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Traditional target detection (TD) algorithms for hyperspectral imagery (HSI) typically suffer from background interference. To alleviate this problem, we propose a novel preprocessing method based on tensor principal component analysis (TPCA) to separate the background and target apart. With the use of TPCA, HSI is decomposed into a principal component part and a residual part with the spatial-spectral information of the HSI being fully exploited, and TD is performed on the latter. Moreover, an effective distinction in scheme can be made between a HSI tensor’s spatial and spectral domains, which is in line with the physical meanings. Experimental results from both synthetic and real hyperspectral data show that the proposed method outperforms other preprocessing methods in improving the TD accuracies. Further, target detectors that combine the TPCA preprocessing approach with traditional target detection methods can achieve better results than those of state-of-the-art methods aiming at background suppression.

The effect of an external magnetic field on the evolution of the self-generated electromagnetic field during laser ablation is investigated by using the Vlasov–Fokker–Planck simulations. It is found that the self-generated field is rotated and distorted under an external magnetic field, and for highly magnetized plasma, the rotation of the electric field becomes stable after the laser ablation. The theoretical analysis indicates that the rotation and tortuosity are primarily attributed to the advection of the Nernst effect and the Righi–Leduc (RL) flux. The curl of the self-generated field increases with the Hall parameter χ e and reaches a peak at χ e = 0.075 , then it decreases with the χ e continuous increase. As the Hall parameter increases, the RL flux contributes more than 60% to the rotation of the electric field. Furthermore, the distortion of the electric field continues to rotate after the laser ablation due to the cross-gradient Nernst transport. These findings provide theoretical references for the evolution of the self-generated electromagnetic field in laser-driven magnetized plasmas.

Hydrogel microspheres are a novel functional material, arousing much attention in various fields. Microfluidics, a technology that controls and manipulates fluids at the micron scale, has emerged as a promising method for fabricating hydrogel microspheres due to its ability to generate uniform microspheres with controlled geometry. With the development of microfluidic devices, more complicated hydrogel microspheres with multiple structures can be constructed. This review presents an overview of advances in microfluidics for designing and engineering hydrogel microspheres. It starts with an introduction to the features of hydrogel microspheres and microfluidic techniques, followed by a discussion of material selection for fabricating microfluidic devices. Then the progress of microfluidic devices for single‐component and composite hydrogel microspheres is described, and the method for optimizing microfluidic devices is also given. Finally, this review discusses the key research directions and applications of microfluidics for hydrogel microsphere in the future. The review summarizes the features of hydrogel microspheres and microfluidic technique, followed by the discussion of material selection in fabricating microfluidic device. Then the progress of microfluidic devices for both single‐component and composite hydrogel microspheres is described. Finally, this review discusses the key research direction and application of microfluidics for hydrogel microsphere in the future.

Denervation can activate the catabolic pathway in skeletal muscle and lead to progressive skeletal muscle atrophy. At present, there is no effective treatment for muscle atrophy. Histone deacetylase 4 (HDAC4) has recently been found to be closely related to muscle atrophy, but the underlying mechanism of HDAC4 in denervation-induced muscle atrophy have not been described clearly yet. In this study, we found that the expression of HDAC4 increased significantly in denervated skeletal muscle. HDAC4 inhibition can effectively diminish denervation-induced muscle atrophy, reduce the expression of muscle specific E3 ubiquitin ligase (MuRF1 and MAFbx) and autophagy related proteins (Atg7, LC3B, PINK1 and BNIP3), inhibit the transformation of type I fibers to type II fibers, and enhance the expression of SIRT1 and PGC-1 α. Transcriptome sequencing and bioinformatics analysis was performed and suggested that HDAC4 may be involved in denervation-induced muscle atrophy by regulating the response to denervation involved in the regulation of muscle adaptation, cell division, cell cycle, apoptotic process, skeletal muscle atrophy, and cell differentiation. STRING analysis showed that HDAC4 may be involved in the process of muscle atrophy by directly regulating myogenin (MYOG), cell cycle inhibitor p21 (CDKN1A) and salt induced kinase 1 (SIK1). MYOG was significantly increased in denervated skeletal muscle, and MYOG inhibition could significantly alleviate denervation-induced muscle atrophy, accompanied by the decreased MuRF1 and MAFbx. MYOG overexpression could reduce the protective effect of HDAC4 inhibition on denervation-induced muscle atrophy, as evidenced by the decreased muscle mass and cross-sectional area of muscle fibers, and the increased mitophagy. Taken together, HDAC4 inhibition can alleviate denervation-induced muscle atrophy by reducing MYOG expression, and HDAC4 is also directly related to CDKN1A and SIK1 in skeletal muscle, which suggests that HDAC4 inhibitors may be a potential drug for the treatment of neurogenic muscle atrophy. These results not only enrich the molecular regulation mechanism of denervation-induced muscle atrophy, but also provide the experimental basis for HDAC4-MYOG axis as a new target for the prevention and treatment of muscular atrophy.

A novel multipoint fiber loop ringdown (FLRD) strain sensing system using frequency-shifted interferometry (FSI) is proposed and experimentally validated. Compared to conventional multipoint FLRD techniques, this scheme measures the decay rate of the continuous wave (CW) light in the space domain and thus greatly reduces the cost without the requirement of expensive devices. A serial dual-point strain sensing system was experimentally constructed and a biconical tapered multimode fiber (MMF) as the sensor head was used for obtaining the large measuring range. By applying different strains on the sensor heads through translation stages, a linear response between strain and additional loss induced by strain sensor was obtained, and the static strain sensitivities of 0.13676 dB/mε and 0.19665 dB/mε were achieved, corresponding to the detection limit of 0.0123 dB and 0.0360 dB, respectively. Moreover, a large measuring range of approximately 6 mε was achieved for both strain sensors. The experimental results indicate that our proposed method offers a promising multipoint strain sensor which has the advantages of low cost, a simple sensing structure and a large measuring range.

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease with the progressive loss of motor neurons, leading to a fatal paralysis. According to whether there is a family history of ALS, ALS can be roughly divided into two types: familial and sporadic. Despite decades of research, the pathogenesis of ALS is still unelucidated. To this end, we review the recent progress of ALS pathogenesis, biomarkers, and treatment strategies, mainly discuss the roles of immune disorders, redox imbalance, autophagy dysfunction, and disordered iron homeostasis in the pathogenesis of ALS, and introduce the effects of RNA binding proteins, ALS-related genes, and non-coding RNA as biomarkers on ALS. In addition, we also mention other ALS biomarkers such as serum uric acid (UA), cardiolipin (CL), chitotriosidase (CHIT1), and neurofilament light chain (NFL). Finally, we discuss the drug therapy, gene therapy, immunotherapy, and stem cell-exosomal therapy for ALS, attempting to find new therapeutic targets and strategies. A challenge is to study the various mechanisms of ALS as a syndrome. Biomarkers that have been widely explored are indispensable for the diagnosis, treatment, and prevention of ALS. Moreover, the development of new genes and targets is an urgent task in this field.

Optimizing nitrogen sources and rootstock selection is crucial for sustainable watermelon production. However, the synergistic mechanisms between organic nitrogen forms and rootstocks remain poorly understood. This study investigates whether glycine, as an organic nitrogen source, modulates root-associated bacterial communities through rootstock-mediated effects to enhance watermelon growth. Grafted watermelon plants (scion: watermelon; rootstocks: self-grafted watermelon (CK), wild watermelon (T1), bottle gourd (T2), pumpkin (T3) were cultivated under glycine (G) or ammonium nitrate (A) treatments for 25 days. Plant growth, soil enzyme activity, rhizosphere bacterial communities (16S rRNA sequencing), and root metabolomes (UPLC-MS/MS) were analyzed. Relative to ammonium nitrate, glycine to some extent increased bacterial α-diversity but there was no significant difference and altered β-diversity, whereas enhancing microbial network complexity. Rootstock genotype is the main driver of bacterial α diversity and shaped the bacterial network architecture: T1-supported networks exhibited strong associations enriched in two-component systems, whereas T3 networks reflected intensified resource competition. Rootstock identity also influenced root exudate profiles. T3 secreted high levels of amino acids and nucleotides with metabolic and defensive roles, correlating with the abundance of and . In contrast, T1 increased abundance via lipid secretion. The rootstock-bacteria-metabolite interplay modulated soil enzyme activities, supported photochemical efficiency, and promoted biomass accumulation. These findings demonstrate the potential of glycine as a sustainable nitrogen source and identify compatible scion-rootstock combinations that enhance rhizosphere microbial dynamics and plant performance. The study provides mechanistic insights into how root exudates shape bacterial community assembly, although further work is needed to elucidate the complexity of microbe-microbe interactions.

Background Denervation-induced muscle atrophy is complex disease involving multiple biological processes with unknown mechanisms. N6-methyladenosine (m6A) participates in skeletal muscle physiology by regulating multiple levels of RNA metabolism, but its impact on denervation-induced muscle atrophy is still unclear. Here, we aimed to explore the changes, functions, and molecular mechanisms of m6A RNA methylation during denervation-induced muscle atrophy. Methods During denervation-induced muscle atrophy, the m6A immunoprecipitation sequencing (MeRIP-seq) as well as enzyme-linked immunosorbent assay analysis were used to detect the changes of m6A modified RNAs and the involved biological processes. 3-deazidenosine (Daa) and R-2-hydroxyglutarate (R-2HG) were used to verify the roles of m6A RNA methylation. Through bioinformatics analysis combined with experimental verification, the regulatory roles and mechanisms of m6A RNA methylation had been explored. Results There were many m6A modified RNAs with differences during denervation-induced muscle atrophy, and overall, they were mainly downregulated. After 72 h of denervation, the biological processes involved in the altered mRNA with m6A modification were mainly related to zinc ion binding, ubiquitin protein ligase activity, ATP binding and sequence-specific DNA binding and transcription coactivator activity. Daa reduced overall m6A levels in healthy skeletal muscles, which reduced skeletal muscle mass. On the contrary, the increase in m6A levels mediated by R-2HG alleviated denervation induced muscle atrophy. The m6A RNA methylation regulated skeletal muscle mass through ubiquitin–proteasome pathway. Conclusion This study indicated that decrease in m6A RNA methylation was a new symptom of denervation-induced muscle atrophy, and confirmed that targeting m6A alleviated denervation-induced muscle atrophy.

Acute pancreatitis (AP) is characterised by inflammation and cell death in pancreatic tissue, with ferroptosis playing a critical role in its pathophysiology by mediating cellular damage and exacerbating inflammation. This study investigated the role of human leukocyte antigen (HLA)-F adjacent transcript 10 (FAT10) in AP, specifically its involvement in ferroptosis within pancreatic acinar cells. We observed that FAT10 expression was significantly elevated in AP tissues, which correlated with increased ferroptosis. Overexpression of FAT10 in pancreatic acinar cells enhances ferroptosis, whereas its knockdown reduced levels of ferroptosis markers. Furthermore, we confirmed that FAT10 enhanced ferroptosis in pancreatic acinar cells primarily by upregulating nuclear receptor coactivator 4 (NCOA4) expression. Mechanistic investigations revealed that FAT10 regulates NCOA4 expression to promote ferroptosis in a complex manner. FAT10 inhibits NCOA4 ubiquitination by reducing ubiquitin-NCOA4 complexes. Meanwhile, NCOA4 expression increased alongside the increase in FAT10-NCOA4 complexes, which are resistant to proteasomal degradation. Notably, we identified silibinin, a natural compound, as an effective inhibitor of the FAT10-NCOA4 axis, leading to reduced ferroptosis and alleviation of pancreatic damage in vivo. Silibinin treatment decreased the levels of ferroptosis-related proteins and inflammatory markers in both cell and animal models. Our findings highlight the FAT10-NCOA4 axis as a crucial regulator of ferroptosis in pancreatic acinar cells and suggest that targeting this pathway could offer a therapeutic strategy for mitigating AP. This study provides new insights into the regulatory mechanisms of ferroptosis in pancreatic acinar cells, identifying FAT10 as a potential therapeutic target for AP management.

Grouted connections are commonly used in marine engineering, especially on oil platforms, cross-sea bridges, and offshore wind power turbines. The prediction methods for axial carrying capacity of grouted connections with shear keys and their application ranges in current codes were analyzed in this paper. The calculated results by using different codes were compared based on a practical grouted connection between steel piles and the jacket foundation of a wind turbine. The research team conducted axial compression tests on seven specimens, collected a wide range of experimental results to establish a database, and finally compared the standard calculation results with the experimental results. The study indicates that the axial strength of grouted connections predicted by different methods is distinct. The calculation formula of the British Health and Safety Executive (HSE, 2002) has obvious limitations; specifically, with increased shear keys, strength is overestimated, resulting in insecure design outcome of structures. The results calculated by the Norwegian Det Norske Veritas (DNV, 2013) are generally consistent with the experimental results, in which the reduction effect of multiple shear keys was considered. The prediction method of the American Petroleum Institute (API, 2007), which undervalues the bearing performance of connections, is excessively conservative. The method of the combined Norwegian and German Det Norske Veritas–Germanischer Lloyd (DNV-GL, 2016) has wider applicability and is safe, reliable, and economical.