The p66shc adaptor protein controls oxidative stress response and life span in mammals

Gene mutations in invertebrates have been identified that extend life span and enhance resistance to environmental stresses such as ultraviolet light or reactive oxygen species. In mammals, the mechanisms that regulate stress response are poorly understood and no genes are known to increase individual life span. Here we report that targeted mutation of the mouse p66shc gene induces stress resistance and prolongs life span. p66shc is a splice variant of p52shc/p46shc (ref. 2), a cytoplasmic signal transducer involved in the transmission of mitogenic signals from activated receptors to Ras. We show that: (1) p66shc is serine phosphorylated upon treatment with hydrogen peroxide (H2O2) or irradiation with ultraviolet light; (2) ablation of p66shc enhances cellular resistance to apoptosis induced by H2O2 or ultraviolet light; (3) a serine-phosphorylation defective mutant of p66shc cannot restore the normal stress response in p66shc-/- cells; (4) the p53 and p21 stress response is impaired in p66shc-/- cells; (5) p66shc-/- mice have increased resistance to paraquat and a 30% increase in life span. We propose that p66shc is part of a signal transduction pathway that regulates stress apoptotic responses and life span in mammals.     

Simulated and reconstructed winter temperature in the eastern China during the last millennium

Since the 1990s, under the auspicious impetus of two international research programs, the “Past Global Changes” (PAGES) and the “Climate Variability and Pre- dictability” (CLIVAR), massive research work has been carried out on climate and environment changes over the past 2000 years[1-3]. But majority of the studies has been centered on obtaining various kinds of climatic proxy data (such as historical documents, tree rings, ice cores, lake cores) and focused on the reconstruction of…     

筒形件错距旋压的有限元分析及其工艺优化系统

以有限元模拟分析为基础 ,建立了筒形件错距旋压的智能参数优化系统 ,提出了一套切实可行的错距旋压工艺参数优化方案 ,并结合人工神经网络和专家系统技术进行了实施 .系统的相关研究结合试验进行了验证 ,仿真结果同试验结果吻合良好 .     

Myeloid leukaemia inhibitory factor maintains the developmental potential of embryonic stem cells

Embryonic stem (ES) cells, the totipotent outgrowths of blastocysts, can be cultured and manipulated in vitro and then returned to the embryonic environment where they develop normally and can contribute to all cell lineages. Maintenance of the stem-cell phenotype in vitro requires the presence of a feeder layer of fibroblasts or of a soluble factor, differentiation inhibitory activity (DIA) produced by a number of sources; in the absence of DIA the ES cells differentiate into a wide variety of cell types. We recently noted several similarities between partially purified DIA and a haemopoietic regulator, myeloid leukaemia inhibitory factor (LIF), a molecule which induces differentiation in M1 myeloid leukaemic cells and which we have recently purified, cloned and characterized. We demonstrate here that purified, recombinant LIF can substitute for DIA in the maintenance of totipotent ES cell lines that retain the potential to form chimaeric mice.     

基于改进粒子群算法优化的自抗扰控制器（ADRC）及其应用

针对自抗扰控制器参数多,不利于整定的问题,提出了一种基于改进的粒子群算法（PSO）的自抗扰控制器参数整定方法。该方法引入了PSO中各个粒子的惯性权值的自适应调整机制,以此来维持粒子的多样性和加速粒子群算法的收敛性。利用改进粒子群算法优化的二阶自抗扰控制器控制主气温控制系统,仿真结果验证了算法的可行性和有效性。     

Angiotensin-converting enzyme 2 is an essential regulator of heart function

Cardiovascular diseases are predicted to be the most common cause of death worldwide by 2020. Here we show that angiotensin-converting enzyme 2 (ace2) maps to a defined quantitative trait locus (QTL) on the X chromosome in three different rat models of hypertension. In all hypertensive rat strains, ACE2 messenger RNA and protein expression were markedly reduced, suggesting that ace2 is a candidate gene for this QTL. Targeted disruption of ACE2 in mice results in a severe cardiac contractility defect, increased angiotensin II levels, and upregulation of hypoxia-induced genes in the heart. Genetic ablation of ACE on an ACE2 mutant background completely rescues the cardiac phenotype. But disruption of ACER, a Drosophila ACE2 homologue, results in a severe defect of heart morphogenesis. These genetic data for ACE2 show that it is an essential regulator of heart function in vivo.     

高压输电线路防鸟设施应用及效果研究

鸟害闪络是引起高压输电线路跳闸的主要原因之一.采用实地抽样调查的方法,对吉林省9个地区1 518基220kV高压杆塔上防鸟害设施的种类、损毁状况、防鸟效果和存在的问题进行了研究.结果表明:吉林省目前主要应用障碍性防鸟设施防止鸟类在输电杆塔上栖落和筑巢,以风力驱鸟器、鸟刺、滚动针式驱鸟器和防鸟罩为主;调查杆塔安装比例为53.6%,各地区存在差异;平均每基杆塔安装的防鸟设施数量为4.8个;不同类型防鸟设施损毁率不同,平均损毁率约为18.0%,其中带鸟刺风力驱鸟器和普通风力驱鸟器损坏率较高,分别为27.5%和27.3%.安装防鸟设施未能完全阻止鸟类在输电杆塔筑巢,但可在一定程度上改变鸟类在输电杆塔上的筑巢位置进而减少鸟害闪络的发生几率.     

Direct detection of more than 50% of the Duchenne muscular dystrophy mutations by field inversion gels

Duchenne muscular dystrophy (DMD) is an X-linked disorder affecting about 1 in 3,500 males. It is allelic with the milder Becker muscular dystrophy. The biochemical basis for both diseases is unknown and no effective treatment is available. Long-range physical mapping has shown that the DMD gene, localized in Xp21, is extremely large, exceeding 2 million base pairs. Until now, carrier detection and prenatal diagnosis has involved the use of linked restriction fragment length polymorphism markers which detect muscular dystrophy-associated deletions in about 10% of the cases. Field inversion gel electrophoresis (FIGE) allows the detection of structural rearrangements in 21 out of 39 of the DMD patients studied (54%), of which 14 (65%) were not detected by conventional methods. Large deletions seem to make up a much higher fraction of the DMD mutations than so far indicated by other methods. A region prone to deletion was located in the distal half of the gene. FIGE analysis could provide a valuable extension of information for carrier detection and prenatal diagnosis. The technique should be generally applicable to the study of diseases involving structural chromosomal rearrangements.     

The genome sequence of the rice blast fungus Magnaporthe grisea

Magnaporthe grisea is the most destructive pathogen of rice worldwide and the principal model organism for elucidating the molecular basis of fungal disease of plants. Here, we report the draft sequence of the M. grisea genome. Analysis of the gene set provides an insight into the adaptations required by a fungus to cause disease. The genome encodes a large and diverse set of secreted proteins, including those defined by unusual carbohydrate-binding domains. This fungus also possesses an expanded family of G-protein-coupled receptors, several new virulence-associated genes and large suites of enzymes involved in secondary metabolism. Consistent with a role in fungal pathogenesis, the expression of several of these genes is upregulated during the early stages of infection-related development. The M. grisea genome has been subject to invasion and proliferation of active transposable elements, reflecting the clonal nature of this fungus imposed by widespread rice cultivation.