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In cable-stayed bridges, cables are susceptible to fatigue damage due to cyclic traffic loads. The accurate monitoring of cable tension is critical in assessing fatigue damage and ensuring the service performance of cables. The vibration method establishes a formula between the cable tension and its vibration frequency. Therefore, the main challenge in identifying the time-varying cable tension is to determine the instantaneous frequencies (IFs) of the cable. Variational nonlinear chirp mode decomposition (VNCMD) exhibits promising advantages in identifying IFs from measured vibration signals, owing to its robustness against noise interference. However, hyperparameter selection significantly affects the IF identification accuracy of VNCMD, limiting its applicability. In this study, an improved VNCMD, termed variational nonlinear chirp mode extraction (VNCME), is proposed to address this limitation and is used to identify the time-varying cable tension. First, VNCME constructs a novel algorithm framework by modifying the optimisation function of VNCMD, eliminating the need for hyperparameter presetting and enabling the identification of a specific-order IF for the cable. The identified IF is then incorporated into the formula of the vibration method to calculate the time-varying cable tension. Examples of nonstationary signals of a sinusoidal function, finite element model of a cable, and laboratory experiments of scaled cables are used to illustrate the advantages of the proposed method, which proves to be successful in time-varying cable tension identification. In addition, the proposed method is implemented on an actual highway cable-stayed bridge to identify the time-varying cable tension over a 24-h duration. The results demonstrate that the proposed method is practical and reliable, providing a new path for the real-time monitoring of cable tension. [ABSTRACT FROM AUTHOR]

This research aimed to develop a new method for clean utilization and treatment of landfill leachate and solid waste weathered coal. Landfill leachate and weathered coal were adopted for combined anaerobic fermentation for methane production. The characteristics of microbial community, mechanism of biological methane production, and utilization characteristics of fermentation broth and solid residue for co-fermentation were analyzed through metagenomics, soluble organic matter detection and thermogravimetric (TG) analysis. The obtained results revealed that combined anaerobic fermentation increased methane production by 80.1%. Syntrophomonas , Salipiger , Methanosaeta and Methanothrix were highly correlated. Gene abundances of 2-oxoacid ferredoxin oxidoreductase and enolase were increased in methane conversion pathway mainly by acetic acid. Pyruvate-ferroredoxin oxidoreductase, 2-oxoglutarate synthase and succinate dehydrogenase acetate synthase intensified electron transfer pathways among microorganisms. Fulvic acid, tyrosine and tryptophan contents were high in fermentation broth. Volatile decomposition temperature, ignition point and residual char combustion temperature of residual coal were decreased and combustion was more stable. The obtained results showed that the co-fermentation of landfill leachate and weathered coal improved biological methane gas production, degraded weathered coal and improved combustion performance, which provided a new idea for weathered coal clean utilization. [Display omitted] • Combined anaerobic fermentation promotes biomethane conversion. • Key metabolic functions of acetic acid are effectively expressed. • Abundance of enzyme genes related to electron transfer between microorganisms increased. • Combustion performance of solid residue after anaerobic fermentation was improved. [ABSTRACT FROM AUTHOR]

Video content tampering is a growing concern. While tampering, perpetrator needs to decompress and re-compress a video. Thus, detecting whether a video has undergone double compression is an important issue in video forensics. In this paper, a novel method is proposed for the detection of High Efficiency Video Coding (HEVC) double compression. Firstly, theoretical and statistical analysis are stated on the quality degradation during double compression, and the impact of Quantization Parameter (QP) on Transforming Unit (TU) and Discrete Cosine Transform (DCT) coefficients distribution. Then 3 sub-features based on Boundary Effect of TU and Non-Zero DCT Coefficients are calculated. Further, 3 sub-features are combined into a 26-dimension feature as the proposed detection feature, which is finally fed to the Multilayer Perceptron (MLP) classifier. Experiments are conducted on video sets with different settings, and the result proves that our method achieves better performance under several situations compared with two existing methods. • A novel method for HEVC video double compression detection under different QPs. • Boundary effect of TU is proposed to construct sub-feature. • Non-zero DCT coefficient distribution is analyzed for constructing sub-features. • Experimental results address the effectiveness of various video setting. [ABSTRACT FROM AUTHOR]

FGFR3 activating mutations and abnormal expression are linked to tumor development. However, the current state of research on FGFR3 gene expression regulation is relatively insufficient. In this study, we have reported that the FGFR3 promoter's positive strand contains several G-tracts and most likely forms a G-quadruplex (G4) structure. Circular dichroism investigations revealed that oligonucleotides from this region exhibit G-quadruplex-like molar ellipticity. We further validated the G4 structure of the FGFR3 promoter using biochemical and cellular molecular biology techniques. The G-quadruplex mutation enhanced the transcriptional activity of the FGFR3 promoter and DNA replication, suggesting that the G4 structure inhibits its expression. Furthermore, we conducted a preliminary screen for helicases associated with FGFR3 expression and explored their regulatory effects on FGFR3 gene transcription. Subsequently, we investigated the effect of curcumin on the stability of the G4 structure of the FGFR3 promoter and its regulatory effect on FGFR3 expression. • 1.The positive strand of the FGFR3 promoter contains several G-tracts with the capacity to form G-quadruplex structures. • The G-quadruplex negatively regulates FGFR3 promoter-mediated transcription and its DNA replication. • Helicases DDX42 and RTEL1 potentially unwind the G4 structures in the FGFR3 promoter. • Curcumin binds to and stabilizes the FGFR3 promoter G-quadruplexes and inhibits its transcriptional activity. [ABSTRACT FROM AUTHOR]

Colorectal cancer (CRC) is the third most common cancer globally. Regorafenib, a multi-target kinase inhibitor, has been approved for treating metastatic colorectal cancer patients who have undergone at least two prior standard anti-cancer therapies. However, regorafenib efficacy as a single agent remains suboptimal. A promising target at the crossroads of multiple signaling pathways is the Src homology 2 domain-containing protein tyrosine phosphatase (SHP2). However, a combination approach using SHP2 inhibitors (SHP099) and anti-angiogenic drugs (Regorafenib) has not been reported in current research. In this study, we conducted in vitro experiments combining SHP099 and regorafenib and established an MC-38 colon cancer allograft mouse model. Our results revealed that co-treatment with SHP099 and regorafenib significantly inhibited cell viability and altered the biological characteristics of tumor cells compared with treatment alone in vitro. Furthermore, the combination strategy demonstrated superior therapeutic efficacy compared to monotherapy with either drug. This was evidenced by reduced tumor size, decreased proliferation, increased apoptosis, normalized tumor microvasculature, and improved antitumor immune response in vivo. These findings suggest that the combination of an SHP2 inhibitor and regorafenib is a promising therapeutic approach for patients with colorectal cancer. • Regorafenib monotherapy extends colorectal cancer survival, but duration is brief. • SHP2 inhibitors shows encouraging outcomes in multiple clinical trials. • Initial Exploration: Anti-angiogenic drugs combined with SHP099 for anti-tumor effects. • Medications combination boosts anti-tumor effects and enhances immunity. [ABSTRACT FROM AUTHOR]

Rheumatoid arthritis (RA) is currently an autoimmune inflammatory disease with an unclear pathogenesis. Fibroblast-like synoviocytes (FLSs) have tumor-like properties, and their activation and secretion of pro-inflammatory factors are important factors in joint destruction. Wogonin (5,7-dihydroxy-8-methoxyflavone), a natural flavonoid isolated from Scutellaria baicalensis root, has been shown to have significant anti-inflammatory, anti-oxidative stress, and anti-tumor effects in a variety of diseases. However, the role of wogonin in RA has not yet been demonstrated. To investigate the inhibitory effect of wogonin on the invasive behavior of fibroblast-like synoviocytes and to explore the mechanism of action of wogonin in RA. CCK-8, EdU, cell migration and invasion, immunofluorescence staining, RT-qPCR, and protein blot analysis were used to study the inhibitory effects of wogonin on migration, invasion, and pro-inflammatory cytokine overexpression in the immortalized rheumatoid synovial cell line MH7A. The therapeutic effects of wogonin were validated in vivo using arthritis scores and histopathological evaluation of collagen-induced arthritis mice. Wogonin inhibited the migration and invasion of MH7A cells, reduced the production of TNF-α, IL-1β, IL-6, MMP-3 and MMP-9, and increased the expression of IL-10. Moreover, wogonin also inhibited the myofibrillar differentiation of MH7A cells, increased the expression of E-cadherin (E-Cad) and decreased the expression of α-smooth muscle actin (α-SMA). In addition, wogonin treatment effectively ameliorated joint destruction in CIA mice. Further molecular mechanism studies showed that wogonin treatment significantly inhibited the activation of PI3K/AKT/NF-κB signaling pathway in TNF-α-induced arthritic FLSs. Wogonin effectively inhibits migration, invasion and pro-inflammatory cytokine production of RA fibroblast-like synoviocytes through the PI3K/AKT/NF-κB pathway, and thus wogonin, as a natural flavonoid, has great potential for treating RA. [Display omitted] • Wogonin inhibits the migration and invasion of fibroblast-like synoviocytes via PI3K/AKT/NF-κB signaling pathway in RA. • Wogonin treatment ameliorate joint inflammation and bone destruction of mice with CIA. • Wogonin is a potential therapeutic agent against RA. [ABSTRACT FROM AUTHOR]

Intestinal injury is one of the most debilitating side effects of many chemotherapeutic agents, such as irinotecan hydrochloride (CPT-11). Accumulating evidence indicates that neutrophil extracellular traps (NETs) play a critical role in the symptoms of ischemia and inflammation related to chemotherapy. The present study investigated the effects and possible mechanisms of phenethyl isothiocyanate (PEITC) in inhibiting NETs and alleviating chemotherapeutic intestinal injury. CPT-11 induced robust neutrophil activation, as evidenced by increased NETs release, intestinal ischemia, and mRNA expression of inflammatory factors. PEITC prolonged the clotting time of chemotherapeutic mice, improved the intestinal microcirculation, inhibited the expression of inflammatory factors, and protected the tight junctions of the intestinal epithelium. Both in vivo and in vitro experiments revealed that PEITC directly suppresses CPT-11-induced NETs damage to intestinal cells, resulting in significant attenuation of epithelial injury. These results suggest that PEITC may be a novel agent to relieve chemotherapeutic intestinal injury via inhibition of NETs. [Display omitted] • PEITC, a natural isothiocyanate, ameliorated chemotherapy-induced enterocolitis. • PEITC exerts protective effects of intestinal epithelium via the inhibition of NETs. • NETs may be an important target for the treatment of chemotherapeutic injury. [ABSTRACT FROM AUTHOR]

TP53INP2 (tumor protein p53-inducible nuclear protein 2), known as an autophagy protein, is essential for regulating transcription and starvation-induced autophagy, which plays a crucial role in the oncogenesis and progression of various cancers. The present study aims to investigate the expression pattern, function and prognostic value of TP53INP2 in colorectal cancer (CRC). Here, we report that low expression of TP53INP2 correlates with poor survival in CRC patients. TP53INP2 was significantly downregulated in CRC tissues compared with adjacent tissues. As the malignancy of CRC progresses, the expression level of TP53INP2 gradually decreased. Knockdown of TP53INP2 promoted CRC cell proliferation and tumor growth in mice. Mechanistically, TP53INP2 deficiency decreased phosphorylation of β-catenin on S33, S37, and T41, resulting in increased accumulation of β-catenin and enhanced nuclear translocation and transcriptional activity. Moreover, we further demonstrated that TP53INP2 sequestered TIM50, thereby inhibiting its activation of β-catenin. Taken together, our findings indicate that the downregulation of TP53INP2 promotes CRC progression by activating β-catenin and suggest that TP53INP2 may be a candidate therapeutic target for CRC. • Low TP53INP2 expression is associated with poor prognosis in colorectal cancer. • Loss of TP53INP2 function decreases phospho-S33/S37/T41 β-catenin, leading to CRC proliferation and tumor progression. • TP53INP2 sequesters TIM50 to inhibit its activation of β-catenin. • TP53INP2 could be used as a marker for diagnosis and treatment of highly malignant colorectal cancer. [ABSTRACT FROM AUTHOR]