DNA甲基化研究进展

DNA甲基化已成为阐明正常和病理基因表达现象的重要机制,因而已成为当前分子生物学的研究热点之一。对DNA甲基化的转录抑制机制、在肿瘤发生中的作用、与细胞衰老和凋亡的关系、抑制剂以及分析方法等方面的研究新进展进行了综述。     

倾斜煤层开采对底板突水影响的数值模拟

为了研究倾斜煤层开采条件下的突水规律,在考虑原岩应力、地质构造、地下水、采动影响等因素基础上,从应力场和渗流场共同作用的角度出发,研究含底板岩体在内的采场岩体系统的变形与破坏。研究结果表明,随着工作面的推进,底板岩层的破坏深度和范围加速增加。研究结论将数值模拟结果与工程实际进行比较分析,为寻求安全、经济的开采方法提供了理论依据。     

Expression, purification of a synthetic fuse-protein-TSF from PF4 and TSP1 fragments and its effect on angiogenesis and tumor growth

Sequences encoding PF4 (58–70) and TSP1 (429–459) were linked to yield a single gene TSF which encodes the fuse-protein of TSF. The gene was cloned into a pGEX-2T expression vector to generate a protein GST-TSF, which was strongly expressed inE. coli. The purified GST-TSF was degraded with thrombin to generate the protein TSF. With the methods of MTT and wound repair assay, the effects of TSF on the proliferation and migration of EC were detected, respectively. The results showed that TSF significantly suppressed BAEC proliferation and migration in a dose-dependent manner. The fuse protein GST-TSF, and the peptides PF4 (58–70) and TSP1 (429–459) also inhibited BAEC proliferation and migration, respectively, but their inhibition rates were not as high as TSF. Using the CAM assay, it was shown that TSF, GST-TSF, PF4 (58–70) and TSP1 (429–459) inhibited angiogenesis in chick CAM potentially, the effect of TSF was the highest.In vivo, the growth of Lewis lung carcinoma was potently inhibited by TSF treatment, and the inhibition rate was 68.75% at a dose of 1.00 μmol/kg · d. These findings suggest that the design on TSF gene was successful, and TSF with its anti-angiogenic and anti-tumor activity, should be a useful source of the inhibitor.     

DNA甲基化在肿瘤形成中的作用（综述）

DNA甲基化改变是肿瘤细胞中常见的现象,DNA甲基化与肿瘤的发生有密切关系。从以下几方面对此做一综述。（1）简介哺乳动物细胞的DNA甲基化;（2）DNA甲基化与肿瘤基因突变;（3）肿瘤DNA甲基化的基因外作用,其中包括：原癌基因的低甲基化和抑癌基因的高甲基化。     

砷剂化合物作用机制的研究概况（综述）

砷剂对急性早幼粒细胞白血病有良好的疗效,研究发现砷剂的作用机制可能包括：（1）诱导细胞凋亡和部分分化;（2）调控细胞凋亡基因的表达;（3）使线粒体内膜跨膜电位(transmembrane potential,△ψm )下降;（4）阻抑细胞增殖。     

HSP70在肺癌组织中表达水平的研究

采用免疫组织化学ＳＡＢＣ法检测３９例肺部组织中ＨＳＰ７０的表达。结果显示：ＨＳＰ７０在高度分化的肺鳞癌和肺腺癌细胞中的阳性表达率与癌旁正常肺组织之间具有高度显著性差异（Ｐ〈０．０１）,ＨＳＰ７０的表达在高分化的肺鳞癌与肺腺癌之间则无显著性差异（Ｐ〉０．０５）,在低分化的肺鳞癌和肺腺癌组织中,ＨＳＰ７０呈阴性反应,ＨＳＰ７０在肺癌组织中表达水平的高低与肺癌细胞的分化程度密切相关,而与肺癌的组织学类型     

Construction and expression of retroviruses encoding dual drug resistance genes in human umbilical cord blood CD34+ cells

A series of retro viral vectors encoding humanmdr1 gene alone as wetl as in combination with either humanmgmt gene or human mutantSer ³¹-dhfr gene are engineered. The resultant retroviruses are used to transduce human umbilical cord blood CD34⁺ cetls. It has been shown that expression of dual drug resistance genes in transduced cetls confers a broad range of resistance to both kinds of corresponding drugs. These data suggest a rationale for the use of such double chemoresistance gene constructs in anin vivo model in which transduced hematopoietic cetls will acquire multiple protection against the cytotoxic side effects of combination chemotherapy and may have future application in chemoprotection of normal tissues, thus killing tumor cetls more effectivety.     

病毒与人类健康——2008年诺贝尔生理学或医学奖简介

2008年10月6日,诺贝尔生理学或医学奖授予了德国科学家哈拉尔德•楚尔•豪森、法国科学家弗朗索瓦丝•巴尔-西诺西和吕克•蒙塔尼,以表彰他们对揭示病毒感染在肿瘤、传染病等人类重大疾病中的致病机制所做出的突出贡献。本文将就病毒感染与人类健康的密切关系做一简要介绍。     

血管内皮生长因子的研究进展

血管内皮生长因子（Vascular Endothelial Growth Factor,VEGF)家族是一类多功能的细胞因子,在血管生成和淋巴管生成中具有直接和间接的调控作用,可保进内皮细胞增殖,促进血管生成以及增加血管的通透性,对于缺血性疾病,VEGF可促进侧枝循环,从而改善缺血;对于肿瘤相关抗VEGF的治疗,抗肿瘤血管治疗最终必将提高肿瘤的诊治水平。     

Surface molecules regulating rolling and adhesion to endothelium of neutrophil granulocytes and MDA-MB-468 breast carcinoma cells and their interaction

The extravasation of leukocytes and tumor cells is a multi-step process with the involvement of various adhesion molecules depending on the three steps rolling, adhesion, and diapedesis. We have developed an in vitro model, by which we investigated the rolling and adhesion of neutrophil granulocytes and MDA-MB-468 human breast carcinoma cells to lung endothelial cells under physiological flow-conditions. We found that norepinephrine had an inhibitory function on the fMLP-promoted adhesion of neutrophil granulocytes due to a down-regulation of β2-integrin. Furthermore, neutrophil granulocytes serve as linking cells for the interaction of the MDA-MB-468 cells with the endothelium, which are both β2-integrin negative, but express the β2-integrin ligand ICAM-1. In addition, we show here that N-cadherin is up-regulated on the endothelial cells and on neutrophil granulocytes in response to fMLP. This up-regulation resulted in a significant increase of adherent MDA-MB-468 cells, which are also N-cadherin positive. Received 3 September 2007; received after revision 17 October 2007; accepted 22 October 2007