产生诱导作用的

Sanchez ET ,Botella LM ,Velasco B ,et al. Synergistic cooperation between hypoxia and transforming growth factor2beta pathways on humanvascular endothelial growth factor gene expression. J Biol Chem ,2001,19,276:38527238535.[3] Blancher C,Moore JW,Talks kl,et al.Relationship of hyposia-inducible factor HIF-1alpha expression to vascular endothelial growth factor I nduction and hypoxia survival in human breast cancer cell lines.

肝细胞癌中缺氧诱导因子-1α、热休克蛋白70的表达】；综上所述，肝细胞癌发生后，由于血供不足诱导HIF-1α过度表达，应激状态下产生的HSP70通过减轻缺血性损伤，增加毛细血管的生成及减轻细胞凋亡等途径使肿瘤细胞的增殖、移行加快，促进恶性肿瘤的生长、浸润和转移，使肿瘤细胞在适应缺氧、能量代谢、细胞凋亡及转移中起重要作用。

Five models were used to investigate the "Changdong"" s anti-tumor effect: mice S180 sarcoma solid model, mice liver cancer H22 solid model, mice Lewis lung cancer model, as well as human liver cancer QGY and colon cancer LOVO implanted in naked mice; mice liver cancer H22 was also used to evaluate the enhancive effect of "Changdong" when it was co-applied with other anti-tumor agent or with radiotherapy; The "Changdong"" s cytotoxic effect in vitro on such tumors as QGY, LOVO, lung cancer A549, breast cancer MCF-7, as well as mice leukemia P388 was observed through MTT method. And investigate the effect of "Changdong" on proliferation of spleen lymphocyte, on activity of NK cell and on synthesis of IL-2 in mice bearing Lewis lung cancer, respectively. With propidium iodide straining, cell aigptosis and cell circle were analyzed by flow cytometry. Result:"Changdong" has an evident tumor inhibitive effect on mice tumor model as well as human tumor implanted in naked mice with a quantity-effect relationship.

使用小鼠S180肉瘤、小鼠肝癌H22实体瘤和小鼠Lewis肺癌模型，以及人体肝癌QGY和人体肠癌LOVO裸鼠异种移植模型，进行"长动"的抗肿瘤药效学研究：用小鼠肝癌H22进行"长动"合并放疗和化疗的增效作用研究；用MTT法进行"长动"对肝癌QGY、肠癌LOVO、肺癌A549、乳腺癌MCF-7、小鼠白血病P388等10株人体和动物肿瘤细胞的体外细胞毒性作用研究；用淋巴细胞转化试验、小鼠NK细胞活性试验、小鼠胸腺细胞增殖法分别测定"长动"对荷Lewis肺癌小鼠的脾淋巴细胞增殖的影响、自然杀伤细胞活性的影响和对小鼠产生白介素-2(IL-2)的影响；用流式细胞仪PI单染色法进行"长动"对人体肝癌QGY细胞的体外诱导凋亡作用和对肿瘤细胞周期的影响的研究。

Furthermore, treatment of the cultured tobacco cells with ABA also resulted in obvious increase in plasma membrane NADPH oxidase activity, and these enhanced effects of H2O2 production and NADPH oxidase activity induced by ABA were pronouncedly inhibited by two widely used mammalian neutrophil NADPH oxidase inhibitors, diphenylene iodonium and imidazole.

进一步研究发现，ABA能够显著升高质膜NADPH氧化酶的活性，而且ABA诱导H_(来源：A79BC论文网www.abclunwen.com)2O_2和NADPH氧化酶活性增加的效应能够被两个常用的NADPH氧化酶抑制剂碘二苯和咪唑显著抑制，这些结果说明，质膜NADPH氧化酶在悬浮细胞ABA诱导的H_2O_2快速产生中起重要作用。

The former stimulates the cells and transfer the signals into the cells through the ligation with receptors on the cell membrane. The latter, a derivative of nucleotide, causes a cytotoxic effect to suppress thymidylate synthetase activity, and, therefore, to damnify RNA and DNA synthesis.

前者通过与细胞表面的受体结合，把胞外刺激传递到胞内，诱导免疫受体介导的信号级联放大作用，引起一系列免疫效应；后者是是小分子的核苷酸衍生物，可直接进入细胞内，通过抑制胸苷酸合成酶及损伤RNA、DNA等对基因转录和核苷酸代谢产生影响，最后产生细胞毒效应。

In addition, like ascorbic acid, an important reducing substrate for H2O2 removal, but unlike diphenylene iodonium, an inhibitor of the H2O2-generating enzyme NADPH oxidase, PD98059 and TFP not only reduced exogenous H2O2 levels in guard cells in light, but also eliminated the H2O2 that had been generated during a dark period and promoted stomatal opening.

另外，和H2O2的产生有关的NADPH氧化酶的抑制剂二苯基碘的作用效果不同，而和H2O2的清除剂抗坏血酸的作用效果类似，PD98059和TFP不仅能够降低光下保卫细胞的外加的H2O2水准，而且还能清除由黑暗条件诱导的已经产生的H2O2，并能引起气孔开放。

Mechanistically, expression of a molecule known as P-selectin by the platelets was crucial for mediating the platelet-neutrophil interaction, which induced platelets to produce proinflammatory factors such as TXA2. The authors therefore suggest that disrupting the platelet-neutrophil interaction or blocking the proinflammatory factors produced as a result of this interaction might provide new therapeutic targets for the treatment of individuals with ALI.

具体来说，体现在分子水平上就是由血小板产生的血小板蛋白对于调解血小板和中性粒细胞交互影响起着关键作用，它能够诱导血小板产生致炎因素如血栓素A2等，该文作者因此认为，或许破坏血小板与中性粒细胞间的相互作用或者阻断相互作用所产生的致炎因素可以提供一种新的方法用于治疗急性肺损伤。

Our results indicate that 1 NSC606985, at nanomolar level, can effectively induce apoptosis in AML cells NB4 and U937 and significantly inhibit the proliferation without cell death in breakpoint cluster region–Abelson murine leukemia kinase-carrying leukemic K562 cells; 2 At such low concentrations, this agent also significantly inhibits the clonogenic activity of hematopoietic progenitors from patients with AML; 3 For apoptosis induction, NSC606985 rapidly induces the proteolytic activation of protein kinase Cδ with loss of mitochondrial transmembrane potential and caspase-3 activation; 4 Co-treatment with rottlerin, a PKCδ-specific inhibitor, completely blocks NSC606985-induced mitochondrial m loss and caspase-3 activation, while the

结果显示：(1)纳摩尔浓度的NSC606985即可有效诱导AML细胞系NB4和U937细胞凋亡并显著抑制含有bcr-abl融合蛋白激酶的K562细胞的增殖；(2)低浓度的NSC606985也显著抑制来自AML病人骨髓的新鲜白血病细胞的克隆形成能力；(3)除了迅速诱导线粒体跨膜电位的崩塌及Caspase-3的活化外，NSC60698也导致蛋白激酶Cδ的水解激活；(4)PKCδ特异的抑制剂rottlerin能够完全抑制NSC606985诱导的线粒体跨膜电位的崩塌和Caspase-3的活化，而Caspase-3特异的抑制剂z-DEVD-fmk仅能部分削弱PKCδ的活化及细胞的凋亡；(5)以移植PML-RARα转基因小鼠产生的白血病细胞建立的模型研究了该化合物对白血病可能的治疗作用。

79Cm and 3. 78cm from M,, M2 to M3 respectively which cannot reach 1/3 height of the control averagely. The seedlings irradiated by 80 X1015 NYcmgave birth to some flower buds without floral shoots and their seed setting rate was lower than that of control obviously. Some M3 plants irradiated by 60X1015 NVcm2grow into bunches which did not appear in M, and M2. Moreover, some phenotypic variations could be inherited stably in subsequent generations. For instance, the dwarf character in the plants treated with the dose of 80 X1015 was stable in inheritance in consecutive three generations.

再次，对不同剂量的低能N~+处理的拟南芥的M_2代试管苗的叶片外植体愈伤组织的诱导和耐盐性进行了比较和分析，发现经不同剂量的低能离子处理的M_2代试管苗的叶片外植体，离子处理影响其出愈率，高剂量处理会抑制愈伤的诱导，但低剂量离子注入对愈伤组织的增殖有一定的促进作用；愈伤组织的耐盐性也与剂量相关，低剂量的耐盐能力比对照的低，但是高剂量处理反而提高愈伤的耐盐性，这间接表明低能离子引起了拟南芥的生理状态的变化，产生了生理效应。

However, it synergizes with γ-radiation in the induction and enhancement of apoptosis. TFAR19 protein; Breast neoplasms; Cell cycle; Apoptosis

rhTFAR19 蛋白对γ射线诱导的MCF-7细胞周期无明显影响，其对细胞凋亡的促进作用可能是通过放大或增强γ射线诱导细胞凋亡的信号产生。

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。

Since historical times,England ,where the early inhabitants were Celts, has been conquered three times .

从有历史以来，英国，在此地早期居住的是凯尔特人，已经被征服了三次。

Bluetooth OBEX File Transfer Enables the sending and receiving of files on your phone via Bluetooth.

蓝牙OBEX文件移动允许经过蓝牙传送和接受文件。。。。