11,282 research outputs found

    The effect of manganese oxide on the sinterability of hydroxyapatite

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    The sinterability of manganese oxide (MnO2) doped hydroxyapatite (HA) ranging from 0.05 to 1 wt% was investigated. Green samples were prepared and sintered in air at temperatures ranging from 1000 to 1400 °C. Sintered bodies were characterized to determine the phase stability, grain size, bulk density, hardness, fracture toughness and Young's modulus. XRD analysis revealed that the HA phase stability was not disrupted throughout the sintering regime employed. In general, samples containing less than 0.5 wt% MnO2 and when sintered at lower temperatures exhibited higher mechanical properties than the undoped HA. The study revealed that all the MnO2-doped HA achieved >99% relative density when sintered at 1100–1250 °C as compared to the undoped HA which could only attained highest value of 98.9% at 1150 °C. The addition of 0.05 wt% MnO2 was found to be most beneficial as the samples exhibited the highest hardness of 7.58 GPa and fracture toughness of 1.65 MPam1/2 as compared to 5.72 GPa and 1.22 MPam1/2 for the undoped HA when sintered at 1000 °C. Additionally, it was found that the MnO2-doped samples attained E values above 110 GPa when sintered at temperature as low as 1000 °C if compared to 1050 °C for the undoped HA

    Shallow Triple Stream Three-dimensional CNN (STSTNet) for Micro-expression Recognition

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    In the recent year, state-of-the-art for facial micro-expression recognition have been significantly advanced by deep neural networks. The robustness of deep learning has yielded promising performance beyond that of traditional handcrafted approaches. Most works in literature emphasized on increasing the depth of networks and employing highly complex objective functions to learn more features. In this paper, we design a Shallow Triple Stream Three-dimensional CNN (STSTNet) that is computationally light whilst capable of extracting discriminative high level features and details of micro-expressions. The network learns from three optical flow features (i.e., optical strain, horizontal and vertical optical flow fields) computed based on the onset and apex frames of each video. Our experimental results demonstrate the effectiveness of the proposed STSTNet, which obtained an unweighted average recall rate of 0.7605 and unweighted F1-score of 0.7353 on the composite database consisting of 442 samples from the SMIC, CASME II and SAMM databases.Comment: 5 pages, 1 figure, Accepted and published in IEEE FG 201

    GFTSM-based Model Predictive Torque Control for PMSM Drive System With Single Phase Current Sensor

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    Copyright © 2017 Acta Automatica Sinica. All rights reserved. A global fast terminal sliding mode (GFTSM)-based model predictive torque control (MPTC) strategy is developed for permanent magnet synchronous motor (PMSM) drive system with only one phase current sensor. Generally two phase-current sensors are indispensable for MPTC. In response to only one phase current sensor available and the change of stator resistance, a novel adaptive observer for estimating the remaining two phase currents and time-varying stator resistance is proposed to perform MPTC. Moreover, in view of the variation of system parameters and external disturbance, a new GFTSM-based speed regulator is synthesized to enhance the drive system robustness. In this paper, the GFTSM, based on sliding mode theory, employs the fast terminal sliding mode in both the reaching stage and the sliding stage. The resultant GFTSM-based MPTC PMSM drive system with single phase current sensor has excellent dynamical performance which is very close to the GFTSM-based MPTC PMSM drive system with two-phase current sensors. On the other hand, compared with proportional-integral (PI)-based and sliding mode (SM)-based MPTC PMSM drive systems, it possesses better dynamical response and stronger robustness as well as smaller total harmonic distortion (THD) index of three-phase stator currents in the presence of variation of load torque. The simulation results validate the feasibility and efiectiveness of the proposed scheme

    Escherichia coli K1 RS218 Interacts with Human Brain Microvascular Endothelial Cells via Type 1 Fimbria Bacteria in the Fimbriated State

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    Escherichia coli K1 is a major gram-negative organism causing neonatal meningitis. E. coli K1 binding to and invasion of human brain microvascular endothelial cells (HBMEC) are a prerequisite for E. coli penetration into the central nervous system in vivo. In the present study, we showed using DNA microarray analysis that E. coli K1 associated with HBMEC expressed significantly higher levels of the fim genes compared to nonassociated bacteria. We also showed that E. coli K1 binding to and invasion of HBMEC were significantly decreased with its fimH deletion mutant and type 1 fimbria locked-off mutant, while they were significantly increased with its type 1 fimbria locked-on mutant. E. coli K1 strains associated with HBMEC were predominantly type 1 fimbria phase-on (i.e., fimbriated) bacteria. Taken together, we showed for the first time that type 1 fimbriae play an important role in E. coli K1 binding to and invasion of HBMEC and that type 1 fimbria phase-on E. coli is the major population interacting with HBMEC

    In vivo effects on intron retention and exon skipping by the U2AF large subunit and SF1/BBP in the nematode Caenorhabditis elegans

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    The in vivo analysis of the roles of splicing factors in regulating alternative splicing in animals remains a challenge. Using a microarray-based screen, we identified a Caenorhabditis elegans gene, tos-1, that exhibited three of the four major types of alternative splicing: intron retention, exon skipping, and, in the presence of U2AF large subunit mutations, the use of alternative 3' splice sites. Mutations in the splicing factors U2AF large subunit and SF1/BBP altered the splicing of tos-1. 3' splice sites of the retained intron or before the skipped exon regulate the splicing pattern of tos-1. Our study provides in vivo evidence that intron retention and exon skipping can be regulated largely by the identities of 3' splice sites

    How Chromatin Is Remodelled during DNA Repair of UV-Induced DNA Damage in Saccharomyces cerevisiae

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    Global genome nucleotide excision repair removes DNA damage from transcriptionally silent regions of the genome. Relatively little is known about the molecular events that initiate and regulate this process in the context of chromatin. We've shown that, in response to UV radiation–induced DNA damage, increased histone H3 acetylation at lysine 9 and 14 correlates with changes in chromatin structure, and these alterations are associated with efficient global genome nucleotide excision repair in yeast. These changes depend on the presence of the Rad16 protein. Remarkably, constitutive hyperacetylation of histone H3 can suppress the requirement for Rad7 and Rad16, two components of a global genome repair complex, during repair. This reveals the connection between histone H3 acetylation and DNA repair. Here, we investigate how chromatin structure is modified following UV irradiation to facilitate DNA repair in yeast. Using a combination of chromatin immunoprecipitation to measure histone acetylation levels, histone acetylase occupancy in chromatin, MNase digestion, or restriction enzyme endonuclease accessibility assays to analyse chromatin structure, and finally nucleotide excision repair assays to examine DNA repair, we demonstrate that global genome nucleotide excision repair drives UV-induced chromatin remodelling by controlling histone H3 acetylation levels in chromatin. The concerted action of the ATPase and C3HC4 RING domains of Rad16 combine to regulate the occupancy of the histone acetyl transferase Gcn5 on chromatin in response to UV damage. We conclude that the global genome repair complex in yeast regulates UV-induced histone H3 acetylation by controlling the accessibility of the histone acetyl transferase Gcn5 in chromatin. The resultant changes in histone H3 acetylation promote chromatin remodelling necessary for efficient repair of DNA damage. Recent evidence suggests that GCN5 plays a role in NER in human cells. Our work provides important insight into how GG-NER operates in chromatin
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