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.     

水分和热胁迫对苗木针叶可溶性糖含量的影响

以杉木、马尾松、花旗松和北美乔柏为对象，研究了在水分和热胁迫下，苗木生长期间针叶内可溶性糖含量的变化。结果表明：(1)水分和热胁迫处理对杉木针叶果糖含量的影响不明显，但对杉木针叶葡萄糖和蔗糖的含量却有显影响。水分胁迫和热胁迫的交互作用对杉苗针叶的蔗糖含量也有显影响。随着水分胁迫程度的加深，葡萄糖含量提高了11．80％，蔗糖含量提高幅度达318．86％。随着热胁迫程度的加深，葡萄糖含量提高了16．54％，蔗糖含量提高幅度为169．83％；(2)水分胁迫处理对马尾松苗木针叶葡萄糖和蔗糖含量的影响显，而热胁迫则对葡萄糖和果糖含量影响显。水分和热胁迫处理对马尾松苗木针叶3种可溶性糖含量的影响均呈上升趋势，其中水分胁迫条件下葡萄糖含量提高了45．92％，果糖含量提高了34．01％，蔗糖含量提高了138．32％。热胁迫条件下葡萄糖含量提高了36．07％，果糖含量提高了28．01％，蔗糖含量提高了22．82％；(3)水分和热胁迫尽管对花旗松苗木针叶的3种可溶性糖含量均有较显影响，但随着水分胁迫程度的加深，3种可溶性糖含量均未表现出明显的上升趋势。只有随着热胁迫程度的加深，花旗松苗木针叶的3种可溶性糖含量才呈现出上升趋势；(4)水分和热胁迫对北美乔柏苗木针叶可溶性糖含量均有显影响。其中随着水分胁迫程度的加深，葡萄糖含量提高了89．46％，果糖含量提高了90．32％，蔗糖含量提高了71.68％。随着热胁迫程度的加深，葡萄糖含量提高了21.18％，果糖含量提高了45．97％，蔗糖含量提高了107．67％。水分胁迫和热胁迫的交互作用对北美乔柏苗木针叶的蔗糖含量有显影响。     

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.     

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...     

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。     

Peripheral SMN restoration is essential for long-term rescue of a severe spinal muscular atrophy mouse model

Spinal muscular atrophy (SMA) is a motor neuron disease and the leading genetic cause of infant mortality; it results from loss-of-function mutations in the survival motor neuron 1 (SMN1) gene. Humans have a paralogue, SMN2, whose exon 7 is predominantly skipped, but the limited amount of functional, full-length SMN protein expressed from SMN2 cannot fully compensate for a lack of SMN1. SMN is important for the biogenesis of spliceosomal small nuclear ribonucleoprotein particles, but downstream splicing targets involved in pathogenesis remain elusive. There is no effective SMA treatment, but SMN restoration in spinal cord motor neurons is thought to be necessary and sufficient. Non-central nervous system (CNS) pathologies, including cardiovascular defects, were recently reported in severe SMA mouse models and patients, reflecting autonomic dysfunction or direct effects in cardiac tissues. Here we compared systemic versus CNS restoration of SMN in a severe mouse model. We used an antisense oligonucleotide (ASO), ASO-10-27, that effectively corrects SMN2 splicing and restores SMN expression in motor neurons after intracerebroventricular injection. Systemic administration of ASO-10-27 to neonates robustly rescued severe SMA mice, much more effectively than intracerebroventricular administration; subcutaneous injections extended the median lifespan by 25 fold. Furthermore, neonatal SMA mice had decreased hepatic Igfals expression, leading to a pronounced reduction in circulating insulin-like growth factor 1 (IGF1), and ASO-10-27 treatment restored IGF1 to normal levels. These results suggest that the liver is important in SMA pathogenesis, underscoring the importance of SMN in peripheral tissues, and demonstrate the efficacy of a promising drug candidate.     

Catalytic activity of the caspase-8-FLIP(L) complex inhibits RIPK3-dependent necrosis

Caspase-8 has two opposing biological functions--it promotes cell death by triggering the extrinsic pathway of apoptosis, but also has a survival activity, as it is required for embryonic development, T-lymphocyte activation, and resistance to necrosis induced by tumour necrosis factor-α (TNF-α) and related family ligands. Here we show that development of caspase-8-deficient mice is completely rescued by ablation of receptor interacting protein kinase-3 (RIPK3). Adult animals lacking both caspase-8 and RIPK3 display a progressive lymphoaccumulative disease resembling that seen with defects in CD95 or CD95-ligand (also known as FAS and FASLG, respectively), and resist the lethal effects of CD95 ligation in vivo. We have found that caspase-8 prevents RIPK3-dependent necrosis without inducing apoptosis by functioning in a proteolytically active complex with FLICE-like inhibitory protein long (FLIP(L), also known as CFLAR), and this complex is required for the protective function.