Magnetic vortex core reversal by excitation with short bursts of an alternating field

The vortex state, characterized by a curling magnetization, is one of the equilibrium configurations of soft magnetic materials and occurs in thin ferromagnetic square and disk-shaped elements of micrometre size and below. The interplay between the magnetostatic and the exchange energy favours an in-plane, closed flux domain structure. This curling magnetization turns out of the plane at the centre of the vortex structure, in an area with a radius of about 10 nanometres--the vortex core. The vortex state has a specific excitation mode: the in-plane gyration of the vortex structure about its equilibrium position. The sense of gyration is determined by the vortex core polarization. Here we report on the controlled manipulation of the vortex core polarization by excitation with small bursts of an alternating magnetic field. The vortex motion was imaged by time-resolved scanning transmission X-ray microscopy. We demonstrate that the sense of gyration of the vortex structure can be reversed by applying short bursts of the sinusoidal excitation field with amplitude of about 1.5 mT. This reversal unambiguously indicates a switching of the out-of-plane core polarization. The observed switching mechanism, which can be understood in the framework of micromagnetic theory, gives insights into basic magnetization dynamics and their possible application in data storage.     

中国-东盟自由贸易区框架协议:21世纪中国-东盟关系的新发展

在回顾中国—东盟自由贸易区构建历程的基础上,对中国、东盟各方从中的获益性做出了分析,指出中国—东盟的共同利益将是贸易区发展的推动力。     

Failure of familial Alzheimer's disease to segregate with the A4-amyloid gene in several European families

The gene coding for the amyloid protein, a component of neuritic plaques found in brain tissue from patients with Alzheimer's disease, has been localized to chromosome 21, and neighbouring polymorphic DNA markers segregate with Alzheimer's disease in several large families. These data, and the association of Alzheimer's disease with Down's syndrome, suggest that overproduction of the amyloid protein, or production of an abnormal variant of the protein, may be the underlying pathological change causing Alzheimer's disease. We have identified a restriction fragment length polymorphism of the A4-amyloid gene, and find recombinants in two Alzheimer's disease families between Alzheimer's disease and the A4-amyloid locus. This demonstrates that the gene for plaque core A4-amyloid cannot be the locus of a defect causing Alzheimer's disease in these families. These data indicate that alterations in the plaque core amyloid gene cannot explain the molecular pathology for all cases of Alzheimer's disease.     

Sequence of cDNA encoding human insulin-like growth factor I precursor

Somatomedins (SM) or insulin-like growth factors (IGF) constitute a heterogeneous group of peptides with important growth-promoting effects in vitro as well as in vivo. Amino acid sequences have been determined for only two of them, IGF-I and IGF-II, which are highly homologous. IGF-I, which is identical with SM-C, is composed of 70 amino acid residues and IGF-II contains 73 amino acids and may be identical with SM-A. Other peptides with different charge properties but with similar SM-like or insulin-like behaviour in biological and receptor assays, have been described but have not yet been fully characterized. The liver is known to be a major site of production of these peptides, but many other tissues--especially in the fetus--may synthesize them as well. We report here the nucleotide sequence of a human liver cDNA encoding the complete amino acid sequence of IGF-I. The IGF-I coding region is flanked by sequences encoding an amino-terminal peptide of at least 25 amino acid residues and a carboxyl-terminal peptide of 35 amino acids. This provides evidence that IGF-I is synthesized as a precursor protein and that formation of IGF-I from this precursor requires proteolytic processing at both ends.     

Controlling the dynamics of spontaneous emission from quantum dots by photonic crystals

Control of spontaneously emitted light lies at the heart of quantum optics. It is essential for diverse applications ranging from miniature lasers and light-emitting diodes, to single-photon sources for quantum information, and to solar energy harvesting. To explore such new quantum optics applications, a suitably tailored dielectric environment is required in which the vacuum fluctuations that control spontaneous emission can be manipulated. Photonic crystals provide such an environment: they strongly modify the vacuum fluctuations, causing the decay of emitted light to be accelerated or slowed down, to reveal unusual statistics, or to be completely inhibited in the ideal case of a photonic bandgap. Here we study spontaneous emission from semiconductor quantum dots embedded in inverse opal photonic crystals. We show that the spectral distribution and time-dependent decay of light emitted from excitons confined in the quantum dots are controlled by the host photonic crystal. Modified emission is observed over large frequency bandwidths of 10%, orders of magnitude larger than reported for resonant optical microcavities. Both inhibited and enhanced decay rates are observed depending on the optical emission frequency, and they are controlled by the crystals' lattice parameter. Our experimental results provide a basis for all-solid-state dynamic control of optical quantum systems.