Optically programmable electron spin memory using semiconductor quantum dots

The spin of a single electron subject to a static magnetic field provides a natural two-level system that is suitable for use as a quantum bit, the fundamental logical unit in a quantum computer. Semiconductor quantum dots fabricated by strain driven self-assembly are particularly attractive for the realization of spin quantum bits, as they can be controllably positioned, electronically coupled and embedded into active devices. It has been predicted that the atomic-like electronic structure of such quantum dots suppresses coupling of the spin to the solid-state quantum dot environment, thus protecting the 'spin' quantum information against decoherence. Here we demonstrate a single electron spin memory device in which the electron spin can be programmed by frequency selective optical excitation. We use the device to prepare single electron spins in semiconductor quantum dots with a well defined orientation, and directly measure the intrinsic spin flip time and its dependence on magnetic field. A very long spin lifetime is obtained, with a lower limit of about 20 milliseconds at a magnetic field of 4 tesla and at 1 kelvin.     

Spink5-deficient mice mimic Netherton syndrome through degradation of desmoglein 1 by epidermal protease hyperactivity

Mutations in SPINK5, encoding the serine protease inhibitor LEKTI, cause Netherton syndrome, a severe autosomal recessive genodermatosis. Spink5(-/-) mice faithfully replicate key features of Netherton syndrome, including altered desquamation, impaired keratinization, hair malformation and a skin barrier defect. LEKTI deficiency causes abnormal desmosome cleavage in the upper granular layer through degradation of desmoglein 1 due to stratum corneum tryptic enzyme and stratum corneum chymotryptic enzyme-like hyperactivity. This leads to defective stratum corneum adhesion and resultant loss of skin barrier function. Profilaggrin processing is increased and implicates LEKTI in the cornification process. This work identifies LEKTI as a key regulator of epidermal protease activity and degradation of desmoglein 1 as the primary pathogenic event in Netherton syndrome.     

南堡2、3号构造中深层硬脆性泥岩漏失机理

冀东油田南堡2、3号构造中深层钻井液漏失问题突出,为科学认识其漏失机理,对该区块岩样开展微组构分析及理化性能测试,并结合现场统计资料分析了该区块钻井液漏失机理.研究结果表明:南堡2、3号构造中深层岩性以硬脆性泥岩为主,其水敏性不强,呈现出一定的硬脆性.岩样微裂缝发育,钻井液相沿裂缝侵入,造成岩样整体胶结强度减弱,易产生沿裂缝面的张性劈裂破坏.结合现场资料判断认为该区块漏失主要类型为张开型裂缝性漏失,钻井液侵入地层导致力学强度降低,引发水力尖劈作用而造成地层破碎,导致漏失程度增加.针对南堡2、3号构造复杂漏失原因,提出了针对不同漏失原因的应对措施.研究结果为科学认识该区块钻井液漏失机理、降低钻井成本提供了技术参考.     

An extrasolar planetary system with three Neptune-mass planets

Over the past two years, the search for low-mass extrasolar planets has led to the detection of seven so-called 'hot Neptunes' or 'super-Earths' around Sun-like stars. These planets have masses 5-20 times larger than the Earth and are mainly found on close-in orbits with periods of 2-15 days. Here we report a system of three Neptune-mass planets with periods of 8.67, 31.6 and 197 days, orbiting the nearby star HD 69830. This star was already known to show an infrared excess possibly caused by an asteroid belt within 1 au (the Sun-Earth distance). Simulations show that the system is in a dynamically stable configuration. Theoretical calculations favour a mainly rocky composition for both inner planets, while the outer planet probably has a significant gaseous envelope surrounding its rocky/icy core; the outer planet orbits within the habitable zone of this star.     

Presynaptic induction of heterosynaptic associative plasticity in the mammalian brain

The induction of associative synaptic plasticity in the mammalian central nervous system classically depends on coincident presynaptic and postsynaptic activity. According to this principle, associative homosynaptic long-term potentiation (LTP) of excitatory synaptic transmission can be induced only if synaptic release occurs during postsynaptic depolarization. In contrast, heterosynaptic plasticity in mammals is considered to rely on activity-independent, non-associative processes. Here we describe a novel mechanism underlying the induction of associative LTP in the lateral amygdala (LA). Simultaneous activation of converging cortical and thalamic afferents specifically induced associative, N-methyl-D-aspartate (NMDA)-receptor-dependent LTP at cortical, but not at thalamic, inputs. Surprisingly, the induction of associative LTP at cortical inputs was completely independent of postsynaptic activity, including depolarization, postsynaptic NMDA receptor activation or an increase in postsynaptic Ca2+ concentration, and did not require network activity. LTP expression was mediated by a persistent increase in the presynaptic probability of release at cortical afferents. Our study shows the presynaptic induction and expression of heterosynaptic and associative synaptic plasticity on simultaneous activity of converging afferents. Our data indicate that input specificity of associative LTP can be determined exclusively by presynaptic properties.     

光学遥感影像土地利用分类方法综述

土地是实现经济社会高质量发展的基础性资源,光学遥感影像以时间、空间、光谱等特有的优势为土地利用变化的发现、识别、分析提供了很好的支持,利用光学遥感技术提取土地利用变化信息已经成为重要的研究领域。论文以近年来土地利用分类相关文献为基础,分别从数据源、处理流程、处理精度、计算效率等角度对土地利用分类应用较为广泛的目视解译、监督分类、非监督分类、深度学习等四类方法进行了分析和总结。最后展望了光学遥感影像土地利用分类方法的发展方向     

Dominant role of the niche in melanocyte stem-cell fate determination

Stem cells which have the capacity to self-renew and generate differentiated progeny are thought to be maintained in a specific environment known as a niche. The localization of the niche, however, remains largely obscure for most stem-cell systems. Melanocytes (pigment cells) in hair follicles proliferate and differentiate closely coupled to the hair regeneration cycle. Here we report that stem cells of the melanocyte lineage can be identified, using Dct-lacZ transgenic mice, in the lower permanent portion of mouse hair follicles throughout the hair cycle. It is only the population in this region that fulfils the criteria for stem cells, being immature, slow cycling, self-maintaining and fully competent in regenerating progeny on activation at early anagen (the growing phase of hair follicles). Induction of the re-pigmentation process in K14-steel factor transgenic mice demonstrates that a portion of amplifying stem-cell progeny can migrate out from the niche and retain sufficient self-renewing capability to function as stem cells after repopulation into vacant niches. Our data indicate that the niche has a dominant role in the fate determination of melanocyte stem-cell progeny.     

Wound repair and regeneration

The repair of wounds is one of the most complex biological processes that occur during human life. After an injury, multiple biological pathways immediately become activated and are synchronized to respond. In human adults, the wound repair process commonly leads to a non-functioning mass of fibrotic tissue known as a scar. By contrast, early in gestation, injured fetal tissues can be completely recreated, without fibrosis, in a process resembling regeneration. Some organisms, however, retain the ability to regenerate tissue throughout adult life. Knowledge gained from studying such organisms might help to unlock latent regenerative pathways in humans, which would change medical practice as much as the introduction of antibiotics did in the twentieth century.     

基于不同对流下加热系统的数值模拟与实验研究

采用多孔介质导热方程、DO辐射模型以及标准κ-ε湍流模型,建立三维热物理模型。应用有限体积法计算了室内沙疗室气固耦合传热问题。首先在自然对流条件下,即沙疗室不开风扇、处于无风状态时,改变其加热方式,分别为单面加热和双面加热。对比分析不同加热方式下,空气层以及沙体层温度场的变化。其次在双面加热条件下,改变其对流方式,分别为自然对流与强制对流。对比分析不同对流方式下,空气层温度场、速度场的变化,以及沙体层温度场的变化。最后,通过实验加以验证。研究发现强制对流条件下的双面加热能够加快空气热对流速度及沙体传热速度,使沙体层温度分布均匀化,进而提高沙体的传热效率。     

DCC constrains tumour progression via its dependence receptor activity

The role of deleted in colorectal carcinoma (DCC) as a tumour suppressor has been a matter of debate for the past 15 years. DCC gene expression is lost or markedly reduced in the majority of advanced colorectal cancers and, by functioning as a dependence receptor, DCC has been shown to induce apoptosis unless engaged by its ligand, netrin-1 (ref. 2). However, so far no animal model has supported the view that the DCC loss-of-function is causally implicated as predisposing to aggressive cancer development. To investigate the role of DCC-induced apoptosis in the control of tumour progression, here we created a mouse model in which the pro-apoptotic activity of DCC is genetically silenced. Although the loss of DCC-induced apoptosis in this mouse model is not associated with a major disorganization of the intestines, it leads to spontaneous intestinal neoplasia at a relatively low frequency. Loss of DCC-induced apoptosis is also associated with an increase in the number and aggressiveness of intestinal tumours in a predisposing APC mutant context, resulting in the development of highly invasive adenocarcinomas. These results demonstrate that DCC functions as a tumour suppressor via its ability to trigger tumour cell apoptosis.