空肠弯曲菌细胞毒素研究

<正> 空肠弯曲菌是世界性流行胞泻的一个重要原因,许多地方的急性肠炎与之有关,然而人们对其发病机制所知甚少。因为它与炎性胞泻有关,我们推测它可能产生一种细胞毒素,类似于引起炎性腹泻的志贺氏痢疾杆菌或新近出现的引起出白性肠炎的大肠杆菌0.57所产生的毒素。 分离的10株空肠弯曲菌的菌体先经多粘菌素B处理,然后离心过滤得到无细胞滤液,将此滤液稀释后接种到Hela单层细胞(此法比前用于检测志贺氏毒素的细胞毒效应)及新鲜的中国地鼠卵巢单层细胞上,24小时后经苔盼蓝摄取试验确定引起50％细胞死亡的稀释度(CD_(50))。其中5个分离株的10~9细菌/ml处理源滤液CD_(50)为1:4,与Hela细胞与地鼠卵巢细胞结果类似(地鼠     

多种天敌控制多种害虫的模糊数学模型

从生态经济学的原理出发，利用模糊集理论，探讨如何评价天敌控制多种害虫的为害作用，提出了多种天敌控制多种害虫的模糊数学模型。同时又得到了天敌对害虫的控制能力C，影响率G，影响强度H，及权数ω(x)的计算公式，以及在天敌作用下安全度的讨论与分析。     

EAAT expression by macrophages and microglia: still more questions than answers

Glutamate is the main excitatory amino acid, but its presence in the extracellular milieu has deleterious consequences. It may induce excitotoxicity and also compete with cystine for the use of the cystine–glutamate exchanger, blocking glutathione neosynthesis and inducing an oxidative stress-induced cell death. Both mechanisms are critical in the brain where up to 20% of total body oxygen consumption occurs. In normal conditions, the astrocytes ensure that extracellular concentration of glutamate is kept in the micromolar range, thanks to their coexpression of high-affinity glutamate transporters (EAATs) and glutamine synthetase (GS). Their protective function is nevertheless sensitive to situations such as oxidative stress or inflammatory processes. On the other hand, macrophages and microglia do not express EAATs and GS in physiological conditions and are the principal effector cells of brain inflammation. Since the late 1990s, a number of studies have now shown that both microglia and macrophages display inducible EAAT and GS expression, but the precise significance of this still remains poorly understood. Brain macrophages and microglia are sister cells but yet display differences. Both are highly sensitive to their microenvironment and can perform a variety of functions that may oppose each other. However, in the very particular environment of the healthy brain, they are maintained in a repressed state. The aim of this review is to present the current state of knowledge on brain macrophages and microglial cells activation, in order to help clarify their role in the regulation of glutamate under pathological conditions as well as its outcome.