负载抗原的DC与CIK共培养对耐药乳腺癌细胞的杀伤作用

目的:观察负载抗原的树突状细胞(dendritic cell,DC)与细胞因子诱导的杀伤细胞(cytokine-induced killer cell,CIK)对高表达P-糖蛋白(P-glycoprotein,P-gp)的多药耐药(multidrug resistance,MDR)人乳腺癌MCF-7/ADR细胞的杀伤作用。方法:提取健康人外周血单个核细胞,常规诱导出CIK及DC;制备MCF-7/ADR细胞冻融抗原后冲击DC,并与CIK共培养作为实验组(冻融物DC-CIK组),未负载抗原的DC与CIK共培养作为对照组(DC-CIK组),同时设单独培养的CIK组或DC组作为空白对照组。流式细胞术分析细胞的表型及P-gp表达,ELISA法测定细胞上清中IL-12、IFN-γ水平,MTT法检测对MCF-7/ADR及MCF-7细胞株的杀伤活性。结果:冻融物DC-CIK组、DC-CIK组细胞增殖活性均大于CIK组(P<0.05)。冻融物DC-CIK组对MCF-7/ADR、MCF-7细胞的杀伤活性在效靶比10∶1、20∶1、40∶1时分别为(44.29±1.39)%、(58.24±3.52)%、(68.9±2.83)%和(33.51±2.18)、(40.43±2.3)%、(44.62±1.19)%,均高于DC-CIK组及CIK组(P<0.05);冻融物DC-CIK组对MCF-7/ADR耐药细胞株的杀伤活性高于非耐药细胞株MCF7(P<0.05);而对于非耐药株MCF-7细胞的杀伤活性,冻融物DC-CIK组和DC-CIK组之间差异无统计学意义(P>0.05)。结论:DC与CIK共培养细胞增殖活性和细胞毒活性均强于CIK,经冻融抗原冲击的DC与CIK共培养可以显著提高对MCF-7/ADR耐药细胞株的杀伤活性。     

两种微创治疗方法在盘源性腰痛治疗中的应用

目的比较水冷式双极射频纤维环成形术和椎间盘内电热疗法治疗盘源性腰痛的临床效果及其并发症。方法 80例盘源性腰痛患者,随机分为A、B两组,每组40例,分别采用水冷式双极射频纤维环成形术和椎间盘内电热疗法进行治疗,观察两组患者手术前后VAS疼痛评分、Oswestry功能障碍指数评定的功能状态以及手术并发症等情况变化。结果经两种微创方法治疗后,两组患者疼痛评分均明显降低,功能状态显著改善,无严重并发症发生。结论水冷式双极射频纤维环成形术和椎间盘内电热疗法均能快速缓解患者疼痛,显著改善患者功能状态,并发症少,两者都是治疗盘源性腰痛的安全、有效的方法。     

2004-2009年广西靖西县淋病、梅毒、AIDS/HIV流行状况分析

目的了解位于中越边境的靖西县2004-2009年梅毒、淋病、艾滋病感染及发病情况,分析其流行特征和规律,为制订性病艾滋病防治策略和措施提供科学依据。方法收集该县2004-2009年的梅毒、淋病、AIDS/HIV病例疫情资料,采用Excel软件进行统计分析。结果全县人口数为61.7万,近6年报告梅毒、淋病、AIDS/HIV阳性病例共767例,人群发病率为21.68/10万,男性高于女性,其中淋病118例、梅毒595例、艾滋病11例(死亡6例)、HIV阳性43例(死亡10例)。以上3种疾病高发年龄在15～44岁年龄组,占总发病率的68.06%。农民发病人数占59.06%。梅毒病例数2007年后增多明显。自1997年发现HIV感染者后,2004-2009年AIDS/HIV患者每年有所增加,病死率呈逐年上升,平均病死率为29.63%。结论该县2004-2009年梅毒患者增加较快,AIDS/HIV阳性病例有所增多,防治工作应进一步加强。     

开通闭塞冠状动脉策略的全球性研究 GUSTO—Ⅱb（亚组研究）

病人资料 3 289例因急性冠脉综合征而接受溶栓治疗的患者,2274例接受t－PA治疗,1015例接受链激酶治疗。     

以IgA沿肾小球毛细血管襻沉积为主的急进性肾小球肾炎

目的:明确以IgA沿肾小球毛细血管襻沉积为主的急进性肾小球肾炎的临床与病理特点。方法:分析解放军总医院全军肾脏病研究所收治的1例以IgA沿肾小球毛细血管襻沉积为主的急进性肾小球肾炎病例,分析其临床特点、病理与电镜特征,以及对强化免疫抑制治疗的反应。结果:该病例临床表现为急进性肾炎综合征,肾功能恶化发展迅速。但无肺出血及全身性血管炎症状。血清自身抗体系列、抗GBM抗体与ANCA均为阴性。病理光镜示肾小球环绕型新月体形成,肾小血管无炎症改变。冰冻切片与石蜡微波修复直接免疫荧光示IgA沿肾小球毛细血管襻细颗粒状沉积,间接免疫荧光法检测血清IgA型抗GBM为阴性;电镜示节段性上皮下、基底膜内及系膜区电子致密物沉积。对强化激素冲击与免疫抑制剂治疗效果欠佳。结论:本病例为特殊类型的急进性肾小球肾炎,根据其临床特点、血清学检测、免疫荧光及电镜检查结果,无法归于目前急进性肾炎的分型,对其临床特点应予重视。     

Interleukin-6 is not involved in the interleukin-1-induced production of colony-stimulating factors by human bone marrow stromal cells and fibroblasts

Interleukin-6 (IL-6) is a multifunctional cytokine that plays a role in regulation of hematopoiesis. Because IL-6 is coinduced with colony- stimulating factors (CSFs) by various cell types in response to stimulation with IL-1, we investigated whether IL-6 is involved in the IL-1-induced production of CSF by human bone marrow (BM) cells in long- term culture or human fibroblasts. We showed that IL-6 does not induce CSF production by these cells. Neither addition of exogenous IL-6 nor neutralization of endogenous production of IL-6 by an anti-IL-6 monoclonal antibody (MoAb) diminished the IL-1-induced colony- stimulating activity (CSA), indicating that IL-6 did not act synergistically with IL-1. Finally, IL-6 did not influence the kinetics of IL-1-induced CSA production by human fibroblasts. We conclude that IL-6, either alone or in combination with IL-1, does not induce CSF production by human BM stromal cells or fibroblasts.     

小藤铃儿草的生物碱成分

自小藤铃儿草Dactylicapnos torulosa(Hook.f ct Thomas.)Hutchins中分得六个单体,通过UV,IR,MS,~1HNMR和~(13)CNMR解析,鉴定了四个,其中一个为新化合物,命名为紫金龙碱(zijinlongine,Ⅰ),其他三个为已知化合物:氯化1-甲氧基小檗碱(1-methoxylberberium chloride,Ⅱ),氯化三乙基苯胺(triethylphcnylamium chloride,Ⅲ)和异紫堇定(isocorydine,Ⅳ)。Ⅱ和Ⅲ系首次从植物中得到。     

米非司酮抗人子宫内膜癌裸鼠移植瘤作用的实验研究

目的：观察米非司酮抗人子官内膜癌裸鼠移植瘤的作用，为临床应用提供依据。方法：将裸鼠分为米非司酮、三苯氧胺、米非司酮＋三苯氧胺、对照４组，用药并观察移植瘤生长情况，电镜观察移植瘤，测定裸鼠血清雌二醇。结果：米非司酮抗癌作用与三苯氧胺相似，二者联合作用增强。米非司酮使癌细胞坏死，内质网及线粒体肿胀，使裸鼠血清雌二醇升高。结论：米非司酮有抗子宫内膜癌作用，与三苯氧胺联合作用增强。     

Interleukin-4 induces a substance in bone marrow stromal cells that reversibly inhibits factor-dependent and factor-independent cell proliferation

Bone marrow-derived stromal cell monolayers pretreated with recombinant interleukin-4 (IL-4) inhibit the growth of hematopoietic cells. This was demonstrated by inhibition of fresh bone marrow-derived, IL-3- induced soft agar colonies as well as by inhibition of proliferation of IL-3-dependent cell lines and of a Friend virus-transformed erythroleukemic cell line. Pretreatment of stromal cells with IL-4 for five to seven days induced the inhibitory activity. IL-4 could then be removed before "plating" the bone marrow cells in soft agar, indicating that the inhibitory activity did not depend on the action of IL-4 on the precursors of the soft agar colonies. The inhibitory activity appears to be mediated by a soluble factor since inhibition was achieved even if the stromal cell layer was separated from the colony forming cells by an "empty" agar layer. However, supernatants of IL-4- induced stromal cell layers had no detectable inhibitory activity. The inhibitory action of the IL-4-pretreated stromal cell lines was not the result of killing of the precursor cells since it could be reversed if the agar layer containing the colony-forming cells was removed from the stromal cell layer and cultured with IL-3. Hydrocortisone (HC) blocked the inhibitory effect if added either in the IL-4 preincubation phase or during the colony formation stage, implying that HC blocked both induction of the inhibitory activity and its release or its effector function. A homogenous long-term stromal cell line could not be induced to exert the inhibitory activity; partial inhibition could be achieved with pure macrophages stimulated with IL-4 and CSF-1, suggesting that the inhibitory activity induced by IL-4 in mixed stromal cell layers may depend on a complex mechanism involving more than one cell type. Northern analysis of RNA from IL-4-induced and uninduced stromal cells indicated that IL-4 did not upregulate expression of CSF-1 or transforming growth factor-beta (TGF-beta) and only modestly increased expression of tumor necrosis factor, suggesting that these cytokines were not responsible for the inhibitory activity. The capacity of IL-4 to induce inhibitory activity in stromal cell layers suggests that IL-4 may play a role in the regulation of hematopoiesis.