在Visual Studio 2008开发环境中,选择ASP.NET 3.5、C#编程语言和SQL Server 2005数据库管理系统开发杂草信息咨询网站。采用表示层、业务逻辑层和数据访问层组成的三层结构,充分利用母页模板、自定义类、ObjectDataSource控件等新技术...在Visual Studio 2008开发环境中,选择ASP.NET 3.5、C#编程语言和SQL Server 2005数据库管理系统开发杂草信息咨询网站。采用表示层、业务逻辑层和数据访问层组成的三层结构,充分利用母页模板、自定义类、ObjectDataSource控件等新技术,提高网站开发效率和性能,并采用数据库绑定的动态网页技术获得了理想的查询效果。展开更多
基于WEB技术开发的在线考试系统可以充分发挥网络的优势，建立大型、高效、共享的题库，实现随时随地进行考试，降低考试成本，减少人为干扰，减轻教师负担，使教师把更多的精力投入到护理及医学教育研究中去，真正实现教考分离，为教...基于WEB技术开发的在线考试系统可以充分发挥网络的优势，建立大型、高效、共享的题库，实现随时随地进行考试，降低考试成本，减少人为干扰，减轻教师负担，使教师把更多的精力投入到护理及医学教育研究中去，真正实现教考分离，为教学内容和教学方法改革奠定基础。本研究把Visual Studio 2008作为主要开发工具，利用最新的ASP．NET3,5动态网页技术和饼程序语言、JavaScript脚本语言、HTML超文本语言，展开更多
Downregulation of the inwardly rectifying potassium channel Kir4.1 is a key step for inducing retinal Müller cell activation and interaction with other glial cells,which is involved in retinal ganglion cell apopt...Downregulation of the inwardly rectifying potassium channel Kir4.1 is a key step for inducing retinal Müller cell activation and interaction with other glial cells,which is involved in retinal ganglion cell apoptosis in glaucoma.Modulation of Kir4.1 expression in Müller cells may therefore be a potential strategy for attenuating retinal ganglion cell damage in glaucoma.In this study,we identified seven predicted phosphorylation sites in Kir4.1 and constructed lentiviral expression systems expressing Kir4.1 mutated at each site to prevent phosphorylation.Following this,we treated Müller glial cells in vitro and in vivo with the m Glu R I agonist DHPG to induce Kir4.1 or Kir4.1 Tyr^(9)Asp overexpression.We found that both Kir4.1 and Kir4.1 Tyr^(9)Asp overexpression inhibited activation of Müller glial cells.Subsequently,we established a rat model of chronic ocular hypertension by injecting microbeads into the anterior chamber and overexpressed Kir4.1 or Kir4.1 Tyr^(9)Asp in the eye,and observed similar results in Müller cells in vivo as those seen in vitro.Both Kir4.1 and Kir4.1 Tyr^(9)Asp overexpression inhibited Müller cell activation,regulated the balance of Bax/Bcl-2,and reduced the m RNA and protein levels of pro-inflammatory factors,including interleukin-1βand tumor necrosis factor-α.Furthermore,we investigated the regulatory effects of Kir4.1 and Kir4.1 Tyr^(9)Asp overexpression on the release of pro-inflammatory factors in a co-culture system of Müller glial cells and microglia.In this co-culture system,we observed elevated adenosine triphosphate concentrations in activated Müller cells,increased levels of translocator protein(a marker of microglial activation),and elevated interleukin-1βm RNA and protein levels in microglia induced by activated Müller cells.These changes could be reversed by Kir4.1 and Kir4.1 Tyr^(9)Asp overexpression in Müller cells.Kir4.1 overexpression,but not Kir4.1 Tyr^(9)Asp overexpression,reduced the number of proliferative and migratory microglia induced by activated Müller cells.Collectively,these results suggest that the tyrosine residue at position nine in Kir4.1 may serve as a functional modulation site in the retina in an experimental model of glaucoma.Kir4.1 and Kir4.1 Tyr^(9)Asp overexpression attenuated Müller cell activation,reduced ATP/P2X receptor–mediated interactions between glial cells,inhibited microglial activation,and decreased the synthesis and release of pro-inflammatory factors,consequently ameliorating retinal ganglion cell apoptosis in glaucoma.展开更多
文摘在Visual Studio 2008开发环境中,选择ASP.NET 3.5、C#编程语言和SQL Server 2005数据库管理系统开发杂草信息咨询网站。采用表示层、业务逻辑层和数据访问层组成的三层结构,充分利用母页模板、自定义类、ObjectDataSource控件等新技术,提高网站开发效率和性能,并采用数据库绑定的动态网页技术获得了理想的查询效果。
文摘基于WEB技术开发的在线考试系统可以充分发挥网络的优势，建立大型、高效、共享的题库，实现随时随地进行考试，降低考试成本，减少人为干扰，减轻教师负担，使教师把更多的精力投入到护理及医学教育研究中去，真正实现教考分离，为教学内容和教学方法改革奠定基础。本研究把Visual Studio 2008作为主要开发工具，利用最新的ASP．NET3,5动态网页技术和饼程序语言、JavaScript脚本语言、HTML超文本语言，
基金supported by the National Natural Science Foundation of China,Nos.32271043(to ZW)and 82171047(to YM)the both Science and Technology Major Project of Shanghai,No.2018SHZDZX01 and ZJLabShanghai Center for Brain Science and Brain-Inspired Technology(to ZW)。
文摘Downregulation of the inwardly rectifying potassium channel Kir4.1 is a key step for inducing retinal Müller cell activation and interaction with other glial cells,which is involved in retinal ganglion cell apoptosis in glaucoma.Modulation of Kir4.1 expression in Müller cells may therefore be a potential strategy for attenuating retinal ganglion cell damage in glaucoma.In this study,we identified seven predicted phosphorylation sites in Kir4.1 and constructed lentiviral expression systems expressing Kir4.1 mutated at each site to prevent phosphorylation.Following this,we treated Müller glial cells in vitro and in vivo with the m Glu R I agonist DHPG to induce Kir4.1 or Kir4.1 Tyr^(9)Asp overexpression.We found that both Kir4.1 and Kir4.1 Tyr^(9)Asp overexpression inhibited activation of Müller glial cells.Subsequently,we established a rat model of chronic ocular hypertension by injecting microbeads into the anterior chamber and overexpressed Kir4.1 or Kir4.1 Tyr^(9)Asp in the eye,and observed similar results in Müller cells in vivo as those seen in vitro.Both Kir4.1 and Kir4.1 Tyr^(9)Asp overexpression inhibited Müller cell activation,regulated the balance of Bax/Bcl-2,and reduced the m RNA and protein levels of pro-inflammatory factors,including interleukin-1βand tumor necrosis factor-α.Furthermore,we investigated the regulatory effects of Kir4.1 and Kir4.1 Tyr^(9)Asp overexpression on the release of pro-inflammatory factors in a co-culture system of Müller glial cells and microglia.In this co-culture system,we observed elevated adenosine triphosphate concentrations in activated Müller cells,increased levels of translocator protein(a marker of microglial activation),and elevated interleukin-1βm RNA and protein levels in microglia induced by activated Müller cells.These changes could be reversed by Kir4.1 and Kir4.1 Tyr^(9)Asp overexpression in Müller cells.Kir4.1 overexpression,but not Kir4.1 Tyr^(9)Asp overexpression,reduced the number of proliferative and migratory microglia induced by activated Müller cells.Collectively,these results suggest that the tyrosine residue at position nine in Kir4.1 may serve as a functional modulation site in the retina in an experimental model of glaucoma.Kir4.1 and Kir4.1 Tyr^(9)Asp overexpression attenuated Müller cell activation,reduced ATP/P2X receptor–mediated interactions between glial cells,inhibited microglial activation,and decreased the synthesis and release of pro-inflammatory factors,consequently ameliorating retinal ganglion cell apoptosis in glaucoma.
