γ-Glutamyl-transpeptidase in lymphatic tissues ofMastomys natalensis during an infection withAcanthocheilonema viteae

Summary DuringAcanthocheilonema viteae infection, the specific activity of -glutamyltranspeptidase (-GT) increased in peritoneal exudate cells and bone marrow and decreased in lymphnodes ofMastomys natalensis throughout the course of infection. However, though there was an increase in specific activity of -GT in thymus and spleen during the prepatent phase ofA. viteae infection, the level either returned to normal or decreased during the latent phase of infection. A close correlation was observed between the host's immune status duringA. viteae infection and the level of -GT in lymphoid tissues.Communication No. 4535 from Central Drug Research Institute, Lucknow.     

光系统核心天线CP43, CP47 中b-Car 与Chl a分子间的能量传递

以纯化的核心天线ＣＰ４３和Ｃ灾材料产荧光激发光谱比较的方法,计算出在３和ＣＰ４７中β－Ｃａｒ到Ｃｈｌａ分子之间的能量传递效率分别为２９．１％和６２．８％,证明了在常温下,ＣＰ４３和Ｃ宫都存在着β－Ｃａｒ到Ｃｈｌａ分子之间的能量传递,为期人能量传递可能以“Ｄｅｘｔｅｒ的电子交换机制”进行,还对ＣＰ４３和ＣＰ４７中β－Ｃａｒ和Ｃｈｌａ分子之间的空间位置关系进行了讨论。     

第43届世界体操锦标赛男子体操比赛成绩分析——兼论2012年伦敦奥运会男子体操比赛格局

运用文献资料法、录像观察法、数理统计法对第43届世界体操锦标赛男子体操比赛情况进行了统计分析,并分析展望了伦敦奥运会我国男子体操的竞争实力。结果表明:1)男子团体比赛中,中国男团实力强大且发挥稳定,日本队步步逼近,中日竞争尤为激烈,美国队进步较快,俄罗斯强劲复苏;2)在全能比赛中,日本队的实力较为明显,中国队缺少全能型选手;3)单项比赛的争夺呈现出百花齐放的态势,19枚奖牌被11个国家瓜分,中国队的吊环、单杠具有较大优势,但是跳马、鞍马有待提升实力;4)提高强项的稳定性和创新性,提升弱项的实力是中国男队再创伦敦奥运会佳绩的关键。     

糖尿病性勃起功能障碍多因素发病机制研究

从神经、血管、代谢、离子通道等多个角度出发,研究糖尿病性勃起功能障碍(DMED)的发病机制,为开展DMED的综合治疗临床研究提供前期研究基础.成年雄性SD大鼠50只,随机取35只大鼠用于制作糖尿病模型,其余大鼠作为正常对照.饲养8周后,用阿朴吗啡法筛选DMED大鼠,用电刺激勃起神经测定海绵体内压(ICP)方法评价勃起功能.取正常组和DMED组大鼠的阴茎海绵体组织,分成若干份,用免疫组化法测定海绵体组织一氧化氮合酶(NOS)的3种亚型(nNOS,eNOS,iNOS)的变化;用Western Blot法测定神经生长因子(NGF)在海绵体组织的表达差异;用放射免疫法测定海绵体组织血管紧张素II(AngII)含量差异;用Western Blot法测定血管内皮生长因子(VEGF)和缝隙连接蛋白Connexin-43含量差异.与正常对照组相比,DMED大鼠ICP测定值明显降低;海绵体组织中nNOS、eNOS表达明显降低,而iNOS表达明显增加;NGF蛋白表达明显增加;血管紧张素II水平显著升高;VEGF蛋白表达明显减少;Connexin-43蛋白表达减少.以上试验结果说明DMED发病机制复杂,与神经、血管、代谢、离子通道等均有关.提示在今后临床治疗研究和实践中,应该从各个角度出发,针对多因素发病机制,采用综合治疗的方法,以提高疗效.     

Alteration of cadherin isoform expression and inhibition of gap junctions in stomach carcinoma cells

To explore cell malignant phenotype correlated changes of cell surface adhesion molecules and cell-cell communication in carcinogenesis, human stomach transformed and cancer cell lines were investigated. Expressions of E-cadherin, N-cadherin,α-catenin, β-catenin as well as gap junction (GJ) protein Cx32 were studied by utilization of immunoblotting, immunocytochemical and fluorescent dye transfer methods. Mammalian normal stomach mucosal cells expressed E-cadherin but not N-cadherin. E-cadherin im-munofluorescence was detected at cell membranous adher-ens junctions (AJ) where colocalization with immunofluo-rescent staining of inner surface adhesion plaque proteins αnd β-catenins was observed. The existence of E-cadherin/ catenin (α-, β-) protein complexes as AJ was suggested. In transformed and stomach cancer cells E-cadherin was inhibited, instead, N-cadherin was expressed and localized at membranous AJ where co-staining with α- and β-catenin fluorescence was observed. Formation of N-cadherin/catenin (α-, β-) protein complex at AJs of transformed and cancer cells was suggested. The above observations were further supported by immunoblotting results. Normal stomach muscosal and transformed cells expressed Cx32 at membranous GJ and were competent of gap junction communication (GJIC). In stomach cancer cells, Cx32 was inhibited and GJIC was defective. The results suggested that changes of signal pathways mediated by both cell adhesion and cell communication systems are associated intracellular events of stomach carcinogenesis. The alteration of cadherin isoform from E- to N-cadherin in transformed and stomach cancer cells is the first report.     

Retinoic acid modulates gap junctional intercellular communication in hepatocytes and hepatoma cells

Gap junctional communication permits the direct exchange of small molecules and ions and has been implicated in tissue homeostasis/metabolite exchange. The lack of gap junctional intercellular communication (GJIC) plays important roles in the promotion and progression of carcinogenesis. In the present study, we demonstrate that treatment of human hepatoma Hep G2 cells with retinoic acid (RA) results in increased amounts and phosphorylation of connexins, their stabilisation in plasma membrane plaques and enhanced GJIC. In cultured fetal hepatocytes, which represent a non-transformed, proliferating and incompletely differentiated liver system, the effects of RA are limited to the establishment of connexin in areas of cell-cell contact and the improvement of GJIC. This suggests that modulation of cell-cell channel communication by RA occurs differently in these two experimental models: while RA is able to revert cell transformation in Hep G2 cells, in fetal hepatocytes it may induce the expression of a more differentiated phenotype. Received 19 June 2002; received after revision 29 July 2002; accepted 8 August 2002 RID="*" ID="*"Corresponding author.     

Fe_(57)Al_(43)合金中的Zener弛豫

考察了Fe57Al43合金的内耗特征。对于空冷和炉冷的样品,在520℃左右观察到一个弛豫型内耗峰,该峰在升降温测量过程中都能出现。根据该内耗峰的激活能,该峰可归因为Zener弛豫,产生于Fe-Al合金中Al原子对的重新取向。     

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弱光和Tris处理条件下PSⅡ放氧核心复合物的损伤

弱光条件下(120μmol·m-2·s-1)用Tris(0.8mol/L,pH6.5～10.0)处理具有放氧活性的PSⅡ核心复合物,可引起33kD锰稳定蛋白的释放和锰复合物的破坏,并导致核心复合物的结构发生明显的改变.温和电泳、SDS-PAGE和双向电泳分析表明,主要是PSⅡ核心复合物的二聚体和单体减少,并且复合物部分解体;除反应中心D1和D2蛋白外,核心天线CP43和CP7的量也减少,33kD锰稳定蛋白要发生降解.避光时,PSⅡ核心复合物不受影响.