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促进...的生长

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The extract from bergamot and boxthorn plays an active role in skin and the promotion of hair growth.

佛手和枸杞提取物具有良好营养皮肤和促进毛发生长的作用。

Fuwankia organic potash fertilizer can improve vegetable growth and increase the yield of cucumber, small cabbage, and celery in sunlight greenhouse.

西芹的株高、茎粗、地上植株、地下根重以及总生物量增加。富万钾有机钾肥能明显促进蔬菜生长,提高产量。

The research focuses on the sulfonamides and chloramphenicol, which are used frequently as human and animal medicines.

抗生素不但在世界范围内用于人类和动物治疗感染疾病,而且还作为畜牧业的生长促进剂使用。

It could draw a conclusion that the Bt crystal proteins had the effect of prevention and treatment of avian coccidiosis and improved the growth of chicken.

试验表明,苏云金杆菌晶体蛋白对雏鸡球虫病有防治作用,并有促进雏鸡生长的作用。

These live rocks provide the foundation for most of the living corals and also helped to seed the exhibit with a wide diversity of micro-fauna and flora, including coralline algae.

这些活石为大部分活珊瑚提供生存基础,也有助于促进各式各样微型动植物的生长,其中包括珊瑚藻等。

BMP production systems will encourage quicker ground cover, more crop residues, greater root growth and more leaf area, all of which will improve N use efficiency and reduce erosion.

最佳管理措施生产体系将有助于迅速覆盖地表,产生较多的作物残留,促进根系生长和增加叶面积,这些都会提高氮素利用率同时降低侵蚀。

A monument was set up as a memorial to the dead soldiers.

为阵亡将士立了一个纪念碑。光是促进植物生长的一个因素。

Objective:To investigate the growth promoting effect of earthworm on fetal rat with IUGR.

目的:研究地龙提取物对大鼠胎仔的生长促进作用。

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。

Result 1 Magnetic nanoparticles, magnetic nanoparticles modified with antisense oligodeoxynucleotide of human telomerase reverse transcriptase induced HL-60 tumor cells to apoptosis, we could see typical morphologic change of apoptosis cells: karyopyknosis, chromation"s condensing and aggregation in nuclear, forming crescent-shaped or annulus structures to lean on edge of cell nucleus"s membrane and posing apoptosis body by Atomic Force Microscope, Fluorescence microscope, transmission electron Microscope 2 There was a significant difference compared with control group(p.01), inhibition ratio had significant positive correlation with medication dosage and time ;during 0.8-8μM dosage amplitude, inhibition ratio accrescenced by dosages increasing. However, the inhibition ratio would decrease when dosage over 8-80μM.

结果 1 磁性纳米粒子、修饰有端粒酶反义寡核苷酸的磁性纳米粒子诱导HL-60细胞发生凋亡,原子力显微镜、光学显微镜、荧光显微镜和透射电镜下均观察到HL-60细胞呈现典型的凋亡细胞的形态变化:细胞核固缩,核内染色质浓缩、凝聚、形成新月形或环状结构紧靠在细胞核膜边缘,并形成凋亡小体。2 磁性纳米粒子、修饰有端粒酶反义寡聚脱氧核苷酸的磁性纳米粒子对HL-60肿瘤细胞的生长和增殖有明显的抑制作用,与对照组相比有显著性差异(p<0.01),在剂量为0.8-8μmol/L范围内,抑制率随剂量的增加而增加,当剂量超过8μmol/L时,抑制率反而下降;3 磁性纳米粒子、修饰有端粒酶反义寡聚脱氧核苷酸的磁性纳米粒子可增强p53基因的表达活性,引起DNA降解损伤,反向调节细胞周期活动,促使细胞从G0期进入G1期,抑制肿瘤细胞的生长。4 修饰有端粒酶反义寡聚脱氧核苷酸的量子点能通过内吞作用进入HL-60肿瘤细胞的细胞核,可以在细胞内进行定位和促进HL-60肿瘤细胞的凋亡。

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