Objective:To investigate the role of alkylation repair homolog 5(ALKBH5)-mediated N6-methyladenosine(m6A)modifi-cation in endometrial decidualization.Methods:The mouse models of pregnancy and pseudopregnancy were established,and quantita-tive real-time PCR and Western blot were used to measure the expression pattern of ALKBH5 in the endometrium.The mouse and cell models of artificially induced decidualization were established,and quantitative real-time PCR,Western blot,and immunohistochemis-try were used to measure the expression levels of decidualization-related markers.The EpiQuik m6A RNA methylation quantification kit was used to measure the level of m6A.The mouse and cell models of artificially induced decidualization with interference of ALKBH5 expression were established,and quantitative real-time PCR,Western blot,and immunohistochemistry were used to measure the expression levels of decidualization-related markers,cell proliferation marker molecules,and apoptosis molecules.Flow cytometry was used to measure cell apoptosis rate.Results:In the mouse model of pregnancy,the expression level of ALKBH5 at the uterine em-bryo implantation site was significantly higher than that adjacent to the implantation site,and in the mouse and cell models of artifi-cially induced decidualization,compared with the control group,the induction group had a significant increase in the expression level of ALKBH5 and a significant reduction in the level of m6A.Inhibiting the expression of ALKBH5 led to an increase in the level of m6A,which in turn inhibited the proliferation of stromal cells,induced cell apoptosis,and ultimately impaired the normal process of en-dometrial decidualization.Conclusion:ALKBH5 deficiency leads to an increase in the level of m6A and decidualization injury in the en-dometrium,which lays a foundation for the research on m6A modifi-cation in decidualization.

Objective To investigate the effect of tamoxifen on pituitary tumor transforming gene ex-pression in C6 cell and tumor growth of glioma in vivo. Methods Animal models were established on 32 SD rats with C6 cells of glioma. The rats bearing with C6 glioma were divided into 4 groups randomly, which were treated without tamoxifen or with different doses of tamoxifen(0. 02 mg · kg-1 · d-1, 0. 2 mg · kg-1 · d-1, 2mg · kg-1 · d-1) once a day for 20 days. The dimension of tumors were measured, the tumor inhibition rates were caculated, and living state of the rats were observed. The expression of PTTG mRNA was detected by RTPCR. Results All kinds of doses of tamoxifen could inhibit the tumors growth in rats with C6 glioma, and the tumor volume were reduced by 47.6%, 35.5% and 21.2% in the high-, middle-and low-dose groups respec-tively, there were significantly differences among the 4 groups ( P < 0. 05 ). Low-, middle- and high- dose of tamoxifen all could inhibit the expression of PTTG mRNA, and there were significantly differences among the 4 groups in PTTG mRNA expression ( P < 0. 05 ). Conclusion Tamoxifen can inhibit PTTG expression and the growth of glioma cell line C6 in vivo significantly in dose-dependent manner, which provides a theory basis for clicinal use of tamoxifen in patients with gliomas.

BACKGROUND: A stable and exact animal model is the necessary tool and basis for studying hemorrhagic cerebrovascular diseases.OBJECTIVE: To establish and evaluate the intracerebral capsular hemorrhage models in rats.DESIGN: A randomized and controlled animal experiment.SETTING: Second Hospital Affiliated to Xuzhou Medical College; First Hospital Affiliated to Nanjing Medical University.MATERIALS: This experiment was carried out in the animal experimental center of Nanjing Medical University during May to November 2002.Totally 35 SD rats were randomized into two groups: experimental group (n=30) and sham-operation group (n=5).METHODS: ① Autoblood was injected into the intracerebral capsule of rats to create intracerebral capsule hemorrhage models with stereotaxy in the experiment group. ②Scoring was conducted according to 5-point neurological scoring criteria from ZeaLonga, somatic sensation and motor function of rats were observed. ③Somatosensory evoked potential(SEP) of rats was detected pre- and post-operation under anesthetic state. ④ After determination of SEP, the rats were sacrificed under anesthetic state. Brains were taken out to made slices, then sections were stained with haematoxylin and eosin. Changes in haematoma and histomorphology were observed at the largest focus under optical microscope.MAIN OUTCOME MEASURES: ①Nerve function scoring; ②Latent period of various waves of SEP; ③ Observation of brain tissue morphology.RESULTS: Totally 35 rats entered the stage of result analysis. ①Appearance of obvious paralysis of the rats suggested the modeling was successful. The successful rate of this experiment was 93.3%(28/30). Significant difference existed in neurological scoring between experimental group [(2.74±0.46)points] and sham-operation group (0 point)(P＜0.05). ②SEP showed that the latent periods of various waves of experimental group after operation were significantly delayed than those before operation and those of sham-operation group [P1: (15.72±0.78) ms, (10.69±0.52) ms, (10.73±0.48) ms;Nl: (17.95±1.27) ms,(13.21±1.31) ms, (13.34±1.27) ms;N2:(21.16±1.62) ms, (15.42±1.46) ms,(15.58±1.44) ms;N3:(24.86±1.58) ms, (18.72±1.76) ms, (18.99±1.67) ms,P＜0.05]. ③In the shamoperation group, a few red blood cells were scattered in the peripheral area of needle channel were found, but hemorrhagic focus was not; In the experimental group, irregular or oval blood clots presented in the left internal capsule area. In about a low-fold visual field, brain tissue in the surrounding of hemorrhagic focus was loosened and swelled, and pathological changes were obviously severer than those in the sham-operation group.CONCLUSION: Intracerebral capsular hemorrhage induced by injection of autoblood with stereotaxy is more close to clinical situation, and it is easy to operate and has good reproducibility.

Objective To study the sensitivity of radiotherapy on the cells in midsection and edge of glioma. Methods The glioma models were established in SD rats and exposed to X radiation. Proliferating cell nuclear antigen (PCNA), apoptosis rate and cell phase of the cells in the midsection and edge of glioma were detected by immunohistochemical assay, terminal transferase dUTP nick ending labeling (TUNEL) and flow cytometry. Results Immunohistochemical assay showed that PCNA-LI of the edge cells was significantly lower than that of midsection cells ((P