Nonlinear equations systems(NESs)are widely used in real-world problems and they are difficult to solve due to their nonlinearity and multiple roots.Evolutionary algorithms(EAs)are one of the methods for solving NESs,...Nonlinear equations systems(NESs)are widely used in real-world problems and they are difficult to solve due to their nonlinearity and multiple roots.Evolutionary algorithms(EAs)are one of the methods for solving NESs,given their global search capabilities and ability to locate multiple roots of a NES simultaneously within one run.Currently,the majority of research on using EAs to solve NESs focuses on transformation techniques and improving the performance of the used EAs.By contrast,problem domain knowledge of NESs is investigated in this study,where we propose the incorporation of a variable reduction strategy(VRS)into EAs to solve NESs.The VRS makes full use of the systems of expressing a NES and uses some variables(i.e.,core variable)to represent other variables(i.e.,reduced variables)through variable relationships that exist in the equation systems.It enables the reduction of partial variables and equations and shrinks the decision space,thereby reducing the complexity of the problem and improving the search efficiency of the EAs.To test the effectiveness of VRS in dealing with NESs,this paper mainly integrates the VRS into two existing state-of-the-art EA methods(i.e.,MONES and DR-JADE)according to the integration framework of the VRS and EA,respectively.Experimental results show that,with the assistance of the VRS,the EA methods can produce better results than the original methods and other compared methods.Furthermore,extensive experiments regarding the influence of different reduction schemes and EAs substantiate that a better EA for solving a NES with more reduced variables tends to provide better performance.展开更多
Elaidic acid(EA)stimulation can lead to endoplasmic reticulum stress(ERS),accompanied by a large release of Ca^(2+),and ultimately the activation of NLRP3 inflammasome in Kupffer cells(KCs).Mitochondrial instability o...Elaidic acid(EA)stimulation can lead to endoplasmic reticulum stress(ERS),accompanied by a large release of Ca^(2+),and ultimately the activation of NLRP3 inflammasome in Kupffer cells(KCs).Mitochondrial instability or dysfunction may be the key stimulating factors to activate NLRP3 inflammasome,and sustained Ca^(2+)transfer can result in mitochondrial dysfunction.We focused on KCs to explore the damage to mitochondria by EA.After EA stimulation,cells produced an oxidative stress(OS)response with a significant increase in ROS release.Immunoprecipitation experiments and the addition of inhibitors revealed that the increase in the level of intracellular Ca^(2+)led to Ca^(2+)accumulation in the mitochondrial matrix via mitochondria-associated membranes(MAMs).This was accompanied by a significant release of m ROS,loss of MMP and ATP,and a significant increase in mitochondrial permeability transition pore opening,ultimately leading to mitochondrial instability.These findings confirmed the mechanism that EA induced mitochondrial Ca^(2+)imbalance in KCs via MAM,ultimately leading to mitochondrial dysfunction.Meanwhile,EA induced OS and the decrease of MMP and ATP in rat liver,and significant lesions were found in liver mitochondria.Swelling of the inner mitochondrial cristae and mitochondrial vacuolization occurred,with a marked increase in lipid droplets.展开更多
Using pseudorabies virus Ea strain as material,we inserted LacZ gene expression cassette into gE gene.After blue plaque and plaque purification,a recombinant virus PRVEa TK+-/gE+-/LacZ++ generated.Utilizing EcoR I sit...Using pseudorabies virus Ea strain as material,we inserted LacZ gene expression cassette into gE gene.After blue plaque and plaque purification,a recombinant virus PRVEa TK+-/gE+-/LacZ++ generated.Utilizing EcoR I site in LacZ gene, digested PRVEa TK+-/gE+-/LacZ++ genome DNA was cotransfected into PK-15 cells with plasmid pFBBS,then PRVEa TK+-/gE+-/gp63+- generated after plaque purification.Four pairs of primers amplification demonstrated the virus was pure TK+-/gE+-/gp63+- mutant virus.PCR product sequence indicates there were 205bp deletion in TK gene;1247bp deletion in gE,gp63 and intergenic region of PRVEa TK+-/gE+-/gp63+- mutant virus genome DNA.Inoculation to Balb/C mice with PRVEa TK+-/gE+-/gp63+- indicates the virulence is reduced greatly.展开更多
基金This work was supported by the National Natural Science Foundation of China(62073341)in part by the Natural Science Fund for Distinguished Young Scholars of Hunan Province(2019JJ20026).
文摘Nonlinear equations systems(NESs)are widely used in real-world problems and they are difficult to solve due to their nonlinearity and multiple roots.Evolutionary algorithms(EAs)are one of the methods for solving NESs,given their global search capabilities and ability to locate multiple roots of a NES simultaneously within one run.Currently,the majority of research on using EAs to solve NESs focuses on transformation techniques and improving the performance of the used EAs.By contrast,problem domain knowledge of NESs is investigated in this study,where we propose the incorporation of a variable reduction strategy(VRS)into EAs to solve NESs.The VRS makes full use of the systems of expressing a NES and uses some variables(i.e.,core variable)to represent other variables(i.e.,reduced variables)through variable relationships that exist in the equation systems.It enables the reduction of partial variables and equations and shrinks the decision space,thereby reducing the complexity of the problem and improving the search efficiency of the EAs.To test the effectiveness of VRS in dealing with NESs,this paper mainly integrates the VRS into two existing state-of-the-art EA methods(i.e.,MONES and DR-JADE)according to the integration framework of the VRS and EA,respectively.Experimental results show that,with the assistance of the VRS,the EA methods can produce better results than the original methods and other compared methods.Furthermore,extensive experiments regarding the influence of different reduction schemes and EAs substantiate that a better EA for solving a NES with more reduced variables tends to provide better performance.
基金supported by fund from the National Natural Science Foundation of China(32172322)。
文摘Elaidic acid(EA)stimulation can lead to endoplasmic reticulum stress(ERS),accompanied by a large release of Ca^(2+),and ultimately the activation of NLRP3 inflammasome in Kupffer cells(KCs).Mitochondrial instability or dysfunction may be the key stimulating factors to activate NLRP3 inflammasome,and sustained Ca^(2+)transfer can result in mitochondrial dysfunction.We focused on KCs to explore the damage to mitochondria by EA.After EA stimulation,cells produced an oxidative stress(OS)response with a significant increase in ROS release.Immunoprecipitation experiments and the addition of inhibitors revealed that the increase in the level of intracellular Ca^(2+)led to Ca^(2+)accumulation in the mitochondrial matrix via mitochondria-associated membranes(MAMs).This was accompanied by a significant release of m ROS,loss of MMP and ATP,and a significant increase in mitochondrial permeability transition pore opening,ultimately leading to mitochondrial instability.These findings confirmed the mechanism that EA induced mitochondrial Ca^(2+)imbalance in KCs via MAM,ultimately leading to mitochondrial dysfunction.Meanwhile,EA induced OS and the decrease of MMP and ATP in rat liver,and significant lesions were found in liver mitochondria.Swelling of the inner mitochondrial cristae and mitochondrial vacuolization occurred,with a marked increase in lipid droplets.
文摘Using pseudorabies virus Ea strain as material,we inserted LacZ gene expression cassette into gE gene.After blue plaque and plaque purification,a recombinant virus PRVEa TK+-/gE+-/LacZ++ generated.Utilizing EcoR I site in LacZ gene, digested PRVEa TK+-/gE+-/LacZ++ genome DNA was cotransfected into PK-15 cells with plasmid pFBBS,then PRVEa TK+-/gE+-/gp63+- generated after plaque purification.Four pairs of primers amplification demonstrated the virus was pure TK+-/gE+-/gp63+- mutant virus.PCR product sequence indicates there were 205bp deletion in TK gene;1247bp deletion in gE,gp63 and intergenic region of PRVEa TK+-/gE+-/gp63+- mutant virus genome DNA.Inoculation to Balb/C mice with PRVEa TK+-/gE+-/gp63+- indicates the virulence is reduced greatly.
