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Your search keyword '"Tang, Yunlong"' showing total 124 results
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37. Molecular dynamics simulations to understand the mechanical behavior of functional gradient nano-gyroid structures.

Author

Dai, Rui, Li, Dawei, Liao, Wenhe, Sun, Haofan, Tang, Yunlong, and Nian, Qiong

Subjects
MOLECULAR dynamics, SPECIFIC gravity, STRESS concentration, MECHANICAL energy
Abstract

Gyroid structure, a nature inspired cellular architecture, is under extensive exploration recently due to its structure continuity, uniform stress distribution under compression, and stable collapse mechanism during deformation. However, when combining with a functional gradient, the Gyroid structure can perform much different mechanical behavior from its homogeneous counterpart. Herein, bottom-up computational modeling is performed to investigate the mechanics of functional gradient nano-gyroid structure made of copper (Cu). Our work reveals that its mechanical properties degrade with a density that is much slower than those of homogeneous gyroid structure. The scaling of yield strength (σ y) to the relative density (ρ ′ ) for the functional gradient gyroid structure is in the factor of 1.5. Moreover, the layer-by-layer collapsing mechanism yields significantly better mechanical energy absorption ability. This study not only leads to insightful understanding of the deformation mechanisms in nonuniform gyroid structures but also promotes the development of the functional gradient cellular materials. [ABSTRACT FROM AUTHOR]

Published
2022
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38. Evodiamine attenuates oxidative stress and ferroptosis by inhibiting the MAPK signaling to improve bortezomib‐induced peripheral neurotoxicity.

Author

Tang, Yunlong, Gu, Weiying, and Cheng, Lingling

Subjects
OXIDATIVE stress, MITOGEN-activated protein kinases, NEUROTOXICOLOGY, DORSAL root ganglia, REACTIVE oxygen species, NERVOUS system regeneration
Abstract

Background: Bortezomib (BTZ) is a commonly used antitumor drug, but its peripheral neuropathy side effect poses a limitation on its dosage. Evodiamine (EVO) exhibits various biological activities, including antioxidant, anti‐inflammatory, and anticancer effects. The purpose of this investigation is to confirm the impact of EVO on BTZ‐induced peripheral neurotoxicity. Methods: GeneCards and HERB were applied to analyze the targets of peripheral neurotoxicity and EVO. The Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways enrichment analysis of the hub genes were identified by DAVID. Rat dorsal root ganglion neurons (DRGs) and rat RSC96 Schwann cells (SCs) were treated with BTZ to simulate peripheral neurotoxicity. BTZ‐induced peripheral neurotoxicity was assessed by detecting cell viability, proliferation, oxidative stress, and ferroptosis in DRGs and SCs. The mitogen‐activated protein kinase (MAPK) signaling was scrutinized by Western blot assay. Results: The Venn diagram for the overlapping targets of EVO and peripheral neurotoxicity showed that EVO might regulate peripheral neurotoxicity by influencing cell oxidative stress, ferroptosis, and MAPK signaling pathway. EVO attenuated BTZ‐induced toxicity in DRGs and SCs. EVO attenuated BTZ‐induced oxidative stress damage in DRGs and SCs by reducing reactive oxygen species and malondialdehyde levels and enhancing glutathione level. EVO attenuated BTZ‐induced ferroptosis in DRGs and SCs. EVO inhibited BTZ‐induced activation of the MAPK signaling in DRGs and SCs. Activation of the MAPK signaling reversed the neuroprotective effect of EVO on BTZ‐induced oxidative stress injury and ferroptosis. Conclusion: EVO attenuated oxidative stress and ferroptosis by inhibiting the MAPK signaling to improve BTZ‐induced peripheral neurotoxicity. [ABSTRACT FROM AUTHOR]

Published
2024
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