In order to study the molecular immune-pathological mechanism of spontaneous abortion (SA), immunohistochemistry techniques were used to detect the FasL expression of first trimester trophoblast in the SA patients and normal controls. High precise color-image measure system for immuno-histochemistry (HPIS) was used to determine the quantity of FasL expression. The results showed that the scale and intensity of FasL expression on the trophoblasts in SA group were significantly lower than in the control group. It is indicated that abnormal expression of FasL on trophoblasts, which damages the immunological tolerance between mother and fetus, may be one of the important mechanisms of development of SA. To induce the expression of FasL or to regulate the immunological tolerance will be a new way to treat SA.

The anti-tumor effect and mechanism of the staphylococcal enterotoxin A (SEA) were studied. The mouse gastric tumor model was produced by subcutaneously inoculating gastric tumor cells (MGC80-3). The experimental group was treated with SEA, and the control group was treated with normal saline. The percentage of tumor generation and tumor mass was measured. The results showed that the percentage of the tumor generation in the SEA-treated mice was lower than in the control group, but there was no significant difference (P>0.05). However, the tumor mass in the experimental group was significantly lighter than in the control group, with the difference being very significant (P<0.001). There were more CD₄⁺ T cells and CD_s⁺ T cells in the tumor of the mice treated with SEA than those of the control group. SEA has an obvious anti-tumor effect on mice gastric tumor. The mechanism might be that SEA induces the effect of superantigen-dependent cell mediated cytotoxicity to the tumor cells.

To investigate the effects of Cyclin D1 antisense oligodeoxyneucleotides (ASODN) on the growth, cell cycle progression and expression of G₁ phase regulators in human gastric carcinoma cell lines SGC7901 and HS746T, phosphorothioate-modified Cyclin D1 ASODN were encapsulated by Lipofect AMINE2000 and transfected into gastric carcinoma cells. Dose-dependent inhibitory effects were induced by Cyclin D1 ASODN in two gastric carcinoma cell lines. Treatment of gastric carcinoma cells with 0.2 μmol/L CycliN D1 ASODN for 24 h could significantly inhibit their growthin vitro andin vivo, reduce expression of Cyclin D1mRNA to 26.3% (SGC7901) and 17.3% (HS746T) respectively. The percentage of cells in G₀/G₁ phase was increased as revealed by flow cytometry. Immunohistochemical staining showed that the expression of p21 was increased and the expression of Cyclin D1 and pRb was decreased in the two cell lines; the expression of p27 was increased in HS746T, but unchanged in SGC7901. Cyclin D1 ASODN could inhibit the growth and the expression of Cyclin D1 mRNA in gastric carcinoma cells, influence the cell cycle and expression of its regulators.