线粒体

MRS2 encode a magnesium transporter protein in Saccharomyces cerevisiae and deletion of MRS2 gene results in decrease in mitochondrial magnesium concentration, Group II RNA splicing defect and growth defect on nonfermentable carbon source.

MRS2 基因编码线粒体镁离子转运蛋白，MRS2缺失会导致酵母线粒体镁离子浓度下降、线粒体内II型内含子剪接缺陷和非发酵碳源上的生长缺陷。

Light microscope and transmission electron microscopy showed that SMMC-7721 cells induced by SAHA had undergone the restorational alteration in morphology and ultrastructure, which were different from those of nontreated cells but were similar to those of normal cells, and the changes were as follows: the cells turned to be flat and spread; the nucleo-cytoplasmic ratio lessened and nuclear shape became rather regular; the number of nucleolus reduced and its volume lessened; euchromatin increased while heterochromatin decreased in nucleus; in the cytoplasm, mitochondria grew in number with relatively consistent structure and well-developed mitochondria cristae; Golgi complex turned to be well-developed and typical; rough endoplasmic reticulum increased. Immunocytochemistry assay showed that the expression of AFP and PCNA were declined significantly. FCM analysis showed SAHA could arrest SMMC-7721 cells in G0/G1 phase, with an accumulation of the cells in G0/G1 phase while a decrease of cells in S phase. Semi-quantitative RT-PCR detection revealed that the expression of p21WAFl mRNA was upregulated remarkably in the cells treated with SAHA.

结果：倒置显微镜和透射电镜观察显示，经SAHA处理的细胞增殖速度显著减慢，细胞体积增大，细胞核较小，形状较为规则，核仁数量减少、体积变小，核内常染色质增多而异染色质减少，核质比例减小，细胞质内线粒体数量增多、线粒体嵴发达，高尔基体较为典型，粗糙型内质网增多，呈现出与正常上皮细胞相似的形态变化；MTT比色法测定结果显示不同浓度(2.5、5.0、7.5、10.0uM)SAHA对SMMC-7721细胞的增殖均有抑制作用，并有明显的剂量依赖和时间依赖关系；免疫细胞化学检测显示SAHA能显著降低PCNA和AFP在SMMC-7721细胞中的表达；流式细胞仪检测结果显示，SMMC-7721细胞经SAHA处理后，G0/G1期细胞明显增加，S期细胞则明显减少，细胞被阻滞于G0/G1期；RT-PCR检测结果表明，SAHA作用12h后SMMC-7721细胞中p21WAF1 mRNA的表达即有增加，24h后更为明显。

Usually, anti-apoptotic protein is insulated in organella, restraining the release of pro-apoptotic factor and controlling cell apoptosis. however, interacting with pro-apoptotic protein, it can not restrain apoptosis, induce the loss of mitochondrial function, accelerate the release of pro-apoptotic factor and result in apoptosis.

抑凋亡蛋白平时被隔离在线粒体等细胞器内抑制促凋亡因子的释放，具有抑制细胞凋亡的功能，但一旦与激活的促凋亡蛋白发生相互作用后，便丧失了对细胞凋亡的抑制作用，造成线粒体等细胞器的功能丧失和细胞器内促凋亡因子的释放，导致细胞凋亡。

Anti-apoptotic and pro-apoptotic factors have synergistic effect and play a switch role. Usually, anti-apoptotic protein is insulated in organella, restraining the release of pro-apoptotic factor and controlling cell apoptosis.

抑凋亡蛋白平时被隔离在线粒体等细胞器内抑制促凋亡因子的释放，具有抑制细胞凋亡的功能，但一旦与激活的促凋亡蛋白发生相互作用后，便丧失了对细胞凋亡的抑制作用，造成线粒体等细胞器的功能丧失和细胞器内促凋亡因子的释放，导致细胞凋亡。

Combining electron microscopy observation with DNA fluoresence detecting technique, it is systematically studied the ultrastructure of microspore, the distribution of plastid and mitochondria and the changes of organelle DNA at different developing stages in Phaseolus vulgaris, Pisum sativum, and Lilium Spec.(L. davidii and L. regale).

基于上述的情况，本研究应用电镜和DNA荧光技术系统研究了菜豆、豌豆及百合属中王百合和兰州百合这些植物种小孢子发育的超微结构，质体和线粒体的分布形式及其DNA的变化情况与遗传的关系，并应用RFLP分析了兰州百合的质体遗传方式，同时对另一种可遗传的细胞器——线粒体的遗传方式也进行了研究。

An application of the test to the comparisons of the eleven sequenced arthropod mtDNAs revealed that most of the observed evolutionary models were homogeneous between the two mosquitoes but not between Daphnia pulex or Artemia Franciscan and the other arthropod, probably due to shifts to a high AT content.

在真实数据中，用11种节肢动物线粒体DNA的比较中发现，水蚤或卤虫与其他9种节肢动物以高百分比违背了同质性进化模型假设，显然是由于AT含量高而引起的，且在两种蚊子的线粒体DNA比较中发现，其满足同质性假设仅有7.69%。

The lung arterial smooth muscle cells are pycnosis, nuclear membrane spaces are enlargement, some mitochondrias are diminution, somes are swelling.

冬凌草甲素组可以发现肺小动脉平滑肌细胞核固缩，核膜间隙增大，线粒体浓聚，部分线粒体肿胀。

In PN group, the light microscopic findings included inflammation cells infiltration and hepatic steatosis, and electron microscopy showed vacuole change in cytosol and rarefactive microvillus in micro-bile duct. Conclusion PN-associated liver dysfunction was related with hepatocyte oxidative injury and apoptosis.

PN肝脏损伤机制可能是PN某些配方成分应用中，脂质过氧化导致肝细胞氧化损伤，同时损伤线粒体膜，促使线粒体膜通透性增加，释放细胞色素C等凋亡相关因子，激发caspase-3等级联反应，产生肝细胞凋亡，导致肝损伤。

In electron microscopy endothelial cell of capillary and mitochondrial was edematous obviously, the basement membranes were thickened. RGCs were vacuolated, chromatin of nucleus aggregated marginally decreased and densification. Some of RGCs were necrosis, nucleus were dissolved, mitochondria was edematous, the rough endoplasmic reticula decreased obviously.

电镜下视网膜毛细血管内皮细胞明显肿胀，胞体变圆，突向管腔，线粒体肿胀，空泡化，基底膜增厚，视网膜神经节细胞胞体变形，核明显固缩，核膜消失，胞浆空泡化，线粒体肿胀，细胞表面突起减少，多聚核糖体及粗面内质网显著减少。

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。

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。