星形神经胶质细胞摄取谷氨酸与环境因子和离子运输的关系

本文以星形神经胶质细胞为对象,用同位素示踪技术较详细地研究了介质中Na、、K~+和CL~-、不同浓度的卡因酸以及几种抑制剂对L-谷氨酸摄取的影响;并观察了L-谷氨酸对星形神经胶质细胞膜运输Na~+、K~+、Cl~-和Ca~(2+)等的作用.结果表明:L-谷氨酸的摄取依赖于介质中是否存在Na~+ ,在缺Na~+介质中对Cl~-的依赖性也较明显,但在正常Na~+浓度下,含Cl~_和缺Cl~_没有明显差别.当增加介质中K~+浓度引起膜的去极化时,则能降低L~_谷氨酸的摄取.反过来,L-谷氨酸的摄取也对Na~+、K~+、Cl~-等的运输起刺激作用.此外,卡因酸及所用的几种抑制剂对谷氨酸的摄取办有明显抑制作用.     

胶质细胞源神经营养因子研究进展

叙述了新近纯化的胶质细胞源神经营养因子（ＧＤＮＦ）的生物功能及其在鼠胚胎的分布,着重介绍了该因子对损伤的多巴胺能神经元及运动神经元促进存活,修复损伤及再生的活性。     

星形胶质细胞的生物学功能

人类大脑由两类细胞组成:一类是神经元,另一类是神经胶质细胞。神经胶质细胞的数量约为神经元的10倍,但其作用长期以来一直被认为仅限于在神经元之间充当填充物,填满大脑中的剩余空间,同时为神经元提供营养。但近年来认识到神经胶质细胞的主要成员星形胶质细胞能够感知外界刺激,它的反应选择性甚至高于相邻神经元。神经元的反应活动很多都要经过星形胶质细胞的介导才能完成。本文介绍了星形胶质细胞在神经调制、突触调节和神经血管系统偶联方面的一些新进展,以期在不久的将来对星形胶质细胞的功能有更深入的了解,并能应用于临床实践。     

星形胶质细胞诱导成年神经干细胞的神经发生

在中枢神经系统 ,成年后新神经元发生主要见于两个脑区 ,即室管下区 (ｓｕｂｖｅｎｔｒｉｃｕｌａｒｚｏｎｅ)与海马的颗粒下区 (ｓｕｂｇｒａｎｕｌａｒｚｏｎｅ)。正常情况下 ,除上述脑区外的其它脑区能够产生神经胶质细胞 ,但是不能产生神经元。为了研究神经元和 /或神经胶质细胞对来源于成年的神经干细胞分化的影响 ,Ｓｏｎｇ等分离了成年大鼠海马的神经元和星形胶质细胞 ,将其分别或联合与来自成年的、依赖ＦＧＦ 2的神经干细胞共培养 ,意外地发现神经元促进神经干细胞分化为少突胶质细胞 ,而星形胶质细胞则促进神经干细胞分化为神经…     

胶质细胞的神经干细胞/祖细胞特性

近年来,关于胶质细胞有许多令人惊奇的发现。其中最令人感兴趣的是部分胶质细胞在体内外都表现出神经千细胞／祖细胞的特性,在适当条件下能分化成神经元、星形胶质细胞和／或少突胶质细胞。不仅存在于非哺乳类脊椎动物整个生命周期的放射胶质显示出这一特性,存在于成年哺乳动物脑室下区和颗粒下层的星形胶质细胞也是如此。在体外培养中,部分胶质细胞具有形成多潜能神经球的能力。在体内,胶质细胞充当前驱细胞时的命运受到细胞间相互作用、细胞因子、血脉系统、胞外基质以及基膜等所构建的微环境的影响。胶质细胞的这些特性将对神经修复产生深远影响。     

胶质细胞衍生的神经营养因子与神经退行性性疾病

胶质细胞衍生的神经营养因子（ＧＤＮＦ）是多巴胺神经元及运动神经元的营养因子,对由于损伤引起的多巴胺神经元及运动神经元的变性有保护及修复作用,因而可能用于临床治疗ＰＤ和ＡＬＳ这类神经退行性疾病。     

运动性骨骼肌疲劳亚细胞机制的探讨

本实验采用持续性下坡跑运动,观察大鼠骨骼肌运动后不同时相线粒体形态、代谢、机能等指标的变化,结果表明：大鼠运动后即刻线粒体钙含量、细胞膜丙二醛（ＭＤＡ）值明显增加,ＡＴＰ含量和细胞膜Ｎａ＋,Ｋ＋－ＡＴＰ酶活性下降;运动后２４ｈ线粒体钙含量、ＭＤＡ值增加最明显,ＡＴＰ含量仍未恢复,细胞膜Ｎａ＋,Ｋ＋－ＡＴＰ酶活性基本恢复,线粒体体密度、平均体积比运动前明显增加,比表面缩小;运动后４８ｈＡＴＰ含量完全恢复,线粒体钙含量、ＭＤＡ值开始恢复。本研究结果提示,急性运动引起的细胞膜脂质过氧化加强、线粒体形态、代谢机能异常抑制线粒体氧化磷酸化过程、减少ＡＴＰ生成可能是运动性骨骼肌疲劳的亚细胞机制之一。耐力训练可以通过改善线粒体形态、代谢、机能提高机体的运动能力。     

胶质细胞参与神经病理痛的机制

神经病理痛是由于躯体感觉系统的损伤或疾病所引起的疼痛。胶质细胞主要包括中枢神经系统的星形胶质细胞和小胶质细胞,以及外周神经系统的施旺细胞和卫星胶质细胞。胶质细胞在神经受损后被激活,发生形态变化并上调特定蛋白表达,通过与神经元的相互作用,在神经病理痛的初始和维持阶段发挥重要作用。本文综述近年来胶质细胞参与神经病理痛的研究成果。     

Palladin regulates cell and extracellular matrix interaction through maintaining normal actin cytoskeleton architecture and stabilizing beta1-integrin

Cell and extracellular matrix (ECM) interaction plays an important role in development and normal cellular function. Cell adhesion and cell spreading on ECM are two basic cellular behaviors related to cell-ECM interaction. Here we show that palladin, a novel actin cytoskeleton-associated protein, is actively involved in the regulation of cell-ECM interaction. It was found that palladin-deficient mouse embryonic fibroblasts (MEFs) display decreased cell adhesion and compromised cell spreading on various ECMs. Disorganized actin cytoskeleton architecture characterized by faint stress fibers, less lamellipodia and focal adhesions can account for the weakened cell-ECM interaction in palladin(-/-) MEFs. Furthermore, decreased polymerized filament actin and increased globular actin can be observed in palladin(-/-) MEFs, strongly suggesting that palladin is essential for the formation or stabilization of polymerized filament actin. Elevated phospho-cofilin level and proper responses in cofilin phosphorylation to either Rho signal agonist or antagonist in palladin(-/-) MEFs indicate that disrupted stress fibers in palladin(-/-) MEFs is not associated with cofilin phosphorylation. More interestingly, the protein level of ECM receptor beta1-integrin is dramatically decreased in MEFs lacking palladin. Down-regulation of beta1-integrin protein can be restored by proteasome inhibitor MG-132 treatment. All these data implicate that palladin is essential for cell-ECM interaction through maintaining normal actin cytoskeleton architecture and stabilizing beta1-integrin protein.     

Movement of different-shaped particles in a pan-coating device using novel video-imaging techniques

The purpose of this study was to investigate the effects of particle shape on the movement of particles in a pan-coating device using novel video-imaging techniques. An area scan CCD camera was installed inside a 24-in pan coater at the same location as that of a spray nozzle, and the movement of particle was tracked using machine vision. A white tracer particle was introduced inside a bed of black-coated particles. The effects of pan loading, pan speed, and particle shape on the movement of particles was studied. The response variables were circulation time, surface time, projected area of particle per pass, dynamic angle of repose, cascading velocity, and dispersion coefficient. Experiments were conducted at 3 different pan speeds, 6, 9, and 12 rpm, and 2 fill levels (ratio of bed depth to pan diameter), one eighth and one quarter, and data were collected over a 30-minute time period. The differences in circulation times of spheres and tablets, with similar volume equivalent diameter as that of the sphere, were found to be insignificant at the 95% confidence interval. The circulation time ranged from 2.8 to 10.8 seconds depending on the operating condition and increased with increasing pan load and decreasing pan speed. The distributions of circulation time, surface time, and projected surface area were found to be nonnormal. The dynamic angle of repose for tablets was higher than for spheres. Also, the bed surface for spheres was much flatter in comparison with tablets where the bed shape attained a “wave-like” form. The average velocity of tablets in the cascading layer was found to be significantly higher than spheres. A linear model (R ²>0.98) best described the variation of velocity as a function of pan speed for all of the operating conditions. Published: October 6, 2005     

Leaflet Movement of Robinia pseudoacacia in Response to a Changing Light Environment

Diurnal and nocturnal leaflet movement of black locust （Robinia pseudoacacia L.） was investigated under three light schemes： 100% natural irradiance, 50% shading, and 90% shading. Changes in leaf mid-vein angle were described by measurements of two planes： （i） β, the angle formed by the bottom of the petiolule and its relation to the horizontal plane; and （ii） θ, the angle between the petiolule and the main leaflet vein. The two highest light regimens had a significant effect on β. Variation in β tends to make the leaflet more erect, thereby minimizing any negative impact of high irradiance on leaf lamina. Light-dark rhythms induced variation in θ （termed nyctinastic movement）. Nyctinastic movement is important during the low light levels experienced by leaflets in early morning and late afternoon. At low light levels, the leaflet stopped nyctinastic movement and θ was fixed at an angle that may have enabled the leaf lamina to maximize light interception. After the light-dark cycle was reestablished, nyctinastic movement was restored. Taken together, our results suggest that irradiance induces variation in β leading to diurnal leaflet movement （diaheliotropism）, whereas the light-dark cycle influences θ, which results in nocturnal leaflet movement. Both angles are important for describing patterns of leaf movement in R. pseudocacia.     

Palladin is a novel binding partner of ILKAP in eukaryotic cells

Palladin was a novel binding partner of ILKAP in eukaryotic cells. Palladin’s C-terminal fragment including only its last three Ig domains (residues 710–1106) and the PP2C domain of ILKAP (residues 108–392) were necessary and sufficient for their interaction. The biological significance of the interaction between palladin and ILKAP was that palladin recruited the cytoplasmic ILKAP to initiate ILKAP-induced apoptosis. Our results suggested that palladin played a specific role in modulating the subcellular localization of the cytoplasmic ILKAP and promoting the ILKAP-induced apoptosis.     

The Cell Adhesion Molecule Necl-4/CADM4 Serves as a Novel Regulator for Contact Inhibition of Cell Movement and Proliferation

Contact inhibition of cell movement and proliferation is critical for proper organogenesis and tissue remodeling. We show here a novel regulatory mechanism for this contact inhibition using cultured vascular endothelial cells. When the cells were confluently cultured, Necl-4 was up-regulated and localized at cell–cell contact sites where it cis-interacted with the vascular endothelial growth factor (VEGF) receptor. This interaction inhibited the tyrosine-phosphorylation of the VEGF receptor through protein-tyrosine phosphatase, non-receptor type 13 (PTPN13), eventually reducing cell movement and proliferation. When the cells were sparsely cultured, Necl-4 was down-regulated but accumulated at leading edges where it inhibited the activation of Rho-associated protein kinase through PTPN13, eventually facilitating the VEGF-induced activation of Rac1 and enhancing cell movement. Necl-4 further facilitated the activation of extracellular signal-regulated kinase 1/2, eventually enhancing cell proliferation. Thus, Necl-4 serves as a novel regulator for contact inhibition of cell movement and proliferation cooperatively with the VEGF receptor and PTPN13.     

N-Acetylglucosamine 6-O-sulfotransferase-1 is required for brain keratan sulfate biosynthesis and glial scar formation after brain injury

Keratan sulfate (KS) is a glycosaminoglycan composed of repeating disaccharide units with sulfate residues at the C6 positions of galactose and N-acetylglucosamine (GlcNAc). The N-acetylglucosamine 6-O-sulfotransferase(s) (GlcNAc6ST) involved in the synthesis of KS in the central nervous system (CNS) has long been unidentified. Here, we report that a deficiency of GlcNAc6ST-1 leads to loss of 5D4-reactive brain KS and reduction of glial scar formation after cortical stab injury in mice. During the development of mice deficient in GlcNAc6ST-1, KS expression in the brain was barely detectable with the KS-specific antibody 5D4. The reactivity of 5D4 antibody with protein tyrosine phosphatase zeta (PTPzeta), a KS proteoglycan (KSPG), was abolished in the deficient mice. In adults, brain injury induced 5D4-reactive KS synthesis in the wounded area in wild-type (WT) mice but not in the deficient mice. Glial scar is formed via the accumulation of reactive astrocytes and is a major obstacle to axonal regeneration by injured neurons. Reactive astrocytes appeared to similar extents in the two genotypes, but they accumulated in the wounded area to a lesser extent in the deficient mice. Consequently, the deficient mice exhibited a marked reduction of scarring and enhanced neuronal regeneration after brain injury. These findings highlight the indispensable role of GlcNAc6ST-1 in brain KS biosynthesis and glial scar formation after brain injury.     

大麦黄矮病毒运动蛋白是RNA沉默抑制因子

大麦黄矮病毒(barley yellow dwarf virus,BYDV)属黄症病毒科家族,其基因组包含6个开放阅读框(open reading frames,ORFs).将BYDV的6个基因分别克隆到pWEIMING101载体上,得到重组基因.电击转化农杆菌后,利用农杆菌瞬时表达方法渗透注射转GFP基因的本氏烟草16c植株的叶片,在长波长紫外灯下观察GFP的表达,并通过Northern blot证明所得现象.研究结果表明,BYDV的PAV株系ORF4编码的运动蛋白(movement protein,MP)是RNA沉默抑制因子,其表达可以抑制局部和系统RNA沉默.BYDV-MP与GFP的双链RNA(dsGFP)共表达后仍能抑制RNA沉默,荧光强度与叶片中GFP的mRNA和其沉默降解形成的siRNA的量有对应关系,其N端核定位序列对抑制局部基因沉默起主要作用,第5、6位氨基酸是抑制基因沉默的关键氨基酸.BYDV-MP单独渗透注射的部位均产生细胞死亡.     

Solvent Effects on the Shape of a Tetramer

Abstract

The solvent effect on the shape of a tetramer with increasing temperature is analyzed. For this purpose models of an isolated chain and a chain immersed in a solvent have been simulated by Molecular Dynamics. A solvent model represented by stochastic forces has been tested against molecular dynamics results. The behaviour of the mean-square end-to-end distance 〈R ²〉 and 〈l ₁ ³ S ²〉 with increasing temperature are shown. where l ₁ is the longest eigenvalue of the moment of inertia tensor and S is the radius of gyration. All the chain models studied show different behaviour of these quantities at low temperature compared to high temperature where the shape of the tetramer is temperature insensitive. The main solvent effect is to pospone the transition to higher temperature. The stochastic solvent model qualitatively agrees with molecular dynamics results.