泛代数上的Groebner-Shirshov基理论

综述了域上或交换代数上的线性（-）代数的相应的簇（范畴）的 Groebner-Shirshov 基理论的新成果，如:结合代数（包括群（半群）代数），自由代数的张量积，李代数，Di-代数，pre-李代数，Rota-Baxter代数，metabelian李代数，L-代数，半环代数，范畴代数，等．以上结果包含了许多应用，尤其是给出了一些著名结论的新的证明．     

关于太平洋安全的中欧对话：展望太平洋：看得到合作的希望吗？

太平洋地区正呈现出紧张局势，这不仅体现在关键的中美关系上，而且也体现在中国与其东部和南中国海周边国家的关系上。正如白宫、美国外交部和五角大楼在2012年初正式宣布且具体实施的那样，美国注意力、行动和军力分配向太平洋地区的“再平衡”战略转移，及此战略背后的真实意图，都引起北京方面的关注。中国担心，美国从大西洋到太平洋的整体“战略转移”，     

分析系统动力学 建模与仿真

本书是结合分析力学和系统动力学发展起来的一种新的多学科动力学系统建模方法。这种新的建模技术基于拉格朗日能量法，依次生成一系列适合数值积分的微分代数方程。本书适用的建模方法是能建模和仿真的六连杆闭链机构或晶体管功率放大器等系统。     

基于OBB层次结构碰撞检测的改进算法

方向包围盒（Oriented bounding box：OBB）的构造以及包围盒的相交测试的计算量都比较大，严重影响了在模拟、仿真的应用，尤其是有变形物体的场景。引入近似凸包的思想提出一种快速构造方向包围盒算法，很大程度上减少了构造方向包围盒（0BB）层次结构的顶点数，改进后的算法在降低构造层次结构时间的同时，对方向包围盒的紧密性代价几乎没有影响，在有些时候还提高了包围盒的紧密性。在包围盒相交测试方面，提留了一种基于筒单羽以爱的相交须刿方击，该算法在检测过程中省去了大量包围盒的相交测试计算，提高了相交测试的速度。最后将两种改进算法联合的碰撞检测框架与常用的基于均值和协方差矩阵的包围盒构造和基于分裂轴的算法进行比较，证明了算法具有高效性。     

A very faint core-collapse supernova in M85

An anomalous transient in the early Hubble-type (S0) galaxy Messier 85 (M85) in the Virgo cluster was discovered by Kulkarni et al. on 7 January 2006 that had very low luminosity (peak absolute R-band magnitude M(R) of about -12) that was constant over more than 80 days, red colour and narrow spectral lines, which seem inconsistent with those observed in any known class of transient events. Kulkarni et al. suggest an exotic stellar merger as the possible origin. An alternative explanation is that the transient in M85 was a type II-plateau supernova of extremely low luminosity, exploding in a lenticular galaxy with residual star-forming activity. This intriguing transient might be the faintest supernova that has ever been discovered.     

Strong dipolar effects in a quantum ferrofluid

Symmetry-breaking interactions have a crucial role in many areas of physics, ranging from classical ferrofluids to superfluid (3)He and d-wave superconductivity. For superfluid quantum gases, a variety of new physical phenomena arising from the symmetry-breaking interaction between electric or magnetic dipoles are expected. Novel quantum phases in optical lattices, such as chequerboard or supersolid phases, are predicted for dipolar bosons. Dipolar interactions can also enrich considerably the physics of quantum gases with internal degrees of freedom. Arrays of dipolar particles could be used for efficient quantum information processing. Here we report the realization of a chromium Bose-Einstein condensate with strong dipolar interactions. By using a Feshbach resonance, we reduce the usual isotropic contact interaction, such that the anisotropic magnetic dipole-dipole interaction between 52Cr atoms becomes comparable in strength. This induces a change of the aspect ratio of the atom cloud; for strong dipolar interactions, the inversion of ellipticity during expansion (the usual 'smoking gun' evidence for a Bose-Einstein condensate) can be suppressed. These effects are accounted for by taking into account the dipolar interaction in the superfluid hydrodynamic equations governing the dynamics of the gas, in the same way as classical ferrofluids can be described by including dipolar terms in the classical hydrodynamic equations. Our results are a first step in the exploration of the unique properties of quantum ferrofluids.     

South-polar features on Venus similar to those near the north pole

Venus has no seasons, slow rotation and a very massive atmosphere, which is mainly carbon dioxide with clouds primarily of sulphuric acid droplets. Infrared observations by previous missions to Venus revealed a bright 'dipole' feature surrounded by a cold 'collar' at its north pole. The polar dipole is a 'double-eye' feature at the centre of a vast vortex that rotates around the pole, and is possibly associated with rapid downwelling. The polar cold collar is a wide, shallow river of cold air that circulates around the polar vortex. One outstanding question has been whether the global circulation was symmetric, such that a dipole feature existed at the south pole. Here we report observations of Venus' south-polar region, where we have seen clouds with morphology much like those around the north pole, but rotating somewhat faster than the northern dipole. The vortex may extend down to the lower cloud layers that lie at about 50 km height and perhaps deeper. The spectroscopic properties of the clouds around the south pole are compatible with a sulphuric acid composition.     

Glucose sensing by POMC neurons regulates glucose homeostasis and is impaired in obesity

A subset of neurons in the brain, known as 'glucose-excited' neurons, depolarize and increase their firing rate in response to increases in extracellular glucose. Similar to insulin secretion by pancreatic beta-cells, glucose excitation of neurons is driven by ATP-mediated closure of ATP-sensitive potassium (K(ATP)) channels. Although beta-cell-like glucose sensing in neurons is well established, its physiological relevance and contribution to disease states such as type 2 diabetes remain unknown. To address these issues, we disrupted glucose sensing in glucose-excited pro-opiomelanocortin (POMC) neurons via transgenic expression of a mutant Kir6.2 subunit (encoded by the Kcnj11 gene) that prevents ATP-mediated closure of K(ATP) channels. Here we show that this genetic manipulation impaired the whole-body response to a systemic glucose load, demonstrating a role for glucose sensing by POMC neurons in the overall physiological control of blood glucose. We also found that glucose sensing by POMC neurons became defective in obese mice on a high-fat diet, suggesting that loss of glucose sensing by neurons has a role in the development of type 2 diabetes. The mechanism for obesity-induced loss of glucose sensing in POMC neurons involves uncoupling protein 2 (UCP2), a mitochondrial protein that impairs glucose-stimulated ATP production. UCP2 negatively regulates glucose sensing in POMC neurons. We found that genetic deletion of Ucp2 prevents obesity-induced loss of glucose sensing, and that acute pharmacological inhibition of UCP2 reverses loss of glucose sensing. We conclude that obesity-induced, UCP2-mediated loss of glucose sensing in glucose-excited neurons might have a pathogenic role in the development of type 2 diabetes.