Primary polypeptide hormones and mucin-producing malignant carcinoid of the larynx

A case of primary malignant laryngeal carcinoid with dual endocrine and mucous differentiation i s reported. Histologically the tumor showed a characteristic organoid pattern and exhibited Alcian-blue, periodic acidschiff, and Grimelius silver positivity. By the immunoperoxidase technique cal citoni n, ACTH, and or-hCG subunit were demonstrated in the tumor cells. ELectron microscopy revealed two different types of endocrinelike cells: mucous cells and occasional cells containing both endocrinelike granules and mucin droplets. Diagnostic morphologic criteria of this rare tumor entity are discussed and reference t o biologic behavior and possible h istogenesis is made.     

Capsaicin-sensitive non-cholinergic excitatory innervation of the guinea-pig tracheobronchial smooth muscle

Field stimulation of the isolated main bronchi of the guinea-pig results in a rapid contraction followed by a sustained contractile response. Tetrodotoxin abolished these effects. The first phase was strongly inhibited by hyoscine, indicating that it was mediated mainly by excitation of cholinergic nerves. The lasting contraction was abolished by capsaicin tachyphylaxis but it was resistant to the effects of hyoscine, hexamethonium or physostigmine. It is suggested that capsaicin-sensitive non-cholinergic nerves have major excitatory effect on the guinea-pig bronchial smooth muscle and there is also evidence for their influence on the trachea.     

长托宁用于喉罩全麻术前用药的临床观察

目的研究选择性M受体拮抗剂长托宁用于喉罩全麻术前用药的临床效果。方法选取ASAⅠ～Ⅱ级行择期腹腔镜下胆囊切除术患者90例，随机分为3组（每组30例）：对照组（A组），术前不应用任何抗胆能药；阿托品组（B组）和长托宁组（C组），麻醉诱导前30min肌肉注射阿托品或长托宁0．01mg／kg，麻醉诱导后置入标准型喉罩后接麻醉机行机械通气；分别记录气管插管后5min（T1）、气管插管后30min（T2）、气管拨管前（T3）气道内分泌物量以及心率变化。结果在T1、T2、T3三个时点，B组和C组患者的气道分泌物明显少于A组（P〈0．05）；B组在T1时间点的心率明显高于A组与C组（P〈0．05）。结论长托宁用于喉罩全麻术前用药临床效果较好。     

声带鳞状细胞癌早期改变的病理学观察

目的探讨声带鳞状细胞癌早期病理学的特点，提高病理诊断水平。方法总结89例声带鳞状细胞癌早期改变病例的病理资料，对其石蜡切片进行HE染色、PAS染色及p53、Ki-67免疫组化染色；以59例声带角化症（分为单纯增生组40例和异型增生组19例）和30例声带浸润癌（浸润深度〉3mm的癌）作为对照。结果在HE染色下，声带鳞状细胞癌的早期改变可区分为两种类型：Ⅰ型为上皮全层癌变型，占67．4％（60／89）；Ⅱ型为上皮基底层及副基底层癌变型，占32．6％（29／89），又可分为Ⅱa和Ⅱb两个亚型。HE染色显示有可疑微小浸润者52例，PAS染色示其中的43例（83％）的可疑病灶周边基膜样物质消失，有微浸润，Ⅰ型微浸润的比例较Ⅱ型明显偏低（P=0．007）。HE染色下3例（3．4％，3／89）认为无微浸润者经深切证实有浸润，并经PAS染色确认。Ⅰ型和Ⅱ型的p53表达率差异无显著性（P=0．445），而Ki-67阳性率Ⅰ型高于Ⅱ型（P=0．048）。癌早期改变组的p53阳性率高于声带角化症伴单纯增生组（P=0．008），而与声带角化症异型增生组和声带进展癌组之间的差异无统计学意义（P=0．240，P=0．268）。癌早期改变组的Ki-67阳性率明显低于浸润癌组（P=0．000），并明显高于角化症伴单纯增生组（P=0．001），但与角化症伴异型增生组之间差异无显著性（P=0．248）。结论声带鳞状细胞癌早期改变可区分为Ⅰ型和Ⅱ型，Ⅱ型癌变可在不累及上皮全层的情况下，由上皮的基底层和（或）副基底层细胞直接向固有膜内增生及癌变，此型占全部病例的近1／3，早期浸润是Ⅱ型诊断的可靠依据；Ⅱ型的存在提示声带鳞状细胞癌的早期发生和演进可能存在不同的机制；PAS染色和p53、Ki-67免疫组化染色有助于声带鳞状细胞癌Ⅱ型早期的诊断。     

Role of mitogen-activated protein kinases in influenza virus induction of prostaglandin E2 from arachidonic acid in bronchial epithelial cells

BACKGROUND: Influenza virus (IV) infection causes airway inflammation; however, it has not been determined whether IV infection could catabolize arachidonic acid cascade in airway epithelial cells. In addition, the responsible intracellular signalling molecules that catabolize arachidonic acid cascade have not been determined. OBJECTIVE: In the present study, to clarify these issues, we examined the cyclooxygenase (COX) expression, cytosolic phospholipase A2 (cPLA2) phosphorylation and prostaglandin E2 (PGE2) release in human bronchial epithelial cells (BEC) upon IV infection, and the role of mitogen-activated protein kinase (MAPK) including extracellular signal-regulated kinase (ERK), p38 MAPK and c-Jun-NH2-terminal kinase (JNK) in catabolizing arachidonic acid cascade in BEC. METHODS: COX-2 expression, phosphorylation of cPLA2 and phosphorylation of ERK, JNK and p38 MAPK were determined by Western blot. The concentrations of PGE2 were determined by ELISA. PD 98059 as a specific inhibitor of MAPK kinase-1 (MEK-1), an up-stream kinase of ERK, SB 203580 as a specific inhibitor of p38 MAPK and CEP-11004 as a specific inhibitor of JNK cascade were used to investigate the role of ERK, p38 MAPK and JNK in catabolizing arachidonic acid cascade in BEC. RESULTS: The results showed that (1) IV infection increases COX-2 expression, cPLA2 phosphorylation and PGE2 release, (2) ERK, p38 MAPK and JNK were phosphorylated, (3) CEP-11004 and PD 98059 predominantly attenuated COX-2 expression and cPLA2 phosphorylation, respectively, (4) SB 203580 did not remarkably affect COX-2 expression and cPLA2 phosphorylation, and (5) each inhibitor dose-dependently attenuated PGE2 release by various extents. CONCLUSION: These results indicate that IV infection activates three distinct MAPKs, ERK, p38 MAPK and JNK, to participate to various extents in the induction of PGE2 synthesis from arachidonic acid in BEC.     

Matrix metalloproteinase-2 from bronchial epithelial cells induces the proliferation of subepithelial fibroblasts

BACKGROUND: In bronchial asthma, subepithelial fibrosis in the conducting airways is associated with increased numbers of subepithelial fibroblasts. OBJECTIVE: This study examined the hypothesis that MMP-2 from airway epithelial cells induces the proliferation of subepithelial fibroblasts. METHODS: Using primary bronchial epithelial cells MMP-2, MT1-MMP and TIMP-2 mRNA expression were assessed by Northern blotting and RT-PCR. Primary bronchial epithelial cells transfected with constructs encoding pro-MMP-2 and MT1-MMP (MMP-14). RESULTS: Transfected cells showed enhanced expression of the appropriate mRNA species by RT-PCR and enhanced MMP-2 or MT1-MMP activity by zymography. Active MMP-2 levels in epithelial supernatants were increased most by cotransfection with pro-MMP-2 and MT1-MMP encoding constructs. By measuring tritiated thymidine incorporation, supernatants from transfected cells were found to enhance DNA synthesis of primary airway fibroblast cultures compared with controls. There was a strong correlation (r = 0.9, P < 0.01) between MMP-2 levels in epithelial cell conditioned media and fibroblast proliferation as indicated by DNA synthesis. The MMP inhibitor 1,10-phenanthroline attenuated the increased proliferation, while the addition of exogenous purified MMP-2 alone also increased fibroblast proliferation. CONCLUSIONS: Our results support a role for MMP-2 in mediating cross-talk between epithelial cells and myofibroblasts.     

XRCC1、hOGG1基因多态性与喉癌遗传易感性的关系

目的 探讨X线修复交叉互补组1基因(X-ray repair cross complementing group 1,XRCC1)、8-羟基鸟嘌呤修复酶基因(human 8-oxoguanine glycosylase I,hOGG1)多态性与喉癌遗传易感性的关系.方法 采用病例-对照设计,应用聚合酶链反应-限制性片段长度多态性分析法检测了72例经病理确诊的喉癌患者和随机抽样的72例无肿瘤、无遗传病对照者XRCC1-Arg399Gln、hOGG1-Ser326Cys多态性.结果 病例组XRCC1第399位密码子杂合型(Arg/Gln)及突变型(Gln/Gln)和hOGG1第326位密码子杂合型(Ser/Cys)及突变型(Cys/Cys)分布频率均高于对照组(P＜0.05),与携带XRCC1-399野生型(Arg/Arg)、hOGG1-326野生型(Ser/Ser)个体相比,携带该基因型的个体喉癌的发病风险分别升高了3.37和2.54倍.交互作用分析显示,吸烟组与不吸烟组相比,携带XRCC1、hOGG1各基因型的个体的喉癌发病风险差异未发现存在统计学意义(xH12=0.15,xH22=0.28,P＞0.05).结论 XRCC1-399位点Arg→Gln和hOGG1-326位点Ser→Cys的氨基酸替换可能导致喉癌的发病风险增加,XRCC1-Arg399Gln、hOGG1-Ser326Cys多态性可能与喉癌的遗传易感性有关.