金针菇多糖改善小鼠学习记忆功能

研究金针菇多糖对正常小鼠学习记忆的影响。利用三等分辐射式迷宫箱训练小鼠,检测每实验日正确反应率、达标小鼠的比率及达标所需训练次数,训练结束后取脑,用紫外分光光度计检测各项指标的OD值,测得超氧化物歧化酶（SOD）和丙二醛（MDA）含量。结果显示低剂量金针菇多糖可显著提高小鼠的达标率,显著降低小鼠达标的训练次数,金针菇多糖对SOD含量水平均有显著的提高作用（p〈0.05）,低剂量的金针菇多糖明显提高大脑海马组织中蛋白质的含量（p〈0.05）并能显著降低MDA含量（p〈0.05）。这表明金针菇多糖对小鼠的学习记忆有一定的促进作用,并能显著提高大脑海马组织中的蛋白质含量,提高SOD活力,降低MDA含量,表现出明显的抗氧化作用。     

振动控制的发展及趋势

 描述了振动控制的主要发展过程及最新发展动向,介绍了机敏材料与智能结构,主动与半主动振动控制和杂合技术,同时还指出新的研究方向:形状记忆合金在振动控制研究的应用研究。     

英语词汇联想记忆方法分析

从英语词汇的构成特点和人类心理记忆规律出发,分析了英语词汇的联想记忆规律,详细讨论了利用联想规律记忆词汇、有效增加词汇量的 7种方法,从而达到有效开发和利用人的记忆潜能和扩大词汇量的目的     

红外遥控LED显示屏

采用CRT显示技术，选用8031单片机为CPU，通过红外遥控操作，实现了多种显示效果。系统内置硬字库和时钟电路。     

胚胎期暴露氰戊菊酯对中年CD-1小鼠 空间学习记忆能力的影响

本研究旨在探讨胚胎期暴露氰戊菊酯对中年CD-1小鼠空间学习记忆能力的影响。利用六臂辐射状水迷宫任务检测胚胎期暴露氰戊菊酯组与暴露乳剂的对照组13月龄CD-1小鼠的空间学习记忆能力。结果表明,在辐射状水迷宫任务的学习期和记忆期中,氰戊菊酯组的错误数和潜伏期均显著高于对照组(Ps<0.05)。因此,胚胎期暴露氰戊菊酯可加速中年CD-1小鼠年龄相关性空间学习记忆能力减退的出现。     

中年ICR小鼠学习记忆损害与血清甲状腺素的关系

研究中年ICR小鼠在新物体再认任务和六臂辐射状水迷宫(RAWM)中的学习记忆能力变化及其与血清甲状腺素(TH)的相关性。结果表明,新物体再认试验中12月龄与6月龄ICR小鼠间的成绩无显著性差异;RAWM中,12月龄小鼠较6月龄小鼠空间学习记忆能力减退;12月龄小鼠血清TH水平(FT3,FT4)低于6月龄小鼠,且FT3水平既与小鼠的空间性学习能力相关,又与记忆能力相关,而FT4仅与空间性学习能力相关。这些结果提示血清TH水平下降可能参与了中年ICR小鼠空间学习记忆能力减退。     

竹笋禾夜蛾的发生与防治

对上海为害竹笋的竹笋禾夜蛾从形态特征、生物学特性、生长发育、为害特点等方面进行研究,并从农业防治和化学防治方面论述了竹笋禾夜蛾的预防措施.     

Effect of vitamin C on expansion of CD4+ effector memory T cells in vitro

AIM：To investigate the effect of vitamin C (VC), a small-molecule compound, on the expansion of CD4+ effector memory T cells (TEM) in vitro and to improve the effect of adoptive immunotherapy. METHODS：Normal human peripheral blood CD4+ T-lymphocytes were isolated and randomly divided into 2 groups: control group and experiment group. VC was added into experimental group. Thereafter, the expansion of CD4+ TEM in the 2 groups was detected by cell counter and flow cytometry. RESULTS：VC did not significantly affect the total number of CD4+ T cells, while it raised the ratio of TEM in CD4+ T cells at an optimal concentration of 100 mg/L. After 10 days of the expansion of CD4+ T cells, the number of CD4+ TEM in experiment group was (3.56±0.35)×106, significantly larger than that in control group ［(1.22±0.15)×106, P<0.01］. CONCLUSION: VC can effectively promote the expansion of CD4+ TEM in vitro, which provides a simple, safe and effective expansion method for adoptive immunotherapy.     

Intervention of hydrogen on memory damage induced by chronic hypoxia-hypercapnia in rats

AIM: To investigate the effects of hydrogen on the memory damage caused by chronic hypoxia-hypercapnia in rats. METHODS: Twenty-four SD rats trained by eight-arm radial maze test were randomly divided into 3 groups:normal control group (NC), hypoxia-hypercapnia+saline group (MS) and hypoxia-hypercapnia+ hydrogen group (MH). The rats in the latter 2 groups were placed in a closed cabin for 8 h/day,6 days/week and lasted for 4 weeks, in which O₂ was 9％-11％ and CO₂ was 5％-6％. In every time after the animals were out of the cabin, the MS rats were intraperitoneally injected with saline (5 mL/kg) and the MH rats were intraperitoneally injected with hydrogen solution at the same dose. The learning and memory function, the activity of superoxide dismutase (SOD), the content of malondialdehyde (MDA) and 8-hydroxydeoxyguanosine (8-OHdG) were examined after the cabin training. The ultramicrostructures of hippocampus were also observed. RESULTS: (1) Compared with NC group, the number of working memory errors, the total errors, the content of hippocampus 8-OHdG and serum MDA in MS and MH groups were higher and the activity of serum SOD was lower (P<0.05). The hippocampus structure was destroyed and some degree of edema and more apoptosis in the neurons were obserued in MS group and MH group. (2) Compared with MS group, the number of working memory errors(WME), the total errors, the content of hippocampus 8-OHdG and serum MDA were lower and the activity of serum SOD was higher in MH group (P<0.05). In MH group, the morphology of hippocampus structures kept nearly normal arrangement and the only mild edema and fewer apoptosis in the neurons were found. CONCLUSION: Hydrogen may attenuate chronic hypoxia-hypercapnia-induced memory damage in rats by inhibiting apoptosis of the neurons and decreasing detrimental free radicals reaction.