基于微丝的PDMS微流动通道制作技术

微流动通道是微流控芯片的重要组成部分, 其加工技术的每一步进化或简化一直为国际学术界与工业界所重视. 提出了一种基于微丝的PDMS微流动通道制作技术. 该技术利用一些简单的模具辅助固定和布置微丝, 然后将PDMS预聚物浇注于模具中浸没微丝并固化, 固化后抽出微丝形成PDMS微通道或通道阵列, 在与通道垂直的方向上打孔并封装, 形成与通道外部物质交换的接口. 实际制作通道时可采用商用化的金属微丝(如不锈钢微丝), 直径从100~20 μm不等. 较为详细地介绍了利用这种技术来构建多种拓扑结构的二维或三维通道或通道阵列, 例如直通道、交叉通道、弯曲通道等的能力. 进一步, 基于金属微丝的电磁特性, 这样的微通道制作工艺还被应用来构建出适于电磁控制和温度控制的微流动通道装置. 最后, 通过圆截面微通道的光路分析、微通道内粒子流动的图像测速(Micro-PIV)与微液滴形成实验及分析进一步印证了这种微流动通道制作技术的可行性和适用性.     

A frameshift mutation in NOD2 associated with susceptibility to Crohn's disease

Crohn's disease is a chronic inflammatory disorder of the gastrointestinal tract, which is thought to result from the effect of environmental factors in a genetically predisposed host. A gene location in the pericentromeric region of chromosome 16, IBD1, that contributes to susceptibility to Crohn's disease has been established through multiple linkage studies, but the specific gene(s) has not been identified. NOD2, a gene that encodes a protein with homology to plant disease resistance gene products is located in the peak region of linkage on chromosome 16 (ref. 7). Here we show, by using the transmission disequilibium test and case-control analysis, that a frameshift mutation caused by a cytosine insertion, 3020insC, which is expected to encode a truncated NOD2 protein, is associated with Crohn's disease. Wild-type NOD2 activates nuclear factor NF-kappaB, making it responsive to bacterial lipopolysaccharides; however, this induction was deficient in mutant NOD2. These results implicate NOD2 in susceptibility to Crohn's disease, and suggest a link between an innate immune response to bacterial components and development of disease.     

A preliminary note on the relationship between the number of adultPrays oleae Bern. caught in pheromone traps and the resulting level of infestation

Summary Preliminary studies in Granada, Spain, have shown a highly significant correlation between the number of adult malePrays oleae caught in pheromone traps and the resulting level of infestation in all the 3 annual generations of this species.The authors want to acknowledge Dr Owen T. Jones, Southampton University, for his assistance in drafting this paper.     

Generation of pathogenic T(H)17 cells in the absence of TGF-β signalling

CD4(+) T-helper cells that selectively produce interleukin (IL)-17 (T(H)17), are critical for host defence and autoimmunity. Although crucial for T(H)17 cells in vivo, IL-23 has been thought to be incapable of driving initial differentiation. Rather, IL-6 and transforming growth factor (TGF)-β1 have been proposed to be the factors responsible for initiating specification. Here we show that T(H)17 differentiation can occur in the absence of TGF-β signalling. Neither IL-6 nor IL-23 alone efficiently generated T(H)17 cells; however, these cytokines in combination with IL-1β effectively induced IL-17 production in naive precursors, independently of TGF-β. Epigenetic modification of the Il17a, Il17f and Rorc promoters proceeded without TGF-β1, allowing the generation of cells that co-expressed RORγt (encoded by Rorc) and T-bet. T-bet(+)RORγt(+) T(H)17 cells are generated in vivo during experimental allergic encephalomyelitis, and adoptively transferred T(H)17 cells generated with IL-23 without TGF-β1 were pathogenic in this disease model. These data indicate an alternative mode for T(H)17 differentiation. Consistent with genetic data linking IL23R with autoimmunity, our findings re-emphasize the importance of IL-23 and therefore may have therapeutic implications.     

广域差分系统中的卫星钟差改正方法

在深入分析星钟和星历分离的广域差分原理的基础上, 利用简易的广域差分仿真平台, 分析了这种原理在差分站时间同步时采用的绝对分离, 以及在主差分站同步、副差分站时间不同步时采用相对分离这两种方法的异同, 分两步给出了副差分站不同步时卫星钟差一站式改正方法, 提出并重点讨论了星钟二次改正的逆向推理算法. 仿真分析得出当差分站采用码相位的伪距测量时, 采用这种钟差改正方法可以实现5~7 ns的授时精度, 当差分站采用载波相位平滑伪距时, 这种钟差改正方法可以实现1~3 ns的授时精度.     

A threshold of transmembrane potential is required for mitochondrial dynamic balance mediated by DRP1 and OMA1

As an organellar network, mitochondria dynamically regulate their organization via opposing fusion and fission pathways to maintain bioenergetic homeostasis and contribute to key cellular pathways. This dynamic balance is directly linked to bioenergetic function: loss of transmembrane potential across the inner membrane (Δψ _m) disrupts mitochondrial fission/fusion balance, causing fragmentation of the network. However, the level of Δψ _m required for mitochondrial dynamic balance, as well as the relative contributions of fission and fusion pathways, have remained unclear. To explore this, mitochondrial morphology and Δψ _m were examined via confocal imaging and tetramethyl rhodamine ester (TMRE) flow cytometry, respectively, in cultured 143B osteosarcoma cells. When normalized to the TMRE value of untreated 143B cells as 100%, both genetic (mtDNA-depleted ρ⁰) and pharmacological [carbonyl cyanide m-chlorophenyl hydrazone (CCCP)-treated] cell models below 34% TMRE fluorescence were unable to maintain mitochondrial interconnection, correlating with loss of fusion-active long OPA1 isoforms (L-OPA1). Mechanistically, this threshold is maintained by mechanistic coordination of DRP1-mediated fission and OPA1-mediated fusion: cells lacking either DRP1 or the OMA1 metalloprotease were insensitive to loss of Δψ _m, instead maintaining an obligately fused morphology. Collectively, these findings demonstrate a mitochondrial ‘tipping point’ threshold mediated by the interaction of Δψ _m with both DRP1 and OMA1; moreover, DRP1 appears to be required for effective OPA1 maintenance and processing, consistent with growing evidence for direct interaction of fission and fusion pathways. These results suggest that Δψ _m below threshold coordinately activates both DRP1-mediated fission and OMA1 cleavage of OPA1, collapsing mitochondrial dynamic balance, with major implications for a range of signaling pathways and cellular life/death events.     

A substantial amount of hidden magnetic energy in the quiet Sun

Deciphering and understanding the small-scale magnetic activity of the quiet solar photosphere should help to solve many of the key problems of solar and stellar physics, such as the magnetic coupling to the outer atmosphere and the coronal heating. At present, we can see only approximately 1 per cent of the complex magnetism of the quiet Sun, which highlights the need to develop a reliable way to investigate the remaining 99 per cent. Here we report three-dimensional radiative transfer modelling of scattering polarization in atomic and molecular lines that indicates the presence of hidden, mixed-polarity fields on subresolution scales. Combining this modelling with recent observational data, we find a ubiquitous tangled magnetic field with an average strength of approximately 130 G, which is much stronger in the intergranular regions of solar surface convection than in the granular regions. So the average magnetic energy density in the quiet solar photosphere is at least two orders of magnitude greater than that derived from simplistic one-dimensional investigations, and sufficient to balance radiative energy losses from the solar chromosphere.     

Modelling conservation in the Amazon basin

Expansion of the cattle and soy industries in the Amazon basin has increased deforestation rates and will soon push all-weather highways into the region's core. In the face of this growing pressure, a comprehensive conservation strategy for the Amazon basin should protect its watersheds, the full range of species and ecosystem diversity, and the stability of regional climates. Here we report that protected areas in the Amazon basin--the central feature of prevailing conservation approaches--are an important but insufficient component of this strategy, based on policy-sensitive simulations of future deforestation. By 2050, current trends in agricultural expansion will eliminate a total of 40% of Amazon forests, including at least two-thirds of the forest cover of six major watersheds and 12 ecoregions, releasing 32 +/- 8 Pg of carbon to the atmosphere. One-quarter of the 382 mammalian species examined will lose more than 40% of the forest within their Amazon ranges. Although an expanded and enforced network of protected areas could avoid as much as one-third of this projected forest loss, conservation on private lands is also essential. Expanding market pressures for sound land management and prevention of forest clearing on lands unsuitable for agriculture are critical ingredients of a strategy for comprehensive conservation.