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Industrial development and population expansion has had serious negative impacts on the water ecological environment, and enhancing water ecological resilience (WER) has become a new sustainable development goal. Current research on WER is mostly about ecological resilience assessment including water systems. In order to explore the WER of the Yangtze River Economic Belt (YREB), ecological resilience and water ecology were combined to form the concept of WER. Based on the "social-ecological" resilience perspective, a DCSMI (Driving Force—Carrying Capacity—State—Management—Innovation) WER evaluation index system was constructed, which consists of five subsystems. The WER of the YREB from 2011 to 2022 was measured by using game-theoretic combination weights and the comprehensive evaluation method, which were then combined with the kernel density (KD) estimation, the Thiel index, and the center of gravity-standard deviation ellipse (SDE) method to reveal the WER differences and spatial evolution characteristics of the YREB. Finally, the key factors influencing WER were explored using the BP-DEMATEL model. It was found that (1) the average value of WER in the YREB has declined from 0.4562 to 0.4442, the polarization of WER is obvious, the overall gap is on a widening trend, and the gap between different basins is the main reason for the differences in WER in the YREB. (2) The WER of the YREB presents an asymmetric U-shaped distribution pattern with the downstream optimal, upstream medium, and midstream worst, and the spatial evolution presenting a northwestern–southeastern pattern. (3) The key factors of the top-ranked provinces in the WER index are concentrated in the layer of the State (S) indicators, the middle-ranked provinces and the back-ranked provinces are more influenced by the Driving Force (D) and the Carrying Capacity (C) indicators, respectively, and the Management (M) and Innovation (I) indicators are distributed in several provinces. These results can provide theoretical support for the construction of "resilient cities" and water ecology optimization in the YREB. [ABSTRACT FROM AUTHOR]

The formation of ice on the surface of the metallic casing of high-end equipment poses a potential threat to its operational safety and stability. One important factor that contributes to bonding failure at the ice-metal interface is stress concentration. This paper aims to investigate the effect of stress concentration on the bonding failure behavior at the ice-metal interface through numerical analysis. First, the forms of bonding failure are categorized. Afterwards, the stress distribution state at the corners of the ice-metal interface is determined by the interfacial stress singularity. Finally, numerical analysis is carried out to investigate the thermal stress distribution law at the corners of the interface during the cooling process of the ice-metal bonding, so as to elucidate the induced mechanism of the interfacial stress state on the bonding failure. This study can provide some reference and guidelines for the study of bonding failure at the ice-metal interface. [ABSTRACT FROM AUTHOR]

Lung cancer and asthma are both global health problems with significant economic consequences. Recent studies have demonstrated that asthma may be a risk factor for lung cancer. The present study aimed to explore the pathogenesis between these two diseases through a comprehensive analysis. Differentially expressed genes (DEGs) screened in the asthma-related GSE165934 dataset were analyzed to find relevant inflammatory pathways. Overlapping genes regulated by inflammatory pathways and lung cancer-DEGs from The Cancer Genome Atlas (TCGA) were obtained and subjected to survival and gene-wide mutation analyses, and nomogram construction to determine the hub gene. The hub gene was further analyzed through expression validation, immunoassays and functional experiments to investigate its role and mechanism in lung cancer. Functional enrichment analysis showed that 1,275 DEGs from GSE165934 were closely associated with the Toll-like receptor signaling pathway, and 8 overlapping genes were identified from 12 genes regulated by the Toll-like receptor signaling pathway and 3,134 TCGA-DEGs. After a series of bioinformatics analyses, it was found that triggering receptor expressed on myeloid cells 1 (TREM1) was the hub gene involved in the mechanism of asthma and lung cancer. TREM1 was also found to be a suppressor gene in lung cancer correlated with immune cells, immune checkpoint-related genes and tumor mutational burden score. Additionally, the results of Cell Counting Kit-8 and Transwell experiments demonstrated that overexpression of TREM1 could significantly inhibit the invasion, proliferation and migration of lung cancer cells. Reverse transcription-quantitative PCR and western blotting demonstrated that the overexpression of TREM1 could also significantly reduce the level of Toll-like receptor signaling pathway proteins. The present findings suggest that TREM1 is associated with the mechanism of asthma and lung cancer through its regulation of the Toll-like receptor signaling pathway. Furthermore, TREM1 may serve as a potential treatment target and prognostic indicator for patients with lung cancer. [ABSTRACT FROM AUTHOR]

Yeast cell walls (YCW) are promising bio-based elicitors for controlling post-harvest fruit decay. In this study, 1% YCW induction increased the resistance of cherry tomato fruits, reducing disease incidence by 66%. This study aimed to explore the interaction of hormones and crosstalk with MAPKs (mitogen-activated protein kinases) in the early response of resistance regulation in cherry tomato fruits treated with YCW and U0126. We analyzed the temporal changes in hormone content, the expression of critical genes involved in phytohormone biosynthesis, and signal transduction in cherry tomato fruits response to the induction. Results revealed that jasmonic acid (JA) and brassinosteroids (BR) significantly regulated early resistance response in fruit induced by 1% YCW. The salicylic acid (SA) pathway is inhibited by the activation of the JA pathway. JA and SA signaling pathway crosstalk with the MAPK3 pathway. BR plays an essential role in the regulation of fruit resistance. The BR pathway may function independently when JA/SA and MAPK3 pathways are inhibited., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2022 The Authors. Published by Elsevier Ltd.)

Background: Acute pulmonary embolism (APE) is a prevalent reason of cardiovascular morbidity and mortality. Recent studies have underscored the positive effects of microRNAs (miRNAs) on many diseases. The present study aimed to identify the critical miRNA with differential expressions and explore its role in APE., Methods: The critical miRNA with its target gene was screened by bioinformatics analysis. Their binding relationship was analyzed by TargetScan, Dual-luciferase reporter and RNA pull-down assays. A rat model of APE was established by self-blood coagulum. Human pulmonary artery smooth muscle cells (PASMCs) were exposed to platelet-derived growth factor (PDGF-BB) for excessive proliferation, and transfected with miR-34a-3p mimic. Mean pulmonary arterial pressure (mPAP) of rat was measured, and the pulmonary tissues were used for the pathological observation by Hematoxylin-Eosin (H&E) staining. Cell viability and proliferation were detected by Cell Counting Kit-8 (CCK-8) and EdU assays. The expressions of miR-34a-3p with its target genes (including dual-specificity phosphatase-1 (DUSP1)), neuron-derived orphan receptor-1 (NOR-1) and proliferating cell nuclear antigen (PCNA) were determined by quantitative reverse transcription polymerase chain reaction (RT-qPCR) or/and Western blot., Results: MiR-34a-3p expression was down-regulated in APE patients, which attenuated the increment of mPAP and thickening of the pulmonary arterial walls in APE rats, accompanied with regulation of NOR-1 and PCNA levels. MiR-34a-3p suppressed DUSP1 expression by directly binding to its 3'-untranslated region (UTR), and attenuated cell viability, proliferation, and the expressions of NOR-1 and PCNA in PDGF-BB-induced PASMCs by inhibiting DUSP1 expression., Conclusion: Up-regulated miR-34a-3p negatively regulates DUSP1 expression to inhibit PASMC proliferation, which, thus, may act on APE treatment by negatively regulating pulmonary vascular proliferation., (© 2021 The Author(s).)

Background: There is a close relationship between neutrophil extracellular traps (NETs) and venous thromboembolism (VTE). The regulatory role and mechanism of glucocorticoids (GC) in the formation of NETs are unclear., Objective: This study was conducted to assess the effect of GC on the formation of NETs., Methods: We constructed a mouse VTE model and treated them with GC to observe the effect of GC on the formation of NETs. In this regard, peripheral blood neutrophils were isolated, and the effect and mechanism of GC in neutrophil activation were analyzed., Results: Following LPS treatment, the colony-forming ability of neutrophils and their ability to form NETs increased significantly. The analysis of cytokine changes by RT-PCR combined with ELISA showed that the level of inflammatory factors in LPS-activated neutrophils increased significantly; however, these factors were significantly inhibited after GC treatment, and the inhibitory effect was positively correlated with the concentration of GC. LPS treatment was able to activate the production of ROS and lipid peroxides, however, this activation was significantly inhibited after GC treatment, and the inhibition increased with increasing doses of GC. Further examination of the changes in NF-κB signaling activation revealed that LPS-induced NF-κB signaling was significantly inhibited after GC treatment, and this inhibition increased with increasing the GC concentration., Conclusion: Glucocorticoids were able to inhibit neutrophil activation and reduce the formation of NETs. The research results provided a new research direction for clinical antithrombotic treatment.

Excessive inflammation is predominantly involved in the pathogenesis of acute lung injury (ALI). Recently, microRNAs (miRNAs) have been shown to act as an important regulator of inflammation. Hence, we investigated the levels of miR-182-5p and its functional role about regulating inflammation in LPS-induced ALI mice and RAW264.7 cells. Here, LPS induced-ALI model was established in male mice. By qRT-PCR, we found that the expression of miR-182-5p was significantly downregulated in lung tissue and bronchoalveolar lavage fluid (BALF), as well as decreased in LPS-treated RAW264.7 cells. In vitro, overexpression of miR-182-5p suppressed the inflammatory response, as evidenced by reduction of pro-inflammatory cytokines including interleukin (IL)-6, IL-1β, and tumor necrosis factor-α (TNF-α). Further experiments revealed that toll-like receptor 4 (TLR4) was the target of miR-182-5p, which was confirmed by luciferase activity assay. Moreover, RAW264.7 cells transfected with pcDNA-TLR4 plasmid abrogated the protective effects of miR-182-5p against LPS-induced inflammatory response. Additionally, we observed that overexpression of miR-182-5p blocked LPS-induced activation of the NF-κB signaling pathway by targeting TLR4. Collectively, the findings of our study indicate that miR-182-5p inhibits the inflammatory response by modulating TLR4/NF-κB signaling pathway in LPS-treated RAW264.7 cells., Competing Interests: None., (IJCEP Copyright © 2018.)