恶性肿瘤患者血清层粘蛋白含量的初步研究

利用酶联免疫吸咐法（ＥＬＩＳＡ）检测了１３５例恶性肿瘤患者清中层粘蛋白的含量。比较了良恶性肿瘤及健康成人血清ＬＮ的差别，对ＬＮ在癌变中的机制进行了初步探讨。结果表明，所有恶性肿瘤患者清ＬＮ值均高于健康对照（Ｐ＜０．００１），并且高于良性肿瘤患者（Ｐ＜０．００１），良性肿瘤和健康组之间没有差别（Ｐ＞０．０５）。以正常人ＬＮ值上限为界，恶性肿瘤阳性分布率为７４．８％，良性肿瘤１３％，正常人假阳性为８．     

层粘素和纤粘素在胃癌中的分布

采用层粘素（ＬＮ）多抗和纤粘素（ＦＮ）多抗检测７６例胃癌。证实癌细胞分化程度越低和局部浸润能力越强，造成的基底膜（ＢＭ）缺损越严重。证明反应性间质增生与癌肿的浸润转移趋势有关。癌细胞穿透基底膜进入间质，引起间质反应性增生，后者可促进癌细胞的浸润和转移。     

Expression of Laminin in Hepatocellular Carcinoma: An Adjunct for Its Histological Diagnosis

In general, hepatocytes lack basement membrane structures andtherefore no laminin expression is seen around hepatic cords.To determine whether or not laminin expression appears whenhepatic tissue becomes carcinomatous, we carried out immunohistochemicalstaining of hepatic tissues excised surgically from 35 patientswith hepatocellular carcinoma, 18 with metastatic colon carcinoma,two with adenomatous hyperplasia, and 10 without any nodularlesions. Among the various conditions of hepatic tissue, lamininexpression was detected only in hepatocellular carcinoma with86% positivity. The result was not dependent on the degree ofdifferentiation. Therefore, it was confirmed that immunohistochemicaldetection of laminin provides a useful adjunct for the diagnosisof hepatocellular carcinoma, and this was verified by a studyusing needle biopsy samples. In addition, our results suggestedthat the basement membranes are derived from endothelial cellsof either portal veins or hepatic arteries.     

福辛普利对肾小球系膜细胞层粘连蛋白及mRNA表达的影响

目的 观察新一代血管紧张素转化酶抑制剂（ACEI）福辛普利（FOS）对体外培养的大鼠肾小球系膜细胞（GMC）产生的细胞外基质（ECM）成分层粘连蛋白（LN）的影响及FOS防治肾小球硬化的机制。方法 按经典方法体外培养大鼠GMC，转种培养后分为对照组、脂多糖（LPS）组和LPS＋FOs组。采用ELISA法测定GMC培养上清液LN含量，荧光半定量PCR方法检测LNmRNA的表达。结果 LPS组GMC分泌LN蛋白及mRNA的表达明显高于对照组（P〈0．05），LPS＋FOS组GMC分泌LN蛋白及mRNA的表达较LPS组明显下降（P〈0．05）。结论 FOS从蛋白和mRNA两个水平对体外培养大鼠GMC产生的LN有明显的抑制作用，提示FOS抑制GMC产生ECM可能是延缓肾小球硬化的重要作用机制之一。     

层粘连蛋白LN及其受体LN-R在髓母细胞瘤中的表达

目的测定Laminin(LN)／Laminin Receptor(LN-R)在髓母细胞瘤中的表达情况，进一步探讨其与该肿瘤浸润、转移的关系。方法通过免疫组化方法测定LN和LN-R在70例髓母细胞瘤和10例正常小脑组织中的表达情况。结果LN-R在10例正常小脑组织及70例髓母细胞瘤中表达均为阴性，LN在髓母细胞瘤中低表达。结论LN及其受体在髓母细胞瘤中低表达，其中LN-R不表达可能为原发性中枢神经系统肿瘤不易发生颅外转移的原因之一。     

上皮性卵巢肿瘤细胞外基质的表达及意义

目的 :探讨上皮性卵巢肿瘤细胞外基质重要成分纤连蛋白、层粘蛋白和IV型胶原蛋白成分表达及改变的意义。方法 :采用免疫组化S P法分别研究在良性卵巢上皮瘤、交界性卵巢上皮瘤及上皮性卵巢癌中纤连蛋白、层粘蛋白和IV型胶原蛋白的表达。结果 :1.良性卵巢上皮瘤、交界性卵巢上皮瘤及上皮性卵巢癌中 ,这 3种成分表达呈由高向低的趋势 ,呈连续线形、间断线形、碎片状及缺失表达 (P <0 .0 5 ) ;2 .上皮性卵巢癌纤连蛋白、层粘蛋白和IV型胶原蛋白表达与临床分期、病理分级、转移及预后有关 (P <0 .0 5 ) ,三者表达与病理类型无关 (P >0 .0 5 ) ;3.上皮性卵巢癌中纤连蛋白、层粘蛋白和IV型胶原蛋白表达呈一致性 (P <0 .0 5 )。结论 :纤连蛋白、层粘蛋白和IV型胶原蛋白的改变与上皮性卵巢癌的病理分级、临床分期、转移和预后有关 ,三者对肿瘤细胞均有屏障作用 ,其阳性表达减低或缺失表达表明基膜受损严重 ,预后差 ,可作为判断预后的指标之一。     

胆脂瘤上皮过度增殖行为的免疫组化研究

目的　探讨中耳胆脂瘤上皮的过度增殖性和生长方式。方法　用免疫组化SP法观察了表皮生长因子受体 (epidermalgrowthfactorreceptor,EGFR) ,增殖细胞核抗原Ki6 7、Ⅳ型胶原蛋白(collagenIV)和层粘连蛋白 (laminin ,LN)在 18例胆脂瘤标本的表达 ,并与 8例外耳道正常皮肤相比较。结果　EGFR有两种染色图案 ,棕黄色的线状或颗粒状胞膜强染色和颗粒状的胞浆染色 ,胆脂瘤标本染色均强于皮肤。在Ki6 7的免疫染色中 ,阳性细胞核为棕黄色 ,胆脂瘤上皮的阳性细胞核比皮肤多。CollagenIV和LN图案极其相似 ,为连续的棕黄色线状和 (或 )带状图案。 4例胆脂瘤上皮基膜下结缔组织中的血管比皮肤丰富。结论　EGFR和Ki6 7在胆脂瘤上皮的表达从不同角度反映了胆脂瘤上皮的过度增殖性。CollagenIV和LN的表达说明胆脂瘤属良性病变 ,血液供应可能比皮肤丰富     

Localization of laminin isoforms in the guinea pig cochlea

OBJECTIVE: To elucidate the pathogenesis of inner ear disorders by examining the distribution of a major component of basement membranes, the glycoprotein laminin. STUDY DESIGN: Animal model. METHODS: Adult guinea pig cochleae were fixed with methanol and sectioned. Sections were examined for the presence of laminins alpha2, alpha5, beta1, and gamma1 using immunohistochemistry. RESULTS: Laminins alpha2, alpha5, and beta1 were not detected. Laminin gamma1 was found in the limbus, spiral ligament, and stria vascularis. CONCLUSIONS: Anti-laminin antibodies have been found in patients with inner ear disorders. Laminin gamma1 demonstrates specific staining at multiple sites in the guinea pig cochlea. These structures may be targets of antibodies causing sensorineural hearing loss.     

Immunohistochemical study of merosin-negative congenital muscular dystrophy: laminin α2 deficiency in skin biopsy

We studied the immunohistochemical expression of laminin subunits α2, α1, β1 in muscle and skin biopsy samples from three patients with congenital muscular dystrophy (CMD), and from ten control patients investigated for various neuromuscular disorders. Merosin α2 chain was not detectable in the basement membrane of muscle fibers, or in the nerve endings, cutaneous nerves, and corium in the skin of the CMD patients, whereas it was clearly expressed in the skin biopsy samples from control patients, especially in the nerve endings of the arrector pili muscles. Laminin α1 chain was expressed in the corium, in the muscle fiber membranes of arrector pili muscles and in cutaneous nerve fibers, perineurium and blood vessels in controls and in CMD patients. Laminin β1 chain was faintly expressed in the corium, and a diffuse labeling was detected on arrector pili muscle with enhanced expression at nerve endings, intracutaneous nerves and capillaries, with similar findings in all biopsy specimens. For merosin-negative CMD patients, skin biopsy may provide a diagnostic alternative to muscle biopsy since merosin deficiency can be demonstrated in the skin neural structures, and in particular in the nerve endings of the arrector pili smooth muscles. Received: 29 October 1996 / Revised, accepted: 27 January 1997     

GFAP,FVIII/RAg,Laminin, and fibronectin in gliosarcomas: An immunohistochemical study

Summary GFAP, Factor VIII/RAg, laminin, and fibronectin were immunohistochemically investigated in 15 glioblastomas and 15 gliosarcomas. GFAP was found variably positive in the glial areas. F VIII/RAg characterizes the endothelial cells and in gliosarcomas suggests the origin of the sarcomatous component from the endothelial proliferations. Laminin separates the two components and characterizes the inner and the outer basement membranes in the vessels. It is multiplied and thickened in endothelial proliferations, while it is often fragmented in the larger vessel wall proliferations. Our observations confirm that gliosarcoma represents the last stage of a process which starts with the endothelial hyperplasia of glioblastoma.Partially supported by CNR, Special Project Center, Grant no. 82.00410.96