重度间歇性低氧对大鼠认知功能及海马超微结构的影响

目的通过模拟阻塞性睡眠呼吸暂停低通气综合征(OSAHS)的发病特征,建立大鼠间歇性低氧(IH)模型,观察重度间歇低氧(50mL/L)条件下不同暴露时间对大鼠学习记忆功能的影响和海马CA1区超微结构的改变。方法成年雄性Wistar大鼠48只分为对照(UC)组和50mL/L间歇性低氧(50mL/L IH)组。UC组放入舱内仅给予压缩空气,50mL/L IH组大鼠每日放入自制低氧舱内予间歇低氧暴露8h,分别干预2、4、6、8周。采用Morris水迷宫检测各组大鼠学习记忆功能,电镜观察海马区神经细胞超微结构。结果与UC组比较,50mL/L IH组中随低氧时间延长,神经细胞核、线粒体、粗面内质网、突触等超微结构损伤明显,水迷宫检测动物逃避潜伏期时间随缺氧时间增加而延长[从2周(49.17±8.87)s到8周的(68.42±7.91)s],均长于UC组[2周和8周分别为(25.66±2.97)s,(25.29±3.07)s];50mL/L IH组的穿台次数也随缺氧时间增加而减少(从2周7.68±1.6到8周的2.87±0.92),均少于UC组(2周和8周分别为11.57±2.18,10.65±1.26)。结论间歇性低氧可造成认知功能障碍,与海马区神经细胞超微结构损伤有关。     

移居高原罹患矽肺矿工20年心血管X线改变的动态观测

选择移居2500m高原63名矽肺矿工，连续20年摄后前位胸片，按居住年限分组，自身对照，观察矽肺与肺动脉高压的演变过程．分析矽肺X线心血管4项指标的改变。结果表明：动态观察矽肺X线及心血管各指标的改变，对预测高原人体矽肺的发生，评定矽肺的发展程度，观察疗效和对矽肺愈后判定有着非常重要的临床应用价值。     

人体低氧状态心血管功能代偿水平的个体差异

为探讨人体低氧条件下循环功能的代偿水平，进行了有关测试。结果显示：高海拔区在总体适应水平上每搏量减少（P＜0．01），心输出量及平均动脉压增加（P＜0．01），且随高度增加，后两项均需增加（P＜0．05）。对于不同群体来说，适应良好者每搏量及总外周阻力不变，心输出量增加（P＜0．01）；适应不良者每搏量减少（P＜0．05），总外周阻力增加，心输出量亦增加但显著性稍差（P＜0．05）。推测人体在不同低氧条件下具有不同的心血管适应能力，且该适应能力具有个体差异。     

Benthic habitat quality assessment of an oxygen stressed fjord by surface and sediment profile images

In May and October 1994 the benthic habitats in Havstensfjord (26 km²), a seasonally oxygen stressed stratified fjord, were classified by taking sediment surface and sediment profile images (SPI) at 90 stations, randomized into nine strata. Qualitative grab samples for faunal inspection were taken at about of the stations in both May and October to help to identify objects in the images. The images give information on sediment characteristics (texture, oxic/anoxic conditions, lamination) which often can be related to functional properties of the macrofauna (burrows, tubes, feeding voids, reworked sediment) or to observations on benthic epifauna. In combination, such variables mirror the quality of the benthic habitat. Analysis of sediment profile images was done with multivariate methods [Benthic Habitat Quality (BHQ) index] and univariate statistical methods to describe differences between areas and depths. Variance analysis of BHQ indices indicated a significant interaction between area and depth. In both the northeast and northwest strata the oxygen stress had induced a habitat degradation at depths deeper than 25 m compared to shallower northwest and northeast strata and all south depth strata. No significant difference in mean BHQ index was found between May and October. We discuss the potential application of the SPI technique for efficient monitoring oxygen stressed marine coastal areas.     

移居高原罹患矽肺矿工20年心血管X线改变的动态观测

选择移居2500m高原63名矽肺矿工，连续20年摄后前位胸片，按居住年限分组，自身对照，观察矽肺与肺动脉高压的演变过程．分析矽肺X线心血管4项指标的改变。结果表明：动态观察矽肺X线及心血管各指标的改变，对预测高原人体矽肺的发生，评定矽肺的发展程度，观察疗效和对矽肺愈后判定有着非常重要的临床应用价值。     

Gli-1在缺氧诱导乳腺癌MDA-MB-231细胞上皮-间质转分化中的重要作用

目的探讨Gli-1在缺氧诱导乳腺癌MDA-MB-231细胞上皮-间质转分化(EMT)及侵袭中的重要作用。方法通过缺氧培养乳腺癌MDA-MB-231细胞,以常氧培养作为对照。Transwell小室侵袭试验检测各组MDAMB-231细胞的侵袭能力;Western blot检测HIF-1α、Gli-1、E-Cadherin和vimentin蛋白的表达水平。通过shRNA稳定转染乳腺癌细胞,再次通过Transwell小室侵袭试验检测缺氧对乳腺癌细胞侵袭能力的影响,Western blot检测HIF-1α、Gli-1、E-Cadherin和vimentin蛋白的表达水平。结果缺氧可明显诱导乳腺癌MDA-MB-231细胞侵袭,并上调HIF-1α、Gli-1和vimentin蛋白,下调E-cadherin蛋白。靶向沉默Gli-1基因后,缺氧失去了对乳腺癌细胞侵袭和EMT的诱导作用。结论缺氧通过上调Gli-1表达活化Hedgehog通路,诱导乳腺癌细胞侵袭及EMT过程。     

双靶向诱导超抗原TSST-1基因重组逆转录病毒的包装及鉴定

目的包装出携5拷贝缺氧反应元件(5 HRE)增强子和癌胚抗原启动子(CEAp)联合调控的超抗原中毒性休克综合征毒素-1(TSST-1)基因的逆转录病毒,并建立稳定表达TSST-1的人结肠癌Lovo细胞株。方法应用已构建好的逆转录病毒载体pLEGFP-N1-5 HRE-CEAp-TSST-1-linker-CD80TM,与辅助质粒pMB-MLV、pMB-G共转染入293T细胞,LaSRT法检测病毒滴度。包装出的逆转录病毒感染CEA阳性的人结肠癌细胞株Lovo和CEA阴性的人宫颈癌细胞株Hela。应用RT-PCR和免疫组化方法鉴定TSST-1的表达。结果获得重组逆转录病毒滴度约为1×106CFU/mL。RT-PCR及免疫组化证实经病毒感染的Lovo细胞在mRNA和蛋白水平均有TSST-1表达,缺氧环境中的mRNA表达量更高,且细胞传代20次后依然有TSST-1 mRNA表达;经病毒感染的Hela细胞在常氧或缺氧状态下均无TSST-1 mRNA及蛋白表达。结论包装出较高滴度重组逆转录病毒,并能靶向性在CEA阳性肿瘤内稳定表达TSST-1,为后续检验TSST-1对肿瘤的杀伤效应奠定了基础。     

Hypoxia-induced enhancement of cell invasiveness in SMMC7721 hepatocellular carcinoma cells

Objective To explore the effects of hypoxia (1% O2) on the ability of cell invasiveness and expression of KAI1/CD82 in SMMC7721 hepatocellular carcinoma cells. Methods SMMC7721 hepatocellular carcinoma cells were cultured by hypoxia ( 1% O2) in vitro, and the ability of cell invasiveness was analyzed by cell invasion assay.Immunohistochemistry staining technique was used to evaluate the protein expression of KAI1/CD82. Results Cell invasion assay revealed that hypoxia enhanced the ability of invasiveness of hepatocellular carcinoma cells. In addition,KAI1/CD82 protein expression was positive in cultured SMMC7721 hepatocellular carcinoma cells, and it was located diffusedly in the cytoplasm and on the membrane. KAI1/CD82 protein expression was down-regulated when mediated by hypoxia; at the same time, it showed a time-effect relationship. Conclusion Hypoxia can enhance invasiveness of hepatocellular carcinoma cells. The down-regulation of KAI1/CD82 expression may play a certain role in those courses.     

Marine Biodiversity and Institutional Interplay

The interplay between the biodiversity regime and fisheries management and conservation regimes is not a critically important phenomenon at this point in time. For now, the institutions most relevant for the management of marine and coastal biodiversity are entrenched in conventional fisheries management structures. Biodiversity-oriented institutions appear to be less in touch with the practical aspects of resource management. The most significant interplay occurs at the global level, where several oceans-related regimes appear to be affected by the concerns raised by the CBD. The important question with regard to the longer term, is what impact the creation and operation of the CBD will have on various fisheries regimes in the future.     

腺苷对正常及模拟缺血缺氧状态下豚鼠心肌细胞动作电位及L型钙通道电流的影响

目的　研究腺苷 (Ado)在正常和缺血缺氧时对心室肌细胞跨膜动作电位 (AP)和L 型钙电流 (ICa .L)的影响。方法　用离体心室肌和酶解法分离得到单个豚鼠心室肌细胞 ,应用细胞内微电极和全细胞膜片钳技术记录动作电位和电流。结果　Ado对正常心室肌跨膜动作电位无明显影响 ,但在缺血缺氧状态下 ,动作电位时程(APD)各参数的缩短较对照组更显著 ,Ado在 10 0 μmol·L-1时 ,APD各参数的缩短程度同对照组比较具有显著性差异 (P <0 0 1)。再灌注后APD未能恢复到原来的水平 ,而表现出的明显的迟后恢复。Ado对正常心室肌细胞ICa .L无明显影响 ;在缺血缺氧时ICa.L受到明显抑制 ,其抑制率为 (38± 11) % ,再灌注后ICa .L可基本恢复 ;而Ado并无增大心肌细胞在缺血缺氧时ICa.L减小的作用 ,其抑制率为 (42± 9) % ,但无明显统计学意义 (P >0 0 5 ) ,而再灌注后ICa.L的恢复比较缓慢。结论　①Ado在正常条件下对豚鼠心室肌细胞动作电位和ICa.L无明显作用 ;②Ado在缺血缺氧时可使APD的缩短明显增大 ,再灌注时APD恢复明显延迟 ;③Ado并不能加重心肌在缺血时ICa .L的减小 ;④心肌缺血缺氧时Ado增大APD的缩短与ICa .L的变化可能无明显平行关系