外泌体miRNA在卵巢癌中的研究进展

卵巢癌(ovarian cancer,OC)致死率在女性生殖系统肿瘤中位居第一,因其早期无典型症状,大多数患者在晚期才得到诊断。此外,由于癌细胞易对化疗药物产生耐药,多数患者会出现复发,导致患者预后很差。因此寻找有效的早期诊断及治疗方法对OC的早期预测、疗效评估、预后及复发判断等具有重要意义。外泌体(exosome)是近年来研究的热点,其富含脂质、蛋白质、RNA和DNA,通过与细胞膜融合将内容物释放到细胞外环境,影响相邻或远处细胞的生物学行为。研究认为外泌体可参与肿瘤微环境中细胞间通讯,通过传递癌或抑癌信息分子,影响肿瘤的进程。微小RNA(miRNA)可被包裹在外泌体中传递至受体细胞,影响肿瘤细胞的增殖、转移、耐药等,在肿瘤进展中发挥重要作用。本文对外泌体miRNA在OC中的研究进行综述。     

lncRNA作为ceRNA在卵巢癌中的研究进展

人类基因组中大部分为非编码区，转录产生非编码RNA（non-coding RNA，ncRNA）。ncRNA 虽然不能翻译成蛋白，但可通过对mRNA直接或间接地调控影响人体生理、病理过程。长链非编码RNA（long non-coding RNA，lncRNA）是ncRNA的重要分类，越来越多的研究表明lncRNA参与癌细胞增殖、迁移、侵袭、凋亡和耐药等，影响肿瘤的发生和发展，lncRNA可作为肿瘤早期诊断、治疗和判断预后的潜在靶向标记物。竞争性内源RNA（competitive endogenous RNA，ceRNA）假说的提出使人们对肿瘤发生机制有了进一步的了解。在ceRNA的形成中，lncRNA有着重要作用。近年lncRNA作为ceRNA在卵巢癌中的研究日益增多。本文就lncRNA形成的ceRNA网络在卵巢癌的发生发展过程中的研究进展进行综述。     

转录因子YY1在妇科肿瘤和妊娠疾病中的作用

转录因子Ying-Yang1(YY1)是正常细胞和癌组织中普遍表达的多功能转录调控蛋白,其参与调控多种细胞正常生理过程,如胚胎发育、细胞骨架蛋白结构和功能、染色体失活和修复、肿瘤发生和浸润转移等过程,在生物体内发挥着重要作用.已有大量证明YY1在多种肿瘤中有异常表达,并通过多种途径调控肿瘤的增殖过程,如宫颈癌、乳腺癌、卵巢癌等,在某些癌症类型中YY1的高表达可提高患者生存预后.并且,近年来YY1在妊娠中的作用也备受关注,以下将重点就YY1的作用机制和在妇科肿瘤方面和妊娠疾病中的研究进展作一综述.     

从学生视角探讨医学生在实习轮转中存在的问题

临床实习是医学理论联系实践的桥梁,是培养学生临床理论、临床实际操作能力和临床思维的重要时期。文章旨在对全日制医学实习生实习轮转中出现问题的原因进行分析,为完善医学生实习、提高教学医院临床教学质量提供参考,并以此探讨适合以两周为轮转周期的全日制医学实习生的实习规划。     

应用辅助材料行修补术治疗阴道前壁脱垂的有效性及安全性的Meta分析

目的研究应用辅助材料行盆底修补术治疗阴道前壁脱垂的有效性及安全性。方法计算机检索Pubmed、Embase、Ovid数据库1980年至2012年符合条件的英文随机对照试验的文献,进行质量评估,并对解剖学失效率、手术时间、术中出血量、周围脏器损伤及术后盆腔痛、泌尿系感染、材料暴露、材料侵蚀、新发生的尿失禁及新发生的性生活困难共10项行Meta分析。结果共检索到符合条件的20篇随机对照文献,纳入受试者共2313例,平均随访时间3～36个月。经Meta分析,应用辅助材料的修补术与不应用辅助材料的修补术治疗阴道前壁膨出相比,辅助材料组表现为更低的解剖学失效率、更长的手术时间、更多的术中出血量及更低的泌尿系感染发生率,效应量分别为（P〈0．01,RR=0．51,95％CI：0．41～0．64）、（P〈0．01,加权均数差=16．25,95％CI：8．07～24．43）、（P=0．01,加权均数差=35．00,95％CI：6．90～63．11）及（P=0．03,RR=0．51,95％CI：0．28—0．93）;但两组在周围脏器损伤、术后疼痛、新发生的尿失禁及新发生的性生活困难的比较差异无统计学意义,P值分别为0．07、0．58、0．54及0．67,辅助材料暴露及突出的平均发生率分别为4．37％（27／618）及7．69％（24／312）。结论辅助材料在阴道前壁修补手术中的应用能改善术后复发率,但并发症的发生总体上与单纯修补术相比未见明显差异。     

Tacolimus postconditioning alleviates apoptotic cell death in rats after spinal cord ischemia-reperfusion injury via up-regulating protein-serine-threonine kinases phosphorylation

The effects of tacrolimus postconditioning on protein-serine-threonine kinases （Akt） phos- phorylation and apoptotic cell death in rats after spinal cord ischemia-reperfusion injury were investi- gated. Ninety male SD rats were randomly divided into sham operation group, ischemia-reperfusion group and tacrolimus postconditioning group. The model of spinal cord ischemia was established by means of catheterization through femoral artery and balloon dilatation. The spinal cord was reperfused 20 min after ischemia via removing saline out of balloon. The corresponding spinal cord segments were excised and determined for Akt activity in spinal cord tissue by using Western blotting at 5, 15, and 60 min after reperfusion respectively. Spinal cord tissue sections were stained immunohistochemically for detection of the phosphorylated Akt expression at 15 min after reperfusion. Flow cytometry was applied to assess apoptosis of neural cells, and dry-wet weights method was employed to measure water content in spinal cord tissue at 24 h after reperfusion. The results showed that the activities of Akt in tarcolimus postconditioning group were significantly higher than those in ischemia-reperfusion group at 5, 15, and 60 min after reperfusion （P〈0.05, P〈0.01）. The Akt activities reached the peak at 15 min after reperfu- sion in ischemia-reperfusion group and tacrolimus postconditioning group. The percentage of apoptotic cells and water content in spinal cord tissue were significantly reduced （P〈0.01） in tacrolimus postcon- ditioning group as compared with those in ischemia-reperfusion group at 24 h after reperfusion. It is concluded that tacrolimus postconditioning can increase Akt activity in spinal cord tissue of rats, inhibit apoptosis of neural cells as well as tissue edema, and thereby alleviate spinal cord ischemia-reperfusion injury.     

人乳头状瘤病毒18型阳性肿瘤疫苗的构建及体外活性鉴定

目的: 制备人乳头状瘤病毒（human papilloma virus, HPV）18型阳性的肿瘤疫苗，并观察其体外活性。方法:利用昆虫杆状病毒(简称Bac to Bac)表达系统，将HPV18L1基因重组入穿梭质粒pFastBacHtb，构建HPV18 L1Htb，通过转座反应,将目的基因片段重组入杆状病毒基因     

选择性环氧合酶抑制剂NS398对子宫内膜癌细胞株的影响

目的探讨环氧合酶抑制剂NS398对子宫内膜癌细胞株的生物学行为的影响。方法2005年9月至2006年11月于华中科技大学同济医学院附属同济医院妇产科实验室用MTT、DNA梯度降解试验及流式细胞仪等方法,研究NS398体外对子宫内膜癌细胞系Ishikawa的抑制增殖、促进凋亡作用。结果NS398对Ishikawa细胞产生明显的生长抑制作用,且表现为剂量依赖性(F=36.598,P<0.01);DNA梯度降解试验、流式细胞仪分析NS398浓度依赖性地诱导了Ishikawa细胞凋亡(F=11.342,P<0.01),且凋亡与细胞周期受阻有关(F=22.445,P<0.01)、主要阻止在G1/S期即DNA合成期。结论NS398对Ishikawa细胞具有显著浓度依赖性的体外生长抑制、诱导凋亡、阻滞DNA合成作用。     

Induction of SiHa Cells Apoptosis by Nanometer Realgar Suspension and Its Mechanism

The effects of nanometer realgar uterine cervix cancer cell line SiHa cells and suspension on proliferation and apoptosis of human oncogenic genes HPV16E6/E7 were investigated. A ＂micro-jet effiux＂ strategy was used for the preparation of nanometer realgar suspension. SiHa cells were treated with nanometer Realgar suspension in various concentrations （6.25, 12.5, 25 and 50 mg/L） for different durations （12, 24, 48 and 72 h）. The inhibitive effect of nanometer realgar suspension on growth of SiHa cells was detected by MTT method. Special morphological changes of apoptosis were observed by transmission electron microscopy （TEM） and DNA fragments electrophoresis. The apoptotic rate was quantified by flow cytometry （FCM）. The expression of HPV 16E6/E7 mRNA and protein was assayed by RT-PCR and Western blot respectively. The results showed after being treated with 25--50 mg/L nanometer realgar suspension for 48 h, the survival rate of SiHa cells was decreased, and apoptotic rate markedly increased in a time- and concentration-dependent manner. TEM and DNA electrophoresis revealed the special morphological changes of apoptosis. The apoptotic rate of SiHa cells treated with nanometer realgar suspension was significantly higher than in the control group （P〈0.01）, and G0/G1 phase arrest appeared following treatment with nanometer realgar suspension in 25 and 50 mg/L for 48 h. RT-PCR and Western blot assay indicated that nanometer realgar suspension reduced the HPV16E6/E7 gene expression. Nanometer realgar suspension could inhibit the proliferation and induce apoptosis of SiHa cells. The mechanism may be related to the down-regulation of the HPV16E6/E7 gene expression.