Accurate design of spatially separated double active site in Bi_(4)NbO_(8)Cl single crystal to promote Z-Scheme photocatalytic overall water splitting

The efficiency of photocatalytic overall water splitting was mainly limited by the slow reaction kinetics of water oxidation.How to design effective surface active site to overcome the slow water oxidation reaction was a major challenge.Here,we propose a strategy to accelerate surface water oxidation through the fabrication spatially separated double active sites.FeCoPi/Bi_(4)NbO_(8)Cl-OVs photocatalyst with spatially separated double active site was prepared by hydrogen reduction photoanode deposition method.Due to the high matching of the spatial loading positions of FeCoPi and OVs with the photogenerated charge distribution of Bi_(4)NbO_(8)Cl and corresponding reaction mechanisms of substrate,the FeCoPi and OVs on the(001)and(010)crystal planes of Bi_(4)NbO_(8)Cl photocatalyst provided surface active site for water oxidation reaction and electron shuttle reaction(Fe^(3+)/Fe^(2+)),respectively.Under visible light irradiation,the evolution O_(2)rate of FeCoPi/Bi_(4)NbO_(8)Cl OVs was 16.8μmol h^(-1),as 32.9 times as Bi_(4)NbO_(8)Cl.Furthermore,a hydrogen evolution co-catalyst PtRu@Cr_(2)O_(3)was prepared by sequential photodeposition method.Due to the introduction of Ru,the Schottky barrier between PbTiO_(3)and Pt was effectively reduced,which promoted the transfer of photogenerated electrons to PtRu@Cr_(2)O_(3)thermodynamically,the evolution H_(2)rate on PtRu@Cr_(2)O_(3)/PbTiO_(3)increased to 664.8 times.On based of the synchronous enhancement of the water oxidation performance on FeCoPi/Bi_(4)NbO_(8)Cl-OVs and water reduction performance on PtRu@Cr_(2)O_(3)/PbTiO_(3),a novel Z-Scheme photocatalytic overall water splitting system(FeCoPi/Bi_(4)NbO_(8)Cl-OVs)mediated by Fe^(3+)/Fe^(2+)had successfully constructed.Under visible light irradiation,the evolution rates of H_(2)and O_(2)were 2.5 and 1.3μmol h^(-1),respectively.This work can provide some reference for the design of active site and the controllable synthesis of OVs spatial position.On the other hand,the hydrogen evolution co catalyst(PtRu@Cr_(2)O_(3))and the co catalyst FeCoPi for oxygen evolution contributed to the construction of an overall water splitting system.

THE USING O THE LIGHT WORKSHOP APPARATUS IN HAND INJURIES

ＴＨＥＵＳＩＮＧＯＴＨＥＬＩＧＨＴＷＯＲＫＳＨＯＰＡＰＰＡＲＡＴＵＳＩＮＨＡＮＤＩＮＪＵＲＩＥＳＴＨＥＵＳＩＮＧＯＴＨＥＬＩＧＨＴＷＯＲＫＳＨＯＰＡＰＰＡＲＡＴＵＳＩＮＨＡＮＤＩＮＪＵＲＩＥＳＷａｎｇＣｕｉｌａｎ；ＨａｎｇＭｉｎｑｉ；ＳｈｉＪｉａｎ；...

公路浆砌片石挡土墙的质量控制与病害处理综述

针对公路工程中应用最为广泛的浆砌片石挡土墙,从原材料和施工工艺上综述了浆砌片石挡土墙的质量控制要点,归纳了浆砌片石挡土墙常见的病害表现形式和病害处理措施,同时整理了近年来浆砌片石挡土墙加固方面的最新成果,以供广大工程技术人员参考,旨在提高浆砌片石挡土墙的整体建造水平。

山区农村公路线形设计浅析

以山区农村公路为研究对象,概述了农村公路线形设计的主要规范,同时从平面线形、纵断面线形以及平、纵组合线形三个方面分析了山区农村公路在线形设计中需要注意的地方,并结合工程实践经验总结了山区农村公路设计中需要考虑的工程造价、协调难度等问题,以供相关农村公路设计人员参考。

CD97 negatively regulates the innate immune response against RNA viruses by promoting RNF125-mediated RIG-I degradation

The G protein-coupled receptor ADGRE5(CD97)binds to various metabolites that play crucial regulatory roles in metabolism.However,its function in the antiviral innate immune response remains to be determined.In this study,we report that CD97 inhibits virus-induced type-I interferon(IFN-I)release and enhances RNA virus replication in cells and mice.CD97 was identified as a new negative regulator of the innate immune receptor RIG-I,and RIG-1 degradation led to the suppression of the IFN-I signaling pathway.Furthermore,overexpression of CD97 promoted the ubiquitination of RIG-I,resulting in its degradation,but did not impact its mRNA expression.Mechanistically,CD97 upregulates RNF125 expression to induce RNF125-mediated RIG-I degradation via K48-linked ubiquitination at Lys181 after RNA virus infection.Most importantly,CD97-deficient mice are more resistant than wild-type mice to RNA virus infection.We also found that sanguinarine-mediated inhibition of CD97 effectively blocks VSV and SARS-CoV-2 replication.These findings elucidate a previously unknown mechanism through which CD97 negatively regulates RIG-I in the antiviral innate immune response and provide a molecular basis for the development of new therapeutic strategies and the design of targeted antiviral agents.

某斜交实心板桥极限承载能力研究

以湖北省五峰土家族自治县某斜交实心板桥为工程背景,考虑混凝土的材料的非线性,分析斜交实心板桥在极限承载状态下的受力状况,同时研究汽车荷载加载过程中结构挠度、应力和裂缝的变化规律。分析结果表明:当汽车荷载达到公路-Ⅱ级的60%时,斜交实心板桥的结构受力进入非线性;当汽车荷载达到公路-Ⅱ级的2.364倍时斜交实心板桥达到极限承载能力,斜交实心板桥具有足够的安全储备;随着荷载的增大,斜交实心板桥的挠度、应力、裂缝宽度最大值均逐渐增大,且存在较为明显的非线性关系;随着荷载的增大,裂缝的顺桥向分布宽度逐渐增大,横桥向分布走向不完全平行于桥梁端部,稍向斜交板钝角方向偏转。

SARS-CoV-2 ORF10 suppresses the antiviral innate immune response by degrading MAVS through mitophagy

The global coronavirus disease 2019(COVID-19)pandemic caused by severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)has caused severe morbidity and mortality in humans.It is urgent to understand the function of viral genes.However,the function of open reading frame 10(ORF10),which is uniquely expressed by SARS-CoV-2,remains unclear.In this study,we showed that overexpression of ORF10 markedly suppressed the expression of type I interferon(IFN-I)genes and IFN-stimulated genes.Then,mitochondrial antiviral signaling protein(MAVS)was identified as the target via which ORF10 suppresses the IFN-I signaling pathway,and MAVS was found to be degraded through the ORF10-induced autophagy pathway.Furthermore,overexpression of ORF10 promoted the accumulation of LC3 in mitochondria and induced mitophagy.Mechanistically,ORF10 was translocated to mitochondria by interacting with the mitophagy receptor Nip3-like protein X(NIX)and induced mitophagy through its interaction with both NIX and LC3B.Moreover,knockdown of NIX expression blocked mitophagy activation,MAVS degradation,and IFN-I signaling pathway inhibition by ORF10.Consistent with our observations,in the context of SARS-CoV-2 infection,ORF10 inhibited MAVS expression and facilitated viral replication.In brief,our results reveal a novel mechanism by which SARS-CoV-2 inhibits the innate immune response;that is,ORF10 induces mitophagy-mediated MAVS degradation by binding to NIX.

A review on the influence of intelligent power consumption technologies on the utilization rate of distribution network equipment

The economy of distribution networks largely depends on the utilization rate of distribution network equipment.Most of the emerging intelligent power consumption technologies have a positive effect on equipment utilization and their use can save investment of distribution networks.In this paper,the influence of intelligent power consumption technologies on the utilization rate of distribution network equipment is reviewed.The evaluation methods and indexes are assessed first and then intelligent power consumption equipment with energy storage function,vehicle-to-grid(V2G)technology and time-of-use(TOU)tariff are reviewed respectively.It is concluded that these intelligent power consumption technologies and measures have great potential to improve utilization rate of distribution network equipment because of their effective improvement to power load.Meanwhile,recommendations on how to utilize these intelligent power consumption technologies to improve utilization rate of distribution network equipment are proposed.

Synthetic vitamin K analogs inhibit inflammation by targeting the NLRP3 inflammasome

Vitamin K refers to a group of structurally similar vitamins that are essential for proper blood coagulation,as well as bone and cardiovascular health.Previous studies have indicated that vitamin K may also have anti-inflammatory properties,although the underlying mechanisms of its anti-inflammatory effects remain unclear.The NLRP3 inflammasome is a multiprotein complex,and its activation leads to IL-1βand IL-18 secretion and contributes to the pathogenesis of various human inflammatory diseases.Here,we show that synthetic vitamins K3 and K4 are selective,potent inhibitors of the NLRP3 inflammasome and specifically block the interaction between NLRP3 and ASC,thereby inhibiting NLRP3 inflammasome assembly.Moreover,we show that treatment with vitamin K3 or K4 attenuates the severity of inflammation in a mouse model of peritonitis.Our results demonstrate that vitamins K3 and K4 exert their anti-inflammatory effects by inhibiting NLRP3 inflammasome activation and indicate that vitamin K supplementation may be a treatment option for NLRP3-associated inflammatory diseases.

Theoretical study on characteristic ionic radii

The characteristic radii for univalent cations and anions were defined by the classical turning point of the electron movement in an ion. The numerical results of the elements from first- to third-rows in the periodic table were obtained using %ab initio% method. The results correlate quite well with Pauling ionic radii and Shannon and Prewitt ionic radii.

RRx-001 ameliorates inflammatory diseases by acting as a potent covalent NLRP3 inhibitor

The NLRP3 inflammasome plays a crucial role in innate immune-mediated inflammation and contributes to the pathogenesis of multiple autoinflammatory,metabolic and neurodegenerative diseases,but medications targeting the NLRP3 inflammasome are not available for clinical use.RRx-001 is a well-tolerated anticancer agent currently being investigated in phase III clinical trials,but its effects on inflammatory diseases are not known.Here,we show that RRx-001 is a highly selective and potent NLRP3 inhibitor that has strong beneficial effects on NLRP3-driven inflammatory diseases.RRx-001 inhibits the activation of the canonical,noncanonical,and alternative NLRP3 inflammasomes but not the AIM2,NLRC4 or Pyrin inflammasomes.Mechanistically,RRx-001 covalently binds to cysteine 409 of NLRP3 via its bromoacetyl group and therefore blocks the NLRP3-NEK7 interaction,which is critical for the assembly and activation of the NLRP3 inflammasome.More importantly,RRx-001 treatment attenuates the symptoms of lipopolysaccharide(LPS)-induced systemic inflammation,dextran sulfate sodium(DSS)-induced colitis and experimental autoimmune encephalomyelitis(EAE)in mice.Thus,our study identifies RRx-001 as a new potential therapeutic agent for NLRP3-driven diseases.