The Internet of Vehicles(IoV)operates in highly dynamic and open network environments and faces serious challenges in secure and real-time authentication and consensus mechanisms.Existing methods often suffer from com...The Internet of Vehicles(IoV)operates in highly dynamic and open network environments and faces serious challenges in secure and real-time authentication and consensus mechanisms.Existing methods often suffer from complex certificate management,inefficient consensus protocols,and poor resilience in high-frequency communication,resulting in high latency,poor scalability,and unstable network performance.To address these issues,this paper proposes a secure and efficient distributed authentication scheme for IoV with reputation-driven consensus and SM9.First,this paper proposes a decentralized authentication architecture that utilizes the certificate-free feature of SM9,enabling lightweight authentication and key negotiation,thereby reducing the complexity of key management.To ensure the traceability and global consistency of authentication data,this scheme also integrates blockchain technology,applying its inherent invariance.Then,this paper introduces a reputation-driven dynamic node grouping mechanism that transparently evaluates and groups’node behavior using smart contracts to enhance network stability.Furthermore,a new RBSFT(Reputation-Based SM9 Friendly-Tolerant)consensus mechanism is proposed for the first time to enhance consensus efficiency by optimizing the PBFT algorithm.RBSFT aims to write authentication information into the blockchain ledger to achieve multi-level optimization of trust management and decision-making efficiency,thereby significantly improving the responsiveness and robustness in high-frequency IoV scenarios.Experimental results show that it excels in authentication,communication efficiency,and computational cost control,making it a feasible solution for achieving IoV security and real-time performance.展开更多
Downregulation of the inwardly rectifying potassium channel Kir4.1 is a key step for inducing retinal Müller cell activation and interaction with other glial cells,which is involved in retinal ganglion cell apopt...Downregulation of the inwardly rectifying potassium channel Kir4.1 is a key step for inducing retinal Müller cell activation and interaction with other glial cells,which is involved in retinal ganglion cell apoptosis in glaucoma.Modulation of Kir4.1 expression in Müller cells may therefore be a potential strategy for attenuating retinal ganglion cell damage in glaucoma.In this study,we identified seven predicted phosphorylation sites in Kir4.1 and constructed lentiviral expression systems expressing Kir4.1 mutated at each site to prevent phosphorylation.Following this,we treated Müller glial cells in vitro and in vivo with the m Glu R I agonist DHPG to induce Kir4.1 or Kir4.1 Tyr^(9)Asp overexpression.We found that both Kir4.1 and Kir4.1 Tyr^(9)Asp overexpression inhibited activation of Müller glial cells.Subsequently,we established a rat model of chronic ocular hypertension by injecting microbeads into the anterior chamber and overexpressed Kir4.1 or Kir4.1 Tyr^(9)Asp in the eye,and observed similar results in Müller cells in vivo as those seen in vitro.Both Kir4.1 and Kir4.1 Tyr^(9)Asp overexpression inhibited Müller cell activation,regulated the balance of Bax/Bcl-2,and reduced the m RNA and protein levels of pro-inflammatory factors,including interleukin-1βand tumor necrosis factor-α.Furthermore,we investigated the regulatory effects of Kir4.1 and Kir4.1 Tyr^(9)Asp overexpression on the release of pro-inflammatory factors in a co-culture system of Müller glial cells and microglia.In this co-culture system,we observed elevated adenosine triphosphate concentrations in activated Müller cells,increased levels of translocator protein(a marker of microglial activation),and elevated interleukin-1βm RNA and protein levels in microglia induced by activated Müller cells.These changes could be reversed by Kir4.1 and Kir4.1 Tyr^(9)Asp overexpression in Müller cells.Kir4.1 overexpression,but not Kir4.1 Tyr^(9)Asp overexpression,reduced the number of proliferative and migratory microglia induced by activated Müller cells.Collectively,these results suggest that the tyrosine residue at position nine in Kir4.1 may serve as a functional modulation site in the retina in an experimental model of glaucoma.Kir4.1 and Kir4.1 Tyr^(9)Asp overexpression attenuated Müller cell activation,reduced ATP/P2X receptor–mediated interactions between glial cells,inhibited microglial activation,and decreased the synthesis and release of pro-inflammatory factors,consequently ameliorating retinal ganglion cell apoptosis in glaucoma.展开更多
基金supported by the National Natural Science Foundation of China(Grant No.61762071,Grant No.61163025).
文摘The Internet of Vehicles(IoV)operates in highly dynamic and open network environments and faces serious challenges in secure and real-time authentication and consensus mechanisms.Existing methods often suffer from complex certificate management,inefficient consensus protocols,and poor resilience in high-frequency communication,resulting in high latency,poor scalability,and unstable network performance.To address these issues,this paper proposes a secure and efficient distributed authentication scheme for IoV with reputation-driven consensus and SM9.First,this paper proposes a decentralized authentication architecture that utilizes the certificate-free feature of SM9,enabling lightweight authentication and key negotiation,thereby reducing the complexity of key management.To ensure the traceability and global consistency of authentication data,this scheme also integrates blockchain technology,applying its inherent invariance.Then,this paper introduces a reputation-driven dynamic node grouping mechanism that transparently evaluates and groups’node behavior using smart contracts to enhance network stability.Furthermore,a new RBSFT(Reputation-Based SM9 Friendly-Tolerant)consensus mechanism is proposed for the first time to enhance consensus efficiency by optimizing the PBFT algorithm.RBSFT aims to write authentication information into the blockchain ledger to achieve multi-level optimization of trust management and decision-making efficiency,thereby significantly improving the responsiveness and robustness in high-frequency IoV scenarios.Experimental results show that it excels in authentication,communication efficiency,and computational cost control,making it a feasible solution for achieving IoV security and real-time performance.
基金supported by the National Natural Science Foundation of China,Nos.32271043(to ZW)and 82171047(to YM)the both Science and Technology Major Project of Shanghai,No.2018SHZDZX01 and ZJLabShanghai Center for Brain Science and Brain-Inspired Technology(to ZW)。
文摘Downregulation of the inwardly rectifying potassium channel Kir4.1 is a key step for inducing retinal Müller cell activation and interaction with other glial cells,which is involved in retinal ganglion cell apoptosis in glaucoma.Modulation of Kir4.1 expression in Müller cells may therefore be a potential strategy for attenuating retinal ganglion cell damage in glaucoma.In this study,we identified seven predicted phosphorylation sites in Kir4.1 and constructed lentiviral expression systems expressing Kir4.1 mutated at each site to prevent phosphorylation.Following this,we treated Müller glial cells in vitro and in vivo with the m Glu R I agonist DHPG to induce Kir4.1 or Kir4.1 Tyr^(9)Asp overexpression.We found that both Kir4.1 and Kir4.1 Tyr^(9)Asp overexpression inhibited activation of Müller glial cells.Subsequently,we established a rat model of chronic ocular hypertension by injecting microbeads into the anterior chamber and overexpressed Kir4.1 or Kir4.1 Tyr^(9)Asp in the eye,and observed similar results in Müller cells in vivo as those seen in vitro.Both Kir4.1 and Kir4.1 Tyr^(9)Asp overexpression inhibited Müller cell activation,regulated the balance of Bax/Bcl-2,and reduced the m RNA and protein levels of pro-inflammatory factors,including interleukin-1βand tumor necrosis factor-α.Furthermore,we investigated the regulatory effects of Kir4.1 and Kir4.1 Tyr^(9)Asp overexpression on the release of pro-inflammatory factors in a co-culture system of Müller glial cells and microglia.In this co-culture system,we observed elevated adenosine triphosphate concentrations in activated Müller cells,increased levels of translocator protein(a marker of microglial activation),and elevated interleukin-1βm RNA and protein levels in microglia induced by activated Müller cells.These changes could be reversed by Kir4.1 and Kir4.1 Tyr^(9)Asp overexpression in Müller cells.Kir4.1 overexpression,but not Kir4.1 Tyr^(9)Asp overexpression,reduced the number of proliferative and migratory microglia induced by activated Müller cells.Collectively,these results suggest that the tyrosine residue at position nine in Kir4.1 may serve as a functional modulation site in the retina in an experimental model of glaucoma.Kir4.1 and Kir4.1 Tyr^(9)Asp overexpression attenuated Müller cell activation,reduced ATP/P2X receptor–mediated interactions between glial cells,inhibited microglial activation,and decreased the synthesis and release of pro-inflammatory factors,consequently ameliorating retinal ganglion cell apoptosis in glaucoma.
