Introduction of the photothermal effect into transition-metal oxide photoanodes has been proven to be an effective method to improve the photoelectrochemical(PEC)water-splitting performance.However,the precise role of...Introduction of the photothermal effect into transition-metal oxide photoanodes has been proven to be an effective method to improve the photoelectrochemical(PEC)water-splitting performance.However,the precise role of the photothermal effect on the PEC performance of photoanodes is still not well understood.Herein,spinel-structured ZnFe_(2)O_(4)nanoparticles are deposited on the surface of hematite(Fe_(2)O_(3)),and the ZnFe_(2)O_(4)/Fe_(2)O_(3)photoanode achieves a high photocurrent density of 3.17 mA cm^(-2)at 1.23 V versus a reversible hydrogen electrode(VRHE)due to the photothermal effect of ZnFe_(2)O_(4).Considering that the hopping of electron small polarons induced by oxygen vacancies is thermally activated,we clarify that the main reason for the enhanced PEC performance via the photothermal effect is the promoted mobility of electron small polarons that are bound to positively charged oxygen vacancies.Under the synergistic effect of oxygen vacancies and the photothermal effect,the electron conductivity and PEC performance are significantly improved,which provide fundamental insights into the impact of the photothermal effect on the PEC performance of small polaron-type semiconductor photoanodes.展开更多
Vision depends on accurate signal conduction from the retina to the brain through the optic nerve,an important part of the central nervous system that consists of bundles of axons originating from retinal ganglion cel...Vision depends on accurate signal conduction from the retina to the brain through the optic nerve,an important part of the central nervous system that consists of bundles of axons originating from retinal ganglion cells.The mammalian optic nerve,an important part of the central nervous system,cannot regenerate once it is injured,leading to permanent vision loss.To date,there is no clinical treatment that can regenerate the optic nerve and restore vision.Our previous study found that the mobile zinc(Zn^(2+))level increased rapidly after optic nerve injury in the retina,specifically in the vesicles of the inner plexiform layer.Furthermore,chelating Zn^(2+)significantly promoted axonal regeneration with a long-term effect.In this study,we conditionally knocked out zinc transporter 3(ZnT3)in amacrine cells or retinal ganglion cells to construct two transgenic mouse lines(VGAT^(Cre)ZnT3^(fl/fl)and VGLUT2^(Cre)ZnT3^(fl/fl),respectively).We obtained direct evidence that the rapidly increased mobile Zn^(2+)in response to injury was from amacrine cells.We also found that selective deletion of ZnT3 in amacrine cells promoted retinal ganglion cell survival and axonal regeneration after optic nerve crush injury,improved retinal ganglion cell function,and promoted vision recovery.Sequencing analysis of reginal ganglion cells revealed that inhibiting the release of presynaptic Zn^(2+)affected the transcription of key genes related to the survival of retinal ganglion cells in postsynaptic neurons,regulated the synaptic connection between amacrine cells and retinal ganglion cells,and affected the fate of retinal ganglion cells.These results suggest that amacrine cells release Zn^(2+)to trigger transcriptomic changes related to neuronal growth and survival in reginal ganglion cells,thereby influencing the synaptic plasticity of retinal networks.These results make the theory of zinc-dependent retinal ganglion cell death more accurate and complete and provide new insights into the complex interactions between retinal cell networks.展开更多
基金This work was supported by the National Natural Science Foundation of China(51902297,52002361,52003300,and 22109120)the Zhejiang Provincial Natural Science Foundation of China(LQ21B030002)the fund of the Key Laboratory of Catalysis and Energy Materials Chemistry of Ministry of Education,and Hubei Key Laboratory of Catalysis and Materials Science.
文摘Introduction of the photothermal effect into transition-metal oxide photoanodes has been proven to be an effective method to improve the photoelectrochemical(PEC)water-splitting performance.However,the precise role of the photothermal effect on the PEC performance of photoanodes is still not well understood.Herein,spinel-structured ZnFe_(2)O_(4)nanoparticles are deposited on the surface of hematite(Fe_(2)O_(3)),and the ZnFe_(2)O_(4)/Fe_(2)O_(3)photoanode achieves a high photocurrent density of 3.17 mA cm^(-2)at 1.23 V versus a reversible hydrogen electrode(VRHE)due to the photothermal effect of ZnFe_(2)O_(4).Considering that the hopping of electron small polarons induced by oxygen vacancies is thermally activated,we clarify that the main reason for the enhanced PEC performance via the photothermal effect is the promoted mobility of electron small polarons that are bound to positively charged oxygen vacancies.Under the synergistic effect of oxygen vacancies and the photothermal effect,the electron conductivity and PEC performance are significantly improved,which provide fundamental insights into the impact of the photothermal effect on the PEC performance of small polaron-type semiconductor photoanodes.
基金the National Key R&D Project of China,No.2020YFA0112701(to YZ)the National Natural Science Foundation of China,Nos.82171057(to YZ),81870657(to YL)+1 种基金Science and Technology Program of Guangzhou of China,No.202206080005(to YZ)the Natural Science Foundation of Guangdong Province of China,No.2022A1515012168(to YL)。
文摘Vision depends on accurate signal conduction from the retina to the brain through the optic nerve,an important part of the central nervous system that consists of bundles of axons originating from retinal ganglion cells.The mammalian optic nerve,an important part of the central nervous system,cannot regenerate once it is injured,leading to permanent vision loss.To date,there is no clinical treatment that can regenerate the optic nerve and restore vision.Our previous study found that the mobile zinc(Zn^(2+))level increased rapidly after optic nerve injury in the retina,specifically in the vesicles of the inner plexiform layer.Furthermore,chelating Zn^(2+)significantly promoted axonal regeneration with a long-term effect.In this study,we conditionally knocked out zinc transporter 3(ZnT3)in amacrine cells or retinal ganglion cells to construct two transgenic mouse lines(VGAT^(Cre)ZnT3^(fl/fl)and VGLUT2^(Cre)ZnT3^(fl/fl),respectively).We obtained direct evidence that the rapidly increased mobile Zn^(2+)in response to injury was from amacrine cells.We also found that selective deletion of ZnT3 in amacrine cells promoted retinal ganglion cell survival and axonal regeneration after optic nerve crush injury,improved retinal ganglion cell function,and promoted vision recovery.Sequencing analysis of reginal ganglion cells revealed that inhibiting the release of presynaptic Zn^(2+)affected the transcription of key genes related to the survival of retinal ganglion cells in postsynaptic neurons,regulated the synaptic connection between amacrine cells and retinal ganglion cells,and affected the fate of retinal ganglion cells.These results suggest that amacrine cells release Zn^(2+)to trigger transcriptomic changes related to neuronal growth and survival in reginal ganglion cells,thereby influencing the synaptic plasticity of retinal networks.These results make the theory of zinc-dependent retinal ganglion cell death more accurate and complete and provide new insights into the complex interactions between retinal cell networks.
