丝状伪足

Induced activation of Rac1,Cdc42 signal transduction pathway, monitoring the transfer of living cells activated sheet pseudopodium emerged and filopodia obvious morphological changes,such as measured values or fluorescence imaging of fluorescence intensity over time to continuously reduce until almost see the determination or observation.

诱导激活的Rac1、Cdc42信号转导通路，监测到转染激活的活细胞中出现片状伪足和丝状伪足等明显的形态变化，测定荧光值或者成像的荧光强度随着时间推移不断降低，直至几乎测定或观察不到。

To investigate the effect of p38MAPK signal conducting pathway on livercancinoma cell's malignant phenotype induced by VEGF,we take theexperiment with cell growth test,scanning microscope and laser scanningconfocal microscope so that observe effect of p38MAPK signal conductingpathway on liver cancinoma cell growth,pseudopodium formation andframework of cytoskeleton induced by VEGF.results indicate that the cellbecame ellipse and there were more and thick pseudopodium in the cell'ssurface after being treated by VEGF,and destroyed framework ofcytoskeleton,which can be blocked by pretreated with a special inhibitor ofp38MAPK SB203580 so that VEGF promote metastasis by enhancing livercell migration and movement via p38MAPK signal conducting pathway,butVEGF promote cell growth without p38MAPK signal conducting pathway.

为进一步探讨VEGF通过p38信号传导通路诱导肝癌细胞转移时，对肝癌细胞恶性表型的影响，采用细胞增殖实验、扫描电子显微镜、激光扫描共聚焦显微镜观察VEGF对肝癌细胞增殖作用、细胞伪足形成、细胞骨架微丝结构的影响以及p38MAPK信号通路调控作用。结果显示，VEGF能够不通过p38信号通路促进肝癌细胞增殖；VEGF诱导肝癌细胞丝状伪足增多、增长，使细胞骨架微丝结构破坏、甚至消失。阻断p38MAPK信号通路，可以抑制VEGF诱导的肝癌细胞伪足形成，细胞骨架丝状结构呈束状，排列较规整。上述结果表明，VEGF可以通过p38信号传导通路诱导肝癌细胞伪足增多、增长，促使细胞骨架微丝结构破坏，使肝癌细胞迁移、运动能力增加，促进肿瘤转移。VEGF并不通过p38信号通路诱导肝癌细胞增殖作用。

The activated Rac1 and Cdc42 signaling pathways led to the formation of lamelliopodia and filopodia in the transfected cells respectively.

诱导激活的Rac1、Cdc42信号转导通路，分别导致转染的活细胞中出现片状伪足和丝状伪足。

The cells were shuttle-like, the lamellipodia and many filopodia were extended from the cells.

细胞变为梭形，伸出板状伪足和许多丝状伪足。

These structures include filopodia, lamellipodia, stress fiber and focal adhesion.

已知与肌动蛋白相关的细胞结构主要有：丝状伪足、板状伪足、粘着斑和张力纤维。

Cdc42 and Rac1 have similar effects on cytoskeleton. They both promote the actin polymerization in the cell and profit the formation of filopodia and lamelipodia respectively.

Cdc42和Rac促进细胞内肌动蛋白聚合，分别有利于丝状伪足和片状伪足的形成；而RhoA可能具有与Cdc42 和Rac相反的效果，通常造成细胞边缘和突起的收缩及胞体变圆。

Thus the actin-based structures which have tight relation with the migration of VSMC take part in the development of restenosis. These structures include filopodia, lamellipodia, stress fiber and focal adhesion.

已知与肌动蛋白相关的细胞结构主要有：丝状伪足、板状伪足、粘着斑和张力纤维。

Recent studies showed that Rho GTPase played a key role in the reorganization of cytoskeleton and in Swiss 3T3 cells, Cdc42, Rac1 and RhoA, three members of Rho superfamily of small GTPase, regulated the polymerization of actin to produce filopodia , lamellipodia, stress fiber and focal adhension, respectively.

近年来的研究表明，Rho家族小G蛋白是细胞骨架肌动蛋白的重要调节因子，目前众多的研究集中在Rho小G蛋白家族成员中的Cdc42、Rac1和RhoA，其中Cdc42促进丝状伪足的形成，Rac1调节板装伪足的生成和膜皱缩，RhoA则促进粘着斑连接和张力纤维的装配。

Before treatment,there are abundant microvtlli on the cell surface,many filoplodia on the cell rim,few of endoplasmic reticulums , Golgi complexes and mitochondrions with abnormal structure and lots of free ribosomes in the cytoplasm. The shape of nucleus is irregular with high nuclear-cytoplasmic ratio, many dark pellets of heteromatin and a few of nucleoluses in which there ar...

经1.5×10~2g/L地塞米松处理后，细胞表面微绒毛和丝状伪足显著减少或消失，出现皱褶状和小泡状结构；细胞核形规则，核质比值减小，异染色质团块减少，核仁数目减少、结构致密；细胞质中粗糙型内质网、高尔基体、线粒体数量增多，形态结构典型，游离核糖体减少，这些变化说明地塞米松改变了MGc80-3细胞的超微结构特征，具有明显的诱导分化作用。

The morphology and structure of reconstructed tissue was detected by microscope and scanning electron microscope.Results:(1) Compared with the control group, the cellular proportion of laminin group increased in 62 ~M phase, and decreased in Go~Gi phase significantly. As shown by the microscope, the cells of control group were in low density. The cells in mass connected tightly. The microfilament appeared reticular formation. The nucleus were the same in size. The cells of laminin group were in high density and put out so many lamellipodia, filopodia, which connected with the surrounding cells. The microfilament increased, elongated, and changed from reticulodromous to sarciniform, which reached to the pseudopods. The nucleus were different in size .(2) As shown by the inverted microscope and the cell growth curve, comparing with the controlgroup, cells of each test group increased evidently. The cellular proportion of each test group increased in S phase and G2 ~M phase, and decreased in Go~Gi phase significantly, but there was no considerable interations between LN and EGF;(3) As shown by the morphological observations, the cultured cat corneal endothelial cells formed an integrated membrane, and attached to the Descemets membrane closely, which was similar to the natural tissue. The cells connected tightly to each other, and some of them arranged in hexagon approximately.

结果：(1)层粘连蛋白组处于G_2～M期细胞比例较对照组显著提高，Go～G_1期细胞比例显著下降，提示层粘连蛋白促进内皮细胞DNA合成，及细胞分裂增殖；光镜下，对照组细胞分布成团状，细胞密度较低，细胞间连接紧密，细胞内微丝结成网状，细胞核大小一致；与对照组相比，层粘连蛋白组细胞生长旺盛，细胞密度高，向周边伸出大量板状及丝状伪足，细胞内微丝增多、拉长、集结成束，伸入伪足中，细胞核形状大小不一致；(2)倒置显微镜观察及细胞生长曲线显示，各组细胞数目随时间增加而明显增多，各实验组较对照组增生显著，EGF和LN联合应用组各时间点细胞数目最高；实验组处于S期和G_2～M期细胞数目增加，Go～G_1期细胞数目减少；提示EGF、LN单独及联合应用均可促进细胞增殖，但尚不能认为二者有交互作用；(3)倒置显微镜下，组织培养的猫角膜内皮细胞排列成密集的单层，细胞间连接紧密；组织学观察发现，培养的猫角膜内皮细胞形成完整的内皮层，贴附于脱水基质的后弹力膜上，与正常的角膜内皮组织结构相似；扫描电镜下，组织培养的猫角膜内皮细胞间紧密镶嵌排列，可见某些细胞呈近似六边形排列，细胞大小不甚一致，胞核清晰。

This paper discusses design and realizable methods of remote test output interface from logical design angle.

本文从逻辑设计的角度讨论遥测输出接口的设计及实现方法。

This also 星体投射plies to buildings, structures and geological features.

这也适用于建筑物和地质特征。