest cells

Neural crest cells are motile and mitotic, whereas their neuronal derivatives are terminally post-mitotic and consist of stationary cell body from which processes grow. The present study documents changes in the cytoskeleton that occur during neurogenesis in cultures of avain neural crest cells. The undifferentiated neural crest cells contain dense bundles of actin filaments throughout their cytoplasm, and a splayed array of microtubules attached to the centrosome. In newly differentiating neurons, the actin bundles are disrupted and most of the remaining actin filaments are reorganized into a cortical layer underlying the plasma membrane of the cell body and processes. Microtubules are more abundant in newly-differentiating neurons than in the undifferentiated cells, and individual microtubules can be seen dissociated from the centrosome. Neuron-specific beta-III tubulin appears in some crest cells prior to cessation of motility and cell division, and expression increases with total microtubule levels during neurogenesis. To investigate how these early cytoskeletal changes might contribute to alterations in morphology during neurogenesis, we have disrupted the cytoskeleton with pharmacologic agents. Microfilament disruption by cytochalasin immediately arrests the movement of neural crest cells and causes them to round-up, but does not significantly change the morphology of the immature neurons. Microtubule depolymerization by nocodazole slows the movement of undifferentiated cells and causes retraction of processes extended by the immature neurons. These results suggest that changes in the actin and microtubule arrays within neural crest cells govern distinct aspects of their morphogenesis into neurons.     

高职教育只有特色办学才有竞争力

在我国虽然高等职业教育发展势头强劲,但仍属于新生事物。面对高等教育激烈的竞争态势,如何扬长避短,办出自己的特色,是诸多新建高职院校应致力思考的一个重要问题。     

Efficacy of monensin for the prevention of subclinical ketosis in lactating dairy cows

A total of 1010 dry cows and pregnant heifers was randomly selected from 25 dairy farms near Guelph, Ontario, Canada to receive either a controlled-release capsule of monensin or a placebo at 3 wk prior to expected calving. Serum samples were obtained at the time of treatment administration, and both serum and milk samples were collected at wk 1, 2, 3, 6, and 9 postcalving. The threshold used to define subclinical ketosis was selected a priori at a concentration of > or = 1200 mumol/L of beta-hydroxybutyrate. Using this threshold, the prevalence and incidence of subclinical ketosis were significantly reduced (50%) by monensin treatment. The duration of subclinical ketosis for cows that had been treated with monensin was also shorter than that for cows treated with the placebo. Monensin treatment significantly reduced the incidence of subclinical ketosis when the threshold was defined using higher concentrations of serum beta-hydroxybutyrate (1400 and 2000 mumol/L). In addition, monensin significantly reduced the prevalence of positive milk ketone tests.     

Chronic hepatitis in children after liver transplantation: role of hepatitis C virus and hepatitis G virus infections

BACKGROUND/AIMS: Chronic graft hepatitis occurs in 20-30% adults after liver transplantation but the prevalence and causes in children are not known. In adults, hepatitis C virus infection is prevalent prior to transplantation and recurrent infection is a frequent cause of graft dysfunction. The significance of the recently described hepatitis G virus infection remains unproven. The aim of this study was to examine the role of hepatitis C virus and hepatitis G virus infection in chronic graft hepatitis after paediatric liver transplantation. METHODS: The prevalence of graft hepatitis and the role of hepatitis C virus and hepatitis G virus infections in 80 children after liver transplantation have been studied, with a median follow up of 4.4 years (range 0.4 to 10.7), and the persistence of hepatitis G infection in the presence of immunosuppression has been determined. RESULTS: Chronic graft hepatitis was diagnosed in 19/80 (24%) children and was most frequently seen in children transplanted for cryptogenic cirrhosis (71%). There was no significant difference in the prevalence of chronic hepatitis in those transplanted before or after donor anti-HCV screening. Hepatitis C infection occurred in three children transplanted prior to donor screening but in only one was associated with chronic hepatitis. Hepatitis G infection was found in 22/79 (28%) transplant recipients but was not associated with graft hepatitis. In 17/21 children hepatitis G infection persisted for a median of 5.2 years after transplantation. CONCLUSION: Chronic hepatitis occurred in 24% of children after liver transplantation, a similar prevalence to that in adults. Cryptogenic liver disease predisposed to graft hepatitis, but neither hepatitis C nor hepatitis G infection was associated. Hepatitis G virus caused a frequent and usually persistent infection after transplantation.