细胞凋亡与衰老关系的研究

文章阐述细胞凋亡与衰老、细胞凋亡与免疫衰老、细胞凋亡与心血管疾病、细胞凋亡与衰老相关疾病的关系及细胞凋亡在修复中的作用.     

基于GIS非点源污染模型的地形因子分析

在地理信息系统软件ＡＲＣ／ＩＮＦＯ支持下，构造了土壤侵蚀及搬运的非点源污染分布式参数模型，以广东省大亚湾经济技术开发区为例，对模型参数（地形因子Ｔ）作灵敏度分析，计算了Ｔ时考虑了各种不规则地形的影响，根据５０，１００，２００ｍ栅格大小计算的Ｔ分布差异较大，结合野外实验，最后确定５０ｍ栅格大小为最优，能表征的精确的Ｔ值。     

盆炎净颗粒的免疫调节作用研究

目的研究盆炎净颗粒的免疫调节作用。方法观察盆炎净颗粒对非特异性免疫、细胞免疫及体液免疫的影响。即对环磷酰胺所致免疫功能低下小鼠腹腔巨噬细胞吞噬能力的影响、对2,4-二硝基氯苯所致小鼠迟发型超敏反应的影响以及对环磷酰胺所致免疫功能低下小鼠血清溶血素生成的影响。结果盆炎净颗粒有明显提高环磷酰胺所致的免疫功能低下小鼠腹腔巨噬细胞吞噬能力的作用,对2,4-二硝基氯苯所致小鼠迟发型超敏反应有明显抑制作用,而对环磷酰胺所致免疫功能低下小鼠血清溶血素的生成没有影响。结论盆炎净颗粒具有提高机体非特异性免疫和细胞免疫的作用。     

A novel graphite/phenolic resin bipolar plate modified by doping carbon fibers for the application of proton exchange membrane fuel cells

In this study, the carbon fibers treated by three methods were selected as a reinforcement to investigate the influence on the properties of composite bipolar plates. The properties and microstructure of the composite bipolar plate were characterized by the four-point probe, universal test machine, contact angle tester and scanning electron microscopy. The optimum treatment methods and the fiber content were analysed. The results showed that the carbon fibers treated by Fenton reagent for 2 ​h exhibited the best performance, which could improve the electrical conductivity and the flexural strength for composite bipolar plate. Besides, the optimal content content of carbon fibers treated by Fenton reagent was 4%. The maximum power density of the PEMFC with the composite bipolar plates could reach 662.75 ​mW ​cm⁻² in H₂-air conditions. Therefore, the phenolic resin/graphite composite bipolar plate modified by doping carbon fibers was a promising candidate for bipolar plate materials for PEMFC.     

细胞凋亡的分子遗传学

介绍了细胞凋良的一些特点以及细胞生长过程中发生的凋亡现象,并从凋亡相关基因的角度,对这些基因所编码的蛋白酶在凋亡中的作用进行了概述。     

Differential insult-dependent recruitment of the intrinsic mitochondrial pathway during neuronal programmed cell death

Programmed cell death contributes to neurological diseases and may involve mitochondrial dysfunction with redistribution of apoptogenic proteins. We examined neuronal death to elucidate whether the intrinsic mitochondrial pathway and the crosstalk between caspase-dependent/-independent injury was differentially recruited by stressors implicated in neurodegeneration. After exposure of cultured cerebellar granule cells to various insults, the progression of injury was correlated with mitochondrial involvement, including the redistribution of intermembrane space (IMS) proteins, and patterns of protease activation. Injury occurred across a continuum from Bax- and caspase-dependent (trophic- factor withdrawal) to Bax-independent, calpain-dependent (excitotoxicity) injury. Trophic-factor withdrawal produced classical recruitment of the intrinsic pathway with activation of caspase-3 and redistribution of cytochrome c, whereas excitotoxicity induced early redistribution of AIF and HtrA2/Omi, elevation of intracellular calcium and mitochondrial depolarization. Patterns of engagement of neuronal programmed cell death and the redistribution of mitochondrial IMS proteins were canonical, reflecting differential insult-dependencies. Received 14 August 2008; received after revision 02 October 2008; accepted 23 October 2008     

FHA-RING ubiquitin ligases in cell division cycle control

Despite the common occurrence of forkhead associated (FHA) phosphopeptide-binding domains and really interesting new gene (RING) E3 ubiquitin ligase domains, gene products containing both an N-terminal FHA domain and C-terminal RING domain constitute a highly distinctive intersection. Characterized FHA-RING ligases include the two vertebrate proteins, Checkpoint with FHA and RING (Chfr) and RING finger 8 (Rnf8), as well as three fungal proteins, Defective in mitosis (Dma1), Chf1 and Chf2. These FHA-RING ligases play roles in negative regulation of the cell division cycle, apparently by coupling protein phosphorylation events to specific ubiquitylation of target proteins. Here, the available data on upstream and downstream regulation of and by FHA-RING ligases are reviewed. Received 24 April 2008; received after revision 18 June 2008; accepted 20 June 2008     

体外培养人涎腺多形性腺瘤细胞及表面标记物的初步研究

体外培养15例人涎腺多形性腺瘤原发肿瘤组织,探讨体外培养的细胞与原发肿瘤组织的表面标志物表达情况。运用免疫组化法检测CK5/6、CK7、CK8/18、CK14、CK20,vimentin及肌上皮表面标记物α-SMA、calponin及p63在细胞和肿瘤组织中的表达。结果发现体外培养的多形性腺瘤细胞呈多样形,可同时表达角蛋白、肌上皮表面标记物及波形蛋白,与原发肿瘤表达基本一致。提示体外培养的多形性腺瘤细胞可能大部分来源于肌上皮细胞及导管上皮细胞等,这为研究涎腺多形性腺瘤肿瘤生物学多样性提供了实验依据。     

Cell fate determination during G1 phase progression

During the cell cycle, a cell may encounter one of five different fates: it can proliferate, differentiate, become quiescent or senescent, or go into apoptosis. The initiation of such fates is often seen in the G1 phase. The aim of this review is to describe an integrative model of G1 phase progression and cell fate determination. Along the G1 phase, the cell will encounter an early checkpoint after which apoptosis can result. For a quiescent state and for differentiation, the cell will exit G1 before the restriction point and a subsequent differentiation checkpoint will decide the fate of the cell, quiescence or differentiation. After the restriction point, the cell can be arrested in response to stress stimuli, such as telomere depletion, and a decision between senescence and apoptosis occurs. Received 19 June 2007; received after revision 23 July 2007; accepted 17 August 2007     

交叉口信号控制方案评价指标动态估计模型

对评价指标在周期内的实时变化进行动态估计是交叉口交通信号动态控制的关键。应用计算机仿真模拟方法以仿真步长为间隔建立了停车延误、停车次数、排队车辆数等常用控制目标与信号灯状态及持续时间之间的动态迭代估计模型,机动车流在路段上的运行特征用CTM描述,在交叉口上的演化规律用微观交通状态描述。以单个进口道的直行车流为研究对象,对经典延误模型进行对比分析,发现随着饱和度增大,各个模型的估计偏差有逐渐增大的趋势,基于仿真步长的迭代估计累积结果基本上处于经典延误模型计算结果的变化范围内。对于单个交叉口而言,迭代算法的时间复杂度为O(n)。