跖疣合并化脓性肉芽肿1例

<正>患者男,38岁,自由职业者。因左足跖部增生性疣状斑块1年,中央红丘疹伴出血、疼痛2个月就诊。患者1年前左足跖部出现肤色斑丘疹,无明显不适,在当地医院曾诊断为"跖疣",未予治疗。近2个月,斑块上出现一红色丘疹,质地软,有压痛,时有出血。体格检查:系统检查未见异常。皮肤科检查:左侧足跖中部可见一约0.8 cm×0.8 cm的疣状斑块,表面浸渍发白,中央约绿豆大的红色丘疹(图1A),质地软,触     

副乳腺

<正>患者女,15岁。主诉:左侧腋前一褐色结节5年。现病史:患者于5年前发现左侧腋前一绿豆大的褐色丘疹,无明显自觉症状,后逐渐增大至黄豆大,于2016年8月22日来我院就诊。既往史、个人史及家族史:均无特殊。体格检查:一般情况良好,全身系统检查均正常。     

糖尿病人群空腹血糖水平与新发脑梗死事件的相关性研究

目的 探讨糖尿病人群空腹血糖水平与新发脑梗死事件的相关性.方法 采用前瞻性队列研究方法,以空腹血糖≥7.0 mmol/L或＜7.0 mmol/L但已确诊为糖尿病、正在使用降糖药物的8 306例糖尿人群作为观察队列,随访(48.01 ±3.14)个月,随访期间每半年收集一次新发脑梗死事件情况.分析糖尿病人群空腹血糖水平与新发脑梗死事件的相关性.结果 (1)随访结束时,随着基线空腹血糖水平的增高,研究对象的总胆固醇、甘油三酯的水平逐渐增高[总胆固醇:(4.93±1.15,510±1.20,5.15± 1.28,5.33±1.35) mmol/L,甘油三酯:(1.70±1.26,1.83± 1.29,2.18±1.76,2.41±2.08) mmol/L,P＜0.05];低密度脂蛋白胆固醇、收缩压、舒张压、体重指数的水平也增高(P＜0.05).(2) 7.0 mmol/L≤空腹血糖＜9.0mmol/L组累积发生脑梗死事件率最低(2.1％,P＜0.01).校正年龄、性别、收缩压、舒张压、总胆固醇、甘油三酯、低密度脂蛋白胆固醇、高密度脂蛋白胆固醇、体重指数、吸烟、糖尿病病程及降糖治疗因素,Cox比例风险回归分析表明,相对于7.0 mmol/L≤空腹血糖＜9.0 mmoL/L组,6.1 mmol/L≤空腹血糖＜7.0mmol/L组和空腹血糖≥9 mmol/L两组发生脑梗死事件的相对危险(RR)各分别增加1.85倍(95％CI 1.09～3.15,P＜0.05)、1.54倍(95％CI 1.16～2.05,P＜0.01).结论 糖尿病人群空腹血糖控制在7.0 ～9.0 mmol/L水平者似新发生脑梗死事件率最低.     

健康教育对高血压病患者治疗的影响

目的 :探讨健康教育对高血压病患者生活方式、服药率、血压控制率及并发症发生率的影响。方法 :2 84例高血压病患者随机分为教育组和对照组 ,均接受临床常规药物治疗 ;教育组根据患者心脑血管病危险因素及高血压病认知水平的调查情况进行针对性的健康教育。通过随访 ,比较 2组患者在生活方式、服药率、血压控制率及并发症发生率方面的变化。结果 :教育组在吸烟、饮酒、低盐饮食、体育锻炼、服药率及血压控制率方面均较干预前有明显改善 (均P <0 .0 0 1) ,与对照组比较差异有显著性 (P <0 .0 0 1) ;经干预后 ,教育组并发症发生率 10 .9% ,对照组 30 .5 % (P <0 .0 0 1)。结论 :针对性健康教育是高血压病防治工作中的一项重要干预措施     

TAP1-EGFP和TAP2-EGFP融合蛋白在恶性黑素瘤细胞系中的表达

目的 探讨pTAP1-EGFP和(或)pTAP2-EGFP转入恶性黑素瘤细胞株后TAP表达的变化,观察TAP在A375中表达后的业细胞定位.方法 在恶性黑素瘤细胞株A375中转入pTAP1-EGFP和(或)pTAP2-EGFP,G418筛选稳定转染细胞株,检测转染后TAP1和TAP2表达水平的变化.将pDsRed2-ER和pTAP1-EGFP或pTAP2-EGFP共转染入A375细胞内,激光共聚焦显微镜下观察TAP1-EGFP和TAP2-EGFP融合蛋白的亚细胞定位.流式细胞仪检测转染前后细胞表面HIA-Ⅰ的表达.结果 将pTAP1-EGFP和(或)pTAP2-EGFP转染A375细胞株后筛选出稳定克隆.转染pTAP1-EGFP和(或)pTAP2-EGFP后能明显增加A375细胞TAP1和TAP2在蛋白水平的表达,并能增加细胞表面HLA-Ⅰ的表达.共转染pDsRed2-ER和pTAP1-EGFP或pTAP2-EGFP后,在激光共聚焦显微镜下观察,发现TAP1-EGFP和TAP2-EGFP融合蛋白的绿色荧光能够与pDsRed2-ER的红色荧光重叠.结论 构建的pTAP1-EGFP和(或)pTAP2-EGFP质粒在A375细胞系中表达成为TAP1-EGFP和TAP2-EGFP融合蛋白后,能准确定位在内质网上,为研究TAP诱导的后续免疫效应提供基础.     

内皮素受体B在黑素瘤中的表达及内皮素3对黑素瘤细胞A375的体外促生长效应

目的 研究内皮素受体B（ETR－B）在人恶性黑素瘤中的表达及内皮素3对黑素瘤细胞A375的体外促生长效应。方法 采用免疫组化SP法检测ETR－B在黑素瘤组织中的表达，用RT-PCR法检测ETR－B基因在人恶性黑素瘤细胞A375和SK－mel－1中的表达，用MTT比色法检测不同浓度内皮素3对黑素瘤细胞A375的体外促增殖活性。结果 ETR-B在41例恶性黑素瘤和23例色素痣中的阳性率分别为78.05%和8.69%，两组间差异有统计学意义，P < 0.05。15例原位和26例Ⅰ ~ Ⅳ期恶性黑素瘤ETR-B阳性表达率分别为53.33%和92.31%，两组比较，P < 0.05。13例转移性恶性黑素瘤（Ⅲ ~ Ⅳ期）中ETR-B阳性表达率100%，28例未转移者（0 ~ Ⅱ期）的阳性表达率为67.86%，两组比较，P < 0.05。ETR－B基因在人恶性黑素瘤细胞A375和SK－mel－1中均有表达；内皮素3对黑素瘤细胞A375在体外具有很强的促增殖作用，且促增殖能力呈内皮素3浓度依赖性。结论 内皮素3/ETR－B在促黑素瘤细胞生长中有重要作用     

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.     

凋亡抑制蛋白c-FLIP在带状疱疹患者细胞免疫中作用的研究

目的探讨凋亡抑制蛋白c-FLIP在抗水痘-带状疱疹病毒(VZV)免疫中的作用。方法采用流式细胞术检测30例无恶性肿瘤的带状疱疹患者、17例伴恶性肿瘤的带状疱疹患者和20例正常对照者外周血T细胞和B细胞内c-FLIP蛋白表达阳性率和CD3+T细胞阳性率。结果急性期伴有恶性肿瘤的带状疱疹患者外周血T细胞内c-FLIP表达明显低于无恶性肿瘤和正常对照组(P<0.05,P<0.01),无恶性肿瘤组明显低于正常对照组(P<0.05);恢复期无恶性肿瘤的带状疱疹患者外周血T细胞内c-FLIP表达明显增加,与急性期相比有明显差异(P<0.01),但恢复期的伴恶性肿瘤和急性期相比无明显差异(P>0.05);外周血B细胞内c-FLIP表达在急性期和恢复期的带状疱疹患者中无明显差异(P>0.05)。CD3+T细胞在带状疱疹患者外周血中的阳性率与c-FLIP有相似的表达趋势,两者呈正相关(r分别为0.806和0.534,P均<0.05)。结论凋亡抑制蛋白c-FLIP在急性期带状疱疹患者外周血T细胞内低表达,恢复期则高表达,且与T细胞数量明显正相关,表明其可能参与带状疱疹患者T细胞的增殖,在带状疱疹发生、发展中发挥一定的作用。     

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.