基于捷联惯性/GPS组合的伺服跟踪系统软件设计

介绍了数字伺服跟踪系统的组成和控制原理,讨论了影响微控制器选择的几个要素,以任务分类和软件模块化为设计思路研究了系统管理软件模块、捷联惯性/GPS组合的伺服控制算法模块、伺服控制测试模块。最后将设计的软件加载到微控制器中对伺服跟踪系统进行验证。实验结果表明,该伺服跟踪系统软件设计方法好,有工程推广应用价值。     

偏振三维成像仪的相对偏振方向定标方法

在介绍偏振三维成像机理、四孔径偏振三维成像仪组成的基础上,开展四孔径相对偏振方向对偏振三维成像精度影响分析,确定四孔径相对偏振方向精度要求。制定了四孔径镜头偏振片相对偏振方向定标方法和四孔径偏振三维成像仪相对偏振方向定标方法,搭建了定标装置,在实验室内开展了相对偏振方向定标。四孔径镜头偏振片相对偏振方向定标误差为±0.5o,四孔径偏振三维成像仪相对偏振方向误差为±1o,从而可保证偏振三维反演的法向量误差为-5.47%~5.80%,为偏振三维成像仪高质量成像提供保障。     

SINS/GPS 组合导航卡尔曼滤波算法研究

针对单独使用某一种的导航设备都无法满足机载火控系统和飞行系统要求的问题,推导出 SINS/GPS 组合导航中的一种新的卡尔曼滤波算法.将有色噪声的白化处理引入到卡尔曼滤波器,设计了一套动态车载组合导航试验系统,给出了基于有色噪声白化的卡尔曼滤波器算法的具体步骤,以动态车载 SINS/GPS 组合导航系统试验的数据分析验证了此算法的正确性和合理性.分析结果表明:基于有色噪声白化的卡尔曼滤波器可以很好地解决有色噪声的影响,弥补了传统卡尔曼滤波器的不足,提高了导航结果的精确度.     

砂岩储层烃类不混溶包裹体特征、成因及地质意义

为了系统研究储层中鲜有关注却较为普遍检测到的一种包裹体类型——烃类不混溶包裹体,采集了多个沉积盆地的大量砂岩样品,利用包裹体岩相学、显微荧光、显微测温、包裹体气液比和水油比检测等一系列手段,研究了天然形成的烃类不混溶包裹体特征与成因:(1)油气不混溶包裹体为天然气气侵原油,因压力变化引起的油气相态分离而非均一捕获形成,具有异常高均一温度和变化的气液比与捕获相态;(2)沥青-油和(或)气不混溶包裹体成因是油包裹体被均一捕获后热裂解、气相逃逸或者油藏水洗、生物降解、气侵和热裂解等生成的沥青与油(气)非均一捕获,前者具有相似的沥青含量,后者沥青从不含到富有均有分布;(3)包裹式水膜和与水相呈分离式接触的水-烃包裹体反映油气充注储层驱替地层水的过程,微量水对均一温度影响甚微;(4)薄油膜的油-水包裹体反映水与烃类流体的相互作用,指示古油藏破坏而残余油与地层水非均一捕获或以生气为主的超压沉积盆地,携带轻烃的天然气溶解于水,"萃取油相"与地层水非均一捕获;(5)气-水不混溶包裹体表明储层中水溶气存在,具有异常高均一温度和变化的气液比,形成于压力变化引起的天然气与水的相分离过程。沉积盆地的有机质类型、构造和热演化历史,决定烃类流体的类型、成熟度、以及之间的相互作用、储层流体所处的温度和压力条件以及稳定性,这些从根本上控制着不混溶包裹体发育及类型。     

梯形透水潜坝附近水面线及透水率

为研究结构物的透水特性和水动力特性,利用PIV流场测量系统专用水槽物理模型试验与Flow3D数值模拟相结合的方法研究均匀开孔的梯形透水潜坝附近水面线及坝体透水率的变化规律。结果表明:潜坝附近壅水及水跌高度随透空率的增大而减小,不同透空率潜坝坝后水面均出现"逆坡现象"。相同断面平均流速条件下,水深越大,相对壅水高度越小;当水深大于2倍坝高时,坝体壅水效果逐渐消失。相同坝前远端水深条件下,随着断面平均流速增大,坝后水跌高度增大。最后利用数模计算结果经回归拟合得到透水率的综合计算公式,经验证该经验公式计算结果和实测值最大偏差不超过5%,具有一定的可靠性。     

黄磷中有机杂质的脱除

综述了工业黄磷中有机杂质的净化方法.     

Haploinsufficiency of a Circadian Clock Gene Bmal1 (Arntl or Mop3) Causes Brain-Wide mTOR Hyperactivation and Autism-like Behavioral Phenotypes in Mice

Approximately 50–80% of children with autism spectrum disorders (ASDs) exhibit sleep problems, but the contribution of circadian clock dysfunction to the development of ASDs remains largely unknown. The essential clock gene Bmal1 (Arntl or Mop3) has been associated with human sociability, and its missense mutation is found in ASD. Our recent study found that Bmal1-null mice exhibit a variety of autism-like phenotypes. Here, we further investigated whether an incomplete loss of Bmal1 function could cause significant autism-like behavioral changes in mice. Our results demonstrated that heterozygous Bmal1 deletion (Bmal1^+/−) reduced the Bmal1 protein levels by ~50–75%. Reduced Bmal1 expression led to decreased levels of clock proteins, including Per1, Per2, Cry 1, and Clock but increased mTOR activities in the brain. Accordingly, Bmal1^+/− mice exhibited aberrant ultrasonic vocalizations during maternal separation, deficits in sociability and social novelty, excessive repetitive behaviors, impairments in motor coordination, as well as increased anxiety-like behavior. The novel object recognition memory remained intact. Together, these results demonstrate that haploinsufficiency of Bmal1 can cause autism-like behavioral changes in mice, akin to those identified in Bmal1-null mice. This study provides further experimental evidence supporting a potential role for disrupted clock gene expression in the development of ASD.     

Genetic Deletion of HLJ1 Does Not Affect Blood Coagulation in Mice

HLJ1 (also called DNAJB4) is a member of the DNAJ/Hsp40 family and plays an important role in regulating protein folding and activity. However, there is little information about the role of HLJ1 in the regulation of physiological function. In this study, we investigated the role of HLJ1 in blood coagulation using wild-type C57BL/6 mice and HLJ1-null (HLJ1^-/-) mice. Western blot analysis and immunohistochemistry were used to assess the expression and distribution of HLJ1 protein, respectively. The tail bleeding assay was applied to assess the bleeding time and blood loss. A coagulation test was used for measuring the activity of extrinsic, intrinsic and common coagulation pathways. Thromboelastography was used to measure the coagulation parameters in the progression of blood clot formation. The results showed that HLJ1 was detectable in plasma and bone marrow. The distribution of HLJ1 was co-localized with CD41, the marker of platelets and megakaryocytes. However, genetic deletion of HLJ1 did not alter blood loss and the activity of extrinsic and intrinsic coagulation pathways, as well as blood clot formation, compared to wild-type mice. Collectively, these findings suggest that, although HLJ1 appears in megakaryocytes and platelets, it may not play a role in the function of blood coagulation under normal physiological conditions.