过氧钒烟酸对糖尿病鼠苯丙氨酸羟化酶活性的影响

目的　探讨过氧钒烟酸（ Ｐ Ｏ Ｖ） 的降血糖作用的分子生物学机制。方法　选用 Ｓ Ｄ 大鼠用链脲佐菌素诱导产生糖尿病鼠动物模型，观察用 Ｐ Ｏ Ｖ 和美迪康（ Ｍｅｔ） 治疗后各组大鼠血、尿糖水平及血肝细胞质中苯丙氨酸羟化酶（ Ｐ Ａ Ｈ） 活性改变情况，并进行比较。结果　糖尿病鼠 Ｐ Ａ Ｈ 活性明显增高，用 Ｐ Ｏ Ｖ治疗４ 周后活性受到抑制，血糖水平明显下降，临床症状得以改善。结论　 Ｐ Ｏ Ｖ 的降糖作用优于美迪康，且未见明显毒副作用。     

改进实验考核方法对学生成绩的影响

目的:改进传统实验考核方法,建立平时考查和期末考核相结合的实验考核方法。方法:选择06级学生为实验组,05级学生为对照组进行实验考核。结果:实验组平均成绩呈正态分布,成绩分布更为合理;对照组平均成绩呈明显偏态分布,且实验组的实验成绩与理论成绩有相关性。     

真核表达载体Rc／LTR携带的报告基因可在Hela细胞中高效表达

利用基因重组技术构建了荧光酶报告基因ｌｕｃ和真表达载体Ｒｃ／ＬＴＲ的重组子Ｒｃ／ＬＴＲ－ｌｕｃ。将此重组子转染Ｈｅｌａ细胞后，ｌｕｃ基因在Ｈｅｌａ细胞中得到高效表达。蛋白激酶Ｃ激活剂ＴＰＡ可使ｌｕｃ基因的表达成增加。结果表明，ＨＩＶ－ＬＴＲ可用作真核细胞内外源基因表达的有效启动子。     

家族性高胆固醇血症患者低密度脂蛋白受体及其基因缺陷

LDLR 是一种细胞表面糖蛋白,因介导血浆 LDL 和β-VLDL 的摄取和细胞内降解而在维持血浆脂蛋白代谢平衡中起重要作用。组成 LDLR 蛋白的5个功能区与 LDLR 基因结构之间有密切的对应关系。FH 是 LDLR 基因突变所致的遗传性疾病,已发现的突变形式有缺失,错义突变,无义突变和插入4种。这些突变导致 LDLR 的4种不同类型的功能障碍。由基因突变引起的脂代谢紊乱,是 FH 患者易发动脉粥样硬化的原因。     

塞来昔布对人鼻咽癌CNE-2细胞生长抑制及放射增敏研究

Objective To investigate the growth inhibition and radiosensitization of Celecoxib in hu-man nasopharyngeal carcinoma cell line CNE-2. Methods CNE-2 growth inhibition by Celecoxib was eval-uated by MTT method. Apoptosis-related changes in morphology were observed by transmission electron mi-croscopy (TEM). Cell cycle distribution and apoptosis rate were measured by flowcytometry (FCM). The ex-pression of COX-2 protein was observed by SP method after the treatment of Celecoxib. Cells were randomly planted into four groups: irradiation control(Ci), drug group(Cd), irradiation group(R), and Celecoxib plus irradiation group(D+R). Single irradiation of 2,4,6,8,and 10 Gy were administered for colonogenic assay. Cell cycle distribution and apoptosis rate were analyzed at 6 Gy irradiation. Results The growth of CNE-2 cell was inhibited by celecoxib in a dose-and time-dependent manner, the IC50 was 80 μmol/L After the treatment, cell ratio of GO and G, phases was increased (47.03±2.76 vs 56.17±1.95, t=4.68, P= 0.010), whereas the ratio of S and G2/M phases was decreased (33.07±1.86 vs 24.87±1.76, t=5.54, P = 0.010; 19.30±0.53: 17.73±0.83, t=2.75, P=0.050), and the apoptosis rate was increased (1.57±0.47:10.47±0.31, t = 27.39, P = 0.000) in a dose-dependent manner. Apoptosis with nuclear chromatin condensation, fragmentation and cell shrinkage was found by TEM. SP method showed that Celeib decreased COX-2 expression (17.48±0.34 vs 12.82±0.51,t=13.20,P =0.00). The sensitivity ratio(D0) was 1.15. FCM showed that the percentage of cells in G2/M phase was significanty more in R and D+R groups than in Ci and Cd groups (68.00±1.65,54.27±5.74,17.60±0.80,14.86±1.23, t=47.70,P=0.000; t=11.63, P=0.000), and also significantly different between R group and D + R group (t=3.99, P= 0.020). The apoptosis rate was higher in R and D + R groups than Ci and Cd groups(4.83±0.97,9.50± 1.35,1.33±0.86 and 2.28±0.42,t=4.67,P=0.010;t=8.81, P=0.000), D + R group than R group(t =4.85,P=0.010). Conclusions Celecoxib can markedly inhibit the growth and induce apoptosis in CNE-2 cells,which may depend on COX-2 pathway. Celeeoxib potently enhances the radiosensitivity of CNE-2 cells,which may due to the repair inhibit of radiation-induced DNA damage, inhibit of cell proliferation,and enhancement of cell apoptosis after irradiation.     

多胺类似物四丁基丙二胺对人A549肺癌细胞的影响

目的:研究新多胺类似物四丁基丙二胺(tetrabutyl propanediamine,TBP)对人A549肺癌细胞增殖、细胞迁移能力和多胺代谢的影响及其机制.方法:MTT法用于分析细胞增殖；流式细胞术用于分析细胞周期；QT-RT-PCR技术用于分析多胺代谢酶的表达水平；高效液相色谱用于检测细胞内多胺含量.结果:TBP处理A549细胞后导致:(1)显著抑制人A549细胞增殖,其抑制效应呈浓度和时间的依赖性；(2)G1期和G2期细胞显著减少,但S期细胞显著性增加；(3)显著诱导多胺降解代谢限速酶SSAT的表达,但对其他酶影响较小；(4)细胞内多胺含量显著性下降.结论:上述研究结果提示TBP具有抑制人A549肺癌细胞增殖的药理活性,有作为肺癌治疗药物的潜在临床应用前景.其机制可能与干扰DNA复制、抑制细胞周期和降低细胞内多胺水平相关.     

急性黄疸型病毒性肝炎病人血清过氧化脂质含量及其与胆红素含量间的关系

脂质过氧化在某些疾病的发生和发展过程中的重要作用,日益受到临床工作者的重视。多种因素引起的肝损伤,如酒精性肝炎和血色病等,其发病过程均与脂质过氧化密切相关。本文研究通过测定急性黄疸型病毒性肝炎病人血清过氧化脂质(LPO)和胆红素水平,分析二者间的相关性,以了解LPO测定在诊断和分析该病病情中的意义。材料和方法一.检测对象急性黄疸型病毒性肝炎85例(男48例,女37例),病程在15天内,平均8.9天,年龄5～50岁;急性无黄