针对空间战场三维图像显示技术的需求,采用MultiGen Creator作为建模工具,Vega作为实时仿真驱动软件,在SGI图形工作站上开发了虚拟机群作战视景仿真系统,设计了系统软硬件体系结构,解决了地形分块、地形LOD(Level of Detail,层次细节)...针对空间战场三维图像显示技术的需求,采用MultiGen Creator作为建模工具,Vega作为实时仿真驱动软件,在SGI图形工作站上开发了虚拟机群作战视景仿真系统,设计了系统软硬件体系结构,解决了地形分块、地形LOD(Level of Detail,层次细节)等大规模地形管理以及与飞行仿真系统的广播内存实时网络接口连接等技术,实现了空间战场环境、特效的逼真显示。仿真结果表明,该系统满足仿真实时性和逼真度指标要求,增加了飞行视景仿真的"沉浸"感。展开更多
AIMTo explore the effect of hydrogen sulfide (H<sub>2</sub>S) on restraint water-immersion stress (RWIS)-induced gastric lesions in rats and the influence of adenosine triphosphate (ATP)-sensitive potassiu...AIMTo explore the effect of hydrogen sulfide (H<sub>2</sub>S) on restraint water-immersion stress (RWIS)-induced gastric lesions in rats and the influence of adenosine triphosphate (ATP)-sensitive potassium (K<sub>ATP</sub>) channels and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway on such an effect.METHODSMale Wistar rats were randomly divided into a control group, a physiological saline (PS) group, a sodium hydrosulfide (NaHS) group, a glibenclamide (Gl) group, Gl plus NaHS group, a pyrrolidine dithiocarbamate (PDTC) group, and a PDTC plus NaHS group. Gastric mucosal injury was induced by RWIS for 3 h in rats, and gastric mucosal damage was analyzed after that. The PS, NaHS (100 μmol/kg body weight), Gl (100 μmol/kg body weight), Gl (100 μmol/kg or 150 μmol/kg body weight) plus NaHS (100 μmol/kg body weight), PDTC (100 μmol/kg body weight), and PDTC (100 μmol/kg body weight) plus NaHS (100 μmol/kg body weight) were respectively injected intravenously before RWIS.RESULTSRWIS induced serious gastric lesions in the rats in the PS pretreatment group. The pretreatment of NaHS (a H<sub>2</sub>S donor) significantly reduced the damage induced by RWIS. The gastric protective effect of the NaHS during RWIS was attenuated by PDTC, an NF-κB inhibitor, and also by glibenclamide, an ATP-sensitive potassium channel blocker, in a dose-dependent manner.CONCLUSIONThese results suggest that exogenous H<sub>2</sub>S plays a protective role against RWIS injury in rats, possibly through modulation of K<sub>ATP</sub> channel opening and the NF-κB dependent pathway.展开更多
文摘针对空间战场三维图像显示技术的需求,采用MultiGen Creator作为建模工具,Vega作为实时仿真驱动软件,在SGI图形工作站上开发了虚拟机群作战视景仿真系统,设计了系统软硬件体系结构,解决了地形分块、地形LOD(Level of Detail,层次细节)等大规模地形管理以及与飞行仿真系统的广播内存实时网络接口连接等技术,实现了空间战场环境、特效的逼真显示。仿真结果表明,该系统满足仿真实时性和逼真度指标要求,增加了飞行视景仿真的"沉浸"感。
基金Natural Science Foundation of Shandong Province,No.ZR2015CL016 and No.ZR2011CL012Colleges and Universities of Shandong Province Science and Technology Plan Projects,No.J11LC17
文摘AIMTo explore the effect of hydrogen sulfide (H<sub>2</sub>S) on restraint water-immersion stress (RWIS)-induced gastric lesions in rats and the influence of adenosine triphosphate (ATP)-sensitive potassium (K<sub>ATP</sub>) channels and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway on such an effect.METHODSMale Wistar rats were randomly divided into a control group, a physiological saline (PS) group, a sodium hydrosulfide (NaHS) group, a glibenclamide (Gl) group, Gl plus NaHS group, a pyrrolidine dithiocarbamate (PDTC) group, and a PDTC plus NaHS group. Gastric mucosal injury was induced by RWIS for 3 h in rats, and gastric mucosal damage was analyzed after that. The PS, NaHS (100 μmol/kg body weight), Gl (100 μmol/kg body weight), Gl (100 μmol/kg or 150 μmol/kg body weight) plus NaHS (100 μmol/kg body weight), PDTC (100 μmol/kg body weight), and PDTC (100 μmol/kg body weight) plus NaHS (100 μmol/kg body weight) were respectively injected intravenously before RWIS.RESULTSRWIS induced serious gastric lesions in the rats in the PS pretreatment group. The pretreatment of NaHS (a H<sub>2</sub>S donor) significantly reduced the damage induced by RWIS. The gastric protective effect of the NaHS during RWIS was attenuated by PDTC, an NF-κB inhibitor, and also by glibenclamide, an ATP-sensitive potassium channel blocker, in a dose-dependent manner.CONCLUSIONThese results suggest that exogenous H<sub>2</sub>S plays a protective role against RWIS injury in rats, possibly through modulation of K<sub>ATP</sub> channel opening and the NF-κB dependent pathway.