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1.
Biomimetics (Basel) ; 8(2)2023 May 23.
Artigo em Inglês | MEDLINE | ID: mdl-37366810

RESUMO

Countersunk head bolted joints are one of the main approaches to joining carbon fiber-reinforced plastics, or CFRP. In this paper, the failure mode and damage evolution of CFRP countersunk bolt components under bending load are studied by imitating water bears, which are born as adult animals and have strong adaptability to life. Based on the Hashin failure criterion, we establish a 3D finite element failure prediction model of a CFRP-countersunk bolted assembly, benchmarked with the experiment. The analysis shows that the simulation results under specified parameters have a good correlation with the experimental results, and can better reflect the three-point bending failure and fracture of the CFRP-countersunk bolted assembly. Based on the specified parameter of the carbon lamina material change, we used the countersunk bolt preload to investigate the stress distribution near the counterbore zone, and to investigate the effect of bolt load on the three-point bending limit load. The results obtained using FEA calculations indicate that the stress distribution around the countersunk hole is related to the laminate direction. The bolt preloading force increasing reduces the load value at the initial damage, and the appropriate preload force will increase the ultimate load of the joint.

2.
Polymers (Basel) ; 15(7)2023 Mar 26.
Artigo em Inglês | MEDLINE | ID: mdl-37050261

RESUMO

In this research, the fatigue damage behavior under three-point bending of a composite joint incorporating a single countersunk fastener is investigated. Firstly, a self-developed fatigue test system was set up to test the fatigue characteristics of CFRP-countersunk bolted assembly under the displacement amplitude cycles of 103 to 106 to study the formation and expansion rule of damage and cracks. It found two typical damage processes, both of which involve some formal interface damage between fiber and matrix. Based on the experiment, a finite element fatigue damage analysis on this assembly was carried out according to the Hashin failure criterion. The simulation result shows an identical fatigue damage location and fatigue life with the experimental phenomenon. Moreover, it predicted the final fatigue life of the specimen under 10 hz cyclic loading with 1 mm displacement and 10 Nm bolt preloading. This research provides guidance for the engineering fatigue issues of single-bolted joint composite connection structures and provides a reference for the corresponding technical specifications formulation.

3.
PLoS One ; 8(8): e70658, 2013.
Artigo em Inglês | MEDLINE | ID: mdl-23940615

RESUMO

OBJECTIVE: This study was to investigate the molecular mechanisms underlying the 27nt-miRNA-mediated regulation of expression of the endothelial nitric oxide synthase (eNOS) gene. METHODS: Cell lines overexpressing 27nt-miRNA or its mutant were established by transfecting the miRNA expression vector into the endothelial cells. eNOS mRNA and protein expression were examined by RT-PCR and Western Blotting, respectively. Luciferase activity reporter system was used to study the target of 27nt-miRNA. RESULTS: The results showed that overexpression of 27nt-miRNA significantly inhibited eNOS mRNA level and protein expression, and reduced the eNOS transcriptional efficiency. Such inhibitory effects of 27nt-miRNA were attenuated by the sequence mutations in 27nt-miRNA. Interestingly, the transcription factor SP-1 expression was reduced by 27nt-miRNA. Meanwhile, overxpression of SP-1 protein partially restored eNOS expression, and rescued the 27nt-miRNA-mediated reduction of endothelial cell proliferation. Moreover, certain sites in the SP-1 mRNA were found to be the direct target of 27nt-miRNA by a luciferase reporter system. CONCLUSIONS: These results demonstrate that the 27nt-miRNA suppresses eNOS gene expression and SP-1 expression in vascular endothelial cells. The 27nt-miRNA directly target to SP-1 mRNA, thereby contributing to proliferation of endothelial cells.


Assuntos
Proliferação de Células , Células Endoteliais/enzimologia , MicroRNAs/genética , Óxido Nítrico Sintase Tipo III/genética , Fator de Transcrição Sp1/genética , Aorta/citologia , Células Cultivadas , Células Endoteliais/fisiologia , Endotélio Vascular/citologia , Repressão Enzimática , Expressão Gênica , Humanos , Íntrons , Interferência de RNA , Fator de Transcrição Sp1/metabolismo
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