男性非淋菌性尿道炎患者支原体对抗菌药物的敏感性

目的:了解支原体在男性非淋菌性尿道炎(NGU)的作用和体外对药物敏感性。方法:对864例疑为NGU的男性患者泌尿生殖道标本进行了支原体型别鉴定,用微量肉汤稀释法对支原体进行9种抗菌药物的敏感性测定。结果:272例(31.4%)支原体培养阳性,其中解脲支原体(Uu)176例,人型支原体(Mh)9例;Uu Mh混合感染87例。97.2%的支原体对9种抗菌药物有不同程度的耐药。Uu Mh混合感染的耐药率明显高于单纯Uu感染。结论:Uu Mh混合感染耐药性升高并发生耐药谱变化。对支原体的定期耐药性监测,对临床用药有重要指导意义。     

挥发性有机物引起荨麻疹机制的实验研究

目的探讨挥发性有机物(VOC)诱发慢性荨麻疹的发病机制。方法以36只Wistar大鼠为研究对象,采用大气采样机采取混有VOC的空气样本,作用于大鼠长期接触组(VOCL组),3个月后再取尘螨、蟑螂、蚕丝变应原液注射于大鼠,观察皮肤及胸腺组织改变。并与双蒸水组、短期接触组(VOCS组)对照。结果VOCL组真皮浅层水肿,可见炎性细胞浸润,同时可见少数嗜酸性粒细胞,其胸腺组织CD4,CD8阳性表达细胞减少,阳性表达细胞的百分比降低,CD8的百分比较CD4的百分比高;双蒸水组、VOCS组炎性细胞较少;VOCS组有少许炎性细胞浸润,CD4,CD8阳性表达细胞增多,阳性细胞的百分比增高。结论VOC低水平长时间作用可导致机体的超敏反应,使变应原诱发慢性荨麻疹发生成为可能,同时对人体的免疫功能有抑制作用。     

抗原致敏树突状细胞抗小鼠白念珠菌系统感染的实验研究

目的研究不同形态白念珠菌致敏的小鼠骨髓来源树突状细胞(DC)对免疫抑制小鼠白念珠菌系统感染的免疫保护作用及所对应的细胞因子改变。方法孢子相和菌丝相白念珠菌在体外分别致敏小鼠骨髓来源的DC(BM-DC),测定混合培养上清IL-12水平;尾静脉回输免疫抑制小鼠体内后,ELISA法测定各组小鼠脾IFN-γ及IL-4水平,并检测肾携菌量。结果DC孢子致敏组上清IL-12水平(380.2±104.13)pg/mL明显高于DC菌丝致敏组和对照组(P<0.05);而DC菌丝致敏组(74.79±23.47)pg/mL与单纯DC培养组上清IL-12水平(19.71±9.21)pg/mL差异无统计学意义(P>0.05)。孢子致敏DC、菌丝致敏DC分别过继免疫小鼠后,前者脾脏IFN-γ水平(269.43±17.34)pg/g明显高于其他组(P<0.05),IL-4水平(6.23±0.37)pg/g则明显低于其他对照组(P<0.05);荷菌一周后孢子致敏DC回输组小鼠肾携菌量(3.58±2.32)×102CFUs与健康小鼠荷菌组比较无统计学意义(P>0.05);其他各组间肾携菌量比较则有统计学意义(P<0.05)。结论尾静脉回输白念珠菌孢子体外致敏的小鼠骨髓来源DC可有效诱导免疫抑制小鼠抗白念珠菌保护性免疫。     

内皮素对黑素瘤A375细胞转化生长因子-β1及磷酸化Smad 3蛋白表达的调节

Objective To investigate the effects ofendothelin-1 (ET-1) and endothelin-3 (ET-3) on the expression of transformation growth factor-beta 1 (TGF-β1) and phosphorylation of Smad 3 in malignant melanoma cell line, A375. Methods Cultured A375 cells were classified into 5 groups, i.e. control group (no stimulation), ET-1 group (stimulated with ET-1), ET-1+BQ123 group (treated with ET-1 and BQ123),ET-1 + BQ788 group (treated with ET-1 and BQ788), ET-3 group (stimulated with ET-3), to receive different stimulation. The working concentrations were 0, 0.1, 1, 10, 100 nmol/L for ET-1 and ET-3, 10 μmol/L for BQ123 and BQ788. After another 12- and 24-hour culture, ELISA, RT-PCR and Western blot were used to detect the expression of TGF-β1 protein and mRNA as well as phosphorylated Smad 3 (P-Smad 3). Results The expression of TGF-β1 in A375 cells was up-regulated by ET-1, but down-regulated by ET-3, and both of the effects were in a concentration-dependent manner. Under the stimulation with ET-1 and ET-3 of 100 nmol/L, the level of TGF-β1 reached 1289.38 ± 89.42 ng/L per 105 cells and 85.09 ± 9.37 ng/L per 105 cells, respectively, significantly different from that in unstimulated cells (both P < 0.05). BQ123 signifi-cantly blocked the up-regnlatory effect of ET-1 on the expression TGF-β1 protein(P < 0.05), but BQ788 had no significant influence on the effect, so was the case with TGF-β1 mRNA. Western blot revealed that ET-1significantly elevated the expression of P-Smad 3 in A375 cells (P <0.05), and the elevation was significantly inhibited by BQ123, but not by BQ788. The expression of P-Smad 3 was statistically decreased by ET-3 in A375 cells (P <0.05). Conclusions The expression of TGF-β1 could be enhanced by ET-1, but suppressed by ET-3. It is likely that endothelin receptor A mediates the phosphorylation of Smad 3 induced by ET-1.     

内皮素对黑素瘤A375细胞转化生长因子-β1及磷酸化Smad 3蛋白表达的调节

Objective To investigate the effects ofendothelin-1 (ET-1) and endothelin-3 (ET-3) on the expression of transformation growth factor-beta 1 (TGF-β1) and phosphorylation of Smad 3 in malignant melanoma cell line, A375. Methods Cultured A375 cells were classified into 5 groups, i.e. control group (no stimulation), ET-1 group (stimulated with ET-1), ET-1+BQ123 group (treated with ET-1 and BQ123),ET-1 + BQ788 group (treated with ET-1 and BQ788), ET-3 group (stimulated with ET-3), to receive different stimulation. The working concentrations were 0, 0.1, 1, 10, 100 nmol/L for ET-1 and ET-3, 10 μmol/L for BQ123 and BQ788. After another 12- and 24-hour culture, ELISA, RT-PCR and Western blot were used to detect the expression of TGF-β1 protein and mRNA as well as phosphorylated Smad 3 (P-Smad 3). Results The expression of TGF-β1 in A375 cells was up-regulated by ET-1, but down-regulated by ET-3, and both of the effects were in a concentration-dependent manner. Under the stimulation with ET-1 and ET-3 of 100 nmol/L, the level of TGF-β1 reached 1289.38 ± 89.42 ng/L per 105 cells and 85.09 ± 9.37 ng/L per 105 cells, respectively, significantly different from that in unstimulated cells (both P < 0.05). BQ123 signifi-cantly blocked the up-regnlatory effect of ET-1 on the expression TGF-β1 protein(P < 0.05), but BQ788 had no significant influence on the effect, so was the case with TGF-β1 mRNA. Western blot revealed that ET-1significantly elevated the expression of P-Smad 3 in A375 cells (P <0.05), and the elevation was significantly inhibited by BQ123, but not by BQ788. The expression of P-Smad 3 was statistically decreased by ET-3 in A375 cells (P <0.05). Conclusions The expression of TGF-β1 could be enhanced by ET-1, but suppressed by ET-3. It is likely that endothelin receptor A mediates the phosphorylation of Smad 3 induced by ET-1.     

万乃洛韦治疗带状疱疹疗效观察

盐酸万乃洛韦(alaciclovir hydrochloride)是阿昔洛韦的L-缬氨酸酯的盐酸盐,口服后吸收迅速,并在体内很快转化为阿昔洛韦,从而发挥其抗病毒作用.我们自1998年9～12月,对该药治疗带状疤疹进行了临床观察,并与静脉滴注阿昔治韦或病毒唑治疗作比较,取得良好疗效,现报道如下.     

外阴鳞状细胞癌中人乳头瘤病毒感染与端粒酶和生存素的关系

目的:探讨人乳头瘤病毒(HPV)6/11、16/18在外阴鳞状细胞癌(vulvarsquamouscellcarcinoma,VSCC)组织中的感染情况及其与人端粒酶逆转录酶(hTERT)和凋亡抑制基因生存素(survivin)表达的关系。方法:采用PCR检测HPV6/11、16/18在31例VSCC及13名正常人皮肤组织中的感染情况,同时用原位杂交法检测hTERTmRNA的表达,免疫组化法检测生存素蛋白的表达。结果:①HPV6/11、16/18在VSCC患者的阳性率分别为25.81%和38.17%,正常对照者为阴性。VSCC患者与正常对照者HPV16/18阳性率的差异有统计学意义(P<0.05)。②VSCC患者hTERTmRNA、生存素蛋白表达的阳性率与正常对照者比较,差异均有统计学意义(P<0.05),且VSCC患者hTERTmRNA表达与生存素蛋白表达的阳性率呈明显的正相关(P<0.05)。③hTERTmRNA在HPV16/18阳性组中的表达明显强于HPV16/18阴性组,生存素蛋白在HPV16/18阳性组中的表达低于其在HPV16/18阴性组中的表达。结论:HPV感染及hTERT、生存素表达在VSCC发生发展中起一定作用;VSCC中hTERT与生存素的表达具有一定的相关性。     

Construction of Prokaryotic Expression Plasmid of mtrC Protein of Neisseria gonorrhoeae and Its Expression in E. Coli

Summary： In order to provide a rational research basis for detection of resistance of Neisseria gonorrhoeae to antimierobial hydrophobie agents and study on the resistant mechanism of multiple transferable resistance （mtr） efflux system, plasmid pET-28a（＋） encoding mtrC gene was constructed and the related target protein was expressed in Escherichia colt （E. cold DE3. The fragments of mtrC gene of Neisseria gonorrhoeae from the standard strains were amplified and cloned into prokaryotic expression plasmid pET-28a（＋） with restriction endonuelease to construct recombinant pET-mtrC which was verified by restriction endonuelease and DNA sequencing. The recom- binant was transformed into E. coli DE3 to express the protein mtrC induced by IPTG. The results showed mtrC DNA fragment was proved correct through restriction endonuelease and DNA sequencing. hs sequence was 99.5 % homologus to that published on GeneBank （U14993）. A 48.5 kD fusion protein which was induced by IPTG was detected by SDS-PAGE. It was concluded that the construction of prokaryotic expression plasmid of mtrC protein of Neisseria gonorrhoeae was correct and the fusion protein was successively expressed in E. coli.