查询词典 cell

Results are as followed:1 Exposure of HELF cells to BP caused c-Jun activation,and increased the activity of MAPK,PI-3K,p53 and cyclin D1 pathway.2 BP-induced c-Jun activation was inhibited by dominant negative mutants of extracellular signal-regulated protein kinase or c-Jun NH_2-terminal kinase,but not by p38,impling that JNK and ERK pathways medicate c-Jun activation induced by BP.3 Overexpression of dominant-negative mutants PI-3K and Akt potently blocked phosphorylations of c-Jun and ERK,but not JNK in response to BP,suggesting that PI-3K/Akt pathway positively regulates BP-induced c-Jun activation through ERK.4 Inhibition of p53 by its chemical or molecular inhibitor markedly increased the phosphorylation levels of c-Jun,Akt and ERK upon BP stimulation,indicating that p53 negatively medicates BP-induced c-Jun activation through PI-3K/Akt/ERK pathway.5 The cell lines expressed TAM67 exhibits no significant affecting normal cell growth properties.6 TAM67 was able to significantly block G_1-S transition and subsequent cell proliferation,suggesting that c-Jun is essential for cell cycle alternations elicited by BP.7 Overexpression of TAM67 impaired BP-induced cyclin D1 activation,decreasing expression of E2F1 and pRb,indicating that c-Jun participates in the modulation of BP-induced activation of cyclin D1/pRb/E2F1 pathway.8 Stably expression of TAM67 led to the increases in the expression levels of p53 and p21,elevating phosphorylation level of p53,clearly indicating that c-Jun regulates p53/p21 pathway activation induced by BRCollectively,PI3K/Akt/ERK pathway mediated BP-induced c-Jun activation through p53-dependent mechanism.

结果显示：1BP刺激细胞可促进c-Jun活化，并伴随着MAPK、PI-3K、p53和cyclinD1通路各组成成分的活性增强。2利用MAPK通路的显性失活突变体分别阻断细胞外信号调节激酶和c-Jun氨基末端激酶活性，均可明显抑制BP诱导的c-Jun活化，但阻断p38活性对BP引起的c-Jun活化无明显影响，提示JNK和ERK通路参与调控BP诱导的c-Jun活化。3过表达PI-3K和Akt的显性失活突变体也可显著抑制BP诱导的c-Jun活化，并降低磷酸化ERK的表达水平，但对磷酸化JNK的表达水平无明显影响，说明PI-3K/Akt通路通过ERK正性调控了BP诱导的c-Jun活化。4p53的化学/分子抑制剂能使BP作用的细胞内c-Jun活性明显增加，并同时诱导Akt和ERK的磷酸化水平的升高，表明p53可通过PI-3K/Akt/ERK通路对BP诱导的c-Jun活化进行负性调控。5随后观察转染细胞的生长情况，发现TAM67对细胞正常生长和形态无明显影响。6稳定表达TAM67可有效抑制BP诱导的S期细胞数的增加，提示c-Jun在BP致细胞周期改变的过程中发挥了重要作用。7TAM67过表达能够抑制BP诱导的cyclin D1活化，降低磷酸化Rb以及E2F1蛋白表达水平，表明c-Jun参与调控BP诱导的cyclin D1/Rb/E2F1通路的活化。8过表达TAM67可使BP刺激的细胞中p53、p21总蛋白以及p53磷酸化的表达水平明显升高，可见c-Jun也参与调控BP诱导的p53/p21通路活化。

In the second part of our research, YC-1, an indazole derivative, displayed impressive selective toxicity against the human lung squamous carcinoma cell line NCI-H226 and human kidney tumor cell lines RXF-631L by a panel of 39 human cancer cell lines (JFCR39) screening. Therefore, the molecular mechanism by which YC-1 affects NCI-H226 cell growth was studied.

在本论文的第二部份中，吲唑类化合物YC-1经利用日本JFCR39癌细胞株之抗癌活性筛选后发现，YC-1对於人类肺鳞状上皮细胞癌细胞NCI-H226以及人类肾癌细胞RXF-631L具有高度的抑制选择性，於是我们选择NCI-H226细胞株做为YC-1对抗肺癌之抗癌机制探讨模式细胞。

The distribution of PTA1 molecule on NK cell, NK cell lines and NK cell clone was detected by indirected immunofluorescence staining and FCM analysis. The results showed that PTA1 expression rate on activated NK cell in MLC was above 60%.

结果证明这种方法能够稳定获得NK细胞克隆，应用流式细胞仪检测获得的一株NK细胞克隆表型为 CD56CD3－。

Microtubules and their textural composite hydrate system, nuclear envelope inside the cell, the places of plasma membrane infolding and cell junction and cell adhesion outside the cell possess lots of nano-scale (100-103 nm) narrow spaces.

在细胞内部的微管及其织构复合水化体系、核膜以及在细胞外部的质膜内褶和细胞连接粘连之处都可以发现许多纳米尺度(100~103 nm)缝隙空间。

After 6 to 7 days of culture, Eleven ES cell lines were selected and explanted. At last we obtained 4,3,4 and 3 ES cell lines separately. One of the B6C3F_1×B6D2F_1 ES cell lines was selected to future study its competent for germline transmission.We founded the ES cell line has normal karyotype on the chromosome analyse.In teratoma experiment by injected ESCs into C57 mices inguen, we gained teratoma contained cells come from all three embryonic germ layers.

选择一株具有高度杂合背景的B6C3F_1×B6D2F_1 ES细胞系进行核型分析、畸胎瘤实验后与ICR品系2n胚胎构建嵌合体并得到具有生殖系传递能力的嵌合体小鼠，证明此细胞系具有生殖系嵌合能力。

ResultsThe glandular cell in the endometrial implant after therapy with middle or high-dose of (10,15 gkg-1d-1) XiaoChaiHu Decoction showed characteristic features of apoptosis which displayed by the cell decreased in size, karyopyknosis , cytoplasmic and nuclear chromatin condensation , density increased and a lot of apoptotic bodies among cell. Whereas some stromal cell displayed degeneration and necrosis. The protein expression of Fas and Caspase-3 in endometriotic tissue of XiaoChaiHu Decoction group was higher than that in the endometrium.

结果中、高剂量小柴胡汤（10，15 gkg-1d-1）治疗后，异位内膜有较多腺上皮细胞出现凋亡的特征，表现为细胞体积变小，核固缩，胞浆和核染色质凝集，密度增高，细胞间凋亡小体，同时间质细胞中可见一些坏死细胞；异位内膜Fas蛋白、Caspase-3蛋白的表达水平明显高于其在位内膜。

And the long axis of simple pit Varied along with CMfs orientation of each secondary wall.This paper proposed a structure model of Phyllostachys pubescens cell wall,based on the results of CMfs deposition and thickness of each secondary wall.Secondly, it was a multilamellate structure of parenchyma cell wall,but its thin and thick lamellate was not evident.CMfs orientation on primary wall of parenchyma cell was perpendicular to cell axis.

纤维的细胞壁为典型的薄厚层相间的同心圆多层结构，初生壁CMfs排列方向与细胞轴向垂直90°次生壁中厚层的CMfs均以接近平行的小角度(0～5°沉积；薄层一般以大角度沉积，且薄层的CMfs角度由壁外侧向细胞腔里逐渐增加，直到完全垂直。

The results show that when the cathode humidified temperature increase, the humidification of membrane and fuel cell performance improved at lower current density, while the saturation in diffusion layer increase and the performance decreases at higher current density. Humidification of membrane and fuel cell performance improved when the anode humidified temperature increase, the saturation in diffusion layer decrease and fuel cell performance improved when the fuel cell working temperature increase, the resistance of diffusion layer decrease and the performance improved when the porosity largen. At last, the simulation results are compared with the experimental results and they are basically the same.

结果表明随阴极加湿温度的提高，在低电流密度运行时膜的润湿条件改善，燃料电池性能提高，在高电流密度运行时扩散层中液态饱和度增加，燃料电池性能下降；随阳极加湿温度的提高，膜的润湿条件改善，燃料电池性能提高；随燃料电池运行温度的提高，扩散层中液态饱和度下降，燃料电池性能提高；随气体扩散层孔隙率增加，气体扩散层阻力减小，燃料电池性能提高。

Leucocytic differentiation antigen 40 sign-al access participates in regulation of inflammatory reaction accommodation of major cell component (vascular endothelial cell、vascular smooth muscle cell and macrophage), it is playing critical role in AS process, participates ather-osclerotic occurrence and development ,reside in atherosclerotic plaque cell thro-ugh CD40-CD40L interaction, induce activate by itself , express and secrete profit to happen immune response、inflammatory reaction、hemagglutination t-hrombogenic proteo-cytokine.

白细胞分化抗原40 (CD40)信号通路参与了动脉粥样硬化斑块内主要细胞成分(血管内皮细胞、血管平滑肌细胞以及巨噬细胞)炎症反应的调节，其在AS进程中扮演着关键性的角色，参与了动脉粥样硬化的发生和发展；存在于AS斑块内的细胞通过CD40-CD40L相互作用，导致自身活化，表达和分泌了有利于免疫应答发生、炎症反应、血凝和血栓形成的蛋白质细胞因子，如激活在AS斑块中的关键性细胞成分如黏附分子、炎症因子、基质金属蛋白酶等的产生，导致斑块的不稳定和破裂，而最终导致粥样硬化斑块病变的恶化。

Compared with the corresponding BEAS-2B cells, the shape of cell clone, the way of cell growth, the shape and quantity of cell and nuclear were not significantly changed in the 1st, 2nd, 5th passage BEAS-2BNNK cells. The shapes of cells and its nuclears of the 10th, 15th, 20th, 25th passage BEAS-2BNNK cells became round gradually, and the way of cell growth became from radio-form into membraniform and more than one nucleolus appeared.

BEAS-2BNNK细胞在第1、2、5代时细胞克隆形态及生长方式、细胞形态、细胞核形态及数目与相应代BEAS-2B无明显差异；第10、15、20、25代时细胞及胞核逐渐变圆，出现多个核仁，细胞由放射状生长逐渐变为膜状生长。

I didn't watch TV last night, because it .

昨晚我没有看电视，因为电视机坏了。

Since this year, in a lot of villages of Beijing, TV of elevator liquid crystal was removed.

今年以来，在北京的很多小区里，电梯液晶电视被撤了下来。