The ultracold neutron(UCN)transport code,MCUCN,designed initially for simulating UCN transportation from a solid deuterium(SD_2)source and neutron electric dipole moment experiments,could not simulate UCN storage and ...The ultracold neutron(UCN)transport code,MCUCN,designed initially for simulating UCN transportation from a solid deuterium(SD_2)source and neutron electric dipole moment experiments,could not simulate UCN storage and transportation in a superfluid^(4)He(SFHe,He-Ⅱ)source accurately.This limitation arose from the absence of an^(4)He upscattering mechanism and the absorption of^(3)He.And the provided source energy distribution in MCUCN is different from that in SFHe source.This study introduced enhancements to MCUCN to address these constraints,explicitly incorporating the^(4)He upscattering effect,the absorption of^(3)He,the loss caused by impurities on converter wall,UCN source energy distribution in SFHe,and the transmission through negative optical potential.Additionally,a Python-based visualization code for intermediate states and results was developed.To validate these enhancements,we systematically compared the simulation results of the Lujan Center Mark3 UCN system by MCUCN and the improved MCUCN code(iMCUCN)with UCNtransport simulations.Additionally,we compared the results of the SUN1 system simulated by MCUCN and iMCUCN with measurement results.The study demonstrates that iMCUCN effectively simulates the storage and transportation of ultracold neutrons in He-Ⅱ.展开更多
目的探讨星状神经节阻滞(SGB)通过长链非编码RNA(lncRNA)牛磺酸上调基因1(TUG1)-NOD样受体热蛋白结构域相关蛋白3(NLRP3)轴在体外脑缺血再灌注模型中对炎症反应和自噬溶酶体形成的调节作用。方法培养大鼠海马神经元细胞系H19-7,并将细...目的探讨星状神经节阻滞(SGB)通过长链非编码RNA(lncRNA)牛磺酸上调基因1(TUG1)-NOD样受体热蛋白结构域相关蛋白3(NLRP3)轴在体外脑缺血再灌注模型中对炎症反应和自噬溶酶体形成的调节作用。方法培养大鼠海马神经元细胞系H19-7,并将细胞分为8组:(i)正常对照组:正常培养的神经元细胞;(ii)氧-糖剥夺/复氧(OGD/R)组:采用氧-糖剥夺/复氧法模拟脑缺血再灌注损伤;(iii)OGD/R+SGB组:OGD/R联合麻醉药0.5%布比卡因用于体外模拟SGB;(iv)OGD/R+SGB+TUG1过表达阴性对照组:OGD/R联合布比卡因并联合TUG1过表达阴性对照质粒转染细胞;(v)OGD/R+SGB+TUG1过表达组:OGD/R联合布比卡因并联合TUG1过表达质粒转染细胞;(vi)OGD/R+SGB+TUG1过表达+MCC950组:OGD/R联合布比卡因、TUG1过表达质粒转染及NLRP3抑制剂MCC950处理细胞;(vii)OGD/R+TUG1过表达组:OGD/R联合TUG1过表达质粒转染细胞;(viii)OGD/R+MCC950组:OGD/R联合NLRP3抑制剂MCC950处理细胞。进一步通过实时定量PCR(Quantitative Real Time PCR,qRTPCR)实验检测细胞中lncRNATUG1的表达;利用Western blot法检测细胞中NLRP3、微管相关蛋白1轻链3(LC3)-I、LC3-II、自噬相关基因5(Atg5)、苄氯素1(beclin1)、自噬接头蛋白(p62)、溶酶体相关膜蛋白1(LAMP1)的表达水平;利用透射电镜(TEM)检测自噬溶酶体的数量;并用酶联免疫吸附测定(ELISA)法检测细胞培养上清中白细胞介素(IL)-1β、IL-6、IL-18、肿瘤坏死因子(TNF)-α的含量。结果与正常对照组相比,OGD/R组lncRNA TUG1、NLRP3、Atg5、beclin1、p62、LAMP1的表达水平以及LC3-II/I比值均显著上调(^(均)P<0.05),自噬溶酶体数量增加(P<0.05),IL-1β、IL-6、IL-18、TNF-α的含量显著升高(^(均)P<0.05)。与OGD/R组相比,OGD/R+SGB组的上述指标均显著下调(P<0.05)。与OGD/R+SGB+TUG1过表达阴性对照组相比,OGD/R+SGB+TUG1过表达组的lncRNA TUG1、NLRP3、Atg5、beclin1、p62、LAMP1的表达水平以及LC3-II/I比值均显著上调(^(均)P<0.05),自噬溶酶体数量增加(P<0.05),IL-1β、IL-6、IL-18、TNF-α的含量显著升高(^(均)P<0.05),然而,加入NLRP3的抑制剂MCC950后,除lncRNA TUG1外其余指标均显著下调(^(均)P<0.05)。另外,与OGD/R组比,OGD/R+TUG1过表达组的上述指标进一步上调(^(均)P<0.05)。与OGD/R组比,OGD/R+MCC950组则抑制了除lncRNA TUG1外的其余指标(^(均)P<0.05)。结论星状神经节阻滞通过调节lncRNA TUG1-NLRP3轴有效减轻体外脑缺血再灌注损伤引起的炎症反应和自噬溶酶体形成,提示其可能作为治疗缺血性脑损伤的潜在策略。展开更多
通过三维离散元分析软件3DEC(3 Dimensional Distinct Element Code),针对卸压孔在不同孔径下的围岩变形情况,较为详细地分析了钻孔卸压在深部巷道中的效果。模拟结果表明,对巷道两帮钻孔卸压以后,应力集中区域由两帮转移到了围岩深部,...通过三维离散元分析软件3DEC(3 Dimensional Distinct Element Code),针对卸压孔在不同孔径下的围岩变形情况,较为详细地分析了钻孔卸压在深部巷道中的效果。模拟结果表明,对巷道两帮钻孔卸压以后,应力集中区域由两帮转移到了围岩深部,且集中在了卸压孔的末端,对深部巷道起到了很好的保护作用,为深部高应力巷道卸压支护提供了依据。展开更多
基金the National Key R&D Program of China(No.2024YFE0110001)the National Natural Science Foundation of China(U1932219)the Mobility Programme endorsed by the Joint Committee of the Sino-German Center(M0728)。
文摘The ultracold neutron(UCN)transport code,MCUCN,designed initially for simulating UCN transportation from a solid deuterium(SD_2)source and neutron electric dipole moment experiments,could not simulate UCN storage and transportation in a superfluid^(4)He(SFHe,He-Ⅱ)source accurately.This limitation arose from the absence of an^(4)He upscattering mechanism and the absorption of^(3)He.And the provided source energy distribution in MCUCN is different from that in SFHe source.This study introduced enhancements to MCUCN to address these constraints,explicitly incorporating the^(4)He upscattering effect,the absorption of^(3)He,the loss caused by impurities on converter wall,UCN source energy distribution in SFHe,and the transmission through negative optical potential.Additionally,a Python-based visualization code for intermediate states and results was developed.To validate these enhancements,we systematically compared the simulation results of the Lujan Center Mark3 UCN system by MCUCN and the improved MCUCN code(iMCUCN)with UCNtransport simulations.Additionally,we compared the results of the SUN1 system simulated by MCUCN and iMCUCN with measurement results.The study demonstrates that iMCUCN effectively simulates the storage and transportation of ultracold neutrons in He-Ⅱ.
文摘目的探讨星状神经节阻滞(SGB)通过长链非编码RNA(lncRNA)牛磺酸上调基因1(TUG1)-NOD样受体热蛋白结构域相关蛋白3(NLRP3)轴在体外脑缺血再灌注模型中对炎症反应和自噬溶酶体形成的调节作用。方法培养大鼠海马神经元细胞系H19-7,并将细胞分为8组:(i)正常对照组:正常培养的神经元细胞;(ii)氧-糖剥夺/复氧(OGD/R)组:采用氧-糖剥夺/复氧法模拟脑缺血再灌注损伤;(iii)OGD/R+SGB组:OGD/R联合麻醉药0.5%布比卡因用于体外模拟SGB;(iv)OGD/R+SGB+TUG1过表达阴性对照组:OGD/R联合布比卡因并联合TUG1过表达阴性对照质粒转染细胞;(v)OGD/R+SGB+TUG1过表达组:OGD/R联合布比卡因并联合TUG1过表达质粒转染细胞;(vi)OGD/R+SGB+TUG1过表达+MCC950组:OGD/R联合布比卡因、TUG1过表达质粒转染及NLRP3抑制剂MCC950处理细胞;(vii)OGD/R+TUG1过表达组:OGD/R联合TUG1过表达质粒转染细胞;(viii)OGD/R+MCC950组:OGD/R联合NLRP3抑制剂MCC950处理细胞。进一步通过实时定量PCR(Quantitative Real Time PCR,qRTPCR)实验检测细胞中lncRNATUG1的表达;利用Western blot法检测细胞中NLRP3、微管相关蛋白1轻链3(LC3)-I、LC3-II、自噬相关基因5(Atg5)、苄氯素1(beclin1)、自噬接头蛋白(p62)、溶酶体相关膜蛋白1(LAMP1)的表达水平;利用透射电镜(TEM)检测自噬溶酶体的数量;并用酶联免疫吸附测定(ELISA)法检测细胞培养上清中白细胞介素(IL)-1β、IL-6、IL-18、肿瘤坏死因子(TNF)-α的含量。结果与正常对照组相比,OGD/R组lncRNA TUG1、NLRP3、Atg5、beclin1、p62、LAMP1的表达水平以及LC3-II/I比值均显著上调(^(均)P<0.05),自噬溶酶体数量增加(P<0.05),IL-1β、IL-6、IL-18、TNF-α的含量显著升高(^(均)P<0.05)。与OGD/R组相比,OGD/R+SGB组的上述指标均显著下调(P<0.05)。与OGD/R+SGB+TUG1过表达阴性对照组相比,OGD/R+SGB+TUG1过表达组的lncRNA TUG1、NLRP3、Atg5、beclin1、p62、LAMP1的表达水平以及LC3-II/I比值均显著上调(^(均)P<0.05),自噬溶酶体数量增加(P<0.05),IL-1β、IL-6、IL-18、TNF-α的含量显著升高(^(均)P<0.05),然而,加入NLRP3的抑制剂MCC950后,除lncRNA TUG1外其余指标均显著下调(^(均)P<0.05)。另外,与OGD/R组比,OGD/R+TUG1过表达组的上述指标进一步上调(^(均)P<0.05)。与OGD/R组比,OGD/R+MCC950组则抑制了除lncRNA TUG1外的其余指标(^(均)P<0.05)。结论星状神经节阻滞通过调节lncRNA TUG1-NLRP3轴有效减轻体外脑缺血再灌注损伤引起的炎症反应和自噬溶酶体形成,提示其可能作为治疗缺血性脑损伤的潜在策略。
文摘通过三维离散元分析软件3DEC(3 Dimensional Distinct Element Code),针对卸压孔在不同孔径下的围岩变形情况,较为详细地分析了钻孔卸压在深部巷道中的效果。模拟结果表明,对巷道两帮钻孔卸压以后,应力集中区域由两帮转移到了围岩深部,且集中在了卸压孔的末端,对深部巷道起到了很好的保护作用,为深部高应力巷道卸压支护提供了依据。
