异烟肼-柚皮素共晶的表征及其性能研究

以抗结核药异烟肼和黄酮类天然产物柚皮素为原料,采用混悬法制得异烟肼-柚皮素的药物-药物共晶。通过XRPD、DSC、FTIR、SSNMR和LNMR等分析技术对共晶产物进行了表征,分析了共晶分子间的氢键作用,确定了共晶中异烟肼和柚皮素的比例;对异烟肼、柚皮素和共晶在模拟生理液中的表观平衡溶解度进行了比较研究。结果表明,异烟肼的酰肼基和吡啶氮与柚皮素上的3个羟基在共晶中形成了新的氢键,共晶产物中异烟肼与柚皮素的摩尔比为1∶1;共晶能大幅降低异烟肼的表观平衡溶解度,提高柚皮素的表观平衡溶解度,说明所得共晶能够在保留异烟肼抗结核药效的同时,减弱肝损伤,药理作用明显。     

大型基础下含软弱夹层的层状砂土变形计算

基于饱和土的相关理论,推导了大型基础下层状地基的沉降计算模型.考虑不同的土性,根据修正剑桥模型和摩尔-库伦模型,推导了K_○0条件下且能够考虑其塑性变形的压缩模量.基于平面网格子域法结合分层总和法建立了一个完整的、更加贴近工程实际的大型基础下含软弱夹层的层状砂土地基沉降计算模型.研究结果表明:该模型的计算结果与模拟结果很贴近,且能够突出体现出软弱夹层的变形特性.研究结论可为含软弱夹层的大型基础地基沉降计算提供直接参考依据.     

双稳系统中布洛赫波峰湍流的统计性质

双稳系统中的布洛赫波峰的横向失稳可以引起波峰湍流,其不规则运动体现为斑图中的漩涡自发而不规则地产生和湮灭.本文以受驱动系统的复Ginzburg-Landau方程为模型,研究了布洛赫波峰湍流的统计性质.计算了漩涡产生速率和湮灭速率,以漩涡数量时间序列为基础,给出了漩涡动力学变化遵循的主方程.对湍流中漩涡对关联函数的计算表明,漩涡产生/湮灭速率中各幂次项来源于漩涡产生/湮灭事件与周围不同数量的漩涡的短程相互作用.     

《计量地理学》分段式教学探讨

顺应大学生加强实践教学环节的时代要求,《计量地理学》由过去讲授为主的专业基础课程,改革为实践课程。依据《计量地理学》自身学科发展及学习思维认知理论,提出新的分段式课程教学方案:讲授—验证学习阶段、启发—引导学习阶段、指导—自主学习阶段、评测—互助教学阶段以及综合应用阶段。实现了从知识讲授到能力培养的转变,以实现实践课的目的要求。     

柏拉图对诗中英雄形象的尽善尽美为何行不通——以革命样板戏中“高大全”式英雄形象的失败为参照

出于建设理想国度、教化公民的政治目的,柏拉图在《理想国》卷二至卷三中,对诗中的英雄形象提出了尽善尽美的要求。柏拉图心目中的完美英雄形象与新中国革命样板戏中的"高大全"式英雄形象有着许多相似处,后者在文艺史中的失败,虽然间接却十分充分地说明柏拉图对诗中英雄形象的尽善尽美要求行不通。柏拉图对"理想国"中的公民缺乏信心,担心公民会受不好的文艺、教育影响,因此他强调诗人的教化职责,要求诗中的英雄形象必须尽善尽美。     

多边矩阵框架的基阵表示和数据挖掘 ——处理复杂系统的新思维系列之二十七

作为系列论文的第27篇,介绍了多边矩阵框架的基阵表示概念,给出了多边矩阵框架的基阵表示的基本性质.作为应用,研究了多边矩阵框架的基阵表示和数据挖掘之间的关系.     

Incoherent control of two classes of finite-level quantum systems

The incoherent control of finite-level quantum systems is investigated.Following a brief introduction to coherent control paradigms in quantum control,a control problem that can not be accomplished using only coherent control is presented.For such a control problem,it is proved that it can be accomplished using incoherent control based on projective measurement and coherent control for two classes of finite-level quantum systems,i.e.,eigenstate controllable quantum systems and wavefunction controllable quantum systems.     

Simultaneous mineralization of CO2 and recovery of soluble potassium using earth-abundant potassium feldspar

CO2 capture and storage(CCS) is an important strategy in combatting anthropogenic climate change.However,commercial application of the CCS technique is currently hampered by its high energy expenditure and costs.To overcome this issue,CO2 capture and utilization(CCU) is a promising CO2 disposal method.We,for the first time,developed a promising method to mineralize CO2 using earth-abundant potassium feldspar in order to effectively reduce CO2 emissions.Our experiments demonstrate that,after adding calcium chloride hexahydrate as an additive,the K-feldspar can be transformed to Ca-silicates at 800 C,which can easily mineralize CO2 to form stable calcium carbonate and recover soluble potassium.The conversion of this process reached 84.7%.With further study,the pretreatment temperature can be reduced to 250 C using hydrothermal method by adding the solution of triethanolamine(TEA).The highest conversion can be reached 40.1%.The process of simultaneous mineralization of CO2 and recovery of soluble potassium can be easily implemented in practice and may provide an economically feasible way to tackle global anthropogenic climate change.     

商科院校基础化学实验教学体系创新探讨

在实验室管理体系创新、实践教学体系创新两个方面介绍了哈尔滨商业大学化学中心多年来创建的以＂一体化、多层次、开放式＂为主线的实践教学体系的人才培养模式。     

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.