Multistage heat treatment involving quenching(Q),lamellarizing(L),and tempering(T)is applied to marine 10Ni5CrMoV steel.The microstructure and mechanical properties were studied by multiscale characterizations,and the...Multistage heat treatment involving quenching(Q),lamellarizing(L),and tempering(T)is applied to marine 10Ni5CrMoV steel.The microstructure and mechanical properties were studied by multiscale characterizations,and the kinetics of reverse austenite transformation,strain hardening behavior,and toughening mechanism were further investigated.The lamellarized specimens possess low yield strength but high toughness,especially cryogenic toughness.Lamellarization leads to the development of film-like reversed austenite at the martensite block and lath boundaries,refining the martensite structure and lowering the equivalent grain size.Kinetic analysis of austenite reversion based on the JMAK model shows that the isothermal transformation is dominated by the growth of reversed austenite,and the maximum transformation of reversed austenite is reached at the peak temperature(750℃).The strain hardening behavior based on the modified Crussard-Jaoul analysis indicates that the reversed austenite obtained from lamellarization reduces the proportion of martensite,significantly hindering crack propagation via martensitic transformation during the deformation.As a consequence,the QLT specimens exhibit high machinability and low yield strength.Compared with the QT specimen,the ductile-brittle transition temperature of the QLT specimens decreases from-116 to-130℃due to the low equivalent grain size and reversed austenite,which increases the cleavage force required for crack propagation and absorbs the energy of external load,respectively.This work provides an idea to improve the cryogenic toughness of marine 10Ni5CrMoV steel and lays a theoretical foundation for its industrial application and comprehensive performance improvement.展开更多
Retinitis pigmentosa is a group of inherited diseases that lead to retinal degeneration and photoreceptor cell death.However,there is no effective treatment for retinitis pigmentosa caused by PDE6B mutation.Adeno-asso...Retinitis pigmentosa is a group of inherited diseases that lead to retinal degeneration and photoreceptor cell death.However,there is no effective treatment for retinitis pigmentosa caused by PDE6B mutation.Adeno-associated virus(AAV)-mediated gene therapy is a promising strategy for treating retinitis pigmentosa.The aim of this study was to explore the molecular mechanisms by which AAV2-PDE6B rescues retinal function.To do this,we injected retinal degeneration 10(rd10)mice subretinally with AAV2-PDE6B and assessed the therapeutic effects on retinal function and structure using dark-and light-adapted electroretinogram,optical coherence tomography,and immunofluorescence.Data-independent acquisition-mass spectrometry-based proteomic analysis was conducted to investigate protein expression levels and pathway enrichment,and the results from this analysis were verified by real-time polymerase chain reaction and western blotting.AAV2-PDE6B injection significantly upregulated PDE6βexpression,preserved electroretinogram responses,and preserved outer nuclear layer thickness in rd10 mice.Differentially expressed proteins between wild-type and rd10 mice were closely related to visual perception,and treating rd10 mice with AAV2-PDE6B restored differentially expressed protein expression to levels similar to those seen in wild-type mice.Kyoto Encyclopedia of Genes and Genome analysis showed that the differentially expressed proteins whose expression was most significantly altered by AAV2-PDE6B injection were enriched in phototransduction pathways.Furthermore,the phototransductionrelated proteins Pde6α,Rom1,Rho,Aldh1a1,and Rbp1 exhibited opposite expression patterns in rd10 mice with or without AAV2-PDE6B treatment.Finally,Bax/Bcl-2,p-ERK/ERK,and p-c-Fos/c-Fos expression levels decreased in rd10 mice following AAV2-PDE6B treatment.Our data suggest that AAV2-PDE6B-mediated gene therapy promotes phototransduction and inhibits apoptosis by inhibiting the ERK signaling pathway and upregulating Bcl-2/Bax expression in retinitis pigmentosa.展开更多
基金financially supported by the National Key K&D Program of China(No.2023YFE0200300)the National Natural Science Foundation of China(Nos.52174303and 51874084)the Program of Introducing Talents of Discipline to Universities(No.B21001)。
文摘Multistage heat treatment involving quenching(Q),lamellarizing(L),and tempering(T)is applied to marine 10Ni5CrMoV steel.The microstructure and mechanical properties were studied by multiscale characterizations,and the kinetics of reverse austenite transformation,strain hardening behavior,and toughening mechanism were further investigated.The lamellarized specimens possess low yield strength but high toughness,especially cryogenic toughness.Lamellarization leads to the development of film-like reversed austenite at the martensite block and lath boundaries,refining the martensite structure and lowering the equivalent grain size.Kinetic analysis of austenite reversion based on the JMAK model shows that the isothermal transformation is dominated by the growth of reversed austenite,and the maximum transformation of reversed austenite is reached at the peak temperature(750℃).The strain hardening behavior based on the modified Crussard-Jaoul analysis indicates that the reversed austenite obtained from lamellarization reduces the proportion of martensite,significantly hindering crack propagation via martensitic transformation during the deformation.As a consequence,the QLT specimens exhibit high machinability and low yield strength.Compared with the QT specimen,the ductile-brittle transition temperature of the QLT specimens decreases from-116 to-130℃due to the low equivalent grain size and reversed austenite,which increases the cleavage force required for crack propagation and absorbs the energy of external load,respectively.This work provides an idea to improve the cryogenic toughness of marine 10Ni5CrMoV steel and lays a theoretical foundation for its industrial application and comprehensive performance improvement.
基金supported by the National Natural Science Foundation of China,Nos.82071008(to BL)and 82004001(to XJ)Medical Science and Technology Program of Health Commission of Henan Province,No.LHGJ20210072(to RQ)Science and Technology Department of Henan Province,No.212102310307(to XJ)。
文摘Retinitis pigmentosa is a group of inherited diseases that lead to retinal degeneration and photoreceptor cell death.However,there is no effective treatment for retinitis pigmentosa caused by PDE6B mutation.Adeno-associated virus(AAV)-mediated gene therapy is a promising strategy for treating retinitis pigmentosa.The aim of this study was to explore the molecular mechanisms by which AAV2-PDE6B rescues retinal function.To do this,we injected retinal degeneration 10(rd10)mice subretinally with AAV2-PDE6B and assessed the therapeutic effects on retinal function and structure using dark-and light-adapted electroretinogram,optical coherence tomography,and immunofluorescence.Data-independent acquisition-mass spectrometry-based proteomic analysis was conducted to investigate protein expression levels and pathway enrichment,and the results from this analysis were verified by real-time polymerase chain reaction and western blotting.AAV2-PDE6B injection significantly upregulated PDE6βexpression,preserved electroretinogram responses,and preserved outer nuclear layer thickness in rd10 mice.Differentially expressed proteins between wild-type and rd10 mice were closely related to visual perception,and treating rd10 mice with AAV2-PDE6B restored differentially expressed protein expression to levels similar to those seen in wild-type mice.Kyoto Encyclopedia of Genes and Genome analysis showed that the differentially expressed proteins whose expression was most significantly altered by AAV2-PDE6B injection were enriched in phototransduction pathways.Furthermore,the phototransductionrelated proteins Pde6α,Rom1,Rho,Aldh1a1,and Rbp1 exhibited opposite expression patterns in rd10 mice with or without AAV2-PDE6B treatment.Finally,Bax/Bcl-2,p-ERK/ERK,and p-c-Fos/c-Fos expression levels decreased in rd10 mice following AAV2-PDE6B treatment.Our data suggest that AAV2-PDE6B-mediated gene therapy promotes phototransduction and inhibits apoptosis by inhibiting the ERK signaling pathway and upregulating Bcl-2/Bax expression in retinitis pigmentosa.
