一种新型多燃料油炉的开发

介绍了所设计的新型多燃料油炉的基本结构和主要性能 .在该多燃料油炉中 ,应用旋焰燃烧理论解决了油炉在低温环境和高海拔缺氧环境中点火困难的问题 ,并应用安全阀技术解决了油炉“回火”和“非正常熄火”等关键问题     

谐波对电能计量影响的分析及对策研究

本文介绍了谐波产生的原因及其对感应式电能表和电子式电能表的影响 ,从感应式电能表和电子式电能表频率响应曲线入手 ,分析了由于谐波的存在而引起的电能计量仪表误差的变化情况 ,并提出了减小电能计量误差的方法和对策     

Twisted gastrulation can function as a BMP antagonist

Bone morphogenetic proteins (BMPs), including the fly homologue Decapentaplegic (DPP), are important regulators of early vertebrate and invertebrate dorsal-ventral development. An evolutionarily conserved BMP regulatory mechanism operates from fly to fish, frog and mouse to control the dorsal-ventral axis determination. Several secreted factors, including the BMP antagonist chordin/Short gastrulation (SOG), modulate the activity of BMPs. In Drosophila, Twisted gastrulation (TSG) is also involved in dorsal-ventral patterning, yet the mechanism of its function is unclear. Here we report the characterization of the vertebrate Tsg homologues. We show that Tsg can block BMP function in Xenopus embryonic explants and inhibits several ventral markers in whole-frog embryos. Tsg binds directly to BMPs and forms a ternary complex with chordin and BMPs. Coexpression of Tsg with chordin leads to a more efficient inhibition of the BMP activity in ectodermal explants. Unlike other known BMP antagonists, however, Tsg also reduces several anterior markers at late developmental stages. Our data suggest that Tsg can function as a BMP inhibitor in Xenopus; furthermore, Tsg may have additional functions during frog embryogenesis.     

教育本质：知识论的困惑与存在论的彰显－兼论教育本质探讨思路的转向

教育本质的论争之所以陷入“疑无路”的境地,根本在于论争只是囿于探究知识论的“教育是什么”而遗忘了追寻存在论的“怎样教育”这一教育之“根”与“本”,以致教育之本质与语言遭际异化。缘此,本文拟在反思以往教育本质论争的基础上,试图走向“怎样教育”,以期扬弃异化,返朴归真。     

基于个体的两凿岩机械手合作任务规划

文章在分析凿岩机械手的机构结构的基础上,求出机械手在工作面上的最大最小工作区间,然后运用模糊理论的相关知识将两凿岩机械手的工作区间进行合理分区,确定两钻臂在这些区域产生碰撞的模糊隶属度,从而引入"区域避碰”理论进行合作任务规划.在考虑两机械手工作进度产生一定变化和机械手在运动中所有关节变化量最小的基础上,引入双向A*算法搜寻最优路径.通过仿真研究证明,文章提出的方法计算简单,规划的路径在一定程度上可满足实际工作的需要.     

Ordering and manipulation of the magnetic moments in large-scale superconducting pi-loop arrays

The phase of the macroscopic electron-pair wavefunction in a superconductor can vary only by multiples of 2pi when going around a closed contour. This results in quantization of magnetic flux, one of the most striking demonstrations of quantum phase coherence in superconductors. By using superconductors with unconventional pairing symmetry, or by incorporating pi-Josephson junctions, a phase shift of pi can be introduced in such loops. Under appropriate conditions, this phase shift results in doubly degenerate time-reversed ground states, which are characterized by the spontaneous generation of half quanta of magnetic flux, with magnitude 1/2 Phi(0)(Phi(0) = h/2e = 2.07 x 10(-15) Wb) (ref. 7). Until now, it has only been possible to generate individual half flux quanta. Here we report the realization of large-scale coupled pi-loop arrays based on YBa2Cu3O7-Au-Nb Josephson contacts. Scanning SQUID (superconducting quantum interference device) microscopy has been used to study the ordering of half flux quanta in these structures. The possibility of manipulating the polarities of individual half flux quanta is also demonstrated. These pi-loop arrays are of interest as model systems for studying magnetic phenomena--including frustration effects--in Ising antiferromagnets. Furthermore, studies of coupled pi-loops can be useful for designing quantum computers based on flux-qubits with viable quantum error correction capabilities.     

Homocysteine increases the synthesis of adrenomedullin in vascular fibroblasts of rats

Homocysteine (Hcy), a highly reactive sulfur- containing amino acid, is an intermediate product of methionine metabolism. Elevation of plasma Hcy has been widely studied as an independent risk factor for many cardiovascular diseases such as atherosclerosis, thrombosis, etc.[1]. Inherited hyperhomocysteinemia cases usually suffer from occlusion or thrombosis in arteries and large veins before the age of 20. Hyperhomocysteinemia significantly reduces the survival rate[2] and dilatation functi…     

The exocyst complex is required for targeting of Glut4 to the plasma membrane by insulin

Insulin stimulates glucose transport by promoting exocytosis of the glucose transporter Glut4 (refs 1, 2). The dynamic processes involved in the trafficking of Glut4-containing vesicles, and in their targeting, docking and fusion at the plasma membrane, as well as the signalling processes that govern these events, are not well understood. We recently described tyrosine-phosphorylation events restricted to subdomains of the plasma membrane that result in activation of the G protein TC10 (refs 3, 4). Here we show that TC10 interacts with one of the components of the exocyst complex, Exo70. Exo70 translocates to the plasma membrane in response to insulin through the activation of TC10, where it assembles a multiprotein complex that includes Sec6 and Sec8. Overexpression of an Exo70 mutant blocked insulin-stimulated glucose uptake, but not the trafficking of Glut4 to the plasma membrane. However, this mutant did block the extracellular exposure of the Glut4 protein. So, the exocyst might have a crucial role in the targeting of the Glut4 vesicle to the plasma membrane, perhaps directing the vesicle to the precise site of fusion.     

A mouse model for spinal muscular atrophy

The survival motor neuron gene is present in humans in a telomeric copy, SMN1, and several centromeric copies, SMN2. Homozygous mutation of SMN1 is associated with proximal spinal muscular atrophy (SMA), a severe motor neuron disease characterized by early childhood onset of progressive muscle weakness. To understand the functional role of SMN1 in SMA, we produced mouse lines deficient for mouse Smn and transgenic mouse lines that expressed human SMN2. Smn-/- mice died during the peri-implantation stage. In contrast, transgenic mice harbouring SMN2 in the Smn-/- background showed pathological changes in the spinal cord and skeletal muscles similar to those of SMA patients. The severity of the pathological changes in these mice correlated with the amount of SMN protein that contained the region encoded by exon 7. Our results demonstrate that SMN2 can partially compensate for lack of SMN1. The variable phenotypes of Smn-/-SMN2 mice reflect those seen in SMA patients, providing a mouse model for this disease.