Interaction of aloe-emodin with human serum albumin

The presence of several high affinity binding sites on human serum albumin (HSA) makes it a possible target for many drugs. This study is designed to examine the effect of aloe-emodin on HSA by fluo-rescence, CD spectroscopy and molecular modeling. The results of fluorescence measurements sug-gested that the hydrophobic interaction was the predominant intermolecular force stabilizing the AE-HSA complex, which was in good agreement with the result of molecular modeling study. And the enthalpy change ΔH0 and the entropy change ΔS0 were calculated to be -7.041 kJ·mol-1 and 76.619 J·mol-1·K-1 according to the Van't Hoff equation. The alterations of protein secondary structure in the presence of AE in aqueous solution were quantitatively calculated from CD spectra, and the content of α-helices obviously increased.     

Evidence for existence of a close association between CD14 and CXCR4 on monocytic cell line U937

The surface expression of HIV-1 coreceptors (CXCR4 and CCR5) on monocytes can be regulated by the ligand of CD14, and the susceptibility of the cells to HIV-1 is then changed. Our previous study found that monoclonal antibody against CD14 could dramatically inhibit CXCR4-mediated chemotaxis and cell-cell fusion. Based on these studies, we explored potential relationship between CD14 and CXCR4 on monocytic cell line U937. Flow cytometry analysis showed that anti-CXCR4 monoclonal antibody (mAb) 12G5 strongly inhibited binding of the FITC-conjugated anti-CD14 monoclonal antibodies (TUK4 and UCHM1) to U937, while another CXCR4-specific mAb B-R24 did not show any effect on this binding. On the other hand, two anti-CD14 monoclonal antibodies (TUK4 and UCH-M1) obviously inhibited the binding of the PE-conjugated anti-CXCR4 mAb 12G5 to U937 but did not inhibit the binding of mAb 12G5 to CXCR4-transfected 3T3 cells (3T3.T4.CXCR4), which indicates that the blocking of mAb 12G5 binding to CXCR4 by CD14-specific mAbs is not involved in the possibility that CD14-specific mAbs directly bind to CXCR4. These results suggested existence of a close association between CD14 and CXCR4 on monocytic cell line U937.     

CD40L对B淋巴细胞表面分子及分泌IL-12的影响

在体外使用CD40L作用于B淋巴细胞使之活化,通过测定B淋巴细胞表面分子及分泌细胞因子的变化,探讨B淋巴细胞作为抗原递呈细胞在抗肿瘤免疫中的优势,为B淋巴细胞特异性活化细胞毒T淋巴细胞(cytotoxic T lymphocyte,CTL)进而发挥其肿瘤细胞杀伤效应奠定基础.取7名健康成人外周静脉血,经淋巴细胞分离液分离人外周血单个核细胞(PBMC),分为对照组和实验组,实验组培养液中加入加入CD40L和IL-4,共培养21 d.观察B淋巴细胞生长状况,并在第7 d、第14 d和第21 d,用流式细胞仪(FCAS)测定其表面分子CD80、CD86和CD19,在第21 d,使用酶联免疫吸附法(ELISA)测定培养液中的IL-12水平.结果显示,在CD40L的作用下,B淋巴细胞呈克隆样增殖,并高表达表面分子CD80/CD86和CD19,和对照组相比,B淋巴细胞分泌IL-12水平升高(P＜0.05).上述实验结果说明通过CD40L的刺激,B淋巴细胞得到了活化,提示通过该途径活化的B淋巴细胞具备了作为抗原递呈细胞而发挥其抗肿瘤免疫治疗的能力.     

光盘刻录机性能研究

研究了光盘刻录机的性能,从光盘刻录机的使用入手,给出高性能刻录机应具备的性能参数.     

一种新型的局部地区网络结构——总线环网(Bus-Ring)

本文介绍了一种新的局部网结构—Bus-Ring和介质送取控制方式—TOKEN CAPTURE,新网的外形结构仍是环形的,但每个结点的接口处理机有一个三态门来旁路,这样,报文经过每个结点时没有延迟,报文在网络中被所有结点同时收到,基于这种网络结构,可以实现令牌截取控制方式,在网络中,令牌不是逐个结点地顺序转送,而是由要求发送信息的结点在环路上截取令牌,建立令牌时采用侦听和碰撞检测技术,如同CSMA/CD,这样,在网络轻载时,可以使用CSMA/CD方式,重载时,使用TOKEN CAPTURE方式,这种新型网络增加了送取方式的灵活性,减少了报文经过每个结点的延迟和令牌传递时间,计算机仿真结果表明Bus-Ring网络性能优于总线网。     

以太网CSMA/CD工作原理研究

针对目前关于CSMA／CD协议工作过程的不同解释，在CSMA／CD协议概念模型和二进制指数退避算法的基础上，分析了CSMA／CD协议的工作过程，指出了它们之间在解释上的差异，并给出了CSMA／CD协议的正确工作过程。     

随书光盘资源的集中与分层管理模式探讨

随书光盘资源是图书资料的有益补充,在学生学习过程中发挥着重要作用。通过对重庆邮电大学图书馆馆藏光盘资源及其管理模式和利用情况的分析,提出了随书光盘资源的集中管理与分层管理相结合的模式,对如何提高光盘资源的使用率进行了积极思考。     

一种三项CD共轭梯度法及其全局收敛性

在前人提出的三项PRP共轭梯度法的基础上,提出了一种三项CD共轭梯度法.与以往求解无约束优化问题的经典二项共轭梯度法不同,该算法的搜索方向是三项的,且在任何线性搜索下都具有充分下降性.在适当的条件下,证明了三项CD共轭梯度法在强Wolfe线性搜索下具有全局收敛性.     

Metformin targets liver tumor-initiating cells through the PI3K/Akt/mTOR survival pathway

Liver tumor-initiating cells （T-ICs） are thought to be inherently resistant to the cytotoxic effects of chemo- therapy, and can self-renewal and maintain tumor-initiating potential. Therefore, effective anticancer research strategies should target the unique properties of T-ICs. In this study, we found that metformin, a first-line drug of choice for the treatment of type 2 diabetes, inhibited liver T-ICs both in vivo and in vitro. Metformin inhibited the formation of hepato- spheres and epithelial-specific antigen-positive （ESA, CD133＋） cell colonies by hepatocellular carcinoma （HCC） cell lines. Metformin also downregulated the expression of several T-IC-related genes which are involved in the signal- ing pathways, governing the self-renewal, proliferation and differentiation of T-ICs. Furthermore, the targeting of liver T-ICs by metformin was PI-3-kinase-Akt-mTOR （PI3K/Akt/ mTOR）-pathway dependent. The PI3K/Akt/mTOR inhibitorLY294002 and rapamycin abolished the inhibitory effect of metformin on CD133＋ cells, and the PI3K/Akt/mTOR stimulator EGF promoted the inhibitory effect of mefformin on CD 133＋ cells. Metformin also dramatically decreased the tumor volume and number of CD133 expressing tumor cells in a xenograft mouse model. Mefformin exerted a synergistic effect with cisplatin to target both T-ICs and non-T-ICs, and resulted in the smallest tumor volume and lowest number of CD133 expressing tumor cells. This study indicates that the antidiabetic drug metformin could potentially be used in combination therapy with chemotherapeutic agents to improve the treatment of liver cancer.     

浅议随书光盘管理模式

分析了网络环境下图书馆光盘管理模式存在的不足,通过比较分析光盘的传统管理模式和网络管理的优点、缺点,建议采用两者结合的光盘管理模式。