磁刺激用平面线圈结构的优化研究

文中建立了采用任意形状平面线圈磁刺激仪的RLC模型，给出了模型参数的计算方法。为了优化线圈，将磁刺激仪线圈的性能指标分为反映线圈输出性能的峰值磁能和反映线圈结构的几何变量。在磁刺激激活函数达到阈值条件下，调整平面螺旋线圈的结构并计算出依赖于线圈结构参数的输出性能值，从而，寻找最优的线圈几何参数。优化结果表明：线圈外半径是关键因素，给定阈值条件，选择合适的线圈外半径，可以大大降低线圈峰值磁能；另外，现在使用的圆环线圈并非最优，D形线圈优于圆环线圈。     

CVB3-VP1基因免疫诱导特异性抗病毒免疫应答及保护作用

目的 :构建表达柯萨奇病毒B3(CVB3)主要包膜蛋白VP1的基因疫苗 ,并研究该疫苗诱导CVB3特异性免疫应答及免疫保护的作用。方法 :抽提CVB3RNA ,以RT PCR扩增VP1基因 ,克隆于真核表达载体 pcDNA3中 ,构建质粒pcDNA3 VP1。将该质粒转染Hela细胞 ,观察其表达情况 ;以 5 0 μgpcDNA3 VP1质粒DNA肌注免疫BALB/c小鼠 3次 ,检测CVB3特异性体液和细胞免疫应答。间隔 4wk以 5×LD50 的CVB3攻击小鼠 ,观察攻击后小鼠的存活情况。结果 :构建了重组质粒 pcDNA3 VP1,并在体外获得有效表达。以该质粒肌肉免疫BALB/c小鼠 ,可诱生高水平的IgM和IgG ,VP1多肽特异性淋巴细胞增殖反应及CTL活性均显著高于 pcDNA3免疫的对照组。病毒攻击试验表明 ,pcDNA3 VP1免疫组33.3%小鼠可长期存活 ,其心肌组织未见明显的病理学改变 ;而对照小鼠平均仅存活 6 .7d ,心肌显示大量的局灶性坏死和炎性细胞浸润。结论 :pcDNA3 VP1免疫可诱生CVB3特异性体液及细胞免疫应答 ,保护免疫小鼠抵抗CVB3的致死性攻击     

人胎儿睾丸发生过程中表皮生长因子与细胞增殖核抗原的表达

目的　观察表皮生长因子 (EGF)与细胞增殖核抗原 (PCNA)在人胎儿睾丸发生过程中的表达特征 ,探讨两者在睾丸发生中的作用。　方法　用SP免疫细胞化学技术检测了人胎儿 12～ 32周睾丸间质细胞、支持细胞、生殖细胞EGF、PCNA阳性细胞表达率。　结果　EGF在胎儿 12周龄睾丸组织未见表达 ,16～ 32周龄睾丸间质细胞呈阳性表达 ,16～ 2 0周为表达高峰 ,随着胎龄的增长呈逐渐下降趋势 (P <0 0 1) ;PCNA在胎儿睾丸间质细胞、支持细胞和生殖细胞均有不同程度表达 ,16～ 2 0周为表达高峰 ,随着胎龄的增长呈逐渐下降趋势 (P <0 0 1)。　结论　EGF与PCNA在人胎儿睾丸发育过程中有不同程度的表达 ,表明EGF与PCNA在睾丸发育过程中起着一定的作用     

人缺血脑组织中TNF-α和IL-1β的表达

目的 :检测人缺血脑组织中TNF α和IL 1β的表达。 方法 :将 13例脑梗死的死亡病例按发病时间分成 <2d、3～ 5d、 >5d3个组 ,以非缺血侧半球作为对照 ,用免疫组化染色法检测缺血脑组织中TNF α和IL 1β的表达。结果 :人脑缺血后缺血病灶中TNF α和IL 1β呈高表达 ,与正常侧脑组织相比较有极显著差异。TNF α和IL 1β表达细胞的分布与缺血灶相一致 ,呈局灶性分布。TNF α的表达高峰在病后 2d内。IL 1β表达高峰在病后 3～ 5d。在病后 5d ,缺血侧TNF α和IL 1β的表达与正常侧无显著差异。结论 :人类脑缺血组织中TNF α和IL 1β的表达与动物实验的结果相似 ,提示TNF α和IL 1β参与了脑缺血损伤 ,有助于临床建立新的有针对性的治疗措施     

关于乳腺普通性增生、不典型增生和原位癌相互关系及鉴别诊断的探讨

目的 探讨各种类型乳腺增生症的发病特点、形态学分类、不典型增生与乳腺癌的关系以及不典型增生与乳腺原位癌的鉴别诊断标准。方法 (1)观察本院300例乳腺良性增生性病变的临床发病特点及其病理形态改变。(2)观察86例大切片乳腺癌旁不典型增生病灶与癌灶的关系。结果 乳腺增生症中,纤维腺瘤为主型好发于21～30岁年龄组,而不典型增生病变则多见于40～60岁组。其中囊肿病仅占6．0％,而纤维腺瘤变达25．4％;癌旁组织中不典型增生发生率为65．1％,其中以导管原位癌发生率最高,达74．9％。结论 研究证实了1997年(舟山)“乳腺增生症的组织学分类”(推荐方案)的可行性。乳腺不典型增生与乳腺癌的发生密切相关。乳腺增生症可归纳为普通性增生和不典型增生。不典型增生的特殊增生细胞具有特别的诊断价值。重度不典型增生与原位癌的鉴别诊断有一定困难,但大部分可分。     

Significance of beta-catenin and pRB pathway components in malignant ovarian germ cell tumours: INK4A promoter CpG island methylation is associated with cell proliferation

To clarify the mechanisms underlying cell cycle promotion in malignant germ cell tumours of the ovary (MGCTOs), beta-catenin and components of the pRB pathway, cyclin D1 and p16, were analysed in relation to cell proliferation. Immunohistochemically, p16 protein was not expressed in a number of MGCTOs (9 of 42 tumours: 21.4%) and was associated with p16 gene (INK4A) promoter 5'-CpG islands methylation. Amplification of the cyclin D1 gene (CCND1) was detected in a small number of MGCTOs (5 of 42 tumours: 13.5%). Reduced expression of p16 due to promoter methylation correlated significantly with increased cell proliferation as evidenced by Ki-67 labelling index (p < 0.001) and mitotic index (p < 0.01). In some tumour types, nuclear localization of beta-catenin has been reported to be associated with beta-catenin gene (CTNNB1) mutation, cyclin D1 overexpression, and increased cell proliferation. Nuclear localization of beta-catenin, which was observed in MGCTOs other than dysgerminoma, was not associated with cyclin D1 expression and increased cell proliferation, but appeared to be related to tumour differentiation. Furthermore, CTNNB1 mutations were not detected in any of the MGCTOs examined. Our results suggest that reduced expression of p16 due to INK4A promoter methylation is one of the principal factors that promote cell proliferation in MGCTOs. Thus, p16 may be a novel target for gene therapies to treat MGCTOs.     

A new microcellular cytotoxicity test based on calcein AM release

We present a microtest for cell-mediated immunity, based on the use of the Tarasaki tray and calcein AM vital dye. The number of target cells needed has been reduced to 500 per test with a corresponding tenfold reduction in the number of effector cells needed. Results were read at the rate of 1 second per test using a fluorimeter attached to a microscope. Each reaction was also confirmed visually with the use of ethidium bromide as a counterstain for dead cells. The calcein AM dye used to stain the living cells was shown to have a low spontaneous leakage rate—less than 15% in 4 hours at 37°C. Dilutions of targets stained by calcein AM had a linear relationship with measured fluorescence values. NK cells, LAKs, and CTLs were readily detectable by this microtest. Quantitation of killing and kinetic analysis was readily performed with this test system. A significant positive correlation to ⁵¹Cr-release results was found. We conclude that the microtest should find wide application in studies of cell-mediated immunity.