67 research outputs found

    Modeling and inverse feedforward control for conducting polymer actuators with hysteresis

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    Conducting polymer actuators are biocompatible with a small footprint, and operate in air or liquid media under low actuation voltages. This makes them excellent actuators for macro- and micro-manipulation devices, however, their positioning ability or accuracy is adversely affected by their hysteresis non-linearity under open-loop control strategies. In this paper, we establish a hysteresis model for conducting polymer actuators, based on a rate-independent hysteresis model known as the Duhem model. The hysteresis model is experimentally identified and integrated with the linear dynamics of the actuator. This combined model is inverted to control the displacement of the tri-layer actuators considered in this study, without using any external feedback. The inversion requires an inverse hysteresis model which was experimentally identified using an inverse neural network model. Experimental results show that the position tracking errors are reduced by more than 50% when the hysteresis inverse model is incorporated into an inversion-based feedforward controller, indicating the potential of the proposed method in enabling wider use of such smart actuators

    Interleukin 6-regulated macrophage polarization controls atherosclerosis-associated vascular intimal hyperplasia

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    Vascular intimal hyperplasia (VIH) is an important stage of atherosclerosis (AS), in which macrophages not only play a critical role in local inflammation, but also transform into foam cells to participate into plaque formation, where they appear to be heterogeneous. Recently, it was shown that CD11c+ macrophages were more associated with active plaque progression. However, the molecular regulation of phenotypic changes of plaque macrophages during VIH has not been clarified and thus addressed in the current study. Since CD11c- cells were M2a-polarized anti-inflammatory macrophages, while CD11c+ cells were M1/M2b-polarized pro-inflammatory macrophages, we used bioinformatics tools to analyze the CD11c+ versus CD11c- plaque macrophages, aiming to detect the differential genes associated with M1/M2 macrophage polarization. We obtained 122 differential genes that were significantly altered in CD11c+ versus CD11c- plaque macrophages, regardless of CD11b expression. Next, hub genes were predicted in these 122 genes, from which we detected 3 candidates, interleukin 6 (Il6), Decorin (Dcn) and Tissue inhibitor matrix metalloproteinase 1 (Timp1). The effects of these 3 genes on CD11c expression as well as on the macrophage polarization were assessed in vitro, showing that only expression of Il6, but not expression of Dcn or Timp1, induced M1/M2b-like polarization in M2a macrophages. Moreover, only suppression of Il6, but not suppression of either of Dcn or Timp1, induced M2a-like polarization in M1/M2b macrophages. Furthermore, pharmaceutical suppression of Il6 attenuated VIH formation and progression of AS in a mouse model that co-applied apolipoprotein E-knockout and high-fat diet. Together, our data suggest that formation of VIH can be controlled through modulating macrophage polarization, as a promising therapeutic approach for prevent AS

    Transcription-associated mutation promotes RNA complexity in highly expressed genes - a major new source of selectable variation

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    Alternatively spliced transcript isoforms are thought to play a critical role for functional diversity. However, the mechanism generating the enormous diversity of spliced transcript isoforms remains unknown, and its biological significance remains unclear. We analyzed transcriptomes in saker falcons, chickens, and mice to show that alternative splicing occurs more frequently, yielding more isoforms, in highly expressed genes. We focused on hemoglobin in the falcon, the most abundantly expressed genes in blood, finding that alternative splicing produces 10-fold more isoforms than expected from the number of splice junctions in the genome. These isoforms were produced mainly by alternative use of de novo splice sites generated by transcription-associated mutation (TAM), not by the RNA editing mechanism normally invoked. We found that high expression of globin genes increases mutation frequencies during transcription, especially on nontranscribed DNA strands. After DNA replication, transcribed strands inherit these somatic mutations, creating de novo splice sites, and generating multiple distinct isoforms in the cell clone. Bisulfate sequencing revealed that DNA methylation may counteract this process by suppressing TAM, suggesting DNA methylation can spatially regulate RNA complexity. RNA profiling showed that falcons living on the high Qinghai–Tibetan Plateau possess greater global gene expression levels and higher diversity of mean to high abundance isoforms (reads per kilobases per million mapped reads ≥18) than their low-altitude counterparts, and we speculate that this may enhance their oxygen transport capacity under low-oxygen environments. Thus, TAM-induced RNA diversity may be physiologically significant, providing an alternative strategy in lifestyle evolution

    Enhanced transcriptomic resilience following increased alternative splicing and differential isoform production between air pollution conurbations

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    Adversehealth outcomes caused by ambient particulate matter (PM) pollution occur in a 16progressive process, with neutrophils eliciting inflammation or pathogenesis. We investigated the 17toxico-transcriptomic mechanisms of PM in real-life settings by comparing healthy residents living 18in Beijing and Chengde, the opposing ends of a well-recognised air pollution (AP) corridor in China. 19Beijing recruits (BRs) uniquelyexpressed ~12,000 alternativesplicing (AS)-derived transcripts, 20largely elevating the proportion of transcripts significantly correlated with PM concentration. BRs 21expressed PM-associated isoforms (PMAIs) of PFKFB3and LDHA,encoding enzymes responsible 22for stimulatingand maintaining glycolysis. PMAIsof PFKFB3featured different COOH-terminals, 23targeting PFKFB3 to different sub-cellular functional compartments and stimulating glycolysis. 24PMAIs of LDHAhavelonger 3’UTRs relative to those expressed in Chengderecruits (CRs),allowing 25glycolysis maintenance by enhancing LDHAmRNA stability and translational efficiency. PMAIs 26weredirectly regulated by different HIF-1Aand HIF-1Bisoforms. BRs expressed more non-func-27tional Fasisoforms and a resultant reduction of intact Fasproportion is expectedto inhibit the trans-28mission of apoptotic signals and prolong neutrophil lifespan. BRs expressed both membrane-bound 29and soluble IL-6Risoforms insteadof only one in CRs. The presence of both IL-6Risoforms sug-30gested a higher migration capacity of neutrophils in BRs. PMAIs of HIF-1Aand PFKFB3were down-31regulated inChronic Obstructive Pulmonary Disease patients compared with BRs, implying HIF-1 32mediated defective glycolysis may mediate neutrophil dysfunction. PMAIs could explain large var-33iances of different phenotypes, highlighting their potential application as biomarkers and therapeu-34tic targets in PM-induced diseases, which remain poorly elucidated

    Peregrine and saker falcon genome sequences provide insights into evolution of a predatory lifestyle

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    As top predators, falcons possess unique morphological, physiological and behavioral adaptations that allow them to be successful hunters: for example, the peregrine is renowned as the world's fastest animal. To examine the evolutionary basis of predatory adaptations, we sequenced the genomes of both the peregrine (Falco peregrinus) and saker falcon (Falco cherrug), and we present parallel, genome-wide evidence for evolutionary innovation and selection for a predatory lifestyle. The genomes, assembled using Illumina deep sequencing with greater than 100-fold coverage, are both approximately 1.2 Gb in length, with transcriptome-assisted prediction of approximately 16,200 genes for both species. Analysis of 8,424 orthologs in both falcons, chicken, zebra finch and turkey identified consistent evidence for genome-wide rapid evolution in these raptors. SNP-based inference showed contrasting recent demographic trajectories for the two falcons, and gene-based analysis highlighted falcon-specific evolutionary novelties for beak development and olfaction and specifically for homeostasis-related genes in the arid environment–adapted saker

    Comparative genomics reveals insights into avian genome evolution and adaptation

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    Birds are the most species-rich class of tetrapod vertebrates and have wide relevance across many research fields. We explored bird macroevolution using full genomes from 48 avian species representing all major extant clades. The avian genome is principally characterized by its constrained size, which predominantly arose because of lineage-specific erosion of repetitive elements, large segmental deletions, and gene loss. Avian genomes furthermore show a remarkably high degree of evolutionary stasis at the levels of nucleotide sequence, gene synteny, and chromosomal structure. Despite this pattern of conservation, we detected many non-neutral evolutionary changes in protein-coding genes and noncoding regions. These analyses reveal that pan-avian genomic diversity covaries with adaptations to different lifestyles and convergent evolution of traits

    Modeling Progressive Damage and Failure of Single-Lap Thin-Ply-Laminated Composite-Bolted Joint Using LaRC Failure Criterion

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    Thin-ply composite failure modes also significantly differ from conventional ply composite failure modes, with the final failure mechanism switching from irregular progressive failure to direct fracture characterized by a uniform fracture with the reduction of the ply thickness. When open holes and bolt joints are involved, thin-ply-laminated composites exhibit more complex stress states, damage evolution, and failure modes. Compared to the experimental study of thin-ply-laminated composite-bolted joints, there are few reports about numerical analysis. In order to understand the damage evolution and failure mechanism of thin-ply-laminated composites jointed by single-lap bolt, a progressive damage model based on three-dimensional (3D) LaRC failure criterion combined with cohesive element is constructed. Through an energy-based damage evolution method, this model can capture some significant mechanical characteristics in thin-ply-laminated structures, such as the in situ effect, delamination inhibition, and fiber compressive kinking failure. The comparisons between the numerical predictions and experimental observations are made to verify the accuracy of the proposed model. It is found that the predicted stress-displacement curves, failure modes, damage morphologies, etc., are consistent with the experimental results, indicating that the presented progressive damage analysis method displays excellent accuracy. The predicted stress at the onset of delamination is 50% higher than that of the conventional thick materials, which is also consistent with experimental results. Moreover, the numerical model provides evidence that the microstructure of thin-ply-laminated composite performs better in uniformity, which is more conducive to inhibiting the intra-layer damage and the expansion of delamination damage between layers. This study on the damage inhibition mechanism of thin-ply provides a potential analytical tool for evaluating damage tolerance and bearing capabilities in thin-ply-laminated composite-bolted joints

    Adaptive sliding mode control of tri-layer conjugated polymer actuators

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    This paper proposes an adaptive sliding mode control methodology to enhance the positioning ability of conducting polymer actuators typified by tri-layer conjugated polymer actuators. This is motivated by the search for an effective control strategy to command such actuators to a desired configuration in the presence of parametric uncertainties and unmodeled disturbances. After analyzing the stability of the adaptive sliding mode control system, experiments were conducted to demonstrate its satisfactory tracking ability, based on a series of experimental results. Implementation of the control law requires a valid model of the conducting polymer actuator and boundaries of the uncertainties and disturbances. Based on the theoretical and experimental results presented, the adaptive sliding mode control methodology is very attractive in the field of smart actuators which contain significant uncertainties and disturbances. © 2013 IOP Publishing Ltd

    Establishment and experimental verification of a prandtl–ishlinskii hysteresis model for tri-layer conducting polymer actuators

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    In this paper, a Prandtl–Ishlinskii hysteresis model (PI) is used to build a rate-independent hysteresis model for a class of conducting polymer actuators typified by tri-layer conjugated polymer actuators. Firstly, an off-line method is proposed to identify a discretization density function for the hysteresis model, and then a linear transfer function for the actuator is identified using the PI inverse model. Secondly, a neural network approach is proposed to realize an adaptive on-line identification method for the density function of the PI hysteresis model. In the back propagation (BP) algorithm for the neural network, the discretization PI operator is considered as an operational function of the neural network and the density function is considered as the power value. Finally, the simulation and experimental results are presented to demonstrate the validity of the model identification method and the actuator model

    A methodology to establish a hysteresis model for trilayer conducting polymer actuators

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    Conducting polymer actuators which are capable of operating in air or liquid media under low actuation voltages can be used as macro and micromanipulation devices. However, their positioning accuracy is adversely affected by their hysteresis nonlinearity. In this paper, we establish a Duhem hysteresis model for conducting polymer actuators, which is a rate-independent hysteresis model. The hysteresis model is experimentally identified and integrated with the linear transfer function of the actuator to build a more accurate actuator model
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