Objective To introduce a simple and easy method for cell apoptosis analysis as an example with artemisinin to induce apoptosis of human U251 cells. Methods Human U251 cells,cultured in suspension and treated with artemisinin,were freeze-thawed. 30 ?L of 3 mmol/L PI was then added and mixed. After being placed under room temperature for 5 min,the cellular ploidy was analyzed by flow cytometry,and the ratio of cell apoptosis was calculated. Results The ratio of human U251 cell apoptosis induced by artemisinin at a dose of 1?10-4,1?10-5 and 1?10-6mol/L was 33.2%,24.0% and 8.0%,respectively. Conclusion The results showed that artemisinin significantly induced the apoptosis of human U251 cells in a dose-dependent manner. Using this method to analyze cell apoptosis can reduce the procedure of cell treatment and avoid many influential factors. Therefore,it can be regarded as a simple,accurate and rapid method for detecting cell apoptosis.

In discussing scientific and ethical issues,problems arising from the proposal to formulate ethical norms for scientists are useful ones of professional ethics framework.Is science a career? If the answer is yes,then should the professional ethics of science be autogenous or allogenous? This paper clarifies the very nature of "good" professional ethics in scientific world.It is feasible to consider science as a public product of imparting knowledge and explaining the diversity of natural world,but we can never ignore to give scientific response to basic philosophical questions such as human desires.

Objective To demonstrate the role of innate immunity reaction in rheumatoid arthritis and other autoimmune diseases by studying the expression of toll-like receptor 4(TLR4) by peripheral blood mononuclear cell(PBMC) in rats with adjuvant-induced arthritis(AIA) and analyzing the relationship between expression of TLR4 by PBMC and score of arthritis severity.Methods Both the proportion of CD14+TLR4+ cells in CD14+ cells and the mean intensity of fluorescence(MIF) of TLR4+ cells were analyzed by flow cytometry.Expression of TLR4 mRNA by PBMC was determined by Northern blot.CD14+TLR4+/CD14+ ratio,TLR4 MIF and expression of TLR4 mRNA by PBMC in the model group at 15 days after AIA were compared,respectively,with normal control group and model group at 25 days.The correlation between TLR4 MIF and score of arthritis severity was analyzed by Mann-Whitey U test.Results CD14+TLR4+/CD14+ ratio,TLR4 MIF and TLR4 mRNA expression in model group at 15 days after AIA were obviously increased compared with those in control and model groups at 25 days(P0.05).It indicated that TLR4 participated in the pathogenesis of rheumatoid arthritis.Conclusion TLR4 expressed by PBMC is closely associated with pathogenesis and pathophysiology of rheumatoid arthritis,which suggests that innate immunity response plays an important role in pathogenesis of RA and other autoimmune diseases.

Objective To study the therapeutic effect of Fumaderm in Freund' complete adjuvant-induced arthritis (AIA) in Spraque-Dawley rats. Methods Adjuvant-induced arthritis (AIA) was established by intradermal injection of 0.1 mL of Freund' complete adjuvant (CFA) in the palmar surface of the right hindpaw and Fumaderm was delivered by oral gavage for 28 days. After CFA injection, the edema of the hindpaw was determined every two days. On 28 days after CFA injection, the lymphocyte subsets of peripheral blood and the cytokines were determined by flow cytometry, meanwhile the histopathological examination of ankle-joints of the animals was performed. Results Fumaderm had a significant therapeutic effect on AIA. The hindpaw swelling was reduced significantly in a dose-dependent manner. The ratio of peripheral blood T lymphocytes was improved obviously. Multiparameter cytokine analysis from peripheral blood CD4+ T cells showed a decrease of proinflammatory cytokines and an increase of anti-inflammatory cytokines in Fumaderm treated animals. A strongly reduced inflammatory response in the joint synovium was observed. Conclusion Fumaderm has potential anti-inflammatory effects on AIA rats. Further investigation is needed to elucidate the molecular mechanism involved in the clinical effect observed in the AIA model.