Density-dependent mortality and the latitudinal gradient in species diversity

Ecologists have long postulated that density-dependent mortality maintains high tree diversity in the tropics. If species experience greater mortality when abundant, then more rare species can persist. Agents of density-dependent mortality (such as host-specific predators, and pathogens) may be more prevalent or have stronger effects in tropical forests, because they are not limited by climatic factors. If so, decreasing density-dependent mortality with increasing latitude could partially explain the observed latitudinal gradient in tree diversity. This hypothesis has never been tested with latitudinal data. Here we show that several temperate tree species experience density-dependent mortality between seed dispersal and seedling establishment. The proportion of species affected is equivalent to that in tropical forests, failing to support the hypothesis that this mechanism is more prevalent at tropical latitudes. We further show that density-dependent mortality is misinterpreted in previous studies. Our results and evidence from other studies suggest that density-dependent mortality is important in many forests. Thus, unless the strength of density-dependent mortality varies with latitude, this mechanism is not likely to explain the high diversity of tropical forests.     

The role of the thermohaline circulation in abrupt climate change

The possibility of a reduced Atlantic thermohaline circulation in response to increases in greenhouse-gas concentrations has been demonstrated in a number of simulations with general circulation models of the coupled ocean-atmosphere system. But it remains difficult to assess the likelihood of future changes in the thermohaline circulation, mainly owing to poorly constrained model parameterizations and uncertainties in the response of the climate system to greenhouse warming. Analyses of past abrupt climate changes help to solve these problems. Data and models both suggest that abrupt climate change during the last glaciation originated through changes in the Atlantic thermohaline circulation in response to small changes in the hydrological cycle. Atmospheric and oceanic responses to these changes were then transmitted globally through a number of feedbacks. The palaeoclimate data and the model results also indicate that the stability of the thermohaline circulation depends on the mean climate state.     

Scalable architecture in mammalian brains

Comparison of mammalian brain parts has often focused on differences in absolute size, revealing only a general tendency for all parts to grow together. Attempts to find size-independent effects using body weight as a reference variable obscure size relationships owing to independent variation of body size and give phylogenies of questionable significance. Here we use the brain itself as a size reference to define the cerebrotype, a species-by-species measure of brain composition. With this measure, across many mammalian taxa the cerebellum occupies a constant fraction of the total brain volume (0.13 +/- 0.02), arguing against the hypothesis that the cerebellum acts as a computational engine principally serving the neocortex. Mammalian taxa can be well separated by cerebrotype, thus allowing the use of quantitative neuroanatomical data to test evolutionary relationships. Primate cerebrotypes have progressively shifted and neocortical volume fractions have become successively larger in lemurs and lorises, New World monkeys, Old World monkeys, and hominoids, lending support to the idea that primate brain architecture has been driven by directed selection pressure. At the same time, absolute brain size can vary over 100-fold within a taxon, while maintaining a relatively uniform cerebrotype. Brains therefore constitute a scalable architecture.     

Interaction of reelin signaling and Lis1 in brain development

Loss-of-function mutations in RELN (encoding reelin) or PAFAH1B1 (encoding LIS1) cause lissencephaly, a human neuronal migration disorder. In the mouse, homozygous mutations in Reln result in the reeler phenotype, characterized by ataxia and disrupted cortical layers. Pafah1b1(+/-) mice have hippocampal layering defects, whereas homozygous mutants are embryonic lethal. Reln encodes an extracellular protein that regulates layer formation by interacting with VLDLR and ApoER2 (Lrp8) receptors, thereby phosphorylating the Dab1 signaling molecule. Lis1 associates with microtubules and modulates neuronal migration. We investigated interactions between the reelin signaling pathway and Lis1 in brain development. Compound mutant mice with disruptions in the Reln pathway and heterozygous Pafah1b1 mutations had a higher incidence of hydrocephalus and enhanced cortical and hippocampal layering defects. Dab1 and Lis1 bound in a reelin-induced phosphorylation-dependent manner. These data indicate genetic and biochemical interaction between the reelin signaling pathway and Lis1.     

Signal transduction mechanisms in plants: an overview

This article provides an overview on recent advances in some of the basic signalling mechanisms that participate in a wide variety of stimulus-response pathways. The mechanisms include calcium-based signalling, G-protein-mediated-signalling and signalling involving inositol phospholipids, with discussion on the role of protein kinases and phosphatases interspersed. As a further defining feature, the article highlights recent exciting findings on three extracellular components that have not been given coverage in previous reviews of signal transduction in plants, extracellular calmodulin, extracellular ATP, and integrin-like receptors, all of which affect plant growth and development.     

Genomic analysis of metastasis reveals an essential role for RhoC

The most damaging change during cancer progression is the switch from a locally growing tumour to a metastatic killer. This switch is believed to involve numerous alterations that allow tumour cells to complete the complex series of events needed for metastasis. Relatively few genes have been implicated in these events. Here we use an in vivo selection scheme to select highly metastatic melanoma cells. By analysing these cells on DNA arrays, we define a pattern of gene expression that correlates with progression to a metastatic phenotype. In particular, we show enhanced expression of several genes involved in extracellular matrix assembly and of a second set of genes that regulate, either directly or indirectly, the actin-based cytoskeleton. One of these, the small GTPase RhoC, enhances metastasis when overexpressed, whereas a dominant-negative Rho inhibits metastasis. Analysis of the phenotype of cells expressing dominant-negative Rho or RhoC indicates that RhoC is important in tumour cell invasion. The genomic approach allows us to identify families of genes involved in a process, not just single genes, and can indicate which molecular and cellular events might be important in complex biological processes such as metastasis.     

基于混沌时间序列的误差纠错预测模型

提出了一种新型的非常实用的非线性时间序列的预测模型,即误差纠错预测模型(EAM),并从概率统计的角度严格证明了该方法的可靠性,同时分析了受噪声扰动的时间序列的预测.先按一般方法确定嵌入维数与时间步长,在每个当前时刻,先用局域线性回归方法得到预测点的预测值,根据信息在非线性演化中产生的失真误差大小予以修正得到修正值,并以该点为新的基点作进一步预测.该方法具备了滑动窗口二次自回归模型(MWDAR)的适用于小数据集且对大数据集具有高效率的优点,而且克服了MWDAR方法中一次项和二次项阶数及滑动窗口长度等参数难以确定,从而会导致预测恶化,使得应用受到限制的缺点.分别用Logistic方程产生的小数据集和大数据集的混沌时间序列数据作了预测,结果良好.     

基于理想点的三角模糊数多指标决策法

研究了属性权重和属性值均以三角模糊数形式给出的模糊多指标决策问题,定义了三角模糊数正理想方案和负理想方案,由此给出了三角模糊数多指标决策问题的理想点法。该方法简单实用,所需信息小.最后用该方法分析了一个实际问题。