采用X射线衍射(XRD)和固体魔角核磁共振硅谱(^(29)Si MAS NMR)技术,研究了不同养护温度下MgO/SiO_2体系水化产物的结构特征.结果表明:死烧MgO比轻烧MgO衍射峰强度更大;水化硅酸镁(M-S-H)凝胶呈结晶性较差、短程有序的层状硅酸盐结构;M-...采用X射线衍射(XRD)和固体魔角核磁共振硅谱(^(29)Si MAS NMR)技术,研究了不同养护温度下MgO/SiO_2体系水化产物的结构特征.结果表明:死烧MgO比轻烧MgO衍射峰强度更大;水化硅酸镁(M-S-H)凝胶呈结晶性较差、短程有序的层状硅酸盐结构;M-S-H含量随着养护温度的升高而增多,相同养护温度下M-S-H的含量随着龄期的延长而增多,50℃下养护28d的试样M-S-H含量最多;养护温度过高会抑制M-S-H的生成;高温养护有利于Q^1向Q^2、Q^2向Q^3转化,使得M-S-H硅氧四面体聚合度提高.展开更多
利用初等方法研究了类似广义Dedekind和S2(h,m,n,k)的算术性质.借助Bernoulli多项式及三角恒等式,探究了S2(qh,m,n,qk)与S2(h,m,n,k)的关系,以及当p为奇素数时sum from b=0 to (p-1) S2(h+bk,m,n,pk)与S2(h,m,n,k)和S2(ph,m,n,k)的关系...利用初等方法研究了类似广义Dedekind和S2(h,m,n,k)的算术性质.借助Bernoulli多项式及三角恒等式,探究了S2(qh,m,n,qk)与S2(h,m,n,k)的关系,以及当p为奇素数时sum from b=0 to (p-1) S2(h+bk,m,n,pk)与S2(h,m,n,k)和S2(ph,m,n,k)的关系,提出并证明了两个恒等式,推广了有关文献的结论.展开更多
TMEM16F is involved in many physiological processes such as blood coagulation,cell membrane fusion and bone mineralization.Activation of TMEM16F has been studied in various central nervous system diseases.High TMEM16F...TMEM16F is involved in many physiological processes such as blood coagulation,cell membrane fusion and bone mineralization.Activation of TMEM16F has been studied in various central nervous system diseases.High TMEM16F level has been also found to participate in microglial phagocytosis and transformation.Microglia-mediated neuroinflammation is a key factor in promoting the progression of Alzheimer’s disease.However,few studies have examined the effects of TMEM16F on neuroinflammation in Alzheimer’s disease.In this study,we established TMEM16F-knockdown AD model in vitro and in vivo to investigate the underlying regulatory mechanism about TMEM16F-mediated neuroinflammation in AD.We performed a Morris water maze test to evaluate the spatial memory ability of animals and detected markers for the microglia M1/M2 phenotype and NLRP3 inflammasome.Our results showed that TMEM16F was elevated in 9-month-old APP/PS1 mice.After TMEM16F knockdown in mice,spatial memory ability was improved,microglia polarization to the M2 phenotype was promoted,NLRP3 inflammasome activation was inhibited,cell apoptosis and Aβplaque deposition in brain tissue were reduced,and brain injury was alleviated.We used amyloid-beta(Aβ_(25-35))to stimulate human microglia to construct microglia models of Alzheimer’s disease.The levels of TMEM16F,inducible nitric oxide synthase(iNOS),proinflammatory cytokines and NLRP3 inflammasome-associated biomarkers were higher in Aβ_(25-35) treated group compared with that in the control group.TMEM16F knockdown enhanced the expression of the M2 phenotype biomarkers Arg1 and Socs3,reduced the release of proinflammatory factors interleukin-1,interleukin-6 and tumor necrosis factor-α,and inhibited NLRP3 inflammasome activation through reducing downstream proinflammatory factors interleukin-1βand interleukin-18.This inhibitory effect of TMEM16F knockdown on M1 microglia was partially reversed by the NLRP3 agonist Nigericin.Our findings suggest that TMEM16F participates in neuroinflammation in Alzheimer’s disease through participating in polarization of microglia and activation of the NLRP3 inflammasome.These results indicate that TMEM16F inhibition may be a potential therapeutic approach for Alzheimer’s disease treatment.展开更多
Lycium barbarum(LB)is a traditional Chinese medicine that has been demonstrated to exhibit a wide variety of biological functions,such as antioxidation,neuroprotection,and immune modulation.One of the main mechanisms ...Lycium barbarum(LB)is a traditional Chinese medicine that has been demonstrated to exhibit a wide variety of biological functions,such as antioxidation,neuroprotection,and immune modulation.One of the main mechanisms of Alzheimer’s disease is that microglia activated by amyloid beta(Aβ)transform from the resting state to an M1 state and release pro-inflammatory cytokines to the surrounding environment.In the present study,immortalized microglial cells were pretreated with L.barbarum extract for 1 hour and then treated with oligomeric Aβfor 23 hours.The results showed that LB extract significantly increased the survival of oligomeric Aβ-induced microglial cells,downregulated the expression of M1 pro-inflammatory markers(inducible nitric oxide synthase,tumor necrosis factorα,interleukin-6,and interleukin-1β),and upregulated the expression of M2 anti-inflammatory markers(arginase-1,chitinase-like protein 3,and interleukin-4).LB extract also inhibited the oligomeric Aβ-induced secretion of tumor necrosis factorα,interleukin-6,and interleukin-1βin microglial cells.The results of in vitro cytological experiments suggest that,in microglial cells,LB extract can inhibit oligomeric Aβ-induced M1 polarization and concomitant inflammatory reactions,and promote M2 polarization.展开更多
文摘采用X射线衍射(XRD)和固体魔角核磁共振硅谱(^(29)Si MAS NMR)技术,研究了不同养护温度下MgO/SiO_2体系水化产物的结构特征.结果表明:死烧MgO比轻烧MgO衍射峰强度更大;水化硅酸镁(M-S-H)凝胶呈结晶性较差、短程有序的层状硅酸盐结构;M-S-H含量随着养护温度的升高而增多,相同养护温度下M-S-H的含量随着龄期的延长而增多,50℃下养护28d的试样M-S-H含量最多;养护温度过高会抑制M-S-H的生成;高温养护有利于Q^1向Q^2、Q^2向Q^3转化,使得M-S-H硅氧四面体聚合度提高.
文摘利用初等方法研究了类似广义Dedekind和S2(h,m,n,k)的算术性质.借助Bernoulli多项式及三角恒等式,探究了S2(qh,m,n,qk)与S2(h,m,n,k)的关系,以及当p为奇素数时sum from b=0 to (p-1) S2(h+bk,m,n,pk)与S2(h,m,n,k)和S2(ph,m,n,k)的关系,提出并证明了两个恒等式,推广了有关文献的结论.
基金supported by the National Natural Science Foundation of China,No.82072941(to QHX)Liaoning Province Key R&D Program Guidance Project,No.2020JH2/10300044Science and Technology Plan Project of Shenyang,No.20-205-4-050(both to XHS)。
文摘TMEM16F is involved in many physiological processes such as blood coagulation,cell membrane fusion and bone mineralization.Activation of TMEM16F has been studied in various central nervous system diseases.High TMEM16F level has been also found to participate in microglial phagocytosis and transformation.Microglia-mediated neuroinflammation is a key factor in promoting the progression of Alzheimer’s disease.However,few studies have examined the effects of TMEM16F on neuroinflammation in Alzheimer’s disease.In this study,we established TMEM16F-knockdown AD model in vitro and in vivo to investigate the underlying regulatory mechanism about TMEM16F-mediated neuroinflammation in AD.We performed a Morris water maze test to evaluate the spatial memory ability of animals and detected markers for the microglia M1/M2 phenotype and NLRP3 inflammasome.Our results showed that TMEM16F was elevated in 9-month-old APP/PS1 mice.After TMEM16F knockdown in mice,spatial memory ability was improved,microglia polarization to the M2 phenotype was promoted,NLRP3 inflammasome activation was inhibited,cell apoptosis and Aβplaque deposition in brain tissue were reduced,and brain injury was alleviated.We used amyloid-beta(Aβ_(25-35))to stimulate human microglia to construct microglia models of Alzheimer’s disease.The levels of TMEM16F,inducible nitric oxide synthase(iNOS),proinflammatory cytokines and NLRP3 inflammasome-associated biomarkers were higher in Aβ_(25-35) treated group compared with that in the control group.TMEM16F knockdown enhanced the expression of the M2 phenotype biomarkers Arg1 and Socs3,reduced the release of proinflammatory factors interleukin-1,interleukin-6 and tumor necrosis factor-α,and inhibited NLRP3 inflammasome activation through reducing downstream proinflammatory factors interleukin-1βand interleukin-18.This inhibitory effect of TMEM16F knockdown on M1 microglia was partially reversed by the NLRP3 agonist Nigericin.Our findings suggest that TMEM16F participates in neuroinflammation in Alzheimer’s disease through participating in polarization of microglia and activation of the NLRP3 inflammasome.These results indicate that TMEM16F inhibition may be a potential therapeutic approach for Alzheimer’s disease treatment.
基金supported by Midstream Research Program for UniversitiesHong Kong Special Administrative Region,China,No.MRP-092-17X。
文摘Lycium barbarum(LB)is a traditional Chinese medicine that has been demonstrated to exhibit a wide variety of biological functions,such as antioxidation,neuroprotection,and immune modulation.One of the main mechanisms of Alzheimer’s disease is that microglia activated by amyloid beta(Aβ)transform from the resting state to an M1 state and release pro-inflammatory cytokines to the surrounding environment.In the present study,immortalized microglial cells were pretreated with L.barbarum extract for 1 hour and then treated with oligomeric Aβfor 23 hours.The results showed that LB extract significantly increased the survival of oligomeric Aβ-induced microglial cells,downregulated the expression of M1 pro-inflammatory markers(inducible nitric oxide synthase,tumor necrosis factorα,interleukin-6,and interleukin-1β),and upregulated the expression of M2 anti-inflammatory markers(arginase-1,chitinase-like protein 3,and interleukin-4).LB extract also inhibited the oligomeric Aβ-induced secretion of tumor necrosis factorα,interleukin-6,and interleukin-1βin microglial cells.The results of in vitro cytological experiments suggest that,in microglial cells,LB extract can inhibit oligomeric Aβ-induced M1 polarization and concomitant inflammatory reactions,and promote M2 polarization.
