MDM2 was transfected to acute lymphoblastic leukemia (ALL) line EU-4 cell which lacks P53 expression and expresses very low levels of MDM2. The results showed that MDM2 upregulated P65 expression in mRNA level and protein level. The effect of adriamycin (ADM) on MDM2-transfected EU-4 cell was detected by MTT assay. It was found that MDM2 transfection could increase drug resistance of EU-4 cells to ADM as compared with parent cells. Since the expression of E-selectin is P65 dependent, E-selectin promoter-CAT construct and P65 and MDM2 expression plasmids were co-transfected to EU-4 cells, revealing that MDM2 increased P65-mediated transactivation of E-selectin promoter. In the absence of P65, MDM2 had no effect on the transactivation of E-selectin. Moreover, MDM2 antisense couldn’t change the transactivation of E-selectin. It was concluded that MDM2 could up-regulate transcriptionally P65 expression; MDM2 increased drug resistance of leukemia cells to ADM; MDM2 elevated NF-kappaB activity in a P53-independent manner.

To study the expression of mTR gene in the testis of SD rats with varied ages and its significance,in situ hybridization (ISH) techniques were applied to detect the expression of telomerase gene mTR mRNA in the testis of SD rats. The expression of mTR was found in testes of differentage male SD rats. There was a positive correlation between the expression of mTR and the location of germ cells (spermatogonia, spermatocyte, spermatid). In Setoli cells, leydig cell and spermatozoa, no telomerase mTR was detectable. Type A spermatogonia expressed the highest level of telomerase mTR mRNA. It was suggested that the expression of mTR gene in the testis of SD rats is of lifetime and coincides with the telomerase activity.

To investigate the effects of estrogen (E₂) on telomerase activity and its mechanism in human breast cancer cells, estrogen receptor positive MCF-7 cells were treated with different concentrations of E₂. Telomerase activity was measured by using TRAP-ELISA method, the cell cycle phases analyzed by using flow cytometry, and the expression of Cyclin D₁ detected by using immunohistochemistry method. The results showed that telomerase activity levels were increased in MCF-7 cells treated with 10⁻⁸ mol/L E₂ during the observed period (P<0.05), and E₂ increased telomerase activity levels in a dose-dependent manner (10⁻¹⁰-10⁻⁸ mol/L); Simultaneously, the cell cycle phases of MCF-7 cells treated with 10⁻⁸ mol/L E₂ were changed significantly: G₀/G₁ phase decreased from 60.52% to 50.93%, S phase increased from 29.03% to 30.83%; However, the expression of Cyclin D₁ was decreased. It was concluded that estrogen can upregulate telomerase activity of MCF-7 cells, and the effect can be blocked by antiestrogen tamoxifen. Its mechanism may be closely associated with modulation of cell cycle phases.

To study the characteristics of acute rejection after limb allotransplantation, 29 male Sprague-Dawley rats were randomly divided into 2 groups, with 15 rats in control group and 14 rats in experimental group. Each rat in control group underwent limb replantation. Each rat in experimental group received limb transplantation from Wistar rat. No immnosuppressive drugs were used after operation. The circulation of the transplanted limb, time and signs of rejection, histopathological changes in the tissues of the limb graft when rejected and survival time of limb grafts were evaluated. In the control group, no signs of rejection were observed, the circulation of each replanted limb was normal, it could survive for a longer time. The experimental group showed clinical signs of rejection (sub dermal edema and erythema) after a mean time of 3.36±1.15 days, and the mean survival time of the allografts was only 7±0.78 days. Histopathological examination showed most violent rejection reaction in skin. It is concluded that with Wistar-to-SD limb transplantation without use of immunosuppression, rejection of the grafts would occur after a mean time of 3, 36±1, 15 days; the earliest signs of rejection were edema and erythema of the skin, being the most representative component of limb graft rejection.