探讨基于4M1E管理法(人、机、料、法、环)的干预措施对检验科采血窗口服务质量的影响,建立“技术-服务”协同优化的实证模型。方法:采用回顾性研究,通过RCA(根本原因分析,Root Cause Analysis)思维框架分析2018年-2024年采血窗口的投诉...探讨基于4M1E管理法(人、机、料、法、环)的干预措施对检验科采血窗口服务质量的影响,建立“技术-服务”协同优化的实证模型。方法:采用回顾性研究,通过RCA(根本原因分析,Root Cause Analysis)思维框架分析2018年-2024年采血窗口的投诉案例(n=11),从4M1E五个维度进行分段式改进。采用满意度(年均≥500例)和年投诉总数评估最终效果。结果:患者满意度稳定在96.96%~98.45%;投诉量从5例(2018年)降至0例(2022年-2023年),2024年因流程漏洞回升至3例。结论:4M1E法能系统性提升采血窗口服务质量,但还需要持续优化工作流程与智能化建设,加强医患沟通效率。本研究为检验科质量前管理提供了“技术规范+人文服务”的双轨优化模范。展开更多
Optic nerve injury leads to axonal degeneration and the death of retinal ganglion cells,which ultimately causes vision loss.Notably,current treatments are limited.In the present study,we explored whether neurogenic di...Optic nerve injury leads to axonal degeneration and the death of retinal ganglion cells,which ultimately causes vision loss.Notably,current treatments are limited.In the present study,we explored whether neurogenic differentiation factor 1(NeuroD1 or ND1)overexpression in retinal Müller cells may repair the retina after optic nerve crush in mice.Adult mice were subjected to optic nerve crush followed by intravitreal AAV-7m8-GFAP-GFP-ND1 virus injection.Immunofluorescent staining,multi-electrode array recording,electroretinogram,and visual behavior tests were then performed to examine retinal and optic nerve structure and retinal function at various post-optic nerve crush and virus injection times.Western blot analysis and quantitative reverse transcription polymerase chain reaction were performed to explore the possible mechanisms.Compared with the control virus,specific overexpression of ND1 in Müller cells greatly improved the light responses of retinal ganglion cells and retinal neurons in optic nerve crush-injured mice as early as 1-2 weeks post-virus injection and lasted for up to 4 weeks.Neuronal survival in the ganglion cell layer and synaptic connections in the inner retina were slightly improved at 2 weeks;however,visual behavior,retinal ganglion cell survival,and optic nerve structure were not improved.ND1 transiently enhanced glial cell-derived neurotrophic factor expression in the optic nerve crush-injured retina but hardly inhibited retinal inflammation within 2 weeks.Together,our data indicate that ND1 overexpression in Müller cells improves retinal function in the optic nerve crush-injured retina,and suggest that its neuroprotective effect may be caused by enhanced glial cell-derived neurotrophic factor release.展开更多
文摘探讨基于4M1E管理法(人、机、料、法、环)的干预措施对检验科采血窗口服务质量的影响,建立“技术-服务”协同优化的实证模型。方法:采用回顾性研究,通过RCA(根本原因分析,Root Cause Analysis)思维框架分析2018年-2024年采血窗口的投诉案例(n=11),从4M1E五个维度进行分段式改进。采用满意度(年均≥500例)和年投诉总数评估最终效果。结果:患者满意度稳定在96.96%~98.45%;投诉量从5例(2018年)降至0例(2022年-2023年),2024年因流程漏洞回升至3例。结论:4M1E法能系统性提升采血窗口服务质量,但还需要持续优化工作流程与智能化建设,加强医患沟通效率。本研究为检验科质量前管理提供了“技术规范+人文服务”的双轨优化模范。
基金supported by the Guangdong Grant Key Technologies for Treatment of Brain Disorders,China,No.2018B030332001(to GC)the Natural Science Foundation of Guangdong Province,China,No.2023A1515012397(to YX).
文摘Optic nerve injury leads to axonal degeneration and the death of retinal ganglion cells,which ultimately causes vision loss.Notably,current treatments are limited.In the present study,we explored whether neurogenic differentiation factor 1(NeuroD1 or ND1)overexpression in retinal Müller cells may repair the retina after optic nerve crush in mice.Adult mice were subjected to optic nerve crush followed by intravitreal AAV-7m8-GFAP-GFP-ND1 virus injection.Immunofluorescent staining,multi-electrode array recording,electroretinogram,and visual behavior tests were then performed to examine retinal and optic nerve structure and retinal function at various post-optic nerve crush and virus injection times.Western blot analysis and quantitative reverse transcription polymerase chain reaction were performed to explore the possible mechanisms.Compared with the control virus,specific overexpression of ND1 in Müller cells greatly improved the light responses of retinal ganglion cells and retinal neurons in optic nerve crush-injured mice as early as 1-2 weeks post-virus injection and lasted for up to 4 weeks.Neuronal survival in the ganglion cell layer and synaptic connections in the inner retina were slightly improved at 2 weeks;however,visual behavior,retinal ganglion cell survival,and optic nerve structure were not improved.ND1 transiently enhanced glial cell-derived neurotrophic factor expression in the optic nerve crush-injured retina but hardly inhibited retinal inflammation within 2 weeks.Together,our data indicate that ND1 overexpression in Müller cells improves retinal function in the optic nerve crush-injured retina,and suggest that its neuroprotective effect may be caused by enhanced glial cell-derived neurotrophic factor release.
