基于NSGA-Ⅱ的IPMC机器鱼动态多目标相容优化控制

实际控制问题中往往有多个控制目标需要兼顾,且多个目标通常情况下是冲突的。根据相邻控制步之间系统状态和控制输入的连续性,提出了一个基于NSGA-II的动态迭代多目标相容优化控制算法,并且这一算法有能力处理目标空间为非凸的控制问题和提高在线优化速度。考虑到IPMC驱动机器鱼在运行过程中能耗和速度两个关键且冲突的目标,建立IMPC驱动机器鱼的运动及能耗模型,将所提算法进行了应用。仿真结果表明了控制算法的有效性及其在慢复杂系统动态控制中的应用潜力。     

Inflammation and immune system interactions in atherosclerosis

Cardiovascular disease (CVD) is the leading cause of mortality worldwide, accounting for 16.7 million deaths each year. The underlying cause of the majority of CVD is atherosclerosis. In the past, atherosclerosis was considered to be the result of passive lipid accumulation in the vessel wall. Today’s picture is far more complex. Atherosclerosis is considered a chronic inflammatory disease that results in the formation of plaques in large and mid-sized arteries. Both cells of the innate and the adaptive immune system play a crucial role in its pathogenesis. By transforming immune cells into pro- and anti-inflammatory chemokine- and cytokine-producing units, and by guiding the interactions between the different immune cells, the immune system decisively influences the propensity of a given plaque to rupture and cause clinical symptoms like myocardial infarction and stroke. In this review, we give an overview on the newest insights in the role of different immune cells and subtypes in atherosclerosis.     

Civic Meaningfulness: The Political Dimension—A Reply to Lena Dominelli

This article argues, firstly, that voluntary civic practices are not doomed to fall prey to a Big Society rhetoric and a cynical politics of cuts in social spending. It all depends on how these civic practices are promoted and what kind of civic discourse is communicated through the channels of social media and public opinion. Secondly, the author highlights the political importance of connecting meaningfulness with citizenship.     

A classifying procedure for signalling turning points

A Hidden Markov Model (HMM) is used to classify an out‐of‐sample observation vector into either of two regimes. This leads to a procedure for making probability forecasts for changes of regimes in a time series, i.e. for turning points. Instead of estimating past turning points using maximum likelihood, the model is estimated with respect to known past regimes. This makes it possible to perform feature extraction and estimation for different forecasting horizons. The inference aspect is emphasized by including a penalty for a wrong decision in the cost function. The method, here called a ‘Markov Bayesian Classifier (MBC)’, is tested by forecasting turning points in the Swedish and US economies, using leading data. Clear and early turning point signals are obtained, contrasting favourably with earlier HMM studies. Some theoretical arguments for this are given. Copyright © 2004 John Wiley & Sons, Ltd.     

Transient expression of a surface antigen on a small subset of neurones during embryonic development

During development, neurones find and interconnect with their targets in a remarkably precise way. The unfolding of neuronal specificity involves a series of highly specific recognition events which are likely to be coordinated by the spatial and temporal expression of many different surface molecules. At early stages of development, neuronal recognition occurs most dramatically at the tips of growing axons, at growth cones and their filopodia. Previous studies on the grasshopper embryo suggest that specific filopodial contacts lead to the stereotyped patterns of selective axonal fasciculation; these results support the 'labelled pathways' hypothesis which predicts that the different neighbouring axon fascicles in the embryonic neuropil within filopodial grasp are differentially labelled. To uncover the molecular labels on fasciculating embryonic axons, we screened 2,000 monoclonal antibodies generated against the embryonic neuroepithelium. Here we describe three antibodies which reveal surface antigens whose temporal and spatial expression during embryogenesis correlate with the predictions of the model. In particular, the Mes-2 antibody recognizes an antigen which is transiently expressed on the surface of only 4 out of approximately 1,000 neurones in each metathoracic hemisegment during a short period of embryogenesis. The growth cones of two of these neurones fasciculate in the periphery and innervate the same target. Moreover, they transiently express the Mes-2 surface antigen while doing so.     

Linking climate change to lemming cycles

The population cycles of rodents at northern latitudes have puzzled people for centuries, and their impact is manifest throughout the alpine ecosystem. Climate change is known to be able to drive animal population dynamics between stable and cyclic phases, and has been suggested to cause the recent changes in cyclic dynamics of rodents and their predators. But although predator-rodent interactions are commonly argued to be the cause of the Fennoscandian rodent cycles, the role of the environment in the modulation of such dynamics is often poorly understood in natural systems. Hence, quantitative links between climate-driven processes and rodent dynamics have so far been lacking. Here we show that winter weather and snow conditions, together with density dependence in the net population growth rate, account for the observed population dynamics of the rodent community dominated by lemmings (Lemmus lemmus) in an alpine Norwegian core habitat between 1970 and 1997, and predict the observed absence of rodent peak years after 1994. These local rodent dynamics are coherent with alpine bird dynamics both locally and over all of southern Norway, consistent with the influence of large-scale fluctuations in winter conditions. The relationship between commonly available meteorological data and snow conditions indicates that changes in temperature and humidity, and thus conditions in the subnivean space, seem to markedly affect the dynamics of alpine rodents and their linked groups. The pattern of less regular rodent peaks, and corresponding changes in the overall dynamics of the alpine ecosystem, thus seems likely to prevail over a growing area under projected climate change.     

The diploid genome sequence of an Asian individual

Here we present the first diploid genome sequence of an Asian individual. The genome was sequenced to 36-fold average coverage using massively parallel sequencing technology. We aligned the short reads onto the NCBI human reference genome to 99.97% coverage, and guided by the reference genome, we used uniquely mapped reads to assemble a high-quality consensus sequence for 92% of the Asian individual's genome. We identified approximately 3 million single-nucleotide polymorphisms (SNPs) inside this region, of which 13.6% were not in the dbSNP database. Genotyping analysis showed that SNP identification had high accuracy and consistency, indicating the high sequence quality of this assembly. We also carried out heterozygote phasing and haplotype prediction against HapMap CHB and JPT haplotypes (Chinese and Japanese, respectively), sequence comparison with the two available individual genomes (J. D. Watson and J. C. Venter), and structural variation identification. These variations were considered for their potential biological impact. Our sequence data and analyses demonstrate the potential usefulness of next-generation sequencing technologies for personal genomics.     

Synergistic response to oncogenic mutations defines gene class critical to cancer phenotype

Understanding the molecular underpinnings of cancer is of critical importance to the development of targeted intervention strategies. Identification of such targets, however, is notoriously difficult and unpredictable. Malignant cell transformation requires the cooperation of a few oncogenic mutations that cause substantial reorganization of many cell features and induce complex changes in gene expression patterns. Genes critical to this multifaceted cellular phenotype have therefore only been identified after signalling pathway analysis or on an ad hoc basis. Our observations that cell transformation by cooperating oncogenic lesions depends on synergistic modulation of downstream signalling circuitry suggest that malignant transformation is a highly cooperative process, involving synergy at multiple levels of regulation, including gene expression. Here we show that a large proportion of genes controlled synergistically by loss-of-function p53 and Ras activation are critical to the malignant state of murine and human colon cells. Notably, 14 out of 24 'cooperation response genes' were found to contribute to tumour formation in gene perturbation experiments. In contrast, only 1 in 14 perturbations of the genes responding in a non-synergistic manner had a similar effect. Synergistic control of gene expression by oncogenic mutations thus emerges as an underlying key to malignancy, and provides an attractive rationale for identifying intervention targets in gene networks downstream of oncogenic gain- and loss-of-function mutations.