增殖的

Bend chorda vertebralis can also be observed in stronglyaffected zebrafish embryos. 2. We alse isolated the mouse PNAS-4 (mPNAS-4) gene. Cell proliferation activity analysis in vitro found overexpression of mPNAS-4 caninhibit mouse LL2 and CT26 tumor cell growth.

分离了小鼠的PNAS-4(mPNAS-4)基因，体外细胞增殖活性实验发现，mPNAS-4基因的过表达能够抑制小鼠肺癌LL2和结肠癌CT26细胞的增殖，PI染色和DNA片段化分析表明，mPNAS-4基因的过表达能够促进LL2和CT26细胞的凋亡。

In T cells,TGF-beta1 can inhibit their proliferation,inhibit the differentiation of Th1 and Th2,inhibit the differentiation of CTL,induce the generation of regulatory T cellsTregin B cells,TGF-beta1 can inhibit their proliferation,induce IgA class switch,it also can induce the apoptosis of immature and resting B cells;in NK cells,TGF-beta1 can inhibit the secretion of IFN-γand the cytolytic function of NK cells.

对T细胞，TGF-beta1可以抑制其增殖，抑制Th1和Th2细胞的分化，抑制CTL的分化，诱导调节性T细胞的产生；对B细胞，TGF-beta1可以抑制B细胞的增殖，诱导IgA的类别转换，还可以诱导不成熟和静息B细胞的凋亡。

Epidermal cells near the wound dedifferentiate and proliferate forming blastema and/or migrate to the wound plane forming a pre-epidermis consisting of several layers of stem cells covering the wound plane, which then re-differentiates further forming fully developed epidermis. Cells in the parietal peritoneum are also induced by injury to dedifferentiate into stem cells which then proliferate and migrate along the parietal peritoneum to the wound place forming a pre-peritoneum which re-differentiates into fully developed parietal peritoneum.

伤口愈合包括伤口闭合、顶端表皮层及体腔上皮的新生：创伤后的前4 d，残腕顶端的肌肉组织向伤口处迁移并重排使伤口闭合；创伤附近的表皮层细胞发生脱分化并增殖后迁移到创伤面形成由数层干细胞组成的前表皮层，之后进一步分化形成表皮层；而体腔上皮细胞在创伤诱导下也脱分化并增殖，然后沿体腔上皮迁移到创伤处形成&前体腔上皮&，经再分化形成新的体腔上皮。

RESULTS:Isoalantolactone exhibited excellent anti-proliferative activities on HeLa, SHIN3 and HOC-21 and HAC-2 cell lines, while 1-O-acetylbritannilactone and britannilactone demonstrated weak anti-proliferative activities on HeLa, SHIN3, HOAC-21 and HAC-2 cell lines even at the concentration of 100 μmol/L. The apoptotic rate in isoalantolactone group with the concentration of 12.5 μmol/L was higher than that in PBS group.

结果： 异土木香内酯对上述5种肿瘤细胞的增殖均有明显的抑制作用，1-氧-乙酰大花旋覆花内酯和大花旋覆花内酯即使在100 μmol/L的高浓度下，对5种妇科肿瘤细胞的增殖不显示抑制活性；流式细胞学检查发现异土木香内脂处理后的HeLa细胞出现凋亡现象。

Image analysis system was used for semi-quantitive assay of TGF-βRⅠ and R Ⅱexpression, and microphotography was used to record the morphologic changes of culturedchondrocytes. The results are:1. TGF-〓 showed sequentially inhibitory and promotive effects on the proliferation of human articular chondrocytes of two week monolayer culture from one passage to eight passage.

本研究采用CellTiter 96〓单溶液细胞增殖分析试剂盒测定体外培养中的软骨细胞的增殖活细胞数量；免疫组化法测定软骨细胞TGF-βR Ⅰ、R Ⅱ，Ⅱ型胶原和S-100蛋白的定性表达；酶免分析法测定TGF-〓作用后的Ⅱ型胶原定量表达；通过图象分析仪，对TGF-βRⅠ、R Ⅱ的免疫组化染色结果进行半定量分析；本研究的实验结果如下：1。

Results Cells cultured in serum-free medium AIMV could proliferate,kill target cellsand express CD11 c well enough to substitute the cells cultured in standard serum-containing medium.Proliferation,cytotoxicity and expression of CD11 c of A-NK were better than nonadherent natural killer cells.Death patterns of tumor target cells were necrosis and apoptosis.

结果 与完全培养基培养细胞相比，AIMV培养细胞增殖能力、杀伤肿瘤细胞的能力、表达CD11 c 的能力与之相当；在同一培养条件下A-NK细胞的增殖能力、杀伤活性及表达CD11 c 的能力明显强于NA-NK细胞；被A-NK细胞杀伤的肿瘤细胞死亡形式是溶解坏死和凋亡。

Results Cells cultured in serum-free medium AIMV could proliferate,kill target cellsand express CD11 c well enough to substitute the cells cultured in standard serum-containing medium.Proliferation,cytotoxicity and expression of CD11 c of A-NK were better than nonadherent natural killer cells.Death patterns of tumor target cells were necrosis and apoptosis.

结果 与完全培养基培养细胞相比，AIMV培养细胞增殖能力、杀伤肿瘤细胞的能力、表达CD11 c 的能力与之相当；在同培养条件下A-NK细胞的增殖能力、杀伤活性及表达CD11 c 的能力明显强于NA-NK细胞；被A-NK细胞杀伤的肿瘤细胞死亡形式是溶解坏死和凋亡。

Based on these results and inferred to related reports from other labratories, it was possible to make some analyses and conclusions or inferrences:(1) CD〓AK with tumoricidal activity were induced and expanded in number througth costimulation of PBMC with anti-CD〓 McAb . and r IL-2 ;(2) CD〓AK induced and expanded in such manner did exibit more potent proliferation·ability and cytotoxicity which maintained for lonser time than those of LAK cells, thus CD〓AK was a new variety of antitumor effector cells worth to be explored;(3) CD〓AK could mediate MHC nonrestricted cytotoxicity and kill tumor target cells through inducing necrosis and apoptosis;(4) Normal mature lymphocytes of PBMC could be induced to proliferate and /or to die from apoptosis when they were costimulated by anti-CD〓McAb and rIL-2. Both proliferation and apoptosis were existing in the same cultivation system sugsesting that the presence of rIL- 2 might provide some accessary signals for apoptosis.

以这些结果为基础并参考其它有关文献可能做出如下分析与结论或推论：(1)用抗CD〓单抗和rIL-2共刺激外周血单个核细胞能诱生扩增出具有杀瘤活性的CD〓AK细胞，(2)与LAK相比，用这种方法诱生扩增的CD〓AK增殖能力强、细胞毒活性强而且维持时间长；CD〓AK是一类值得开发的抗瘤效应细胞；(3)CD〓AK能够介导MHC非限制性细胞毒活性，可以通过诱导靶细胞坏死和/或凋亡杀伤肿瘤细胞；(4)正常外周血单个核细胞中的成熟淋巴细胞在受到抗CD〓单抗和rIL-2共同刺激后既可诱导增殖也可诱导凋亡，两者并存于同一体系，推测rIL-2的存在可能为细胞凋亡提供一些辅助信号。

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。

The human cartilages are composed of chondrocyte and extracellular matrix,the form of chondrocytes are hypertrophy and the quantity are less;the ECM of cartilage are compised of type II collagen and proteoglycan. Articular cartilages are all hyaline with little fibers. Trauma and arthritis are the main cause of cartilage injury,the ommilayer injury ofcartilage can be recovered by marrow,but because of without stimulation mechanism,the new tissues are merely fibrocartilages,they can not be coincide with hyaline cartilage in menchanics;the purely damage of articular cartilage can not stimulate chondrocyte to regenerate because of without blood circulation,thus,the plerosis of articular catilage can not depend on the proliferation of local chondrocyte.Ever since,people tried their best to find a way to reconstruct articular cartilage.

造成人体关节软骨损伤的原因主要为创伤和关节炎，关节软骨全层损伤可由于骨髓中间充质干细胞的高速增殖修复，但这种修复由于缺乏相应的刺激机制，只能形成纤维软骨，而不能形成符合关节生理、力学要求的透明软骨；单纯软骨部分损伤软骨组织内无血管，软骨细胞迁移迟缓，无法使损伤区域软骨细胞再生，因此，关节炎及关节创伤后的软骨修复不能依赖于软骨细胞的增殖和迁移。

In the negative and interrogative forms, of course, this is identical to the non-emphatic forms.

。但是，在否定句或疑问句里，这种带有"do"的方法表达的效果却没有什么强调的意思。

Go down on one's knees;kneel down

屈膝跪下。。。下跪祈祷