A laboratory analogue of the event horizon using slow light in an atomic medium.

Singularities underlie many optical phenomena. The rainbow, for example, involves a particular type of singularity-a ray catastrophe-in which light rays become infinitely intense. In practice, the wave nature of light resolves these infinities, producing interference patterns. At the event horizon of a black hole, time stands still and waves oscillate with infinitely small wavelengths. However, the quantum nature of light results in evasion of the catastrophe and the emission of Hawking radiation. Here I report a theoretical laboratory analogue of an event horizon: a parabolic profile of the group velocity of light brought to a standstill in an atomic medium can cause a wave singularity similar to that associated with black holes. In turn, the quantum vacuum is forced to create photon pairs with a characteristic spectrum, a phenomenon related to Hawking radiation. The idea may initiate a theory of 'quantum' catastrophes, extending classical catastrophe theory.     

Reverse engineering of regulatory networks in human B cells

Cellular phenotypes are determined by the differential activity of networks linking coregulated genes. Available methods for the reverse engineering of such networks from genome-wide expression profiles have been successful only in the analysis of lower eukaryotes with simple genomes. Using a new method called ARACNe (algorithm for the reconstruction of accurate cellular networks), we report the reconstruction of regulatory networks from expression profiles of human B cells. The results are suggestive a hierarchical, scale-free network, where a few highly interconnected genes (hubs) account for most of the interactions. Validation of the network against available data led to the identification of MYC as a major hub, which controls a network comprising known target genes as well as new ones, which were biochemically validated. The newly identified MYC targets include some major hubs. This approach can be generally useful for the analysis of normal and pathologic networks in mammalian cells.     

Positional identification of TNFSF4, encoding OX40 ligand, as a gene that influences atherosclerosis susceptibility

Ath1 is a quantitative trait locus on mouse chromosome 1 that renders C57BL/6 mice susceptible and C3H/He mice resistant to diet-induced atherosclerosis. The quantitative trait locus region encompasses 11 known genes, including Tnfsf4 (also called Ox40l or Cd134l), which encodes OX40 ligand. Here we report that mice with targeted mutations of Tnfsf4 had significantly (P 相似文献   

采用应变梯度硬化模型预测黄铜薄板微弯曲弯矩

通过黄铜板料微弯曲实验,发现其弯曲弯矩存在明显的尺寸效应现象,随板料厚度的减小,弯曲弯矩增大.采用经典塑性理论和不同的应变梯度理论对微弯曲弯矩进行了预测,对比分析结果表明：修正的Nix Gao模型的预测结果更接近于实验结果,并且得出了合理的内禀尺寸表达式;该内禀尺寸与材料的剪切模量、初始屈服极限、柏氏矢量和板料厚度方向上的孪晶数有关.