Allowed and forbidden transitions in artificial hydrogen and helium atoms

The strength of radiative transitions in atoms is governed by selection rules that depend on the occupation of atomic orbitals with electrons. Experiments have shown similar electron occupation of the quantized energy levels in semiconductor quantum dots--often described as artificial atoms. But unlike real atoms, the confinement potential of quantum dots is anisotropic, and the electrons can easily couple with phonons of the material. Here we report electrical pump-and-probe experiments that probe the allowed and 'forbidden' transitions between energy levels under phonon emission in quantum dots with one or two electrons (artificial hydrogen and helium atoms). The forbidden transitions are in fact allowed by higher-order processes where electrons flip their spin. We find that the relaxation time is about 200 micro s for forbidden transitions, 4 to 5 orders of magnitude longer than for allowed transitions. This indicates that the spin degree of freedom is well separated from the orbital degree of freedom, and that the total spin in the quantum dots is an excellent quantum number. This is an encouraging result for potential applications of quantum dots as basic entities for spin-based quantum information storage.     

关于停时的一个注记

对任意停时T,定义A(T)={停时S:S≤T,在{T>0}上S相似文献   

A large-scale RNAi screen in human cells identifies new components of the p53 pathway

RNA interference (RNAi) is a powerful new tool with which to perform loss-of-function genetic screens in lower organisms and can greatly facilitate the identification of components of cellular signalling pathways. In mammalian cells, such screens have been hampered by a lack of suitable tools that can be used on a large scale. We and others have recently developed expression vectors to direct the synthesis of short hairpin RNAs (shRNAs) that act as short interfering RNA (siRNA)-like molecules to stably suppress gene expression. Here we report the construction of a set of retroviral vectors encoding 23,742 distinct shRNAs, which target 7,914 different human genes for suppression. We use this RNAi library in human cells to identify one known and five new modulators of p53-dependent proliferation arrest. Suppression of these genes confers resistance to both p53-dependent and p19ARF-dependent proliferation arrest, and abolishes a DNA-damage-induced G1 cell-cycle arrest. Furthermore, we describe siRNA bar-code screens to rapidly identify individual siRNA vectors associated with a specific phenotype. These new tools will greatly facilitate large-scale loss-of-function genetic screens in mammalian cells.     

Transport and Anderson localization in disordered two-dimensional photonic lattices

One of the most interesting phenomena in solid-state physics is Anderson localization, which predicts that an electron may become immobile when placed in a disordered lattice. The origin of localization is interference between multiple scatterings of the electron by random defects in the potential, altering the eigenmodes from being extended (Bloch waves) to exponentially localized. As a result, the material is transformed from a conductor to an insulator. Anderson's work dates back to 1958, yet strong localization has never been observed in atomic crystals, because localization occurs only if the potential (the periodic lattice and the fluctuations superimposed on it) is time-independent. However, in atomic crystals important deviations from the Anderson model always occur, because of thermally excited phonons and electron-electron interactions. Realizing that Anderson localization is a wave phenomenon relying on interference, these concepts were extended to optics. Indeed, both weak and strong localization effects were experimentally demonstrated, traditionally by studying the transmission properties of randomly distributed optical scatterers (typically suspensions or powders of dielectric materials). However, in these studies the potential was fully random, rather than being 'frozen' fluctuations on a periodic potential, as the Anderson model assumes. Here we report the experimental observation of Anderson localization in a perturbed periodic potential: the transverse localization of light caused by random fluctuations on a two-dimensional photonic lattice. We demonstrate how ballistic transport becomes diffusive in the presence of disorder, and that crossover to Anderson localization occurs at a higher level of disorder. Finally, we study how nonlinearities affect Anderson localization. As Anderson localization is a universal phenomenon, the ideas presented here could also be implemented in other systems (for example, matter waves), thereby making it feasible to explore experimentally long-sought fundamental concepts, and bringing up a variety of intriguing questions related to the interplay between disorder and nonlinearity.     

可编程逻辑互连网络的设计

半导体技术的迅速进步要求数字系统设计过程的同步提升。例如英特尔4004处理器这样的早期集成电路完全是手工设计的，其中包括了布局工艺图。对于在1971年利用100m技术工艺过程构建的2300个晶体管晶件而言，这是一个合理的努力。与之形成对照的是2002年7月公布的最新的英特尔奔腾2微处理器。它包含了2．2亿个晶体管，使用了0．180m工艺过程，设计这样一个大型器件要求几百个工程师依靠高级的CAD工具来处理其复杂性。在过去的5至10年内，每一个新的英特尔处理器都是设计的顶峰，为其他器件的跟进设置了标准。随着当前制造技术达到了深一亚微层次，为创建一个可以工作的设计所要求的低层次设计努力就越来越多。同时可编程逻辑器件的功能已经提升。目前的现场可编程门阵列（FPGA）可以实现整个数字系统，它们对于系统层次设计者的吸引力在不断地增加。但是在许多情况中，它们的性能是不够的，或者它们没有包含足够的内存，或者缺乏关键的知识产权核心。因此存在着不断增加的需求，要把可编程逻辑技术与客户化的亚微VLSI技术相结合。如果说在可编程逻辑中存在着一个没有被完全理解的具体方面的话，那就是互连。它占用了最大的面积而且要为大多数的延时负责。可编程逻辑器件的90％是布局，10％是逻辑。本书把焦点放在了90％上面，即可编程布局上。它介绍了互连设计的最新研究成果，重点是互连结构自动生成的知识与工具。     

Defense-related phenylpropanoid biosynthetic gene clusters in rice

Since colonising land,plants have undergone massive metabolic diversification.This is reflected by the numbers of metabolites that they collectively produce (es...     

Thymic selection threshold defined by compartmentalization of Ras/MAPK signalling

A healthy individual can mount an immune response to exogenous pathogens while avoiding an autoimmune attack on normal tissues. The ability to distinguish between self and non-self is called 'immunological tolerance' and, for T lymphocytes, involves the generation of a diverse pool of functional T cells through positive selection and the removal of overtly self-reactive thymocytes by negative selection during T-cell ontogeny. To elucidate how thymocytes arrive at these cell fate decisions, here we have identified ligands that define an extremely narrow gap spanning the threshold that distinguishes positive from negative selection. We show that, at the selection threshold, a small increase in ligand affinity for the T-cell antigen receptor leads to a marked change in the activation and subcellular localization of Ras and mitogen-activated protein kinase (MAPK) signalling intermediates and the induction of negative selection. The ability to compartmentalize signalling molecules differentially in the cell endows the thymocyte with the ability to convert a small change in analogue input (affinity) into a digital output (positive versus negative selection) and provides the basis for establishing central tolerance.     

The sirtuin SIRT6 regulates lifespan in male mice

The significant increase in human lifespan during the past century confronts us with great medical challenges. To meet these challenges, the mechanisms that determine healthy ageing must be understood and controlled. Sirtuins are highly conserved deacetylases that have been shown to regulate lifespan in yeast, nematodes and fruitflies. However, the role of sirtuins in regulating worm and fly lifespan has recently become controversial. Moreover, the role of the seven mammalian sirtuins, SIRT1 to SIRT7 (homologues of the yeast sirtuin Sir2), in regulating lifespan is unclear. Here we show that male, but not female, transgenic mice overexpressing Sirt6 (ref. 4) have a significantly longer lifespan than wild-type mice. Gene expression analysis revealed significant differences between male Sirt6-transgenic mice and male wild-type mice: transgenic males displayed lower serum levels of insulin-like growth factor 1 (IGF1), higher levels of IGF-binding protein 1 and altered phosphorylation levels of major components of IGF1 signalling, a key pathway in the regulation of lifespan. This study shows the regulation of mammalian lifespan by a sirtuin family member and has important therapeutic implications for age-related diseases.