华北半叶紫菜丝状体细胞凋亡过程的初步研究

本文对华北半叶紫菜丝状体细胞的凋亡过程进行了初步观察并对这一过程中细胞超微形态的变化进行了研究。结果表明，丝状体细胞的凋亡过程是由分枝的端部细胞发生老化开始的，老化细胞的细胞内壁增厚；细胞核内染色质凝缩，核膜溶解；色素体片层结构变形、溶解；红藻淀粉电子密度显著下降，逐渐解体；胞浆中出现不规则形态的囊泡、髓样结构和结构特殊的小体；随着细胞的趋于凋亡，核、色素体、线粒体等细胞器相继溶解消失，细胞结构崩溃，细胞内壁明显增厚。细胞中的囊泡和髓样结构参与了细胞内壁的形成。本研究首次报道紫菜中存在细胞凋亡，并对丝状体细胞凋亡过程的生物学意义及髓样结构的功能进行了讨论。     

细胞凋亡与心血管疾病

目的：评价细胞凋亡与心血管疾病的关系．方法：查阅文献，综合论点．结果：细胞凋亡过程涉及多种心血管疾病．结论：细胞凋亡的形态特征、细胞凋亡的生化过程及其细胞凋亡的诱导因素和基因调控机理的发现，为揭示心血管疾病的发病机制及寻找生物学防治提供了新的思路．     

胚胎发育与细胞凋亡

目的：论述在胚胎发育过程中细胞凋亡的发生及其作用；方法：通过光盘检索相关资料，进行综合评述：结果：在胚胎器官系统的发生过程中，有凋亡细胞的出现及异常凋亡能引起器官发育异常；结论：细胞凋亡在胚胎发育和器官形成过程中起重要作用。     

细胞凋亡与肿瘤治疗

细胞凋亡与许多疾病特别是肿瘤的发生发展有关，许多癌基因与抑癌基因参与细胞凋亡过程。对细胞凋亡以及在肿瘤治疗中的有关系进行了综述。     

细胞凋亡的简要分子基础

细胞凋亡的过程极为复杂，涉及一系列调控因子，本文除了介绍控制该过程的核心组分胱天酶外，还介绍了细胞凋亡的内部途径和外部途径。     

哺乳动物卵子发生过程中细胞凋亡的研究进展

细胞凋亡是发育过程中的基本生命现象,是多细胞生物体一种重要的自我稳定机制．除各种体细胞凋亡外,生殖细胞在其发生过程中也有细胞凋亡现象产生．对许多脊椎动物和无脊椎动物的研究发现,有大量生殖细胞在其发育的不同阶段丢失．对近10年来哺乳动物卵子发生过程中细胞凋亡的研究进行了综述,主要描述了哺乳动物卵子发生过程中的细胞凋亡及其调控以及凋亡的意义．     

敏感和抗性的白血病HL60细胞对staurosporine诱导 …

用对蛋白激酶具有强烈抑制、作用广泛的抑制剂ｓｔａｕｒｏｓｐｏｒｉｎｅ（Ｓｔａ），研究敏感和抗三尖杉酯碱的人白血病ＨＬ６０细胞中凋亡和多药抗药性的关系。Ｓｔａ均能诱导２种细胞发生典型的凋亡，但抗性细胞发生凋亡需更长的时间、凋亡的细胞数减少。Ｓｔａ增加柔红霉素在抗性细胞内的积聚，说明其能逆转多药抗药性，在抗性细胞凋亡过程中，ｍｄｒｌ基因表达没有变化，ｃ－ｍｙｃ稍有增加，结果显示：Ｓｔａ能诱导敏感和抗三     

人脐带静脉血管内皮细胞的体外培养及其凋亡的研究

本文从提取生长因子入手，建立人脐带静脉血管内皮细胞系，用电镜进行了细胞鉴定，然后用去除生长因子（FGF和胎牛血清）的方法诱导细胞凋亡，利用荧光显微技术、DNA凝胶电泳、电镜技术和流式细胞分光光度技术，研究了血管内皮细胞凋亡过程中超微结构和细胞周期的变化。发现去除生长因子3h后，在细胞发生明显的DNA片段化和形成凋亡小体的同时，细胞核与细胞质的超微结构发生了明显的变化，S期细胞显著减少，G1期无明显变化，G2细胞显著增多，说明用去除生长因子的方法诱导血管内皮细胞凋亡时，细胞从G2期脱离细胞周期进入凋亡程序，本文的人血管内皮细胞在体外的成功培养和对该细胞凋记的研究对深入研究其凋亡的分子调控机制具有重要的参考价值。     

病毒感染与细胞凋亡

阐述了细胞凋亡的概念，与细胞凋亡相关的病毒和基因，病毒调控细胞凋亡的机制和研究病毒感染与细胞凋亡关系的意义，以增进人们对病毒和细胞之间关系的理解。     

细胞凋亡机制简述

细胞死亡有坏死、凋亡等多种方式。细胞凋亡和细胞坏死有很大的区别。细胞凋亡是指一种受基因调节的细胞自主控制的自杀过程,它是一个井然有序的过程,大量的分子和途径参与了细胞凋亡发生。     

Retinal pigmented epithelial cells induced to transdifferentiate to neurons by laminin

Although the regeneration of nervous tissue in the vertebrate is very limited, there are a few remarkable examples of this process. Understanding the factors that regulate CNS regeneration in those areas of the nervous system where it occurs, will doubtless provide generally applicable, essential information about the process. It has been known for some time that the amphibian retina regenerates following its destruction. Transplant studies, confirmed later by in vitro experiments, have shown that one source of new neurons in regenerating retina is the retinal pigmented epithelium (RPE). RPE cells can transdifferentiate to either neurons or lens cells in culture, but little is known about the factors that regulate this process. A recent study in vivo of retinal regeneration provided evidence that the association of RPE cells with the retinal vascular membrane is an important step in transdifferentiation. We report here that transdifferentiation in vitro is profoundly influenced by the substrate on which the cells are cultured; RPE cells plated on laminin-containing substrates frequently transdifferentiate into neurons. In addition, we have found a high concentration of laminin in the Rana retinal vascular membrane. Therefore, we propose that retinal regeneration is initiated by changes in the composition of the extracellular matrix that RPE cells contact early in the process.     

Selective immortalization of murine macrophages from fresh bone marrow by a raf/myc recombinant murine retrovirus

Myeloid precursors can be grown in vitro in the presence of specific growth factors; however, their expansion is limited by a competing process of terminal differentiation. Proto-oncogenes seem to be involved in cellular proliferation and/or differentiation and may also play a role in the myelopoietic process. Murine myeloid precursors which are grown in vitro with growth factors respond with augmented self-renewal upon infection with recombinant retroviruses carrying the v-myc or v-src oncogenes, suggesting a synergism or complementation between some viral oncogenes (v-onc) and certain growth factors. We now show that the combination of two v-onc genes (raf and myc) induces the selective proliferation of monocytic cells from fresh murine bone marrow (BM) in the absence of a specific growth factor supplement. Depending on the culture conditions these cells can either differentiate and cease to proliferate or grow continuously, thus mimicking the alternative pathways that can be followed by committed BM stem cells in vivo.     

Haemopoietic colony stimulating factors promote cell survival by suppressing apoptosis.

The survival, differentiation, proliferation and development of haemopoietic precursor cells and the functional activity of mature blood cells are all influenced by colony stimulating factors (CSFs). As haemopoietic cells rapidly die in the absence of appropriate CSF, the promotion of cell survival mediated by CSFs, or growth factors, is fundamental to all the other effects exerted by these factors. This enhancement of cell survival is distinct from the stimulation of proliferation. Here we show that the death of haemopoietic precursor cells on withdrawal of the relevant CSF. is due to active cell death, or apoptosis, indicating that CSFs promote cell survival by suppression of the process of apoptosis. The existence of a positive control mechanism regulating precursor cell survival has important implications both for the regulation of normal haemopoiesis and for tumorigenesis.     

Intrinsic and extrinsic control of haematopoietic stem-cell self-renewal

When stem cells divide, they can generate progeny with the same developmental potential as the original cell, a process referred to as self-renewal. Self-renewal is driven intrinsically by gene expression in a cell-type-specific manner and is modulated through interactions with extrinsic cues from the environment, such as growth factors. However, despite the prevalence of the term self-renewal in the scientific literature, this process has not been defined at the molecular level. Haematopoietic stem cells are an excellent model for the study of self-renewal because they can be isolated prospectively, manipulated relatively easily and assessed by using well-defined assays. Establishing the principles of self-renewal in haematopoietic stem cells will lead to insights into the mechanisms of self-renewal in other tissues.     

废旧锌锰电池的回收利用

分析了我国废旧电池的回收利用现状。阐述了废旧电池对生态环境造成的危害和回收利用废旧电池的重大意义。介绍了回收利用废旧锌锰电池的工艺流程和实验原理。在现有的实验条件下,初步研究了利用废旧锌锰电池制备高锰酸钾、氯化锌、氯化铵等物质的实验方法;分析讨论了制备高锰酸钾的各种影响因素,如反应物的量、反应温度等。     

绒山羊曲细精管生殖细胞的长期培养和精子发生过程的观察

哺乳动物精子发生过程是生殖生物学的重要研究课题之一.为了开展对山羊精子发生过程的研究,我们首次建立了绒山羊睾丸生殖细胞原代培养方法.原代生殖细胞和支持细胞(Sertolicells)由绒山羊睾丸曲细精管组织块产生,在体外共培养超过三个月.在共培养期间,观察到绒山羊的精原干细胞分化为精母细胞和精子细胞的形态变化过程.这一方法的建立为山羊精子发生过程的研究和应用打下了基础.实验结果显示,在没有添加任何生长因子的条件下,绒山羊睾丸生殖细胞长期增生分化,不断产生精子细胞.这一结果暗示了组织块和共生的支持细胞为生殖细胞的增生和分化提供了营养因子和调节因子.生成的游离精子细胞最后全部死亡,暗示这一共培养体系不能提供变态过程所需因子.     

端粒,端粒酶与细胞衰老

细胞衰老是指正常细胞的有限增殖性,放多因素影响或控制着细胞衰老的发生,发展。端粒是染色体的末端,具有保护端粒ＤＮＡ的功能,随着ＤＮＡ不断复制和细胞分裂,端粒长度会逐渐缩短,而细胞衰老的过程也就开始,端粒酶活性和端粒长度呈正相关,间接地影响了细胞的衰老过程。     

血管内皮细胞凋亡过程中几种癌基因表达的研究

为了研究细胞凋亡的分子调控机制 ,用光学显微技术、DNA凝胶电泳和Northernblot方法 ,研究了去除生长因子 (FGF和血清 )和蛇毒诱导的两个血管内皮细胞凋亡系统中 p53、c H ras、c myc和bcl 2基因的表达 .发现去除生长因子诱导的细胞凋亡过程中 ,p53基因表达显著增加 ,c H ras和c myc基因表达无变化 ;蛇毒诱导细胞凋亡过程中 ,p53基因表达显著增加 ,c H ras和c myc基因表达无变化 .在正常生长和凋亡细胞中均未检测到bcl 2基因的明显表达 .实验结果表明 :p53基因参与上述两种细胞凋亡诱导系统的分子调控 ;c H ras基因只参与去除生长因子诱导的细胞凋亡过程 ,而不参与蛇毒诱导的细胞凋亡过程 ;这两种细胞凋亡诱导系统均与c myc基因表达无关 ;未见bcl 2基因明显参与血管内皮细胞的凋亡过程 .