基于GIS、GPS、GSM的救护车智能管理系统研究

文章提出了一种救护车智能管理系统。该系统基于GIS、GPS、GSM技术,它能在发生紧急事故时,提供救护车到达出事地点,再从出事地点到达最近医院的最佳路径,该系统能够使救护车始终处于监控之下。我们通过设计有效的数据结构和算法来实现系统的上述功能。     

建党百年来愚公移山精神的历史演进及现实意义

作为中华民族的宝贵精神财富的愚公移山精神,在中国共产党带领全国人民进行革命、建设、改革和中国特色社会主义新时代各项事业的进程中都发挥了重要的精神引领作用,已经成为中国共产党人的红色基因.回顾愚公移山精神在建党百年来的历史演进过程,可看出精神引领是其赓续的逻辑宗旨,历史使命是其赓续的时代标识,困难险阻是其赓续的不竭动力....     

约束的移动对象最近邻轨迹查询

提出了一种新的查询概念,即约束的移动对象最近邻轨迹(constrained nearest neighbor search on moving objects trajectories,简称CNNMOT)查询.针对两阶段算法分阶段处理最近邻查询和范围查询的缺陷,对传统空间最近邻算法进行了改进和扩展,使其能够合并到一步完成,并对传统的mindist定义进行了修改.实验结果表明:该改进算法能较好地克服两阶段算法的缺陷,并在数据量较大时仍保持较高的性能.     

变电站并联电容器谐波放大及改进措施

提出了谐波等值网络化简法,分析各奇次谐波下随电容器组投入情况不同,变电站等值网络的变化过程,研究了电容器支路发生谐波谐振放大的各种可能性.并在此基础上,指出电容器组须按照分析结果进行投运,以避开谐振点,从而避免谐波电流放大的发生.对驻马店变电站实际运行电容器组进行的仿真分析,证明了所提出分析方法的正确性和有效性.该方法对实际生产运行具有指导意义,可避免传统方法所造成的设备浪费,对多数带并联补偿的三绕组电力变压器都适用,并可作为校验方法供设计时使用.     

纳米TiO2的应用

纳米TiO2因其具有更为独特的性能,例如优异的紫外屏蔽作用、透明无毒、奇特的颜色及光催化作用等,引起了人们的普遍关注,对它的制备、性能和应用展开了深入的研究.本文概述了纳米TiO2在有机和无机废水处理、杀菌、空气净化、紫外屏蔽、表面自清洁材料、高级涂料、静电屏蔽、红外吸收、红外反射、隐身材料及增强增韧材料等方面的应用和最新研究进展.     

公路交通事故黑点总体特征分析

采用改进的事故频数法选取了江苏、安徽两省部分二级以上公路事故黑点,运用事故数及致死事故率2个指标对事故黑点数据进行统计分析.得出了公路事故黑点总体特征表明:公路事故黑点所占里程短、事故数集中,事故致死率略大于一般路段;各等级公路事故黑点在事故时间分布、季节及气候影响、事故的道路线形分布等特征方面具有相似性,在事故类型分布、事故形态分布、事故空间分布等方面又具有不同特征.     

IFT54 regulates IFT20 stability but is not essential for tubulin transport during ciliogenesis

Intraflagellar transport (IFT) is required for ciliogenesis by ferrying ciliary components using IFT complexes as cargo adaptors. IFT54 is a component of the IFT-B complex and is also associated with cytoplasmic microtubules (MTs). Loss of IFT54 impairs cilia assembly as well as cytoplasmic MT dynamics. The N-terminal calponin homology (CH) domain of IFT54 interacts with tubulins/MTs and has been proposed to transport tubulin during ciliogenesis, whereas the C-terminal coiled-coil (CC) domain binds IFT20. However, the precise function of these domains in vivo is not well understood. We showed that in Chlamydomonas, loss of IFT54 completely blocks ciliogenesis but does not affect spindle formation and proper cell cycle progression, even though IFT54 interacts with mitotic MTs. Interestingly, IFT54 lacking the CH domain allows proper flagellar assembly. The CH domain is required for the association of IFT54 with the axoneme but not with mitotic MTs, and also regulates the flagellar import of IFT54 but not IFT81 and IFT46. The C-terminal CC domain is essential for IFT54 to bind IFT20, and for its recruitment to the basal body and incorporation into IFT complexes. Complete loss of IFT54 or the CC domain destabilizes IFT20. ift54 mutant cells expressing the CC domain alone rescue the stability of IFT20 and form stunted flagella with accumulation of both IFT-A component IFT43 and IFT-B component IFT46, indicating that IFT54 also functions in IFT turn-around at the flagellar tip.     

Granzyme B is recovered by natural killer cells via clathrin-dependent endocytosis

When they recognize a target cell, natural killer (NK) cells mount an attack to kill the target by exerting their cytotoxicity via the exocytosis of cytotoxic granules. Although the details of this process (which includes the movement of cytotoxic granules in the immune synapse and their fusion with the plasma membrane, releasing granzymes and perforin into the synaptic cleft) are relatively better understood, the post-exocytosis regulation of the process is still largely unknown. Here we show that a clathrin-dependent endocytosis stimulated by target cell occurs in NK92 cell line, which is closely correlated with granzyme B recovery. Inhibition of the endocytosis significantly attenuates the cytotoxicity of NK92 cells. The NK cell recovery of its released effector molecules, in turn, suggests that endocytosis may well play a key role in the post exocytosis regulation of immune cells.     

A genome-wide association study in Han Chinese identifies new susceptibility loci for ankylosing spondylitis

To identify susceptibility loci for ankylosing spondylitis, we performed a two-stage genome-wide association study in Han Chinese. In the discovery stage, we analyzed 1,356,350 autosomal SNPs in 1,837 individuals with ankylosing spondylitis and 4,231 controls; in the validation stage, we analyzed 30 suggestive SNPs in an additional 2,100 affected individuals and 3,496 controls. We identified two new susceptibility loci between EDIL3 and HAPLN1 at 5q14.3 (rs4552569; P = 8.77 × 10(-10)) and within ANO6 at 12q12 (rs17095830; P = 1.63 × 10(-8)). We also confirmed previously reported associations in Europeans within the major histocompatibility complex (MHC) region (top SNP, rs13202464; P < 5 × 10(-324)) and at 2p15 (rs10865331; P = 1.98 × 10(-8)). We show that rs13202464 within the MHC region mainly represents the risk effect of HLA-B*27 variants (including HLA-B*2704, HLA-B*2705 and HLA-B*2715) in Chinese. The two newly discovered loci implicate genes related to bone formation and cartilage development, suggesting their potential involvement in the etiology of ankylosing spondylitis.     

Cdk5 targets active Src for ubiquitin-dependent degradation by phosphorylating Src(S75)

The non-receptor tyrosine kinase Src is a critical regulator of cytoskeletal contraction, cell adhesion, and migration. In normal cells, Src activity is stringently controlled by Csk-dependent phosphorylation of Src(Y530), and by Cullin-5-dependent ubiquitinylation, which affects active Src(pY419) exclusively, leading to its degradation by the proteosome. Previous work has shown that Src activity is also limited by Cdk5, a proline-directed kinase, which has been shown to phosphorylate Src(S75). Here we show that this phosphorylation promotes the ubiquitin-dependent degradation of Src, thus restricting the availability of active Src. We demonstrate that Src(S75) phosphorylation occurs in vivo in epithelial cells, and like ubiquitinylation, is associated only with active Src. Preventing Cdk5-dependent phosphorylation of Src(S75), by site-specific mutation of S75 or by Cdk5 inhibition or suppression, increases Src(Y419) phosphorylation and kinase activity, resulting in Src-dependent cytoskeletal changes. In transfected cells, ubiquitinylation of Src(S75A) is about 35% that of wild-type Src-V5, and its half-life is approximately 2.5-fold greater. Cdk5 suppression leads to a comparable decrease in the ubiquitinylation of endogenous Src and a similar increase in Src stability. Together, these findings demonstrate that Cdk5-dependent phosphorylation of Src(S75) is a physiologically significant mechanism of regulating intracellular Src activity.