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METHODS: After AIF△1-120 gene was successfully cloned, the shorter truncated human AIF gene (AIF△1-400) was constructed by deleting the Nterminal mitochondrial localization sequence, the coding sequence of flavine adenine dinucleotide binding domain and nicotinamide adenine dinucleotide binding domain of AIF protein.The truncated human AIF gene (AIF△1-400) was inserted into the pIRES2EGFP and pcDNA3 eukaryotic expression vectors, and the coexpression vectors were then transfected into HeLa cells with LipofectAMINE.

在AIF△1-120基因克隆成功的基础上进一步改造,构建截去AIF基因线粒体定位信号,FAD结合结构域和NADH结合结构域(1-400位氨基酸)编码序列的AIF△1-400基因,将其克隆入pcDNA3和pIRES2EGFP真核表达载体,用脂质体法转染HeLa细胞,通过荧光显微镜观察,MTT检测等方法检测该基因在转染细胞中的表达及其对肿瘤细胞的促凋亡活性。

METHODS: After AIF△1-120 gene was successfully cloned, the shorter truncated human AIF gene (AIF△1-400) was constructed by deleting the Nterminal mitochondrial localization sequence, the coding sequence of flavine adenine dinucleotide binding domain and nicotinamide adenine dinucleotide binding domain of AIF protein.

在AIF△1-120基因克隆成功的基础上进一步改造,构建截去AIF基因线粒体定位信号,FAD结合结构域和NADH结合结构域(1-400位氨基酸)编码序列的AIF△1-400基因,将其克隆入pcDNA3和pIRES2EGFP真核表达载体,用脂质体法转染HeLa细胞,通过荧光显微镜观察,MTT检测等方法检测该基因在转染细胞中的表达及其对肿瘤细胞的促凋亡活性。

It was found that theintrduction of polar phosphatidylcholine to LLA chains had largely changed thehydrophilicity of the synthesized polymers. And from the research ofendothelioid cell (ECV304) compatibility and adhesion of blood platelet, wefound that the cells adhesion of ECV304 on the films of PLLA-PC-PLLA lagedcomparing to PLLA, but then could proliferate and cover the films in total,PLLA-PC-PLLA, the same as PLLA are not cytotoxicity and ECV304 canattach and proliferate on them, and PLLA-PC-PLLA can reduce the adhesion ofblood platelet.

结果表明:由于聚乳酸中磷脂酰胆碱结构的引入,使得该材料的亲水性得到很大的改善,并且随着聚合物中磷脂结构单元比例的增高其亲水性能就越好;通过对该材料进行细胞亲和性的实验研究,发现这种材料能够使细胞锚着并支持细胞的增殖;而血小板黏附的实验结果初步显示了该材料具有较好的抗血小板黏附的性质。

As the development that studies to structure of protective screen of kidney spherule filtration and function, it is normal to realise VEGFR of sufficient cell surface shares sufficient cell gradually of structure and function maintain, mix in injury sufficient cell wither dies certain effect is produced in the process.

随着对肾小球滤过屏障结构和功能探究的深入,逐渐熟悉到足细胞表面VEGFR参和足细胞正常结构和功能的维持,在损伤和足细胞凋亡过程中发挥一定功能。

Covers cells and tissues of the immune system, lymphocyte development, the structure and function of antigen receptors, the cell biology of antigen processing and presentation including molecular structure and assembly of MHC molecules, the biology of cytokines, leukocyte-endothelial interactions, and the pathogenesis of immunologically mediated diseases.

课程涵盖免疫系统的细胞和组织,淋巴球的发育过程,抗原受体的结构和功能,抗原反应过程的细胞生物学以及抗原的呈现,其中包括MHC分子的结构与组合,细胞激素的生物学,白血球和内皮组织的互动关系,以及免疫相关疾病的致病机转。

Microscope examination:in group A,at 2 weeks,a few inflamatory cells appeared in the holes with many osteoblasts and ostoid appeared around the drilled holes.At 8 weeks,marrow formed in the drilled holes in group B,at 2 weeks,there were a large amount of osteoblasts in the drilled holes and some ostoid formed around thc drilled holes.At 4 weeks,the drilled holes were full of trabeculae.At 8 weeks,the trabeculae matured with the marrow appeared in the intertrabecular space.

组织学结果:2周时A组钻孔区出现少许炎症细胞,边缘出现较多成骨细胞并有骨组织形成,至8周时,钻孔区内形成骨髓组织,只在边缘形成骨小梁结构。2周时B组钻孔区有大量的成骨细胞,边缘有较多骨组织形成,4周时钻孔区内充满重生骨小梁结构,8周时钻孔区内骨小梁成熟,小梁有骨髓组织填充。

Microscope examination:in group a,at 2 weeks,a few inflamatory cells appeared in the holes with many osteoblasts and ostoid appeared around the drilled holes.at 8 weeks,marrow formed in the drilled holes in group b,at 2 weeks,there were a large amount of osteoblasts in the drilled holes and some ostoid formed around thc drilled holes.at 4 weeks,the drilled holes were full of trabeculae.at 8 weeks,the trabeculae matured with the marrow appeared in the intertrabecular space.

组织学结果:2周时a组钻孔区出现少许炎症细胞,边缘出现较多成骨细胞并有骨组织形成,至8周时,钻孔区内形成骨髓组织,只在边缘形成骨小梁结构。2周时b组钻孔区有大量的成骨细胞,边缘有较多骨组织形成,4周时钻孔区内充满新生骨小梁结构,8周时钻孔区内骨小梁成熟,小梁有骨髓组织填充。[结论]骨髓基质干细胞对兔股骨头缺血性坏死有良好的修复作用。

In the other hard, it is reported that caspase - 3 has important effect in cell apotosis by destroyiny the cell anti - apoptosis factors ( eg: bcl - 2 ), cell framework (eg: frame protein actin, fodrin, lamin).

此外文献报道,CasPase一3还通过破坏细胞抗凋亡因素(如bel一2),破坏细胞的结构(如结构蛋白aetin、fodrin、larnin)在细胞凋亡中发挥作用。

Results Infected by this peptide, cell viability decreased 28.9%. Under light microscope, cells were shrinked and rounded, many cells were divorced from plate wall, some neuraxon shortened and broke. Apoptotic cells which nucleolus shrinked and rounded could be coloured orange by fluorescent colouration. Under electron microscope, chromatin gathered along the inside of the nuclear membrane, vacuole bodies appeared. Apoptotic peak was detected by flow cytometry and the ladder band appeared in DNA electrophoresis.

结果:细胞接触肽段后存活率下降28.9%;光镜下可见细胞贴壁不良,胞体缩小,细胞突起断裂缩短;荧光染色可见细胞突起缩短、胞核固缩、胞质染成橘红色的凋亡细胞;电镜下可见胞质中出现空泡样结构,细胞染色质浓集于核膜内侧并裂解成碎块状;流式细胞仪检测细胞出现亚二倍体峰,DNA电泳出现梯状带。

The results indicated that the typical apoptosis was induced by PRRSV in lungs and uteri. The ultrastructural changes showed different characterizations at different stages of the infection. During the early stage from 8th h to day 3 postinfection,the apoptosis cells shrank,the cytoplasm concentrated,the chromatin condensed,the kernel disaggregated and the endoplasmic reticulum dilated. During the middle stage from day 5 to day 9 postinfection,the apoptosis cells evidently shrank,the cell membranes protu berated,the plastosome manifolded,and apoptosis bodies were found. During the last stage from day 10 upwards postinfection,the apoptosis bodies degenerated and disappeared,and no inflammation occurred. Few apoptosis cells were necrotic.

结果表明,PRRSV可诱导宿主肺和子宫发生典型的细胞凋亡,表现为细胞的超微形态结构随着病毒感染进程出现不同的特征性变化,早期(感染后第8 h至第3 d)凋亡细胞多表现为细胞体积缩小,细胞质密度增强,染色质浓缩,核仁解体,内质网扩张;中期(感染后第5 d至第9 d)凋亡细胞体积显著缩小,细胞膜突起,线粒体增多,有凋亡小体形成;晚期(感染后第10 d以后)凋亡细胞形态多表现为凋亡小体降解和消失,少数凋亡细胞在凋亡晚期表现为坏死细胞。

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