细胞发生

A malignant transformant line 3T3 (T24) was obtained by transfection of mouse fibroblast NIH3T3 cells with pMAMneo-T24-ras plasmid. 3T3 (T24) cells were cultured continuously in the presence of benzamide , an NAD site inhibitor of poly polymerase .

将12位密码子突变的活化ras癌基因全cDNA序列克隆到真核表达载体pSV2neo和pMAMneo上，获得了相应的重组质粒pSV2neo-T24-ras和pMAMneo-T24-ras，将pMAMneo-T24-ras质粒利用基因转移方法导入小鼠成纤维细胞NIH3T3中，活化的ras癌基因可使受体细胞发生恶性转化。

The drug resistance of tumour is one of the major reasons of chemotherapeutic failure.

肿瘤细胞发生耐药是化疗失败的主要原因之一，而p73蛋白的某些亚型被证明与肿瘤细胞耐药密切相关。

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。

Objective Establishment of a hybridoma cell line secreting a monoclonal antibody to facilitate iˉdentification of human tissue kallikrein（KLK1gene,hK1protein）.Methods Mice were immunized with E.coli-exˉpressed GST-hK1fusion protein and their spleen cells were fused with SP2/0myeloblastoma cells.Specificity of the monoclonal antibody was shown by Western blotting and by immunofluorescence.Results The monoclonal antibody reacted specifically to E.coli-expressed hK1and with the KLK1cDNA-transfected COS-1cells.

目的 将人组织激肽释放酶（基因命名 KLK1，酶命名为hK1）cDNA克隆入肠杆菌表达质粒，以重组菌表达的GST-hK1融合蛋白免疫小鼠，获得了分泌hK1特异单克隆抗体的杂交瘤细胞株方法将KLK1cDNA克隆入真核表达质粒，用获得的重组质粒转染COS-1细胞，经间接免疫荧光试验证明，上述单克隆抗体能与转染细胞发生特异反应。

Five pieces of genes, HIP2, UBE2D3, Apaf-1, BCL10 and TRAF-3, associated with APO expressed divergently.

BEL-7402细胞发生凋亡后，有5条与凋亡相关的基因发生了差异性表达，其中HIP2表达降低，UBE2D3，Apaf-l，BCL10，TRAF-3表达增加。

A clear cause-and-effect relationship between excessive myocardial MMP-1 activity, increased mysial collagen degradation, and progression to systolic HF has been shown experimentally through the use of transgenic models and the use of pharmacological MMP activators.53,54 In addition, experimental evidence has been provided showing that following chronic neurohormonal activation, increased synthesis and release of MMPs into the local extracellular matrix of the cardiomyocyte occurs,55 which in turn could contribute to endomysial and perimysial collagen degradation and disruption.

一个明显的因果过多的心肌MMP-1关系活动， mysial增加胶原蛋白的降解和进展收缩性心力衰竭已被证明试验，通过使用转基因模型和使用的MMP药理作用此外，activators.53，54实验证据下面被提供显示慢性神经激活时，增加的MMPs合成和释放到当地的细胞外基质的心肌细胞发生，55反过来有助于人肌内膜和 perimysial胶原退化和破坏。

It was found that exogenic gene could start-up the expression of neural stem cell specific marker, nestin, and raise neural polar changes on ES cell.

发现外源性ibeB基因的转染能启动ES细胞表达神经干细胞标志蛋白nestin，并使ES细胞发生神经细胞样极性变化。

Ultraviolet radiation can induce HaCaT cells apoptosis.One of morphological feature of cells apoptosis is karyopyknosis and clumped chromatin and formming circularity or crescent.

紫外线辐射HaCaT细胞可诱导凋亡，细胞发生凋亡的形态学特点之一是细胞核固缩，染色质浓缩，凝集，形成环状或新月体结构。

Signs of DNA laddering were observed in lung tissue of positive group.

光气染毒可造成小鼠肺水肿，引起肺Ⅱ型细胞发生DNA损伤和肺脏细胞凋亡。

BACKGROUND: Lipopexia induced by glucocorticoid is fat precipitation in marrow due to abnormal lipometabolism, or differentiation of cells resulting from hormone-affected bone marrow mesenchymal cells.

摘要背景：糖皮质激素引起的髓内脂肪蓄积是由机体脂肪代谢异常在髓内形成的脂肪沉淀，还是由于激素直接作用于骨髓间充质细胞使细胞发生了分化，以及具体生成的过程目前还没有定论。

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。