Experimental study on vibration serviceability of cold-formed thin-walled steel floor

Bin Chen,Liang Cao,Faming Lu,Y. Frank Chen 국제구조공학회 2023 Steel and Composite Structures, An International J Vol.46 No.4

In this study, on-site testing was carried out to investigate the vibration performance of a cold-formed thin-walled steel floor system. Ambient vibration, walking excitation (single and double persons), and impulsive excitation (heel-drop and jumping) were considered to capture the primary vibration parameters (natural frequencies, damping ratios, and mode shapes) and vertical acceleration response. Meanwhile, to discuss the influence of cement fiberboard on structural vibration, the primary vibration parameters were compared between the systems with and without the installation of cement fiberboard. Based on the experimental analysis, the cold-formed thin-walled steel floor possesses high frequency (> 10 Hz) and damping (> 2%); the installed cement fiberboard mainly increases the mass of floor system without effectively increasing the floor stiffness and may reduce the effects of primary vibration parameters on acceleration response; and the human-structure interaction should be considered when analyzing the vibration serviceability. The comparison of the experimental results with those in the AISC Design Guide indicates that the cold-formed thin-walled steel floor exhibits acceptable vibration serviceability. A crest factor βrp (ratio of peak to root-mean-square accelerations) is proposed to determine the root-mean-square acceleration for convenience.

Stochastic approximation Monte Carlo importance sampling for approximating exact conditional probabilities

Cheon, Sooyoung,Liang, Faming,Chen, Yuguo,Yu, Kai Springer-Verlag 2014 Statistics and computing Vol.24 No.4

ETV4 facilitates proliferation, migration, and invasion of liver cancer by mediating TGF-β signal transduction through activation of B3GNT3

Zhou Zhongcheng,Wu Bin,Chen Jing,Shen Yiyu,Wang Jing,Chen Xujian,Fei Faming,Li Liang 한국유전학회 2023 Genes & Genomics Vol.45 No.11

Background Metastasis of liver cancer (LC) is the main cause of its high mortality. ETV4 is a critical regulatory factor in promoting LC progression, but the mechanism that ETV4 impacts LC proliferation, migration, and invasion is poorly understood. Objective Investigation of the molecular mechanism of LC metastasis is conducive to developing effective drugs that prevent LC metastasis. Methods Expression of ETV4 and its target gene B3GNT3 in LC tissue was analyzed by bioinformatics, and the result was further verified in LC cells by qRT-PCR. In vitro cellular assays evaluated the impact of ETV4 on the proliferation, migration, and invasion of LC cells. Chromatin immunoprecipitation (ChIP) and dual-luciferase reporter gene assay were conducted to analyze the interaction between B3GNT3 and ETV4. SB525334 suppressor was used to treat and access the activation of ETV4 on the TGF-β pathway. Results We discovered that ETV4 and B3GNT3 were evidently up-regulated in LC, and high expression of ETV4 was coupled to the increase of proliferation, migration, and invasion of LC cells and epithelial-mesenchymal transition ability. Besides, ETV4 could bind to the B3GNT3 promoter and activate its transcription. Knockdown of B3GNT3 could prominently suppress the effect of up-regulated ETV4 on LC cells. Meanwhile, ETV4 could activate the TGF-β signaling pathway via B3GNT3, while SB525334 treatment notably repressed the functions of ETV4. Conclusion ETV4 emerges as a driven oncogene in LC, and the ETV4/B3GNT3-TGF-β pathway promotes proliferation, migration, invasion, and epithelial-mesenchymal transition progress of LC. Inhibition of the pathway may provide an underlying method for the prevention and treatment of LC metastasis.

Controlled Synthesis of Pt–Pd Nanoparticle Chains with High Electrocatalytic Activity Based on Insulin Amyloid Fibrils

LI HOU,Yunfeng Niu,Yan Wang,YANG JIANG,Rongna Chen,Tianran Ma,FAMING GAO 성균관대학교(자연과학캠퍼스) 성균나노과학기술원 2016 NANO Vol.11 No.6

Here, we present a simple and novel method based on using insulin amyloid fibrils (INSAFs) as sacrificial templates for the construction of Pt–Pd nanoparticle chains (Pt–PdNPCs) under mild conditions. By incubating INSAFs in metal salt solution and then reduction, Pt–Pd nanoparticles with an uniform particle size of around 2.5 nm nucleated and grew along the axial direction of INSAFs, and thus formed a long chain structure with length up to several micrometers. The as-prepared Pt–PdNPCs exhibit an improved catalytic activity for lowtemperature CO and methanol oxidation and possess greater CO tolerance compared with the commercial Pt/C catalyst, which makes them promising for a variety of possible catalytic applications.

Hypoxia Mediates Runt-Related Transcription Factor 2 Expression via Induction of Vascular Endothelial Growth Factor in Periodontal Ligament Stem Cells

Xu, Qian,Liu, Zhihua,Guo, Ling,Liu, Rui,Li, Rulei,Chu, Xiang,Yang, Jiajia,Luo, Jia,Chen, Faming,Deng, Manjing Korean Society for Molecular and Cellular Biology 2019 Molecules and cells Vol.42 No.11

Periodontitis is characterized by the loss of periodontal tissues, especially alveolar bone. Common therapies cannot satisfactorily recover lost alveolar bone. Periodontal ligament stem cells (PDLSCs) possess the capacity of self-renewal and multilineage differentiation and are likely to recover lost alveolar bone. In addition, periodontitis is accompanied by hypoxia, and hypoxia-inducible $factor-1{\alpha}$ ($HIF-1{\alpha}$) is a master transcription factor in the response to hypoxia. Thus, we aimed to ascertain how hypoxia affects runt-related transcription factor 2 (RUNX2), a key osteogenic marker, in the osteogenesis of PDLSCs. In this study, we found that hypoxia enhanced the protein expression of $HIF-1{\alpha}$, vascular endothelial growth factor (VEGF), and RUNX2 ex vivo and in situ. VEGF is a target gene of $HIF-1{\alpha}$, and the increased expression of VEGF and RUNX2 proteins was enhanced by cobalt chloride ($CoCl_2$, $100{\mu}mol/L$), an agonist of $HIF-1{\alpha}$, and suppressed by 3-(5'-hydroxymethyl-2'-furyl)-1-benzyl indazole (YC-1, $10{\mu}mol/L$), an antagonist of $HIF-1{\alpha}$. In addition, VEGF could regulate the expression of RUNX2, as RUNX2 expression was enhanced by human VEGF ($hVEGF_{165}$) and suppressed by VEGF siRNA. In addition, knocking down VEGF could decrease the expression of osteogenesis-related genes, i.e., RUNX2, alkaline phosphatase (ALP), and type I collagen (COL1), and hypoxia could enhance the expression of ALP, COL1, and osteocalcin (OCN) in the early stage of osteogenesis of PDLSCs. Taken together, our results showed that hypoxia could mediate the expression of RUNX2 in PDLSCs via $HIF-1{\alpha}$-induced VEGF and play a positive role in the early stage of osteogenesis of PDLSCs.

Hypoxia Mediates Runt-Related Transcription Factor 2 Expression via Induction of Vascular Endothelial Growth Factor in Periodontal Ligament Stem Cells

Manjing Deng,Qian Xu,Zhihua Liu1,Ling Guo,Rui Liu,Rulei Li,Xiang Chu,Jiajia Yang,Jia Luo,Faming Chen 한국분자세포생물학회 2019 Molecules and cells Vol.42 No.11

Periodontitis is characterized by the loss of periodontal tissues, especially alveolar bone. Common therapies cannot satisfactorily recover lost alveolar bone. Periodontal ligament stem cells (PDLSCs) possess the capacity of self-renewal and multilineage differentiation and are likely to recover lost alveolar bone. In addition, periodontitis is accompanied by hypoxia, and hypoxia-inducible factor-1α (HIF-1α) is a master transcription factor in the response to hypoxia. Thus, we aimed to ascertain how hypoxia affects runt-related transcription factor 2 (RUNX2), a key osteogenic marker, in the osteogenesis of PDLSCs. In this study, we found that hypoxia enhanced the protein expression of HIF-1α, vascular endothelial growth factor (VEGF), and RUNX2 ex vivo and in situ. VEGF is a target gene of HIF-1α, and the increased expression of VEGF and RUNX2 proteins was enhanced by cobalt chloride (CoCl2, 100 μmol/L), an agonist of HIF-1α, and suppressed by 3-(5′-hydroxymethyl-2′-furyl)-1-benzyl indazole (YC-1, 10 μmol/L), an antagonist of HIF-1α. In addition, VEGF could regulate the expression of RUNX2, as RUNX2 expression was enhanced by human VEGF (hVEGF165) and suppressed by VEGF siRNA. In addition, knocking down VEGF could decrease the expression of osteogenesis-related genes, i.e., RUNX2, alkaline phosphatase (ALP), and type I collagen (COL1), and hypoxia could enhance the expression of ALP, COL1, and osteocalcin (OCN) in the early stage of osteogenesis of PDLSCs. Taken together, our results showed that hypoxia could mediate the expression of RUNX2 in PDLSCs via HIF-1α-induced VEGF and play a positive role in the early stage of osteogenesis of PDLSCs