细胞

He expression levels of TGF-β3 decreased in descending order of endotenon tenocytes (42.5%), tendon sheath fibroblasts (41.2%), and epitenon tenocytes (33.3%).

GF-β1 表达平均降低程度从大到小依次为腱鞘细胞（36.1%）、腱内膜细胞（31.2%）、腱外膜细胞（31.0%），TGF-β2依次为腱鞘细胞（37.9%）、腱外膜细胞（32.1%）、腱内膜细胞（27.0%），TGF-β3 依次为腱内膜细胞（42.5%）、腱鞘细胞（41.2%）及腱外膜细胞（33.3%）。

Immunohistochemistrical section: observe the VEGF protein expression in different cells, the positive ratio detected by a morphometrical analysis system was used as the amount of the VEGF protein expression.

免疫组化染色切片：观察不同给药时间股骨头内VEGF的表达情况；高倍视野下（400倍）沿骨小梁表面计数50个成骨细胞中的阳性细胞数，VEGF成骨细胞阳性率=阳性成骨细胞数/50×100％，3次取平均值；计数每个高倍视野软骨细胞中的阳性细胞数，VEGF软骨细胞阳性率=阳性软骨细胞数/软骨细胞总数×100％，5次取平均值。

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。

Comparing with control group, CD4~+ T cells of AIDS patient were markedly depleted in gastro-mucosal tissues(P＜0.01), but in presymptomatic patients CD4~+ T cells were not significantly different. CD3~+ T cells, CD8~+ T cells and NK. cells were notably increased (P.01), and they severely infiltrated glands and epitheliums in gastro-mucosal tissues. And the quantity and distribution of CD20~+ B cells between patients and control group were not obviously different.

HIV感染无症状者和AIDS患者胃黏膜活检组织中CD3~+T细胞、CD4~+T细胞、CD8~+T细胞、NK细胞、B细胞的数量及分布：与非HIV感染对照组相比，(1)AIDS患者胃黏膜内CD4~+T细胞显著减少(P＜0.01)，而无症状者与对照组无显著差异(P＞0.05)；(2)胃黏膜内CD3~+T细胞、CD8~+T细胞、NK细胞(CD57~+)显著增加(P＜0.01)，并呈现较明显普遍性噬胃黏膜上皮和腺体现象；(3)各组胃黏膜内CD20~+B淋巴细胞的数量分布变化不明显。3。

Results:①The amount of human colon carcinoma cell line SW480 treated by quercetin decreased. The morphology of partial SW480 cells was shrunk volume, integrated cell membrane, condensed cytoplasm, pyknotic chromatin, nuclear fragmentation. Apoptotic Corpuscles were found by electron microscope.②MTT colorimetric assay showed quercetin inhibited the growth of human colon carcinoma cell line SW480 in a time- and dose-dependent manner when the concentration of quercetin was 30、60、90μmol/L.③Flow cytometry analysis showed the cell cycle of SW480 cell was restricted in G1/S. G0/G1 phase rate increased and S phase rate decreased with increasing concentration of quercetin and time lasting.④ Zymogram analysis assay showed the secretion of matrix metalloproteinases in human colon carcinoma cell line SW480 treated by quercetin decreased. With increasing concentration of quercetin, the secretion of MMP-2 and MMP-9 decreased.⑤Immunohistochemistry method demonstrated the position expression of Cathepsin-D in SW480 cell was suppressed by quercetin in a time- and dose-dependent manner.

研究结果：经槲皮素处理的人结肠癌SW480细胞数量减少，部分细胞体积缩小，细胞膜完整，胞浆浓缩，核染色质固缩，细胞核碎裂，形成凋亡小体；MTT法检测显示当作用浓度为30μmol/L~90μmol/L时，槲皮素对人结肠癌SW480细胞的生长有抑制作用，其抑制作用随着作用浓度的增加和作用时间的延长而增强；流式细胞学发现槲皮素主要作用于人结肠癌SW480细胞周期的G1/S期，大部分细胞被阻断于S期，随药物浓度的升高和作用时间的延长，G0/G1期细胞比例逐渐增加，S期细胞比例逐渐减少；酶谱分析法检测显示不同浓度的槲皮素能够抑制人结肠癌SW480细胞分泌MMP-2及MMP-9，随浓度的升高，MMP-2及MMP-9的分泌量减少；免疫组织化学法显示不同浓度的槲皮素处理人结肠癌SW480细胞后，Cathepsin-D的表达随药物浓度的升高和作用时间的延长而降低。

The survival rates of CEM cells cultured with cis-diamminedichicloroplatinum added 24 h later were higher than that cultured with hTERT ASODN and DDP added 24 h later. The survival rates of CEM cells cultured with DDP were similar with that cultured with hTERT SOND and DDP. In morphological observation of apoptotic cells using Giemsa staining, cells treated with DDP or DDP combined with hTERT ASODN ro SODN at 48 h, displayed classic apoptotic changes. Apoptosis rates of CEM cells treated with DDP for 48 h after 24 h of exposure to ASODN significantly increased. There was significant difference in the percentage of apoptotic cells of CEM cells between hTERT ASODN plus DDP and SODN plus DDP or DDP alone, respectively.

结果： hTERT ASODN作用于CEM细胞24 h再加入柔红霉素、长春新碱、足叶乙甙，对细胞生长的抑制分别与单用柔红霉素、长春新碱、足叶乙甙及hTERT正义寡核苷酸联合柔红霉素、长春新碱、足叶乙甙组相比，统计学上无显著差异(P＞0.05)。hTERT反义核酸作用于CEM细胞24 h加入顺铂，再共同作用48 h，CEM活细胞均数为2.318×108 cells/L，与单用顺铂组(3.250×108 cells/L)及hTERT正义核酸联用顺铂组(3.175×108 cells/L)相比，对细胞抑制明显增强(P＜0.05)。hTERT ASODN作用于CEM细胞24 h再加入顺铂作用48 h，细胞出现典型的凋亡形态学改变。hTERT ASODN与2.5 μmol/L顺铂联合作用于CEM细胞48 h的凋亡细胞百分率(19.47%)分别同SODN与顺铂联合作用组(6.97%)、单用顺铂作用组(6.02%)进行比较有显著差异(P＜0.01)。

In this thesis, we find that dlg is indispensible in the establishment of anterior-posterior and dorsal-ventral polarity of drosophila oocyte. Removal of Dlg function from the posterior follicle cells using the FLP/FRT system leads to disruption of oocyte skeleton reconstruction that is elicited by the failure of those posterior cells to differentiate normally in mid-oogenesis. We demonstrate that abnormity of Notch, JAK-STAT and EGFR signal pathway in dlg mutants contributes to this aberrant differentiation. dlg null mutant also blocks the normal differentiation of two groups of anterior follicle cell-stretched cell and centripetal cell, but not border cell, with a lower penetrance. However unlike the result in posterior follicle cells, Notch and JAK-STAT signaling are both undisrupted in all mutant anterior follicle cells, implying other fate determinants may be involved.

我们的研究发现，后端滤泡细胞中的Dlg在果蝇卵子发生中期卵母细胞前后轴和背腹轴建立过程中也是必须的，PFC中dlg完全缺失型突变引起PFC的分化异常，导致卵子发生中期卵母细胞骨架重组异常，Stau、Grk等极性决定蛋白定位错误。dlg突变阻碍了Notch、JAK-STAT、EGFR等调节PFC分化的信号通路的激活。dlg突变的PFC也没有获得前端滤泡细胞命运。dlg突变不影响前端滤泡细胞群中边界细胞的分化，但是在一定程度上影响伸展细胞和向心细胞的分化，并且这种影响不依赖于前端滤泡细胞Notch或JAK-STAT信号激活的异常。

Additionally XBP1 mRNA which functioned as centrally regulating molecule during ER stress was spliced partially,while it was completely spliced in positive control cells and unspliced in H7721.These results gave the proof that blocking expression of GnT-V caused H7721"s ER stress and response was more weak than that caused by DTT. It may be the chronic process.Additionally,previous studies reported that the ds-RNA may activate the kinase PKR which phosphorylated eIF2 α and inhibited synthesis of proteins.In this paper the antisense cDNA of GnT-V was integrated with GnT-V-AS/H7721"s gene and functioned through the binding of antisense RNA and mRNA of GnT-V.Additionally,the integration of GnT-V cDNA in genome also may be a non-specific factor.

对这三种ER stress关键分子的检测发现：和阴性细胞相比较，实验细胞中BIP的表达无论是蛋白水平还是转录水平都有明显的上调，但上调程度都要低于DTT处理的ER stress阳性细胞；XBP-1 mRNA在实验细胞中部分被剪接，在阳性细胞中XBP-1 mRNA完全被剪接，而在阴性细胞中其以非剪接形态存在；此外和DTT处理的ER stress阳性细胞相似，实验细胞中的PERK发生磷酸化，表明ER stress过程中通过磷酸化eIF2α抑制蛋白合成机制的活化，这和芯片所检测到的GnT-V-AS／H7721细胞蛋白合成系统水平下调相一致。

Electron microscopic findings were: 1. alveolar type I cells were degenerated、 broken-down and desquamated, endothelial cells were swelled, with inter cellular tight junction shortened, alveolar type II cells hyperplastic, basement membrane thinned and deformed; 2. alveolar macrophages and interstitial macrophages were hyperplastic; 3.mast cells were infiltrated and degranulated; 4.electron-dense deposits were present at alveolar wall; 5. myofibroblasts 、fibroblasts、 collagen and basement membrane like material were hyperplastic.

电镜观察可见：(1)I型肺泡上皮细胞变性、崩解和脱落，内皮细胞肿胀，细胞间紧密连接短小，II型肺泡上皮细胞增生，基底膜变薄和破坏；(2)肺泡巨噬细胞、间质巨噬细胞增多；(3)肥大细胞浸润并见脱颗粒现象；(4)肺泡壁电子致密物沉积；(5)肌纤维母细胞、纤维母细胞、胶原原纤维及基底膜样物质增生。

Following chemical activation, blastocysts rate of the treated oocytes was similar to untreated oocytes.8 Following fertilization, however, few oocytes inhibited with CHX developed into morulae/blastocysts, due to a high incidence of polyspermy.9 Cortical granule migration occurred during inhibition, but CHX inhibition impaired CG migration, significantly no oocytes inhibited by CHX completed CG migration after maturation.10 CHX inhibition had no effects onα-microtubles and microfilaments of goat oocytes.

抑制24h转为正常培养24h，不影响卵母细胞的成熟和孤雌激活能力，并且CHX抑制后再成熟的卵母细胞经孤雌激活发育到囊胚的比例与对照组卵母细胞相似。8、体外受精后，CHX抑制后再成熟卵母细胞的多精受精现象显著增加，发育到桑椹胚/囊胚的比例显著低于对照组。9、CHX抑制过程中皮质颗粒仍能发生迁移，但是CHX抑制会对皮质颗粒的迁移造成不可恢复的损伤，使再成熟的卵母细胞内皮质颗粒不能完全迁移。10、CHX抑制对山羊卵母细胞α-微管和微丝都没有影响，无论是抑制后处于生发泡期的卵母细胞，还是抑制后再成熟的卵母细胞，微管和微丝的分布都与对照卵母细胞相似。

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。