次氯酸钠/过氧化氢法处理含铜绿微囊藻原水

以铜绿微囊藻实验室单培养液及其10倍稀释液为原水,pH分别为7.3、7.6,用NaOCl和H2O2作氧化剂,以663nm吸光度变化百分率为指标,分别研究了单独氧化及先应用NaOCl后续H2O2氧化处理、再对已处理过的水样分别投加PAC混凝去除铜绿微囊藻的效果.结果表明:在水中NaOCl、H2O2浓度分别为2.0、1.5mg/L条件下,NaOCl、H2O2、联合氧化处理原水和稀释水的去除率分别为82.2%、50%,83.3%、57.1%,92.2%、78.5%;再分别投加PAC,浓度为40mg/L,混凝沉淀后,单独投加氧化剂的水样的去除率均不超过90%,联合氧化后的水样的去除率达到100%.NaOCl或H2O2刺激藻细胞分泌保护性粘性物质,这些粘性物质包裹藻细胞形成沉降性能良好的聚集体,但对PAC混凝有不利影响,联合氧化改善了这些物质的特性而促进了混凝效果.     

Na2SO3/H2O体系引发MMA聚合

实现了亚硫酸钠水溶液可以引发甲基丙烯酸甲酯(MMA)的聚合,并进一步研究了各种因素对聚合速率和聚合物分子量的影响.结果表明:亚硫酸钠水溶液可以有效引发甲基丙烯酸甲酯聚合;聚合动力学方程为Rp=kp[MMA]1.6[Na2SO3]0.44,聚合反应的总的活化能为81.7kJ/mol,所得到的聚合物分子量可达1.36x105,单体转化率高达86.7%.初步讨论了该引发体系可能的机理.     

5-氯-2-(4-氯-苯氧基)-苯酚的合成

以对二氯苯为起始原料,经过乙酰基化、醚化、过氧乙酸氧化、水解得到5-氯-2-(4-氯-苯氧基)-苯酚,改良后的工艺使终产品收率达32.9%,醚化反应改用氢氧化钾代替碳酸钾与对氯苯酚反应制备亲核试剂,均三甲苯代替二甲苯为溶剂,醚化产物收率达到69.2%。氧化反应使用乙酸酐与过氧化氢(w=0.30)反应制备氧化剂,乙酸为溶剂,氧化反应收率达到72.7%。     

程序升温热重法研究神府高温煤焦-CO2气化反应性

在制焦温度为1223~1773 K内,制备了慢速和快速神府煤焦,采用程序升温热重法研究了煤焦-CO2高温气化反应性。主要研究了升温速率、制焦温度和热解速率对煤焦反应性的影响,并对一种高温慢速热解焦(制焦温度为1573 K)的程序升温和等温动力学进行了比较。结果表明:升温速率对煤焦-CO2气化反应有明显影响;制焦温度较高的煤焦反应性较低;快速热解有利于提高煤焦的反应性;由程序升温法和等温法所得活化能随转化率变化呈现不同的趋势,但所得活化能的平均值分别为160.13 kJ/mol和163.21 kJ/mol,十分接近。     

在J2EE架构中数据对象的设计与实现

从数据流角度出发,基于MVC模式设计要求,对数据对象在不同层之间的传输和转换问题进行了深入分析,设计出基于对象化数据在不同层之间的实现思路,基于网络传输和跨平台性考虑,提出了VO和XAO的解决方案,并采用了COMMAND模式进行设计实现。     

对耦合板间接静电放电辐射场的数值分析

静电放电(ESD)抗扰度实验是电磁兼容(EMC)实验和测试技术的一项非常重要的实验之一,主要用于测试电子器件及设备的电磁敏感度.目前该标准规定了2种放电方式:直接放电和间接放电.其中间接放电模拟的是带电操作人员对受试器件放电的情形,这在实际生活中经常发生.本文基于IEC61000-4-2中规定的抗扰度实验平台,采用时域有限差分法(FDTD),结合脉冲函数形式的放电电流波形表达式,在对垂直耦合板实施间接放电情形下,对其附近空间的瞬态辐射场作了数值分析与计算.     

CNTF信号转导途径上游的新支路

用活细胞内荧光探针Ｆｕｒａ２／ＡＭ检测ＣＮＴＦ对谷氨酸引起的海马神经细胞内游离Ｃａ＾２＋浓度升高的快速影响,并观察Ｇ蛋白是否参与。结果表明,谷氨酸可引起海马神经细胞内游离Ｃａ＾２＋浓度快速升高,并在５００μｍｏｌ／Ｌ范围内呈剂量相关性。ＣＮＴＦ对静息条件下海马神经细胞内的游离Ｃａ＾２＋浓度无显著性改变。但ＣＮＴＦ孵育５ｍｉｎ后,可快速压抑谷氨酸引起的胞内游离Ｃａ＾２＋浓度升高,这一过程有ＰＴＸ敏感     

How do Shp2 mutations that oppositely influence its biochemical activity result in syndromes with overlapping symptoms?

Activating and inactivating mutations of SHP-2 are responsible, respectively, for the Noonan (NS) and the LEOPARD (LS) syndromes. Clinically, these developmental disorders overlap greatly, resulting in the apparent paradox of similar diseases caused by mutations that oppositely influence SHP-2 phosphatase activity. While the mechanisms remain unclear, recent functional analysis of SHP-2, along with the identification of other genes involved in NS and in other related syndromes (neurofibromatosis-1, Costello and cardio-facio-cutaneous syndromes), strongly suggest that Ras/MAPK represents the major signaling pathway deregulated by SHP-2 mutants. We discuss the idea that, with the exception of LS mutations that have been shown to exert a dominant negative effect, all disease-causing mutations involved in Ras/MAPK-mediated signaling, including SHP-2, might lead to enhanced MAPK activation. This suggests that a narrow range of MAPK signaling is required for appropriate development. We also discuss the possibility that LS mutations may not simply exhibit dominant negative activity. Received 30 November 2006; received after revision 8 February 2007; accepted 13 March 2007     

Surface molecules regulating rolling and adhesion to endothelium of neutrophil granulocytes and MDA-MB-468 breast carcinoma cells and their interaction

The extravasation of leukocytes and tumor cells is a multi-step process with the involvement of various adhesion molecules depending on the three steps rolling, adhesion, and diapedesis. We have developed an in vitro model, by which we investigated the rolling and adhesion of neutrophil granulocytes and MDA-MB-468 human breast carcinoma cells to lung endothelial cells under physiological flow-conditions. We found that norepinephrine had an inhibitory function on the fMLP-promoted adhesion of neutrophil granulocytes due to a down-regulation of β2-integrin. Furthermore, neutrophil granulocytes serve as linking cells for the interaction of the MDA-MB-468 cells with the endothelium, which are both β2-integrin negative, but express the β2-integrin ligand ICAM-1. In addition, we show here that N-cadherin is up-regulated on the endothelial cells and on neutrophil granulocytes in response to fMLP. This up-regulation resulted in a significant increase of adherent MDA-MB-468 cells, which are also N-cadherin positive. Received 3 September 2007; received after revision 17 October 2007; accepted 22 October 2007