18 research outputs found

    Study on Typhoon Characteristic Based on Bridge Health Monitoring System

    Get PDF
    Through the wind velocity and direction monitoring system installed on Jiubao Bridge of Qiantang River, Hangzhou city, Zhejiang province, China, a full range of wind velocity and direction data was collected during typhoon HAIKUI in 2012. Based on these data, it was found that, at higher observed elevation, turbulence intensity is lower, and the variation tendency of longitudinal and lateral turbulence intensities with mean wind speeds is basically the same. Gust factor goes higher with increasing mean wind speed, and the change rate obviously decreases as wind speed goes down and an inconspicuous increase occurs when wind speed is high. The change of peak factor is inconspicuous with increasing time and mean wind speed. The probability density function (PDF) of fluctuating wind speed follows Gaussian distribution. Turbulence integral scale increases with mean wind speed, and its PDF does not follow Gaussian distribution. The power spectrum of observation fluctuating velocity is in accordance with Von Karman spectrum

    S2^2MAT: Simultaneous and Self-Reinforced Mapping and Tracking in Dynamic Urban Scenariosorcing Framework for Simultaneous Mapping and Tracking in Unbounded Urban Environments

    Full text link
    Despite the increasing prevalence of robots in daily life, their navigation capabilities are still limited to environments with prior knowledge, such as a global map. To fully unlock the potential of robots, it is crucial to enable them to navigate in large-scale unknown and changing unstructured scenarios. This requires the robot to construct an accurate static map in real-time as it explores, while filtering out moving objects to ensure mapping accuracy and, if possible, achieving high-quality pedestrian tracking and collision avoidance. While existing methods can achieve individual goals of spatial mapping or dynamic object detection and tracking, there has been limited research on effectively integrating these two tasks, which are actually coupled and reciprocal. In this work, we propose a solution called S2^2MAT (Simultaneous and Self-Reinforced Mapping and Tracking) that integrates a front-end dynamic object detection and tracking module with a back-end static mapping module. S2^2MAT leverages the close and reciprocal interplay between these two modules to efficiently and effectively solve the open problem of simultaneous tracking and mapping in highly dynamic scenarios. We conducted extensive experiments using widely-used datasets and simulations, providing both qualitative and quantitative results to demonstrate S2^2MAT's state-of-the-art performance in dynamic object detection, tracking, and high-quality static structure mapping. Additionally, we performed long-range robotic navigation in real-world urban scenarios spanning over 7 km, which included challenging obstacles like pedestrians and other traffic agents. The successful navigation provides a comprehensive test of S2^2MAT's robustness, scalability, efficiency, quality, and its ability to benefit autonomous robots in wild scenarios without pre-built maps.Comment: homepage: https://sites.google.com/view/smat-na

    Synergistic Effects of Apigenin and Paclitaxel on Apoptosis of Cancer Cells

    Get PDF
    BACKGROUND: It was well known that the clinical use of chemotherapeutic drugs is restricted by severe adverse reactions and drug resistances. Thus it is necessary to figure out a strategy to increase the specific anti-tumor efficiency of chemotherapeutic drugs. Apigenin, a kind of flavonoids, has been reported to possess anticancer activities with very low cytotoxicity to normal tissue. METHODOLOGY/PRINCIPAL FINDINGS: Our results from cell viability assay, western-blots and TdT-mediated dUTP-biotin nick end labeling (TUNEL) assay demonstrated the synergistic pro-apoptotic effects of a low dose of apigenin and paclitaxel in human cancer cell lines. To analyze the underlying mechanism, we examined reactive oxygen species (ROS) staining after cells were treated with a combination of apigenin and paclitaxel, or each of them alone. Data from flow-cytometry showed that superoxides but not reduction of peroxides accumulated in HeLa cells treated with apigenin or a combination of apigenin and paclitaxel. Apigenin and paclitaxel-induced HeLa cell apoptosis was related to the level of ROS in cells. We further evaluated activity and protein level of superoxide dismutase (SOD). Apigenin significantly inhibited SOD activity but did not alter the SOD protein level suggesting that apigenin promoted ROS accumulation through suppressing enzyme activity of SOD. Addition of Zn(2+), Cu(2+) and Mn(2+) to cell lysates inhibited apigenin's effects on SOD activity. At the same time, data from caspase-2 over-expression and knocked-down experiments demonstrated that caspase-2 participated in apigenin and paclitaxel-induced HeLa cell apoptosis. CONCLUSIONS/SIGNIFICANCE: Taken together, our study demonstrated that apigenin can sensitize cancer cells to paclitaxel induced apoptosis through suppressing SOD activity, which then led to accumulation of ROS and cleavage of caspase-2, suggesting that the combined use of apigenin and paclitaxel was an effective way to decrease the dose of paclitaxel taken

    Investigations into the cumulative fatigue life of an AISI 304L austenitic stainless steel used for pressure water reactors: Application of a double linear damage rule

    No full text
    International audienceIn order to investigate cumulative damage in fatigue, a multi-level fatigue programme has been carried out on an austenitic stainless steel AISI 304L. All the tests have been performed under controlled strain-amplitude conditions, with several changes of levels up to rupture; values of strain-amplitude were included between 0.20% and 0.80%. The present experimental programme shows that applying a linear damage rule (LDR), also referred to as Palmgren–Miner’s rule, has been demonstrated to be unreliable in some cases. A loading sequence (loading history) effect is clearly shown for the two-level sequence tests; application of the LDR leads to residual fatigue-life overestimation for high-to-low loading (H–L) sequences whereas residual fatigue-life is underestimated for low-to-high loading (L–H) sequences. The multi-level and block tests, undertaken in this campaign, confirm also a possible non-verification of the LDR.Within this framework, the double linear damage rule (DLDR) has been tested. Its application would seem to be promising as an additional approach in certain situations. However, complex sequences and random fatigue tests are still needed to draw a conclusion, and to more clearly evaluate the conditions where use of the LDR would not be sufficient

    A novel mutation in exon 11 of COMP gene in a Chinese family with pseudoachondroplasia

    No full text
    Pseudoachondroplasia (PSACH) is a relatively common skeletal dysplasia characterized by disproportionate short stature, joint laxity, early-onset osteoarthrosis, and dysplasia of the spine, epiphysis, and metaphysis. It is known as an autosomal dominant disease which results exclusively from mutations in the gene for Cartilage Oligomeric Matrix Protein (COMP). We have identified a five year old Chinese boy who was diagnosed as pseudoachondroplasia according to clinical manifestations and X-ray symptoms. His mother seems like another effected individual because of the apparent short stature. Genomic DNA was extracted from peripheral blood lymphocytes. DNA sequencing analysis of the COMP gene revealed a heterozygous mutation (c.1219 T > C,p.Cys407Arg) in the patient. His mother was also affected with the same genetic change. Mutations in COMP gene is proved to change the Cartilage Oligomeric Matrix Protein. This missense mutation (c.1219 T > C) has not been reported before and it is not belongs to polymorphism sites. Our results extend the spectrum of mutations in COMP gene leading to pseudoachondroplasia. Keywords: COMP, Novel mutation, Skeletal dysplasia, Pseudoachondroplasia, Therap

    Spectral Representation via Data-Guided Sparsity for Hyperspectral Image Super-Resolution

    No full text
    Hyperspectral imaging is capable of acquiring the rich spectral information of scenes and has great potential for understanding the characteristics of different materials in many applications ranging from remote sensing to medical imaging. However, due to hardware limitations, the existed hyper-/multi-spectral imaging devices usually cannot obtain high spatial resolution. This study aims to generate a high resolution hyperspectral image according to the available low resolution hyperspectral and high resolution RGB images. We propose a novel hyperspectral image superresolution method via non-negative sparse representation of reflectance spectra with a data guided sparsity constraint. The proposed method firstly learns the hyperspectral dictionary from the low resolution hyperspectral image and then transforms it into the RGB one with the camera response function, which is decided by the physical property of the RGB imaging camera. Given the RGB vector and the RGB dictionary, the sparse representation of each pixel in the high resolution image is calculated with the guidance of a sparsity map, which measures pixel material purity. The sparsity map is generated by analyzing the local content similarity of a focused pixel in the available high resolution RGB image and quantifying the spectral mixing degree motivated by the fact that the pixel spectrum of a pure material should have sparse representation of the spectral dictionary. Since the proposed method adaptively adjusts the sparsity in the spectral representation based on the local content of the available high resolution RGB image, it can produce more robust spectral representation for recovering the target high resolution hyperspectral image. Comprehensive experiments on two public hyperspectral datasets and three real remote sensing images validate that the proposed method achieves promising performances compared to the existing state-of-the-art methods

    Characterization of fusion boundary between low alloy steel and stainless steel cladding

    No full text
    The microstructure and hardness of fusion boundary (FB) and near FB of a low alloy steel (LAS) 16MND5 welding cladded with stainless steel 308L for nuclear reactor pressure vessel were investigated by using modern electron microscopes and nano-indenter. The wavy morphology of fusion line results in changes of nearby microstructures of both cladding 308L and substrate 16MND5 along the FB. The microstructure of the cladding 308L is composed of columnar grains adjacent most of the FB, but it is equiaxed grains at the valley of the wavy fusion line with large curvature. The microstructures of 16MND5 near the FB are ferrite at the wavy fusion line with large curvature, martensite at the wavy fusion line with small curvature, and transition mixed structure between them. A carbide-depleted zone adjacent to the FB was observed in the 16MND5 side, of which the hardness is lower than both FB and 16MND5 base metal. Three types of FB can be observed according to the width, being narrow or sharp FB, needle-like martensite FB, and partially-mixed zone FB. The FB includes high density of carbides of M7C3 and M3C, leading to a hardness peak at FB

    Luteolin inhibits activation of STAT3 in carcinoma cells.

    No full text
    <p>A, HeLa cells were treated with indicated concentrations of luteolin for 24 h and then were subjected to Western blot for measuring protein levels of phosphor-STAT3 (tyr705), phosphor-STAT3 (ser727), STAT3 and c-myc respectively. B, HeLa cells were treated with 50 µM luteolin for different time and then were subjected to Western blot by using phosphor-STAT3 (tyr705), phosphor-STAT3 (ser727), STAT3 or c-myc antibody respectively. C, MCF-7 cells were treated with indicated dose of luteolin, and then subjected to Western blot for detecting protein levels of phosphor-STAT3 (tyr705), phosphor-STAT3 (ser727) and STAT3. D, Hep3B cells treated with indicated dose of luteolin and then subjected to Western blot for detecting protein levels of phosphor-STAT3 (tyr705), phosphor-STAT3 (ser727) and STAT3. E, HeLa cells were treated with indicated dose of luteolin respectively for 24 h and then were subjected used for measuring the nuclear and cytoplasmic fraction of STAT3. F, HeLa cells were transfected with STAT3 luciferase reporter plasmids for 24 hours and then treated with luteolin for 24 hours. Luciferase activity was measured by Luminometer TD-20/20. Values were obtained from three independent experiments. _*<i>P</i><0.05, **<i>P</i><0.001, compared with the control.</p

    Luteolin induced carcinoma cells apoptosis.

    No full text
    <p>A, Carcinoma cells (HeLa, HepG2), and normal cells (WRL-68, HEK293, XJH B) were treated with 20, 30, 40, 50, 60 µM luteolin for 24 h and followed by CytoTox-Glo™ cytotoxicity assays. The data above are plotted as “dead cell” rate versus the concentration of Luteolin. B. HeLa cells were treated with indicated concentration of luteolin for 24 h and subjected to immunoblot analysis for pro-caspase3 and PARP. C. HeLa cells were treated with indicated concentration of luteolin for 24 h and were harvested, and then stained with propidium iodidle and AnnexinV-FITC for detecting the apoptosis by flow cytometry. D. HeLa cells were transfected with indicated concentration of HA-Hsp90 and 24 h after transfection cells were treated with 50 µM luteolin for 24 h and were harvested, and then stained with propidium iodidle and AnnexinV-FITC for detecting the apoptosis by flow cytometry. E. HeLa cells were treated with 50 µM luteolin and 10 µM GA, for 24 h, and then cells were incubated with primary antibodies against PARP. HeLa cells were immunostained with anti-mouse alexa fluor 488 secondary antibody and then stained with DAPI and Alexa Fluor 555 phalloidin derivatives for labeling F-actin. The specimens were visualized by confocal laser scanning microscopy. Blue depicts the nucleus, red depicts localization of F-actin and green depicts localization of cleaved-PARP. F. HeLa cells were pretreated with 25 µM z-VAD-fmk for 1 h and then treated with 50 µM luteolin for 24 h followed by immunoblotting with pro-caspase3 and cleaved PARP antibodies.</p
    corecore