结节性黄瘤1例

临床资料患者男,17岁。因臀部和四肢多个黄色结节10余年于2007年2月1日就诊于我科门诊。患者10余年前无明显诱因发现臀部出现多个黄色的境界清楚的略隆起的豌豆大小球形结节,后逐渐增多增大,个别如鸡蛋大小,随后双侧膝关节及肘关节伸侧亦发现数个黄色的略隆起的圆形小结节。无明显瘙痒、疼痛。未进行特殊治疗。患者既往体健,无高血压、糖尿病、高血脂病史,家族中无类似病史。体检:一般情况尚可,各系统未见明显异常。皮肤科检查:臀部、大腿后部、窝、双侧膝关节及肘部伸侧可见片状黄色的境界清楚的略隆起的斑块,臀沟处及大腿后部可见豌豆至…     

人食管不典型增生上皮与原位癌的计算机纹理分析研究

采用计算机图象纹理分析和相关点阵检测技术,对人食管正常粘膜、不典型增生上皮及原位癌的不同纹理特征进行了观察。观察样品为常规病理切片,用计算机图象分析系统检测了组织的纹理特征。对受检图象建立了三种灰色分层关系矩阵,同时计算了8种纹理测度。结果显示,在重度不典型增生上皮和原位癌之间,其纹理测度和相关点阵检测数据均有显著性差异(P<0.05)。全部测量数据经计算机多元逐步判别分析,其正判率达90%以上。本研究结果表明,计算机纹理分析方法可正确地判别食管癌前病变和原位癌的组织结构异型性。提示本技术在食管癌的早期诊断方面具有肯定的实用性价值。     

Marshall-White综合征10例临床分析

Marshall-White综合征临床少见,近几年来报道逐渐增多,自1994年以来国内已有20例报道[1-4]。为分析该综合征的临床特点,我们对协和医院皮肤科门诊1999年10月至2006年6月所诊治的10例该综合征患者进行分析,现报道如下。1临床资料10例患者中男性7例,女性3例。年龄19～37岁,平均年龄(29.4±5.5)岁。其中2例为学生,2例为公司职员,其余6例为工人。病程1～3年。所有患者均因无明显诱因出现上下肢白斑而就诊。皮肤科检查:四肢(以前臂及小腿伸侧为主,包括手背和足背)呈淡红色或暗红色斑,其上散在直径1～2cm苍白色斑点,边界清,形状不规则,似大理石样…     

IL-8及瘦素在硬皮病小鼠模型体内的表达和相关性

目的通过建立硬皮病小鼠模型,检测模型小鼠血清及皮肤组织中IL-8及瘦素的表达水平,探讨IL-8及瘦素在硬皮病发病机制中的作用。方法实验用博莱霉素(BLM)造模方法,将小鼠随机分为二组:模型组小鼠每日用BLM在小鼠背部皮肤皮下注射,对照组小鼠每日用磷酸盐缓冲液(PBS)于背部相同部位皮下注射,连续4周后分别取小鼠背部皮肤及肺组织、血清。采用HE染色观察皮肤及肺的组织病理变化特点,并测量两组小鼠真皮厚度。采用酶联免疫吸附法分别检测两组小鼠血清IL-8及瘦素浓度,采用免疫组化法检测IL-8及瘦素在皮肤中的定位及表达。结果与对照组比较,模型组小鼠皮肤组织呈典型的硬皮病病理学改变,同时模型组小鼠肺组织切片HE染色结果显示肺泡间隔增宽以及大量单个核细胞浸润。模型组小鼠真皮(135.60±3.71)μm较PBS对照组(84.94±1.75)μm显著增厚(P0.01)。酶联免疫吸附法测得硬皮病模型小鼠血清中IL-8及瘦素表达水平上升(P0.01),两者呈正相关性(r=0.84,P0.01)。免疫组化结果显示IL-8及瘦素在硬皮病模型皮肤中表达阳性,且表达均高于对照组。结论博莱霉素反复皮下注射可诱导建立硬皮病小鼠模型。硬皮病小鼠血清及皮肤组织中IL-8及瘦素水平较对照组升高且呈正相关性,提示这些因子在硬皮病发病中可能发挥重要作用。     

早期先天梅毒1例

报告1例早期先天梅毒。患儿女,70d。发热、背部及四肢起暗红色斑伴脱屑1周。患儿及其父母快速血浆反应素环状卡片试验RPR均阳性(1∶16),梅毒微粒凝集试验TPPA阳性。给予水剂青霉素G5万U/kg·d,连续用药14d全身皮疹完全消退。     

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.     

孤立性毛发上皮瘤1例

患者女,80岁.因鼻右侧结节2年,渐增大半年,于2010年11月14日于我科门诊就诊.患者2年前无明显诱因右侧鼻翼上方出现一丘疹,因无自觉症状,未予治疗,近半年因增大而就诊.患者既往体健,家族中无类似病史,无外伤史.