细胞黏附分子(ICAM-1)在大鼠弥漫性脑损伤中的表达意义

目的探讨ICAM—1在大鼠弥漫性脑损伤中的表达及意义。方法采用Marmarou方法获得大鼠弥漫性脑损伤模型．实时定量RT—PCR、S—P免疫组化法分别测定ICAM—1蛋白和mRNA在外伤后不同时间点的表达变化．干湿重法测脑组织含水量．组织切片苏木精一伊红染色观测炎性细胞浸润情况。结果外伤组与假手术对照组比较，ICAM—1蛋白表达分别于伤后6h明显升高．72h达到高峰（P〈0.05），ICAM—ImRNA表达3h即明显升高，72h达最高峰，其后下降。7d时仍高于假手术对照组（P〈0．01）。伤后脑组织含水量较假手术对照组高，同时炎性细胞大量聚集。结论大鼠脑外伤诱导了ICAM—1的表达．ICAM—1通过介导炎性细胞的浸润可能参与了伤后脑水肿的形成过程．     

PCR-SSP法HLA-A、B基因分型与血清学分型的比较

目的比较聚合酶链反应-序列特异性引物(PCR-SSP)进行HLA-Ⅰ类A、B抗原位点分型的准确性,并探讨血清学分型错误发生的原因。方法用PCR-SSP以及单克隆抗体血清学分型技术对HLA-A、B分型并比较。结果34例样本PCR-SSP基因分型无假阳性和假阴性出现。PCR-SSP法与血清学比较,血清学检出错误或漏检率分别为HLA-A位点23.5%,B位点26.5%。血清学发生错误或易混淆的抗原有:A2和A68、A32和A33,B5、B60和61。结论PCR-SSP法进行HLA-A、B抗原等位基因分型具有分辨率高、特异性强、重复性好、实验过程简捷快速、分型结果较血清学更加准确可靠的优点。     

1 240例女性生殖道支原体感染分析

目的 为了解生殖道支原体在晚期孕妇、育龄妇女、念珠菌性阴道炎和淋球菌性阴道炎患者中的感染状况。方法 采用套式聚合酶链反应技术，对962例晚期孕妇、85例育龄妇女、90例念珠菌性阴道炎和103例淋球菌性阴道炎患者的宫颈拭子标本进行了生殖道支原体检测。结果 在晚期孕妇、育龄妇女、念珠菌性阴道炎和淋球菌性阴道炎患者中生殖道支原体的检出率分别为4．16％、3．52％、11．1l％和13．59％。结论 生殖道支原体在晚期孕妇、育龄妇女、念珠菌性阴道炎和淋球菌性阴道炎妇女中均有一定的检出率。     

宫颈癌细胞中DAPK1基因CpG岛甲基化及其表达

目的 :探讨宫颈癌细胞中凋亡相关蛋白激酶 1(DAPK1 )基因CpG岛甲基化及其表达与宫颈癌的相关性 .方法 :应用甲基化特异性PCR和SABC免疫组化方法 ,检测 32(鳞癌 1 8,腺癌 1 4 )例宫颈癌组织DAPK1基因CpG岛甲基化修饰及蛋白表达 .结果 :宫颈癌中DAPK1基因甲基化扩增阳性率明显增高 5 6 .3% ,与正常宫颈比较有显著性差异 (P <0 .0 5 ) ,鳞癌与腺癌甲基化扩增阳性率无显著差异 (P >0 .0 5 ) ;宫颈癌中DAPK1蛋白表达阳性率降低 1 5 .6 3% ,与正常宫颈比较有显著性差异 (P <0 .0 5 ) ,鳞癌和 7例与腺癌无显著性差异 (P >0 .0 5 ) .结论 :DAPK1基因CpG岛异常甲基化修饰能抑制DAPK1的转录 ,使DAPK1蛋白不表达 ,丧失抑癌作用 ,是促进正常宫颈上皮细胞癌变的一个重要因素     

B细胞淋巴瘤石蜡包埋组织克隆性重链基因重排检测

目的 探讨克隆性重链基因重排检测在B细胞淋巴瘤(B—NHL)诊断中的价值。方法 用半巢式聚合酶链反应(semi—nested PCR)、聚丙烯酰胺凝胶电泳(PAGE)及银染技术，检测经形态学及免疫组织化学确诊的23例B—NHL石蜡包埋组织标本的克隆性免疫球蛋白第三互补决定区(IgHCDR3)重排基因，对照组为7例T细胞淋巴瘤(T—NHL)及6例反应性增生或肉芽肿性淋巴结炎。结果 B—NHL IgHCDR3检出的阳性率87．0％(20／23)，假阳性率7．7％(1／13)，假阴性率13．0％(3／23)。结论 检测克隆性IgHCDR3重排为B—NHL的诊断及鉴别诊断提供有效的辅助手段。     

D1S549等6个短串重复序列基因座在河南汉族群体的遗传多态性

目的　探讨河南汉族群体的D1S5 49、D3S175 4、D2 2S683和CSF1PO、TPOX、TH0 1基因座遗传多态性分布。方法　ACD抗凝血样采自 2 19名无血缘关系汉族个体 ,酚 氯仿法提取DNA ,应用复合扩增技术对D1S5 49等 6个短串重复序列 (STR)基因座进行扩增 ,采用高分辨率的聚丙烯酰胺凝胶电泳分离、银染法显影技术。统计各基因频率、计算杂合度、多态信息含量、个人识别概率及亲权否定概率。结果　 6个STR基因座基因频率的分布均符合Hardy Weinberg平衡 ,各基因座的杂合度分别为 0 .7964、0 .72 3 1、0 .815 9、0 .75 81、0 .65 2 3、0 .6816;非父排除概率为 0 .62 46、0 .4914、0 .65 0 1、0 .5 2 3 6、0 .40 98、0 .42 87;个人识别机率为 0 .8996、0 .8781、0 .92 3 1、0 .8896、0 .8167、0 .83 92 ;多态信息含量为 0 .72 16、0 .6994、0 .742 1、0 .7169、0 .65 17、0 .710 6。结论　D1S5 49等 6个STR基因座是一组高度多态性的遗传标记系统 ,在人类遗传学及法医学研究中具有重要意义     

Concurrent oral and genital infection with HPV DNA types 6 and 11 in a heterosexual male

Objective Detection of HPV DNA in oral and genital lesions of a heterosexual male. 4 months after oral and vaginal intercourse with a woman with vulvar warts. Passible modes of acquisition of oral HPV infection in the male sexual partner are discussed. Setting Genitourinary Medicine clinic. Methods Polymerase chain reaction amplification of genomic DNA from oral and genital lesions. HPV DNA typing by dot blot hybridization. Results HPV DNA types 6 and 11 were identified in a polypoid tongue lesion and in a penile wart from the male sexual partner. Conclusions The acquisition of oral HPV infection in the male sexual partner may have resulted from genital-oral HPV transfer, either by direct contact with vulvar warts or by digital self-inoculation.     

RAPD技术用于结核病交叉感染的鉴别

目的：调查RAPD技术用于结核菌株DNA指纹鉴定的效果。方法：采用多重PCR方法对一组2例母女同时发病的肺结核患者和一组2例先后发病的兄妹肺结核患者的病原菌进行了菌种鉴定。采用RAPD技术对它们的基因组DNA进行指纹多态性分析。结果：4株病原菌均为结核分支杆菌。经RAPD分型，其中母女组2菌株的DNA指纹图谱完全相同，兄妹组2菌株的DNA指纹图谱有所不同。证明母女组所染病原菌的同源性很好，很可能为同一感染源，母女之间交叉感染的可能性很大；兄妹组病原菌的同源性较差，为非交叉感染。结论：RAPD技术适用于结核分支杆菌流行病学调查，特别是交叉感染的鉴别。     

多抗甲素对人NK细胞活性的作用机理研究

作者应用单细胞细胞毒试验及形态学观察，研究多抗甲素（ＰＡＡ）对人体自然杀伤（ＮＫ）细胞活性的作用机理。结果表明：ＰＡＡ能增强食道癌患者淋巴细胞（ＰＢＬ）明显低下的结合率（Ｂ％）和杀伤率（Ｋ％），也可增强正常人ＰＢＬ的Ｋ％，但对正常人ＰＢＬ的Ｂ％无影响。形态学观察发现：与靶细胞结合的ＰＢＬ除大颗粒ＰＢＬ外，尚有普通的非颗粒ＰＢＬ，结合的靶细胞损伤首先表现为线粒体肿胀、空泡变，然后核固缩，核膜损伤，细胞严重空泡变性等，偶见靶细胞与自然杀伤细胞结合部质膜破损的现象。经ＰＡＡ预处理的靶效细胞结合的形态改变无明显差异，但食道癌组的杀伤作用出现较早，且明显增强。     

The relationship of gingival crevicular fluid short chain carboxylic acid concentration to gingival inflammation

Abstract Short-chain carboxylic acids (SCCA; C≤5: e.g., lactic acid, propionic acid, butyric acid) are metabolic by-products of bacterial metabolism which accumulate in the gingival crevice, and exhibit significant biological activity, including the ability to alter gene expression. It has been hypothesized that among the activities of SCCAs are their ability to contribute to gingival inflammation. This concept complements the notion that specific periodontal pathogens are the causative agents of gingival inflammation. To begin testing these 2 hypotheses, we examined the relationship between SCCA concentrations, specific putative periodontal pathogens, and gingival inflammation in medically healthy periodontally diseased subjects. We reasoned that if SCCAs and/or specific periodontal pathogens were causative gingival inflammatory agents, gingival inflammation should increase with increasing concentration of the inflammatory mediator. We also recognized that other clinical variables needed to be controlled for, and an objective quantitative assessment of gingival inflammation used. To accomplish these tasks, sites within subjects were stratified by location and pocket depth, and the following quantified: bacteria] presence; SCCA concentration: and gingival inflammation. The results indicated that gingival inflammation directly and significantly correlated with SCCA concentrations in the maxillary and mandibular molars, incisors and canines (all r≥0.47; all p≤ 0.015; too few bicuspids were available for complete analysis). The relationship between gingival inflammation and SCCA concentration was best described by a natural log relationship. Gingival inflammation did not, however, correlate positively with either the total number of specific putative periodontal pathogens, or the sum of subsets of these pathogens (?0.31 ≤r≤ 0.39; 0.08 ≤p 0.75) for any of the locations. Finally, the SCCA concentration did not correlate with the level of individual or groups of pathogens. These data, together with historical work and other preliminary data, support the hypothesis that SCCA, rather than specific putative periodontal pathogens, may be a causative agent in gingival inflammation. This work may, in part, begin to explain the apparent lack of a direct relationship between current gingival inflammation and the prediction of bacterially mediated periodontal attachment loss.