Adaptogenic functions of extracellular autoregulators of microorganisms

Information about the functions of extracellular autoregulators, which adapt microorganisms to the stresses “scheduled” in the development cycle of microbial cultures (stresses of new medium, starvation, or space exhaustion (high cell density)) is summarized in the review. In a number of bacteria and yeasts, derivatives of alkylhydroxybenzenes (AHB), particularly of the class of alkyl resorcinols, act as autoregulators with adaptogenic functions. The chemical structure of AHB determines their amphiphility; capacity for physical and chemical interaction with membrane lipids, proteins, and DNA; properties as natural modifiers of biological membranes and enzymes; and the expression of antioxidant activity. Increase of AHB concentration up to the critical level (10^?5-10^?4 M) results in cessation of cell division and in transition of the microbial culture to the stationary phase; further increase to 10^?4-10^?3 M induces a transition of some of the cells of a post-stationary culture to the anabiotic state with the formation of cystlike resting cells (CRC), even in non-spore-forming bacteria. AHB participate in the regulation of the phenotypic variability of bacteria. The dynamics of extra-and intracellular concentrations of AHB in growing microbial cultures and the polymodality of their effect determine the adaptogenic functions of AHB as autoinhibitors of culture growth, autoinducers of anabiosis, and autoinhibitors of germination of resting forms. Manifestation of any given function depends on the concentration of AHB, the physiological state of the recipient cells, and on environmental factors. The species nonspecificity of AHB effects points to their significant role in the regulation of the development and functioning of microbial communities.     

Meeting Report: The 24th Fungal Genetics Conference at Asilomar, California, USA

<正>The 24~(th) Fungal Genetics Conference was recently held at the Asilomar Conference Center in the coastal town of Pacific Grove,Monterey County,California,USA,between March 20~(th) and 25~(th),2007.At this conference,there were 750 participants representing 33 countries,with the number of participants reaching the maximum holding capacity of the conference center.About 200 people were on the waiting list and could not attend the meeting because of space limitations.     

城市绿地的生态环境效应研究进展

工业化的快速发展和城市化进程的加剧,使得城市生态环境的破坏和污染愈来愈严重,加速了城市的“生态环境危机”.城市绿地能够通过植被的光合作用、吸收作用、隔离阻挡作用、蒸腾以及蒸散作用改善城市的生态环境.目前研究主要集中在降温、增湿、固碳释氧、降噪、抗污染、生物多样性保护等6个方面.关于城区绿地对6种生态环境要素的改善程度、影响范围、机理问题以及不同植被种类生态环境效应的差异情况等,国内外学者都进行了大量详细的研究.基于传统实地观测数据进行城市绿地的生态环境效应研究是目前主要使用的研究方法,部分学者开始使用遥感技术手段研究城区绿地的降温增湿效应.在总结和分析前人研究成果的基础上,从研究内容的不同着手,主要总结并系统评估了目前关于城市绿地6种生态环境效应的研究,为今后相关研究提供参考.     

基于GIS的城市绿地景观引力场研究——以宁波市为例

城市绿地是城市用地的重要组成部分 ,也是城市生态系统的一个子系统。城市绿地景观的评价是城市生态系统研究的重要课题之一。在 GIS技术支持下 ,对城市绿地景观进行了研究。在研究过程中 ,将物理学中“场”的相关理论引入城市绿地景观的研究 ,提出绿地景观引力场的概念及评价方法。绿地景观引力场是城市绿地系统为城市居民提供服务能力的大小或潜力 ,其主要影响因素有绿地景观本身的质量、城市人口分布状况、城市土地利用现状、城市主要交通设施等。在研究中需要建立以下相关模型 :城市阻力的空间分布模型、城市人口的空间分布模型、城市公共绿地的空间分布模型、城市绿地景观引力场的空间分布评价模型。研究结果得出以下结论 :(1)景观引力场用于城市绿地系统的评价 ,能够更好地反映城市绿地的空间分布格局 ;(2 )丰富了城市绿地系统评价的指标内容和评价方法 ;(3)该方法从景观设计上提供了一个可供决策参考的依据 ;(4 )景观引力场还可用于城市其它服务设施的合理性与有效性的评价与研究。     

高频激光-DNA分子相互作用体系相空间的局域特征

利用激光与DNA分子相互作用的动力学模型,借助适当的数值方法,讨论了系统动力学演化及相空间特性。结果表明：高频激光可使DNA分子的运动状态发生变化;特别地,相空间分析表明,高频激光的作用会使DNA分子运动在一些特定状态之间转变。从而可说明高频激光作用下DNA分子呈现新的有序运动现象。     

Matrix metalloproteinases and angiogenesis

Matrix metalloproteinases (MMPs) are a family of enzymes that proteolytically degrade various components of the extracellular matrix (ECM). Angiogenesis is the process of forming new blood vessels from existing ones and requires degradation of the vascular basement membrane and remodeling of the ECM in order to allow endothelial cells to migrate and invade into the surrounding tissue. MMPs participate in this remodeling of basement membranes and ECM. However, it has become clear that MMPs contribute more to angiogenesis than just degrading ECM components. Specific MMPs have been shown to enhance angiogenesis by helping to detach pericytes from vessels undergoing angiogenesis, by releasing ECM-bound angiogenic growth factors, by exposing cryptic proangiogenic integrin binding sites in the ECM, by generating promigratory ECM component fragments, and by cleaving endothelial cell-cell adhesions. MMPs can also contribute negatively to angiogenesis through the generation of endogenous angiogenesis inhibitors by proteolytic cleavage of certain collagen chains and plasminogen and by modulating cell receptor signaling by cleaving off their ligand-binding domains. A number of inhibitors of MMPs that show antiangiogenic activity are already in early stages of clinical trials, primarily to treat cancer and cancer-associated angiogenesis. However, because of the multiple effects of MMPs on angiogenesis, careful testing of these MMP inhibitors is necessary to show that these compounds do not actually enhance angiogenesis.     

高相对分子质量裂褶多糖的制备与结构鉴定

以裂褶菌（Schizophyllum commune）发酵生产的培养物为研究对象,经过活性炭脱色、Sevag法脱杂蛋白、乙醇沉淀得粗多糖,再经Sephadex G-200柱层析分离纯化得裂褶多糖纯品.通过Sephadex G-200凝胶层析法测得其平均分子质量为436kDa;由气相色谱、红外光谱、高碘酸氧化、Smith降解、^13C核磁共振等方法表征其化学结构,推测其结构为具有（1→6）分支的β-〔1-3）-D-葡聚糖：其组成重复单元应该含有3个主链糖基和一个单糖分支,主链的取代发生在C-1和C-3之间,即为1→3糖苷键;分支发生在C-1和C-6之间,即为1→6糖苷键,其中分支点在主链糖基的C-6上.     

胞外ATP对壳聚糖诱导的ROS和PAL活性变化的影响

以烟草BY-2悬浮细胞为材料,探讨了胞外ATP对壳聚糖引起的活性氧(reactive oxygen species,ROS)水平和苯丙氨酸解氨酶(phenylalanine ammonia-lyase,PAL)活性变化的影响。结果表明,5~20μg·mL^-1壳聚糖处理导致了烟草悬浮细胞细胞内ROS水平逐渐增加;壳聚糖也导致了PAL活性的增加,其活性在15μg·mL^-1壳聚糖处理下达到峰值,此后有所降低。10~40μmol·L^-1外源ATP处理未引起烟草悬浮细胞内ROS水平和PAL活性的显著变化。细胞外ATP水平则随壳聚糖浓度的增加而逐渐下降。本文进一步分析了细胞外ATP对壳聚糖引起的ROS水平和PAL活性变化的影响。结果显示,外源施加20μmol·L^-1ATP可以有效降低壳聚糖诱导的烟草悬浮细胞ROS水平上升,同时外源ATP也明显减缓了壳聚糖所诱导的PAL活性的上升。上述结果表明,细胞外ATP水平能够影响壳聚糖引起的ROS水平和PAL活性的变化。     

Microtubule destruction induces tau liberation and its subsequent phosphorylation

Neurofibrillary tangle-bearing neurons, a pathological hallmark of Alzheimer’s disease, are mostly devoid of normal microtubule (MT) structure and instead have paired helical filaments that are composed of abnormal hyperphosphorylated tau. However, a causal relationship between tau phosphorylation and MT disruption has not been clarified. To examine whether MT disruption induces tau phosphorylation, stathmin, an MT-disrupting protein, was co-expressed with tau in COS-7 cells. Stathmin expression induced apparent MT catastrophe and tau hyperphosphorylation at Thr-181, Ser-202, Thr-205, and Thr-231 sites. In contrast, c-Jun N-terminal kinase activation, or phosphatase inhibition, led to significant tau phosphorylation without affecting MT structure. These findings suggest that MT disruption induces subsequent tau phosphorylation.