边坡变形时序分析的进化-自适应神经模糊推理模型

变形监测与预报是保证边坡工程施工安全与工程质量的重要措施,但由于位移时间序列的强非线性,边坡变形预报成为非常困难的问题．自适应模糊神经推理系统（ANFIS）有优越的学习和泛化性能,而遗传算法（GA）是优秀的全局优化工具．采用遗传算法优化ANFIS参数,并编制了相应的计算程序．结合三峡工程永久船闸施工变形监测和新滩滑坡变形监测,建立了边坡变形时序分析的GA-ANFIS智能模型．为了对比该模型的预测精度,采用GA优化支持向量回归（SVR）和BP神经网络的模型参数,编制了GA-SVR及GA-BP程序,对相同的算例进行了变形预测分析．按滚动预测法对三峡永久船闸高边坡和新滩滑坡的计算结果表明,文中提出的GA-ANFIS模型能够获得比GA-SVR和GA-BP模型更高的预测精度,可以应用于边坡工程变形监测预报分析,并为类似工程提供参考．     

钙依赖途径在高糖致心肌细胞肥大中的作用

目的探讨体外培养条件下钙调神经磷酸酶(CN)和钙调蛋白激酶Ⅱ(CaMKⅡ)是否参与高糖诱导的心肌细胞的肥大反应。方法新生SD大鼠心肌细胞在含150mL/L的新生牛血清培养48h后,换用无血清培养基培养24h,然后用正常糖(5.5mmol/L的D-葡萄糖)、高糖(25mmol/L的D-葡萄糖)和等渗糖(5.5mmol/L的D-葡萄糖+19.5mmol/L的L-葡萄糖)分别培养48h。检测心肌细胞肥大指标:表面积和蛋白含量;用钙成像技术研究其钙瞬变特点;以及利用CN和CaMKⅡ的阻断剂CsA和KN93验证两种酶在肥大过程中的作用。结果与正常糖组和等渗对照组相比,高糖可以诱导心肌细胞肥大和钙超载,增加了心肌细胞的表面积和蛋白含量。CsA和(或)KN93可明显抑制心肌细胞的肥大。结论 CN和CaMKII在高糖诱导的心肌细胞肥大过程中发挥重要的作用。     

汽车ABS系统传导瞬态抗扰度性能研究

研究某型号ABS系统的瞬态抗扰度性能,分析试验过程中该ABS系统出现的失效状态和毁坏状况产生的原因,并给出了整改措施。对整改后的ABS系统再次进行试验,结果表明,整改后的ABS系统完全满足ISO7637—2最高等级的要求。     

Eukaryotic expression and biological activity analysis of neuroprotective peptide [Gly14]-Humanin

Objective To investigate the expression of neuroprotective peptide [Gly14]-Humanin (HNG) in eukaryotic cells by gene engineering technique and analyze its biological activity. Methods By means of asymmetrical primer/template, double stranded cDNA of HNG with FLAG in its C-terminal was obtained, which was cloned into the plasmid pcDNA3.1(-), and the resultant recombinant vector pcDNA3.1(-)/HNG-FLAG was transfected into PC12 cells. At the same time, the recombinant vector pcDNA3.1(-)/EGFP was transfected to control the efficiency of transfection. The expression of HNG in the cells was determined by immunocytochemistry. In order to analyze the biological activity of the expressed HNG, 25μM Aβ25-35 peptide was added to the culture medium of the transfected cells for 24h, then cell morphology, MTT assay and Hoechst 33258 staining were observed. Results The eukaryotic expression vector of pcDNA3.1(-)/HNG-FLAG was identified by enzyme digestion and sequencing. HNG was highly expressed in PC12 cells. After exposure of PC12 cells to 25μM Aβ25-35 for 24h, cell viability decreased to (65.8±5.3)%, and the dystrophic changes of neuritis and nuclei condensation were obvious. When cells were pre-transfected with pcDNA3.1(-)/HNG-FLAG, Aβ25-35-induced cell death and morphological changes of cells and nuclei were suppressed. In contrast, pre-transfected with empty vector did not protect cells from Aβ25-35-induced toxicity. Conclusion The eukaryotic expression vector for FLAG-tagged HNG was successfully constructed and expressed in PC12 cells. Expressed HNG has biological activity.     

Construction of lentivirus vectors carrying alphastatin gene and its secretion expression in human umbilical vein endothelia cells

Objective To construct lentivirus vectors carrying alphastatin gene, test its secretion expression in human umbilical vein endothelia cells (HUVECs) and observe its effects on growth, migration and tube formation of HUVECs. Methods We constructed recombinant lentivirus vectors of NT4-alphastatin fusion gene containing neurotrophin-4 signal peptide, pro-region sequences and alphastatin, then transfected the recombinant lentivirus vectors into HUVECs to obtain secretory protein alphastatin and test its anti-angiogenic activities in vitro. Results Our data showed that recombinant self-inactivating lentivirus vectors of NT4-alphastatin were successfully constructed, and stable NT4-alphastatin transduced HUVECs were capable of sustainably secreting alphastatin which significantly suppressed HUVECs migration and differentiation but not VEGF-induced proliferation. Conclusion This report represents the first time on the use of lentivirus-based vectors to deliver alphastatin, the endogenous angiogenesis inhibitor, and reveals the potential utility of anti-angiogenic gene therapy with lentivirus vectors for treating cancer.     

城市快速路交通事件检测的自适应算法研究

针对城市快速路交通事件检测问题,提出了-种基于自适应遗传算法与神经网络相结合的自动检测算法.通过改进的自适应遗传算法优化神经网络结构和权值参数,保证了神经网络能以较小规模和最优的权值参数来描述事件发生与交通参数间的映射关系,从而提高检测效果.利用PARAMICS交通软件模拟了北京市京通快速路从大望桥到四惠桥路段间的一组交通数据,仿真结果表明,该算法同现有的典型算法相比较,具有较高的检测率和较快的检测速度.     

消费能力的变动对经济增长的影响机制分析

消费能力是人们对满足自身生存、享受和发展需要的物质资料和劳务在有货币支付能力的转化形式,即消费者的货币支付能力。消费者的消费能力无论对内需的变化还是经济总量的变化都有着重要影响。为此,本文试图从消费者消费能力的变动来讨论消费需求的变化影响经济增长的传导机制。     

Effects of PYY on the interdigestive migrating myoelectric complex in the small intestine in vivo and the neural and endocrinal mechanisms of the effects

Objective To investigate the effects of peptide YY (PYY) on the interdigestive migrating myoelectrlc complex (MMC) in the small intestine in vivo and explore the neural and endecrinal mechanisms of the effects. Methods Spragne-Dawley rats were supplied with a venous catheter and bipolar electrodes in the duodenum and jejunum for electromyography of stomach and small intestine in wake state. PYY, phentolamine, nitro-L-arginine (L-NNA, the inhibitor of nitric oxide synthase) and atropine were served with PYY respectively. The plasma motilin levels before and after the infusion of PYY were observed. Results At all the three recording points, PYY lengthened the drde length of MMC [from (591.90±128.98)s to (999.25±216.59)s, P<0. 01] and lowered the frequency of phase Ⅲ [from (39.28±8.40) min-1 to (22.08±3.13) min-1 , P<0.01], amplitude of phase Ⅲ [from (0. 320±0.060)mV to (0. 179±0.030)mV, P<0.01], and the portion of phase Ⅲ over the whole circle length [from (28. 61 ± 5.84)% to (15.43 ±5.16)% , P<0.01]. Phentolumine had no influence on the role of PYY. Administered L-NNA combined with PYY, the percentage of phase Ⅲ increased [(42. 09±8.67)%] compared with that of control(P<0.01) and compared with that of PYY administered alone (P<0. 01) too. Atropine combined with PYY showed stronger depressing effects on MMC. No significant difference was found between the plasma motilin levels before and after the infusion of PYY. Conclusion PYY my inhibit the interdigestive intestine motility through the none-adrenergic none-choUnergic tract, while the m-receptor tract and circulating motilin are probably not involved In the depressing effect.     

姜黄素和脑源性神经营养因子对阿尔茨海默病记忆的改善作用

目的研究姜黄素对阿尔茨海默病(Alzheimer's disease,AD)模型大鼠学习记忆能力的影响及其作用机制。方法采用脑室内注射Aβ1-42的方法,制备AD动物模型。单次腹腔注射(急性治疗组)或连续6d腹腔注射(慢性治疗组)50、100、300mg/kg剂量的姜黄素,结合海马内微量注射脑源性神经营养因子(brain-derived neurotrophic factor,BDNF)(每侧1.0μg)、BDNF shRNA慢病毒(每侧2.0×105单位),分析大鼠Y迷宫、Morris水迷宫及旷场行为变化,并应用Western blot检测海马BDNF表达变化。结果姜黄素急性治疗对AD模型大鼠自主改变行为、总活动距离、水迷宫潜伏期没有显著作用。300mg/kg姜黄素慢性治疗后AD大鼠自主改变行为(P<0.000 1)及在水迷宫测试中记忆能力(P<0.05)比盐水对照组显著增高。100和300mg/kg姜黄素慢性治疗组海马BDNF表达和盐水对照组相比显著上升(P分别<0.05和<0.000 1)。海马内注射BDNF的AD大鼠水迷宫潜伏期显著下降(F_(4,295)=5.813,P<0.01)。姜黄素慢性治疗+shBDNF组大鼠在2号象限内的游泳时间与盐水对照组无差异(P=0.657),而100mg/kg姜黄素组、BDNF组、假手术组大鼠的停留时间比盐水对照组显著增高(P值分别<0.05、<0.05、<0.000 1)。结论姜黄素可能通过上调BDNF的表达继而激活下游信号通路,最终对Aβ诱导的AD大鼠学习记忆能力起到改善作用。