高层次复合型医学人才是推动我国医疗卫生事业高质量发展的主要动力,是回应未来医学挑战实现“健康中国2030”的关键力量。在新医科背景下进行学科交叉,推动多学科融合对于创新人才培养至关重要。新时代,我国医学教育发展水平虽稳步提高...高层次复合型医学人才是推动我国医疗卫生事业高质量发展的主要动力,是回应未来医学挑战实现“健康中国2030”的关键力量。在新医科背景下进行学科交叉,推动多学科融合对于创新人才培养至关重要。新时代,我国医学教育发展水平虽稳步提高,但仍存在医学学科不断分化、聚力不足、医学人才创新性不够以及医学人才培养质量有待提升等突出问题。通过立足行业特色院校医学教育发展新定位,提出多学科融合视域下的“大学科”“大科学”人才培养模式,基于教学系统设计(instructional system design,ISD)模型设计新医科创新人才教学路径及多学科融合的“未来医学+”课程体系,论证并评价该课程体系实施效果,促进多学科融合及创新育人价值的进一步提升。展开更多
The inflammatory microenvironment and neurotoxicity can hinder neuronal regeneration and functional recovery after spinal cord injury.Ruxolitinib,a JAK-STAT inhibitor,exhibits effectiveness in autoimmune diseases,arth...The inflammatory microenvironment and neurotoxicity can hinder neuronal regeneration and functional recovery after spinal cord injury.Ruxolitinib,a JAK-STAT inhibitor,exhibits effectiveness in autoimmune diseases,arthritis,and managing inflammatory cytokine storms.Although studies have shown the neuroprotective potential of ruxolitinib in neurological trauma,the exact mechanism by which it enhances functional recovery after spinal cord injury,particularly its effect on astrocytes,remains unclear.To address this gap,we established a mouse model of T10 spinal cord contusion and found that ruxolitinib effectively improved hindlimb motor function and reduced the area of spinal cord injury.Transcriptome sequencing analysis showed that ruxolitinib alleviated inflammation and immune response after spinal cord injury,restored EAAT2 expression,reduced glutamate levels,and alleviated excitatory toxicity.Furthermore,ruxolitinib inhibited the phosphorylation of JAK2 and STAT3 in the injured spinal cord and decreased the phosphorylation level of nuclear factor kappa-B and the expression of inflammatory factors interleukin-1β,interleukin-6,and tumor necrosis factor-α.Additionally,in glutamate-induced excitotoxicity astrocytes,ruxolitinib restored EAAT2 expression and increased glutamate uptake by inhibiting the activation of STAT3,thereby reducing glutamate-induced neurotoxicity,calcium influx,oxidative stress,and cell apoptosis,and increasing the complexity of dendritic branching.Collectively,these results indicate that ruxolitinib restores glutamate homeostasis by rescuing the expression of EAAT2 in astrocytes,reduces neurotoxicity,and effectively alleviates inflammatory and immune responses after spinal cord injury,thereby promoting functional recovery after spinal cord injury.展开更多
文摘高层次复合型医学人才是推动我国医疗卫生事业高质量发展的主要动力,是回应未来医学挑战实现“健康中国2030”的关键力量。在新医科背景下进行学科交叉,推动多学科融合对于创新人才培养至关重要。新时代,我国医学教育发展水平虽稳步提高,但仍存在医学学科不断分化、聚力不足、医学人才创新性不够以及医学人才培养质量有待提升等突出问题。通过立足行业特色院校医学教育发展新定位,提出多学科融合视域下的“大学科”“大科学”人才培养模式,基于教学系统设计(instructional system design,ISD)模型设计新医科创新人才教学路径及多学科融合的“未来医学+”课程体系,论证并评价该课程体系实施效果,促进多学科融合及创新育人价值的进一步提升。
基金supported by the National Natural Science Foundation of China,No.82272484(to XC).
文摘The inflammatory microenvironment and neurotoxicity can hinder neuronal regeneration and functional recovery after spinal cord injury.Ruxolitinib,a JAK-STAT inhibitor,exhibits effectiveness in autoimmune diseases,arthritis,and managing inflammatory cytokine storms.Although studies have shown the neuroprotective potential of ruxolitinib in neurological trauma,the exact mechanism by which it enhances functional recovery after spinal cord injury,particularly its effect on astrocytes,remains unclear.To address this gap,we established a mouse model of T10 spinal cord contusion and found that ruxolitinib effectively improved hindlimb motor function and reduced the area of spinal cord injury.Transcriptome sequencing analysis showed that ruxolitinib alleviated inflammation and immune response after spinal cord injury,restored EAAT2 expression,reduced glutamate levels,and alleviated excitatory toxicity.Furthermore,ruxolitinib inhibited the phosphorylation of JAK2 and STAT3 in the injured spinal cord and decreased the phosphorylation level of nuclear factor kappa-B and the expression of inflammatory factors interleukin-1β,interleukin-6,and tumor necrosis factor-α.Additionally,in glutamate-induced excitotoxicity astrocytes,ruxolitinib restored EAAT2 expression and increased glutamate uptake by inhibiting the activation of STAT3,thereby reducing glutamate-induced neurotoxicity,calcium influx,oxidative stress,and cell apoptosis,and increasing the complexity of dendritic branching.Collectively,these results indicate that ruxolitinib restores glutamate homeostasis by rescuing the expression of EAAT2 in astrocytes,reduces neurotoxicity,and effectively alleviates inflammatory and immune responses after spinal cord injury,thereby promoting functional recovery after spinal cord injury.
