Quantum-enhanced positioning and clock synchronization

A wide variety of positioning and ranging procedures are based on repeatedly sending electromagnetic pulses through space and measuring their time of arrival. The accuracy of such procedures is classically limited by the available power and bandwidth. Quantum entanglement and squeezing have been exploited in the context of interferometry, frequency measurements, lithography and algorithms. Here we report that quantum entanglement and squeezing can also be employed to overcome the classical limits in procedures such as positioning systems, clock synchronization and ranging. Our use of frequency-entangled pulses to construct quantum versions of these protocols results in enhanced accuracy compared with their classical analogues. We describe in detail the problem of establishing a position with respect to a fixed array of reference points.     

Noise-resistant and synchronized oscillation of the segmentation clock

Periodic somite segmentation in vertebrate embryos is controlled by the 'segmentation clock', which consists of numerous cellular oscillators. Although the properties of a single oscillator, driven by a hairy negative-feedback loop, have been investigated, the system-level properties of the segmentation clock remain largely unknown. To explore these characteristics, we have examined the response of a normally oscillating clock in zebrafish to experimental stimuli using in vivo mosaic experiments and mathematical simulation. We demonstrate that the segmentation clock behaves as a coupled oscillator, by showing that Notch-dependent intercellular communication, the activity of which is regulated by the internal hairy oscillator, couples neighbouring cells to facilitate synchronized oscillation. Furthermore, the oscillation phase of individual oscillators fluctuates due to developmental noise such as stochastic gene expression and active cell proliferation. The intercellular coupling was found to have a crucial role in minimizing the effects of this noise to maintain coherent oscillation.     

传输带时钟同步的量子测量原理

时钟同步技术不管在民用生活中,还是在军事通信中都起着非常重要的作用。但是,现实中并不存在绝对同步的时钟,所以,测量两地时钟的同步性,是全世界国家所关心和研究的重要课题。在这样的背景下,提出一种传输带时钟同步的方法,此方法并不需要交换信号的传输时间;并基于脉冲纠缠双光子的量子相干性,给出了一种时钟同步的光学实验方案,此方案对介质色散具有很强的扼制效应。     

异步时钟域信号同步的实现

随着数字电子系统设计的快速发展,FPGA(现场可编程门阵列)在一些实际应用系统中通常包含有多个不同时钟,而系统功能实现的前提就是要完成数据在多个不同的时钟域之间进行传输,通常会产生亚稳态危害,为了较小亚稳态风险,本文分析了在跨时钟域时系统可能出现的亚稳态问题,提出了在FPGA工程设计中实现不同时钟域间的数据同步方法,对异步FIFO缓存法做了重点介绍.读写地址指针均采用了格雷码的形式,格雷码的特点是的相邻元之间每一次只有一位数据发生变化,所以系统的亚稳态风险会减小,通过Modelsim软件的仿真,验证了异步FIFO的应用可以有效的解决数据的跨时钟域传输问题.     

基于环状拓扑的网络时钟同步

时钟同步是很多网络应用的基本要求。本文研究并设计实现了基于环状拓扑的分布式多主机时钟同步系统。系统使用面向单向延迟测量的Altair&Vega（A&V）方法支持两主机间的时间同步，利用特有的环状拓扑上的累积误差提高系统的精度。文中详细介绍了动态环状逻辑拓扑的控制方案和高精度的相对时钟偏移修正方案，并对测试结果进行了详细的分析，通积累误差得到毫秒级的同步结果。     

Notch signalling controls pancreatic cell differentiation.

The pancreas contains both exocrine and endocrine cells, but the molecular mechanisms controlling the differentiation of these cell types are largely unknown. Despite their endodermal origin, pancreatic endocrine cells share several molecular characteristics with neurons, and, like neurons in the central nervous system, differentiating endocrine cells in the pancreas appear in a scattered fashion within a field of progenitor cells. This indicates that they may be generated by lateral specification through Notch signalling. Here, to test this idea, we analysed pancreas development in mice genetically altered at several steps in the Notch signalling pathway. Mice deficient for Delta-like gene 1 (Dll1) or the intracellular mediator RBP-Jkappa showed accelerated differentiation of pancreatic endocrine cells. A similar phenotype was observed in mice over-expressing neurogenin 3 (ngn 3) or the intracellular form of Notch3 (a repressor of Notch signalling). These data provide evidence that ngn3 acts as proendocrine gene and that Notch signalling is critical for the decision between the endocrine and progenitor/exocrine fates in the developing pancreas.     

抗时钟漂移的协议同步的设计与实现

通信双方基于时钟漂移破坏协议信息同步问题,提出了一种在时钟漂移下协议信息保持同步的方式。文中首先介绍了现在常用的处理方式,并分析了在时钟漂移下协议同步保持原理,最后根据协议设计在系统设备中进行了验证,证明该方式具备抗时钟漂移的能力。     

Acetylation-dependent regulation of endothelial Notch signalling by the SIRT1 deacetylase

Notch signalling is a key intercellular communication mechanism that is essential for cell specification and tissue patterning, and which coordinates critical steps of blood vessel growth. Although subtle alterations in Notch activity suffice to elicit profound differences in endothelial behaviour and blood vessel formation, little is known about the regulation and adaptation of endothelial Notch responses. Here we report that the NAD(+)-dependent deacetylase SIRT1 acts as an intrinsic negative modulator of Notch signalling in endothelial cells. We show that acetylation of the Notch1 intracellular domain (NICD) on conserved lysines controls the amplitude and duration of Notch responses by altering NICD protein turnover. SIRT1 associates with NICD and functions as a NICD deacetylase, which opposes the acetylation-induced NICD stabilization. Consequently, endothelial cells lacking SIRT1 activity are sensitized to Notch signalling, resulting in impaired growth, sprout elongation and enhanced Notch target gene expression in response to DLL4 stimulation, thereby promoting a non-sprouting, stalk-cell-like phenotype. In vivo, inactivation of Sirt1 in zebrafish and mice causes reduced vascular branching and density as a consequence of enhanced Notch signalling. Our findings identify reversible acetylation of the NICD as a molecular mechanism to adapt the dynamics of Notch signalling, and indicate that SIRT1 acts as rheostat to fine-tune endothelial Notch responses.     

OFDM软件无线电接收机的采样时钟同步

针对正交频分复用(Orthogonal Frequency Division Multiplexing,OFDM)采样时钟同步问题,提出了一种适合于软件无线电(Software-.Defined Radio,SDR)接收机的全数字实现方案.该方案的整体结构基于经典的Gardner环路,借助联合迭代估计算法来进行误差的动态跟踪,并通过对接收信号进行异步重采样来实现采样时钟误差的实时校正.误差检测环节不仅能消除载波频率误差的影响,还可以在维持环路的响应速度的同时提高误差检测的精度.误差校正环节利用一种简单的动态延迟技术来对信号重采样进行直接控制,尽管增加了一些处理延迟,但能使重采样过程平稳进行.理论分析和仿真结果表明,新的采样时钟同步方案在多径信道环境中能有效工作,算法的性能优于其他同类算法.     

单向时延测量的实时时钟同步算法

对已有分段聚类算法进行改进,使用软件方法对单向时延序列进行分析,在线检测时钟调整位置.采用变宽度的滑动窗方法对单向时延数据进行过滤,减少时间序列大小,同时保证时钟调整位置信息不丢失.使用自底向上算法对时间序列进行线性分段,检测时钟调整或时钟频率跳变点,算法的时间复杂度大大降低.针对在线时钟同步的要求,为了消除滑动窗不具有离线算法的全局寻优缺点,提出使用基于滑动窗自底向上算法的实时单向时延时钟同步算法.实际测试实验表明:该算法大大降低了时间复杂度并提高了分段精度.     

The ELF3 zeitnehmer regulates light signalling to the circadian clock

The circadian system regulates 24-hour biological rhythms and seasonal rhythms, such as flowering. Long-day flowering plants like Arabidopsis thaliana, measure day length with a rhythm that is not reset at lights-off, whereas short-day plants measure night length on the basis of circadian rhythm of light sensitivity that is set from dusk, early flowering 3 (elf3) mutants of Arabidopsis are aphotoperiodic and exhibit light-conditional arrhythmias. Here we show that the elf3-7 mutant retains oscillator function in the light but blunts circadian gating of CAB gene activation, indicating that deregulated phototransduction may mask rhythmicity. Furthermore, elf3 mutations confer the resetting pattern of short-day photoperiodism, indicating that gating of phototransduction may control resetting. Temperature entrainment can bypass the requirement for normal ELF3 function for the oscillator and partially restore rhythmic CAB expression. Therefore, ELF3 specifically affects light input to the oscillator, similar to its function in gating CAB activation, allowing oscillator progression past a light-sensitive phase in the subjective evening. ELF3 provides experimental demonstration of the zeitnehmer ('time-taker') concept.     

一种低通信开销联合时钟同步和定位算法

针对无线传感器网络（wireless sensor networks ,WSNs）中降低节点间的通信开销的需求,提出一种基于成对广播同步协议（pairwise broadcast synchronization ,PBS）改进的联合时钟同步和定位算法。在联合时钟同步和定位过程中,锚节点（位置已知,时钟需同步）侦听未知节点（位置未知,时钟需同步）与参考节点（位置已知,时钟为参考时钟）双向交换的时间信息,不用发送额外的信息。因此相比于传统基于双向信息交换方式的联合时钟同步和定位算法可以节省大量的通信开销,同时可以降低同步所需参考节点的数目。该算法不仅对未知节点的位置参数和时钟参数进行联合估计,同时也完成锚节点时钟参数的估计。经过仿真分析,估计值满足所推导的克拉美罗下限（cramer-rao lower bound,CRLB）,且估计精度接近其他两种典型联合算法。综合考虑估计精度和通信开销,所提出的算法优于现有的联合时钟同步和定位算法。     

基于IEEE 1588协议的网络时钟同步系统

提出一种基于IEEE1588协议和卫星授时的局域网内时间同步方案,将FC3180微控制器作为设备的核心控制单元,结合相应的硬件单元实现IEEE1588协议,将通过授时模块获取的卫星上的时间作为基准时间.IEEE1588将此基准时间分布到局域网中,并将各个从时钟设备的时间同步到基准时间源上.实验结果表明,该方案能够实现亚微秒级别的时间同步精度,达到了IEEE1588协议规定的精度,能够满足大部分应用系统对时间同步的要求,具有一定的应用价值.     

Frizzled regulation of Notch signalling polarizes cell fate in the Drosophila eye

The Drosophila eye, a paradigm for epithelial organization, is highly polarized with mirror-image symmetry about the equator. The R3 and R4 photoreceptors in each ommatidium are vital in this polarity; they adopt asymmetrical positions in adult ommatidia and are the site of action for several essential genes. Two such genes are frizzled (fz) and dishevelled (dsh), the products of which are components of a signalling pathway required in R3, and which are thought to be activated by a diffusible signal. Here we show that the transmembrane receptor Notch is required downstream of dsh in R3/R4 for them to adopt distinct fates. By using an enhancer for the Notch target gene Enhancer of split mdelta, we show that Notch becomes activated specifically in R4. We propose that Fz/Dsh promotes activity of the Notch ligand Delta and inhibits Notch receptor activity in R3, creating a difference in Notch signalling capacity between R3 and R4. Subsequent feedback in the Notch pathway ensures that this difference becomes amplified. This interplay between Fz/Dsh and Notch indicates that polarity is established through local comparisons between two cells and explains how a signal from one position (for example, the equator in the eye) could be interpreted by all ommatidia in the field.     

Suppression of Notch signalling by the COUP-TFII transcription factor regulates vein identity

Arteries and veins are anatomically, functionally and molecularly distinct. The current model of arterial-venous identity proposes that binding of vascular endothelial growth factor to its heterodimeric receptor--Flk1 and neuropilin 1 (NP-1; also called Nrp1)--activates the Notch signalling pathway in the endothelium, causing induction of ephrin B2 expression and suppression of ephrin receptor B4 expression to establish arterial identity. Little is known about vein identity except that it involves ephrin receptor B4 expression, because Notch signalling is not activated in veins; an unresolved question is how vein identity is regulated. Here, we show that COUP-TFII (also known as Nr2f2), a member of the orphan nuclear receptor superfamily, is specifically expressed in venous but not arterial endothelium. Ablation of COUP-TFII in endothelial cells enables veins to acquire arterial characteristics, including the expression of arterial markers NP-1 and Notch signalling molecules, and the generation of haematopoietic cell clusters. Furthermore, ectopic expression of COUP-TFII in endothelial cells results in the fusion of veins and arteries in transgenic mouse embryos. Thus, COUP-TFII has a critical role in repressing Notch signalling to maintain vein identity, which suggests that vein identity is under genetic control and is not derived by a default pathway.     

Periodic notch inhibition by lunatic fringe underlies the chick segmentation clock

The segmented aspect of the vertebrate body plan first arises through the sequential formation of somites. The periodicity of somitogenesis is thought to be regulated by a molecular oscillator, the segmentation clock, which functions in presomitic mesoderm cells. This oscillator controls the periodic expression of 'cyclic genes', which are all related to the Notch pathway. The mechanism underlying this oscillator is not understood. Here we show that the protein product of the cyclic gene lunatic fringe (Lfng), which encodes a glycosyltransferase that can modify Notch activity, oscillates in the chick presomitic mesoderm. Overexpressing Lfng in the paraxial mesoderm abolishes the expression of cyclic genes including endogenous Lfng and leads to defects in segmentation. This effect on cyclic genes phenocopies inhibition of Notch signalling in the presomitic mesoderm. We therefore propose that Lfng establishes a negative feedback loop that implements periodic inhibition of Notch, which in turn controls the rhythmic expression of cyclic genes in the chick presomitic mesoderm. This feedback loop provides a molecular basis for the oscillator underlying the avian segmentation clock.     

Notch signalling limits angiogenic cell behaviour in developing zebrafish arteries

Recent evidence indicates that growing blood-vessel sprouts consist of endothelial cells with distinct cell fates and behaviours; however, it is not clear what signals determine these sprout cell characteristics. Here we show that Notch signalling is necessary to restrict angiogenic cell behaviour to tip cells in developing segmental arteries in the zebrafish embryo. In the absence of the Notch signalling component Rbpsuh (recombining binding protein suppressor of hairless) we observed excessive sprouting of segmental arteries, whereas Notch activation suppresses angiogenesis. Through mosaic analysis we find that cells lacking Rbpsuh preferentially localize to the terminal position in developing sprouts. In contrast, cells in which Notch signalling has been activated are excluded from the tip-cell position. In vivo time-lapse analysis reveals that endothelial tip cells undergo a stereotypical pattern of proliferation and migration during sprouting. In the absence of Notch, nearly all sprouting endothelial cells exhibit tip-cell behaviour, leading to excessive numbers of cells within segmental arteries. Furthermore, we find that flt4 (fms-related tyrosine kinase 4, also called vegfr3) is expressed in segmental artery tip cells and becomes ectopically expressed throughout the sprout in the absence of Notch. Loss of flt4 can partially restore normal endothelial cell number in Rbpsuh-deficient segmental arteries. Finally, loss of the Notch ligand dll4 (delta-like 4) also leads to an increased number of endothelial cells within segmental arteries. Together, these studies indicate that proper specification of cell identity, position and behaviour in a developing blood-vessel sprout is required for normal angiogenesis, and implicate the Notch signalling pathway in this process.