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.     

Melatonin and mitochondrial function during ischemia/reperfusion injury

Ischemia/reperfusion (IR) injury occurs in many organs and tissues, and contributes to morbidity and mortality worldwide. Melatonin, an endogenously produced indolamine, provides a strong defense against IR injury. Mitochondrion, an organelle for ATP production and a decider for cell fate, has been validated to be a crucial target for melatonin to exert its protection against IR injury. In this review, we first clarify the mechanisms underlying mitochondrial dysfunction during IR and melatonin’s protection of mitochondria under this condition. Thereafter, special focus is placed on the protective actions of melatonin against IR injury in brain, heart, liver, and others. Finally, we explore several potential future directions of research in this area. Collectively, the information compiled here will serve as a comprehensive reference for the actions of melatonin in IR injury identified to date and will hopefully aid in the design of future research and increase the potential of melatonin as a therapeutic agent.     

非下采样Contourlet HMT模型

非下采样Contourlet变换（NSCT）不仅具有类似传统小波变换和Contourlet变换的多尺度和多方向特性,而且还具有良好的平移不变特性．文中对NSCT变换系数进行研究,获得NSCT变换的方向子带系数同样具有持续性和聚集性的结论;在此基础上结合隐Markov树模型,建立了一种新的基于NSCT域的隐Markov树模型NSCT—HMT,并且给出了该模型的参数结构以及模型参数的训练方法;最后将所提出的模型应用于图像去噪中取得了很好的仿真效果．     

探月工程三期月地高速再入返回飞行器防热系统设计与验证

本文针对月地高速再入返回的高焓、二次大气层再入、高热流密度峰值与长加热时间耦合的气动加热环境特点,提出了飞行器防热系统设计方案,研制了七种新型碳硅复合烧蚀防热材料,建立了防热系统分析模型,并完成了地面试验验证.经对飞行试验数据的详细分析,结果表明防热系统的实际性能与设计预期一致.     

A genetic interaction network of five genes for human polycystic kidney and liver diseases defines polycystin-1 as the central determinant of cyst formation

Autosomal dominant polycystic liver disease results from mutations in PRKCSH or SEC63. The respective gene products, glucosidase IIβ and SEC63p, function in protein translocation and quality control pathways in the endoplasmic reticulum. Here we show that glucosidase IIβ and Sec63p are required in mice for adequate expression of a functional complex of the polycystic kidney disease gene products, polycystin-1 and polycystin-2. We find that polycystin-1 is the rate-limiting component of this complex and that there is a dose-response relationship between cystic dilation and levels of functional polycystin-1 following mutation of Prkcsh or Sec63. Reduced expression of polycystin-1 also serves to sensitize the kidney to cyst formation resulting from mutations in Pkhd1, the recessive polycystic kidney disease gene. Finally, we show that proteasome inhibition increases steady-state levels of polycystin-1 in cells lacking glucosidase IIβ and that treatment with a proteasome inhibitor reduces cystic disease in orthologous gene models of human autosomal dominant polycystic liver disease.     

基于装备体系韧性的作战网络链路重要度评估及恢复策略

韧性可以全面描述装备体系吸收打击或干扰、并从打击或干扰中恢复的能力, 体现了体系的综合性能。针对装备体系的韧性提出了一种量化评价方法, 以对装备体系作战网络链路进行重要度评估。首先给出了装备体系韧性的明确定义, 并建立了量化韧性的数学模型; 其次提出了基于韧性增加值的链路重要度指标, 并构建了一种基于装备体系韧性的作战网络链路重要度评估模型; 然后构建了不同的恢复策略,并分析了其对作战网络性能恢复的影响; 最后通过应用案例验证了所提方法与模型的适用性和合理性, 为优化体系结构、保障和提高体系作战性能提供了理论支撑, 也为进一步开展基于装备体系韧性的作战网络应用研究提供了参考借鉴。     

助成胶作用和氧化镧掺杂对活性氧化铝热稳定性的影响

研究水溶液成胶制备氧化铝过程中,掺杂氧化镧及利用聚乙二醇助成胶对氧化铝热稳定性和比表面的影响。通过XRD表征手段和TG检测方法来检测氧化铝在不同温度焙烧后的晶相改变和热失重情况,并利用BET检测方法检测不同温度焙烧后的比表面。实验结果表明,氧化镧的掺杂可提高氧化铝的热稳定性,利用聚乙二醇助成胶可有效提高氧化铝的比表面。     

P_MOEA：一种多目标决策辅助遗传算法用于服务组合QoS优化

在服务组合场景下,SLA约束下的服务组合优选是实现服务质量管理的重要基础之一．服务组合优选既是一个组合优化问题同时也是多目标决策问题,需要高效的算法以支持大规模的候选组合方案集合,同时也需要有效的评价模型来明确定义候选方案的优劣程度,从而为决策者提供支持．现有的服务组合优选方法多基于两种模型定义其优化目标：线性效用函数和Pareto最优．前者需要量化权重配置以定义效用函数,但是对于用户来说精确的量化权重配置是一个非常困难的任务,特别是在涉及到的QoS维度较多时;后者无需权重配置,将Pareto最优的skyline集合作为优化结果返回给用户,然而skyline集合的规模是不可控的,最优结果集的规模会随着问题的规模增大而显著增大,过大的最优结果集显然难以为决策者提供有效参考,针对上述传统方法的不足,在本文中,我们将PROMETHEE方法弓I入服务组合优选问题,结合Pareto和PROMETHEE两种评价模型,将skyline集合基础上的Top—kPROMETHEE最优方案作为优化目标,提出并实现了一个高效的遗传算法：P—MOEA．算法可以针对大规模问题,高效地返回Top—kPROMETHEE最优组合方案集合,从而为进一步的决策提供有效的参考．我们实验验证了算法的效率和有效性．     

协同多点传输中迫零预编码和天线选择技术

MIMO无线传输技术极大地提高了系统的容量,在实际通信系统中,整个网络是一个干扰受限的系统,小区间干扰对MIMO系统传输的影响是显著的,每个相邻小区的基站天线都可以看成一个干扰源．由于基站端数据处理能力的提升和回程容量的增加,多个小区协同多点传输技术引起了人们的广泛关注．目前的大部分工作都是集中于研究系统的容量（吞吐量）,而在实际系统中,每个用户的接收等效信噪比（即公平性）对系统的性能如误帧率等有重要的影响．对于每个用户为单天线的情形,研究了总功率受限和每天线功率受限下采用迫零预编码的系统容量和公平性．对两种功率约束条件下的公平性进行了分析,得到了公平性算法的闭式表达式．当每个用户为多天线的情形,为了降低计算的复杂度,引入了信道范数最大的接收天线选择算法,把每个用户为多天线的情形转化成等效的每个用户单天线情形,推导的每用户为单天线的公平性算法仍然适用．仿真结果显示,采用迫零预编码的多小区协作可以使系统性能显著提升．在相同的迫零预编码下,不同的功率分配策略对系统的容量和公平性有显著的影响．和用户为单天线相比,采用天线选择算法可以提升系统的容量和公平性．考虑了用户公平性时的吞吐量和最大系统吞吐量之间的折中关系,并给出了仿真结果．