Prussian blue analogs(PBAs)have emerged as environmentally friendly and structurally tunable cathode materials for aqueous ammonium-ion batteries(AIBs).However,the fundamental role of crystalline H_(2)O in regulating ...Prussian blue analogs(PBAs)have emerged as environmentally friendly and structurally tunable cathode materials for aqueous ammonium-ion batteries(AIBs).However,the fundamental role of crystalline H_(2)O in regulating ammonium-ion storage and transport remains poorly understood.In this study,we present a comprehensive comparison between hydrated NH_(4)NiHCF-H_(2)O and its anhydrous counterpart NH_(4)NiHCF,revealing the critical contribution of interstitial water to electrochemical performance.Structural and spectroscopic analyses confirm that interstitial water forms robust hydrogen bonds with NH_(4)+ions,stabilizing the PBA framework and mitigating structural degradation during cycling.Electrochemical measurements show that NH_(4)NiHCF-H_(2)O delivers a significantly higher specific capacity of 61 mA h g^(−1)at 0.2 C and markedly improved rate performance compared to NH_(4)NiHCF(48 mA h g^(−1)at 0.2 C).Kinetic analysis reveals that interstitial water enhances NH_(4)+diffusion,as evidenced by higher diffusion coefficients.Furthermore,density functional theory(DFT)calculations demonstrate that crystal water acts as a hydrogen bond acceptor,preferentially interacting with NH_(4)+and reducing the migration energy barrier,thereby facilitating fast ion transport.This work provides fundamental insights into the role of crystal water in PBAs and offers a rational design strategy for improving the kinetics,structural stability of PBAs cathodes for AIBs.展开更多
Alzheimer’s disease is initially thought to be caused by age-associated accumulation of plaques,in recent years,research has increasingly associated Alzheimer’s disease with lysosomal storage and metabolic disorders...Alzheimer’s disease is initially thought to be caused by age-associated accumulation of plaques,in recent years,research has increasingly associated Alzheimer’s disease with lysosomal storage and metabolic disorders,and the explanation of its pathogenesis has shifted from amyloid and tau accumulation to oxidative stress and impaired lipid and glucose metabolism aggravated by hypoxic conditions.However,the underlying mechanisms linking those cellular processes and conditions to disease progression have yet to be defined.Here,we applied a disease similarity approach to identify unknown molecular targets of Alzheimer’s disease by using transcriptomic data from congenital diseases known to increase Alzheimer’s disease risk,namely Down syndrome,Niemann-Pick type C disease,and mucopolysaccharidoses I.We uncovered common pathways,hub genes,and miRNAs across in vitro and in vivo models of these diseases as potential molecular targets for neuroprotection and amelioration of Alzheimer’s disease pathology,many of which have never been associated with Alzheimer’s disease.We then investigated common molecular alterations in brain samples from a Niemann-Pick type C disease mouse model by juxtaposing them with brain samples of both human and mouse models of Alzheimer’s disease.Detailed phenotypic,molecular,chronological,and biological aging analyses revealed that the Npc1tm(I1061T)Dso mouse model can serve as a potential short-lived in vivo model for brain aging and Alzheimer’s disease research.This research represents the first comprehensive approach to congenital disease association with neurodegeneration and a new perspective on Alzheimer’s disease research while highlighting shortcomings and lack of correlation in diverse in vitro models.Considering the lack of an Alzheimer’s disease mouse model that recapitulates the physiological hallmarks of brain aging,the short-lived Npc1^(tm(I1061T)Dso) mouse model can further accelerate the research in these fields and offer a unique model for understanding the molecular mechanisms of Alzheimer’s disease from a perspective of accelerated brain aging.展开更多
基金supported by the National Natural Science Foundation of China(52172227)the Natural Science Foundation of Hubei Province(2023AFA114)+2 种基金the Guizhou Provincial Key Technology R&D Program(ZD[2025]019)Additional funding was provided by the Startup Fund(20QD80 and 22QD28)The authors also acknowledge support from the Science&Technology Top Talents Program of Guizhou Province([2024]349).We gratefully acknowledge Beijing SciStar Technology Co.,Ltd.for in-situ measurements and analysis.
文摘Prussian blue analogs(PBAs)have emerged as environmentally friendly and structurally tunable cathode materials for aqueous ammonium-ion batteries(AIBs).However,the fundamental role of crystalline H_(2)O in regulating ammonium-ion storage and transport remains poorly understood.In this study,we present a comprehensive comparison between hydrated NH_(4)NiHCF-H_(2)O and its anhydrous counterpart NH_(4)NiHCF,revealing the critical contribution of interstitial water to electrochemical performance.Structural and spectroscopic analyses confirm that interstitial water forms robust hydrogen bonds with NH_(4)+ions,stabilizing the PBA framework and mitigating structural degradation during cycling.Electrochemical measurements show that NH_(4)NiHCF-H_(2)O delivers a significantly higher specific capacity of 61 mA h g^(−1)at 0.2 C and markedly improved rate performance compared to NH_(4)NiHCF(48 mA h g^(−1)at 0.2 C).Kinetic analysis reveals that interstitial water enhances NH_(4)+diffusion,as evidenced by higher diffusion coefficients.Furthermore,density functional theory(DFT)calculations demonstrate that crystal water acts as a hydrogen bond acceptor,preferentially interacting with NH_(4)+and reducing the migration energy barrier,thereby facilitating fast ion transport.This work provides fundamental insights into the role of crystal water in PBAs and offers a rational design strategy for improving the kinetics,structural stability of PBAs cathodes for AIBs.
基金supported by the NIA/NIH(1K01AG060040).Studies performed by JN were funded by the NICHD/NIH(5R00HD096117)Microscopy Core Facility supported,in part,with funding from NIH-NCI Cancer Center Support Grant P30 CA016059.
文摘Alzheimer’s disease is initially thought to be caused by age-associated accumulation of plaques,in recent years,research has increasingly associated Alzheimer’s disease with lysosomal storage and metabolic disorders,and the explanation of its pathogenesis has shifted from amyloid and tau accumulation to oxidative stress and impaired lipid and glucose metabolism aggravated by hypoxic conditions.However,the underlying mechanisms linking those cellular processes and conditions to disease progression have yet to be defined.Here,we applied a disease similarity approach to identify unknown molecular targets of Alzheimer’s disease by using transcriptomic data from congenital diseases known to increase Alzheimer’s disease risk,namely Down syndrome,Niemann-Pick type C disease,and mucopolysaccharidoses I.We uncovered common pathways,hub genes,and miRNAs across in vitro and in vivo models of these diseases as potential molecular targets for neuroprotection and amelioration of Alzheimer’s disease pathology,many of which have never been associated with Alzheimer’s disease.We then investigated common molecular alterations in brain samples from a Niemann-Pick type C disease mouse model by juxtaposing them with brain samples of both human and mouse models of Alzheimer’s disease.Detailed phenotypic,molecular,chronological,and biological aging analyses revealed that the Npc1tm(I1061T)Dso mouse model can serve as a potential short-lived in vivo model for brain aging and Alzheimer’s disease research.This research represents the first comprehensive approach to congenital disease association with neurodegeneration and a new perspective on Alzheimer’s disease research while highlighting shortcomings and lack of correlation in diverse in vitro models.Considering the lack of an Alzheimer’s disease mouse model that recapitulates the physiological hallmarks of brain aging,the short-lived Npc1^(tm(I1061T)Dso) mouse model can further accelerate the research in these fields and offer a unique model for understanding the molecular mechanisms of Alzheimer’s disease from a perspective of accelerated brain aging.
