Morphine 6 glucuronide stimulates nitric oxide release in mussel neural tissues: evidence for a morphine 6 glucuronide opiate receptor subtype

We have previously demonstrated that Mytilus edulis pedal ganglia contain opiate alkaloids, i.e., morphine and morphine 6 glucuronide (M6G), as well as mu opiate receptor subtype fragments exhibiting high sequence similarity to those found in mammals. Now we demonstrate that M6G stimulates pedal ganglia constitutive nitric oxide (NO) synthase (cNOS)-derived NO release at identical concentrations and to similar peak levels as morphine. However, the classic opiate antagonist, naloxone, only blocked the ability of morphine to stimulate cNOS-derived NO release and not that of M6G. CTOP, a mu-specific antagonist, blocked the ability of M6G to induce cNOS-derived NO release as well as that of morphine, suggesting that a novel mu opiate receptor was present and selective toward M6G. In examining a receptor displacement analysis, both opiate alkaloids displaced [³H]-dihydromorphine binding to the mu opiate receptor subtype. However, morphine exhibited a twofold higher affinity, again suggesting that a novel mu opiate receptor may be present. Received 1 November 2001; received after revision 1 February 2002; accepted 1 February 2002     

外源性生长激素对改善腹腔感染时生长激素不敏感状态中的作用

探索了外源性生长激素对改善腹腔感染时生长激素不敏感中的作用。应用盲肠结扎穿孔法（CLP）制备腹腔感染大鼠模型,同时给予外源性生长激素;应用放射免疫法测定血清生长激素（GH）水平;应用逆转录多聚酶链反应（RT-PCR）法测定肝组织胰岛素样生长因子I(IGF-I)、生长激素受体（GHR）和细胞因子信号传导抑制体3(SOCS-3)mRNA的表达;应用ELISA测定血清肿瘤坏死因子α(TNF-α)和白介素6(IL-6)水平。结果表明腹腔感染组大鼠血清生长激素水平与对照组无明显差异,但肝组织IGF-ImRNA表达明显下降;给予外源性生长激素后可明显降低血清TNF-α和IL-6水平,同时可更快地促使GHR和IGF-ImRNA表达的上调及下调SOCS-3mRNA的表达。腹腔感染时机体存在对生长激素的不敏感状态,给予外源性生长激素后可明显地改善感染状态下机体对生长激素的敏感性。     

受体缺乏改变小鼠脑内组胺含量及昼夜节律

在乙谜麻醉下,分别于明时(8:00 a.m.)及暗时(8:00 p.m.)断头处死野生型及组胺H1R基因敲除型小鼠,迅速取出脑组织并分离出皮层、纹状体、海马、下丘脑、丘脑、中脑及脑干等脑区.这些脑组织被制成匀浆并用HPLC荧光检测法测量其组胺含量.结果显示暗时处死时,H1R基因敲除型小鼠海马、丘脑、中脑及脑干中的组胺含量明显低于野生型小鼠.明时处死时,野生型小鼠各脑区组胺含量均较暗时处死显著降低,但这一变化在H1R基因敲除型小鼠中并未观察到.这些表明作为组胺的功能靶,H1R不仅介导组胺的功能,而且调节大脑中组胺含量与释放的昼夜节律.     

Anti-nociceptive role of neuropeptide Y in the nucleus accumbens in rats with inflammation, an effect modulated by mu- and kappa-opioid receptors

Recent study in our laboratory showed that neuropeptide Y (NPY) plays an antinociceptive role in the nucleus accumbens (NAc) in intact rats. The present study was performed to further investigate the effect of NPY in nociceptive modulation in the NAc of rats with inflammation, and the possible interaction between NPY and the opioid systems. Experimental inflammation was induced by subcutaneous injection of carrageenan into the left hindpaw of rats. Intra-NAc administration of NPY induced a dose-dependent increase of hindpaw withdrawal latencies (HWLs) to thermal and mechanical stimulations in rats with inflammation. The anti-nociceptive effect of NPY was significantly blocked by subsequent intra-NAc injection of the Y1 receptor antagonist NPY28-36, suggesting an involvement of Y1 receptor in the NPY-induced anti-nociception. Furthermore, intra-NAc administration of the opioid antagonist naloxone significantly antagonized the increased HWLs induced by preceding intra-NAc injection of NPY, suggesting an involvement of the endogenous opioid system in the NPY-induced anti-nociception in the NAc during inflammation. Moreover, the NPY-induced anti-nociception was attenuated by following intra-NAc injection of the μ-opioid antagonist β-funaltrexamine (β-FNA), and κ-opioid antagonist nor-binaltorphimine (nor-BNI), but not by δ-opioid antagonist naltrindole, indicating that μ- and κ-opioid receptors, not δ-opioid receptor, are involved in the NPY-induced anti-nociception in the NAc in rats with inflammation.     

指数分布下的产品可靠性抽样检验

对于失效时间遵从指数分布,本文提出了定时截尾样本下可靠性抽样检验方案的统计方法.质量统计是不可靠度的矩估计的严格增加函数,利用渐近正态分布样本量和接受常数被近似确定.     

8-（2′-萘磺酰）-胺基喹啉锌荧光探针的合成及其对酵母细胞的染色

合成了一种锌离子荧光探针-8-(2′-萘磺酰)-胺基喹啉(NSQ),NSQ自身具有较弱的荧光,向NSQ溶液中加入Zn2 后,荧光增强5.7倍,并且生物体系中含量较多的碱金属或碱土金属离子几乎不干扰Zn2 的荧光.酵母细胞染色实验表明,NSQ可以对酵母细胞中的锌离子进行荧光显微分析.     

基于VHDL的数字密码锁的设计与实现

数字密码锁主要完成上锁、密码输入、密码核对、开启电锁、密码修改等功能.数字密码锁的设计电路主要包括11个模块,各模块由相应的VHDL程序具体实现并分别进行了MAX＋PLUSⅡ时序仿真.最后,在MAX＋PLUSⅡ环境下进行了整体电路的模拟仿真,结果表明,整个设计满足要求.     

基于质量均匀分布的新型MTMD设计模型

提出了刚度和阻尼保持常量但质量均匀分布的新型MTMD设计模型以控制基底加速度激励下结构的振动，结构用某一受控振型的降阶模型表示.利用数值优化技术，研究了MTMD的最优参数，讨论了它对MTMD有效性和鲁棒性的影响.MTMD参数包括：质量间隔、频率间隔、平均阻尼比、调谐频率比、总质量比和总数.MTMD的优化准则定义为结构最大动力放大系数的最小值的最小化.为进行比较，还考虑了刚度和阻尼保持常量但频率均匀分布的MTMD设计模型.数值分析表明，新型MTMD设计模型不存在近0最优平均阻尼比，而且这种新型MTMD设计模型和频率均匀分布的MTMD设计模型达到近似同样的有效性和鲁棒性.     

Calmodulin modulation of ion channels and receptors

Ion channels and receptors are the structural basis for neural signaling and transmission. Recently, the function of ion channels and receptors has been demonstrated to be modulated by many intracellular and extracellular chemicals and signaling molecules. Increasing evidence indicates that the complexity and plasticity of the function of central nervous system is determined by the modulation of ion channels and receptors. Among various mechanisms, Ca 2+ signaling pathways play important roles in neuronal activity and some pathological changes. Ca 2+ influx through ion channels and receptors can modulate its further influx in a feedback way or modulate other ion channels and receptors. The common feature of the modulation is that Ca 2+ /calmodulin (CaM) is the universal mediator. CaM maintains the coordination among ion channels/receptors and intracellular Ca 2+ homeostasis by feedback modulation of ion channels/receptors activity. This review focuses on the modulating processes of ion channels and receptors mediated by CaM, and further elucidates the mechanisms of Ca 2+ signaling.