Search

This article studies the correlation between ground surface deformation of transmission lines in mining affected areas and various geological and human factors, and it constructs the corresponding numerical models. By analyzing the distribution of goaf areas, geological structures, slope structures, and other factors that affect transmission lines, the tower foundations' deformation characteristics and disaster mechanisms under mining conditions have been clarified. On this basis, research on ground surface deformation risk prediction technology was carried out using monitoring data, and a safety operation risk assessment model was established to achieve rapid identification and accurate prediction and warning of hidden dangers. At the same time, a monitoring, early warning, and risk assessment system has been constructed and demonstrated to be highly accurate and practical in pilot verification. In addition, through the comprehensive application of physical models and numerical simulations, the influence of different ground surface settlements on the deformation of transmission line towers was explored, providing important references for improving the safety of transmission lines. [ABSTRACT FROM AUTHOR]

Objectives Systemic lupus erythematosus (SLE) is a complex autoimmune disease with varying symptoms and multi-organ damage. Relapse-remission cycles often persist for many patients for years with the current treatment. Improved understanding of molecular changes caused by SLE flare and intensive treatment may result in more targeted therapies. Methods RNA sequencing was performed on peripheral blood mononuclear cells (PBMCs) from 65 SLE patients in flare, collected both before (SLE1) and after (SLE2) in-hospital treatment, along with 15 healthy controls (HC). Differentially expressed genes (DEGs) were identified among the three groups. Enriched functions and key molecular signatures of the DEGs were analysed and scored to elucidate the transcriptomic changes during treatment. Results Few upregulated genes in SLE1 vs HC were affected by treatment (SLE2 vs SLE1), mostly functional in interferon signalling (IFN), plasmablasts and neutrophils. IFN and plasmablast signatures were repressed, but the neutrophil signature remained unchanged or enhanced by treatment. The IFN and neutrophil scores together stratified the SLE samples. IFN scores correlated well with leukopenia, while neutrophil scores reflected relative cell compositions but not cell counts. Conclusions In-hospital treatment significantly relieved SLE symptoms with expression changes of a small subset of genes. Notably, IFN signature changes matched SLE flare and improvement, while enhanced neutrophil signature upon treatment suggested the involvement of low-density granulocytes (LDG) in disease development. [ABSTRACT FROM AUTHOR]

We investigate the triple correlation sums of coefficients of Maaß forms in the level aspect. More precisely, letting Π be a Maaß form for |$SL_4({{\mathbb{Z}}})$| and f (resp. g) a holomorphic newform of prime level p (resp. trivial level), we show a strengthened upper bound for the sum |$\sum_{m,n\ge 1} \lambda_{g}(n) \lambda_{\Pi}(m,1,1) \lambda_{f}(m+pn) \,U{\left({m}/{X}\right) }V{\left ({n}/{H}\right)} $|⁠. More generally, for any complex sequence |$\lambda_\star (n)\in {{\mathbb{C}}}$|⁠ , we further obtain a ready-to-use quantitative estimate for the triple correlation sum |$\sum_{m,n\ge 1} \lambda_\star (n) \lambda_{\Pi}(m,1,1)\lambda_{f}(m+pn) \,U{\left({m}/{X}\right) }V{\left ({n}/{H}\right)} $|⁠. As a result, we present that this type of sum is non-trivial in the regime |$p\le X^{1-\varepsilon}$| for any ɛ  > 0; notably, there exists a family of newforms such that the triple sum is non-trivial, as long as |$H\ge X^{\varepsilon}$|⁠. In addition, we obtain an upper bound for the sum of the shape |$\sum_{m,n\ge 1}a(m) b(n) \lambda_{f}(m+pn) \,U{\left({m}/{X}\right) }V{\left ({n}/{H}\right)}$| for any complex sequences |$\mathbf{a}=\{a(m)\}$| and |$\mathbf{b}=\{b(n)\}$|⁠. As an application, we consider certain triple correlation sums corresponding to the configuration |$GL_M \times GL_N\times GL_2$|⁠ , |$M,N\ge3$| and attain the significant cancellations in these sums. [ABSTRACT FROM AUTHOR]

Centromere protein M (CENPM) is essential for chromosome separation during mitosis. However, its roles in lung adenocarcinoma (LUAD) progression and metastasis remain unknown. In this study, we aimed to explore the effects of CENPM on LUAD progression as well as the underlying mechanisms. We analyzed the expression of CENPM and its correlation with clinicopathological characteristics using GEO LUAD chip datasets and TCGA dataset. We further investigated the impact of CENPM on LUAD in vitro and in vivo. In silico analysis and qRT-PCR revealed that CENPM is upregulated in LUAD compared with that in normal lung tissues. Via gain/loss-of-function assays, we further found that CENPM promotes the LUAD cell cycle, cell proliferation, migration and invasion, and inhibits cell apoptosis in vitro. The in vivo study showed that loss of CENPM inhibits the growth of A549 xenografts. Furthermore, we found that CENPM can promote the phosphorylation of mTOR rather than directly affect the mTOR content. Inhibition of mTOR activity abrogates the promoting effects of CENPM on cell cycle progression, cell proliferation, migration and invasion. Taken together, these results show that CENPM plays an important role in the growth and metastasis of LUAD and may be a promising therapeutic target in LUAD.