长江河口中小型浮游动物数量分布、变动及主要影响因素

于1999年枯水期(2～3月份)、丰水期(8月份)、2000年枯水期(2～3月份)对长江河口浮游动物采样调查,研究了长江河口浮游动物的数量分布、变动及主要影响因素.结果表明:1999年枯水期浮游动物平均数量仅为79.07ind/m3,浮游动物在河口内与口外海滨形成两个高丰度区,浮游动物个体数量从口门内向近岸及近外海逐渐递减,优势种数量分布情况决定了该期浮游动物总数量分布.1999年丰水期,浮游动物平均数量高达300.89ind/m3,浮游动物分布不均匀,数量由河口内向近岸水域与近外海水域递增.2000年枯水期,浮游动物数量分布总体趋势与1999年枯水期相同.1999年枯水期、丰水期,2000年3月枯水期,桡足类数量占浮游动物总数量分别为95.54%、85.82%、84.83%,桡足类数量在浮游动物总数量中占绝对优势,并在浮游动物数量分布中起关键作用.浮游动物数量分布受潮周期影响显著,优势种在浮游动物数量潮周期分布中起重要作用.由各样站的浮游动物数量与盐度做回归分析,在枯水期均不成线性关系,在丰水期则成线性相关,回归方程为:y=0.34134 0.0112x(r=0.9341, n=8).此外,长江口浮游动物数量季节变化与温度、径流量、海流及食物等关系密切.     

细胞核CaMK和Calcineurin 对大鼠心肌肥厚发生的作用

目的:研究大鼠心肌肥厚时,钙依赖的蛋白激酶和蛋白磷酸酶在心肌细胞膜、细胞浆和细胞核的分布规律,以探讨核钙信号与核反应在心肌肥厚发生过程中的病理生理意义.方法:制备腹主动脉缩窄大鼠心肌肥厚模型,同位素32P掺入法分别测定心肌细胞核、细胞浆和细胞膜的蛋白激酶活性及用无机磷生成显色法测定其蛋白磷酸酶活性.结果:腹主动脉缩窄术后4周大鼠心肌显著肥厚,伴有明显的血液动力学异常.与正常对照组相比较,腹主动脉缩窄心肌肥厚组心肌细胞核钙调素蛋白激酶(CaMK)活性增加101.1%(P＜0.01),其膜的酶活性升高40.2%(P＜0.01),而胞浆的酶活性不变(P＞0.05);心肌细胞核钙调神经磷酸酶(Calcineurin)活性增加43.6%(P＜0.05),膜和胞浆中其活性增加无显著性(P＞0.05).正常组和腹主动脉缩窄心肌肥厚组心肌细胞CaMK和Calcineurin活性分布为核＞膜＞胞浆(P＜0.01).结论:腹主动脉缩窄心肌肥厚时核内钙依赖的CaMK和Calcineurin活性增加,提示压力超负荷时细胞核内钙调节的蛋白磷酸化和去磷酸化水平增高,可能在介导心肌肥厚的发生中起重要作用.     

Inhibition of dengue virus by targeting viral NS4B protein

We report a novel inhibitor that selectively suppresses dengue virus (DENV) by targeting viral NS4B protein. The inhibitor was identified by screening a 1.8-million-compound library using a luciferase replicon of DENV serotype 2 (DENV-2). The compound specifically inhibits all four serotypes of DENV (50% effective concentration [EC(50)], 1 to 4 μM; and 50% cytotoxic concentration [CC(50)], >40 μM), but it does not inhibit closely related flaviviruses (West Nile virus and yellow fever virus) or nonflaviviruses (Western equine encephalomyelitis virus, Chikungunya virus, and vesicular stomatitis virus). A mode-of-action study suggested that the compound inhibits viral RNA synthesis. Replicons resistant to the inhibitor were selected in cell culture. Sequencing of the resistant replicons revealed two mutations (P104L and A119T) in the viral NS4B protein. Genetic analysis, using DENV-2 replicon and recombinant viruses, demonstrated that each of the two NS4B mutations alone confers partial resistance and double mutations confer additive resistance to the inhibitor in mammalian cells. In addition, we found that a replication defect caused by a lethal NS4B mutation could be partially rescued through trans complementation. The ability to complement NS4B in trans affected drug sensitivity when a single cell was coinfected with drug-sensitive and drug-resistant viruses. Mechanistically, NS4B was previously shown to interact with the viral NS3 helicase domain; one of the two NS4B mutations recovered in our resistance analysis-P104L-abolished the NS3-NS4B interaction (I. Umareddy, A. Chao, A. Sampath, F. Gu, and S. G. Vasudevan, J. Gen. Virol. 87:2605-2614, 2006). Collectively, the results suggest that the identified inhibitor targets the DENV NS4B protein, leading to a defect in viral RNA synthesis.     

Oxytocin, but not arginine vasopressin is involving in the antinociceptive role of hypothalamic supraoptic nucleus

Our pervious study has demonstrated that the hypothalamic supraoptic nucleus (SON) plays a role in pain modulation. Oxytocin (OXT) and arginine vasopressin (AVP) are the important hormones synthesized and secreted by the SON. The experiment was designed to investigate which hormone was relating with the antinociceptive role of the SON in the rat. The results showed that (1) microinjection of l-glutamate sodium into the SON increased OXT and AVP concentrations in the SON perfusion liquid, (2) pain stimulation induces OXT, but not AVP release in the SON, and (3) intraventricular injection (pre-treatment) with OXT antiserum could inhibit the pain threshold increase induced by SON injection of l-glutamate sodium, but administration of AVP antiserum did not influence the antinociceptive role of SON stimulation. The data suggested that the antinociceptive role of the SON relates to OXT rather than AVP.     

大鼠心肌肌浆网和核被膜ryanodine受体动力学特性的比较

目的 :观察大鼠心肌浆网 (sarcoplasmicreticulum ,SR)和核被膜 (nuclearenvelope ,NE)ryanodine受体 (RyR)与配体结合特点及其蛋白质磷酸化调节。方法 :采用差速和等密度梯度离心分离心肌SR和NE ,用放射受体分析法研究RyR的特征。结果 :NE上存在高亲和力RyR ,其最大结合 (Bmax)为SRRyR的 1.7% ,解离常数 (Kd)为SR的6 0 %。分别用PKA和PKC磷酸化后 ,SR上该受体的Bmax各增加 3.7和 1.2倍 ,而NE上的该受体Bmax各增加 2 .2和 3.1倍 ,Kd均无显著改变。结论 :NE上存在比SR密度低但亲和力高的RyR ,能被PKA和PKC激活 ,而且对PKC较PKA更敏感     

Inhibition of interferon signaling by the New York 99 strain and Kunjin subtype of West Nile virus involves blockage of STAT1 and STAT2 activation by nonstructural proteins

The interferon (IFN) response is the first line of defense against viral infections, and the majority of viruses have developed different strategies to counteract IFN responses in order to ensure their survival in an infected host. In this study, the abilities to inhibit IFN signaling of two closely related West Nile viruses, the New York 99 strain (NY99) and Kunjin virus (KUN), strain MRM61C, were analyzed using reporter plasmid assays, as well as immunofluorescence and Western blot analyses. We have demonstrated that infections with both NY99 and KUN, as well as transient or stable transfections with their replicon RNAs, inhibited the signaling of both alpha/beta IFN (IFN-alpha/beta) and gamma IFN (IFN-gamma) by blocking the phosphorylation of STAT1 and its translocation to the nucleus. In addition, the phosphorylation of STAT2 and its translocation to the nucleus were also blocked by KUN, NY99, and their replicons in response to treatment with IFN-alpha. IFN-alpha signaling and STAT2 translocation to the nucleus was inhibited when the KUN nonstructural proteins NS2A, NS2B, NS3, NS4A, and NS4B, but not NS1 and NS5, were expressed individually from the pcDNA3 vector. The results clearly demonstrate that both NY99 and KUN inhibit IFN signaling by preventing STAT1 and STAT2 phosphorylation and identify nonstructural proteins responsible for this inhibition.