细胞的

This account for cytoskeleton and cellular morphology and adhering capacity could be affected by alterative culture medium in the process of the culture.

说明细胞培养过程中，更换细胞生长环境可影响到细胞骨架，进而改变细胞形态及细胞的粘附能力。

Compared with classical cytotoxic T lymphocytes , NK cells are superior in the following aspects: NK cells are among the first cell types to be activated after intracellular pathogen stimuli, the activity of NK cells peaked between 1 to 3 days, retained during the first 7-10 days, and the T cells response emerged only after 7 days when the NK cell responses begin to decline; though comprising of only 10％-15％ of peripheral lymphocytes, NK cells mobilize most of the cell populations in a strong and high level response to different invasions, and act as key factors at early defense before a specific immune response could mount, while only certain clones were involved in T cell response; NK cells kill virus-infected or malignant transformed cells without pre-sensitization and without restriction by major histocompatibility antigen, which is usually a mechanism of immune escape to T cell recognition by virus-infected or tumor cells, thus NK cell in complementary with T cells play crucial roles in tumor and virus eradication.

NK细胞以其强大的细胞毒活性为特征，与细胞毒性T细胞相比，NK细胞具有如下特点：NK细胞虽然只占外周血淋巴细胞的10-15％，但是对刺激性因素产生应答的过程十分迅速，一次可以调动大多数细胞共同参与，而不是几个克隆的活化，免疫应答的强度高；病毒感染或恶性转化细胞的一个主要特征是细胞表达的MHCⅠ类分子下降或消失，并借助这一机制逃避特异性T细胞应答的识别，NK细胞介导的杀伤活性无需抗原刺激，不受MHCⅠ分子表达的限制，从而与T细胞应答互为补充发挥免疫防御的功能；NK细胞的免疫活性可以被多种细胞因子上调，其中IFNα，IL-2，IL-12，IL-15和IL-18具备更强的作用；NK细胞具有强大的细胞因子分泌功能，对于启动T细胞特异性应答必不可少。

Results: Tyroserleutide can significantly increase the life span of H22 tumor-bearing mice by 50-70% in dosages of 20ug/kg/d-80ug/kg/d,specially the high dosage of 80ug/ml can significantly increase the life span by 69.24%; Tyroserleutide can inhibit the growth of transplanted hepatocellular tumor BEL-7402 in nude mice,the rate of tumor inhibition was25-50% in dosages of 40-320ug/ml ,the inhibition rate of 160ng/ml was 44.03%; Tyroserleutide could inhibit the growth of H22 and BEL-7402 tumor in a dose-dependent manner. Simultaneously, tumoricidal activity of tyroserleutide against BEL-7402 cell line in vitro was observed hinger when compared with the control group(P.05).The inhibition effect of 72hrs was higher than 24hrs,48hrs,96hrs.And specially the high dosage of 160ug/ml can significantly inhibit growth of tumor cell by 19.36%. Tyroserleutide can activated PEM and marked enhance cytotoxicity andphagocytosis functions in vitro and in vivo. The OD values of cytotoxicity were observed hinger when compared with the control group(P.05).The cytotoxicity of macrophages activated by tyroserleutide against BEL-7402 and B16-F10 was 35.58%,61.2% in vitro and21.39%,47.63% in vivo. The cytotoxicity rate of nude mice PEM was 32.86%,73.07% in vivo. Furthermore, tyroserleutide alone could stimulated the production of IL-1B TNF- a and NO by M . Tyroserleutide and LPS could synergistically activated M producing more cytotoxicity effectors. Conclusion: Tyroserleutide had inhibition functions against hepatoma carcinoma .Its possible mechanisms were related to the affect that Tyroserleutide could inhibit tumor cell directively and induce tumor cells apoptosis or death effectively.

结果：酪丝亮肽能显著延长腹水型肝癌H_(22)小鼠的生存时间，给药剂量为80μg／kg／d时疗效最显著，达到69.24％，在20μg／kg／d-80μg／kg／d剂量范围内生命延长率为50-70％，给药剂量与荷瘤鼠生存时间呈现一定量效关系；酪丝亮肽能显著抑制人肝癌BEL-7402移植瘤裸鼠的肿瘤生长，给药剂量为160μg／kg／d时疗效最显著，抑制率为44.03％，并且在40-320μg／kg／d剂量范围内抑制率为25-50％，给药剂量与肿瘤抑制率呈现一定量效关系；酪丝亮肽体外对人肝癌BEL-7402细胞生长有一定的抑制作用，在作用72hrs时各浓度酪丝亮肽对肿瘤细胞的抑制作用较24hrs、48hrs、96hrs明显，其中浓度为100μg／ml时抑制率达19.36％；酪丝亮肽体内外均能增强小鼠腹腔巨噬细胞对肿瘤细胞的杀伤：体外作用中巨噬细胞对BEL-7402、B16-F10的杀伤功能明显增强，与效应细胞对照组相比有显著性差异(P＜0.05)杀伤率分别达到35.58％、61.2％；体内作用中巨噬细胞对BEL-7402、B16-F10的杀伤功能明显增强，与生理盐水对照组相比有显著性差异(P 。05)，杀伤率分别达到21.39%、47.63%；裸鼠腹腔巨噬细胞经酪丝亮肤作用后对BEL一7402、B 16一F10杀伤功能明显增强，与生理盐水对照组相比有显著性差异(P.05)，最高杀伤率分别达到32.86%、73.07%；酪丝亮肤能增强单核巨噬细胞系统的吞噬功能，吞噬指数与生理盐水组比较有显著性差异(P.05)；酪丝亮肤体外作用能促进小鼠腹腔巨噬细胞分泌合成细胞毒效应分子IL一lp、TNF一Q和NO，与效应细胞对照组相比有显著性差异(P.05)；酪丝亮肤体内作用能促进小鼠腹腔巨噬细胞分泌合成细胞毒效应分子IL一lp、TNF一Q和NO，与生理盐水对照组相比有显著性差异(P.05)；酪丝亮肤能促进鼠巨噬细胞株R戌W264.7分泌合成IL一1p和NO，IL一1日、NO水平分别在酪丝亮肤作用24hrs、12hrs时达到高峰，酪丝亮肤单独应用能提高巨噬细胞的分泌合成功能，而且酪丝亮肤能与LPS协同作用刺激巨噬细胞的细胞毒效应分子分泌合成。

MTT assay FAK signaling pathway inhibitor genistein on human corneal epithelial cell cytotoxicity;RT-PCR detection of human corneal epithelial cells adhesion to fungus at different times,extracellular matrix protein including laminin,fibronectin,FN glass,Ⅳcollagen,transmembrane protein integrinαⅤ,integrinβ1(ITGβ1),as well as the FAK signaling pathway FAK1,FAK2 and Paxillin gene expression;Western blot detection of the signal transduction pathway adhesion-associated protein ITGβ1,FAK and PAX expression and the inhibition of genistein. Immunocytochemical method was used to observe the LN,FN and FAK expression in human corneal epithelial cells during interaction with the fungues;Laser scanning confocal microscope had a cell positioning on FN,FAK and PAX,observed the changing of the human corneal epithelial cytoskeleton after stimulated by fungues;Quantitatived by flow cytometry to detect of human corneal epithelial cells with PAX at ITGβ1 fungal expression after adhesion;Optical microscopy quantitied the fungues and human corneal epithelial cell adhesion and recorded to determination the integral optical density afrer adhesion;Scanning and transmitted electron microscope observed the changing of cell ultrastructure after fungues and human corneal epithelial cell adhesion.

第一部分真菌激活人角膜上皮细胞FAK信号转导通路的体外实验研究将三种常见致病真菌(白色念珠菌、烟曲霉菌和茄病镰刀菌)分别与人角膜上皮细胞共孵育，MTT法检测FAK信号通路抑制剂染料木黄酮的对人角膜上皮细胞的细胞毒性作用；RT-PCR检测真菌黏附人角膜上皮细胞后不同时间细胞外基质层连蛋白、纤连蛋白、玻连蛋白、Ⅳ型胶原、跨膜蛋白整合素αV、整合素β1(ITGβ1)，以及FAK信号通路中FAK1、FAK2和桩蛋白基因的表达情况；Western blot的方法检测黏附信号转导途径相关蛋白ITGβ1、FAK和PAX的表达，以及染料木黄酮对真菌刺激人角膜上皮细胞FAK信息通路活化的抑制作用；免疫细胞化学方法观察人角膜上皮细胞与真菌相互作用过程中LN、FN和FAK的表达；激光共聚焦显微镜对FN、FAK和PAX进行了细胞定位，并观察真菌刺激后人角膜上皮细胞骨架的变化；流式细胞仪定量检测人角膜上皮细胞ITGβ1与PAX在真菌黏附后表达的改变；光学显微镜观察真菌与人角膜上皮细胞黏附数量，记录并测定了黏附后积分光密度值OD扫描及投射电镜观察了真菌与人角膜上皮细胞黏附后，细胞超微结构的改变。

The EC_(50) of QKL against the formation of syncytia of MT-2 induced by HIV-1_ was 1/198.02 with a SI of 5.36. By detecting the survival rate of co-culturing H9/HIV-1_ cells and MT-2 cells or MT-2 cell direct infected by HIV-1_ QKL was found to be protective to cells. The EC_(50) was 1/166.67 and 1/144.93 with SI of 4.51 and 3.92 respectively. The EC_(50) of QKL against P24 antigen production was 1/175.44 with SI of 4.75. The drug serum of QKL was also found to be effective to inhibit the cell fusion and protect cells infected by HIV-1_.

结果：QKL对H9／HIV-1_细胞和MT-2细胞的CC_(50)分别为1／50.76和1／36.97；抑制H9／HIV-1_细胞和MT-2细胞早期融合的EC_(50)=1／235.29，SI=6.36；抑制HIV-1_细胞诱导MT-2细胞形成合胞体的EC_(50)=1／198.02，SI=5.36；H9／HIV-1_细胞和MT-2细胞混合培养和HIV-1_感染MT-2细胞时，QKL保护病毒感染细胞免于死亡的EC_(50)分别为1／166.67和1／144.93，SI分别为4.51和3.92；抑制p24抗原产生的EC_(50)=1／175.44，SI=4.75；QKL药物血清也可抑制H9／HIV-1_细胞和MT-2细胞的早期融合，保护细胞免于死亡。

Cells were re-suspended and cultured in a humidified incubator with 5%CO_2 at 37℃.

建立巨噬细胞和死亡细胞的共培养模型在96孔板上种植RAW264.7细胞或小鼠腹腔原代巨噬细胞，分为3组，即对照组、凋亡细胞处理组和坏死细胞处理组。

Most 5-HT cells appeared in the base part of gland in the rat, while in the human they were mainly located in the intercellular substance and a few scatted in the glandular epithelium.

方法采用免疫细胞化学方法，检测人和大鼠胃窦部粘膜内生长抑素细胞、胃泌素细胞、5-羟色胺细胞（5-HT细胞）、嗜铬粒素A细胞的分布。

Cell proliferation was measured with cell number,cell metabolic activity (WST-1 cleavage),DNA synthesis and cell cycle assayed with flow cytometry.

进行新西兰白兔心脏心肌成纤维细胞的培养；测定细胞计数，细胞活性（WST－1分解）和DNA合成，并以流式细胞仪测定细胞周期等以表示细胞增殖。

Methods: Cardiac myofibroblasts derived from heart of New Zealand rabbit were cultured and identified. Cell proliferation was measured with cell number,cell metabolic activity (WST-1 cleavage),DNA synthesis and cell cycle assayed with flow cytometry.

进行新西兰白兔心脏心肌成纤维细胞的培养；测定细胞计数，细胞活性（WST－1分解）和DNA合成，并以流式细胞仪测定细胞周期等以表示细胞增殖。

Results were shown as followings:(1) Sodium selenite at 0～2.5 μmol/L significantly increased the antioxidative capacity of L-02 cells without having remarkable impact on SMMC-7721 cells;(2) Sodium selenite at concentrations above significantly increased telomerase activity, hTERT gene expression and telomere length of L-02 cells without significant impact on SMMC-7721 cells;(3) Sodium selenite at higher concentrations (larger than 5 μmol/L) resulted in peroxidation of L-02 cells, while scutellarin significantly counteracted its effect;(4) Selenium-rich amino acids from silkworm pupas in the range of 0.5～2.5 μmol/L Se significantly inhibited SMMC-7721 cell growth, induced apoptosis and cell cycle change, and the generation of reactive oxygen species. In contrast, sodium selenite and selenomethionine only had weak impact on them at the same concentrations;(5) A new selenium-containing protein was found from selenium-rich silkworm pupas, which is worthy to be study further;(6) An expression vector containing ansense RNA of hTERT gene were constructed and used to transfect SMMC-7721 cells. They were observed to inhibit hepatoma cells.

结果如下：（1）0～2.5μmol/L亚硒酸钠显著性增强L-02细胞的抗氧化能力；而对SMMC-7721细胞的作用不显著；（2）该浓度硒显著性提高L-02细胞端粒酶活性、增强hTERT基因表达和延长细胞端粒长度；而对SMMC-7721细胞的作用均不显著；（3）高浓度硒（5μmol/L以上）显著性抑制L-02细胞生长、致细胞过氧化，灯盏花素能拮抗硒所致过氧化、降低硒毒性；（4）0.5～2.5μmol/L富硒蚕蛹氨基酸显著性抑制肝癌细胞SMMC-7721生长、导致细胞凋亡和周期改变、诱导细胞产生活性氧，同浓度亚硒酸钠和硒代蛋氨酸对其抑制不显著；（5）富硒蚕蛹蛋白经分离纯化和鉴定后发现存在一新含硒蛋白，其结构和功能有待研究；（6）通过已有的含hTERT基因质粒，成功构建hTERT反义RNA表达质粒，转染SMMC-7721细胞后对其生长具有抑制作用。

We have no common name for a mime of Sophron or Xenarchus and a Socratic Conversation; and we should still be without one even if the imitation in the two instances were in trimeters or elegiacs or some other kind of verse--though it is the way with people to tack on 'poet' to the name of a metre, and talk of elegiac-poets and epic-poets, thinking that they call them poets not by reason of the imitative nature of their work, but indiscriminately by reason of the metre they write in.

索夫农 、森那库斯和苏格拉底式的对话采用的模仿没有一个公共的名称；三音步诗、挽歌体或其他类型的诗的模仿也没有——人们把&诗人&这一名词和格律名称结合到一起，称之为挽歌体诗人或者史诗诗人，他们被称为诗人，似乎只是因为遵守格律写作，而非他们作品的模仿本质。

The relationship between communicative competence and grammar teaching should be that of the ends and the means.

交际能力和语法的关系应该是目标与途径的关系。