西南岩溶地区黄荆和檵木叶片结构对其生态环境的响应

应用常规石蜡切片法对生长于桂林毛村岩溶区和非岩溶区的黄荆(Vitex negundo)和檵木(Loropetalumchinense)的解剖特征进行了比较研究,并对两区的黄荆叶片表皮形态进行了扫描电镜观察.结果显示:(1)两地的黄荆叶片背面均有浓密的绒毛,但致密程度有差异,岩溶区黄荆叶片的气孔深藏于绒毛间隙,这种结构可减少水分蒸发,降低因岩溶干旱带来的水分缺失.(2)岩溶区黄荆和檵木的叶片厚度、上下表皮厚度、栅栏组织的厚度以及栅栏组织的致密程度均大于非岩溶区,这些特征有利于减少水分蒸腾.(3)岩溶区黄荆和檵木叶片的维管组织发达程度高于非岩溶区,有利于在蒸腾减小的情况下促进水分运输和营养元素的迁移,说明2种植物叶片结构特征在不同生境区的改变是其长期在岩溶区干旱环境条件下形成的适应性变化.     

东亚小花蝽成虫对西花蓟马若虫的捕食功能反应与搜寻效应

为探明东亚小花蝽对西花蓟马的控制效能,开展了东亚小花蝽成虫对西花蓟马若虫的捕食功能反应与搜寻效应研究。结果表明,在供试温度下,该捕食功能反应符合HollingⅡ型方程。在相同温度下,东亚小花蝽成虫的捕食量随着猎物密度的增加而增大,搜寻效应随着猎物密度的增加而降低。在18℃～26℃内,随着温度的升高,东亚小花蝽成虫对西花蓟马若虫的捕食量增加,而在26℃～34℃则有相反的趋势。在相同猎物密度条件下,随着东亚小花蝽成虫密度的增大,其平均捕食量逐渐减少,捕食作用率也相应地降低,东亚小花蝽成虫之间存在分摊竞争。     

温度对拟小食螨瓢虫捕食皮氏叶螨成螨功能反应的影响

在5个温度(16℃、20℃、24℃、28℃和32℃)条件下,测定了拟小食螨瓢虫雌成虫对皮氏叶螨成螨的捕食功能反应。结果表明,在试验温度范围内,各温度下的功能反应均能用Holling圆盘方程(Ⅱ型)拟合,但各温度间功能反应的参数存在差异。以瞬时攻击率和捕食处理时间为评价指标,在16℃～28℃,拟小食螨瓢虫雌成虫对皮氏叶螨成螨的捕食效能随温度的上升而提高,28℃时达到最高,此时的瞬时攻击率和捕食处理时间分别为0.5899和0.0169d。温度上升至32℃时,捕食效能略为下降,此时的瞬时攻击率和捕食处理时间分别为0.5740和0.0184d,与28℃时的瞬时攻击率和捕食处理时间差异不显著。表明较高温度有利于拟小食螨瓢虫发挥对皮氏叶螨成螨的控制作用。在试验的密度和温度范围内,以三次多项方程描述了在不同猎物密度和温度组合下拟小食螨瓢虫雌成虫对皮氏叶螨成螨的捕食作用,以软件Surfer8.0生成了皮氏叶螨成螨密度和温度组合下的拟小食螨瓢虫雌成虫捕食量模拟值等值线图。同时,还对拟小食螨瓢虫在热带作物害虫生物防治中的应用潜力进行了讨论。     

一个具有扩散和时滞的捕食模型的持久性与周期解的存在性

对一类在斑块环境下具有Beddington型功能性反应和时滞现象的非自治捕食系统进行了研究,证明系统在适当的条件下是永久持续生存的;利用重合度理论,得到了一组保证该系统存在正周期解的充分条件．     

A Pseudomonas syringae pv. tomato DC3000 mutant lacking the type III effector HopQ1-1 is able to cause disease in the model plant Nicotiana benthamiana

The model pathogen Pseudomonas syringae pv. tomato DC3000 causes bacterial speck in tomato and Arabidopsis, but Nicotiana benthamiana, an important model plant, is considered to be a non-host. Strain DC3000 injects approximately 28 effector proteins into plant cells via the type III secretion system (T3SS). These proteins were individually delivered into N. benthamiana leaf cells via T3SS-proficient Pseudomonas fluorescens, and eight, including HopQ1-1, showed some capacity to cause cell death in this test. Four gene clusters encoding 13 effectors were deleted from DC3000: cluster II (hopH1, hopC1), IV (hopD1, hopQ1-1, hopR1), IX (hopAA1-2, hopV1, hopAO1, hopG1), and native plasmid pDC3000A (hopAM1-2, hopX1, hopO1-1, hopT1-1). DC3000 mutants deleted for cluster IV or just hopQ1-1 acquired the ability to grow to high levels and produce bacterial speck lesions in N. benthamiana. HopQ1-1 showed other hallmarks of an avirulence determinant in N. benthamiana: expression in the tobacco wildfire pathogen P. syringae pv. tabaci 11528 rendered this strain avirulent in N. benthamiana, and elicitation of the hypersensitive response in N. benthamiana by HopQ1-1 was dependent on SGT1. DC3000 polymutants involving other effector gene clusters in a hopQ1-1-deficient background revealed that clusters II and IX contributed to the severity of lesion symptoms in N. benthamiana, as well as in Arabidopsis and tomato. The results support the hypothesis that the host ranges of P. syringae pathovars are limited by the complex interactions of effector repertoires with plant anti-effector surveillance systems, and they demonstrate that N. benthamiana can be a useful model host for DC3000.     

Immune response to stem cells and strategies to induce tolerance

Although recent progress in cardiovascular tissue engineering has generated great expectations for the exploitation of stem cells to restore cardiac form and function, the prospects of a common mass-produced cell resource for clinically viable engineered tissues and organs remain problematic. The refinement of stem cell culture protocols to increase induction of the cardiomyocyte phenotype and the assembly of transplantable vascularized tissue are areas of intense current research, but the problem of immune rejection of heterologous cell type poses perhaps the most significant hurdle to overcome. This article focuses on the potential advantages and problems encountered with various stem cell sources for reconstruction of the damaged or failing myocardium or heart valves and also discusses the need for integrating advances in developmental and stem cell biology, immunology and tissue engineering to achieve the full potential of cardiac tissue engineering. The ultimate goal is to produce 'off-the-shelf' cells and tissues capable of inducing specific immune tolerance.