Influence of the Luminous Gas Phase into Butane Plasma Polymerization in a Closed Reactor System

High Energy Chemistry - This study investigated the plasma polymerization process of butane in a closed radio frequency plasma reactor system. Optical emission spectra of the luminous gas phase...     

Glucose sensing by POMC neurons regulates glucose homeostasis and is impaired in obesity

A subset of neurons in the brain, known as 'glucose-excited' neurons, depolarize and increase their firing rate in response to increases in extracellular glucose. Similar to insulin secretion by pancreatic beta-cells, glucose excitation of neurons is driven by ATP-mediated closure of ATP-sensitive potassium (K(ATP)) channels. Although beta-cell-like glucose sensing in neurons is well established, its physiological relevance and contribution to disease states such as type 2 diabetes remain unknown. To address these issues, we disrupted glucose sensing in glucose-excited pro-opiomelanocortin (POMC) neurons via transgenic expression of a mutant Kir6.2 subunit (encoded by the Kcnj11 gene) that prevents ATP-mediated closure of K(ATP) channels. Here we show that this genetic manipulation impaired the whole-body response to a systemic glucose load, demonstrating a role for glucose sensing by POMC neurons in the overall physiological control of blood glucose. We also found that glucose sensing by POMC neurons became defective in obese mice on a high-fat diet, suggesting that loss of glucose sensing by neurons has a role in the development of type 2 diabetes. The mechanism for obesity-induced loss of glucose sensing in POMC neurons involves uncoupling protein 2 (UCP2), a mitochondrial protein that impairs glucose-stimulated ATP production. UCP2 negatively regulates glucose sensing in POMC neurons. We found that genetic deletion of Ucp2 prevents obesity-induced loss of glucose sensing, and that acute pharmacological inhibition of UCP2 reverses loss of glucose sensing. We conclude that obesity-induced, UCP2-mediated loss of glucose sensing in glucose-excited neurons might have a pathogenic role in the development of type 2 diabetes.     

凤凰座SX型变星CY Aqr光变周期长期变化研究的新进展

通过对凤凰座SX型变星CY Aqr的观测测定了2个新的光变极大时刻,并利用文献中光变曲线资料得出了3个新的光变极大时刻.结合已发表的数据点,拟合得出新的极大时刻计算公式,并作出了O-C图.用新的数据检验现有的两种解释该星周期变化的理论表明轨道光时效应模型更为合理.     

光学超精密抗振系统的鲁棒控制

将鲁棒控制技术应用于主动抗振控制系统中,并用于解决光学超精密抗振系统的不确定性问题,其中采用小波分析方法将随机振动信号进行时频分析后得到低频全局信息,随后设计鲁棒控制器对低频振动进行抑制,该方法克服了由模型自身和外部干扰所引起的不确定性,使得控制系统能够有效地抑制抗振模型的不确定性和外部振动的干扰,同时也具有很高的控制精度和灵敏度.仿真结果表明,该方法使光学测量设备在外部振动的干扰下具有较好的鲁棒稳定性和控制精度,同时也能较好的抑制低频振动.     

邻甲苯胺在银纳米棒生长中作用的探讨

探讨了邻甲苯胺在制备银纳米棒中的作用.在邻甲苯胺存在下利用乙醇还原硝酸银制备了银纳米棒.产物经过XRD、TEM表征.对比实验表明不加邻甲苯胺或当邻甲苯胺形成配合物(2-(2-甲基苯基)氨基-4-(2-甲基苯基)亚氨基-2-戊烯)后,在类似条件下得到银纳米粒子.     

生物淋滤溶出废旧锂离子电池中钴的研究

考察不同培养条件对生物淋滤溶出钴的影响,研究提高钴生物溶出效率的方法和工艺条件. 研究表明:在硫磺质量浓度为4 g/L,起始pH为2.0,培养温度为27 ℃时,当电极混合材料的质量浓度为1%的条件下,淋滤12 d后钴的溶出质量浓度可达306 mg/L. 降低淋滤体系起始酸度(pH为1.0)和改变淋滤液硫源组合(2 g/L硫磺和2 g/L黄铁矿)可以有效提高钴的生物溶出效率,淋滤12 d后钴的溶出质量浓度高达1 682 mg/L,溶出率超过90%.     

基于模糊概率符号有向图的复杂系统故障诊断

通过分析复杂系统的故障信息传递特性,在符号有向图(SDG)中引入了状态关联概率和模糊信息,并结合面向对象技术提出了一种新的故障描述模型--模糊概率有向图.给出了基于此模型的建模方法和诊断流程.进一步引入消息节点和支路,通过连接各子实体对象的模糊概率SDG模型,构成整个复杂系统的模糊概率SDG系统.该模型能对复杂系统故障诊断中存在的复杂关联关系进行建模与故障诊断.利用该方法建立了某武器平台的故障诊断系统,实验结果表明提出的方法有效且实用.     

网络资源监控系统的设计与实现

结合铁路客票网络应用现状,分析已有监控软件系统的不足,设计出符合实际需求的网络资源监控系统框架,包括控制台端和代理端设计方案,以及辅助管理的故障处理专家知识库。最后按照设计方案,在Unix平台上采用面向对象开发语言C ,完成网络资源监控软件开发,并在实践中得以应用。     

表面等离子共振生物传感器测定人免疫球蛋白的抗原活性

目的:研究人免疫球蛋白质与羧甲基葡聚糖的氨基偶联及其与其他蛋白质的特异结合作用。方法:测定不同条件下人免疫球蛋白G(IgG)在羧甲基葡聚糖表面静电吸附的影响,并采用氨基偶联的方法,将其交联固定于葡聚糖表面,测定其与羊抗人IgG的特异结合。结果:pH及离子强度对蛋白质在羧甲基葡聚糖表面静电吸附有较大的影响,流体速度控制蛋白质的静电吸附动力学过程,并对其静电吸附量产生影响,其与羊抗人IgG有很强的特异结合作用,表现为快结合慢解离的动力学过程。结论:3.0相似文献   

从《唐诗别裁集》对李白诗评注看沈德潜诗论

历代的唐诗选本种类繁多,清人沈德潜编录的《唐诗别裁集》是其中一个影响较大的选本。沈德潜的诗论以"温柔敦厚"为首,主张诗歌要有社会功用,他在《唐诗别裁集》中十分强调这种儒家诗教。李白是沈德潜在《唐诗别裁集》中推崇的大家,他对李白诗的选录与评注,也无一不在阐发其"温柔敦厚"的诗论。