鼻腔恶性淋巴瘤误诊原因分析

鼻腔恶性淋巴瘤 (鼻腔恶性肉芽肿 )是指始于鼻部 ,渐延及面部中线进行性坏死性溃疡为特征的一种肉芽肿。本病病情险恶 ,病因未明。近年来通过临床资料观察发病率有逐年增高的趋势 ,且病理检查缺乏特异性 ,早期症状又多不一 ,缺乏特征 ,常易造成误诊和漏诊。现将我院 1991～ 2 0 0 1年收治和转入诊治的误诊病例报告如下 ,并对误诊原因进行分析 ,以提高对本病的重视。1　临床资料共收治 18例 ,误诊 6例 ,误诊率 3 3 3 %。误诊病例中年龄最小者 15岁 ,最大者 48岁 ,均为男性 ,其中误诊为鼻息肉者 2例 ,慢性鼻窦炎 2例 ,鼻咽癌 1例 ,右鼻腔乳头…     

黏膜黑色素瘤原发部位与转移部位相关性分析

目的:探讨黏膜黑色素瘤的原发部位与转移部位的相关性及基因组学特征。方法:对经病理确诊为黏膜黑色素瘤的92例患者进行流行病学调查,对肿瘤原发部位及转移部位的相关因素进行总结分析。结果:头颈部为黏膜黑色素瘤高发部位46人（50%）,其次为泌尿生殖系统25人（27.17%）,肛管直肠21人（22.83%）。最常见转移部位均为区域淋巴结,头颈部、肛管直肠、泌尿生殖系统分别为63.04%、57.14%、32.00%;其次为肺转移,头颈部、肛管直肠、泌尿生殖系统分别为23.91%、19.05%、32.00%;肛管直肠和泌尿生殖系统来源黑色素瘤还易出现肝转移,分别为28.57%和20.00%。进行基因检测的33人中,BRAF V600E突变2例（6.06%）,CKIT突变1例（3.03%）,NRAS突变4例（12.12%）。结论:淋巴结转移最常见于头颈部黑色素瘤,其次为肛管直肠黑色素瘤,泌尿生殖系统来源黑色素瘤淋巴结转移比例较低;局部复发伴淋巴结转移在头颈部黑色素瘤约占1/3。基因检测及靶向治疗为更多患者带来生存获益。     

氧化应激介导的Ras-ERK信号通路活化参与醛固酮诱导的肾小球系膜细胞增殖

目的 探讨氧化应激介导的Ras-胞外信号调节激酶(ERK1/2)信号通路活化在醛同酮( ALDO)诱导的系膜细胞增殖中的作用.方法 体外培养人肾小球系膜细胞,应用3H-胸腺嘧啶(3H-TdR)掺入法和细胞计数测定系膜细胞增殖;Western印迹检测Ki-RasA、c-Raf、MEK1/2和ERK1/2活化.结果 ALDO可显著促进系膜细胞增殖,抗氧化剂乙酰半胱氨酸(NAC)、过氧化氢酶(CAT)、超氧化物歧化酶(SOD)显著抑制ALDO诱导的系膜细胞增殖(均P＜ 0.01).ALDO刺激系膜细胞3h,活化的Ki-RasA、c-Raf、MEK1/2和ERK1/2表达显著增强,分别是对照组的4.05倍、3.62倍、4.52倍和3.40倍(均P＜0.01).抗氧化剂NAC几乎完全阻断ALDO诱导的Ki-RasA、c-Raf、MEK1/2和ERK 1/2活化(均P＜0.01).Ki-RasA siRNA可呈浓度依赖性降低系膜细胞Ki-RasA表达,并显著抑制ALDO诱导的Ki-RasA活化及系膜细胞增殖(P＜0.01).c-Raf抑制剂GW5074和MEK1/2抑制剂PD98059亦显著抑制ALDO诱导的系膜细胞增殖,其抑制率均达到65％(P＜0.01).Ki- RasA siRNA不能降低ALDO诱导的磷酸肌醇-3激酶( PI3K)磷酸化.联合应用PI3K抑制剂LY294002和MEKl/2抑制剂PD98059可完全阻断ALDO诱导的系膜细胞增殖(P＜0.01).结论 ALDO可通过氧化应激活化Ki-RasA-c-Raf-MEK-ERK信号通路.同时阻断ERK1/2和PI3K信号通路可完全抑制ALDO诱导的系膜细胞增殖.     

卡氏肺孢子虫在实验感染大鼠肺组织内的分布

观察了卡氏肺孢子虫包囊在实验感染大鼠不同5个肺叶的分布。在大鼠右肺副叶,左肺叶,右肺前叶,右肺中叶包囊数较多,右肺后叶包囊数最少,右肺后叶包囊数与其他4个肺叶相比,差异均具显著性。提示采用病原学方法检查大鼠肺组织时,从右肺副叶,左肺叶,右肺前叶,右肺中叶取材检出包囊的阳性率较高。     

张家口市幼儿蛲虫感染情况调查

蛲虫病为一种常见的人体肠道寄生虫病,主要症状为肛门奇痒。若异位寄生于阴道、尿道等处,可致相应部位的炎症。由于蛲虫生活史不受外界气候的影响,所以感染分布很广,其中儿童感染更为多见。为了解本市儿童蛲虫感染情况,我们于1985年9月用透明胶纸肛拭法对8个幼儿园进行抽样调查。其结果如下:1.受检儿童年龄在3.5～6.5岁,共1,060人,其中阳性354人,阳性率达33.4%,低于1983和1984年济南市和南京市的调查(41.8%和41.7%)及我国50年代     

儿童毛细血管内皮细胞增生性紫癜性肾炎的临床病理及预后分析

目的 探讨以弥漫性毛细血管内皮细胞增生为主要病理表现的紫癜性肾炎（DEP-HSPN）的临床、病理及预后。 方法 回顾性分析本院近10年来经肾活检确诊的8例DEP-HSPN患儿临床、病理和预后资料,并分别与同病理级别或具有同等蛋白尿水平（肾病水平蛋白尿）的非DEP-HSPN患儿进行比较。 结果 （1）DEP-HSPN起病急,临床表现重,8例患儿中,4例临床表现为肾炎性肾病,3例表现为肾病水平蛋白尿伴血尿,1例呈急性肾炎综合征,4例患儿合并有肉眼血尿。病理分级均为Ⅲ-b级,光镜主要表现为弥漫性毛细血管内皮细胞和系膜细胞增生,常合并毛细血管袢坏死及肾小球内炎性细胞浸润,4例患儿合并细胞性新月体。（2）与病理为Ⅲ-b级的非DEP-HSPN患儿比较,DEP-HSPN患儿病程较短,临床多见肉眼血尿,24 h尿蛋白量高,更多呈肾炎性肾病表现。病理上,DEP-HSPN肾小球毛细血管袢坏死更常见。与具有肾病水平蛋白尿的非DEP-HSPN患儿相比,DEP-HSPN合并新月体的比例较低。（3）8例患儿均采用口服泼尼松联合静脉滴注环磷酰胺（CTX）冲击,病程早期给予2个疗程甲泼尼龙冲击治疗方案。平均随防（7.00±2.20）月,1例临床痊愈,5例持续镜下血尿,2例微量蛋白尿及持续镜下血尿。两组患儿预后差异无统计学意义。 结论 DEP-HSPN起病较急,临床以大量蛋白尿或肾炎性肾病为主要表现,并且常合并肉眼血尿。病程早期给予积极的免疫抑制剂治疗常能取得较满意的近期疗效。     

NADPH oxidase-derived reactive oxygen species involved in angiotensin Ⅱ-induced monocyte chemoattractant protein-1 expression in mesangial cells

Objective To investigate the origin of oxidative stress induced by angiotensin H (Ang Ⅱ ) in human mesangial cells and the role of reactive oxygen species ( ROS) in Ang Ⅱ -induced monocyte chemoattractant protein-1 (MCP-1) expression.Methods MCP-1 expression was determined by real time RT-PCR.ROS production was measured by DCFDA fluorescence.Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity was examined by lucigenin chemiluminescence.p47phox and p67phox translocation was assayed by Western blot.Twenty-four male mice were randomly divided into three groups; the control,the Ang Ⅱ infusion [ Ang Ⅱ 400 ng/(kg±min) ],and the apocynin treatment.Ang Ⅱ was infused by subcutaneously osmotic minipump for 14 days.Urinary albumin and 8-isoprostane excretion were measured by ELISA.Results In cultured human mesangial cells,Ang Ⅱ induced the MCP-1 expression in a dose-dependent manner with 3.56 fold increase as compared with the control.Ang Ⅱ increased intracellular ROS production as early as 3 min with the peak at 60 min and was in a time and dose-dependent.Incubation with different dosages of Ang Ⅱ ( 1μmol/L,10μmol/L,and 100μmol/L Ang Ⅱ ) for 60 min,ROS production increased at 1.82,2.92,and 4.08 folds respectively.Ang Ⅱ-induced ROS generation was sensitive to diphenyleneiodonium sulfate (DPI,10 μmol/L) and apocynin (500μmol/L) ,two structurally distinct NADPH oxidase inhibitors.In contrast,inhibitors of other oxidant- producing enzymes,including the mitochondrial complex I inhibitor rotenone,the xanthine oxidase inhibitor allopurinol,the cyclooxygenase inhibitor indomethacin,the lipoxygenase inhibitor nordihydroguiaretic acid,the cytochrome P450 oxygenase inhibitor ketoconazole and the nitric oxide synthase inhibitor G-nitro-L- arginine methyl ester were without an effect Ang Ⅱ -induced ROS generation was inhibited by the ATI antagonist losartan (10μmol/L) but not the AT2 antagonist PD123319 (10μmol/L).Ang Ⅱ treatment induced translocation of cytosolic of p47 and p67 to the membrane.The antioxidants almost abolished Ang Ⅱ -induced MCP-1 expression.Ang Ⅱ infusion increased urinary and p67 translocation by 2.69-,2.97-,and 2.67-fold,respectively.Conclusions NADPH oxidase-derived ROS is involved in Ang Ⅱ-induced MCP-1 expression.Inhibition of NADPH oxidase alleviates Ang Ⅱ -induced renal injury.