A quasi-equiatomic CoCrFeCuNi high-entropy alloy(HEA) with a broad-spectrum antibacterial ability and good mechanical properties has been fabricated by selective laser melting(SLM) and in-situ alloying of a blend of p...A quasi-equiatomic CoCrFeCuNi high-entropy alloy(HEA) with a broad-spectrum antibacterial ability and good mechanical properties has been fabricated by selective laser melting(SLM) and in-situ alloying of a blend of pre-alloyed CoCrFeNi powder and Cu elemental powder.The as-built HEA alloy has a homogeneous distribution of Cu and presents a single FCC phase.Compared with the same HEA fabricated using the traditional ingot metallurgy(IM) process,the HEA alloy fabricated by SLM releases more Cu ions to prevent growth and biofilm formation by gram-negative Escherichia coli and gram-positive Staphylococcus aureus,which enhances the applicability of the HEA alloy in potential applications that requires antibacterial ability.The results of this study confirm the feasibility of combining the antibacterial CoCrFeCuNi HEA alloy and SLM technology in fabricating complex shaped parts or structures with a strong antibacterial ability to be used in medical application or other environments desired for antibacterial ability.展开更多
Titanium alloys possess excellent corrosion resistance in marine environments,thus the possibility of their corrosion caused by marine microorganisms is neglected.In this work,microbiologically influenced corrosion(MI...Titanium alloys possess excellent corrosion resistance in marine environments,thus the possibility of their corrosion caused by marine microorganisms is neglected.In this work,microbiologically influenced corrosion(MIC)of TC4 titanium alloy caused by marine Pseudomonas aeruginosa was investigated through electrochemical and surface characterizations during a 14-day immersion test.Results revealed that the unstable surface caused by P.aeruginosa resulted in exposure of Ti_(2)O_(3) and severe pitting corrosion with maximum pit depth of 5.7μm after 14 days of incubation.Phenazine-1-carboxylate(PCN),secreted by P.aeruginosa,promoted extracellular electron transfer(EET)and accelerated corrosion.Deletion of the phzH gene,which codes for the enzyme that catalyzes PCN production,from the P.aeruginosa genome,resulted in significantly decreased rates of corrosion.These results demonstrate that TC4 titanium alloy is not immune to marine MIC,and EET contributes to the corrosion of TC4 titanium alloy caused by P.aeruginosa.展开更多
Extracellular electron transfer(EET)plays a critical role in bioelectrochemical processes,allowing cou-pling between microorganisms and extracellular solid-state electrodes,metals,or other cells in energy metabolism.P...Extracellular electron transfer(EET)plays a critical role in bioelectrochemical processes,allowing cou-pling between microorganisms and extracellular solid-state electrodes,metals,or other cells in energy metabolism.Previous studies have suggested a role for outer-surface c-type cytochromes in direct metal-to-microbe electron transfer by Geobacter sulfurreducens,a model electroactive bacterium.Here,we ex-amined the possibility of other microbially produced electrical contacts by deleting the gene for PilA,the protein monomer that G.sulfurreducens assembles into electrically conductive protein nanowires(e-pili).Deleting pilA gene inhibited electron extraction from pure iron and 316L stainless steel up to 31%and 81%,respectively more than deleting the gene for the outer-surface cytochrome OmcS.This PilA-deficient phenotype,and the observation that relatively thick biofilms(21.7μm)grew on the metal surfaces at multi-cell distances from the metal surfaces suggest that e-pili contributed significantly to microbial cor-rosion via direct metal-to-microbe electron transfer.These results have implications for the fundamental understanding of electron harvest via e-pili by electroactive microbes,their uses in bioenergy production,as well as in monitoring and mitigation of metal biocorrosion.展开更多
Microbes can cause or accelerate metal corrosion,leading to huge losses in corrosion damages each year.Geobacter sulfurreducens is a representative electroactive bacterium in many soils,sediments,and wastew-ater syste...Microbes can cause or accelerate metal corrosion,leading to huge losses in corrosion damages each year.Geobacter sulfurreducens is a representative electroactive bacterium in many soils,sediments,and wastew-ater systems.It has been confirmed to directly extract electrons from elemental metals.However,little is known about the effect of electron shuttles in G.sulfurreducens corrosion on stainless steel.In this study,we report that exogenous flavins promote iron-to-microbe electron transfer,accelerating micro-bial corrosion.G.sulfurreducens caused 1.3 times deeper pits and increased electron uptake(with 2 times increase of i_(corr))from stainless steel when riboflavin was added to the culture medium.OmcS-deficient mutant data suggest that G.sulfurreducens utilizes riboflavin as a bound-cofactor in outer membrane c-type cytochromes.The finding that,in the presence of microbes,riboflavin can substantially accelerate corrosion highlights the role of flavin redox cycling for enhanced iron-to-microbe electron transfer by G.sulfurreducens and provides new insights in microbial corrosion.展开更多
The oil and gas industry requires complex subsea infrastructure in order to develop offshore oil and gas fields.Upon installation,these components may encounter high slamming loads,stemming from impact with the water ...The oil and gas industry requires complex subsea infrastructure in order to develop offshore oil and gas fields.Upon installation,these components may encounter high slamming loads,stemming from impact with the water surface.This paper utilises two different numerical methods,the mesh-free Smoothed Particle Hydrodynamics(SPH)approach and Reynolds Averaged Navier-Stokes(RANS)Volume of Fluid(VOF)method to quantify these loads on a free-falling object.The investigation is also interested in conducting a parameter study and determining the effect of varying simulation parameters on the prediction of slamming event kinematics and forces.The surface impact of a freefalling wedge was introduced as a case study and has been simulated using SPH and RANS,with the results being compared to an experimental investigation.It was found from the SPH simulations that particle resolution and the size of the SPH particle kernel are very important,whilst the diffusion term does not play an important role.The latter is due to the very transient nature of slamming events,which do not allow sufficient time for diffusion in the fluid domain.For the RANS simulations,motion of the wedge was achieved using the overset grid technique,whereby varying the discretising time step was found to have a pronounced impact on the accuracy of the captured slamming event.Through analysing the numerical data,one can observe that the RANS results correlate slightly better with the experimental data as opposed to that obtained from the SPH modelling.However,considering the robustness and quick set up of the SPH simulations,both of these two numerical approaches are considered to be promising tools for modelling more complicated slamming problems,including those potentially involving more intricate structures.展开更多
Notch signaling plays important roles in the regulation of immune cell functioning during the inflammatory response.Activation of the innate immune signaling receptor NLRP3 promotes inflammation in injured tissue.Howe...Notch signaling plays important roles in the regulation of immune cell functioning during the inflammatory response.Activation of the innate immune signaling receptor NLRP3 promotes inflammation in injured tissue.However,it remains unknown whether Jagged1(JAG1)-mediated myeloid Notch1 signaling regulates NLRP3 function in acute liver injury.Here,we report that myeloid Notch1 signaling regulates the NLRP3-driven inflammatory response in ischemia/reperfusion(IR)-induced liver injury.In a mouse model of liver IR injury,Notch1-proficient(Notch1^(FL/FL))mice receiving recombinant JAG1 showed a reduction in IR-induced liver injury and increased Notch intracellular domain(NICD)and heat shock transcription factor 1(HSF1)expression,whereas myeloidspecific Notch1 knockout(Notch1^(M-KO))aggravated hepatocellular damage even with concomitant JAG1 treatment.Compared to JAG1-treated Notch1^(FL/FL) controls,Notch1^(M-KO) mice showed diminished HSF1 and Snail activity but augmented NLRP3/caspase-1 activity in ischemic liver.The disruption of HSF1 reduced Snail activation and enhanced NLRP3 activation,while the adoptive transfer of HSF1-expressing macrophages to Notch1^(M-KO) mice augmented Snail activation and mitigated IR-triggered liver inflammation.Moreover,the knockdown of Snail in JAG1-treated Notch1^(FL/FL) livers worsened hepatocellular functioning,reduced TRX1 expression and increased TXNIP/NLRP3 expression.Ablation of myeloid Notch1 or Snail increased ASK1 activation and hepatocellular apoptosis,whereas the activation of Snail increased TRX1 expression and reduced TXNIP,NLRP3/caspase-1,and ROS production.Our findings demonstrated that JAG1-mediated myeloid Notch1 signaling promotes HSF1 and Snail activation,which in turn inhibits NLRP3 function and hepatocellular apoptosis leading to the alleviation of IR-induced liver injury.Hence,the Notch1/HSF1/Snail signaling axis represents a novel regulator of and a potential therapeutic target for liver inflammatory injury.展开更多
基金financial support to Deliang Zhang by the “Xing Liao Talent Plan” of the Science and Technology Department of Liaoning Province, China (No. XLYC1802080) is gratefully acknowledgedsupported by grants to Dake Xu from the National Natural Science Foundation of China (Nos. U2006219 and 51871050)the Fundamental Research Funds for the Central Universities (Nos. N180203019 and N2002019)。
文摘A quasi-equiatomic CoCrFeCuNi high-entropy alloy(HEA) with a broad-spectrum antibacterial ability and good mechanical properties has been fabricated by selective laser melting(SLM) and in-situ alloying of a blend of pre-alloyed CoCrFeNi powder and Cu elemental powder.The as-built HEA alloy has a homogeneous distribution of Cu and presents a single FCC phase.Compared with the same HEA fabricated using the traditional ingot metallurgy(IM) process,the HEA alloy fabricated by SLM releases more Cu ions to prevent growth and biofilm formation by gram-negative Escherichia coli and gram-positive Staphylococcus aureus,which enhances the applicability of the HEA alloy in potential applications that requires antibacterial ability.The results of this study confirm the feasibility of combining the antibacterial CoCrFeCuNi HEA alloy and SLM technology in fabricating complex shaped parts or structures with a strong antibacterial ability to be used in medical application or other environments desired for antibacterial ability.
基金This work was supported by the National Natural Science Foundation of China(U2006219,U1660118 and 51871050)the Fundamental Research Funds for the Central Universities of the Ministry of Education of China(N180205021,N180203019)Liaoning Revitalization Talents Program(No.XLYC1907158)。
文摘Titanium alloys possess excellent corrosion resistance in marine environments,thus the possibility of their corrosion caused by marine microorganisms is neglected.In this work,microbiologically influenced corrosion(MIC)of TC4 titanium alloy caused by marine Pseudomonas aeruginosa was investigated through electrochemical and surface characterizations during a 14-day immersion test.Results revealed that the unstable surface caused by P.aeruginosa resulted in exposure of Ti_(2)O_(3) and severe pitting corrosion with maximum pit depth of 5.7μm after 14 days of incubation.Phenazine-1-carboxylate(PCN),secreted by P.aeruginosa,promoted extracellular electron transfer(EET)and accelerated corrosion.Deletion of the phzH gene,which codes for the enzyme that catalyzes PCN production,from the P.aeruginosa genome,resulted in significantly decreased rates of corrosion.These results demonstrate that TC4 titanium alloy is not immune to marine MIC,and EET contributes to the corrosion of TC4 titanium alloy caused by P.aeruginosa.
基金supported by the National Natu-ral Science Foundation of China(Nos.U2006219 and 52101078)China Baowu Low Carbon Metallurgy Innovation Foundation(No.BWLCF202120)+2 种基金the National Key Research and Development Pro-gram of China(No.2020YFA0907300)the Fundamental Research Funds for the Central Universities of the Ministry of Education of China(Nos.N2102009 and N2002019)the Liaoning Revitaliza-tion Talents Program(No.XLYC1907158).
文摘Extracellular electron transfer(EET)plays a critical role in bioelectrochemical processes,allowing cou-pling between microorganisms and extracellular solid-state electrodes,metals,or other cells in energy metabolism.Previous studies have suggested a role for outer-surface c-type cytochromes in direct metal-to-microbe electron transfer by Geobacter sulfurreducens,a model electroactive bacterium.Here,we ex-amined the possibility of other microbially produced electrical contacts by deleting the gene for PilA,the protein monomer that G.sulfurreducens assembles into electrically conductive protein nanowires(e-pili).Deleting pilA gene inhibited electron extraction from pure iron and 316L stainless steel up to 31%and 81%,respectively more than deleting the gene for the outer-surface cytochrome OmcS.This PilA-deficient phenotype,and the observation that relatively thick biofilms(21.7μm)grew on the metal surfaces at multi-cell distances from the metal surfaces suggest that e-pili contributed significantly to microbial cor-rosion via direct metal-to-microbe electron transfer.These results have implications for the fundamental understanding of electron harvest via e-pili by electroactive microbes,their uses in bioenergy production,as well as in monitoring and mitigation of metal biocorrosion.
基金supported by the National Natural Science Foundation of China(Nos.52101078,U2006219)the National Key Research and Development Program of China(No.2020YFA0907300)+1 种基金the Fundamental Research Funds for the Central Universities of the Ministry of Education of China(Nos.N2102009,N2002019)Liaoning Revitalization Talents Program(No.XLYC1907158).
文摘Microbes can cause or accelerate metal corrosion,leading to huge losses in corrosion damages each year.Geobacter sulfurreducens is a representative electroactive bacterium in many soils,sediments,and wastew-ater systems.It has been confirmed to directly extract electrons from elemental metals.However,little is known about the effect of electron shuttles in G.sulfurreducens corrosion on stainless steel.In this study,we report that exogenous flavins promote iron-to-microbe electron transfer,accelerating micro-bial corrosion.G.sulfurreducens caused 1.3 times deeper pits and increased electron uptake(with 2 times increase of i_(corr))from stainless steel when riboflavin was added to the culture medium.OmcS-deficient mutant data suggest that G.sulfurreducens utilizes riboflavin as a bound-cofactor in outer membrane c-type cytochromes.The finding that,in the presence of microbes,riboflavin can substantially accelerate corrosion highlights the role of flavin redox cycling for enhanced iron-to-microbe electron transfer by G.sulfurreducens and provides new insights in microbial corrosion.
文摘The oil and gas industry requires complex subsea infrastructure in order to develop offshore oil and gas fields.Upon installation,these components may encounter high slamming loads,stemming from impact with the water surface.This paper utilises two different numerical methods,the mesh-free Smoothed Particle Hydrodynamics(SPH)approach and Reynolds Averaged Navier-Stokes(RANS)Volume of Fluid(VOF)method to quantify these loads on a free-falling object.The investigation is also interested in conducting a parameter study and determining the effect of varying simulation parameters on the prediction of slamming event kinematics and forces.The surface impact of a freefalling wedge was introduced as a case study and has been simulated using SPH and RANS,with the results being compared to an experimental investigation.It was found from the SPH simulations that particle resolution and the size of the SPH particle kernel are very important,whilst the diffusion term does not play an important role.The latter is due to the very transient nature of slamming events,which do not allow sufficient time for diffusion in the fluid domain.For the RANS simulations,motion of the wedge was achieved using the overset grid technique,whereby varying the discretising time step was found to have a pronounced impact on the accuracy of the captured slamming event.Through analysing the numerical data,one can observe that the RANS results correlate slightly better with the experimental data as opposed to that obtained from the SPH modelling.However,considering the robustness and quick set up of the SPH simulations,both of these two numerical approaches are considered to be promising tools for modelling more complicated slamming problems,including those potentially involving more intricate structures.
基金supported by the NIH grants R01AI139552,R21AI146742,R21AI112722,R21AI115133(B.K.),P01AI120944,R01DK062357,R01DK102110,and R01DK107533(J.W.K.-W.)by the Dumont Research Foundation.
文摘Notch signaling plays important roles in the regulation of immune cell functioning during the inflammatory response.Activation of the innate immune signaling receptor NLRP3 promotes inflammation in injured tissue.However,it remains unknown whether Jagged1(JAG1)-mediated myeloid Notch1 signaling regulates NLRP3 function in acute liver injury.Here,we report that myeloid Notch1 signaling regulates the NLRP3-driven inflammatory response in ischemia/reperfusion(IR)-induced liver injury.In a mouse model of liver IR injury,Notch1-proficient(Notch1^(FL/FL))mice receiving recombinant JAG1 showed a reduction in IR-induced liver injury and increased Notch intracellular domain(NICD)and heat shock transcription factor 1(HSF1)expression,whereas myeloidspecific Notch1 knockout(Notch1^(M-KO))aggravated hepatocellular damage even with concomitant JAG1 treatment.Compared to JAG1-treated Notch1^(FL/FL) controls,Notch1^(M-KO) mice showed diminished HSF1 and Snail activity but augmented NLRP3/caspase-1 activity in ischemic liver.The disruption of HSF1 reduced Snail activation and enhanced NLRP3 activation,while the adoptive transfer of HSF1-expressing macrophages to Notch1^(M-KO) mice augmented Snail activation and mitigated IR-triggered liver inflammation.Moreover,the knockdown of Snail in JAG1-treated Notch1^(FL/FL) livers worsened hepatocellular functioning,reduced TRX1 expression and increased TXNIP/NLRP3 expression.Ablation of myeloid Notch1 or Snail increased ASK1 activation and hepatocellular apoptosis,whereas the activation of Snail increased TRX1 expression and reduced TXNIP,NLRP3/caspase-1,and ROS production.Our findings demonstrated that JAG1-mediated myeloid Notch1 signaling promotes HSF1 and Snail activation,which in turn inhibits NLRP3 function and hepatocellular apoptosis leading to the alleviation of IR-induced liver injury.Hence,the Notch1/HSF1/Snail signaling axis represents a novel regulator of and a potential therapeutic target for liver inflammatory injury.
