目的:比较Fuji IX GP玻璃离子水门汀、3M ESPE Filtek^(TM) Bulk Fill Flowable树脂、VOCO Polofil Supra树脂及Beautiful Flow Plus F03树脂修复根面龋的临床疗效。方法:选取后牙根面龋患者128例(422颗患牙),按照充填修复材料分为A组(F...目的:比较Fuji IX GP玻璃离子水门汀、3M ESPE Filtek^(TM) Bulk Fill Flowable树脂、VOCO Polofil Supra树脂及Beautiful Flow Plus F03树脂修复根面龋的临床疗效。方法:选取后牙根面龋患者128例(422颗患牙),按照充填修复材料分为A组(Fuji IX GP玻璃离子水门汀修复)34例、B组(3M ESPE Filtek^(TM) Bulk Fill Flowable树脂修复)29例、C组(VOCO Polofil Supra树脂修复)35例、D组(Beautiful Flow Plus F03树脂修复)30例。手术治疗后随访6个月,比较4组患者牙髓活力、材料密合性、充填物表面磨损及充填物完好性情况。结果:术后6个月,4组患者牙髓活力均正常。A组、B组、C组、D组材料密合性好的患牙占比分别为75.49%、90.74%、88.57%、97.20%,A组低于B组、C组、D组,差异均有统计学意义(P<0.05);B组与D组、C组与D组比较,差异均有统计学意义(P<0.05),B、C组之间差异无统计学意义(P>0.05)。A组、B组、C组、D组充填物表面无磨损的患牙占比分别为77.45%、95.37%、94.29%、99.07%,A组占比低于B组、C组及D组,差异均有统计学意义(P<0.05);B组与C组、B组与D组、C组与D组间比较,差异均无统计学意义(P>0.05)。A组、B组、C组、D组充填物完好的患牙占比分别为91.18%、97.22%、97.14%、99.07%,A组占比低于D组,差异有统计学意义(P<0.05)。其他组之间比较,差异均无统计学意义(P>0.05)。结论:4种材料对牙髓活力均无影响,树脂类材料在密合性、表面磨损情况以及完好性上均优于Fuji IX GP玻璃离子水门汀。三种树脂类材料中Beautiful Flow Plus F03在密闭性方面优于其他两种树脂。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
文摘目的:比较Fuji IX GP玻璃离子水门汀、3M ESPE Filtek^(TM) Bulk Fill Flowable树脂、VOCO Polofil Supra树脂及Beautiful Flow Plus F03树脂修复根面龋的临床疗效。方法:选取后牙根面龋患者128例(422颗患牙),按照充填修复材料分为A组(Fuji IX GP玻璃离子水门汀修复)34例、B组(3M ESPE Filtek^(TM) Bulk Fill Flowable树脂修复)29例、C组(VOCO Polofil Supra树脂修复)35例、D组(Beautiful Flow Plus F03树脂修复)30例。手术治疗后随访6个月,比较4组患者牙髓活力、材料密合性、充填物表面磨损及充填物完好性情况。结果:术后6个月,4组患者牙髓活力均正常。A组、B组、C组、D组材料密合性好的患牙占比分别为75.49%、90.74%、88.57%、97.20%,A组低于B组、C组、D组,差异均有统计学意义(P<0.05);B组与D组、C组与D组比较,差异均有统计学意义(P<0.05),B、C组之间差异无统计学意义(P>0.05)。A组、B组、C组、D组充填物表面无磨损的患牙占比分别为77.45%、95.37%、94.29%、99.07%,A组占比低于B组、C组及D组,差异均有统计学意义(P<0.05);B组与C组、B组与D组、C组与D组间比较,差异均无统计学意义(P>0.05)。A组、B组、C组、D组充填物完好的患牙占比分别为91.18%、97.22%、97.14%、99.07%,A组占比低于D组,差异有统计学意义(P<0.05)。其他组之间比较,差异均无统计学意义(P>0.05)。结论:4种材料对牙髓活力均无影响,树脂类材料在密合性、表面磨损情况以及完好性上均优于Fuji IX GP玻璃离子水门汀。三种树脂类材料中Beautiful Flow Plus F03在密闭性方面优于其他两种树脂。
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.
