Kinetic models for peptide-induced leakage from vesicles and cells

In this article analytical expressions for peptide-induced membrane leakage are presented. Two different models for time-dependent leakage have been developed. In the first, the leakage is assumed to be coupled by pores formed by the peptides. In the second model the peptide is assumed to induce a stress/perturbation in the membrane, and in order to reduce the stress, rearrangements in the membrane are induced. The leakage is coupled to these rearrangements, and when equilibrium is achieved no more leakage occurs. From the kinetic models simple fitting routines have been developed involving only two fitting parameters, and these have been used to fit experimental data for two prion protein-derived peptides as well as the honey bee toxin melittin in both vesicles and erythrocytes with good results. The fitted parameters provide both a quantitative and a qualitative basis for interpreting the experimental results. In addition a model for the peptide concentration-dependent leakage is presented, which was used to fit experimental data for leakage induced by the prion protein-derived peptides. The models presented in this article are compared with other models for peptide-induced membrane leakage.     

Leakage-channel conductance of single (Na+ + K+)-ATPase molecules incorporated into planar bilayers by fusion of liposomes

By fusing liposomes which contain in the mean only one pump unit (one intramembranous particle) to planar bilayers, and provoking the ouabain-blockable leakage conductance by the presence of n-decane, the predominant unit leakage conductance associated with one pump unit was estimated to be 40–50 pS, indicating the channel nature of the leakage pathway.     

Interactions of Gliocladium virens with Rhizoctonia solani and Pythium ultimum in Non-sterile Potting Medium

Interactions of Gliocladium virens with Pythium ultimum and Rhizoctonia solani under simulated in vivo conditions were observed microscopically. Different types of propagules of the three fungi were paired on nitrocellulose membranes and incubated at 25°C in non-sterile potting medium in Petri dishes for 1-5 days. Alginate-wheat bran prill were used as carriers for G. virens. Prill inoculated with G. virens and pre-incubated in potting medium for 3-5 days before placement on membranes did not inhibit the germination of Pythium sporangia, but subsequent Pythium growth was markedly stunted and distorted, with some hyphal collapse and cytoplasmic leakage. G. virens had no visible effect on older Pythium mycelium. Two to 5 days' growth of G. virens caused cytoplasmic leakage of Rhizoctonia mycelium, prevented secondary branching of hyphae and occasionally coiled around Rhizoctonia hyphae. Prill that were newly colonized by G. virens, but not prill pre-incubated for 3 or 5 days, stimulated the growth of Pythium mycelium and sporangia, Rhizoctonia mycelium and unprimed monilioid cells, probably by supplying nutrients. The timing of the interactions and their specificity for the different pathogen propagules were consistent with the production of gliotoxin by G. virens. This view was supported by in vitro experiments, in which pathogen propagules were incubated in a range of concentrations of gliotoxin in potato dextrose broth. Pythium sporangia and mycelium were inhibited by 1 or 2 μmg ml^-1, but Rhizoctonia monilioid cells and mycelium required 3-5 μmg ml^-1 for inhibition. At the lowest effective concentrations the inhibition was sometimes reversible, but propagules were killed at high concentrations of gliotoxin.     

水稻耐铁毒性的生理指标研究

1　引　　言铁毒是热带和亚热带地区水稻栽培中常见的生理病害 ,主要原因是土壤溶液中积累过多的亚铁盐 ,严重影响了稻谷产量 .水稻遭受铁毒的外观症状是叶面产生棕褐色斑点 ,最初以叶片斑点的面积大小衡量铁毒伤害的严重程度[4 ] .但实际操作不方便 ,难以定量比较 ;且有试验表明 ,在部分品种中 ,叶片病斑面积和产量没有相关性[5] .目前普遍采用亚铁胁迫培养下植物干重相对受害 (减少 )率作为评价水稻耐铁毒能力的形态指标[1] ,但测定时会毁损植株 .为了在苗期筛选耐铁毒水稻时不毁损植株 ,建立评价水稻铁毒耐性的生理指标十分必要 .已有研…     

具有leakage时滞与随机干扰的离散神经网络渐近稳定性分析

研究了一类具有leakage时滞与随机干扰的离散型神经网络的全局渐近稳定性问题．利用一种新的时滞分割方法将时滞区间分割为多个区间．通过构造新的Lyapunov泛函得到了基于线性矩阵不等式（LMI）的渐近稳定性判据．该判据在获得更小的保守性同时也降低了计算的复杂度．     

Evaluating Plasmonic Transport in Current-carrying Silver Nanowires

Plasmonics is an emerging technology capable of simultaneously transporting a plasmonic signal and an electronic signal on the same information support^1,2,3. In this context, metal nanowires are especially desirable for realizing dense routing networks⁴. A prerequisite to operate such shared nanowire-based platform relies on our ability to electrically contact individual metal nanowires and efficiently excite surface plasmon polaritons⁵ in this information support. In this article, we describe a protocol to bring electrical terminals to chemically-synthesized silver nanowires⁶ randomly distributed on a glass substrate⁷. The positions of the nanowire ends with respect to predefined landmarks are precisely located using standard optical transmission microscopy before encapsulation in an electron-sensitive resist. Trenches representing the electrode layout are subsequently designed by electron-beam lithography. Metal electrodes are then fabricated by thermally evaporating a Cr/Au layer followed by a chemical lift-off. The contacted silver nanowires are finally transferred to a leakage radiation microscope for surface plasmon excitation and characterization^8,9. Surface plasmons are launched in the nanowires by focusing a near infrared laser beam on a diffraction-limited spot overlapping one nanowire extremity^5,9. For sufficiently large nanowires, the surface plasmon mode leaks into the glass substrate^9,10. This leakage radiation is readily detected, imaged, and analyzed in the different conjugate planes in leakage radiation microscopy^9,11. The electrical terminals do not affect the plasmon propagation. However, a current-induced morphological deterioration of the nanowire drastically degrades the flow of surface plasmons. The combination of surface plasmon leakage radiation microscopy with a simultaneous analysis of the nanowire electrical transport characteristics reveals the intrinsic limitations of such plasmonic circuitry.     

可溶的和纤维化的Aβ1-40对膜脂的通透性的影响

利用光散射,浊度,荧光以及电镜等技术研究了可溶性的A茁1-40聚集形成纤维的动力学过程;用三种水溶性的分子质量不同的荧光探剂ANTS/DPX,Calcein,DextranFD-4包裹在脂质体内,检测可溶的和纤维化的A茁1-40对其内含物漏出的影响。结果表明:可溶性的A茁1-40在pH7.4,37℃温育4天以后开始聚集,7天后形成稳定的纤维;聚集的A茁1-40能够诱导包裹在脂质体内的ANTS/DPX,Calcein的漏出,但不能诱发Dextran(FD-4)的漏出,并初步估算出聚集的A茁1-40在膜上能产生孔径为13-18魡的小孔,而可溶的A茁1-40无此作用。这提示我们,聚集成纤维的A茁1-40能改变膜脂的物理化学性质,并造成内含物的漏出,这些作用可能是造成神经细胞毒性的重要原因。