基于节能偏好的冲突多目标相容温室环境控制

在温室环境控制问题中,传统的控制方法追求精确的点目标控制,而精确的控制精度是以高的能量消耗为代价的。针对温室环境控制这一实际问题,采用多目标相容控制算法来进行控制。因为在相容控制算法中点控制目标被放宽到区间内,所以有很大的余地来协调控制精度和能耗。为了满足相容控制算法在控制过程中节能偏好的需要,对遗传算法进行了改进,把节能这一偏好信息引入到了优化过程中、参与进化寻优。通过对经典温室模型仿真,验证了新算法在节能降耗方面的优势。     

American Pikas ( Ochotona princeps ) in northwestern Nevada: a newly discovered population at a low-elevation site

The central tenet of island biogeography theory—that species assemblages on islands are functions of island area, isolation from mainlands, and vicariance—has been altered by the demonstrable effects that rapid climate change is imposing on insular faunas, at least in isolated mountaintops. Although populations of American pikas ( Ochotona princeps ) continue to suffer extirpations, and although the lower bounds of the pika's elevational distribution are shifting upslope across the Great Basin, we report here on the new discovery of a low-elevation population of pikas in a mountain range from which they had not been reported previously. This discovery, particularly in the context of relatively rapid ecological change, highlights the importance of seeking out original sources of information and performing spatially extensive fieldwork. Results presented here further illustrate that although thermal influences appear to be the single strongest determinant of pika distribution currently, such influences interact with a number of other factors to determine persistence.     

Rationality and irrationality in the history of continental drift: Was the hypothesis of continental drift worthy of pursuit?

The revolution in geology, initiated with Alfred Wegener’s theory of continental drift, has been the subject of many philosophical discussions aiming at resolving the problem of rationality underlying this historical episode. Even though the debate included analyses in terms of scientific methodology, applications of concrete accounts of epistemic justification to this case study have been rare. In particular, the question as to whether Wegener’s theory was epistemically worthy of pursuit in the first half of the twentieth century, that is, in its early development, remained open or inadequately addressed. The aim of this paper is to offer an answer to this question. The evaluation of Drift will be done by means of an account of theory evaluation suitable for the context of pursuit, developed in ?e?elja and Straßer (accepted for publication). We will argue that pursuing the theory of continental drift was rational, i.e., that it was irrational to reject its pursuit as unworthy.     

Action Research in Inter-Organisational Networks: Impartial Studies or the Trojan Horse?

This article addresses the distinct ethical challenges of action research in inter-organisational projects. Traditionally, the literature on action research has distinguished between two researcher roles: The problem-solver and the observer. Based on an action research project in a Danish inter-organisational network, a third role as legitimiser is identified as an ethical challenge. Potentially, the legitimacy that the researchers carry as academic knowledge-generating actors may be used by a particular company to involve other companies in the network. Thus, the researchers may be perceived as bringing into the other organisations a Trojan Horse containing the interests of this particular company. Lack of clarity in defining the role of the action researcher may thus jeopardise the trustworthiness of the researchers and the action research project. On the basis of the case study analysis, the article develops a number of preliminary points of ethical consideration for future research analysis.     

Augmentation of tumor angiogenesis by a Myc-activated microRNA cluster

Human adenocarcinomas commonly harbor mutations in the KRAS and MYC proto-oncogenes and the TP53 tumor suppressor gene. All three genetic lesions are potentially pro-angiogenic, as they sustain production of vascular endothelial growth factor (VEGF). Yet Kras-transformed mouse colonocytes lacking p53 formed indolent, poorly vascularized tumors, whereas additional transduction with a Myc-encoding retrovirus promoted vigorous vascularization and growth. In addition, VEGF levels were unaffected by Myc, but enhanced neovascularization correlated with downregulation of anti-angiogenic thrombospondin-1 (Tsp1) and related proteins, such as connective tissue growth factor (CTGF). Both Tsp1 and CTGF are predicted targets for repression by the miR-17-92 microRNA cluster, which was upregulated in colonocytes coexpressing K-Ras and c-Myc. Indeed, miR-17-92 knockdown with antisense 2'-O-methyl oligoribonucleotides partly restored Tsp1 and CTGF expression; in addition, transduction of Ras-only cells with a miR-17-92-encoding retrovirus reduced Tsp1 and CTGF levels. Notably, miR-17-92-transduced cells formed larger, better-perfused tumors. These findings establish a role for microRNAs in non-cell-autonomous Myc-induced tumor phenotypes.     

A new chromosome 17q21.31 microdeletion syndrome associated with a common inversion polymorphism

Submicroscopic genomic copy number changes have been identified only recently as an important cause of mental retardation. We describe the detection of three interstitial, overlapping 17q21.31 microdeletions in a cohort of 1,200 mentally retarded individuals associated with a clearly recognizable clinical phenotype of mental retardation, hypotonia and a characteristic face. The deletions encompass the MAPT and CRHR1 genes and are associated with a common inversion polymorphism.     

Transformation of amyloid β(1–40) oligomers into fibrils is characterized by a major change in secondary structure

Alzheimer’s disease (AD) is a neurodegenerative disorder occurring in the elderly. It is widely accepted that the amyloid beta peptide (Aβ) aggregation and especially the oligomeric states rather than fibrils are involved in AD onset. We used infrared spectroscopy to provide structural information on the entire aggregation pathway of Aβ(1–40), starting from monomeric Aβ to the end of the process, fibrils. Our structural study suggests that conversion of oligomers into fibrils results from a transition from antiparallel to parallel β-sheet. These structural changes are described in terms of H-bonding rupture/formation, β-strands reorientation and β-sheet elongation. As antiparallel β-sheet structure is also observed for other amyloidogenic proteins forming oligomers, reorganization of the β-sheet implicating a reorientation of β-strands could be a generic mechanism determining the kinetics of protein misfolding. Elucidation of the process driving aggregation, including structural transitions, could be essential in a search for therapies inhibiting aggregation or disrupting aggregates.