Reactive oxygen species play an important role in the mediation of cell killing. But the mechanistic links between reactive oxygen species (ROS) and cell death remains unclear. There was a speculation that ROS, especially hydroxyl radicals can induce necrosis but not apoptosis in cells treated with copper-1,10-phenanthroline, IICu(OP)2. In this paper, liver carcinoma cell line (Bel-7402) was treated with IICu(OP)2 and its effect was examined by several means. Cells were found to undergo changes characteristic of apoptosis. Hoechst staining showed apoptotic body appeared in the cells induced by IICu(OP)2. When DNA extracted from the cells treated with IICu(OP)2 was analyzed by agarose gel electrophoresis it generated 'ladder' pattern of discontinuousDNAfragments. Sub-G1 peakwas detected in treated cells. Furthermore, two different flowcytometric methods were used, each allowing us to relate the apoptotic cells to the position the cell-cycle position. Apoptosis induced by IICu(OP)2 was limited to G1-phase cells. Using cyclin analysis, the expression of cyclin E in G1 was blocked. Thus, it was concluded that IICu(OP)2 can induceG1-phase specific apoptosis in Bel-7402.

Hyperthermia is a useful adjunct in cancer therapy, as it can increase the effectiveness and decrease the toxicity of currently available cancer treatments such as chemotherapy and radiation. In this study we determined the power-time curves of U-937 cell line treated by the combination of hyperthermia and Carmofur by using an LKB 2277 Bioactivity Monitor. The maximal thermal power and the heat production were used to evaluate the antitumor effect. Our results show that the combined treatment of hyperthermia and Carmofur had a synergistic antitumor effect, which is consistent with the apoptosis ratio obtained by TUNEL assay. The results also indicate that the metabolic activity of apoptotic cells is lower than that of normal cells. Thus microcalorimetry is a powerful tool in fields of hyperthermia.

Four DTPA and DOTA derivative ligands containing sulfonamide groups and their gadolinium complexes were prepared and characterized. Relaxivity studies showed that these gadolinium complexes possessed higher relaxation effectiveness than those of the corresponding ionic gadolinium complex Gd-DTPA and Gd-DOTA, respectively. In vitro cytotoxicity assay demonstrated that these gadolinium complexes have low cytotoxicity to the human liver cells (L-02). Magnetic resonance imaging (MRI) and experimental data of biodistribution in mice indicated that these gadolinium complexes containing sulfonamide groups could be used as the potential MRI contrast agents for Hepatoma (H22) and Ehrlich ascites carcinoma (EAC) in mice and specific organs such as the liver and could be mostly excreted by the kidneys.

猪瘟病毒在离体细胞培养条件下不引起宿主细胞病变，病毒与宿主细胞之间相互作用的研究一直没有合适的模型以猪瘟病毒中国标准强毒石门株为材料，通过基因工程的手段，在构建全基因组感染性克隆的基础上，对全基因组进行部分缺失，获得了7.5kh的亚基因组.以携带野生型猪瘟病毒的PK-15细胞为宿主，用亚基因组进行转染，获得到了能够诱导PK-15细胞产生CPE的亚基因组病毒，检测显示产生CPE的细胞培养物中野生型基因组和亚基因组共同存在猪瘟病毒致细胞病变模型的构建，为进一步研究其致病的分子机制开辟了新的方向。

Severe acute respiratory syndrome (SARS) coronavirus (SARS-CoV) is a newly identified member of Family Coronaviridae. Coronavirus envelope spike protein S is a class I viral fusion protein which is characterized by the existence of two heptad repeat regions (HR1 and HR2) (forming a complex called fusion core). Here we report that by using in vitro bio-engineering techniques, SARS-CoV HR1 and HR2 bind to each other and form a typical 6-helix bundle. The HR2, either as a synthetic peptide or as a GSTfusion polypeptide, is a potent inhibitor of virus entry. The results do show that SARS-CoV follows the general fusion mechanism of class I viruses and this lays the ground for identification of virus fusion/entry inhibitors for this devastating emerging virus.