细胞发生

Results indicated that the variation was significant from treatment to treatment. S-deficiency caused bulging chloroplasts, loosening and dishevelled grana lamella, reducing organelle, and damaged chondriosome in mesophyll cells of the leaves, and empty cells of the roots, while S-excess, however, led to densification, condensation and randomization of grana lamella of the chloroplasts of the leaves, and separation of cytoplasms from walls of the cells of the roots.

结果表明，受S素营养胁迫的水稻，其根系及叶片的超微结构均发生了显著的变化：低S胁迫会造成水稻叶片叶肉细胞内的叶绿体结构肿胀，基粒片层松驰、散乱，细胞器减少，线粒体结构被破坏，根系细胞内几乎没有内含物；S浓度高则会使叶片叶绿体基粒片层致密、浓缩，无规则化，根系细胞发生质壁分离。

Beijingensis under three droughttreatments, normal, moderate and severe stresses. The results showed:(1) the canker disease ofboth cultivars was serious gradually with increased drought;(2) the bark tissue cells sufferedplasmolysis, more evident with the severity of drought stress;(3) under the drought andinoculation with B. dothidea, cells of two cultivars damaged at different degree, mailyrepresented in the changes of organelles, such as chloroplast swollen and distorted, number ofmitochondria increased and membrane system indistinct; then organelles suffered furtherdamagement with inoculation time, thinned mitochondrias stroma, decreased cristae, crumpledand partly broken membrane of chloroplasts with stroma exosmosis. At last, the chloroplastspartly disorganized;(4) the hyphae growed mainly intercellular in resistant cultivar and notonly intercellular but also intracellular in susceptible cultivar, which directly caused thenecrosis of cells;(5) under the severe drought, the damage of cells enhanced the infection ofpathogen and drought and pathogen stressed together and promoted the disease development;the damage from pathogen on cells was more serious than that from drought.

结果显示：(1)随着干旱胁迫程度的增加，2种杨树溃疡病害发生渐趋严重；(2)干旱胁迫下，杨树树皮组织细胞发生质壁分离，并随胁迫程度的增加而严重；(3)干旱胁迫下接种病原菌，2种杨树细胞发生不同程度的损伤，主要表现为细胞器发生较大变化，如出现叶绿体肿胀变形、线粒体数量增多，质膜模糊不清等现象；随接种时间的延长，细胞器受到进一步损伤，叶绿体被膜折皱，严重时局部破裂，基质外渗，并部分最终解体；(4)毛白杨中的菌丝主要在细胞间隙中穿行，而北京杨的菌丝除在细胞间隙中生长之外，侵入细胞内部也较多，直接导致细胞的解体；(5)干旱胁迫下细胞的损伤促进了病原菌的侵染，干旱和病原菌的双重胁迫加剧了病害的发生程度，并且病原菌侵染对细胞的破坏程度大于水分胁迫。

By FCM analy sing, p53 gene can induce cells apoptosis and make it G1 arrest; Cisplatine can induce cell apoptosis and make it G2 arrest.

流式细胞计数证实p53能诱导QBC939细胞发生凋亡并导致其发生G1期阻滞，顺铂能诱导QBC939细胞发生凋亡并导致细胞发生明显的G2期阻滞。

Aligned cells are electroporated and subsequently electrofused within high electric field strength.

细胞电融合利用细胞在相对电极之间的介电电泳，诱导细胞按特定方向排列，通过电极间产生的较高场强的电脉冲使相互接触的细胞发生电穿孔，进而发生电融合。

Results 5C11 induced homotypic aggregation, proliferation arrest and apoptosis in the multiple myeloma cell line XG2 highly expressed CD40. 5C11 induced B lymphoma cell line Daudi homotypic aggregation and proliferation arrest but no apoptosis.

结果 5C11能引起CD40表达强阳性的多发性骨髓瘤细胞XG2发生同型聚集，抑制其生长并介导细胞凋亡；5C11可引起CD40＋的恶性B淋巴瘤细胞株Daudi发生同型聚集，抑制其生长并使细胞发生G2/M期阻滞，但并不介导细胞凋亡。

Result 1 Magnetic nanoparticles, magnetic nanoparticles modified with antisense oligodeoxynucleotide of human telomerase reverse transcriptase induced HL-60 tumor cells to apoptosis, we could see typical morphologic change of apoptosis cells: karyopyknosis, chromation"s condensing and aggregation in nuclear, forming crescent-shaped or annulus structures to lean on edge of cell nucleus"s membrane and posing apoptosis body by Atomic Force Microscope, Fluorescence microscope, transmission electron Microscope 2 There was a significant difference compared with control group(p.01), inhibition ratio had significant positive correlation with medication dosage and time ;during 0.8-8μM dosage amplitude, inhibition ratio accrescenced by dosages increasing. However, the inhibition ratio would decrease when dosage over 8-80μM.

结果 1 磁性纳米粒子、修饰有端粒酶反义寡核苷酸的磁性纳米粒子诱导HL-60细胞发生凋亡，原子力显微镜、光学显微镜、荧光显微镜和透射电镜下均观察到HL-60细胞呈现典型的凋亡细胞的形态变化：细胞核固缩，核内染色质浓缩、凝聚、形成新月形或环状结构紧靠在细胞核膜边缘，并形成凋亡小体。2 磁性纳米粒子、修饰有端粒酶反义寡聚脱氧核苷酸的磁性纳米粒子对HL-60肿瘤细胞的生长和增殖有明显的抑制作用，与对照组相比有显著性差异(p＜0.01)，在剂量为0.8-8μmol／L范围内，抑制率随剂量的增加而增加，当剂量超过8μmol／L时，抑制率反而下降；3 磁性纳米粒子、修饰有端粒酶反义寡聚脱氧核苷酸的磁性纳米粒子可增强p53基因的表达活性，引起DNA降解损伤，反向调节细胞周期活动，促使细胞从G0期进入G1期，抑制肿瘤细胞的生长。4 修饰有端粒酶反义寡聚脱氧核苷酸的量子点能通过内吞作用进入HL-60肿瘤细胞的细胞核，可以在细胞内进行定位和促进HL-60肿瘤细胞的凋亡。

We may well explain why ricin-induced apoptosis showed no typical DNA ladder. The presence of laddering in DNA gels implies an apoptosis process, but its absence does not rule out the apoptosis. The ricin 0.05μmol〓 had no effect on the 〓 phase of cell cycle, but induced 〓 arrest. The ricin may affect the balance of synthesis and destruction of proteins that controlling the cell cycle.

检测到DNA梯度表明细胞发生了细胞凋亡，未检测到DNA梯度不能否认凋亡的存在。0.05μmol.L〓的蓖麻毒素对HeLa细胞周期的G〓/G〓期无影响，而诱导了G〓/M期阻滞，蓖麻毒素可能引起一些控制细胞周期蛋白的合成与降解发生紊乱。

These results revealed that the pollen chamber developmental pattern passed through four phases. Firstly, a group of nucellar cells at the micropylar end elongated longitudinally. Thereafter, the uppermost nucellar cells at the micropylar end initiated PCD; and these elongated cells undergoed PCD in a basally and laterally oriented direction to form a cavity.

贮粉室的形态发生可分为4个阶段：最先是位于珠孔端的几层珠心细胞纵向地伸长；接着，珠孔端最顶部的珠心细胞发生PCD；然后，那些已经纵向伸长的珠心细胞向基地和侧向地依次发生死亡，产生贮粉室空腔；最后，珠孔端的珠心表皮细胞发生开裂，形成贮粉室的开口。

When pea ( Pisum sativum L.,Alaska strain) was grown in short\|day conditions,the apical bud senescence started with the transformation of the bud from vegetative to reproductive growth.DNA fragmentation was detected during the senescence using the terminal deoxynucleotidyl transferase\|mediated dUTP nick end in situ labeling method.The cell ultrastructural changes were similar to apoptosis in animal cells:the apical meristemetic cells underwent the programmed cell death.This wa...

显微、超微结构研究表明，短日照条件下豌豆顶芽的衰老过程是从营养生长锥向花芽的转化，而用DNA原位末端标记、Caspase 8WesternBlot和 14 0bpDNA片断积累的试验结果证明，转化为花芽的整个生长锥细胞发生了编程性死亡，而且其最顶端部分细胞首先发生PCD ，而顶端周围的分生组织细胞逐渐分化出花芽的各部分，但顶芽最后并没有发育成为完整的花，所有细胞就都发生PCD ，从而顶芽衰老

Neural stem cells have a strong self-renew mechanism and it can transform after a little break. Neural stem cells have a long term survival, which mean that it has more probability of wrong copy than mature cells. These cells are formed glioma stem cells in the end. The genes who adjust neural stem cells can express in glioma stem cells, which hold out glioma stem cells from neural stem cells. There is another presume that glioma stem cells come from differentiated cells. Through the gene break of these cells, they can obtain characteristics of stem cells, then form glioma stem cells.

神经干细胞具有很强的自我更新机制，获得较少突变即有可能恶性转化，而且干细胞存活时间较长，这意味着干细胞比成熟细胞发生细胞复制的错误几率更大，因外界环境的刺激而发生突变的机会更多，最终形成脑胶质瘤干细胞，同时调节神经干细胞增殖和自我更新的基因在脑胶质瘤的脑胶质瘤干细胞中也表达，这也是支持神经干细胞是脑胶质瘤干细胞来源的；也有推测认为它可能起源于已分化的细胞，由这些细胞突变发生去分化得来，并通过基因突变而获得了干细胞自我更新的特性，从而形成脑胶质瘤干细胞。

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。