Clinical Features and Surgical Treatment of A-pattern Exotropia

IntroductionAnA鄄patternexotropiashowssignificantlymoreexodeviationindowngazeversusupgaze,inwhichthechangeofbinocularalignmentresemblesthealphaberA.Accordingtopublishedreports[1～4],A鄄patternexotropiaisviewedastheleasttypeofAandVpatterns.However,thepr鄄evalenceofA鄄patternexotropiaratherincreasedinourclinicalstudies[5],inwhichparticularattentionwaspaidtoobservethedeviationindownwardgazeandassesssuperiorobliquefunction.Accordingly,clinicalcharacteristics,surgicaltreatmentandtreatmentoutcome…     

二羟异黄酮对人乳腺癌细胞系MCF-7生长影响

大豆异黄酮是豆科植物的重要成分.近年来研究显示,其具有抗肿瘤作用,尤其对人类乳腺癌细胞株及前列腺癌细胞株均具有明显的体外抗肿瘤作用.献表明,二羟异黄酮可以抑制细胞增殖及阻滞细胞周期.本实验初步探讨二羟异黄酮的抗肿瘤作用.     

稳定表达乙型肝炎病毒含前S2的表面抗原重组细胞系的建立

目的 建立稳定表达含有pre-S2的HBsAg的细胞系。方法 构建在真核细胞表达pre-S2-HB-sAg的重组质粒PCI-HBs2。用此质粒转染HepG2细胞，经克隆化培养以及G418筛选，建立稳定表达HBsAg的细胞系。对其分泌动态、细胞纯度、遗传稳定性等生物学特性做了鉴定。同时对该细胞实验室大量培养的条件进行了优化。结果 成功构建表达pre-S2-HBsAg的重组质粒。转染细胞后筛选到一个稳定表达pre-S2-HBsAg的细胞系3E3。ELISA检测表明该细胞系分泌的HBsAg水平高，生物学性状研究结果表明稳定表达HBsAg的3E3细胞纯度好，遗传性状稳定。结论 成功建立了稳定表达pre-S2-HBsAg的细胞系。该细胞系遗传性质稳定，表达蛋白产量高。此细胞系可用于pre-S2-HBsAg的制备及纯化。     

内皮抑素对荷卵巢上皮性癌细胞系ES-2细胞裸鼠的抗血管生成作用

肿瘤的生长和转移与肿瘤区血管生长有密切关系，分期越晚，分化越差，肿瘤内血管密度（MVD）越高。抑制和破坏肿瘤区新牛血管的生长，阻断其血液供应导致肿瘤细胞坏死，并阻断其转移，成为治疗实体肿瘤的一种新途径。1997年，O’Reilly等体外实验发现，内皮抑素对牛毛细血管内皮细胞有特异的抑制增殖作用，而对非血管内皮细胞、平滑肌细胞等尢抑制作用；体内实验证明，内皮抑素可抑制鸡胚尿囊膜的毛细血管生长：近年来，已有数种作用机理不同的这类药物正在进行临床试验。目前，内皮抑素已应用于多种肿瘤的体内实验。本研究采用裸鼠移植瘤模型，观察内皮抑素对人卵巢上皮性癌（卵巢痛）移植瘤内肿瘤新生血管生成的抑制作用，现报道如下。     

5-杂氮-2′-脱氧胞苷抑制人鼻咽癌CNE细胞生长的机制

目的探讨5-杂氮-2′-脱氧胞苷(5-Aza-CdR)抑制人鼻咽癌CNE细胞系生长增殖的机制,寻找鼻咽癌治疗的新靶点。方法用5-Aza-CdR处理人鼻咽癌CNE细胞,应用MTT试验观察不同浓度的5-Aza-CdR对癌细胞生长增殖的影响。用甲基化特异性PCR(MSP)分析死亡相关蛋白激酶(DAPK)基因甲基化状态;逆转录聚合酶链反应、免疫细胞化学、流式细胞仪检测用药前后DAPK mRNA、蛋白的表达情况及细胞凋亡和细胞周期的变化。结果从CNE细胞生长曲线知各浓度的5-Aza-CdR对细胞生长均有抑制作用。未经5-Aza-CdR处理的CNE细胞中DAPK基因CpG岛过甲基化,且DAPK mRNA不表达。经5-Aza-CdR处理后,甲基化的DAPK基因部分去甲基化,用药组的细胞中均有DAPK mRNA表达,且表达随药物浓度增高而增强。免疫细胞化学结果显示,经药物处理后的CNE细胞中DAPK蛋白表达呈阳性,而对照组不表达。流式细胞分析结果显示,药物处理后细胞凋亡率明显增加,且G0/G1期细胞增加,G2/M期减少。结论5-Aza-CdR对体外培养的鼻咽癌细胞生长增殖的抑制作用,可能是由于其能使因甲基化而失活的DAPK基因再转录,诱导该基因重新表达的结果。     

人胚胎干细胞建系及培养的研究进展

人胚胎干细胞的培养是了解人胚胎发育机制和实现治疗性克隆的前提。在人胚胎干细胞建系和维持过程中，胚胎材料来源、内细胞团分离、扩增传代、冻存复苏等均为难点。从鼠源饲养层、人源饲养层到无饲养层培养系统的发展，以及体细胞核移植技术平台的建立，奠定了治疗性克隆的基础。     

提高对多发性骨髓瘤的警惕性

多发性骨髓瘤(MM)是浆细胞系统的恶性增生性疾病，常侵犯多个系统，临床表现多不典型，易致误诊。国内文献报道误诊率达57．4％～78．8％。本文就其临床表现特点做一概述，以期提高对MM的警惕性，减少误漏诊。     

STAT1对人肾透明细胞癌放射敏感性的影响

目的 研究人肾透明细胞癌信号传递和转录活化因子1(STAT1)表达情况及抑制STAT1对该肿瘤细胞放射敏感性的影响.方法 采用免疫组织化学染色技术对比检测34例人肾透明细胞癌标本和12例正常肾组织标本的STAT1表达.用Western blotting法检测离体培养人肾透明细胞癌细胞(CRL-1932)、纤维母细胞(CCL-116)和wilm's瘤细胞(CRL-1441)的STAT1表达.用氟达拉滨和siRNA抑制CRL-1932细胞STAT1表达,并通过成克隆法和台盼蓝染色计数法研究抑制STAT1对CRL-1932细胞放射敏感性的影响.结果 人肾透明细胞癌标本的总STAT1和磷酸化STAT1表达均明显高于正常肾组织.Western blotting法显示CRL-1932细胞STAT1表达比CRL-1441、CCL-116细胞明显增高;药物氟达拉滨能显著抑制CRL-1932细胞磷酸化STAT1的表达,并显著增加CRL-1932细胞的放射敏感性,且放射增敏程度与药物浓度呈正相关.经STAT1 siRNA处理后CRL-1932细胞总STAT1和磷酸化STAT1的表达均被有效抑制,且细胞在照射后的存活分数显著下降.结论 肾透明细胞癌STAT1呈高表达,抑制STAT1对该细胞有放射增敏作用.     

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.     

Production of neutralizing monoclonal antibody against human vascular endothelial growth factor receptor Ⅱ

AIM: To prepare neutralizing monoclonal antibody (mAb) against extracellular immunoglobulin (Ig)-like domain Ⅲ of vascular endothelial growth factor receptor KDR and study its biological activity. METHODS: Soluble KDR Ig domain III (KDR-Ⅲ) fusion protein was expressed in E Coli and purified from the bacterial periplasmic extracts via an affinity chromatography. Monoclonal antibodies against KDR-Ⅲ were prepared by hybridoma technique. ELISA and FACS analysis were used to identify its specificity. Immunoprecipitation and [^3H]-thymidine incorporation assay were also used to detect the activity of anti-KDR mAb blocking the phosphorylation of KDR tyrosine kinase receptor and the influence on vascular endothelial growth factor-induced mitogenesis of human endothelial cells. RESULTS: A monoclonal antibody, Ycom1D3 (IgG1), was generated from a mouse immunized with the recombinant KDR-Ⅲ protein. YcomlD3 bound specifically to both the soluble KDR-Ⅲ and the cell-surface expressed KDR. Ycom1D3 effectively blocked VEGF/KDR interaction and inhibited VEGF-stimulated KDR activation in human endothelial cells. Furthermore, the antibody efficiently neutralized VEGF-induced mitogenesis of human endothelial cells. CONCLUSION: Our results suggest that the anti-KDR mAb, Ycom1D3, has potential applications in the treatment of cancer and other diseases where pathological angiogenesis is involved.