从团粒结构失稳角度探讨由灌溉引起的黄土湿陷发生机理

利用SEM/EDX等测试手段,探讨了由灌溉引起的黄土湿陷发生机理.结果表明:黄土湿陷过程包括初始快速变形和后续迟缓变形2个阶段,这2个阶段的发生都与黄土的骨架颗粒--团粒有关.前者是由于黄土中非水稳性团粒遇水破坏所至,而后者是因为水的渗透造成黄土团粒主要胶结物碳酸钙的淋溶移动损失,从而导致失稳.黄土中松散结构或架空孔隙的存在是产生湿陷的重要条件,但不是湿陷发生的根本原因.     

地域的履历——浙江省奉化县忠义乡（下）

(接上期)上面提到的非定居移住民,是指从福建及浙江省南部的台州府等地流入奉化县山区的人,即所谓的“棚民”。在位于忠义乡以西的剡源乡,可以见到如下的记事 。剡源向乏水患,亦无劫案。自嘉庆初,闽、台(福建省与浙江省台州府———引用者)棚民相率来剡〔源乡〕,种靛青、种苞芦,日辟日广。如牛山之濯濯水,无所蓄迨。〔嘉庆〕末年,大雨连旬,山水骤注于溪,溪不能容,遂漂没田畴无算。……比年仙居、黄岩无业贫民偕来工作,寓居山厂,一不得食,抢劫之案,层见叠出。由此来看,自嘉庆初年( 1 8世纪末)以降,福建等地的棚民、浙江南部的贫民流入该地山…     

Tristable nematic liquid-crystal device using micropatterned surface alignment

It has long been appreciated that liquid-crystal (LC) devices in which the LC molecules adopt multiple stable orientations could drastically reduce the power consumption required for high-information-content displays. But for the commonly used nematic LCs, which are intrinsically uniaxial in symmetry, no industrially feasible multi-stable LC device has been realized. Recently we demonstrated how bistability can be robustly engineered into a nematic LC device, by patterning a substrate with an orientational chequerboard pattern that enforces orthogonal LC alignment in neighbouring square domains. As a result of the four-fold symmetry of the pattern, the two diagonal axes of the chequerboard become equally stable macroscopic orientations. Here we extend this symmetry approach to obtain a tristable surface-aligned nematic LC. A microscopic pattern exhibiting six-fold symmetry is inscribed on a polyimide surface using the stylus of an atomic force microscope. The hexagonal symmetry of the microscopic orientational domains in turn gives rise to three stable macroscopic LC orientations, which are mutually switchable by an in-plane electric field. The resulting switching mode is surface driven, and hence should be compatible with demanding flexible display applications.     

Suppression of basal autophagy in neural cells causes neurodegenerative disease in mice

Autophagy is an intracellular bulk degradation process through which a portion of the cytoplasm is delivered to lysosomes to be degraded. Although the primary role of autophagy in many organisms is in adaptation to starvation, autophagy is also thought to be important for normal turnover of cytoplasmic contents, particularly in quiescent cells such as neurons. Autophagy may have a protective role against the development of a number of neurodegenerative diseases. Here we report that loss of autophagy causes neurodegeneration even in the absence of any disease-associated mutant proteins. Mice deficient for Atg5 (autophagy-related 5) specifically in neural cells develop progressive deficits in motor function that are accompanied by the accumulation of cytoplasmic inclusion bodies in neurons. In Atg5-/- cells, diffuse, abnormal intracellular proteins accumulate, and then form aggregates and inclusions. These results suggest that the continuous clearance of diffuse cytosolic proteins through basal autophagy is important for preventing the accumulation of abnormal proteins, which can disrupt neural function and ultimately lead to neurodegeneration.     

High entropy state of orientationally-disordered clusters in Zr-based bulk metallic glass

A phase transformation of a metastable Zr2Ni intermetallic crystalline phase to vitrify was studied with molecular dynamics (MD) simulations based on a plastic crystal model (PCM), which utilizes the orientational disorder of molecules of plastic crystals in a class of soft matter. The simulation results show ed that computational operations in MD-PCM for the random rotati ons of the clusters in the crystalline phase around their center of gravity and subsequent annealing lead to form a dense random pa cking structure from the metastable Zr2Ni phase. These randomly-rotated clusters provide high degrees of freedom in terms of atomic positions, which results in enhancing the glass-forming ability of the alloy. The critical fraction of the number of rotated cl usters for forming the glassy phase ( fc^R) is evaluated to be 0.75 ? 0.80. Thus, the critical fraction of the number of un-rotated clusters (fc^U=1?fc^R) is close to the critical concentration of site percolation for metallic materials. The mechanism of the metastable Zr2Ni phase to vitrify with increasing f^R was analyzed with a concept of communal entropy in the free volume theory with solid- and liquid-like cells proposed by Cohen and Grest. The MD-PCM for the metastable Zr2Ni phase suggests that Zr-based bulk metallic glass (BMG) can be regarded as an alloy in a high rotation entropy state of cl usters and that glass transition takes place by percolation of th e nuclei of a liquid-like glassy phase.     

Chenguodaite （Ag9FeTe2S4）： a new tellurosulfide mineral from the gold district of East Shandong Peninsula,China

Chenguodaite, approved by IMA-CNMMN （2004-042a）, was discovered in the Bunan quartz vein-type gold deposit in the gold district of East Shandong Peninsula. The mineral occurs in high grade Au-Ag-Cu ores, coexisting with galena, chalcopyrite, hessite, electrum, unnamed Ag6TeS2 and AglsFeBiTe3Se, enclosed and replaced by native silver and acanthite. In the reflected light microscope, the mineral has light gray color, indistinguishable anistropism and hardness around 2-3. The color indices of chenguodaite relative to ICE C illuminator are： x=0.3027, y=0.3076, Y=25.78%,λd=474 nm, Pe=3.68%, similar to those of canfieldite. The average chemical composition from 16 microprobe analyses is Ag8.97Fe1.00Te1.99S4.04, idealized to AggFeTe2S4. The polycrystalline X-ray diffraction of chenguodaite by Gandolfi camera and synchrotron oscillation photography results in 67 reflections with the 12 strongest being （relative intensity in bracket）： 6.742（69）, 6.416（39）, 5.951（33）, 3.265（100）, 2.981（24）, 2.649（22）, 2.25（24）, 2.188（71）, 2.142（22）, 2.123（31）, 2.044（23）, 1.949（33）, which are indexed to a primitive orthorhombic cell with a=12.769 （2） A, b= 14.814（2） A, c= 16.233 （1） A, V= 3070.6 A^3, Z= 9, Dcal.=6.85 g/cm^3. The name is for the late Prof. Chen Guoda, a famous Chinese geologist and the founder of Diwa-Geodepression theory of tectonics.     

A stress response pathway regulates DNA damage through β2-adrenoreceptors and β-arrestin-1

The human mind and body respond to stress, a state of perceived threat to homeostasis, by activating the sympathetic nervous system and secreting the catecholamines adrenaline and noradrenaline in the 'fight-or-flight' response. The stress response is generally transient because its accompanying effects (for example, immunosuppression, growth inhibition and enhanced catabolism) can be harmful in the long term. When chronic, the stress response can be associated with disease symptoms such as peptic ulcers or cardiovascular disorders, and epidemiological studies strongly indicate that chronic stress leads to DNA damage. This stress-induced DNA damage may promote ageing, tumorigenesis, neuropsychiatric conditions and miscarriages. However, the mechanisms by which these DNA-damage events occur in response to stress are unknown. The stress hormone adrenaline stimulates β(2)-adrenoreceptors that are expressed throughout the body, including in germline cells and zygotic embryos. Activated β(2)-adrenoreceptors promote Gs-protein-dependent activation of protein kinase A (PKA), followed by the recruitment of β-arrestins, which desensitize G-protein signalling and function as signal transducers in their own right. Here we elucidate a molecular mechanism by which β-adrenergic catecholamines, acting through both Gs-PKA and β-arrestin-mediated signalling pathways, trigger DNA damage and suppress p53 levels respectively, thus synergistically leading to the accumulation of DNA damage. In mice and in human cell lines, β-arrestin-1 (ARRB1), activated via β(2)-adrenoreceptors, facilitates AKT-mediated activation of MDM2 and also promotes MDM2 binding to, and degradation of, p53, by acting as a molecular scaffold. Catecholamine-induced DNA damage is abrogated in Arrb1-knockout (Arrb1(-/-)) mice, which show preserved p53 levels in both the thymus, an organ that responds prominently to acute or chronic stress, and in the testes, in which paternal stress may affect the offspring's genome. Our results highlight the emerging role of ARRB1 as an E3-ligase adaptor in the nucleus, and reveal how DNA damage may accumulate in response to chronic stress.     

Molecular evidence on evolutionary switching from particle-feeding to sophisticated carnivory in the calanoid copepod family Heterorhabdidae: drastic and rapid changes in functions of homologues

The oceanic calanoid copepod family Heterorhabdidae is unique in that it comprises both particle-feeding and carnivorous genera with some intermediate taxa. Both morphological and molecular (nuclear 18S and 28S rRNA) phylogenetic analyses of the family suggest that an evolutionary switch in feeding strategy, from transitions of typical particle-feeding through some intermediate modes to sophisticated carnivory, might have occurred with the development of a specially designed ‘poison’ injection system. In view of the small amount of genetic differentiation among genera in this family, the switching of feeding modes and re-colonization from deep to shallow waters might have occurred over a short geological period since the Middle to Late Miocene.     

采用死区补偿和输出电流补偿的数控UPS逆变器

为在不增加传感器的情况下,改善不间断电源(U PS)逆变器的输出动静态性能,提出了一种数字控制策略。该策略利用面积等效原理,将线性负载下的死区等效为方波扰动,利用前馈对其补偿;将输出电流视为对控制系统的扰动,并利用前馈补偿,通过对输出电压的微分运算获得输出滤波电容电流值,从而在不使用电流传感器的情况下,实现了对U PS逆变器的准双环控制。在1 kVA的样机上进行实验研究,其结果在额定阻性负载下的稳态总谐波畸变率(THD)为2.49%,空载与额定负载间阶越变化下的电压调整率为6.75%。结果表明:死区补偿和输出电流补偿有效,整个控制策略的可行。     

Experimental adaptation of an influenza H5 HA confers respiratory droplet transmission to a reassortant H5 HA/H1N1 virus in ferrets

Highly pathogenic avian H5N1 influenza A viruses occasionally infect humans, but currently do not transmit efficiently among humans. The viral haemagglutinin (HA) protein is a known host-range determinant as it mediates virus binding to host-specific cellular receptors. Here we assess the molecular changes in HA that would allow a virus possessing subtype H5 HA to be transmissible among mammals. We identified a reassortant H5 HA/H1N1 virus-comprising H5 HA (from an H5N1 virus) with four mutations and the remaining seven gene segments from a 2009 pandemic H1N1 virus-that was capable of droplet transmission in a ferret model. The transmissible H5 reassortant virus preferentially recognized human-type receptors, replicated efficiently in ferrets, caused lung lesions and weight loss, but was not highly pathogenic and did not cause mortality. These results indicate that H5 HA can convert to an HA that supports efficient viral transmission in mammals; however, we do not know whether the four mutations in the H5 HA identified here would render a wholly avian H5N1 virus transmissible. The genetic origin of the remaining seven viral gene segments may also critically contribute to transmissibility in mammals. Nevertheless, as H5N1 viruses continue to evolve and infect humans, receptor-binding variants of H5N1 viruses with pandemic potential, including avian-human reassortant viruses as tested here, may emerge. Our findings emphasize the need to prepare for potential pandemics caused by influenza viruses possessing H5 HA, and will help individuals conducting surveillance in regions with circulating H5N1 viruses to recognize key residues that predict the pandemic potential of isolates, which will inform the development, production and distribution of effective countermeasures.