VEGF、TGF-β1、NF-κBp65在颅内海绵状血管瘤的表达及意义

目的探讨脑海绵状血管瘤（CCH）组织血管内皮细胞生长因子（VEGF）、转化生长因子β1（TGF-β1）、核转录因子κBp65（NF-κBp65）的表达及意义。方法收集我院2009年6月到2011年12月CCH标本27例,脑动静脉畸形（AVM）标本9例和正常脑组织标本（颅脑损伤或癫痫术中切取的脑组织）6例,用免疫组化方法检测VEGF、TGF-β1、NF-κBp65的表达。结果CCH组织VEGF、NF-κBp65阳性表达率（分别是96．3％和70．4％）显著高于正常脑组织（分别为33．3％和0;P〈0．05）,而与脑AVM组织（分别是77．8％和44．4％）无显著差异（P〉0．05）;脑AVM组织TGF-β1表达阳性率（100％）显著高于CCH组织（33.3％,P〈0．05）和正常脑组织（16．7％,P〈0．05）。结论VEGF、TGF-β1、NF-κBp65在不同组织表达水平不一样,提示VEGF、NF-κBp65与CCH形成有关,而TGF-β1可能在其形成过程中意义不大。     

The role of microRNA profiling in prognosticating progression in Ta and T1 urinary bladder cancer

ObjectiveTo analyze microRNA profile in Ta and T1 urinary bladder cancers in combination and separately and to relate this to the risk of later developing higher-stage disease.Materials and methodsFormalin-fixed, paraffin-embedded samples of 44 Ta and 42 T1 bladder cancers representing cases with and without stage progression during follow-up were collected and microRNA expression levels were measured by microarray analysis.ResultsIn a comparison between the progressors and controls, in the Ta/T1 group, miR-10a-5p and miR-31-5p were differentially expressed. miR-10a-5p was also correlated to time to progression (P = 0.00012). In the subgroup analysis, 3 microRNAs, miR-10a-5p, miR-31-5p, and miR-130a-3p, were differentially expressed among Ta tumors and had a fold change of more than 1.5 (P<0.038). The comparison concerning microRNA expression between the progressors and controls in category T1 cancers revealed no significant differences.ConclusionsProfiling revealed that certain microRNAs predicted the risk of developing higher-stage disease among patients with Ta cancers. Lower miR-10a-5p expression in Ta progressing tumors indicates that this microRNA could be important for later malignant potential among this group of patients.     

血管生成因子在子宫内膜异位症组织中的表达及相关研究

目的：探究表皮生长因子（EGF）、成纤维细胞生长因子（FGF）、肿瘤坏死因子（TNF‐α）和血管内皮生长因子（VEGF）在子宫内膜异位症组织中的表达情况,并探讨其在子宫内膜异位症的发病机制。方法选取45例子宫内膜异位症患者和45例正常子宫内膜患者作为观察组和对照组,采用免疫组化S P法检测观察组患者的在位内膜、异位内膜及对照组正常子宫内膜组中EG F、FG F、TNF‐α和VEGF的表达情况,并进行相关性分析。结果观察组患者在位内膜、异位内膜中 EGF、FGF的阳性率以及观察组TNF‐α和VEGF的灰度值均高于正常对照组（P＜0．05）,且观察组异位内膜中EGF及FGF的阳性率也较在位内膜组高。结论 EGF、FGF、TNF‐α和VEGF在子宫内膜异位症组织中呈较高表达,与子宫内膜异位的血管生成有较高的相关性。     

NGF调控RSV感染大鼠IL-17的表达变化

目的：探讨IL-17在RSV感染大鼠中的表达变化及神经生长因子（NGF）对其调控效应。方法1周龄SD雄性乳鼠共30只,区组随机均分为对照组、RSV感染组和抗NGF抗体组,每组10只。 RSV感染组采用每周1次RSV滴鼻法复制RSV感染模型。抗NGF抗体组先腹膜腔内注射山羊抗大鼠β-NGF抗体,3h后按照RSV感染组相同的方法进行RSV感染。第8周对3组大鼠进行ELISA 检测血清NGF 和IL-17浓度变化并对3组大鼠 NGF 和 IL-17浓度行相关性分析。结果ELISA结果显示：与对照组相比,RSV组血清NGF浓度显著升高（P〈0.05）,抗体组和对照组血清NGF浓度无明显变化。与对照组相比,RSV组血清IL-17显著增高（P〈0.05）,而抗体组与对照组血清IL-17无显著变化。血清NGF蛋白水平与血清IL-17蛋白水平呈正相关（r=0.739,P〈0.01）。结论 IL-17参与RSV感染大鼠发病过程,NGF升高可促进IL-17分泌并促进炎症反应的发生。     

Upregulation of microRNA-93-5p/microRNA-4668-5p,and promoter methylation of matrix metalloproteinase-3 and interleukin-16 genes in Turkish patients with rheumatoid arthritis

Aim of the workTo investigate promoter methylation of matrix metalloproteinase-3 (MMP-3) and interleukin-16 (IL-16) genes with the expression of miRNA-93-5p and miRNA-4668-5p which target these genes in rheumatoid arthritis (RA), respectively.Patients and methodsThe study included 49 RA patients and 38 healthy controls. Promoter methylation of MMP-3 and IL-16 was analyzed by methylation-specific PCR. The expression of miRNA-93-5p and miRNA-4668-5p were determined. Disease activity score (DAS28) was assessed.ResultsThe 49 patients (38 female, 11 male) mean age was 50.4 ± 10.5 years and disease duration of 9.1 ± 7.4 years. The mean DAS28 was 3.9 ± 1.4. The MMP-3 gene methylation frequency was significantly lower in patients (n = 37;75.5%) compared to control (n = 37;97.4%) (p = 0.004) while they were comparable for IL-16 gene (n = 46;93.9% vs n = 37;97.4%)(p = 0.45). The relative normalized expression of miRNA-93-5p and miRNA-4668-5p were significantly increased (p < 0.001) in patients (2.28 ± 3.71 and 2.47 ± 4.17-fold) compared to controls (1.12 ± 0.18 and 1.28 ± 0.53-fold) and both tended to decrease with high disease activity (r =  ? 0.104, p = 0.52; r = ?0.24, p = 0.15, respectively). There was no significant difference of miRNA-93-5p (p = 0.45), and miRNA-4668-5p (p = 0.26) expressions between patients receiving treatment and those not. A negative correlation was observed between disease activity and change in expression levels of miRNA-93-5p (r = ?0.104, p = 0.52) and miRNA-4668-5p (r = ?0.24, p = 0.15). The ROC curve analysis of target miRNAs showed the diagnostic potential of miRNA-93-5p and miRNA-4668-5p (p = 0.003 and p < 0.001 respectively).ConclusionsThe methylation status of MMP-3 promoter and expression levels of miRNA-93-5p and miRNA-4668-5p could be useful biomarkers for the pathogenesis of RA and might reflect disease activity.     

Role of miR-511 in the Regulation of OATP1B1 Expression by Free Fatty Acid

MicroRNAs (miRNAs) are a family of non-coding RNA that are able to adjust the expression of many proteins, including ATP-binding cassette transporter and organic cation transporter. We sought to evaluate the effect of miR-511 on the regulation of OATP1B1 expression by free fatty acids. When using free fatty acids to stimulate Chang liver cells, we found that the expression of miR-511 increased significantly while the expression of OATP1B1 decreased. We also proved that SLCO1B1 is the target gene of miR-511 with a bioinformatics analysis and using the dual luciferase reporter assay. Furthermore, the expressions of SLCO1B1 and OATP1B1 decreased if transfecting Chang liver cells with miR-511, but did not increase when transfecting the inhibitors of miR-511 into steatosis cells. Our study indicates that miR-511 may play an important role in the regulation of OATP1B1 expression by free fatty acids.     

人周围血单核细胞载脂蛋白E基因表达的竞争性逆转录-聚合酶链反应定量分析

为建立人周围血单核细胞载脂蛋白E基因表达检测方法,研究载脂蛋白E基因与儿童健康的关系,我们抽取26例健康儿童外周静脉血,分离血单核细胞,抽提RNA,采用逆转录-聚合酶链式反应检测载脂蛋白E基因表达,并以正常人cDNA作定量标准物,待测样品与定量标准物共扩增,计算出待测样本的个体的mRNA量.研究发现载脂蛋白E基因能在健康儿童周围血单核细胞表达,健康儿童载脂蛋白E基因表达量为0.37±0.15 mol/mol mRNA.表明采用竞争性逆转录-聚合酶链反应方法来检测人周围血单核细胞载脂蛋白E基因表达的分析方法快速、简便、灵敏、实用、可靠,且能准确定量,值得推广应用.     

细小病毒H-1诱导胃癌细胞死亡分子机制的基因表达谱研究

背景：自主性细小病毒H—1在活体组织中具有肿瘤抑制活性，并且在细胞培养中能特异地干扰转化细胞或肿瘤细胞的生存，但其诱导转化细胞死亡的分子机制尚不十分清楚。目的：研究细小病毒H—1诱导人胃癌细胞株HGC—27死亡时HGC—27细胞基因表达的变化，进而为阐明细小病毒H—1的抗肿瘤机制奠定基础。方法：采用四唑蓝(MTT)比色法分析HGC—27细胞在感染细小病毒H—1后不同时间点的存活率；分别收集纯化细小病毒H—1感染前和感染48h后HGC—27细胞的mRNA，应用基因表达谱芯片技术研究HGC—27细胞感染细小病毒H—1后的基因表达变化。结果：HGC—27细胞从感染细小病毒H—1后的第3天开始，细胞存活率呈明显下降趋势；感染细小病毒H—148h后，基因表达谱发生了明显的变化，表达改变基因约占被检测基因的11.5％(920／8000)，363对基因的表达明显下调，557对基因的表达明显上调。其中与细胞信号传导、细胞周期、细胞凋亡相关的部分基因表达改变与细小病毒H—1诱导的细胞死亡通路相关；而与DNA合成和修复、代谢以及蛋白质合成相关的部分基因表达改变可能与细胞对外界刺激的防御反应相关。结论：细小病毒H—1诱导人胃癌HGC—27细胞死亡的过程是以一种细胞依赖的方式进行的，并涉及细胞中多个促进死亡的信号传导通路。细小病毒H—1诱导胃癌细胞死亡以及胃癌细胞自身防御反应中所展示的基因表达差异谱，为研究细小病毒H—1抗肿瘤作用的分子机制提供了初步的线索。