细胞坏死

Discussion TNF-αis an inflammatory cell cytokine,with the properties of autocrine, produced by cadiocyte at the early age of MIRI,inducing myocardial function abnormal and cadiocyte necrosis in MIRI、pyaemia、chronic cardiac insufficiency、viral myocarditis and the homograft rejection of heart.

讨论 TNF-α是心肌缺血再灌注早期心肌细胞产生的炎性细胞因子，是一种自分泌的作用因子，在缺血再灌注损伤、脓毒症、慢性心功能不全、病毒性心肌炎以及心脏同种移植排斥反应中均能导致心肌功能能障碍和心肌细胞坏死。

Observation: Apoptosis was usually proved by elec tron microscopy.

细胞凋亡与细胞坏死在形态学方面有着显著的差别，通常电镜观察结果是证明细胞凋亡的最可靠的证据。

The infected cells grew slowly or did not grow and some of them died. The cytopathological changes were observed using an electron microscope.

感染病毒的培养细胞出现增长缓慢或停止生长的现象，部分细胞坏死；电镜下可以观察到一系列细胞病理变化。

2The animal amount of happening hepatic cell necrosis changes in 2.00g/kg group was lowered,the degree of pathobiological changes was lightened,and the cell necrosis- changed evaluation had dramatical differences compared with the CCl4 control group.

结果 0.67g/kg和2.00g/kg剂量组的血清谷丙转氨酶、谷草转氨酶水平降低，与CCl4对照组比较( P ＜0.05)；2.00g/kg剂量组发生肝细胞坏死的动物例数明显减少，病变程度减轻，坏死评分低于CCl4对照组( P ＜0.01)。

Methods DCs were pre pared from peripherad blood mononuclear induce d with gra-nulocyt e／macrophage colony-stimulating factor and interleukin-4.Apoptosis of he patochlangioma cells were induced with γ-radiation.We design these experiment groups including(1)coculture of DCs and apoptotic cancer cells and T cells,(2)co culture of DCs and necrosis cancer cells and T cells,(3)coculture of DCs and cul tured cancer cell and T cells,(4)cocultu re of DCs and T cell,(5)cocuture of DCs and cultured cancer cell.

用粒-巨噬细胞集落刺激因子加白介素-4(IL-4)从人外周血分化、诱导DCs、γ-射线在体外诱导培养的人胆管癌细胞凋亡，将DCs、T淋巴细胞和凋亡胆管癌细胞共培养，同时设计不同类型肿瘤细胞(坏死胆管癌细胞及培养胆管癌细胞)作对照，7d后，分离、富集DCs、T 淋巴细胞进行免疫应答及肿瘤细胞杀伤试验。

Results:The degenerative changes of articular cartilage in the manipulation group and the sodium hyaluronate group,such as vacuolar degeneration of cytoplasm,decreased quantity and degraded function of orginele,pycnosis of nuclear and necrosis even disintegration of cell,are lesser than that in the group without treatmnet.

结果：手法干预组和透明质酸钠组软骨细胞发生胞浆空泡化，细胞器数量减少，功能减退以及细胞核固缩甚至细胞坏死崩解等退变现象的程度较空白对照组轻，手法组与透明质酸钠组相当。

Acute diffuse lung injury were identified in toxication control group, intra-pulmonary alveoli hemorrage, effusion, inflammotory cell infiltration and inter-pulmonary alveoli, fibroplasia were seen; necrosis and abbscission were seen in of typeⅠand Ⅱ epithelial cells.

结果 中毒组大鼠肺的病理学改变为急性弥漫性肺损伤，表现为肺泡腔内出血、渗出、炎性细胞浸润，肺泡隔炎性细胞浸润及纤维组织增生，Ⅰ型和Ⅱ型上皮细胞坏死脱落。

It is now known that seere hypoxia-ischemia may not cause immediate cell death, but may precipitate a complex biochemical cascade leading to the delayed deelopment of neuronal loss. These phases include a latent phase after reperfusion, with initial recoery of cerebral energy metabolism but EEG suppression, followed by a secondary phase characterized by accumulation of cytotoxins, seizures, cytotoxic edema, and failure of cerebral oxidatie metabolism from 6 to 15 h post insult.

现在认识到严重的局部缺氧有可能不立即引起细胞坏死，但是可能促成一种复杂的生化级联反应，这可能导致神经元丢失，进而导致延缓发育，这些时期包括再灌注后的潜伏期，该期出现早期的脑能量代谢复苏但脑电图却呈抑制状态，紧接着第二期表现为损伤后6－15个小时细胞毒素，癫痫，细胞毒性水肿，脑氧化功能衰竭的累积。

MAIN OUTCOME MEASURES:①The amount of inflammatory cells, epithelization degree and the level of fibrocytes in the section.

苏木精-伊红染色病理切片观察结果：前4组见皮片内细胞水肿，有少量炎性细胞浸润，术后5d发现皮片部分角质细胞坏死脱落。

Apoptosis was detected in both of the cell lines in the absence of folacin, but no necrosis was observed in this experiment.

实验组和对照组中，均未观察到细胞坏死，每种细胞均可看到凋亡细胞；HBL-100在实验组的P53突变型蛋白面积比对照组大（P.05），实验组P53mRNA阳性面积比对照组的大（P.05）。

The split between the two groups can hardly be papered over.

这两个团体间的分歧难以掩饰。

This approach not only encourages a greater number of responses, but minimizes the likelihood of stale groupthink.

这种做法不仅鼓励了更多的反应，而且减少跟风的可能性。