多孔SiO2分子巢制备多功能涤纶纤维试验研究

针对传统PET材料不具备抗菌、不耐洗等问题,以煎煮法为基础,以草珊瑚、艾叶和薄荷为原料,制备含植物活性成分的溶液,其具有抗菌、杀菌的作用;以溶胶-凝胶法为多孔材料制备方法,用十六烷基三甲基溴化铵、十二烷基苯磺酸钠表面活性剂为模板剂,正硅酸乙酯为有机硅源,氨水为催化剂,乙醇和乙醚为助溶剂,在水-乙醇-乙醚体系中合成多孔二氧化硅微球;然后,多孔二氧化硅微球与提取液混合制备含植物活性成分的多孔二氧化硅分子巢;最后以制备的多孔二氧化硅分子巢与普通的聚酯切片用熔融纺丝工艺进行造粒、纺丝,得到具有抗菌、杀菌和耐洗的多功能涤纶纤维.通过SEM微观观察和力学性能测试、抗菌试验、耐洗性测试,对上述制备的多功能涤纶纤维性能进行验证.结果表明:在模板剂总浓度为0.029 mol·L-1、V醇:V醚=20:20、两种表面活性剂比为4:1时,得到的多孔SiO2微球排列规整;当多孔二氧化硅分子巢掺量(质量分数)在0.5％～1％时,通过熔融共混纺丝得到的新型多功能涤纶纤维力学性能表现最优;当多孔二氧化硅分子巢掺量(质量分数)在1％时,得到的新型多功能涤纶纤维的抗菌性能达到87.9％.而二氧化硅分子巢掺量越高,纤维材料越耐洗.以上结果说明本试验制备涤纶纤维的方案可行.     

Theoretical estimation of dielectric loss of oxide glasses using nonequilibrium molecular dynamics simulations

To theoretically explore amorphous materials with a sufficiently low dielectric loss, which are essential for next-generation communication devices, the applicability of a nonequilibrium molecular dynamics simulation employing an external alternating electric field was examined using alkaline silicate glass models. In this method, the dielectric loss is directly evaluated as the phase shift of the dipole moment from the applied electric field. This method enabled us to evaluate the dielectric loss in a wide frequency range from 1 GHz to 10 THz. It was observed that the dielectric loss reaches its maximum at a few THz. The simulation method was found to qualitatively reproduce the effects of alkaline content and alkaline type on the dielectric loss. Furthermore, it reasonably reproduced the effect of mixed alkalines on the dielectric loss, which was observed in our experiments on sodium and/or potassium silicate glasses. Alkaline mixing was thus found to reduce the dielectric loss.     

毫米波三维异质异构集成技术的进展与应用

三维异质异构集成技术是实现电子信息系统向着微型化、高效能、高整合、低功耗及低成本方向发展的最重要方法,也是决定信息化平台中微电子和微纳系统领域未来发展的一项核心高技术。文章详细介绍了毫米波频段三维异质异构集成技术的优势、近年来的发展趋势以及面临的挑战。利用硅基MEMS 光敏复合薄膜多层布线工艺可实现异质芯片的低损耗互连,同时三维集成高性能封装滤波器、高辐射效率封装天线等无源元件,还能很好地处理布线间的电磁兼容和芯片间的屏蔽问题。最后介绍了一款新型毫米波三维异质异构集成雷达及其在远距离生命体征探测方面的应用。     

小型无线场强探测传感器研究

近年来,微波加热因其高效性和清洁无污染等优点广泛应用于各个领域。然而,微波加热的不均匀性限制了微波作为高效加热能源的应用。通过测量和分析加热腔中的电场分布情况可以帮助设计人员改进微波加热腔体设计,提高微波加热的均匀性。现有的场强测量设备均为有线设备,应用场景极为有限。因此,本文提出了一种由探头、接收机和上位机三部分组成的无线场强探测传感器。介绍了无线场强探测传感器的结构和原理,采用横电磁波小室进行校准。通过一系列测量实验表明实测值与标准场强仪测量值一致性较好,可满足工程测量需求。     

线上线下混合"计算机控制技术"教学改革

本文结合"计算机控制技术"课程的授课内容和学校的创新应用型人才培养目标,探索了一种线上线下混合式教学模式,将传统的线下课堂知识点传授与现代线上多媒体、多平台的信息共享、在线视频会议等相互融合,实践表明该教学模式有效调动了学生的学习积极性和主动性,获得了良好的授课效果.     

WSN低功耗低时延路径式协同计算方法

针对云计算应用于无线传感器网络(Wireless Sensor Network,WSN)时延敏感型业务时存在的高传输时延问题,提出了一种WSN低功耗低时延路径式协同计算方法。该方法基于一种云雾网络架构开展研究,该架构利用汇聚节点组成雾计算层;在数据传输过程中基于雾计算层的计算能力分步骤完成任务计算,降低任务处理时延;由于汇聚节点计算能力较弱,时延降低将导致能耗增加,WSN工作寿命减短,为此提出能耗约束下的任务映射策略,并利用离散二进制粒子群优化(Binary Particle Swarm Optimization,BPSO)算法解决能耗约束下的时延优化问题。仿真结果表明,在相同的能耗约束下,对比其他算法,基于BPSO算法得出的映射方案能有效降低业务处理时延,满足时延敏感型业务的需求。     

A Novel LRRK2 Variant p.G2294R in the WD40 Domain Identified in Familial Parkinson’s Disease Affects LRRK2 Protein Levels

Leucine-rich repeat kinase 2 (LRRK2) is a major causative gene of late-onset familial Parkinson’s disease (PD). The suppression of kinase activity is believed to confer neuroprotection, as most pathogenic variants of LRRK2 associated with PD exhibit increased kinase activity. We herein report a novel LRRK2 variant—p.G2294R—located in the WD40 domain, detected through targeted gene-panel screening in a patient with familial PD. The proband showed late-onset Parkinsonism with dysautonomia and a good response to levodopa, without cognitive decline or psychosis. Cultured cell experiments revealed that p.G2294R is highly destabilized at the protein level. The LRRK2 p.G2294R protein expression was upregulated in the patient’s peripheral blood lymphocytes. However, macrophages differentiated from the same peripheral blood showed decreased LRRK2 protein levels. Moreover, our experiment indicated reduced phagocytic activity in the pathogenic yeasts and α-synuclein fibrils. This PD case presents an example wherein the decrease in LRRK2 activity did not act in a neuroprotective manner. Further investigations are needed in order to elucidate the relationship between LRRK2 expression in the central nervous system and the pathogenesis caused by altered LRRK2 activity.