●AIM:To determine the teaching effects of a real-time three dimensional(3D)visualization system in the operating room for early-stage phacoemulsification training.●METHODS:A total of 10 ophthalmology residents of th...●AIM:To determine the teaching effects of a real-time three dimensional(3D)visualization system in the operating room for early-stage phacoemulsification training.●METHODS:A total of 10 ophthalmology residents of the first-year postgraduate were included.All the residents were novices to cataract surgery.Real-time cataract surgical observations were performed using a custom-built 3D visualization system.The training lasted 4wk(32h)in all.A modified International Council of Ophthalmology’s Ophthalmology Surgical Competency Assessment Rubric(ICO-OSCAR)containing 4 specific steps of cataract surgery was applied.The self-assessment(self)and expert-assessment(expert)were performed through the microsurgical attempts in the wet lab for each participant.●RESULTS:Compared with pre-training assessments(self 3.2±0.8,expert 2.5±0.6),the overall mean scores of posttraining(self 5.2±0.4,expert 4.7±0.6)were significantly improved after real-time observation training of 3D visualization system(P<0.05).Scores of 4 surgical items were significantly improved both self and expert assessment after training(P<0.05).●CONCLUSION:The 3D observation training provides novice ophthalmic residents with a better understanding of intraocular microsurgical techniques.It is a useful tool to improve teaching efficiency of surgical education.展开更多
目的研究程序性细胞死亡蛋白4(programmed cell death protein 4,PDCD4)在脓毒症诱导的急性肾损伤(acute kidney injury,AKI)中的作用机制,以及调控PDCD4表达通过丝裂原活化蛋白激酶3(mitogen-activated protein kinase 3,MAP2K3)和p38...目的研究程序性细胞死亡蛋白4(programmed cell death protein 4,PDCD4)在脓毒症诱导的急性肾损伤(acute kidney injury,AKI)中的作用机制,以及调控PDCD4表达通过丝裂原活化蛋白激酶3(mitogen-activated protein kinase 3,MAP2K3)和p38蛋白激酶(p38 mitogen-activated protein kinase,p38 MAPK)对脓毒症AKI起到潜在治疗作用。方法用脂多糖(lipopolysaccharide,LPS)刺激人肾小管上皮细胞(HK-2)构建脓毒症AKI细胞模型。进一步用腺病毒介导siRNA和过表达载体抑制和上调AKI细胞模型中PDCD4的表达;CCK-8法检测细胞增殖;用DCFH-DA及激光共聚焦显微镜检测细胞中ROS水平,用总SOD活性检测试剂和MDA检测试剂盒检测细胞中SOD和MDA水平;免疫共沉淀验证PDCD4和MAP2K3之间的蛋白相互作用;TUNEL染色法检测细胞凋亡;RT-qPCR和Western blot检测PDCD4及相关基因的mRNA和蛋白表达水平;ELISA法检测患者血清中炎症相关因子水平。结果LPS诱导可以促进HK-2细胞中PDCD4表达,下调PDCD4可抑制LPS诱导的HK-2细胞的炎症、氧化应激及细胞凋亡。数据库预测及免疫共沉淀证实PDCD4可以与MAP2K3相互作用,且在LPS诱导的HK-2细胞中,MAP2K3表达水平显著增强。MAP2K3过表达和p38 MAPK激动剂可以减轻PDCD4下调对LPS诱导的细胞炎症和氧化应激的影响并抑制细胞凋亡。结论下调PDCD4可以通过抑制MAP2K3和p38 MAPK从而抑制LPS诱导的肾小管上皮细胞的炎症和凋亡。展开更多
基金Supported by research grants from the National Key Research and Development Program of China(No.2020YFE0204400)the National Natural Science Foundation of China(No.82271042+1 种基金No.52203191)the Zhejiang Province Key Research and Development Program(No.2023C03090).
文摘●AIM:To determine the teaching effects of a real-time three dimensional(3D)visualization system in the operating room for early-stage phacoemulsification training.●METHODS:A total of 10 ophthalmology residents of the first-year postgraduate were included.All the residents were novices to cataract surgery.Real-time cataract surgical observations were performed using a custom-built 3D visualization system.The training lasted 4wk(32h)in all.A modified International Council of Ophthalmology’s Ophthalmology Surgical Competency Assessment Rubric(ICO-OSCAR)containing 4 specific steps of cataract surgery was applied.The self-assessment(self)and expert-assessment(expert)were performed through the microsurgical attempts in the wet lab for each participant.●RESULTS:Compared with pre-training assessments(self 3.2±0.8,expert 2.5±0.6),the overall mean scores of posttraining(self 5.2±0.4,expert 4.7±0.6)were significantly improved after real-time observation training of 3D visualization system(P<0.05).Scores of 4 surgical items were significantly improved both self and expert assessment after training(P<0.05).●CONCLUSION:The 3D observation training provides novice ophthalmic residents with a better understanding of intraocular microsurgical techniques.It is a useful tool to improve teaching efficiency of surgical education.
文摘目的研究程序性细胞死亡蛋白4(programmed cell death protein 4,PDCD4)在脓毒症诱导的急性肾损伤(acute kidney injury,AKI)中的作用机制,以及调控PDCD4表达通过丝裂原活化蛋白激酶3(mitogen-activated protein kinase 3,MAP2K3)和p38蛋白激酶(p38 mitogen-activated protein kinase,p38 MAPK)对脓毒症AKI起到潜在治疗作用。方法用脂多糖(lipopolysaccharide,LPS)刺激人肾小管上皮细胞(HK-2)构建脓毒症AKI细胞模型。进一步用腺病毒介导siRNA和过表达载体抑制和上调AKI细胞模型中PDCD4的表达;CCK-8法检测细胞增殖;用DCFH-DA及激光共聚焦显微镜检测细胞中ROS水平,用总SOD活性检测试剂和MDA检测试剂盒检测细胞中SOD和MDA水平;免疫共沉淀验证PDCD4和MAP2K3之间的蛋白相互作用;TUNEL染色法检测细胞凋亡;RT-qPCR和Western blot检测PDCD4及相关基因的mRNA和蛋白表达水平;ELISA法检测患者血清中炎症相关因子水平。结果LPS诱导可以促进HK-2细胞中PDCD4表达,下调PDCD4可抑制LPS诱导的HK-2细胞的炎症、氧化应激及细胞凋亡。数据库预测及免疫共沉淀证实PDCD4可以与MAP2K3相互作用,且在LPS诱导的HK-2细胞中,MAP2K3表达水平显著增强。MAP2K3过表达和p38 MAPK激动剂可以减轻PDCD4下调对LPS诱导的细胞炎症和氧化应激的影响并抑制细胞凋亡。结论下调PDCD4可以通过抑制MAP2K3和p38 MAPK从而抑制LPS诱导的肾小管上皮细胞的炎症和凋亡。
