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In this work, the effect of gas jets used in the deep vertical vibratory compaction technique are studied. Gas jets play a vital role in treating structured loess foundations by the pneumatic-vibratory probe compaction method. Utilizing the geotechnical particle finite-element method numerically, we estimate the limit gas injection pressure and delineate the injection-induced damage and plastic zones. The behavior of structured soil is described using an elastoplastic constitutive model considering its structure evolution. The analysis of structured loess under gas injection is based on the cavity expansion approach. Experimentally, we performed a scale model test of gas injection to investigate the mechanism of the gas jets on the surrounding soil and compared relevant results with numerical results. Numerical results show that the limit gas injection pressure for structured loess beyond a depth of 8.0 m ranges from 1,409.7 to 1,467.2 kPa, increasing with the increase of overburden depth while the current cavity expansion radius decreases. The radius of the plastic zone induced by cavity expansion is 2.0 to 3.0 times the current cavity radius within this depth range; for the damage zone, however, it ranges from 0.1 to 0.4 times. The horizontal pressure recorded during the model test is observed to be lower compared with the numerical simulation results. This discrepancy can be attributed to factors such as the neglect of gas leakage within the soil and the utilization of a uniform parameter. The gas jets expand soil in cyclic shear form. It goes through a process from destruction of soil structure to compression in the horizontal direction; then, its pressure gradually drops to zero in the expansion direction of the dominant channel in soil. [ABSTRACT FROM AUTHOR]

The vibratory probe compaction method may sometimes fail to proceed smoothly due to the hard layer encountered during treatment of collapsible loess foundation. To this end, high-pressure water jetting around the traveling drill bit was used to soften the soil layer to assist the vibratory probe in sinking. However, due to the shortage of water resources in northwest China, a measure to reduce water consumption and add hydrochloric acid solution was adopted. To clarify the effect of the hydrochloric acid solution on the engineering characteristics of loess, this study conducted a series of geotechnical tests on remolded loess samples mixed with different concentrations of hydrochloric acid solution at the same dry density. The test results showed the pH values of all the sample leachates ranged from 7.83 to 7.64, and they had little effect on the surrounding environment. The coagula generated from the reaction between the acid solution with the original cementing material inside the loess enhanced the cementation between the soil particles and filled the gaps between the particles. The formation of this new structure gave the sample a strong ability to resist collapsing deformation, which was reflected in the acid-added sample having a smaller collapse coefficient than the water-added sample after the last stage of the collapsibility test. However, because the maximum dry density of the mixture increased with the increase of the acid concentration, the degree of compaction of the acid-added sample at the same dry density was insufficient, resulting in considerably bigger and more macro pores than that of water-added sample. It further caused the strength and disintegration characteristics of the sample to deteriorate with the increase of the acid concentration. The application of acid-added loess as a compacted filler is feasible for the construction of the vibratory probe compaction method in the loess area, which provides a new method for the treatment of collapsible loess foundation. [ABSTRACT FROM AUTHOR]

Long noncoding RNAs have been reported to be important regulators in numerous cancers. In this study, we found that HOXC13 antisense RNA (HOXC13‐AS) was highly expressed in head and neck squamous carcinoma (HNSC) tissues in The Cancer Genome Atlas database. Nasopharyngeal carcinoma (NPC) belongs to HNSC. Therefore, we further investigated the potential role of HOXC13‐AS in NPC. Quantitative reverse transcription polymerase chain reaction examination revealed that HOXC13‐AS was markedly upregulated in NPC tissues and cell lines. Furthermore, HOXC13‐AS was identified as an independent prognosis factor by Cox regression analyses. Subsequently, functional assay revealed that knockdown of HOXC13‐AS impaired cell proliferation, migration, and invasion. Mechanistically, RIP and luciferase reporter analysis confirmed that miR‐383‐3p was a target of HOXC13‐AS. Besides, high mobility group AT‐hook 2 (HMGA2) was proved to be a target of miR‐383‐3p in NPC. Finally, rescue assays demonstrated that HOXC13‐AS functioned as a competing endogenous RNAs to enhance the expression of HMGA2 via sponging miR‐383‐3p. This study suggested that HOXC13‐AS exerted oncogenic function in NPC via regulating miR‐383‐3p/HMGA2 axis, indicating HOXC13‐AS may be a potential therapeutic target for patients with NPC. [ABSTRACT FROM AUTHOR]

Cellular heterogeneity in nasopharyngeal cancer (NPC) and oral cancer remains unclear. In the current study, using single‐cell RNA sequencing techniques, we investigated the cellular landscape in NPC and oral cancers. We identified a diverse range of cell types within the tumor microenvironment (TME) and variations in cell infiltration between NPC and oral cancer. In oral cancer, we observed a predominant infiltration of epithelial cells, fibroblasts, and endothelial cells (ECs), while T cells were the main infiltrating cell population in NPCs. We further classified these infiltrating cells into subclusters. Additionally, we observed complex interactions among cells that led to distinct trajectories. In particular, a unique epithelial subcluster with high expression of major histocompatibility complex class II (MHC‐II) molecules was correlated with a favorable outcome and infiltration of CD4+ T cells. In addition, MHC‐II+ epithelial cells inhibited mouse tumor growth and promoted T‐cell infiltration. Consequently, our findings provide a deep understanding of the TME showing a significant prognostic value and therapeutic potential. [ABSTRACT FROM AUTHOR]

Objectives: Laryngeal cancer (LC), with a relatively rare diagnosis, is a primary malignancy originating from laryngeal mucosa. This study investigated the mechanisms of microRNA (miR)- 340-5p in LC cell proliferation and invasion., Methods: The expression patterns of miR-340-5p, long non-coding RNA (lncRNA) nuclear paraspeckle assembly transcript 1 (NEAT1), and matrix metallopeptidase 11 (MMP11) in LC cells, tissues, and para-carcinoma tissues, and human bronchial epithelial cells (HBEC) were examined via RT-qPCR. The effects of elevating or silencing miR-340-5p on LC cell proliferation and invasion were examined. The subcellular localization of lncRNA NEAT1 was determined. The binding relations among miR-340-5p, lncRNA NEAT1, and MMP11 were verified. Functional rescue experiments were designed to verify the functions of lncRNA NEAT1 and MMP11 on LC cell proliferation and invasion. Nude-mouse tumor models were established to assess the role of miR-340-5p in LC in vivo., Results: miR-340-5p was under-expressed in LC, and miR-340-5p overexpression repressed LC cell proliferation and invasion. Mechanically, miR-340-5p decreased lncRNA NEAT1 stability via directly binding to lncRNA NEAT1 and thus declined lncRNA NEAT1 expression in LC cells, while lncRNA NEAT1 accelerated MMP11 transcription via binding to heat shock factor 1 (HSF1). Overexpression of lncRNA NEAT1 or MMP11 reversed the repression of miR-340-5p overexpression on LC cell proliferation and invasion. In vivo, miR-340-5p overexpression repressed the tumor growth., Conclusion: miR-340-5p overexpression reduced lncRNA NEAT1 stability via binding to lncRNA NEAT1, which declined lncRNA NEAT1 expression and reduced the binding of lncRNA NEAT1 to HSF1 to further inhibit MMP11 transcription, thus repressing LC cell proliferation and invasion., (Copyright © 2022 Elsevier GmbH. All rights reserved.)