WNT10A在肾细胞癌组织中的表达及意义

目的 探讨Wnt信号通路分子WNT10A在肾细胞癌(RCC)发生、发展中的作用.方法 选择50例RCC患者的手术标本(RCC组,其中肾透明细胞癌38例、非透明细胞癌12例,临床病理分期Ⅰ期14例、Ⅱ期13例、Ⅲ期13例、Ⅳ期10例);取其癌旁组织标本作为癌旁组;另选15例因外伤、输尿管癌行肾切除术患者的正常肾组织标本作为对照组.采用Real-time RT-PCR法检测各组WNT10A表达,比较不同病理类型及病理分期组织中WNT10A表达的差异.结果 RCC组WNT10A表达量高于癌旁组、对照组(P＜0.01).透明细胞癌组织中WNT10A mRNA的表达量高于非透明细胞癌(P＜0.05).肾癌组织中WNT10A mRNA的表达随病理分期升高呈升高趋势.结论 WNT10A mRNA在RCC中的表达量随病理分期的增高而增高,且在肾透明细胞癌组织中的表达量高于非透明细胞癌.WNT10A mRNA表达可作为诊断RCC的指标.     

肾癌组织中CapG蛋白的表达变化及临床意义

目的观察肾透明细胞癌（肾癌）组织中CapG蛋白的表达变化,并探讨其意义。方法选取132例肾癌标本（观察组）及40例癌旁正常肾组织标本（对照组）,采用免疫组化SP法检测CapG蛋白的表达。结果对照组CapG蛋白阳性表达率为7.5%,明显低于观察组的56.1%,P〈0.001。观察组CapG蛋白表达与淋巴结转移和预后有关（P均〈0.05）,与患者年龄、性别、T分期、病理分级、复发转移无显著相关（P均〉0.05）。结论肾癌组织中CapG蛋白表达上调。其与肾癌的转移和预后有关。     

肾细胞癌及癌旁组织中TIP30蛋白的表达及临床意义

目的 探讨肾细胞癌组织中Tat结合蛋白(TIP30)的表达及其临床意义.方法 采用S-P免疫组织化学染色法对65例肾细胞癌组织及其癌旁组织中TIP30蛋白表达进行检测.同时采用Western印迹方法检测22例肾细胞癌及其癌旁新鲜标本中TIP30蛋白的表达.结果 免疫组化结果显示,TIP30蛋白阴性表达率在肾癌组中为49.2%(32/65),显著高于癌旁组织[10.8% (7/65)](P＜0.01)差异有统计学意义;TIP30蛋白的阴性表达在肾癌各病理类型中差异无统计学意义(P＞0.05);TIP30蛋白在肾细胞癌中的阴性表达与浸润程度(P＜0.01)、淋巴结转移(P＜0.05)以及肾静脉癌栓有关(P＜0.05).Western印迹结果显示在77.3%(17/22)的肾细胞癌组织中有TIP30蛋白低表达.结论 TIP30蛋白的阴性表达与肾细胞癌发生、发展有关;作为抑癌基因产物,TIP30蛋白可在蛋白质水平为临床估计病情及预后提供一个有意义的客观指标.     

葡萄糖转运因子1蛋白在肾癌组织中的表达及意义

目的探讨葡萄糖转运因子1(Glut-1)蛋白在肾透明细胞癌发生、发展中的作用。方法采用免疫组化法检测50份肾透明细胞癌和10份同期距肾癌组织5 cm远的正常肾组织标本中Glut-1蛋白表达。结果 Glut-1蛋白在正常肾组织中无表达,在肾透明细胞癌组织中表达显著增强,阳性表达率为100%,但Glut-1表达与肾癌分级、分期无关。结论 Glut-1在肾癌组织中呈高表达,可能是参与肾癌发生的一个早期指标。     

Six1基因在肺癌组织表达水平及RNA干扰抑制其表达后对肺癌细胞生物学特性的影响

目的探讨Six1基因在肺癌组织表达及抑制其表达后对肺癌细胞增殖凋亡的影响。方法提取肺癌及癌旁组织蛋白,Western印迹检测Six1的表达; Six1-siRNA转染人肺癌A549细胞,分为空白组和阴性对照组(NC组)、Six1-siRNA组,转染48 h后通过Western印迹检测各组细胞Six1的表达; CCK8检测Six1-siRNA转染A549细胞24～72 h的细胞增殖;流式细胞术检测转染48 h的细胞凋亡率; Western印迹检测增殖相关蛋白细胞增殖核抗原(PCNA)、B细胞淋巴瘤/白血病-2(Bcl-2)家族Bcl-2相关X蛋白(Bax)及Notch1信号通路Notch1和Hes1的蛋白表达。结果 Six1在肺癌组织中的表达显著高于癌旁组织(P<0. 05); Six1-siRNA转染能明显降低A549细胞Six1的表达;与空白组比较,Six1-siRNA组细胞24～72 h的细胞增殖均显著降低,在48 h的细胞凋亡率显著升高,PCNA、Notch1和Hes1蛋白表达均显著降低,Bax蛋白表达显著升高(P<0. 05)。结论 Six1在肺癌组织中高表达,通过RNA干扰抑制其表达可通过下调Notch1信号通路降低肺癌细胞增殖及诱导细胞凋亡,对细胞增殖凋亡的影响方式是下调PCNA和上调Bax蛋白表达。     

肾透明细胞癌组织中Id4因子的表达变化及意义

目的观察分化抑制因子4（Id4因子）在肾透明细胞癌组织中的表达,并探讨其临床意义。方法采用免疫组化法检测30例肾透明细胞癌（肾癌组）、10例癌旁（癌旁组）和10例正常肾组织（正常组）中Id4因子,并分析其与肾透明细胞癌病理分级、临床分期的关系。结果肾癌组Id4因子阳性表达率为70％,明显高于癌旁组的30％和正常组的20％（P均〈0．05）;Id4因子的阳性表达率随肾透明细胞癌病理分级、TNM分期的增高而增加,但P〉0．05。结论Id4因子在肾透明细胞癌的组织中表达增强,可能在本病的发病机制中起重要作用。     

肾透明细胞癌组织中CD_（40）、Caspase-7蛋白的表达变化及意义

目的观察肾透明细胞癌组织中CD40和Caspase-7蛋白的表达变化,并探讨其临床意义。方法采用免疫组化法分别检测41例肾透明细胞癌、21例癌旁组织和6例正常肾组织中CD40和Caspase-7蛋白,并分析两者与肿瘤临床分期、病理分级的关系。结果肾癌组中CD40阳性表达率达61.0%（25/41）,显著高于癌旁组9.5%（2/21）和对照组0（0/6）,P均〈0.05;同时CD40的阳性表达率随临床分期及病理分级进展而显著升高,P均〈0.05。肾癌组中Caspase-7阳性表达率为51.2%（21/41）,显著低于癌旁组85.7%（18/21）和对照组83.3%（5/6）的表达率,P均〈0.05。同时Caspase-7的阳性表达率随临床分期及病理分级进展而显著降低,P均〈0.05。结论肾透明细胞癌组织中CD40表达上调,Caspase-7表达下调。二者可能在肾透明细胞癌的发生发展过程中发挥一定作用。     

细胞周期素D1在大肠癌中的表达及意义

目的：探讨细胞周期素D1（CD1）与大肠癌的发生、进展及预后的关系。方法：收集24例手术切除的大肠癌标本,同时取距癌灶5cm以外的癌旁组织及10cm以外的正常组织,用原位杂交的方法检测癌组织、癌旁组织及正常组织中CD1mRNA的表达,同时结合临床病理资料进行分析。结果：24例大肠癌组织中CD1mRNA阳性9例,阳性率37．5％;癌旁组织仅有1例阳性,阳性率4．2％;正常组织未见阳性表达。癌旁组织和正常组织均与癌组织有显著性差异（P＜0．01）。CD1mRNA的表达在浸润至浆膜层组明显高于浸润至肌层组（P＜0．05）;有淋巴结转移组及晚期病变（Dukes B C D期）组亦明显高于无淋巴结转移及早期病变（Dukes A期）组（P＜0．05）。CD1mRNA的表达高低与年龄、性别、癌灶直径大小、分化程度及是否有远处转移无明显关系（P＞0．05）。结论：CD1mRNA过度表达与大肠癌的发生、发展及转移有关。     

非小细胞肺癌组织及癌旁组织VEGF、P16蛋白的表达及意义

目的分析P16蛋白、血管内皮生长因子(VEGF)在非小细胞肺癌(NSCLC)组织及癌旁组织的表达情况。方法应用免疫组化SP法检测NSCLC组织65例,距肿瘤边缘5 cm以上癌旁正常组织20例中VEGF、P16蛋白的表达。结果①VEGF在肺癌组织的阳性表达率72.3%,明显高于癌旁组织的阳性表达率35.0%(P<0.05);P16蛋白在肺癌组织的阳性表达率47.7%,明显低于癌旁组织的阳性表达率85.0%(P<0.05)。②P16蛋白的表达与肺癌淋巴结转移、临床分期、分化程度有关,而与病理类型无关;VEGF的表达与临床分析、淋巴结转移有关。NSCLC组织中P16蛋白与VEGF之间呈负相关(rs=-0.537,P<0.01)。结论 NSCLC组织中存在VEGF与P16蛋白表达的异常,且两者表达呈负相关,推测NSCLC的发病与血管生成及P16表达异常有关。     

胰腺癌p57kip2、视网膜母细胞瘤蛋白和增殖细胞核抗原的表达及与临床病理的关系

目的探讨细胞周期蛋白依赖性激酶抑制因子p57kip2,视网膜母细胞瘤蛋白(Rb)和增殖细胞核抗原(PCNA)在胰腺癌发生发展中的作用.方法应用免疫组化技术,对32例胰腺癌及癌旁组织中p57kip2、Rb蛋白和PCNA表达进行检测.结果 p57kip2蛋白阳性表达率在胰腺癌组织中为46.9%,显著低于癌旁胰腺组织的75.0%(χ2=5.317,P < 0.05),并与胰腺癌组织分化程度有关(P < 0.05),而与淋巴结转移无关(P > 0.05).Rb蛋白阳性表达率在胰腺癌组织中为50%,显著低于癌旁胰腺组织的78.1%(χ2=5.497, P < 0.05).PCNA阳性表达率在胰腺癌组织中为71.9%,显著高于癌旁胰腺组织的43.8%(χ2=5.189, P < 0.05),并与胰腺癌组织分化程度和淋巴结转移均有关(P < 0.05) .p57kip2蛋白阳性表达组Rb蛋白阳性表达率为53.3%;p57kip2蛋白阴性表达组Rb蛋白阳性表达率为47.1%,两组间无相关性(γ=0.16507, P ＞ 0.05).结论 p57kip2、Rb蛋白低表达和PCNA蛋白过度表达与胰腺癌的发生发展有关.     

妊娠时间与肺结核复发的相关性研究及诊治对策

目的 分析肺结核史患者妊娠时间和肺结核复发间相关性.方法 选取我院收治的有肺结核史的妊娠妇女576例作为研究对象,对其妊娠前肺结核治疗、治愈后妊娠时间、妊娠后复发肺结核等进行分析,总结有肺结核史育龄女性的妊娠时间和肺结核复发之间的关系.结果 肺结核治愈后不同时间段妊娠者的结核复发率比较,差异具有显著性（P＜0.05）,停药后间隔时间越久妊娠,肺结核复发的几率越小.结论 加强孕期痰菌检查,及早发现复发肺结核,提高母婴安全.     

我国骨关节结核诊治的回顾与展望

骨关节结核是危害人们健康的严重感染性疾病,近95％由他处结核病继发而来.罹患骨关节结核疾病后几乎均将致残,严重影响人们的健康、工作和生活.建国以来在党和国家的关心和支持下,骨关节结核的诊治水平取得了长足进步.时至今日,由于多种原因,学科发展和被重视程度受到一定的制约,同整个医疗行业的发展不相适应.回顾过去,展望未来,我们需要重新审视骨关节结核的诊治方法,努力推进骨关节结核诊疗技术的科学发展.     

Effect of phosphorylation of MAPK and Stat3 and expression of c-fos and c-jun proteins on hepatocarcinogenesis and their clinical significance

AIM To study the effect of phosphorylation ofMAPK and Stat3 and the expression of c-fos andc-jun proteins on hepatocellular carcinogenesisand their clinical significance.METHODS SP immunohistochemistry was usedto detect the expression of p42/44~(MAPK), p-Stat3,c-fos and c-jun proteins in 55 hepatocellularcarcinomas (HCC) and their surrounding livertissues.RESULTS The positive rates and expressionlevels of p42/44~(MAPK), p-Stat3, c-fos and c-junproteins in HCCs were significantly higher thanthose in pericarcinomatous liver tissues (PCLT).A positive correlation was observed between theexpression of p42/44~(MAPK) and c-fos proteins, andbetween p-Stat3 and c-jun, but there was nosignificant correlation between P42/44~(MAPK) and p-Stat3 in HCCs and their surrounding livertissues.CONCLUSION The abnormalities of Ras/Raf/MAPK and JAKs/ Stat3 cascade reaction maycontribute to malignant transformation ofhepatocytes. Hepatocytes which are positive forp42/ 44~(MAPK), c-fos or c-jun proteins may bepotential malignant pre-cancerous cells.Activation of MAPK and Stat3 proteins may be anearly event in hepatocellular carcinogenesis.     

Overweight and Obesity and Progression of ADPKD

Open in a separate window     

Replication and Inhibitors of Enteroviruses and Parechoviruses

The Enterovirus (EV) and Parechovirus genera of the picornavirus family include many important human pathogens, including poliovirus, rhinovirus, EV-A71, EV-D68, and human parechoviruses (HPeV). They cause a wide variety of diseases, ranging from a simple common cold to life-threatening diseases such as encephalitis and myocarditis. At the moment, no antiviral therapy is available against these viruses and it is not feasible to develop vaccines against all EVs and HPeVs due to the great number of serotypes. Therefore, a lot of effort is being invested in the development of antiviral drugs. Both viral proteins and host proteins essential for virus replication can be used as targets for virus inhibitors. As such, a good understanding of the complex process of virus replication is pivotal in the design of antiviral strategies goes hand in hand with a good understanding of the complex process of virus replication. In this review, we will give an overview of the current state of knowledge of EV and HPeV replication and how this can be inhibited by small-molecule inhibitors.     

Effect of phosphorylation of MAPK and Stat3 and expression of c-fas and c-jun proteins on hepatocarcinogenesis and their clinical significance

AIM To study the effect of phosphorylation ofMAPK and Stat3 and the expression of c-fos andc-jun proteins on hepatocellular carcinogenesisand their clinical significance.METHODS SP immunohistochemistry was usedto detect the expression of p42/44MAPK, p-Stat3,c-fos and c-jun proteins in 55 hepatocellularcarcinomas (HCC) and their surrounding livertissues.RESULTS The positive rates and expressionlevels of p42/44MAPK, p-Stat3, c-fos and c-junproteins in HCCs were significantly higher thanthose in pericarcinomatous liver tissues (PCLT).A positive correlation was observed between theexpression of p42/44MAPK and c-fos proteins, andbetween p-Stat3 and c-jun, but there was nosignificant correlation between p42/44MAPK and p-Stat3 in HCCs and their surrounding livertissues.CONCLUSION The abnormalities of Ras/Rat/MAPK and JAKs/ Stat3 cascade reaction maycontribute to malignant transformation ofhepatocytes. Hepatocytes which are positive forp42/ 44MAPK, c-fos or c-jun proteins may bepotential malignant pre-cancerous cells.Activation of MAPK and Stat3 proteins may be anearly event in hepatocellular carcinogenesis.     

心电图、心电向量图与冠状动脉造影结果对比分析

目的:通过分析心电图(Electrocardiogram,ECG)和心电向量图(Vectorcardiogram,VCG)的改变与冠脉造影（CAG）结果进行对比,探讨ECG、VCG在冠状动脉病变中的诊断价值。方法: 选择2008年1月~2009年12月临床拟诊断为冠心病患者108例,行常规ECG、VCG检查,并于1周内进行CAG,对检查结果依据各自的诊断标准进行判定,以CAG为标准诊断法,利用四格表法,计算相关评价真实性的指标并进行比较。结果: ①VCG检测的灵敏度、特异度、准确度显著高于ECG(P<0.05,P<0．01)。②ECG、VCG阳性率与冠脉病变支数组间比较:在单支病变、双支病变中,VCG阳性率明显高于ECG(P<0.05),左主干或三支病变无统计学意义;组内比较:ECG组左主干或三支病变组较单支病变、双支病变阳性率高(P<0.05,P<0.01);VCG组左主干或三支病变组较单支病变阳性率高(P<0.05);与双支病变阳性率比较无统计学意义;③ECG、VCG阳性率与冠脉病变程度组间比较:冠脉病变狭窄50%～69%的VCG阳性率明显高于ECG (P<0.05),其他两组阳性率比较无统计学意义;组内比较:ECG组冠脉病变狭窄≥90%较50%～69%、70%～89%的阳性率高(P<0.05,P<0.01); VCG组狭窄≥90%较50%～69%阳性率高（P<0.01),其他无统计学意义。结论: VCG对冠心病检测价值显著高于ECG。     

Detection and characterization of the product of hydroethidine and intracellular superoxide by HPLC and limitations of fluorescence

Here we report the structural characterization of the product formed from the reaction between hydroethidine (HE) and superoxide (O(2)(.-)). By using mass spectral and NMR techniques, the chemical structure of this product was determined as 2-hydroxyethidium (2-OH-E(+)). By using an authentic standard, we developed an HPLC approach to detect and quantitate the reaction product of HE and O(2)(.-) formed in bovine aortic endothelial cells after treatment with menadione or antimycin A to induce intracellular reactive oxygen species. Concomitantly, we used a spin trap, 5-tert-butoxycarbonyl-5-methyl-1-pyrroline N-oxide (BMPO), to detect and identify the structure of reactive oxygen species formed. BMPO trapped the O(2)(.-) that formed extracellularly and was detected as the BMPO-OH adduct during use of the EPR technique. BMPO, being cell-permeable, inhibited the intracellular formation of 2-OH-E(+). However, the intracellular BMPO spin adduct was not detected. The definitive characterization of the reaction product of O(2)(.-) with HE described here forms the basis of an unambiguous assay for intracellular detection and quantitation of O(2)(.-). Analysis of the fluorescence characteristics of ethidium (E(+)) and 2-OH-E(+) strongly suggests that the currently available fluorescence methodology is not suitable for quantitating intracellular O(2)(.-). We conclude that the HPLC/fluorescence assay using HE as a probe is more suitable [corrected] for detecting intracellular O(2)(.-).     

Effects of sex and time of day on metabolism and excretion of corticosterone in urine and feces of mice

Non-invasive techniques to monitor stress hormones in small animals like mice offer several advantages and are highly demanded in laboratory as well as in field research. Since knowledge about the species-specific metabolism and excretion of glucocorticoids is essential to develop such a technique, we conducted radiometabolism studies in mice (Mus musculus f. domesticus, strain C57BL/6J). Each mouse was injected intraperitoneally with 740 kBq of 3H-labelled corticosterone and all voided urine and fecal samples were collected for five days. In a first experiment 16 animals (eight of each sex) received the injection at 9 a.m., while eight mice (four of each sex) were injected at 9 p.m. in a second experiment. In both experiments radioactive metabolites were recovered predominantly in the feces, although males excreted significantly higher proportions via the feces (about 73%) than females (about 53%). Peak radioactivity in the urine was detected within about 2h after injection, while in the feces peak concentrations were observed later (depending on the time of injection: about 10h postinjection in experiment 1 and about 4h postinjection in experiment 2, thus proving an effect of the time of day). The number and relative abundance of fecal [3H]corticosterone metabolites was determined by high performance liquid chromatography (HPLC). The HPLC separations revealed that corticosterone was extensively metabolized mainly to more polar substances. Regarding the types of metabolites formed, significant differences were found between males and females, but not between the experiments. Additionally, the immunoreactivity of these metabolites was assessed by screening the HPLC fractions with four enzyme immunoassays (EIA). However, only a newly established EIA for 5alpha-pregnane-3beta,11beta,21-triol-20-one (measuring corticosterone metabolites with a 5alpha-3beta,11beta-diol structure) detected several peaks of radioactive metabolites with high intensity in both sexes, while the other EIAs showed only minor immunoreactivity. Thus, our study for the first time provides substantial information about metabolism and excretion of corticosterone in urine and feces of mice and is the first demonstrating a significant impact of the animals' sex and the time of day. Based on these data it should be possible to monitor adrenocortical activity non-invasively in this species by measuring fecal corticosterone metabolites with the newly developed EIA. Since mice are extensively used in research world-wide, this could open new perspectives in various fields from ecology to behavioral endocrinology.     

大鼠骨髓间充质干细胞的分离培养和外源基因的导入

目的探讨绿色荧光蛋白基因转染骨髓间质干细胞的可行性。方法采用F icoll-PaqueTMP lus淋巴细胞分离液,根据细胞密度梯度原理,分离大鼠骨髓间充质干细胞(rM SC s)并进行体外原代培养和传代扩增,倒置相差显微镜观察细胞生长情况,免疫细胞化学法对其初步鉴定。流式细胞仪分析转染效率。结果原代和传代培养的细胞呈现梭形外观,具有较强的生长增殖能力;细胞均一表达CD44、CD54、CD106、CD29抗原。电穿孔法转染rM SC s转染率为32.8%±3%。结论采用比重为1.077 g/L的F icoll-PaqueTMP lus能分离获得大鼠骨髓间充质干细胞,经原代培养和传代培养能够迅速扩增。电穿孔法具有较高的介导外源基因表达于rM SC s的效率。