基于重构相图相似性检测的单相接地故障选相方法

配电线路在发生单相高阻接地故障时,由于故障特征微弱导致传统以求解电气参量为依据的选相方法存在困难.依据故障支路附加状态的三相电流中健全相与故障相存在幅值相角不一的差异,提出一种利用相空间重构方法对故障附加状态的三相电流进行升维重构,然后依据重构相轨迹图的差异作为故障特征进行单相接地故障选相的新方法.该方法可通过重构相轨...     

关于齿顶边星图的优美性

在齿轮图.的每个齿的齿顶分别加上 m_1,m_2,…,m_n,条悬挂边后构成的图称为齿顶边星图,记为,(m_1,m_2,…,m_n).本文给出了、(m_1,m_2…,m_n)的优美标号,从而证明了.(m_1,m_2,…,m_n)是优美图;当m_1=m_2=…,m_n=k 时,(k,k,…k)即为 k 顶边星图,于是解决了“所有的 k 顶边星图都是优美图”这一猜想.     

关于Pell方程x~2─2y~2＝1与y~2─Dz~2＝4的公解

本文研究Ｐｅｌｌ方程ｘ￣２─２ｙ￣２＝１与ｙ￣２─ＤＺ￣２＝４的公解的问题，完整地证明了当Ｄ无平方因子且至多含三个不同奇素因子时，除开（ｘ，ｙ，ｚ）＝（１７，１２，２）．（Ｄ＝３５）；（ｘ，ｙ，ｚ）＝（１９６０１，１３８６０．２６）．（Ｄ＝２９×４１×２３９）外无其它非平凡解．这个结果加强了Ｍａｈａｎｔｙ￣［１］和陈建华￣［２］的结论．     

不同条件下麝香石竹玻璃苗的诱导形成及其生理特性研究

研究了不同培养基及外植体条件下麝香石竹玻璃苗的诱导形成及玻璃苗部分生理特性。本文研究认为：麝香石竹玻璃的形成是培养基和外植体因素相互作用的结果，培养基极端的水分环境可能是导致玻璃苗形成的外在原因。     

Birth of parthenogenetic mice that can develop to adulthood

Only mammals have relinquished parthenogenesis, a means of producing descendants solely from maternal germ cells. Mouse parthenogenetic embryos die by day 10 of gestation. Bi-parental reproduction is necessary because of parent-specific epigenetic modification of the genome during gametogenesis. This leads to unequal expression of imprinted genes from the maternal and paternal alleles. However, there is no direct evidence that genomic imprinting is the only barrier to parthenogenetic development. Here we show the development of a viable parthenogenetic mouse individual from a reconstructed oocyte containing two haploid sets of maternal genome, derived from non-growing and fully grown oocytes. This development was made possible by the appropriate expression of the Igf2 and H19 genes with other imprinted genes, using mutant mice with a 13-kilobase deletion in the H19 gene as non-growing oocytes donors. This full-term development is associated with a marked reduction in aberrantly expressed genes. The parthenote developed to adulthood with the ability to reproduce offspring. These results suggest that paternal imprinting prevents parthenogenesis, ensuring that the paternal contribution is obligatory for the descendant.     

Epigenetic inactivation of SFRP genes allows constitutive WNT signaling in colorectal cancer

Aberrant WNT pathway signaling is an early progression event in 90% of colorectal cancers. It occurs through mutations mainly of APC and less often of CTNNB1 (encoding beta-catenin) or AXIN2 (encoding axin-2, also known as conductin). These mutations allow ligand-independent WNT signaling that culminates in abnormal accumulation of free beta-catenin in the nucleus. We previously identified frequent promoter hypermethylation and gene silencing of the genes encoding secreted frizzled-related proteins (SFRPs) in colorectal cancer. SFRPs possess a domain similar to one in the WNT-receptor frizzled proteins and can inhibit WNT receptor binding to downregulate pathway signaling during development. Here we show that restoration of SFRP function in colorectal cancer cells attenuates WNT signaling even in the presence of downstream mutations. We also show that the epigenetic loss of SFRP function occurs early in colorectal cancer progression and may thus provide constitutive WNT signaling that is required to complement downstream mutations in the evolution of colorectal cancer.     

BMP signaling inhibits intestinal stem cell self-renewal through suppression of Wnt-beta-catenin signaling

In humans, mutations in BMPR1A, SMAD4 and PTEN are responsible for juvenile polyposis syndrome, juvenile intestinal polyposis and Cowden disease, respectively. The development of polyposis is a common feature of these diseases, suggesting that there is an association between BMP and PTEN pathways. The mechanistic link between BMP and PTEN pathways and the related etiology of juvenile polyposis is unresolved. Here we show that conditional inactivation of Bmpr1a in mice disturbs homeostasis of intestinal epithelial regeneration with an expansion of the stem and progenitor cell populations, eventually leading to intestinal polyposis resembling human juvenile polyposis syndrome. We show that BMP signaling suppresses Wnt signaling to ensure a balanced control of stem cell self-renewal. Mechanistically, PTEN, through phosphatidylinosital-3 kinase-Akt, mediates the convergence of the BMP and Wnt pathways on control of beta-catenin. Thus, BMP signaling may control the duplication of intestinal stem cells, thereby preventing crypt fission and the subsequent increase in crypt number.     

Free fatty acids regulate insulin secretion from pancreatic beta cells through GPR40

Diabetes, a disease in which carbohydrate and lipid metabolism are regulated improperly by insulin, is a serious worldwide health issue. Insulin is secreted from pancreatic beta cells in response to elevated plasma glucose, with various factors modifying its secretion. Free fatty acids (FFAs) provide an important energy source as nutrients, and they also act as signalling molecules in various cellular processes, including insulin secretion. Although FFAs are thought to promote insulin secretion in an acute phase, this mechanism is not clearly understood. Here we show that a G-protein-coupled receptor, GPR40, which is abundantly expressed in the pancreas, functions as a receptor for long-chain FFAs. Furthermore, we show that long-chain FFAs amplify glucose-stimulated insulin secretion from pancreatic beta cells by activating GPR40. Our results indicate that GPR40 agonists and/or antagonists show potential for the development of new anti-diabetic drugs.     

MIMO干扰信道下基于功率分配的干扰抑制算法

为了抑制MIMO干扰信道下的多小区干扰,采用子空间干扰抑制算法和功率分配相结合的干扰抑制方案,该方案充分利用系统总功率,将多小区干扰尽可能地重叠,以提高系统的性能.理论分析及仿真结果表明,与传统干扰抑制方案相比,该方案仅牺牲极微小的系统容量,却明显地降低了系统的干扰功率.