Future 6G communications are envisioned to enable a large catalogue of pioneering applications.These will range from networked Cyber-Physical Systems to edge computing devices,establishing real-time feedback control l...Future 6G communications are envisioned to enable a large catalogue of pioneering applications.These will range from networked Cyber-Physical Systems to edge computing devices,establishing real-time feedback control loops critical for managing Industry 5.0 deployments,digital agriculture systems,and essential infrastructures.The provision of extensive machine-type communications through 6G will render many of these innovative systems autonomous and unsupervised.While full automation will enhance industrial efficiency significantly,it concurrently introduces new cyber risks and vulnerabilities.In particular,unattended systems are highly susceptible to trust issues:malicious nodes and false information can be easily introduced into control loops.Additionally,Denialof-Service attacks can be executed by inundating the network with valueless noise.Current anomaly detection schemes require the entire transformation of the control software to integrate new steps and can only mitigate anomalies that conform to predefined mathematical models.Solutions based on an exhaustive data collection to detect anomalies are precise but extremely slow.Standard models,with their limited understanding of mobile networks,can achieve precision rates no higher than 75%.Therefore,more general and transversal protection mechanisms are needed to detect malicious behaviors transparently.This paper introduces a probabilistic trust model and control algorithm designed to address this gap.The model determines the probability of any node to be trustworthy.Communication channels are pruned for those nodes whose probability is below a given threshold.The trust control algorithmcomprises three primary phases,which feed themodel with three different probabilities,which are weighted and combined.Initially,anomalous nodes are identified using Gaussian mixture models and clustering technologies.Next,traffic patterns are studied using digital Bessel functions and the functional scalar product.Finally,the information coherence and content are analyzed.The noise content and abnormal information sequences are detected using a Volterra filter and a bank of Finite Impulse Response filters.An experimental validation based on simulation tools and environments was carried out.Results show the proposed solution can successfully detect up to 92%of malicious data injection attacks.展开更多
Glycidol is a common lipid-derived foodborne toxicant mainly presents in refined oils and related foodstuffs.Vascular endothelial cells may be potential targets of the deleterious effects associated with glycidol expo...Glycidol is a common lipid-derived foodborne toxicant mainly presents in refined oils and related foodstuffs.Vascular endothelial cells may be potential targets of the deleterious effects associated with glycidol exposure.In human umbilical vein endothelial cells(HUVECs),we found that glycidol treatment promoted endothelialto-mesenchymal transition(EndMT)at a lower concentration(0.5 mmol/L),while induced apoptosis and inflammation at a higher concentration(1 mmol/L).These harmful effects were achieved by the activation of NF-κB/MAPK signaling pathway and were mediated by reactive oxygen species(ROS).In addition,the protective potential of 6-C-(E-2-fluorostyryl)naringenin(6-CEFN)against glycidol was evaluated and compared with naringenin.HUVECs pre-treated with 6-CEFN,but not naringenin,displayed resistance to endothelial dysfunction caused by glycidol.展开更多
Recent studies have suggested that abnormal acidification of lysosomes induces autophagic accumulation of amyloid-βin neurons,which is a key step in senile plaque formation.Therefore,resto ring normal lysosomal funct...Recent studies have suggested that abnormal acidification of lysosomes induces autophagic accumulation of amyloid-βin neurons,which is a key step in senile plaque formation.Therefore,resto ring normal lysosomal function and rebalancing lysosomal acidification in neurons in the brain may be a new treatment strategy for Alzheimer's disease.Microtubule acetylation/deacetylation plays a central role in lysosomal acidification.Here,we show that inhibiting the classic microtubule deacetylase histone deacetylase 6 with an histone deacetylase 6 shRNA or thehistone deacetylase 6 inhibitor valproic acid promoted lysosomal reacidification by modulating V-ATPase assembly in Alzheimer's disease.Fu rthermore,we found that treatment with valproic acid markedly enhanced autophagy.promoted clearance of amyloid-βaggregates,and ameliorated cognitive deficits in a mouse model of Alzheimer's disease.Our findings demonstrate a previously unknown neuroprotective mechanism in Alzheimer's disease,in which histone deacetylase 6 inhibition by valproic acid increases V-ATPase assembly and lysosomal acidification.展开更多
The influence of sodium silicate on the corrosion behaviour of aluminium alloy 7075-T6 in 0.1 M sodium chloride solution was studied by open circuit potential (OCP) and electrochemical impedance spectroscopy (EIS) tec...The influence of sodium silicate on the corrosion behaviour of aluminium alloy 7075-T6 in 0.1 M sodium chloride solution was studied by open circuit potential (OCP) and electrochemical impedance spectroscopy (EIS) techniques. Scanning electron microscopy (SEM) was used to characterize the AA7075-T6 surface. Silicate can significantly reduce corrosion deterioration and the inhibition efficiency increases with the concentration of Na<sub>2</sub>SiO<sub>3</sub>. The corrosion inhibition mechanism involves the formation of a protective film over the alloy surface by adsorption of aluminosilicate anions from solution, as has also been suggested by others in literature.展开更多
Background:Methionine or lysine has been reported to influence DNA methylation and fat metabolism,but their combined effects in N6-methyl-adenosine(m^(6)A)RNA methylation remain unclarified.The combined effects of rum...Background:Methionine or lysine has been reported to influence DNA methylation and fat metabolism,but their combined effects in N6-methyl-adenosine(m^(6)A)RNA methylation remain unclarified.The combined effects of rumen-protected methionine and lysine(RML)in a low-protein(LP)diet on lipid metabolism,m^(6)A RNA methylation,and fatty acid(FA)profiles in the liver and muscle of lambs were investigated.Sixty-three male lambs were divided into three treatment groups,three pens per group and seven lambs per pen.The lambs were fed a 14.5%crude protein(CP)diet(adequate protein[NP]),12.5%CP diet(LP),and a LP diet plus RML(LP+RML)for 60 d.Results:The results showed that the addition of RML in a LP diet tended to lower the concentrations of plasma leptin(P=0.07),triglyceride(P=0.05),and non-esterified FA(P=0.08).Feeding a LP diet increased the enzyme activity or m RNA expression of lipogenic enzymes and decreased lipolytic enzymes compared with the NP diet.This effect was reversed by supplementation of RML with a LP diet.The inclusion of RML in a LP diet affected the polyunsaturated fatty acids(PUFA),n-3 PUFA,and n-6 PUFA in the liver but not in the muscle,which might be linked with altered expression of FA desaturase-1(FADS1)and acetyl-Co A carboxylase(ACC).A LP diet supplemented with RML increased(P<0.05)total m^(6)A levels in the liver and muscle and were accompanied by decreased expression of fat mass and obesity-associated protein(FTO)and alk B homologue 5(ALKBH5).The m RNA expressions of methyltransferase-like 3(METTL3)and methyltransferase-like 14(METTL14)in the LP+RML diet group were lower than those in the other two groups.Supplementation of RML with a LP diet affected only liver YTH domain family(YTHDF2)proteins(P<0.05)and muscle YTHDF3(P=0.09),which can be explained by limited m^(6)Abinding proteins that were mediated in m RNA fate.Conclusions:Our findings showed that the inclusion of RML in a LP diet could alter fat deposition through modulations of lipogenesis and lipolysis in the liver and muscle.These changes in fat metabolism may be associated with the modification of m^(6)A RNA methylation.展开更多
基金funding by Comunidad de Madrid within the framework of the Multiannual Agreement with Universidad Politécnica de Madrid to encourage research by young doctors(PRINCE project).
文摘Future 6G communications are envisioned to enable a large catalogue of pioneering applications.These will range from networked Cyber-Physical Systems to edge computing devices,establishing real-time feedback control loops critical for managing Industry 5.0 deployments,digital agriculture systems,and essential infrastructures.The provision of extensive machine-type communications through 6G will render many of these innovative systems autonomous and unsupervised.While full automation will enhance industrial efficiency significantly,it concurrently introduces new cyber risks and vulnerabilities.In particular,unattended systems are highly susceptible to trust issues:malicious nodes and false information can be easily introduced into control loops.Additionally,Denialof-Service attacks can be executed by inundating the network with valueless noise.Current anomaly detection schemes require the entire transformation of the control software to integrate new steps and can only mitigate anomalies that conform to predefined mathematical models.Solutions based on an exhaustive data collection to detect anomalies are precise but extremely slow.Standard models,with their limited understanding of mobile networks,can achieve precision rates no higher than 75%.Therefore,more general and transversal protection mechanisms are needed to detect malicious behaviors transparently.This paper introduces a probabilistic trust model and control algorithm designed to address this gap.The model determines the probability of any node to be trustworthy.Communication channels are pruned for those nodes whose probability is below a given threshold.The trust control algorithmcomprises three primary phases,which feed themodel with three different probabilities,which are weighted and combined.Initially,anomalous nodes are identified using Gaussian mixture models and clustering technologies.Next,traffic patterns are studied using digital Bessel functions and the functional scalar product.Finally,the information coherence and content are analyzed.The noise content and abnormal information sequences are detected using a Volterra filter and a bank of Finite Impulse Response filters.An experimental validation based on simulation tools and environments was carried out.Results show the proposed solution can successfully detect up to 92%of malicious data injection attacks.
基金supported by the National Key R&D Program of China(2021YFD2100103)the National Natural Science Foundation of China(32101935).
文摘Glycidol is a common lipid-derived foodborne toxicant mainly presents in refined oils and related foodstuffs.Vascular endothelial cells may be potential targets of the deleterious effects associated with glycidol exposure.In human umbilical vein endothelial cells(HUVECs),we found that glycidol treatment promoted endothelialto-mesenchymal transition(EndMT)at a lower concentration(0.5 mmol/L),while induced apoptosis and inflammation at a higher concentration(1 mmol/L).These harmful effects were achieved by the activation of NF-κB/MAPK signaling pathway and were mediated by reactive oxygen species(ROS).In addition,the protective potential of 6-C-(E-2-fluorostyryl)naringenin(6-CEFN)against glycidol was evaluated and compared with naringenin.HUVECs pre-treated with 6-CEFN,but not naringenin,displayed resistance to endothelial dysfunction caused by glycidol.
基金supported by the National Natural Science Foundation of China,No.82201582(to QT)Scientific and Technological Research Program of Chongqing Municipal Education Commission,No.KJQN202200457(to QT)+3 种基金General Project of Changqing Natural Science Foundation,No.cstc2021jcyjmsxmX0442(to ZL)CQMU Program for Youth Innovation in Future Medicine,No.W0044(to ZD and GH)Direct Research Project for PhD of Chongqing,No.CSTB2022BSXM-JCX0051(to ZL)the Project of the Top-Notch Talent Cultivation Program For the Graduate Students of Chongqing Medical University,No.BJRC202310(to CG)。
文摘Recent studies have suggested that abnormal acidification of lysosomes induces autophagic accumulation of amyloid-βin neurons,which is a key step in senile plaque formation.Therefore,resto ring normal lysosomal function and rebalancing lysosomal acidification in neurons in the brain may be a new treatment strategy for Alzheimer's disease.Microtubule acetylation/deacetylation plays a central role in lysosomal acidification.Here,we show that inhibiting the classic microtubule deacetylase histone deacetylase 6 with an histone deacetylase 6 shRNA or thehistone deacetylase 6 inhibitor valproic acid promoted lysosomal reacidification by modulating V-ATPase assembly in Alzheimer's disease.Fu rthermore,we found that treatment with valproic acid markedly enhanced autophagy.promoted clearance of amyloid-βaggregates,and ameliorated cognitive deficits in a mouse model of Alzheimer's disease.Our findings demonstrate a previously unknown neuroprotective mechanism in Alzheimer's disease,in which histone deacetylase 6 inhibition by valproic acid increases V-ATPase assembly and lysosomal acidification.
文摘The influence of sodium silicate on the corrosion behaviour of aluminium alloy 7075-T6 in 0.1 M sodium chloride solution was studied by open circuit potential (OCP) and electrochemical impedance spectroscopy (EIS) techniques. Scanning electron microscopy (SEM) was used to characterize the AA7075-T6 surface. Silicate can significantly reduce corrosion deterioration and the inhibition efficiency increases with the concentration of Na<sub>2</sub>SiO<sub>3</sub>. The corrosion inhibition mechanism involves the formation of a protective film over the alloy surface by adsorption of aluminosilicate anions from solution, as has also been suggested by others in literature.
基金funded by Chinese Academy of Sciences(Strategic Priority Research Program Grant NO.XDA26040304,XDA26050102)CAS Science and Technology Service Network Initiative(KFJ-STS-ZDTP-075)Innovation Province Project(2019RS3021)。
文摘Background:Methionine or lysine has been reported to influence DNA methylation and fat metabolism,but their combined effects in N6-methyl-adenosine(m^(6)A)RNA methylation remain unclarified.The combined effects of rumen-protected methionine and lysine(RML)in a low-protein(LP)diet on lipid metabolism,m^(6)A RNA methylation,and fatty acid(FA)profiles in the liver and muscle of lambs were investigated.Sixty-three male lambs were divided into three treatment groups,three pens per group and seven lambs per pen.The lambs were fed a 14.5%crude protein(CP)diet(adequate protein[NP]),12.5%CP diet(LP),and a LP diet plus RML(LP+RML)for 60 d.Results:The results showed that the addition of RML in a LP diet tended to lower the concentrations of plasma leptin(P=0.07),triglyceride(P=0.05),and non-esterified FA(P=0.08).Feeding a LP diet increased the enzyme activity or m RNA expression of lipogenic enzymes and decreased lipolytic enzymes compared with the NP diet.This effect was reversed by supplementation of RML with a LP diet.The inclusion of RML in a LP diet affected the polyunsaturated fatty acids(PUFA),n-3 PUFA,and n-6 PUFA in the liver but not in the muscle,which might be linked with altered expression of FA desaturase-1(FADS1)and acetyl-Co A carboxylase(ACC).A LP diet supplemented with RML increased(P<0.05)total m^(6)A levels in the liver and muscle and were accompanied by decreased expression of fat mass and obesity-associated protein(FTO)and alk B homologue 5(ALKBH5).The m RNA expressions of methyltransferase-like 3(METTL3)and methyltransferase-like 14(METTL14)in the LP+RML diet group were lower than those in the other two groups.Supplementation of RML with a LP diet affected only liver YTH domain family(YTHDF2)proteins(P<0.05)and muscle YTHDF3(P=0.09),which can be explained by limited m^(6)Abinding proteins that were mediated in m RNA fate.Conclusions:Our findings showed that the inclusion of RML in a LP diet could alter fat deposition through modulations of lipogenesis and lipolysis in the liver and muscle.These changes in fat metabolism may be associated with the modification of m^(6)A RNA methylation.
