中国东北地区流动沙丘生态系统丘间低地地下芽库的时空变化

中国东北地区流动沙丘生态系统丘间低地地下芽库的时空变化 地下芽库在半干旱区沙丘生态系统植被恢复中起着重要作用。然而,目前针对流动沙丘丘间低地地下芽库时空变化的研究却很少。本研究通过调查一个生长季内5个不同面积流动沙丘丘间低地地下芽库的大小和组成,确定流动沙丘丘间低地地下芽库的时空变化。研究结果显示,中等面积丘间低地的总芽库密度与分蘖芽密度最高,茎基部芽密度呈相反趋势,而根茎芽密度不随丘间低地的面积变化而变化。地下芽库大小具有明显的季节变化特征。总芽密度在8月份达到高峰,10月份最低,根茎芽密度变化趋势与总芽密度相似,而茎基芽密度变化趋势与总芽密度相反,分蘖芽密度的变化不明显。以上结果表明,地下芽库密度随丘间低地的面积和季节变化而变化。这一结果有助于认识流动沙丘生态系统中植物生长的适应策略,并可为半干旱区沙丘植被恢复和保护提供理论指导。     

Early detection of field-evolved resistance to Bt cotton in China: cotton bollworm and pink bollworm

Transgenic crops producing Bacillus thuringiensis (Bt) toxins kill some major insect pests, but pests can evolve resistance and thereby reduce the effectiveness of such Bt crops. The main approach for slowing pest adaptation to Bt crops uses non-Bt host plants as "refuges" to increase survival of susceptible pests. To delay evolution of pest resistance to cotton producing Bt toxin Cry1Ac, several countries have required refuges of non-Bt cotton, while farmers in China have relied on "natural" refuges of non-Bt host plants other than cotton. This strategy is designed for cotton bollworm (Helicoverpa armigera), which attacks many crops and is the primary target of Bt cotton in China, but it does not apply to pink bollworm (Pectinophora gossypiella), which feeds almost entirely on cotton in China. Here we review evidence of field-evolved resistance to Cry1Ac by cotton bollworm in northern China and by pink bollworm in the Yangtze River Valley of China. For both pests, results of laboratory diet bioassays reveal significantly decreased susceptibility of field populations to Cry1Ac, yet field control failures of Bt cotton have not been reported. The early detection of resistance summarized here may spur countermeasures such as planting Bt cotton that produces two or more distinct toxins, increased planting of non-Bt cotton, and integration of other management tactics together with Bt cotton.     

甘蔗品种资源的表型遗传多样性

为了提高甘蔗品种资源的利用效率, 为甘蔗遗传育种亲本的选择、杂交组合配制及核心种质构建提供理论指导, 我们利用17个质量性状和5个数量性状分析了来自13个国家共20个地区的1,160份甘蔗品种资源的遗传变异、遗传结构和遗传距离等。结果表明: 5个数量性状在不同来源地品种群体之间的变异系数值(CV)变化较大, 说明不同来源地品种群体的数量遗传变异有较大差异, 其中来自海南的品种其群体遗传变异最丰富。质量性状的Shannon-Wiener多样性指数表明, 来自美国的品种群体遗传多样性最高, 其次为中国台湾, 第三为澳大利亚, 说明上述3个地区的甘蔗种质创新比较活跃, 在遗传育种中使用了更多表型性状多样化的亲本。不同来源地品种其群体的遗传分化系数(Gst)和基因流(Nm)显示甘蔗品种群体表型性状的遗传变异主要来自来源地内部, 且不同来源地品种群体之间存在较大的基因交流。遗传距离和UPGMA聚类分析结果表明, 各来源地品种群体之间遗传距离在0.0261–0.2945之间, 其中以福建和广东的品种最为相似, 其次为古巴和美国、广西和云南、澳大利亚和菲律宾、江西和四川、巴西和法国, 说明上述地区在杂交亲本的选择上比较相近。鉴于此, 在遗传育种中应加大利用具有丰富遗传多样性的品种材料并尽量避免选择同一组的品种相互杂交, 同时对于与其他来源地品种群体遗传距离较远的墨西哥品种群体在亲本选配时应给予更多关注。     

Beam-Scanning Planar Lens Based on Metal–Dielectric–Metal Waveguide Arrays

Under specific illumination conditions, periodic arrays of metal–dielectric–metal (MDM) waveguides act as uniform optical phased-array antenna where the phase of the radiating optical wave can be controlled by modifying the refractive index distribution of the dielectric material. Based on this property, we propose a planar gradient index MDM-based lens which can transform spherical waves of the transverse-magnetic surface plasmon polariton waves to plane waves with specific beam deflections by adjusting the refractive index configurations. Using numerical simulations based on two-dimensional finite-difference time-domain method, it is confirmed that beam focusing and splitting with multiple dflection angles can also be achieved.     

siRNA干扰HIF-1α表达对高糖高胰岛素诱导的肥大心肌细胞的影响

目的 研究胰岛素受体底物1(insulin receptor substrate 1,IRS1)和缺氧诱导因子1a(hypoxia inducible factor 1a,HIF-1a)在高糖高胰岛素诱导的肥大心肌细胞中的表达及其之间的关系;观察siRNA沉默HIF-1a基因对高糖高胰岛素诱导的心肌细胞肥大的影响.方法 新生大鼠心肌细胞培养48h后,换用无血清DMEM培养液并分别加入高糖高胰岛素、高糖高胰岛素+HIF-1a-siRNA培养48h,未加入任何药物的心肌细胞在无血清DMEM培养液中继续培养48h作为对照.通过心肌细胞表面积、总蛋白含量指标检测心肌细胞肥大,并利用Real time PCR检测转染前后HIF-1a mRNA表达变化及免疫细胞化学方法检测HIF-1a及IRS1蛋白水平的表达.结果 高糖高胰岛素可增加心肌细胞表面积、总蛋白含量、HIF-1a mRNA以及HIF-1a表达,并降低IRS1表达.转染siRNA后使HIF-1a基因的表达下降,能部分抑制心肌细胞的肥大,降低心肌细胞表面积和总蛋白含量,但对IRS1表达的影响不明显.在对正常对照组和高糖高胰岛素组中IRS1表达量与HIF-1a表达量进行相关分析表明,两者的表达量成负相关.结论 通过siRNA技术对HIF-1a的有效沉默可明显地抑制高糖高胰岛素诱导大鼠乳鼠心肌细胞肥大,并且这种作用可能是通过作用于IRS1/PI3K/ Akt/MTOR途径来实现的.     

Flavin containing monooxygenase 3 exerts broad effects on glucose and lipid metabolism and atherosclerosis

We performed silencing and overexpression studies of flavin containing monooxygenase (FMO) 3 in hyperlipidemic mouse models to examine its effects on trimethylamine N-oxide (TMAO) levels and atherosclerosis. Knockdown of hepatic FMO3 in LDL receptor knockout mice using an antisense oligonucleotide resulted in decreased circulating TMAO levels and atherosclerosis. Surprisingly, we also observed significant decreases in hepatic lipids and in levels of plasma lipids, ketone bodies, glucose, and insulin. FMO3 overexpression in transgenic mice, on the other hand, increased hepatic and plasma lipids. Global gene expression analyses suggested that these effects of FMO3 on lipogenesis and gluconeogenesis may be mediated through the PPARα and Kruppel-like factor 15 pathways. In vivo and in vitro results were consistent with the concept that the effects were mediated directly by FMO3 rather than trimethylamine/TMAO; in particular, overexpression of FMO3 in the human hepatoma cell line, Hep3B, resulted in significantly increased glucose secretion and lipogenesis. Our results indicate a major role for FMO3 in modulating glucose and lipid homeostasis in vivo, and they suggest that pharmacologic inhibition of FMO3 to reduce TMAO levels would be confounded by metabolic interactions.     

Brain-Derived Neurotrophic Factor Increases Synaptic Protein Levels via the MAPK/Erk Signaling Pathway and Nrf2/Trx Axis Following the Transplantation of Neural Stem Cells in a Rat Model of Traumatic Brain Injury

Brain-derived neurotrophic factor (BDNF) plays an important role in promoting the growth, differentiation, survival and synaptic stability of neurons. Presently, the transplantation of neural stem cells (NSCs) is known to induce neural repair to some extent after injury or disease. In this study, to investigate whether NSCs genetically modified to encode the BDNF gene (BDNF/NSCs) would further enhance synaptogenesis, BDNF/NSCs or naive NSCs were directly engrafted into lesions in a rat model of traumatic brain injury (TBI). Immunohistochemistry, western blotting and RT-PCR were performed to detect synaptic proteins, BDNF-TrkB and its downstream signaling pathways, at 1, 2, 3 or 4 weeks after transplantation. Our results showed that BDNF significantly increased the expression levels of the TrkB receptor gene and the phosphorylation of the TrkB protein in the lesions. The expression levels of Ras, phosphorylated Erk1/2 and postsynaptic density protein-95 were elevated in the BDNF/NSCs-transplanted groups compared with those in the NSCs-transplanted groups throughout the experimental period. Moreover, the nuclear factor (erythroid-derived 2)-like 2/Thioredoxin (Nrf2/Trx) axis, which is a specific therapeutic target for the treatment of injury or cell death, was upregulated by BDNF overexpression. Therefore, we determined that the increased synaptic proteins level implicated in synaptogenesis might be associated with the activation of the MAPK/Erk1/2 signaling pathway and the upregulation of the antioxidant agent Trx modified by BDNF-TrkB following the BDNF/NSCs transplantation after TBI.