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| 1 | Effects of Filler Metal Composition on Inclusions and Inclusion Defects for ER NiCrFe-7 Weldments显示文摘The effects of filler metal(FM) composition on inclusions and inclusion defects for ER NiCrFe-7 weldments have been investigated and analyzed.Results show that as Al,Ti content in FM increases from 0.14 wt%Al,0.30 wt% Ti to 0.42 wt%Al,0.92 wt%Ti,the Al,Ti reduction will increase during welding.Inclusion defects(point-like defects named by welding workers) are prone to form in the high Al,Ti content weldments.Inclusion defects with Mg,Ca,Al,and Ti as major metallic elements have been found on the surface and interior of the weldments,as Al,Ti content in FM is over 0.29 wt%Al,0.62 wt%Ti.Less Ti content in FM cannot prevent ductility-dip-cracking(DDC) through producing enough intragranular precipitates and lessening intergranular M_(23)C_6 precipitates.Nb can be used to replace Ti to reduce the sensitivity of the DDC in the NiCrFe-7 alloy weldments. | Wenlin Mo Shanping Lu Dianzhong Li Yiyi Li | 2013 | Journal of Materials Science & Technology2013，29，5： | 11 |
| 2 | Effects of Boron on the Microstructure,Ductility-dip-cracking,and Tensile Properties for NiCrFe-7 Weld Metal显示文摘The distribution of boron and the microstructure of grain boundary(GB) precipitates(M_(23)(C,B)_6 and M_2B)have been analyzed with their effects on the susceptibility of ductility-dip-cracking(DDC) and tensile properties for NiCrFe-7 weld metal,using optical microscopy(OM),secondary ion mass spectroscopy(SIMS),scanning electron microscopy(SEM),and transmission electron microscopy(TEM).The results show that boron segregates at GBs in NiCrFe-7 weld metal during the welding process.The segregation of boron at GBs promotes the formation of continuous M_(23)(C,B)_6 carbide chains and M_2B borides along GBs.The addition of boron aggravates GB embrittlement and causes more DDC in the weld metal,by its segregation at GBs presenting as an impurity,and promoting the formation of larger and continuous M_(23)(C,B)_6 carbides,and M_2B borides along GBs.DDC in the weld metal deteriorates the ductility and tensile strength of the weld metal simultaneously. | Wenlin Mo Xiaobing Hu Shanping Lu Dianzhong Li Yiyi Li | 2015 | Journal of Materials Science & Technology2015，31，12： | 9 |
| 3 | Experimental investigation and thermodynamic modeling of the U-Nb system显示文摘The phase equilibria and thermodynamic properties of the U-Nb system were investigated through experiments and thermodynamic modeling.In the experiments,a series of samples with different content of Nb were prepared by arc melting.The Nb content covers the entire composition range of the U-Nb binary system.After solidification,the samples were annealed and then analyzed by X-ray diffraction,scanning electron microscopy,energy dispersive X-ray spectroscopy,differential scanning calorimeter and neutron diffraction.The equilibrium phases,including γ1(U-rich bcc),αU,and γ2(U-depleted bcc),were determined in detail from the experimental characterization.The occurrence of the invariant reaction γ1→αU+γ2 was confirmed,and the reaction temperature and composition were accurately identified.Moreover,the experimental findings clarify the dispute between the Dwight and Terekhov theories regarding the phase region(i.e.,whether the phase region is αU+γ1 or βU+γ2).Furthermore,the U-Nb phase diagram was reassessed by incorporating the present experimental data and previously published reliable experimental data from the literature.A set of self-consistent thermodynamic parameters were developed using CALPHAD(Calculation of phase diagrams),and the calculations reasonably agree with the experimental observations. | Chuan Mo Wenlin Mo Peng Zhou BaiXue Bian Yong Du Tao Fa Pengguo Zhang Ruiwen Li Yanzhi Zhang Changsheng Zhang Yuanhua Xia Xiaolin Wang | 2021 | Journal of Materials Science & Technology2021，，22： | 0 |
| 4 | ZBTB7A governs 2-DG-inhibited glycolysis by regulating GLUT1 in nasopharyngeal carcinoma显示文摘Our previous studies suggested a potential interaction between the POK erythroid myeloid ontogenic factor ZBTB7A and glucose transporter 1(GLUT1)in nasopharyngeal carcinoma(NPC).This study was designed to confirm the interaction and further evaluate the precise mechanism by which ZBTB7A and GLUT1 regulate NPC development.The binding sites between ZBTB7A and the promoter of GLUT1 were predicted by bioinformatics.Gene expression was measured by quantitative real-time polymerase chain reaction(qPCR),western blotting,and immunohistochemistry.The activities of key glycolysis enzymes,including hexokinase(HK),pyruvate kinase(PK),lactate dehydrogenase(LDH),and lactate,were detected using specific enzyme-linked immunosorbent assay kits.The connection between ZBTB7A and GLUT1 was analyzed by dual-luciferase reporter assay and chromatin immunoprecipitation-qPCR.The vitality,proliferation,and tumorigenicity of the cells expressing different levels of ZBTB7A were tested by adding the glycolysis inhibitor 2-deoxy-D-glucose(2-DG),followed by MTT,colorimetric focus forming,and xenograft assays,respectively.Our results showed that high expression of GLUT1 was associated with late-stage NPC.After constructing stably transfected cells with lentiviruses,ZBTB7A was effectively knocked down in 5-8F cells(RNAi-5-8F)and overexpressed in 6-10B cells(ZBTB7A-6-10B).The up-or downregulation of GLUT1 secondary to ZBTB7A changes was also limited.The vitality and proliferation of the cells expressing low ZBTB7A were notably blocked by 2-DG.The cells expressing high ZBTB7A were not very sensitive to 2-DG.The growth of RNAi-5-8F xenografts was strongly suppressed by 2-DG.The activities of HK,PK,and LDH were suppressed by 2-DG in the cells expressing low ZBTB7A.RNAi-5-8F cells had the lowest 2-DG-induced lactate production.ZBTB7A directly suppressed the promoter region of GLUT1 to regulate GLUT1 expression.Thus,ZBTB7A controls the 2-DG-induced inhibition of glycolysis by affecting GLUT1. | FEI LIU JIAZHANG WEI JIAO LAN YONGLI WANG JIANXIANG YE CHENG SU MINGZHENG MO FENGZHU TANG BING LI MIN LI WEIMING DENG LINSONG YE WENLIN HUANG JINGJIN WENG WEI JIAO SHENHONG QU | 2022 | BIOCELL2022，46，12： | 0 |
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