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RISS 인기검색어
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- 저자 : Xu Xinrui (검색결과 3 건)
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Required Active Earth Pressure for 3D ERSS Following a Modified Mohr-Coulomb Strength Criterion
Jingshu Xu,Xinrui Wang,Liyun Li,Xiuli Du 대한토목학회 2024 KSCE Journal of Civil Engineering Vol.28 No.7
Exploiting the linear Mohr-Coulomb strength criterion, the stability computation for earth retaining structures (ERSs) by estimating the active earth pressure has been mainly conducted by setting the plane strain 2D. In this research, the modified MC strength criterion with reduced tensile strength is put into use for the stability analysis of ERSs employing a 3D multi-cone collapse analysis mechanism. After computing the coefficient of active earth pressure, the optimal results are captured from a combination of the genetic algorithm and particle swarm optimization. Research findings are validated through comparison, while the influences of soil tensile strength threshold and 3D geometrical features over the stability measures and critical failure modes of ERSs are explored by parametric assessment. It is revealed in this work that the linear MC strength criterion derives conservative estimates of the active earth pressure. The tensile strength threshold of soil has a pronounced effect on both the objective solutions and failure shapes, especially for the ERSs under a greater dimensionless cohesion c/H. This work provides a straightforward approach to perform a 3D stability analysis of ERSs considering a tensile strength cutoff, without a pre-assumed distribution of the rupture angle.
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Liu Junjie,Chu Chenxiao,Qin Xianzhong,Meng Weisong,Xu Xinrui,Wang Bo,Cai Feipeng 한국세라믹학회 2023 한국세라믹학회지 Vol.60 No.3
High nickel ternary cathode materials (Ni ≥ 90%) have great potential for application as power batteries in electric vehicles and have become a hot spot for research on cathode materials. However, the residual Li on the surface of the high Ni ternary cathode materials prepared by solid-phase sintering is one of the main reasons affecting their electrochemical performance. It is found that Li1 + x(Ni0.9Co0.05Mn0.05)1-xO2 with x = 0.3, which has a discharge-specific capacity of 205.74 mAh g −1 at 2.7–4.3 V, 0.1C and 184.1 mAh g −1 at 1 C, retained 89% of its initial discharge capacity after 100 cycles at 1 C. The discharge-specifi c capacity at 10 C was 153.14 mAh g −1. In addition, the Li residue of NCM90-1.03 was 17,189.959 ppm, and the total alkalinity was 4196.896 ppm. The results by X-ray diff raction (XRD) and scanning electron microscope (SEM) showed that when the Li excess was 0.3%, it was possible to obtain uniform particle size, a wider Li layer, and reduced cation mixing. Therefore, choosing the right amount of excess Li can stimulate the application prospect of NCM90 in new energy vehicles.
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Zhang Jintao,Zhang Dong,Pan Yun,Liu Xiaofei,Xu Jiawei,Qiao Xinrui,Cui Wenjing,Dong Liang 대한천식알레르기학회 2022 Allergy, Asthma & Immunology Research Vol.14 No.2
Purpose: Tumor necrosis factor-like ligand 1A (TL1A), especially its secreted form, has been shown to contribute to eosinophilic inflammation and mucus production, cardinal features of asthma, through its receptor, death receptor 3 (DR3). However, the role of the TL1A-DR3 axis in asthma, especially in terms of airway remodeling, has not yet been fully understood. Methods: The present study investigated the expression and secretion of TL1A in the lung and human bronchial epithelial cells. DR3 small interfering RNA (siRNA), TL1A siRNA, and truncated plasmids were used respectively to identify the function of the TL1A-DR3 axis in vitro. To further validate the roles of the TL1A-DR3 axis in asthma, we collected airway biopsies and sputa from asthmatic patients and constructed a mouse model following rTL1A administration, DR3 knockdown, and TL1A knockout, the asthma-related inflammatory response and the pathological changes in airways were analyzed using various experimental methods. Associated signaling pathways downstream of TL1A knockout in the mouse model were analyzed using RNA sequencing. Results: TL1A, especially its non-secreted form (nsTL1A) was involved in the remodeling process in asthmatics’ airways. Knockdown of TL1A or its receptor DR3 decreased the expression of fibrosis-associated protein in BEAS-2B cells. Reversely, overexpression of nsTL1A in airway epithelial cells facilitated the transforming growth factor-β-induced remodeling progress. In the asthma mouse model, activating the TL1A-DR3 axis contributes to airway inflammation, remodeling, and tissue destruction. Reciprocally, DR3 knockdown or TL1A knockout partly reverses airway remodeling in the asthma model induced by ovalbumin. Conclusions: Our results confirm differential TL1A expression (including its secreted and non-secreted form) in asthma, which modulates remodeling. The shared mechanism of action by which nsTL1A and secreted TL1A exert their effects on asthma development might be mediated via the nuclear factor-κB pathway. The TL1A-DR3 axis presents a promising therapeutic target in asthma.
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