9 research outputs found

    Pavement dynamic monitoring data processing based on wavelet decomposition and reconfiguration methods

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    Early damage to asphalt pavements generally occurs due to the increasing traffic flow and the loads of vehicles, coupled with alternating high- and low-temperature cycles, freeze–thaw cycles, ultraviolet radiation, and other harsh environments. Several types of distress, such as rutting, cracking, and other damage, deteriorate the serviceability of asphalt pavements and shorten the road service life. Thus, the long-term structural mechanical response of asphalt pavements under the influence of loads and the environment is crucial data for the road sector, which provides guidance about road maintenance. Effectively processing the pavement dynamic monitoring data is a prerequisite to obtain the dynamic response of asphalt pavement structures. However, the dynamic monitoring data of pavements are often characterized by transient weak signals with strong noises, making it challenging to extract their essential characteristics. In this study, wavelet decomposition and reconstruction methods were applied to reduce the noise of pavement dynamic response data. The parameters of the signal-to-noise ratio (SNR) and root mean square error (RMSE) were introduced to compare and analyze the effect of the decomposition of two different wavelet functions: the symlet (sym) wavelet function and the Daubechies (db) wavelet function. The results showed that both the sym and db wavelet functions can effectively obtain the average similarity information and the detailed information of the dynamic response signals of the pavement, the SNR after the sym wavelet fixed-threshold denoising process is relatively higher, and the RMSE is smaller than that of the db wavelet. Thus, wavelet transformation exhibits good localization properties in both the time and frequency domains for processing pavement dynamic monitoring data, making it a suitable approach for handling massive pavement dynamic monitoring data

    Brahma-related gene 1 acts as a profibrotic mediator and targeting it by micheliolide ameliorates peritoneal fibrosis

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    Abstract Background Progressive peritoneal fibrosis is a worldwide public health concern impacting patients undergoing peritoneal dialysis (PD), yet there is no effective treatment. Our previous study revealed that a novel compound, micheliolide (MCL) inhibited peritoneal fibrosis in mice. However, its mechanism remains unclear. Brahma-related gene 1 (BRG1) is a key contributor to organ fibrosis, but its potential function in PD-related peritoneal fibrosis and the relationship between MCL and BRG1 remain unknown. Methods The effects of MCL on BRG1-induced fibrotic responses and TGF-β1-Smads pathway were examined in a mouse PD model and in vitro peritoneal mesothelial cells. To investigate the targeting mechanism of MCL on BRG1, coimmunoprecipitation, MCL-biotin pulldown, molecular docking and cellular thermal shift assay were performed. Results BRG1 was markedly elevated in a mouse PD model and in peritoneal mesothelial cells cultured in TGF-β1 or PD fluid condition. BRG1 overexpression in vitro augmented fibrotic responses and promoted TGF-β1-increased-phosphorylation of Smad2 and Smad3. Meanwhile, knockdown of BRG1 diminished TGF-β1-induced fibrotic responses and blocked TGF-β1-Smad2/3 pathway. MCL ameliorated BRG1 overexpression-induced peritoneal fibrosis and impeded TGF-β1-Smad2/3 signaling pathway both in a mouse PD model and in vitro. Mechanically, MCL impeded BRG1 from recognizing and attaching to histone H3 lysine 14 acetylation by binding to the asparagine (N1540) of BRG1, in thus restraining fibrotic responses and TGF-β1-Smad2/3 signaling pathway. After the mutation of N1540 to alanine (N1540A), MCL was unable to bind to BRG1 and thus, unsuccessful in suppressing BRG1-induced fibrotic responses and TGF-β1-Smad2/3 signaling pathway. Conclusion Our research indicates that BRG1 may be a crucial mediator in peritoneal fibrosis and MCL targeting N1540 residue of BRG1 may be a novel therapeutic strategy to combat PD-related peritoneal fibrosis
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