细胞

While the tissue spaces surrounding a few blood vessels wasAl and Fg positive,no Al or Fg positive cells were observed.In antemortem injurygroup,diffuse subarachnoid hemorrhage,cerebral edema,swelling or pyknotic neu-rons could be observed.The axons showed irregular swelling and disconnection at1～3h,marked swelling and disconnection at 6h,and retraction ball at 15h whichwas more remarkable at 24h after injury.The space between myelin sheaths andaxons was increased at 3～6h after injury.Tortuous and wavelike myelin sheathswhich adhered on axons incompletely,or even peeled off could be found from 15hto 24h after injury.Perinuclear lysis of Nissl bodies began at 24h after injury.Thenumber of GFAP positive cells in cerebrum and brain-stem increased significantlyfollowed by decrease,and then increased again,but the time courses of the changesin different areas of brain were not same.Al and Fg positive neural cells,mainlysurrounded blood vessels,with diffuse or peripherally distributed positive matter incytoplasm could be observed at 0.5h after injury.The number of Al or Fg positivecells and the intensity of immunoreaction increased with the time of injury.The areaof SYN positivity in medulla oblongata and pons decreased notably 3～6h afterinjury,then return to normal levels and continued to 24h after injury.

生前损伤组，可见广泛蛛网膜下腔出血，脑组织水肿，神经细胞肿胀，晚期神经元固缩；伤后1～3h见部分神经轴突不规则增粗、断裂，伤后6h断端膨大，伤后15h可见收缩球，至伤后24h更为明显；伤后3～6h可见部分神经髓鞘与轴突之间的间隙增宽，伤后15h髓鞘明显曲折，不完全附着在轴突两侧，甚至剥脱，持续到伤后24h；核周尼氏体减少在伤后24h才开始出现；同一部位的GFAP阳性细胞数目随损伤时间发生改变，先增多（最早在伤后0.5h），达到高峰后减少，其后又有增多趋势，但不同部位的GFAP阳性细胞数目增减的时间过程不尽相同，同时，大脑中的GFAP阳性细胞数目也有改变；伤后0.5h，可在脑干组织中见到Al和Fg阳性神经细胞，主要位于血管周围，阳性物在胞浆中呈弥散性分布，但部分细胞的阳性物仅分布于靠近胞膜的胞浆中而呈环状，随损伤时间延长，阳性细胞数目增多，反应强度增加；伤后3～6h，延髓及桥脑中的SYN阳性物面积减少，其后恢复到正常水平，并持续到伤后24h。

The follicle cells of growing follicle were composed of small cells, intermediate cells and pyriform cells.

乌梢蛇生长卵泡的滤泡细胞是由小细胞、中间细胞和梨形细胞组成的异形滤泡细胞。

When cells undergo programmed cell death, cell corpses adopt a refractile and disc like structure. Using this morphological change as a cell death marker, we analyzed the death of the first 13 cells in the AB cell lineage of wild type and cnx-1; crt-1 mutant embryos.

进一步以4D摄影分析线虫AB世系细胞中最早死亡的13颗细胞之相对死亡时间和细胞尸体持续的时间长短的结果则显示，此死亡细胞数量提高的现象应是源於吞噬步骤发生问题而非细胞死亡执行上的问题。

①Rat MSC and VSMC were cultured and identified, respectively. MSC were labeled with DAPI firstly, and then co-cultivated with VSMC. The changes of morphology and ultrastructure of co-cultured cells were observed. Immunfluorescence analysis was performed by using monoclonal antibodies against specific antigen.②We established the regulatable system in two steps: a stable MSC line expressing rtTA has been constructed and characterized firstly by transfected with pUHD 17-1hyg and then selected by hygromycin B; in a second step, this line was used for trandfer the AT2R gene to MSC to get the well establishing double stable MSC lines;③The expression of AT2R regulated by doxycycline was evaluated by western blot;④The MSCs were transduced into rat carotid arteries with regulatable AT2R gene after the establishment of rat carotid balloon injury restenosis model. The intimal/medial area ratio were measured by digital analysis system.

研究方法：(1)密度梯度离心法及胶原酶消化法分别培养原代大鼠MSC及VSMC，细胞共培养并行免疫荧光化学染色和透射电镜观察超微结构；(2)组成受Dox调控的哺乳动物表达系统的四种成分的转化、扩增及提纯并酶切鉴定；(3)采用常规分子生物学方法连续两个回合转染体外培养的MSC，并分别采用发光计检测不同细胞克隆萤光素酶活性改变以及RT-PCR方法检测AT2R目的基因mRNA表达情况，根据各个细胞克隆受Dox调控表达的程度，选择低背景、高诱导表达AT2R的细胞系，作为双重稳定MSC细胞系；蛋白免疫印迹法观察该细胞系在Dox调控下AT2R表达的时相性、持续性及在不同浓度Dox调控下的表达情况；(4)建立大鼠颈动脉球囊损伤动物模型，将双重稳定MSC在术中导入血管，分别于14 d、28 d进行病理切片，检测可调控AT2R对新生内膜增生的影响；采用RT-PCR免疫组织化学免疫荧光等技术观察AT2R基因在新生内膜中的表达以及细胞外基质成分表达的改变，TUNEL法检测血管组织中细胞凋亡的变化情况。

Results After restimulation with antigen, some of the CD4 +T cells were positive either for Th1 or Th2 cytokines, but few cells was positive for both of them.

Th1细胞产生IFN γ、TNF β和IL 2 ，参与细胞介导的免疫反应；而Th2细胞产生IL 4、IL 5、IL 10和IL 13等，参与体液介导的免疫反应；Th0细胞分泌混合型细胞因子，当受特异性抗原的刺激时，在微环境的影响下，可以向Th1方向转化或向Th2方向转化。

On day40 after infection,donor derived Thy-1.1~+ CD8Tm cells were detectable in various organs including peripheral blood,spleen,lymph nodes,and liver.These cells were CD44~,CD62L~/CD62L~ in phenotype and more importantly,these cells were readily detectable for intracellular IFN-γsecretion several hours after ex vivo restimulation with OVA_(257-264) peptide.

感染40天后，可以在包括外周血、脾脏、淋巴结和肝脏在内的脏器中检测到一定比例的Thy-1.1~+ CD8 T细胞，这群细胞具有记忆性CD8T细胞的表型特征，即CD44~，CD62L~/CD62L~，更重要的是，这群细胞在体外OVA_(257-264)肽再刺激数小时后即可检测到细胞内IFN-γ分泌。

Using New Zealand rabbit ears cartilage makes chondrocyte suspension, Fibrinogen was mixed with D-hank's makes a final fibrinogen concentration of 50mg/ml mixture solution, then chondrocytes resuspend with fibrinogen solution, chondrocytes-seeded fibrinogen was mixed with thrombin (25U/ml in 40mM calcium choride) to make chondrocytes/fibrin glue polymer. Pluronic F-127 was mixed with D-hank's makes a final Pluronic F-127 concentration of 400mg/ml mixture solution, then chondrocytes resuspend with Pluronic F-127 solution to make chondrocytes/Pluronic F-127 polymer. The chondrocyte concentrations was 10 million chondrocyte/ml of polymer.

为确定纤维蛋白凝胶与Pluronic F-127在注射方式形成组织工程化软骨过程中的优劣，我们进行了如下实验：应用新西兰大白兔耳软骨获取软骨细胞并体外培养，纤维蛋白原应用D-hank's液配制为50mg/ml，然后以纤维蛋白原溶液重悬软骨细胞，再与40mM的氯化钙配制的25U/ml凝血酶混合形成软骨细胞—纤维蛋白凝胶复合物；Pluronic F-127应用D-hank's液配制为400mg/ml，同样用PluronicF-127溶液重悬软骨细胞而形成软骨细胞—Pluronic F-127凝胶复合物。

Finally, we used GF109203X, Rottlerin, PKC-delta antisense RNA and PKC-epsilon siRNA to inhibit PKC activation or expression, and then observed their effects on TRAIL-induced apoptosis.

当以Rottlerin处理细胞时，均会增加细胞对於TRAIL的感受性。除了H1299细胞，p53能透过藉由Rottlerin抑制PKC-delta的活性，进而增加细胞对TRAIL诱导细胞凋亡的情形。

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。

The result of AKP test showed that the 3D-colony cells taken the russety colour .The other cells including feeder cells and around cells have not been dyed. It suggests that the 3D-colony cells should have a high activity of AKP, might be in the non-differentiation or low differentiation state.

碱性磷酸激酶的染色结果显示这些细胞克隆呈红褐色，而周围细胞和饲养层细胞未着色或着色很浅，说明这些细胞克隆的内源性碱性磷酸酶活性较高，从而表明这些细胞克隆处于未分化或低分化状态。

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。