Solidification cracking(SC)of 2024 high-strength aluminium alloy during fusion welding or additive manufacturing has been a long-term issue.In this work,crack-free weld could be obtained using a Zr-core-Alshell wire(Z...Solidification cracking(SC)of 2024 high-strength aluminium alloy during fusion welding or additive manufacturing has been a long-term issue.In this work,crack-free weld could be obtained using a Zr-core-Alshell wire(ZCASW filler material,a novel filler)coupled with an oscillating laser-arc hybrid welding process,and we investigated the solidification cracking susceptibility(SCS)and cracking behavior of AA2024 weld fabricated with different filler materials.The cracking inhibition mechanism of the weld fabricated with ZCASW filler material was elucidated by combined experiments and phase-field simulation.The results show that the effectiveness of filler materials in reducing the SC gradually improves in the order of ER2319 filler material<ER4043 filler material<ZCASW filler material.The main cracking(when using the ER2319 filler material)branches and the micro cracking branches interact with each other to produce cracking coalescence,which aggravates the cracking propagation.The formation of the Al_(3) Zr phase(when using the ZCASW filler material)promotes heterogeneous nucleation of α-Al,thereby resulting in finer and equiaxed non-dendrite structures,which shortens the liquid phase channels and decreases cracking susceptibility index|d T/d(f_(s))^(1/2)|(T is temperature and f_(s) is solidification fraction)at final solidification.A higher proportion(7.65%area fraction)of inter-dendrite phase with spherical distribution state,a shorter(8.6 mm liquid channel length)inter-dendrite phase coupled with round non-dendrite structure(6μm dendrite size)effectively inhibit the SC.The present study can be a useful database for welding and additive manufacturing of AA2024.展开更多
酰基辅酶A合成酶短链家族成员1(acyl-CoA synthetase short-chain family member 1,ACSS1)是定位于线粒体基质的关键代谢酶,主要功能是通过催化乙酸与辅酶A合成乙酰辅酶A,进入三羧酸(TCA)循环,经氧化分解产生ATP,为机体供能。其在细胞...酰基辅酶A合成酶短链家族成员1(acyl-CoA synthetase short-chain family member 1,ACSS1)是定位于线粒体基质的关键代谢酶,主要功能是通过催化乙酸与辅酶A合成乙酰辅酶A,进入三羧酸(TCA)循环,经氧化分解产生ATP,为机体供能。其在细胞能量稳态、脂质合成和表观遗传调控中发挥主要作用。ACSS1具有明确的基因定位和组织特异性表达模式,其蛋白结构保守。在葡萄糖缺乏或应激状态下,ACSS1可利用乙酸等替代碳源合成乙酰辅酶A,为TCA循环提供底物,维持ATP生成,从而保障心、脑等高耗能组织的能量稳定。其分子结构包含保守的赖氨酸乙酰化位点(小鼠K635/人类K642),该位点受到沉默信息调节转录因子3(Silent information regulator transcript 3,SIRT3)去乙酰化酶的动态调控,尤其在营养剥夺(如禁食)或氧化应激条件下,SIRT3通过去乙酰化激活ACSS1酶活性,促进乙酸利用以维持能量平衡。在正常生理状态下,ACSS1参与饥饿能量维持、肝脏生酮及心脏ATP供应。在病理状态下,ACSS1功能紊乱与多种疾病相关:在肿瘤中支持癌细胞低营养生存;其功能下降可能导致神经退行性疾病中的能量衰竭;此外还与脂肪肝、肌肉减少症等代谢性疾病密切相关。通过对现有研究的系统梳理,本综述旨在为理解ACSS1在能量代谢中的调控通路及分子机制提供理论依据。展开更多
基金financially supported by the National Natural Science Foundation of China under Grant Nos.52305467,52188102,U22A20196,and 52075201the Guangdong Basic and Applied Basic Research Foundation Nos.2023A1515010081 and 2022B1212020003the Fundamental Research Funds for the Central Universities under Grant No.YCJJ20230360.
文摘Solidification cracking(SC)of 2024 high-strength aluminium alloy during fusion welding or additive manufacturing has been a long-term issue.In this work,crack-free weld could be obtained using a Zr-core-Alshell wire(ZCASW filler material,a novel filler)coupled with an oscillating laser-arc hybrid welding process,and we investigated the solidification cracking susceptibility(SCS)and cracking behavior of AA2024 weld fabricated with different filler materials.The cracking inhibition mechanism of the weld fabricated with ZCASW filler material was elucidated by combined experiments and phase-field simulation.The results show that the effectiveness of filler materials in reducing the SC gradually improves in the order of ER2319 filler material<ER4043 filler material<ZCASW filler material.The main cracking(when using the ER2319 filler material)branches and the micro cracking branches interact with each other to produce cracking coalescence,which aggravates the cracking propagation.The formation of the Al_(3) Zr phase(when using the ZCASW filler material)promotes heterogeneous nucleation of α-Al,thereby resulting in finer and equiaxed non-dendrite structures,which shortens the liquid phase channels and decreases cracking susceptibility index|d T/d(f_(s))^(1/2)|(T is temperature and f_(s) is solidification fraction)at final solidification.A higher proportion(7.65%area fraction)of inter-dendrite phase with spherical distribution state,a shorter(8.6 mm liquid channel length)inter-dendrite phase coupled with round non-dendrite structure(6μm dendrite size)effectively inhibit the SC.The present study can be a useful database for welding and additive manufacturing of AA2024.
文摘酰基辅酶A合成酶短链家族成员1(acyl-CoA synthetase short-chain family member 1,ACSS1)是定位于线粒体基质的关键代谢酶,主要功能是通过催化乙酸与辅酶A合成乙酰辅酶A,进入三羧酸(TCA)循环,经氧化分解产生ATP,为机体供能。其在细胞能量稳态、脂质合成和表观遗传调控中发挥主要作用。ACSS1具有明确的基因定位和组织特异性表达模式,其蛋白结构保守。在葡萄糖缺乏或应激状态下,ACSS1可利用乙酸等替代碳源合成乙酰辅酶A,为TCA循环提供底物,维持ATP生成,从而保障心、脑等高耗能组织的能量稳定。其分子结构包含保守的赖氨酸乙酰化位点(小鼠K635/人类K642),该位点受到沉默信息调节转录因子3(Silent information regulator transcript 3,SIRT3)去乙酰化酶的动态调控,尤其在营养剥夺(如禁食)或氧化应激条件下,SIRT3通过去乙酰化激活ACSS1酶活性,促进乙酸利用以维持能量平衡。在正常生理状态下,ACSS1参与饥饿能量维持、肝脏生酮及心脏ATP供应。在病理状态下,ACSS1功能紊乱与多种疾病相关:在肿瘤中支持癌细胞低营养生存;其功能下降可能导致神经退行性疾病中的能量衰竭;此外还与脂肪肝、肌肉减少症等代谢性疾病密切相关。通过对现有研究的系统梳理,本综述旨在为理解ACSS1在能量代谢中的调控通路及分子机制提供理论依据。
