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| 1 | Meta分析系列之三:随机对照试验的质量评价工具显示文摘Meta分析是对原始研究的二次综合分析与评价,其质量受纳入原始研究质量、评价的方法、评价者的知识水平及观点的影响.若Meta分析纳入的原始研究质量低,且未对原始研究方法学质量进行正确评价,Meta分析的结果和结论可能是不正确的,从而对临床实践造成误导[1].因此,对Meta分析纳入的原始研究质量进行严格的评价尤为重要.原始研究质量评价工具主要根据研究设计、实施、结果分析整个过程中可能出现偏倚的各个因素而确定,目前出现的评价工具较多,主要有单个评价条目(components/items)、清单(checklist/list)和量表(scale)三种类型.前面我们已经对Meta分析的类型[2]、Meta分析的软件[3]进行了介绍,本文将在简要回顾原始研究类型的基础上,对随机对照试验(randomized controlled trail,RCT)常用的质量评价工具进行简要分析. | 曾宪涛 包翠萍 曹世义 刘菊英 | 2012 | 中国循证心血管医学杂志2012，4，3： | 240 |
| 2 | Meta分析系列之十三:盲法的评价显示文摘盲法(blinding)起源于Franklin Benjamin及他的同事们:他们让受试者戴上眼罩,使受试者无法看到,从而避免受试者主观因素对催眠术(mesmerism)治疗作用的评估的影响。盲法后来被应用到临床试验中,成为了随机对照试验(randomized controlled trail,RCT)的一个重要且独特的方面。 | 曾宪涛 熊期 沈可 | 2013 | 中国循证心血管医学杂志2013，5，4： | 43 |
| 3 | 痤疮发病机制的研究进展显示文摘痤疮是累及毛囊皮脂腺的慢性炎症性皮肤病,其发病机制复杂,不仅与雄激素介导的皮脂腺分泌增加、皮脂成分改变、毛囊皮脂腺导管角化异常、痤疮丙酸杆菌增殖及炎症反应有关,遗传因素以及饮食习惯也是痤疮发病的重要因素,饮食因素可经胰岛素及IGF-1通过PI3k/Akt信号通路影响痤疮发病,而增强肿瘤坏死因子相关凋亡诱导配体(TRAIL)表达,上调转录因子p53被认为是治疗痤疮的关键。本文综述痤疮各发病机制的最新研究进展,希望能为临床诊治以及科研工作提供新的思路。 | 潘清丽 邵蕾 陈丽洁 王建琴 | 2018 | 皮肤性病诊疗学杂志2018，25，6： | 48 |
| 4 | 肿瘤细胞对TRAIL敏感性与其表面DR5表达水平的相关性研究显示文摘目的 探讨肿瘤细胞表面DR5表达水平与其对肿瘤坏死因子相关的凋亡诱导配体(TRAIL)敏感性之间的关系。方法 利用抗DR5特异性单克隆抗体 ,采用流式细胞仪技术直接检测不同肿瘤细胞系表面DR5的表达水平 ,并采用TRAIL凋亡检测试剂盒检测肿瘤细胞对TRAIL诱导凋亡的敏感性 ,研究两者之间的关系。结果 不同肿瘤细胞表面DR5的表达水平分别为 :U937细胞97.9%、Jurkat细胞 95 .1%、SW4 80细胞 93.8%、HCT116细胞 86 .2 %、HL 6 0细胞 6 4 .2 %、HeLa细胞4 6 .6 %、K5 6 2细胞 13.1% ;TRAIL诱导的细胞凋亡率分别为 :U937细胞 72 .6 %、Jurkat细胞 85 .2 %、SW4 80细胞 78.6 %、HCT116细胞 70 .2 %、HL 6 0细胞 6 0 .1%、HeLa细胞 4 5 .4 %、K5 6 2细胞 12 .3%。经统计学分析 ,两者之间呈现非常明显的正相关 (r=0 .997,P <0 .0 0 1)。结论 肿瘤细胞对TRAIL的敏感性与其表面DR5表达水平有关 。 | 马远方 张军 赵粤萍 杨东亮 陈有海 | 2004 | 中华肿瘤杂志2004，26，9： | 32 |
| 5 | 细胞凋亡的死亡受体途径显示文摘死亡受体信号转导通路是诱导细胞凋亡的主要途径之一,目前已知的死亡受体有8种,其信号转导途径主要有3条,分别为TNFR、TRAIL和Fas/FasL信号途径。本文将就这三条通路的研究概况进行阐述。 | 赵美玲 季宇彬 毕明刚 | 2013 | 黑龙江医药2013，26，2： | 34 |
| 6 | Analysis of TRAIL receptor expression using anti-TRAIL death receptor-5 monoclonal antibodies显示文摘ObjectiveTo establish hybridomas that produce anti-death receptor-5 (DR5) monoclonal antibodies (mAbs) and check the surface expression of DR5 (sDR5) on cell lines.MethodsThe cDNA of human DR5 was cloned into pGAPZα. Recombinant Pichia pastoris clones generated via homologous recombination secreted high levels of sDR5. The sDR5 was purified using a nickel ion column. BALB/c mice were immunized with sDR5 and spleen cells were fused with the SP2/0-Ag 14. Monoclonal antibodies were tested by ELISA for their abilities binding to sDR5 and by flow cytometry for thereactivities to surface DR5 of Jurkat cells. Surface expression of the TRAIL receptor was determined by flow cytometric analysis measuring the binding of anti-DR5 mAb. Resultse to sDR5 as observed through ELISA. It was discovered using flow cytometry that only IgG was able to bind to DR5 on the plasma membrane of Jurkat cells. sDR5was found to completely inhibit anti-DR5 mAb binding to Jurkat cells. Pproximately 95% of Jurkat cells, 98% SW480, 99% U937, 100% U87, 86% HCT116, 64% HL-60, 47% HeLa and 13% K562 cells express membrane DR5. ConclusionsThese results demonstrate that anti-DR5 mAb is able to specifically bind to DR5and that DR5 is expressed at high levels on Jurkat, SW480, U87, U937 and HCT116cell lines, and at medium levels on HL-60 and HeLa cell lines. The expressionof DR5 on K562 cell line is low. | 马远方 杨东亮 陈有海 | 2003 | Chinese Medical Journal2003，，6： | 30 |
| 7 | Expression of TRAIL and TRAIL receptors in normal and malignant tissues显示文摘TRAIL, tumor necrosis factor-related apoptosis-inducing ligand, is a member of the TNF family of proteins.Tumour cells were initially found to have increased sensitivity to TRAIL compared with normal cells, raising hopes thatTRAIL would prove useful as an anti-tumor agent. The production of reliable monoclonal antibodies against TRAIL andits receptors that can stain fixed specimens will allow a thorough analysis of their expression on normal and malignanttissues. Here we report the generation of monoclonal antibodies against TRAIL and its four membrane-bound receptors(TR1–4), which have been used to stain a range of normal and malignant cells, as routinely fixed specimens. Low levelsof TRAIL expression were found to be limited mostly to smooth muscle in lung and spleen as well as glial cells in thecerebellum and follicular cells in the thyroid. Expression of the TRAIL decoy receptors (TR3 and 4) was not aswidespread as indicated by Northern blotting, suggesting that they may be less important for the control of TRAILcytotoxicity than previously thought. TR1 and TR2 expression increases significantly in a number of malignant tissues,but in some common malignancies their expression was low, or patchy, which may limit the therapeutic role of TRAIL.Taken together, we have a panel of monoclonal antibodies that will allow a better assessment of the normal role ofTRAIL and allow assessment of biopsy material, possibly allowing the identification of tumors that may be amenable toTRAIL therapy. | RaymondADANIELS HelenTURLEY FionaCKIMBERLEY XueSongLIU JuthathipMONGKOLSAPAYA3 PaulCH'EN XiaoNingXU BoquanJIN FrancescoPEZZELLA GavinRSCREATON | 2005 | Cell Research2005，15，6： | 22 |
| 8 | Fas FasL TRAIL分子在尖锐湿疣皮损中的分布显示文摘目的 探讨Fas、FasL和TRAIL介导的细胞凋亡在尖锐湿疣发病中的可能作用及意义。方法 用免疫组化方法检测了 30例尖锐湿疣患者皮损中Fas、FasL和TRAIL的表达。结果 所有尖锐湿疣标本 ( 10 0 % )Fas均阳性 ,2 3例 ( 76 .7% )FasL阳性 ,2 1例 ( 70 .0 % )TRAIL阳性 ,三者分布基本一致 ,正常表皮基本不表达。且FasL和TRAIL分子与真皮单一核细胞浸润呈显著负相关 (γ =-0 .5 0 6和γ =-0 .45 0 ,P均 <0 .0 5 )。结论 尖锐湿疣组织中细胞凋亡相关分子Fas、FasL和TRAIL表达异常 ,且Fas、TRAIL分子表达影响局部免疫反应 ,考虑凋亡失控可能参与尖锐湿疣发病 ,引起复发。 | 谢红付 冯浩 范学工 肖满兰 陈翔 施为 | 2003 | 中国皮肤性病学杂志2003，17，3： | 19 |
| 9 | 白附子木脂素化合物调节人胃癌SGC-7901细胞TRAIL及其受体的表达显示文摘目的:探讨白附子木脂素化合物对人胃癌细胞株(SGC-7901)的TRAIL及其受体TRAIL—R1和TRAIL—R2表达的影响。方法:SGC-7901细胞在不同浓度组0.026~26μg·L^-1的白附子木质素化合物中培养24h后,用MTT法检测白附子木脂素化合物对细胞增殖的抑制作用;利用Hoechst33342/PI染色法观察细胞凋亡;采用RT—PCR方法检测不同浓度白附子木脂素化合物对SGC-7901细胞TRAIL及其受体mRNA基因表达。结果:不同浓度组0.026~26μg·L^-1的白附子提取物对SGC-7901细胞增殖的抑制率分别为7.35%,16.11%,27.18%和50.58%;且均导致细胞凋亡的改变;同时其TRAIL及其受体TRIAL—R1和TRAIL—R2 mRNA表达水平明显高于空白对照组。结论:白附子木脂素化合抑制了SGC-7901的增殖并诱导其凋亡。作用机制可能与上调TRAIL及其受体TRAIL—R1和TRAIL-R2有关。 | 马英丽 李艳凤 唐丽萍 艾凤伟 | 2010 | 中国新药杂志2010，19，3： | 18 |
| 10 | Enhanced Effects of TRAIL-endostatin-based Double-gene-radiotherapy on Suppressing Growth, Promoting Apoptosis and Inducing Cell Cycle Arrest in Vascular Endothelial Cells显示文摘This study examined the effects of TRAIL-endostatin-based gene-radiotherapy on cellu-lar growth, apoptosis and cell cycle progression in human vascular endothelial cells ECV304 in vitro. The expression of TRAIL and endostatin protein in ECV304 cells was detected by ELISA after the transfection of recombinant plasmid pshuttle-Egr1-shTRAIL-shES and X-ray irradiation. Then MTT assay was used for determining the cellular proliferation, and flow cytometry (FCM) plus Annexin V and propidium iodide (PI) double-staining or PI single-staining were employed for the detection of apoptosis and cell cycle progression. The results showed that expression of TRAIL and endostatin protein exhibited a time- and dose-dependent change in ECV304 cells after pshut-tle-Egr1-shTRAIL-shES transfection in conjunction with irradiation. In the TRAIL-endostatin-based single- or double-gene-radiotherapy, the cell viability declined in a time- and dose-dependent manner, the percentage of cells at G2/M phase and apoptotic rate was increased, and the percentage of cells at G0/G1 phase was lowered as compared with those receiving radiotherapy alone. Moreover, TRAIL-endostatin-based double-gene-radiotherapy demonstrated better effects on growth inhibition, promotion of apoptosis and induction of cell cycle arrest in ECV304 cells than sin-gle-gene-radiotherapy. | 李艳博 郭彩霞 王志成 龚平生 孙志伟 龚守良 | 2012 | Journal of Huazhong University of Science and Technology(Medical Sciences)2012，32，2： | 16 |
| 11 | 抑制Livin基因对肺腺癌SPC-A1细胞增殖及顺铂敏感性的影响显示文摘目的:Livin是近年来发现的人类凋亡抑制蛋白(inhibitorof apoptosis protein,IAP)家族的新成员,发现在多数肿瘤中表达,与肿瘤发生有密切关系,并可能作为肿瘤诱导凋亡治疗的新靶点。本研究旨在探讨si RNA-Livin和夫拉平度(Flavopiridol,FP)协同凋亡诱导配体(TRAIL)两种方式有效抑制Livin表达,诱导非小细胞肺癌SPC-A1凋亡并增强对化疗药物顺铂的敏感性。方法:si RNA-Livin转染SPC-A1,Real-Time PCR检测Livin基因的表达水平,MTT检测干扰组和干扰加药组肿瘤细胞的增殖及活性;TRAIL、FP单独及联合作用诱导细胞凋亡,蛋白质印迹法检测凋亡抑制蛋白Livin的表达水平,MTT检测各处理组细胞的增殖及活性。结果:100 nmol/LFP处理组(F)细胞存活率为(84.30±1.34)%,100 ng/m LTRAIL处理组(T)为(93.40±1.56)%,FP和TRAIL联合组(F+T)为(48.02±1.35)%,si RNA-Livin处理组为(50.88±1.14)%,1.2μg/m L Cisplatin处理组为(19.30±0.89)%,si RNA-livin+Cisplatin组为(14.37±0.81)%,FP+T+Cisplatin组为(10.86±0.87)%,C组存活率为100%。F+T组对细胞的增殖抑制作用显著高于单独用药组,si RNA-livin+Cisplatin与si RNA-Livin组相比、FP+T+Cisplatin与FP+T组相比都显著增强了化疗药物对SPC-A1的杀伤作用。50μmol/LZ-VAD-FMK预处理后联合用药组细胞的存活率为(88.16±1.64)%,caspase抑制剂能明显抑制F+T联合处理组的凋亡效应。结论:RNA干扰和F+T联合用药都能显著降低凋亡抑制蛋白Livin的表达,有效抑制肿瘤细胞的增殖生长,并增强肿瘤细胞对化疗药物顺铂的敏感性,为肺腺癌的靶向治疗提供新的理论依据。 | 庄莉 董超 杨润祥 高春林 | 2015 | 现代生物医学进展2015，15，6： | 16 |
| 12 | Bcl-2 over-expression and activation of protein kinase C suppress the Trail-induced apoptosis in Jurkat T cells显示文摘Trail, a tumor necrosis factor-related apoptosis-inducing ligand, is a novel potent endogenous activator of the cell death pathway through the activation of cell surface death receptors Trail-R1 and Trail-R2. Its role, like FasL in activation-induced cell death (AICD), has been demonstrated in immune system. However the mechanism of Trail induced apoptosis remains nuclear. In this report, the recombinant Trail protein was expressed and purified. The apoptosis-inducing activity and the regulation mechanism of recombinant Trail on Jurkat T cells were explored in vitro. Trypan blue exclusion assay demonstrated that the recombinant Trail protein actively killed Jurkat T cells in a dose-dependent manner. Trail-induced apoptosis in Jurkat T cells were remarkably reduced by Bcl-2 over expression in BcL-2 gene transfected cells. Treatment with PMA (phorbol 12-myristate 13-acetate), a PKC activator, suppressed nail-induced apoptosis in Jurkat T cells. The inhibition of apoptosis by PMA was abolished by pretreatment with Bis, a PKC inhibitor. Taken together, it was suggested that Bcl-2 over-expression and PMA activated PKC actively down-regulated the Trail-mediated apoptosis in Jurkat T cell. | GuoBC XuYU | 2001 | Cell Research2001，11，2： | 16 |
| 13 | Western medication plus Traditional Chinese Medicine preparations in patients with chronic heart failure:a prospective,single-blind,randomized,controlled,and multicenter clinical trial显示文摘OBJECTIVE: To assess the efficacy and safety in patients with chronic heart failure(CHF) of Western medication plus Traditional Chinese Medicine(TCM) preparations.METHODS: This prospective, single-blind, randomized, controlled, and multicenter clinical trial began on September 17, 2008, and was completed on June 25, 2011. A total of 340 inpatients, aged 40-79 years, with exacerbating CHF from 10 hospitals were enrolled and randomly allocated within 24 h of admission. The trial included three intervention periods. During hospitalization, the control group received western medication for CHF and the treatment group received Danhong injection with Shenfu injection or Shenmai injection. After discharge,all patients were treated with Qiliqiangxin capsules and Buyiqiangxin tablets or a placebo for 6 months. After the 6-month intervention, both groups received only continuous western medication. The primary endpoint was all-cause mortality.The efficacy assessments were as follows: B-type natriuretic peptide(BNP), Lee's HF score, the 6-minute walking test(6 MWT), left ventricular ejection fraction(LVEF), and the Minnesota Living with Heart Failure Questionnaire(MLHFQ). The safety assessments were as follows: blood and urine routine examination, hepatic and renal function, electrolytes in blood and adverse events.RESULTS: Compared with the control group, the treatment group showed a 30.99% reduction in all-cause mortality and an improved survival rate.The treatment group showed greater improvement in 6 MWT(P = 0.02) than the control group on discharge, after 12-month follow-up, there was a time-group interaction for MLHFQ(P = 0.03). Incidence rate of adverse events and other relevant safety indexes were not statistically significant between the two groups.CONCLUSION: Western medication plus TCM treatment can increase 6-minute walking distance(improve exercise tolerance) and quality of life with heart failure patients. | Wang Xianliang Hou Yazhu Mao Jingyuan Zhao Yingqiang Niu Tianfu Yuan Ruyu Wang Yonggang Cui Jin-rong Shi Le Jia Xiuli Fan Ruihong Lin Qian Zhang Yan Li Zhijun Shang Hongcai Wang Baohe Wang Hongwu Wang Henghe Cui Xiaolei Soh Shanbin Ruan Jishou Zhang Boli | 2017 | Journal of Traditional Chinese Medicine2017，37，6： | 15 |
| 14 | TRAIL receptor mediates inflammatory cytokine release in an NF-κB-dependent manner显示文摘在现在的文章,我们报导 DR4 或 DR5 overexpression 戏剧性地在 293T, MDA-MB-231 和 HCT-116 房间以一种 NF-魏 B 依赖者方式激活煽动性的 cytokines IL-8, TNF- 伪, CCL20, MIP-2 和 MIP-1 尾的版本。我们显示出调停受体的信号是的那死亡细胞外域无关,而 DR4 细胞内部的领域的 overexpression 的效果是少得多有势力。表明串联的 TRADD-TRAF2-NIK-IKK 伪 / 尾,在导致 TNF 的 NF-魏 B 激活起一个必要作用,被发现涉及肿瘤坏死因素相关导致 apoptosis ligand (小道) 调停受体的信号 transduction。表明小径的 FADD-caspase,被报导了主要与 apoptosis 有关,作为与表明串联的 TRADD-TRAF2-NIK-IKK 伪 / 尾为 DR4 或 DR5 调停 overexpression 的 NF-魏 B 激活和 cytokine 分泌物和串音是必要的被识别。而且, DR5 论战的抗体(AD5-10 ) 触发了煽动性的 cytokine 版本。这些数据和以前的报告,提供小道和小道受体在发炎起一个重要作用的充分证据。 | Wanhu Tang Weimin Wang Yaxi Zhang Shilian Liu Yanxin Liu Dexian Zheng | 2009 | Cell Research2009，19，6： | 14 |
| 15 | 超声引导下改良腹横肌平面阻滞在胃癌根治术中的应用显示文摘腹横肌平面(TAP)阻滞是近年来提出的一种新的腹壁区域阻滞方法,指在腹内斜肌与腹横肌之间的神经筋膜层注射局麻药可以阻滞前腹壁的神经,提供良好的腹壁镇痛。Trail等在超声引导下将苯胺染料注射在髂嵴上方的腹横肌平面,结果显示染色只影响了T10-L1神经根,提示这项技术可能仅适用于下腹部手术。 | 陈红生 徐兴国 曹苏 | 2015 | 中华临床医师杂志(电子版)2015，9，1： | 14 |
| 16 | 苦参碱对肿瘤细胞获得性多药耐药的逆转作用显示文摘目的观察苦参碱对模拟临床化疗CFP方案诱导的小鼠S180肿瘤细胞获得性多药耐药的逆转作用,明确其对多药耐药逆转的作用及其作用机制。以指导临床应用苦参碱逆转肿瘤患者多药耐药,提高化疗疗效。方法模拟临床CFP方案,分别给予小鼠顺铂3mg·kg-1,ip,每周1次;环磷酰胺和5FU各3mg·kg-1,ig,qd,连续4周,流式细胞术荧光检测观察其对MDR细胞膜糖粘蛋白P170、细胞凋亡及其相关因子Fas、Trail和细胞黏附因子CD54的影响。结果苦参碱抑制P170表达、增加对细胞凋亡因子Fas、Trail表达率,促进耐药S180细胞的凋亡,降低细胞黏附因子CD54的表达。结论说明苦参碱逆转肿瘤获得性多药耐药与对肿瘤多种相关生物分子因子的调节有关。临床可以根据肿瘤多药耐药的性质,通过调节多药耐药相关因子逆转肿瘤化疗耐药性,提高临床化疗疗效。 | 李宏建 李贵海 孙付军 尹格平 | 2005 | 中国医院药学杂志2005，25，5： | 13 |
| 17 | 巴豆生物碱上调TRAIL配体、caspase-8的表达诱导HeLa细胞凋亡的体外研究显示文摘目的研究巴豆生物碱对人宫颈HeLa细胞诱导凋亡作用,并探讨其作用机制。方法 MTT法观察巴豆生物碱对HeLa细胞的抑制率;流式细胞仪检测HeLa细胞TRAIL及其受体DR5的表达及其巴豆生物碱对HeLa细胞TRAIL配体表达的影响;Caspase-8活性检测;RT-PCR检测TRAIL配体及Caspase-8、Caspase-3 mRNA的表达。结果巴豆生物碱对HeLa细胞生长有抑制作用,且呈剂量依赖关系。流式细胞仪检测HeLa细胞TRAIL及其受体DR5的表达阳性,巴豆生物碱处理HeLa细胞后发现TRAIL配体的表达明显上调,Caspase-8活性明显增加,TRAIL配体、Caspase-3及Caspase-8 mRNA高表达。结论巴豆生物碱对人宫颈癌HeLa细胞有增殖抑制和诱导细胞凋亡的作用,其诱导机制可能与上调TRAIL配体和Caspase-8mRNA的表达有关。 | 许群 方轶萍 赵小迎 蔡平生 | 2011 | 海峡药学2011，23，2： | 13 |
| 18 | 肿瘤坏死因子家族新成员——TRAIL显示文摘肿瘤坏死因子相关的凋亡诱导配体(TRAIL)或称凋亡素2配体(Apo2ligand,Apo2L),是TNF家族的新成员.它是从表达序列标签库(expressedsequencedtag,EST)中寻找TNF的同源分子时发现的.TRAIL是一种分子质量为325ku的Ⅱ型跨膜糖蛋白,活性形式呈同源三聚体.TRAIL和可溶性的TRAIL强烈诱导肿瘤细胞株凋亡.新近发现的TRAIL受体DR4和DR5及TRID说明了TRAIL与TNF和Fas/Apo1配体的作用途径是不同的.随着对TRAIL的受体及作用机理研究的深入,TRAIL很可能成为新一代抗肿瘤制剂. | 王梁华 焦炳华 | 1998 | 生物化学与生物物理进展1998，25，5： | 11 |
| 19 | 婴幼儿血管瘤及血管畸形组织中p16及TRAIL的表达及其意义显示文摘目的 检测婴幼儿血管瘤组织中抑癌基因 p1 6及肿瘤坏死因子相关凋亡诱导配体(TRAIL)的表达 ,并探讨它们在血管瘤增生、消退过程中的作用。方法 采用免疫组化SP法检测 32例增生期、2 0例消退期血管瘤及 1 4例血管畸形组织中p1 6和TRAIL的表达。结果 p1 6在增生期和消退期血管瘤组织中阳性表达率分别为 78.1 % (2 5/ 32 )、90 .0 % (1 8/ 2 0 ) ,血管畸形组织中全部为阴性。经秩和检验 :Hc=2 6 .6 ,三者之间差异存在显著性意义 (P <0 .0 1 ) ,两者之间差异有显著性意义(P <0 .0 5)。TRAIL在增生期和消退期血管瘤组织中阳性表达率分别为 2 1 .9% (7/ 32 )、80 .0 % (1 6/2 0 ) ,血管畸形中全部为阴性 ,卡方检验 :χ2 =2 7.8,三者之间差异存在显著性意义 (P <0 .0 1 ) ,两两之间比较经 χ2 分割 ,增生期与消退期之间有差异 (P <0 .0 5) ,消退期与血管畸形之间有差异 (P <0 .0 5) ,增生期与血管畸形之间无差异 (P >0 .0 5) ,血管瘤与血管畸形之间有差异。结论 p1 6和TRAIL的表达水平与血管瘤的增生、消退有关 ,p1 6可抑制内皮细胞的分裂增殖 ,TRAIL可通过诱导内皮细胞凋亡发挥作用 。 | 黄莺 王康敏 康安静 靳耀锋 李恭才 | 2003 | 中华小儿外科杂志2003，24，1： | 11 |
| 20 | 宫颈病变中凋亡调控基因TRAIL及Caspase-3表达与HPV感染的相关性研究显示文摘目的探讨凋亡调控基因TRAIL及Caspase-3在宫颈病变组织中的表达,及其与HPV16/18感染的相关性。方法收集正常宫颈组织(NE)20例,宫颈上皮肉瘤样病变-低度(CIN-L)25例,上皮肉瘤样病变-高度(CIN-H)25例,宫颈鳞状细胞癌组织(SCC)30例,采用免疫组化对各宫颈组织石蜡标本进行TRAIL及Caspase-3的检测,同时采用PCR技术检测HPVI6/18感染情况。结果 TRAIL、Caspage-3在NE组、CIN-L组、CIN-H组和SCC组中的阳性表达率均呈逐渐递减趋势,TRAIL在各组间差异有统计学意义(P<0.05),CIN-H组和SCC组中Caspage-3阳性表达率均明显低于NE组和CIN-L组(P<0.01),HPV16/18在NE组、CIN-L组、CIN-H组和SCC组中的阳性表达率分呈逐渐升高,各组间差异有统计学意义(P<0.05),TRAIL阳性表达率与组织分化程度密切相关,Caspase-3阳性表达与宫颈癌临床分期及组织学分级密切相关,差异有统计学意义(P<0.05),HPV16/18基因的表达阳性率与HPV16/18基因的表达阳性率与SCC的临床病理特征均无关。结论 TRAIL和Caspase-3低表达与宫颈癌的发生有关,且TRAIL和Caspase-3的低表达和HPV16/18感染,在宫颈癌发生发展过程中起协同作用。 | 贾万钧 曹学全 甘梅富 张亚斌 | 2011 | 中华医院感染学杂志2011，21，22： | 11 |
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