Background/Aims: Androgen receptor (AR), estrogen receptor α (ERα) signaling and their interaction with epidermal growth factor receptor (EGFR) signaling pathway is a potential therapeutic target in non-small cell lung cancer (NSCLC). To explore the cross communication between AR, ERα and EGFR signaling pathway, we used RNA silencing technology and sex hormones intervention in NSCLC cell line. Methods: Model system was the well-characterized A549 adenocarcinoma NSCLC cells which can express AR and ERs well. We used different concentrations of testosterone (T), estradiol (E2) intervention cells and small interfering RNA (siRNA) specifically targeting AR, ERα in A549 cells, then examined the expression of AR, ERα and EGFR/PI3K/AKT axis, followed by detection of cells proliferation, apoptosis, migration and invasion. Results: After knocked down the expression of AR, ERα, the EGFR/PI3K/AKT axis was inhibited, and the proliferation decreased, apoptosis increased, migration and invasion decreased in A549 cells. 50µM T and 50µM E2 intervention inhibited AR, ERα and EGFR/PI3K/AKT axis expression, and the proliferation decreased, apoptosis increased, migration and invasion decreased in A549 cells. 10µM T, 10µM E2 and 100µM T, 100µM E2 intervention promoted the expression of AR, ERα and EGFR/PI3K/AKT axis, which enhanced the activity and migration invasiveness of A549 cells. Conclusions: These data provide a rationale for further investigation of the antitumor activity of clinical sex hormones therapy and the development of anticancer drugs targeting sex hormone receptors in the clinic. Future .

目的:研究扶正消癌合剂对肺腺癌A549细胞增殖的影响及PI3K/Akt信号通路的作用机制.方法:制备大鼠含药血清,采用CCK8法对A549进行观察,了解其增殖抑制情况,了解其对细胞周期的影响,以及如何造成细胞凋亡.利用Western-Blot法检测含药血清对PI3K,Akt及P-Akt蛋白表达产生的作用.结果:扶正消癌合剂能抑制A549细胞增殖,呈现时间-浓度依赖关系,与顺铂呈正相关,48 h、72 h、96 h的抑制率分别是28.26％、39.62％和37.89％;扶正消癌合剂可以促进A549细胞发生变化,出现凋亡的情况,并且随着浓度的增高而有所增加,镜下观察G2/M期细胞明显增多,所占的比例也相应增加,相对于另一组来说差异有统计学意义(P＜0.05).其在诱导过程中,随着细胞逐渐凋亡,下调PI3K、P-Akt蛋白表达.结论:扶正消癌合剂可以抑制人肺腺癌细胞A549增殖,可能与抑制PI3K/Akt信号通路中PI3K、P-Akt蛋白表达有关.

目的 探讨小干扰RNA(siRNA)沉默雌激素受体β(ER)表达和雌二醇(E2)干预对非小细胞肺癌细胞系A549的作用及其可能分子机制.方法 siRNA转染实验分为空白对照组(Control组)、siRNA-NC转染组(NC组)、Lipofectamine 2000转染组(Lipo组)和siRNA-ERβ转染组(siRNA组);E2干预实验分为0μmol/L组、10 μmol/L组、50 μmol/L组和100 μmol/L组.采用Western blot和RT-PCR分别检测A549细胞中ERβ、表皮生长因子受体(EGFR)、磷脂酰肌醇3-激酶(PI3K)、Akt的蛋白和mRNA表达,CCK-8法和划痕实验分别检测A549细胞活性和迁移能力的变化.结果 与Control组、NC组和Lipo组相比,siRNA组ERβ、EGFR、PI3K、Akt蛋白和mRNA表达下调,细胞活性和迁移能力降低(P＜0.05).与0 μmol/L组相比,10 μmol/L组ERβ、EGFR、PI3K、Akt蛋白和mRNA表达上调,细胞活性和迁移能力增加(P＜0.05);而50μmol/L组ERβ、EGFR、PI3K、Akt蛋白和mRNA表达下调,细胞活性和迁移能力降低(P＜0.05);100 μmol/L组各指标均无明显变化(P＞0.05).结论 E2及其受体ERβ可能通过EGFR/PI3K/Akt信号通路影响A549细胞的活性及迁移能力,从而参与非小细胞肺癌的发生和发展过程.

Background/Aims: Retinoic acid receptor beta (RAR beta) is a retinoic acid receptor gene that has been shown to play key roles during multiple cancer processes, including cell proliferation, apoptosis, migration and invasion. Numerous studies have found that methylation of the RAR beta promoter contributed to the occurrence and development of malignant tumors. However, the connection between RAR beta promoter methylation and prostate cancer (PCa) remains unknown. This meta-analysis evaluated the clinical significance of RAR beta promoter methylation in PCa. Materials and Methods: We searched all published records relevant to RAR beta and PCa in a series of databases, including PubMed, Embase, Cochrane Library, ISI Web of Science and CNKI. The rates of RAR beta promoter methylation in the PCa and control groups (including benign prostatic hyperplasia and normal prostate tissues) were summarized. In addition, we evaluated the source region of available samples and the methods used to detect methylation. To compare the incidence and variation in RAR beta promoter methylation in PCa and non-PCa tissues, the odds ratio (OR) and 95% confidence interval (CI) were calculated accordingly. All the data were analyzed with the statistical software STATA 12.0. Results: Based on the inclusion and exclusion criteria, 15 articles assessing 1,339 samples were further analyzed. These data showed that the RAR beta promoter methylation rates in PCa tissues were significantly higher than the rates in the non-PCa group (OR=21.65, 95% CI: 9.27-50.57). Subgroup analysis according to the source region of samples showed that heterogeneity in Asia was small (I2=0.0%, P=0.430). Additional subgroup analysis based on the method used to detect RAR beta promoter methylation showed that the heterogeneity detected by MSP (methylation-specific PCR) was relatively small (I2=11.3%, P=0.343). Conclusion: Although studies reported different rates for RAR beta promoter methylation in PCa tissues, the total analysis demonstrated that RAR beta promoter methylation may be correlated with PCa carcinogenesis and that the RAR beta gene is particularly susceptible. Additional studies with sufficient data are essential to further evaluate the clinical features and prognostic utility of RAR beta promoter methylation in PCa.

BACKGROUND/AIMS:BushenShugan Formula (BSF) is a traditional Chinese medicine that has therapeutic effects on middle- and late-stage lung adenocarcinoma in clinical application. It was reported that Bushen Chinese medicine suppressed the onset of pre-metastatic niches in a murine model of spontaneous lung metastasis. However, the mechanisms of BSF on human lung adenocarcinoma remain unknown.METHODS:Cell proliferation was determined by CCK8 and colony formation. Cell apoptosis and cell cycle were detected by flow cytometry. Cancer stem cells properties were examined by spheroid body formation. The migration and invasion abilities were analyzed by wound healing assay and transwell invasion assay. The mRNA expressions were determined by qRT-PCR. Western blotting analysis showed the protein levels.RESULTS:BSF was shown to inhibit the proliferation of A549 cells in time- and concentration-dependent manners. Colony formation assays also indicated the antiproliferative effect of BSF against A549 cells. Cellular mechanistic studies demonstrated that BSF arrested the cell cycle in G2/M phase and induced apoptosis. Importantly, BSF could inhibit the epithelial-mesenchymal transition(EMT) of A549 cells through PI3K/AKT/NF-κB pathway.CONCLUSIONS:BSF effectively inhibited tumour growth, suggesting that it is a promising anticancer treatment for further clinical development.

BACKGROUND/AIMS:In contrast to men, women have experienced a rapid increase in lung cancer mortality. Numerous studies have found that the sex differences in lung cancer are due to reproductive hormones. Experiments in female mice with and without ovariectomy were performed to explore the possible mechanism by which sex hormones (and their receptors) influence lung cancer.METHODS:Twenty-four female C57BL/6 mice aged 56-62 days were randomly divided into the ovariectomized group and the control group. In the ovariectomized group, the bilateral ovaries were removed via the dorsal approach, while the control group underwent a sham operation with bilateral ovarian fat resection at the same sites. After 3 weeks of recovery, Lewis lung cancer cells were transplanted into these mice by subcutaneous inoculation of a tumour cell suspension to establish the ovariectomized lung cancer model. Beginning on the 6th day after subcutaneous inoculation, mouse weight and transplanted tumour volume were measured every 3 days. After 3 weeks, all the mice were killed by cervical dislocation, and we measured the tumour weight. Mouse serum and tumour tissues were removed. Then, the serum levels of E2 (oestradiol) and T (testosterone) were detected by ELISA; the protein expression levels of AR (androgen receptor), ERα (oestrogen receptor α) and ERβ (oestrogen receptor β) were detected by Western Blot and IHC (immunohistochemistry); and the mRNA expression levels of AR, ERα and ERβ were detected by qRT-PCR (quantitative real-time polymerase chain reaction) in the ovariectomized and control groups.RESULTS:Compared with the control group, both mouse weight and transplanted tumour volume increased rapidly in the ovariectomized group, and the transplanted tumour weight was significantly heavier in the ovariectomized group (1.83±0.40 and 3.13±0.43, P<0.05). E2 and T serum levels decreased exponentially in the ovariectomized group, while the E2/T ratio increased compared with the control group (E2: 55.88±11.45 and 78.21±9.37; T: 0.82±0.14 and 1.46±0.16; ratio: 69.62±14.43±29.81 and 52.22±5.42; all P<0.05). The Western blot and IHC results indicated that AR, ERα and ERβ protein expression levels were obviously higher in transplanted tumour and lung tissues from the ovariectomized group, with particular increases in ERβ in transplanted tumour tissue and in ERα in lung tissue. The PCR results also showed markedly higher mRNA expression levels of AR, ERα and ERβ in the ovariectomized group, and in particular, ERβ in transplanted tumour tissue and ERα in lung tissue were significantly increased in the ovariectomized group.CONCLUSION:Ovariectomy decreased E2 and T serum levels and increased the E2/T ratio in mice, and this imbalance in the internal environment promoted the growth of transplanted tumours. Sex hormone disorder not only promoted transplanted tumour growth but also significantly reduced the protein and mRNA expression levels of sex hormone receptors. The metabolism of E2 and T may affect the growth, proliferation and metabolism of lung cancer cells, and the mechanism by which sex hormones and their receptors influence lung cancer is worthy of further research.

Objective:To investigate the difference of tumor growth,the expression levels of sex hormones and their receptors in male castrated mice and normal mice transplanted with Lewis lung cancer,and to explore the possible mechanism of sex hormones in the occurrence of lung cancer.Methods:The male C57BL/6 mice aged 8-9 weeks were randomly divided into the castrated group (n =12) and control group (n =12).The castrated group underwent bilateral orchiectomy via the abdominal approach,while the control group underwent a sham operation of bilateral testicular fat removal at the same sites.After 2 weeks of restorative feeding,these mice were transplanted with Lewis lung cancer tissues by subcutaneous inoculation to establish the kidney deficiency and lung cancer xenograft model.The tumor growth in each mouse was observed,and the tumor size was measured every 5 days.After 3 weeks,all mice were weighed,and their serum was taken.Then the mice were sacrificed to remove the tumor and lung tissues,and the weights of tumor and lung tissues were measured,respectively.The serum levels of estrodiol (E2) and testosterone (T) were detected by ELISA method.The expression levels of androgen receptor (AR) and estrogen receptor α/β (ERα/β) were detected by immunohistochemistry.Resulu:Compared with the control group,the body weight of mice in the castrated group lost more after operation (P ＜ 0.05),while the volume of tumor increased faster (P ＜ 0.05),the weights of tumor and lung tissues increased (both P ＜ 0.05),the number of lung metastatic nodules also increased significantly (P ＜ 0.05),and the serum levels of E2 and T decreased greatly (both P ＜ 0.001).In the lung tissues,the expression levels of AR,ERα and ERβ were all high in the two groups,and the high-expression rates of AR,ERα and ERβ in the castrated group were especially higher than those in the control group (all P ＜ 0.05).In the tumor tissues,the high-expression rate of ERβ in the castrated group was higher than that in the control group (P ＜ 0.05),but the expression levels of AR and ERα in the two groups were not high.Conclusion:The castration may cause the disorder of sex hormone in mice,and abnormal up-regulation of the expression of relative sex hormone receptors,which can make the mice lose weight,promote the growth of transplanted tumor,increase the number of lung metastasis nodules.These suggest that the imbalance of sex hormones and relative receptors may promote the formation and development of lung cancer.

目的 探讨消癌平注射液对肝癌患者血清中肿瘤标志物水平的影响.方法 选取肝癌患者204例,并随机分为两组,对照组87例、治疗组117例.对照组给予常规支持治疗,治疗组在对照组的用药基础上给予消癌平注射液治疗,每日1次,静脉滴注.干预治疗4周后,评价所有患者临床疗效、不良反应发生情况及治疗前后血清肿瘤标志物(AFP、CA199、CEA、AFU、CA125)水平的变化.结果 对照组和治疗组患者总有效率分别为44.8%、79.5%,组间差异具有统计学意义(P<0.05).两组患者治疗后血清AFP、CA199、CEA、AFU、CA125水平均较治疗前显著降低,且除CEA外,治疗组均显著低于对照组(P<0.05).治疗组患者白细胞减少、总胆红素升高、血清丙氨酸氨基转移酶升高的发生率均显著低于对照组(P<0.05).结论 消癌平注射液能降低肝癌患者血清标志物含量,抑制肿瘤细胞的恶性增殖、迁移,临床疗效和安全性均较高.

目的:观察补肾疏肝方对Lewis肺癌生长和转移的抑制作用并探讨其可能存在的机制.方法:选取模型复制成功的C57BL/6小鼠40只,随机分为模型组、顺铂组、中药组、综合组.模型组给予生理盐水灌胃0.4mL.d-1;顺铂组在第1天、第3天、第5天给予顺铂腹腔注射0.5 mL(含顺铂0.1 mg);中药组给予中药灌胃0.4 mL·d-1(含生药0.7g);综合组给予每日中药灌胃(同中药组)同时腹腔注射顺铂(同顺铂组),共干预21 d.第22天处死,剥取肿瘤称质量,计算抑瘤率;计算自发性肺转移灶数,计算肺转移抑制率;用免疫组织化学的方法检测瘤组织微血管密度(microvessel density,MVD)、血管内皮生长因子(vascular endothelial growth factor,VEGF)及基质金属蛋白酶-9(matrix m etalloproteinase-9,MMP-9)的表达.结果:与模型组相比,各用药组均能显著抑制肿瘤生长,差异有统计学意义(P＜0.01);与中药组比较,综合组平均瘤质量显著降低(P＜0.01).与模型组相比,各用药组均能显著抑制肿瘤的自发性肺转移(P＜0.05);与顺铂组和中药组比较,综合组自发性肺转移灶数显著降低(P＜0.05).与模型组相比,各用药组MVD、VEGF均显著降低(P＜0.05);与顺铂组相比,综合组MVD、VEGF降低明显(P＜0.05).与模型组相比,各用药组MMP-9表达显著降低(P＜0.01);与顺铂组和中药组相比,综合组MMP-9表达下降有统计学意义(P＜0.05).结论:补肾疏肝方可显著抑制Lewis肺癌生长和自发性肺转移,与顺铂联合有协同作用,其抑制肿瘤生长和转移的机制之一可能为下调VEGF和MMP-9的表达.

目的 探讨血清神经元特异性烯醇化酶(neuron specific enolase,NSE)、糖类抗原(carbohydrate antigen,CA) 125、癌胚抗原(carcinoembryonic antigen,CEA)、非小细胞肺癌抗原(cytokeratin 19 fragment,CYFRA21-1)联合检测对小细胞肺癌(small cell lung cancer,SCLC)的诊断价值.方法 SCLC患者51例(SCLC组)和同期体检健康者25例(对照组),采用电化学发光法检测2组血清NSE、CA125、CEA、CYFRA21-1、CA19-9、CA72-4水平,应用ROC曲线进行分析和评价.结果 SCLC组NSE[(60.22±19.62) μg/L]、CA125[(49.79±9.78) u/mL]、CEA[(6.46±1.02)μg/L]、CYFRA21-1[(3.95±0.85)μg/L]高于对照组[(13.47±4.41)μg/L、(11.49±3.32)u/mL、(1.93±0.75)μg/L、(2.14±0.64)μg/L],差异有统计学意义(P＜0.01),SCLC组CA19-9[(15.28±4.39) u/mL] 、CA72-4[(2.89±0.36) u/mL]与对照组[(8.42±1.03)u/mL、(1.82±0.41) u/mL]比较差异无统计学意义(P＞0.05);血清NSE、CA125、CEA、CYFRA21-1在SCLC组的AUC分别为0.905、0.853、0.778、0.705;ROC曲线分析显示NSE、CA125、CEA、CYFRA21-1的临床诊断临界点分别为23.23 μg/L、19.71 u/mL、2.64 μg/L、3.24 μg/L,单项检测时,NSE、CA125、CEA、CYFRA21-1的灵敏性分别为74.51％ 、64.71％ 、64.71％ 、50.98％,特异性分别为100.00％、96.00％、88.00％、92.00％,4项指标联合检测时灵敏性为94.12％,特异性为84.00％.结论 血清NSE是诊断SCLC的一个较理想指标;检测血清NSE、CA 125、CEA、CYFRA21-1水平对诊断SCLC有重要意义,4项联合检测灵敏度较单项检测升高,但特异性下降.

Objective To explore clinical effect of the therapeutics of Cytokine - induced Killer( CIK)cell in combination with radiation and chemotherapy on limited stage small cell lung cancer(SCLC). Methods From January 2007 to February 2010,in the First Affiliated Hospital of Zhengzhou University,60 SCLC patients were divided randomly into observation group and control group,30 in each. Control group were given concurrent chemotherapy,observation group were given the same chemotherapy,followed by CIK immunotherapy. The short - term therapy,improvement of life of quality(LOQ),1 - year,2- year survival probabilities and adverse reactions were evaluated. Results The numbers of CR,PR,SD,and PD were 0,15, 1,and 14 in control group,while the numbers of CR,PR,SD,and PD were 2,19,3,6 in observation group. The curative effects were different between 2 groups(u = 2. 058,P < 0. 05). The disease control rate was 80. 0% (24 / 30)in observation group,higher than in control group〔53. 3%(16 / 30),χ2 = 4. 800,P = 0. 028〕. The LOQ improvement were different( u= - 4. 138,P < 0. 01). The incidence of WBC reduction was 50. 0%(15 / 30) in observation group,lower than in control group〔80. 0% (24 / 30),χ2 = 5. 934,P < 0. 05〕. The 1 - year survival probability was 76. 7%(23 / 30)in control group, 83. 3%(25 / 30)in observation group,and 2 - year survival probability 73. 9%(17 / 23),88. 0%(22 / 25),respectively,the difference was not significant(P > 0. 05). Conclusion Biological immune therapy combined with radiation and chemotherapy can improve the control rates of limited SCLC patients,improve their QOL,reduce incidence of part adverse reactions.

目的 探讨非小细胞肺癌(NSCLC)组织中雌激素受体α(ERα)的表达与表皮生长因子受体(EGFR)突变之间的关系.方法 应用免疫组织化学法及实时荧光定量聚合酶链反应法检测286例NSCLC中ERα的表达及EGFR突变情况,并分析其与临床特性的关系.结果 ERα表达阳性率为36.0％ (103/286),在女性患者中的表达要显著高于男性患者(P=0.004),肿瘤最大直径小于或等于3 cm的患者显著高于肿瘤直径大于3 cm的患者(P＜0.01).EGFR基因突变62例(21.7％),在女性、腺癌、肿瘤直径较小的患者显著增多,在ERα表达阳性患者中显著高于ERα阴性者(P=0.001).结论 NSCLC中ERα的阳性表达与EGFR基因突变相关,可能与EGFR信号通路的交叉调控有关.

目的:探讨补肾疏肝方对人肺癌A549细胞及其相关干性因子的影响.方法:SD雄性大鼠随机分为6组,每组10只,分别为补肾疏肝方低、高剂量组(15,30 g·kg-1),顺铂组(8 g·kg-1),低剂量联合顺铂组(联合低剂量组),高剂量联合顺铂组(联合高剂量组),正常组,顺铂组ip给予相应药物,补肾疏肝方ig给予相应药物,正常组给予等体积的生理盐水,制备大鼠含药血清;分别配制10％含补肾疏肝方低、高剂量、顺铂、低剂量联合顺铂、高剂量联合顺铂,分别与肺癌A549细胞共同培养,CCK8法检测补肾疏肝方含药血清对A549增殖的影响;流式细胞术检测含药血清对A549细胞周期的影响;Annexin V/PI双染流式细胞术观察含药血清对A549细胞凋亡的影响;荧光定量PCR检测含药血清对相关mRNA表达的影响;流式细胞术检测含药血清对CD133蛋白表达的影响.结果:补肾疏肝方以时间、剂量依赖方式抑制A549细胞增殖,与顺铂联合有协同增效作用,24,48,72 h高剂量联合顺铂组的抑制率分别为45.39％,54.76％及59.94％;与正常组比较,补肾疏肝方、联合、顺铂含药血清可促进A549细胞凋亡,随着浓度增加,G2/M期细胞的百分比明显增加,明显下调CD133,SOX-2,OCT4 mRNA的表达,明显降低CD133蛋白表达量,均具有明显统计学差异(P ＜0.05,P＜0.01).结论:补肾疏肝方可抑制A549细胞增殖,促进细胞凋亡,与顺铂联合可下调CD133,SOX-2,OCT-4等干性因子的表达.

Objective To explore the effects of Bushenshugan Formula( BSSGF)on the apoptosis of human lung adenocarcinoma A549 cells,the level of TNF - α and the mRNA expression of Survivin and Caspase - 3. Methods BSSGF was used to make low - dose(1. 25 g/ ml),medium - dose(2. 50 g/ ml)and high - dose(3. 75 g/ ml)liquid. Using random number table method,we divided the rats into control group,low - dose group,medium - dose group,high - dose group,DDP group and combined group(medium - dose liquid combined with DDP)with 10 rats in each group. Control group was given 0. 9% sodium chloride solution from day 1 to day 5;low - dose,medium - dose and high - dose groups were given corresponding dose of liquid by 4 ml/ d;DDP group was given 2 ml DDP(20% ) on day 1,day 3 and day 5 by intraperitoneal infection;combined group was given medium - dose liquid by 4 ml/ d from day 1 to day 5 and was also given 2 ml DDP(20% )on day 1,&nbsp;day 3 and day 5 by intraperitoneal infection. Two hours after the last administration,blood samples were taken and serum was separated. A549 cells were added into the serum of each group and were cultured for 72 hours,then observed cell apoptosis by inverted fluorescence microscope. ELISA method was used to determine TNF - α level at 24 h,48 h and 72 h after cultivatation. After 72 hours,fluorogenic quantitative PCR was employed to determine the relative expression of Survivin mRNA and Caspase -3 mRNA. Results After 72 hours' influence of serum on A549 cells,cell apoptosis and karyopyknosis occurred,and the apoptotic cells increased with liquid concentration increasing. At 24 h,48 h and 72 h,the 6 groups were significantly different in the expression of TNF - α(P ﹤ 0. 05). At 24 h,48 h and 72 h,low - dose group,medium - dose group,high - dose group,DDP group and combined group were higher than control group in the expression of TNF - α(P ﹤ 0. 05). The 6 groups were significantly different in the relative expression of Survivin mRNA at 72 h(F = 13. 238,P ﹤ 0. 05). High - dose group, DDP group and combined group were lower(P ﹤ 0. 05)than control group in the relative expression of Survivin mRNA at 72 h. The 6 groups were significantly different in the relative expression of Caspase - 3 mRNA at 72 h( F = 10. 814,P ﹤ 0. 05). Medium - dose group,high - dose group,DDP group and combined group were higher than control group in the relative expression of Caspase - 3 mRNA at 72 h(P ﹤ 0. 05). Conclusion BSSGF could accelerate the apoptosis of A549 cells,and it may induce apoptosis of A549 cells by inhibiting the gene expression of Survivin,promoting the secretion of TNF - α and increasing the expression of Caspase - 3.

Objective: To study the apoptosis inducing effects and apoptosis related genes research of Bushen Shugan Formula on human lung adenocarcinoma A549 cells. Methods: Rat serum concentrating Bushen Shugan Formula was prepared and A549 cells were cultured in the drug serum with different concentrations. The proliferation of cells was detected by MTT assay. The flow cytometry was used to test the A549 cell cycle and cell apoptosis. Western-blot was used to test the expression of protein P53 and Bcl-2. Results: With the increase of Bushen Shugan Formula concentration and the extension of action time,the inhibitory effect on cells more obvious, and the effect of treatment group with DDP combined Bushen Shugan Formula was the most obvious. The inhibition rate of action time 24 h, 48 h and 72 h was 26.71%, 30.86% and 41.74%, respectively. The drug serum could induce the cell apoptosis, and there were significant differences of apoptosis rate between the treatment group and the control group(P0.05). With the increase of Bushen Shugan Formula concentration, the cell percentage in G2/M also increased.Drug could decrease the expression of Bcl-2, and increase the expression of P53. Conclusion: Bushen Shugan Formula could inhibit proliferation of A549 cells and demonstrate a dose and time dependent manner. The mechanism of inducing cell apoptosis and inhibiting cell proliferation with Bushen Shugan Formula might be that it could inhibit the Bcl-2 protein expression and promote P53 protein expression.

目的：探讨特质怒与阿尔茨海默病（ AD）发病的关联，初步分析特质怒与怒的表达在 AD 发病进程中的关系。方法采用同性别、同年龄段（±3岁）、同等文化程度1∶1匹配的病例对照研究，问卷调查，面对面访谈。结果病例组特质怒得分高于对照组（t＝44.784，P＝0.000）， OR＝51.857（14.009，191.954）；病例组怒的表达（AX-O、AX-I）显著高于对照组（P＜0.01），病例组和对照组特质怒与怒表达指数均呈正相关（r＝0.579，P＜0.01；r＝0.372，P＜0.01）。结论特质怒倾向高和怒的表达程度高皆是AD发病的危险因素；特质怒与怒的表达在 AD 发病进程中呈正相关，特质怒倾向高且怒的表达程度高更容易诱发AD。

Objective: To study the apoptosis inducing efects of Fuzheng Xiaoai Mixture on human lung adenocarcinoma A549 cells. Methods: Fuzheng Xiaoai Mixture containing rat serum was prepared and applied on A549. The cell growth inhibition was detected by MTT assay; the apoptosis was detected by Annexin V-FITC/PI staining with low cytometry. The expression of P53, Bcl-2 and Survivin were analyzed by Western Blot. Results: Fuzheng Xiaoai Mixture could inhibit the proliferation of A549 in the time and dose-dependent manner and had synergies combined with DDP. The inhibitory rate was 28.27%, 38.68%and 37.98% respectively for 48h, 72h and 96h. The herb serum could induce apoptosis, later stage apoptosis accounted main part.Apoptosis rate in the treatment group was higher than that of the control group(P0.05). The herb serum could down-regulate the expression of Bcl-2, Survivin protein, while activation of the P53 protein in the process of induction of apoptosis. Conclusion:Fuzheng Xiaoai Mixture can probably induce the apoptosis of A549 by inhibiting the expression of Bcl-2, Survivin protein, while activation of the P53 protein.

目的 观察电针膀胱过度活动症(OAB)的临床疗效,讨论其治疗机理.方法 将我院符合标准的膀胱过度活动症61例,随机分为观察组及对照组,通过比较日间及夜间排尿次数,国际前列腺症状评分表(Ⅰ-PSS评分)及生活质量指数评分(QoL评分)治疗效果比较,通过统计学分析评价疗效.结果 观察组与对照组,在日间及夜间排尿次数,国际前列腺症状评分表(Ⅰ-PSS评分)及生活质量指数评分(QoL评分)均存在有统计学意义差异(P＜005).结论 电针配合艾灸治疗对改善膀胱过度活动症(OAB)患者症状显著疗效.

Objective:To discuss the effects of chronic anger stress on rats' brain aging progress and concentration of plasma monoamine neurotransmitters.Methods:Induced anger stimulation after building D-gal aging and brain aging model,we observed the effects of chronic anger stress on the spatial learning and memory of rats by Morris water maze,and measured the contents of plasma monoamine neurotransmitters:norepinephrine(NE),5-hydroxytryp-tamine(5-HT),dopamine(DA).Results:Compared with the model group,the rats' spatial learning and memory in the angry stress group decreased obviously,the contents of NE and DA in plasma in the angry stress group increased,the contents of 5-HT decreased.Conclusion:The rats' brain aging was aggravated by chronic anger stress,the aging was accelerated;the rat's monoamine neurotransmitters disorder may be one of the mechanisms.

Objective: To discuss the association of tryptophan hydroxylase gene A218C polymorphism and anger started as well as anger control trait.Methods: After the subjects were selected by STAXI-2 questionnaire,blood of them was sampled,DNA was extracted by phenol–chloroform method,genotyped by PCR-LDR method,and data was statistically analyzed.Results: ①For high trait anger subjects,there was statistical significance of the scores of anger control-out(AC-O) of male in three genotype groups(P0.05).②For low trait anger subjects,there was statistical significance of the following scores of the subjects in three genotype groups(P0.05): anger control(AC),anger control-out(AC-0),anger control-in(AC-I) and anger control-out of female(AC-0).Conclusion: There was the association of TPH gene A218C polymorphism with anger control-out trait of normal male college students with high trait anger in China.The locus polymorphism was also related to the following anger traits of normal college students with low trait anger in China: anger control trait,anger control-out trait,anger control-in trait,anger control-out trait of female.