In pressurized nuclear power plants,metallic tubes such as steam generator(SG)tubes are subject to complex mechanical and environmental loads that can lead to crack initiation and propagation.Evaluating the structural...In pressurized nuclear power plants,metallic tubes such as steam generator(SG)tubes are subject to complex mechanical and environmental loads that can lead to crack initiation and propagation.Evaluating the structural integrity of SG tubes requires non-destructive assessment of crack size and location.Current inversion schemes can determine crack shape but lack position information,and reconstruction using a single coil has low efficiency.While array probes improve defect detection,reconstruction research based on array signals is challenging due to the complexity of processing multiple sets of signals.This study proposes a simple and effective array reconstruction scheme utilizing signals from two adjacent coils near the crack,enabling simultaneous determination of both crack shape and location through interpolation techniques.Numerical results validate this new crack sizing method,showing accurate reconstruction of both size and location.展开更多
The dissociation kinetics of noncovalent cross-links play a pivotal role in determining the mechanical performance of supramolecular polymer networks(SPNs).However,achieving effective control over the dissociation kin...The dissociation kinetics of noncovalent cross-links play a pivotal role in determining the mechanical performance of supramolecular polymer networks(SPNs).However,achieving effective control over the dissociation kinetics remains highly challenging.Herein,by incorporating pseudorotaxane stopper with varying sizes,we exploited steric hindrance effects to modulate the dissociation rates of supramolecular cross-links,thereby effectively tuning the mechanical properties of the SPNs.Specifically,SPN-1,whose cross-linkers incorporated smaller terminal stoppers,exhibited a higher dissociation rate constant(>3.5×10^(−3) s^(−1)),while SPN-2,the crosslinker 2 featuring larger terminal stoppers,demonstrated slower dissociation kinetics(6.1×10^(−7) s^(−1)).As a result,SPN-2 showed a slower stress relaxation behavior and better creep resistance in comparison to SPN-1.Furthermore,SPN-2 exhibited superior robustness compared to SPN-1,evidenced by higher breaking stress(14.5 vs 4.1 MPa),fracture strain(549.5%vs 273.5%),and toughness(46.7 vs 9.4 MJ m^(−3)).Thus,our work offers a new strategy for modulating the dissociation kinetics and mechanical performance of SPNs and deepens our insights into the structure-property relationships within dynamic networks.展开更多
Background:Diabetic foot ulcer(DFU)is a common and debilitating complication of diabetes,often leading to delayed wound healing.The peroxisome proliferator-activated receptors(PPARs)play a crucial role in regulating c...Background:Diabetic foot ulcer(DFU)is a common and debilitating complication of diabetes,often leading to delayed wound healing.The peroxisome proliferator-activated receptors(PPARs)play a crucial role in regulating cellular metabolism and promoting angiogenesis.This study aims to elucidate the mechanisms through which the activation of PPARs enhances wound healing,particularly under diabetic conditions,as these mechanisms remain inadequately understood.Methods:Differentially expressed genes in DFU wounds and normal skin tissues were identified using the GEO database.PPAR expression in DFU neovascularization was validated by quantitative reverse transcription polymerase chain reaction,immunofluorescence,and western blotting.In vivo,diabetic mice treated with PPAR agonists(chiglitazar)underwent wound healing assessment,including collagen deposition and angiogenesis.In vitro,advanced glycation end-products(AGEs)-induced endothelial cell models were used to evaluate PPAR activation effects on cell migration,tube formation,and mitochondrial function.Whole transcriptome sequencing and mitochondrial analysis were performed to explore the underlying mechanisms,particularly the sonic hedgehog(SHH)-mitochondrial axis.Results:PPAR expression was significantly downregulated in DFU tissues(p<0.05),and PPAR activation in diabetic mice enhanced wound healing,collagen deposition,granulation tissue proliferation,and angiogenesis(p<0.05).In vitro,PPAR activation protected endothelial cells,promoting vascular endothelial growth factor-A(VEGF-A)and CD31 expression,reducing apoptosis,and enhancing cell migration and tube formation(p<O.05).Mechanistically,PPARs activated mitochondrial oxidative phosphorylation and membrane function through the SHH signaling pathway.SHH gene silencing reversed the effects of PPAR activation on mitochondrial function and angiogenesis.Conclusions:PPAR signaling plays a critical role in DFU healing,with its inhibition linked to vascular dysfunction.Activation of the PPARs/SHH-mitochondrial axis significantly enhances endothelial cell metabolism and angiogenesis.This study provides insights into the molecular mechanisms of diabetic wound healing and supports the clinical potential of PPAR agonists for DFU treatment.展开更多
基金the National Key R&D Program of China(No.2023YFF0615200)the Natural Science Foundation of China(Grant No.52477015,No.U2130206,No.12222207)the General Collaborative Research Project(Project Code:J24I008)of Institute of Fluid Science,Tohoku University,Japan.
文摘In pressurized nuclear power plants,metallic tubes such as steam generator(SG)tubes are subject to complex mechanical and environmental loads that can lead to crack initiation and propagation.Evaluating the structural integrity of SG tubes requires non-destructive assessment of crack size and location.Current inversion schemes can determine crack shape but lack position information,and reconstruction using a single coil has low efficiency.While array probes improve defect detection,reconstruction research based on array signals is challenging due to the complexity of processing multiple sets of signals.This study proposes a simple and effective array reconstruction scheme utilizing signals from two adjacent coils near the crack,enabling simultaneous determination of both crack shape and location through interpolation techniques.Numerical results validate this new crack sizing method,showing accurate reconstruction of both size and location.
基金support from the National Natural Science Foundation of China(NSFC)(grant nos.22471164 and 52421006)the Shanghai Municipal Science and Technology Major Project,the Natural Science Foundation(NSF)of Shanghai,China(grant no.22dz1207603)+4 种基金the Open Project of State Key Laboratory of Supramolecular Structure and Materials,China(sklssm202518)support from the NSFC(grant no.52333001)support of the NSFC(grant no.22475128)support of the NSFC(grant no.22305150)support of the NSFC(grant no.223B2113).
文摘The dissociation kinetics of noncovalent cross-links play a pivotal role in determining the mechanical performance of supramolecular polymer networks(SPNs).However,achieving effective control over the dissociation kinetics remains highly challenging.Herein,by incorporating pseudorotaxane stopper with varying sizes,we exploited steric hindrance effects to modulate the dissociation rates of supramolecular cross-links,thereby effectively tuning the mechanical properties of the SPNs.Specifically,SPN-1,whose cross-linkers incorporated smaller terminal stoppers,exhibited a higher dissociation rate constant(>3.5×10^(−3) s^(−1)),while SPN-2,the crosslinker 2 featuring larger terminal stoppers,demonstrated slower dissociation kinetics(6.1×10^(−7) s^(−1)).As a result,SPN-2 showed a slower stress relaxation behavior and better creep resistance in comparison to SPN-1.Furthermore,SPN-2 exhibited superior robustness compared to SPN-1,evidenced by higher breaking stress(14.5 vs 4.1 MPa),fracture strain(549.5%vs 273.5%),and toughness(46.7 vs 9.4 MJ m^(−3)).Thus,our work offers a new strategy for modulating the dissociation kinetics and mechanical performance of SPNs and deepens our insights into the structure-property relationships within dynamic networks.
基金supported by the Chinese National Nature Science Foundation(Grant No.82370903)the Major Project of Science and Technology Research Program of Chongqing Education Commission of China(Grant No.KJZD-M202400102)+2 种基金the National Key Clinical Specialties(Grant No.GJZDZK202201)the Noncommunicable Chronic Diseases-National Science and Technology Major Project(Grant Nos.2023ZD0509400&02)the Young Project of Scientific and Technological Research Program of Chongqing Municipal Education Commission(Grant No.KJQN202400132).
文摘Background:Diabetic foot ulcer(DFU)is a common and debilitating complication of diabetes,often leading to delayed wound healing.The peroxisome proliferator-activated receptors(PPARs)play a crucial role in regulating cellular metabolism and promoting angiogenesis.This study aims to elucidate the mechanisms through which the activation of PPARs enhances wound healing,particularly under diabetic conditions,as these mechanisms remain inadequately understood.Methods:Differentially expressed genes in DFU wounds and normal skin tissues were identified using the GEO database.PPAR expression in DFU neovascularization was validated by quantitative reverse transcription polymerase chain reaction,immunofluorescence,and western blotting.In vivo,diabetic mice treated with PPAR agonists(chiglitazar)underwent wound healing assessment,including collagen deposition and angiogenesis.In vitro,advanced glycation end-products(AGEs)-induced endothelial cell models were used to evaluate PPAR activation effects on cell migration,tube formation,and mitochondrial function.Whole transcriptome sequencing and mitochondrial analysis were performed to explore the underlying mechanisms,particularly the sonic hedgehog(SHH)-mitochondrial axis.Results:PPAR expression was significantly downregulated in DFU tissues(p<0.05),and PPAR activation in diabetic mice enhanced wound healing,collagen deposition,granulation tissue proliferation,and angiogenesis(p<0.05).In vitro,PPAR activation protected endothelial cells,promoting vascular endothelial growth factor-A(VEGF-A)and CD31 expression,reducing apoptosis,and enhancing cell migration and tube formation(p<O.05).Mechanistically,PPARs activated mitochondrial oxidative phosphorylation and membrane function through the SHH signaling pathway.SHH gene silencing reversed the effects of PPAR activation on mitochondrial function and angiogenesis.Conclusions:PPAR signaling plays a critical role in DFU healing,with its inhibition linked to vascular dysfunction.Activation of the PPARs/SHH-mitochondrial axis significantly enhances endothelial cell metabolism and angiogenesis.This study provides insights into the molecular mechanisms of diabetic wound healing and supports the clinical potential of PPAR agonists for DFU treatment.