Fluorescein-concanavalin A conjugates distinguish between normal and malignant human cells: a preliminary report

A method is described for using a fluorescein isothiocyanate concanavalin A conjugate to stain human cell membranes in formalin fixed paraffin embedded tissue. 57 neoplastic and normal tissue sites were examined. In 54 malignant tumours, bright green fluorescence was confined to the cell membranes while in 23 benign tumours and normal tissue sites, the membranes were unstained or showed a diminished level of fluorescence. The distinction between malignant and hyperplastic or normal cells was clear cut and definite.     

Defying death after DNA damage

DNA damage frequently triggers death by apoptosis. The irreversible decision to die can be facilitated or forestalled through integration of a wide variety of stimuli from within and around the cell. Here we address some fundamental questions that arise from this model. Why should DNA damage initiate apoptosis in the first place? In damaged cells, what are the alternatives to death and why should they be selected in some circumstances but not others? What signals register DNA damage and how do they impinge on the effector pathways of apoptosis? Is there a suborganellar apoptosome complex effecting the integration of death signals within the nucleus, just as there is in the cytoplasm? And what are the consequences of failure to initiate apoptosis in response to DNA damage?     

Fluorescein-concanavalin A conjugates distinguish between normal and malignant human cells: A preliminary report

Summary A method is described for using a fluorescein isothiocyanate concanavalin A conjugate to stain human cell membranes in formalin fixed paraffin embedded tissue. 57 neoplastic and normal tissue sites were examined. In 34 malignant tumours, bright green fluorescence was confined to the cell membranes while in 23 benign tumours and normal tissue sites, the membranes were unstained or showed a diminished level of fluorescence. The distinction between malignant and hyperplastic or normal cells was clear cut and definite.     

新能源转换系统功率模块驱动可靠性分析与试验

目前推挽结构的功率模块驱动可通过减小驱动电阻将导致开通、关断时间的缩短,但同时也将导致开关过程中IGBT功率器件电流、电压热应力的增加,从而使功率模块可靠性降低。对此,在分析功率模块失效机理和热模型的基础上,提出一种基于dSPACE的分段控制算法,通过软件和硬件结合分段控制功率模块开、关断速度。通过实验揭示了功率模块的表面温度变化规律,得出表面温度变化的指数曲线,并证明了该控制方法具有良好的驱动和保护功能,在缩短开关时间的同时可以有效抑制电压、电流应力的增加,并能有效减少新能源转换系统中输出电压和电流的谐波、提高电压利用率和波形质量,使新能源转换系统可靠性得到提高。     

Glucocorticoid-induced thymocyte apoptosis is associated with endogenous endonuclease activation

In near-physiological concentrations, glucocorticoid hormones cause the death of several types of normal and neoplastic lymphoid cell, but the mechanisms involved are unknown. One of the earliest structural changes in the dying cell is widespread chromatin condensation, of the type characteristic of apoptosis, the mode of death frequently observed where cell deletion seems to be 'programmed'. It is shown here that this morphological change is closely associated with excision of nucleosome chains from nuclear chromatin, apparently through activation of an intracellular, but non-lysosomal, endonuclease.