在相对论性激光-等离子体系统中模拟激光参数对等离子弧柱形态的影响

基于相对论性激光-等离子体动力学理论和PIC方法建立了激光入射等离子弧柱的模型,该模型描述了激光入射等离子弧后粒子的运动,并模拟了弧柱形态的变化。通过改变激光的平均功率、脉冲宽度以及重复频率,模拟等离子弧柱形态变化,得到的激光参数对等离子弧柱形态的影响规律。通过控制弧柱的直径可以提高材料的熔积性能。计算结果表明增大激光平均功率、脉冲宽度,可以更深地压缩等离子弧;但是,重复频率的影响则会出现波动现象。激光等离子复合加工更适合于精细加工。     

A New Method with High Confidence for Validation of Computer Simulation Models of Flight Systems

Computer simulation models may by used to gain further information about missile performance variability. Model validation is an important aspect of the test program for a missile system. Validation provides a basis for confidence in the model's results and is a necessary step if the model is to be used to draw inference about the behavior of the real missile. This paper is a review of methods useful for validation of computer simulation models of missile systems and provides a new method with high degree of confidence for validation of computer simulation models of missile systems. Some examples of the use of the new method in validating computer simulation models are given.     

空间n边形中的正弦定理

利用向量代数中的一个基本等式进行推证,得出了在空间 ｎ 边形中正弦定理的表现形式。使文［１］,［２］,［３］更加完整     

Anthropogenic ocean acidification over the twenty-first century and its impact on calcifying organisms

Today's surface ocean is saturated with respect to calcium carbonate, but increasing atmospheric carbon dioxide concentrations are reducing ocean pH and carbonate ion concentrations, and thus the level of calcium carbonate saturation. Experimental evidence suggests that if these trends continue, key marine organisms--such as corals and some plankton--will have difficulty maintaining their external calcium carbonate skeletons. Here we use 13 models of the ocean-carbon cycle to assess calcium carbonate saturation under the IS92a 'business-as-usual' scenario for future emissions of anthropogenic carbon dioxide. In our projections, Southern Ocean surface waters will begin to become undersaturated with respect to aragonite, a metastable form of calcium carbonate, by the year 2050. By 2100, this undersaturation could extend throughout the entire Southern Ocean and into the subarctic Pacific Ocean. When live pteropods were exposed to our predicted level of undersaturation during a two-day shipboard experiment, their aragonite shells showed notable dissolution. Our findings indicate that conditions detrimental to high-latitude ecosystems could develop within decades, not centuries as suggested previously.     

A dipole mode in the tropical Indian Ocean

For the tropical Pacific and Atlantic oceans, internal modes of variability that lead to climatic oscillations have been recognized, but in the Indian Ocean region a similar ocean-atmosphere interaction causing interannual climate variability has not yet been found. Here we report an analysis of observational data over the past 40 years, showing a dipole mode in the Indian Ocean: a pattern of internal variability with anomalously low sea surface temperatures off Sumatra and high sea surface temperatures in the western Indian Ocean, with accompanying wind and precipitation anomalies. The spatio-temporal links between sea surface temperatures and winds reveal a strong coupling through the precipitation field and ocean dynamics. This air-sea interaction process is unique and inherent in the Indian Ocean, and is shown to be independent of the El Ni?o/Southern Oscillation. The discovery of this dipole mode that accounts for about 12% of the sea surface temperature variability in the Indian Ocean--and, in its active years, also causes severe rainfall in eastern Africa and droughts in Indonesia--brightens the prospects for a long-term forecast of rainfall anomalies in the affected countries.     

Prion-like behaviour and tau-dependent cytotoxicity of pyroglutamylated amyloid-β

Extracellular plaques of amyloid-β and intraneuronal neurofibrillary tangles made from tau are the histopathological signatures of Alzheimer's disease. Plaques comprise amyloid-β fibrils that assemble from monomeric and oligomeric intermediates, and are prognostic indicators of Alzheimer's disease. Despite the importance of plaques to Alzheimer's disease, oligomers are considered to be the principal toxic forms of amyloid-β. Interestingly, many adverse responses to amyloid-β, such as cytotoxicity, microtubule loss, impaired memory and learning, and neuritic degeneration, are greatly amplified by tau expression. Amino-terminally truncated, pyroglutamylated (pE) forms of amyloid-β are strongly associated with Alzheimer's disease, are more toxic than amyloid-β, residues 1-42 (Aβ(1-42)) and Aβ(1-40), and have been proposed as initiators of Alzheimer's disease pathogenesis. Here we report a mechanism by which pE-Aβ may trigger Alzheimer's disease. Aβ(3(pE)-42) co-oligomerizes with excess Aβ(1-42) to form metastable low-n oligomers (LNOs) that are structurally distinct and far more cytotoxic to cultured neurons than comparable LNOs made from Aβ(1-42) alone. Tau is required for cytotoxicity, and LNOs comprising 5% Aβ(3(pE)-42) plus 95% Aβ(1-42) (5% pE-Aβ) seed new cytotoxic LNOs through multiple serial dilutions into Aβ(1-42) monomers in the absence of additional Aβ(3(pE)-42). LNOs isolated from human Alzheimer's disease brain contained Aβ(3(pE)-42), and enhanced Aβ(3(pE)-42) formation in mice triggered neuron loss and gliosis at 3 months, but not in a tau-null background. We conclude that Aβ(3(pE)-42) confers tau-dependent neuronal death and causes template-induced misfolding of Aβ(1-42) into structurally distinct LNOs that propagate by a prion-like mechanism. Our results raise the possibility that Aβ(3(pE)-42) acts similarly at a primary step in Alzheimer's disease pathogenesis.     

Human gamma-chain genes are rearranged in leukaemic T cells and map to the short arm of chromosome 7

Three gene families that rearrange during the somatic development of T cells have been identified in the murine genome. Two of these gene families (alpha and beta) encode subunits of the antigen-specific T-cell receptor and are also present in the human genome. The third gene family, designated here as the gamma-chain gene family, is rearranged in murine cytolytic T cells but not in most helper T cells. Here we present evidence that the human genome also contains gamma-chain genes that undergo somatic rearrangement in leukaemia-derived T cells. Murine gamma-chain genes appear to be encoded in gene segments that are analogous to the immunoglobulin gene variable, constant and joining segments. There are two closely related constant-region gene segments in the human genome. One of the constant-region genes is deleted in all three T-cell leukaemias that we have studied. The two constant-region gamma-chain genes reside on the short arm of chromosome 7 (7p15); this region is involved in chromosomal rearrangements identified in T cells from individuals with the immunodeficiency syndrome ataxia telangiectasia and observed only rarely in routine cytogenetic analyses of normal individuals. This region is also a secondary site of beta-chain gene hybridization.     

Bone marrow cells regenerate infarcted myocardium

Myocardial infarction leads to loss of tissue and impairment of cardiac performance. The remaining myocytes are unable to reconstitute the necrotic tissue, and the post-infarcted heart deteriorates with time. Injury to a target organ is sensed by distant stem cells, which migrate to the site of damage and undergo alternate stem cell differentiation; these events promote structural and functional repair. This high degree of stem cell plasticity prompted us to test whether dead myocardium could be restored by transplanting bone marrow cells in infarcted mice. We sorted lineage-negative (Lin-) bone marrow cells from transgenic mice expressing enhanced green fluorescent protein by fluorescence-activated cell sorting on the basis of c-kit expression. Shortly after coronary ligation, Lin- c-kitPOS cells were injected in the contracting wall bordering the infarct. Here we report that newly formed myocardium occupied 68% of the infarcted portion of the ventricle 9 days after transplanting the bone marrow cells. The developing tissue comprised proliferating myocytes and vascular structures. Our studies indicate that locally delivered bone marrow cells can generate de novo myocardium, ameliorating the outcome of coronary artery disease.     

Coherent spin manipulation without magnetic fields in strained semiconductors

A consequence of relativity is that in the presence of an electric field, the spin and momentum states of an electron can be coupled; this is known as spin-orbit coupling. Such an interaction opens a pathway to the manipulation of electron spins within non-magnetic semiconductors, in the absence of applied magnetic fields. This interaction has implications for spin-based quantum information processing and spintronics, forming the basis of various device proposals. For example, the concept of spin field-effect transistors is based on spin precession due to the spin-orbit coupling. Most studies, however, focus on non-spin-selective electrical measurements in quantum structures. Here we report the direct measurement of coherent electron spin precession in zero magnetic field as the electrons drift in response to an applied electric field. We use ultrafast optical techniques to spatiotemporally resolve spin dynamics in strained gallium arsenide and indium gallium arsenide epitaxial layers. Unexpectedly, we observe spin splitting in these simple structures arising from strain in the semiconductor films. The observed effect provides a flexible approach for enabling electrical control over electron spins using strain engineering. Moreover, we exploit this strain-induced field to electrically drive spin resonance with Rabi frequencies of up to approximately 30 MHz.