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1.
Materials (Basel) ; 14(9)2021 Apr 22.
Artigo em Inglês | MEDLINE | ID: mdl-33922060

RESUMO

As is known to all, the incapacity to nucleate holes automatically in the design domain is one of the main issues of the classical level set topology optimization method. To solve the issue of hole nucleation, this paper employs the bi-directional evolutionary structural optimization (BESO) method based on the material removal scheme and the frequently used topological sensitivity and proposes the combining BESO and topological sensitivity (CBT) method for level set topology optimization. This method can replace the existing hole nucleation method for level set topology optimization. First, the topological sensitivity is combined with BESO, and the BESO method based on topological sensitivity is proposed. Second, the method is integrated into level set topology optimization to solve the issue of hole nucleation. Two sensitivity thresholds are defined depending on the evolutionary volume ratio and boundary topological sensitivity, respectively, and the smaller one is used as the sensitivity threshold for hole nucleation. The material is removed from the design domain to nucleate holes based on this threshold. Three classical two-dimensional numerical examples are used to validate the proposed hole nucleation method.

2.
Materials (Basel) ; 12(18)2019 Sep 18.
Artigo em Inglês | MEDLINE | ID: mdl-31540498

RESUMO

In harsh environments, the corrosion damage of steel structures and equipment is a serious threat to the operational safety of service. In this paper, a Zn-Al diffusion layer was fabricated on 45 steel by the Mechanical Energy Aided Diffusion Method (MEADM) at 450 °C. The microstructure and composition, the surface topography, and the electrochemical performance of the Zn-Al diffusion layer were analyzed before and after corrosion. The results show that the Zn-Al diffusion layer are composed of Al2O3 and Γ1 phase (Fe11Zn40) and δ1 phase (FeZn6.67, FeZn8.87, and FeZn10.98) Zn-Fe alloy. There is a transition zone with the thickness of about 5 µm at the interface between the Zn-Al diffusion layer and the substrate, and a carbon-rich layer exists in this zone. The full immersion test and electrochemical test show that the compact corrosion products produced by the initial corrosion of the Zn-Al diffusion layer will firmly bond to the Zn-Al diffusion layer surface and fill the crack, which plays a role in preventing corrosion of the corrosive medium and reducing the corrosion rate of the Zn-Al diffusion layer. The salt spray test reveals that the initial corrosion products of the Zn-Al diffusion layer are mainly ZnO and Zn5(OH)8Cl2H2O. New corrosion products such as ZnAl2O4, FeOCl appear at the middle corrosion stage. The corrosion product ZnAl2O4 disappears, and the corrosion products Zn(OH)2 and Al(OH)3 appear at the later corrosion stage.

3.
Peptides ; 99: 92-98, 2018 01.
Artigo em Inglês | MEDLINE | ID: mdl-29183756

RESUMO

The results of our and other's studies showed that activation of galanin receptor 1 could mitigate insulin resistance via promoting glucose transporter 4 (GLUT4) expression and translocation in the skeletal muscle of rats. But no literature are available regarding the effect of galanin receptor 2 (GALR2) on insulin resistance in skeletal muscle of type 2 diabetes. Herein, in this study we intended to survey the effect of GALR2 and its signal mechanisms in the mice with high fat diet-induced obese. The mice were intraperitoneally injected with vehicle, GALR2 agonist M1145 and antagonist M871 respectively once a day for continuous 21 days. The skeletal muscles were processed for determination of glucose uptake, and GLUT4 mRNA and protein expression levels. The PGC-1α, AKT, p38MAPK, AS160, pAKT, pP38MAPK and pAS160 expression levels were quantitatively assessed too. We found that pharmacological activation of GALR2 enhanced energy expenditure, and increased GLUT4 expression and translocation in skeletal muscle of mice during high-fat diet regimens. Activation of GALR2 alleviated insulin resistance through P38MAPK/PGC-1α/GLUT4 and AKT/AS160/GLUT4 pathway in the skeletal muscle of mice. Overall, these results identify that GALR2 is a regulator of insulin resistance and activation of GALR2 represents a promising strategy against obesity-induced insulin resistance.


Assuntos
Galanina/análogos & derivados , Resistência à Insulina , Proteínas Musculares , Músculo Esquelético/metabolismo , Obesidade/metabolismo , Receptor Tipo 2 de Galanina , Animais , Galanina/farmacologia , Glucose/metabolismo , Masculino , Camundongos , Proteínas Musculares/agonistas , Proteínas Musculares/metabolismo , Músculo Esquelético/patologia , Obesidade/tratamento farmacológico , Obesidade/patologia , Receptor Tipo 2 de Galanina/agonistas , Receptor Tipo 2 de Galanina/metabolismo
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