Crh and Oprm1 mediate anxiety-related behavior and social approach in a mouse model of MECP2 duplication syndrome

Genomic duplications spanning Xq28 are associated with a spectrum of phenotypes, including anxiety and autism. The minimal region shared among affected individuals includes MECP2 and IRAK1, although it is unclear which gene when overexpressed causes anxiety and social behavior deficits. We report that doubling MECP2 levels causes heightened anxiety and autism-like features in mice and alters the expression of genes that influence anxiety and social behavior, such as Crh and Oprm1. To test the hypothesis that alterations in these two genes contribute to heightened anxiety and social behavior deficits, we analyzed MECP2 duplication mice (MECP2-TG1) that have reduced Crh and Oprm1 expression. In MECP2-TG1 animals, reducing the levels of Crh or its receptor, Crhr1, suppressed anxiety-like behavior; in contrast, reducing Oprm1 expression improved abnormal social behavior. These data indicate that increased MeCP2 levels affect molecular pathways underlying anxiety and social behavior and provide new insight into potential therapies for MECP2-related disorders.     

A test of the unified neutral theory of biodiversity

One of the fundamental questions of ecology is what controls biodiversity. Recent theory suggests that biodiversity is controlled predominantly by neutral drift of species abundances. This theory has generated considerable controversy, because it claims that many mechanisms that have long been studied by ecologists (such as niches) have little involvement in structuring communities. The theory predicts that the species abundance distribution within a community should follow a zero-sum multinomial distribution (ZSM), but this has not, so far, been rigorously tested. Specifically, it remains to be shown that the ZSM fits the data significantly better than reasonable null models. Here I test whether the ZSM fits several empirical data sets better than the lognormal distribution. It does not. Not only does the ZSM fail to fit empirical data better than the lognormal distribution 95% of the time, it also fails to fit empirical data better even a majority of the time. This means that there is no evidence that the ZSM predicts abundances better than the much more parsimonious null hypothesis.     

基于热压块的不锈钢粉尘还原实验

为了从不锈钢粉尘中回收利用Fe,Cr和Ni等,对不锈钢粉尘热压块制备及其自还原过程进行了研究.在热压温度为200℃,热压压力为35 MPa条件下,抗压强度达到900 N/个以上.高温条件下,煤热解产生的挥发分可参与不锈钢粉尘还原反应,当还原温度为1 400,1 450℃时,挥发分还原作用率达到0.4.据XRD分析和热力学计算,自还原过程中含铬物质的物相转变顺序为Fe Cr2O4,Cr2O3,Cr7C3,[Cr]Fe-Cr-Ni-C.当还原温度为1 450℃,烟煤中固定碳与粉尘中可去除氧的物质量的比(xc/xo)为0.72时,不锈钢粉尘热压块不能完全还原;当xc/xo大于0.8,还原20 min时,不锈钢粉尘热压块能完全还原.     

本溪地区BIF中玄武质围岩的高场强元素特征

辽宁本溪地区条带状铁矿(BIF)与其玄武质火山围岩之间的时空关联非常密切.对于玄武质火山围岩高场强元素(HFSE)的研究表明:wNb/wTa比值(7.00~19.93)表现出明显的分异,而wZr/wHf比值(33.46~38.28)则变化不大;从弓长岭到南芬、歪头山样品的wNb/wTa比值变化具有明显的循序性.这种高场强元素的迁移和分异特征反映出俯冲作用与盆地演化之间的关联.研究区玄武质火山围岩(wNb/wYb)N比值大于1(1.21~18.45,平均2.72),这进一步表明,其形成的构造背景为陆内弧后盆地提供了有利于BIF形成的条件.     

机器人辅助柔性针穿刺路径的悬臂梁预测模型

路径操控技术是机器人辅助柔性针穿刺的重要技术之一。软组织变形、多层软组织相对滑移和针挠曲是引起靶点位置移动,降低穿刺精度的3个主要原因。该文在研究针受力的基础上,利用柔性针挠曲规律提出了一种预测穿刺路径的悬臂梁模型,通过准静态过程将柔性针分为有限段并将每段都视为一个悬臂梁,从而建立起三维空间中针体路径预测算法。仿真实验表明,该模型能够实现柔性针路径预测功能,为机器人辅助柔性针穿刺路径规划和避障运动提供了理论基础。     

Competition and phylogeny determine community structure in Müllerian co-mimics

Until recently, the study of negative and antagonistic interactions (for example, competition and predation) has dominated our understanding of community structure, maintenance and assembly. Nevertheless, a recent theoretical model suggests that positive interactions (for example, mutualisms) may counterbalance competition, facilitating long-term coexistence even among ecologically undifferentiated species. Müllerian mimics are mutualists that share the costs of predator education and are therefore ideally suited for the investigation of positive and negative interactions in community dynamics. The sole empirical test of this model in a Müllerian mimetic community supports the prediction that positive interactions outweigh the negative effects of spatial overlap (without quantifying resource acquisition). Understanding the role of trophic niche partitioning in facilitating the evolution and stability of Müllerian mimetic communities is now of critical importance, but has yet to be formally investigated. Here we show that resource partitioning and phylogeny determine community structure and outweigh the positive effects of Müllerian mimicry in a species-rich group of neotropical catfishes. From multiple, independent reproductively isolated allopatric communities displaying convergently evolved colour patterns, 92% consist of species that do not compete for resources. Significant differences in phylogenetically conserved traits (snout morphology and body size) were consistently linked to trait-specific resource acquisition. Thus, we report the first evidence, to our knowledge, that competition for trophic resources and phylogeny are pivotal factors in the stable evolution of Müllerian mimicry rings. More generally, our work demonstrates that competition for resources is likely to have a dominant role in the structuring of communities that are simultaneously subject to the effects of both positive and negative interactions.     

Mutations in SOX2 cause anophthalmia

A submicroscopic deletion containing SOX2 was identified at the 3q breakpoint in a child with t(3;11)(q26.3;p11.2) associated with bilateral anophthalmia. Subsequent SOX2 mutation analysis identified de novo truncating mutations of SOX2 in 4 of 35 (11%) individuals with anophthalmia. Both eyes were affected in all cases with an identified mutation.     

Mutations in ENPP1 are associated with 'idiopathic' infantile arterial calcification

Idiopathic infantile arterial calcification (IIAC; OMIM 208000) is characterized by calcification of the internal elastic lamina of muscular arteries and stenosis due to myointimal proliferation. We analyzed affected individuals from 11 unrelated kindreds and found that IIAC was associated with mutations that inactivated ecto-nucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1). This cell surface enzyme generates inorganic pyrophosphate (PP(i)), a solute that regulates cell differentiation and serves as an essential physiologic inhibitor of calcification.