黄参方剂诱导胃癌癌前病变细胞凋亡和影响BCL—2蛋白表达的研究

目的：探讨黄参方剂对胃癌癌前病变细胞凋亡及相关基因表达的影响。方法：将７２例胃癌癌前变患者随机分为２组,治疗组３７例,口服黄参方剂６０ｍｌ／ｄ;对照组３５例,口服维酶素片１２片／天,疗程２月。治疗后胃镜同一部位取材,检测治疗前后细胞凋亡指数和ＢＣＬ－２蛋白的表达。采用原位末端标记法（ＴＵＮＥＬ）检测细胞凋亡,采用免疫组化检测ＢＣＬ－２蛋白的表达。结果：黄参方剂组服药前后细胞凋亡指数分别为（１９．８     

雌激素对氧化型低密度脂蛋白诱导的血管内皮细胞凋亡的影响

目的：观察雌激素（１７β－雌二醇）对氧化型低密度脂蛋白（ｏｘＬＤＬ）诱导人脐静脉内皮细胞（ＨＵＶＥＣ）凋亡的影响。方法 以ＨＵＶＥＣ为对象,观察不同浓度的１７β－雌二醇（１,１０和１００μｍｏｌ／Ｌ）对ｏｘＬＤＬ（４μｇ／Ｌ）诱导的凋亡的影响。结果 不同剂量的１７β－雌二醇对使用ｏｘＬＤＬ诱导的ＨＵＶＥＣ凋亡减少７０％￣９３％,其抑制呈明显的正向量效应关系,１７β－雌二醇１μｍｏｌ／Ｌ组细胞凋亡占     

胸腺细胞凋亡的研究进展

就目前在胸腺细胞凋亡这一方面的国内外研究进展作一简要综述。     

运用原位DNA末端标记法研究细胞凋亡对乳腺癌预后的影响

研究临床乳腺癌标本中细胞凋亡的发生情况,评价其在预测后在的意义。方法搜集９１例浸润性乳腺癌的石蜡组织切片,运用原位ＤＮＡ断裂位点的末端标记法,检测细胞凋亡,计算凋亡细胞占肿瘤细胞的百分比,求得凋亡指数。结果本组病例细胞凋亡发生率为９１．２％,凋亡指数分为两组：０～０．２１和０．２８～０．６２,凋亡指数高低与腋淋巴结转称相关（Ｐ＜０．０１）。生存率单因素分析中,凋亡指数高的病例,无病生存率（Ｐ＝０．００９５）及总生存率（Ｐ＝０．０３４８）均优于凋亡指数低的病例。但Ｃｏｘ模型多因素分析末能指示凋亡指数是一个独立的预后指标。结论在乳腺癌组织中,细胞凋亡是一种自发现象,其发生情况各有不同,研究初步提示了细胞凋亡在乳腺癌预后中的作用,了解了凋亡和腋淋巴结转移的相关性。     

紫杉醇诱发人乳癌细胞凋亡的机制研究

探讨紫杉醇诱发人乳腺癌细胞凋亡的发生机制。方法应用细胞形态观察、琼脂糖凝胶电泳、流式细胞仪、活细胞视频观察和蛋白印迹免疫法进行检测和观察。结果癌细胞在紫杉醇作用下,细胞分裂阻滞在分裂期的中期,并诱导细胞发生凋亡。凋亡细胞表现为细胞固缩,核染色质凝聚或者断裂。细胞ＤＮＡ裂解片段呈现典型的“阶梯状”排列的条带。凋亡抑制基因Ｂｃｌ－２在细胞凋亡过程中呈低表达并发生修饰反应,而凋亡诱导基因Ｂａｘ先呈高表达然后表达降低。结论紫杉醇诱发的人乳癌细胞的凋亡与细胞分裂期阻滞密切相关,Ｂｃｌ－２和Ｂａｘ在紫杉醇诱发的人乳癌细胞凋亡中可能起着重要的调控作用     

Plasma Factor Triggering Alternative Complement Pathway Activation by Liposomes

Several plasma components, such as complement (C) components, play a role in the clearance of liposomes from the circulation. The interactions between liposomes and the C system were investigated in this study. Multilamellar vesicle (MLV) liposomes, which were damaged by activation of the complement, became susceptible depending on the density of cetylmannoside (Man) on the liposome membrane, and activation proceeded through the alternative C pathway as observed for liposomes without Man (PC-MLV) (K. Funato et al, Biochim. Biophys. Acta 1103:198–204, 1992). In addition, the capacity of Man-modified liposomes (Man-MLV) to activate the alternative C pathway was abolished by preadsorption of plasma with Man-MLV but not with PC-MLV. The results suggest that a specific plasma factor adsorbed with Man-MLV was responsible for the augmentation of the C activation and, further, that the rapid clearance of Man-MLV from the circulation is caused by both enhanced C-mediated liposome permeability and enhanced C-mediated phagocytosis of liposomes.     

大鼠三叉神经本体觉中枢传导通路的电生理学证明

近年来形态学上发现了三叉神经领域本体感觉中枢通路,在此基础上,本文用电生理学方法,通过电刺激咬肌神经和压下颌,观察了由四级神经元组成的此通路的二级（三叉神经脊束核吻侧亚核背内侧部及邻接的网状结构）、三级（沿三叉神经感觉主核内缘存在的“带状区”）中继核团以及作为最后驿站的丘脑腹后内侧核等处的单位放电反应;另外又分别刺激或损毁二、三级中继核团,观察了丘脑腹后内侧核的单位放电变化,结果证明电刺激咬肌神经和压下颌,在上述核团都出现对本体觉冲动反应的单位放电,包括兴奋性反应单位、抑制性反应单位和无关单位三种类型,以兴奋性单位为主,占神经元单位放电总数的５２．９％～６７．７％．分别刺激二和三级神经元的所在核团,在丘脑腹后内侧核处发生相应的单位放电效应;损毁二和三级核团,本体觉传入冲动被阻断。本研究结果从电生理学上确证了形态学上发现的三叉神经本体感觉中枢通路的客观存在,从定性研究方面支持了定位研究的结果,并填补了以往生理学上只证明初级传入核团与丘脑腹后内侧核之间存在着一条多突触联系的本体觉传递通路但未能判断其具体行径和中继部位的空白,本研究并对方法论以及一些有关问题进行了讨论．     

Interleukin-1β-converting enzyme and related proteases as potential targets in inflammation and apoptosis

Summary Interleukin-1-converting enzyme (ICE, EC 3.4.22.36) is the cysteine protease responsible for the production of interleukin-1 in monocytes. Since its discovery in 1989, this enzyme has been the subject of enthusiastic investigation because of the suspected role of this cytokine in the pathogenesis of inflammatory diseases such as rheumatoid arthritis. These studies have culminated in the purification and cloning of the enzyme, development of potent inhibitors, determination of its structure by X-ray crystallography and the development of knockout mice, which have confirmed an important role for this protease in inflammation. Late in 1993, the protease became the subject of further interest because of its homology to CED-3, the product of a gene required for programmed cell death in the nematodeC. elegans. It is now clear that ICE is the first identified member of a new cysteine protease family that includes CED-3 and at least four other human homologues. Although the extent to which ICE itself plays a role in mammalian apoptosis remains controversial, it is clear that at least one of these homologues, CPP32, is an important player. The recognition that members of this family play key biological roles in both inflammation and apoptosis, two extremely attractive targets for therapeutic intervention, has led to intense interest in these proteases.     

二甲苯对不同年龄大鼠脑组织形态学及神经细胞凋亡的影响

目的　探讨年龄对二甲苯神经毒作用的影响。方法　采用 Ｈ Ｅ 染色法和 Ｔ Ｕ Ｎ Ｅ Ｌ 技术对不同月龄大鼠的脑组织病理形态学和神经细胞凋亡情况进行了研究。结果　二甲苯５００ ｍ ｇ／ｋｇ 染毒后,２ 月龄组较８ 月龄组大鼠脑组织形态学改变相对严重,２ 月龄组染毒大鼠神经细胞凋亡的发生率为（１ ．５３ ±１ ．０６） 个／ 视野,明显高于同龄对照组的（０ ．９３ ±０ ．７５） 个／ 视野, Ｆ＝ １２ ．６５９ ６ , Ｐ＜ ０ ．００１ ;８ 月龄组染毒大鼠的神经细胞凋亡率为（１ ．６５ ±１ ．１１） 个／ 视野,明显高于同龄对照组的（１ ．１５ ±１ ．０７） 个／ 视野, Ｆ＝ ６ ．２６３ ３ , Ｐ＜ ０ ．０５ 。结论　低龄大鼠对二甲苯的神经毒作用更为敏感     

子宫颈癌组织细胞凋亡、增殖细胞核抗原及P53蛋白表达的实验研究

目的：探讨细胞凋亡及增殖细胞核抗原（ＰＣＮＡ）与子宫颈癌的关系。方法：采用原位末端标记法（ＴＵＮＥＬ）检测细胞凋亡,采用免疫组化技术检测ＰＣＮＡ和Ｐ５３蛋白。结果：３２例子宫颈鳞癌组织中,细胞凋亡、Ｐ５３蛋白和ＰＣＮＡ阳性率分别为６２．５０％,５３．１３％和６５．６３％。表达Ｐ５３蛋白的细胞与表达ＰＣＮＡ细胞分布区域基本一致,与细胞凋亡无明显相关性。正常子宫颈组织只有上皮组织内有少数凋亡细胞和表达ＰＣＮＡ的细胞,显微镜下每视野阳性细胞数均不超过１０％。结论：Ｐ５３蛋白可能通过促进细胞增殖,抑制细胞凋亡而参与子宫颈癌发生与发展。