A microgravity environment has been shown to cause ocular damage and affect visual acuity,but the underlying mechanisms remain unclear.Therefore,we established an animal model of weightlessness via tail suspension to ...A microgravity environment has been shown to cause ocular damage and affect visual acuity,but the underlying mechanisms remain unclear.Therefore,we established an animal model of weightlessness via tail suspension to examine the pathological changes and molecular mechanisms of retinal damage under microgravity.After 4 weeks of tail suspension,there were no notable alterations in retinal function and morphology,while after 8 weeks of tail suspension,significant reductions in retinal function were observed,and the outer nuclear layer was thinner,with abundant apoptotic cells.To investigate the mechanism underlying the degenerative changes that occurred in the outer nuclear layer of the retina,proteomics was used to analyze differentially expressed proteins in rat retinas after 8 weeks of tail suspension.The results showed that the expression levels of fibroblast growth factor 2(also known as basic fibroblast growth factor)and glial fibrillary acidic protein,which are closely related to Müller cell activation,were significantly upregulated.In addition,Müller cell regeneration and Müller cell gliosis were observed after 4 and 8 weeks,respectively,of simulated weightlessness.These findings indicate that Müller cells play an important regulatory role in retinal outer nuclear layer degeneration during weightlessness.展开更多
目的本研究拟通过视频头脉冲试验(video head impulse test,vHIT)建立军事飞行学员动态前庭眼反射功能的生理参考值范围,为优化军事飞行学员前庭功能评估及选拔标准提供客观依据。方法2023年选取276名男性军事飞行学员作为受试者,年龄17...目的本研究拟通过视频头脉冲试验(video head impulse test,vHIT)建立军事飞行学员动态前庭眼反射功能的生理参考值范围,为优化军事飞行学员前庭功能评估及选拔标准提供客观依据。方法2023年选取276名男性军事飞行学员作为受试者,年龄17~22岁,平均年龄(19.09±1.09)岁。分别测试其头脉冲试验(head impulse paradigm,HIMP)和头脉冲抑制试验(suppression head impulse paradigm,SHIMP)两种vHIT模式的前庭眼动参数。在HIMP模式下检测左前、右前、左水平、右水平、左后和右后半规管功能;在SHIMP模式下检测左水平和右水平功能。结果HIMP模式下测试增益值分别为左前0.85(0.79,0.92)、右前(0.90±0.09)、左水平0.92(0.88,0.96)、右水平0.98(0.93,1.02)、左后0.77(0.72,0.82)、右后半规管0.91(0.84,0.98)。增益不对称值分别为右水平/左水平3%(2%~4%)、左前/右后半规管3%(1%~6%)、右前/左后7%(5%~11%)。SHIMP模式下,增益值分别为左水平0.84(0.81,0.88)和右水平0.86(0.82,0.93);增益不对称值为2%(1%~4%)。右侧增益高于左侧(P<0.05),水平半规管增益高于垂直半规管增益(P<0.05),HIMP模式下水平半规管增益值高于SHIMP模式(P<0.05)。结论本研究建立了两种测试模式的军事飞行学员vHIT生理参考值范围,为下一步有关标准制定提供参考。展开更多
目的失重环境下成骨细胞增殖能力下降是引起失重性骨丢失的重要原因之一,然而其具体机制仍不清楚。本文在前期研究基础上,研究CDK12参与模拟失重抑制成骨细胞增殖的作用及机制。方法采用RPM模拟失重条件,以CDK12高/低表达成骨细胞与对...目的失重环境下成骨细胞增殖能力下降是引起失重性骨丢失的重要原因之一,然而其具体机制仍不清楚。本文在前期研究基础上,研究CDK12参与模拟失重抑制成骨细胞增殖的作用及机制。方法采用RPM模拟失重条件,以CDK12高/低表达成骨细胞与对照组成骨细胞为研究对象,分别采用Ed U染色、流式细胞术、细胞免疫荧光染色、Real time PCR和Western Blot检测成骨细胞增殖、细胞周期、CDK12分布,以及CDK12介导的信号转导的变化,并检测CDK12高表达对失重抑制成骨细胞增殖的挽救作用。结果(1)模拟失重条件抑制成骨细胞增殖,改变细胞周期,下调成骨细胞中CDK12表达;(2)CDK12低表达抑制成骨细胞增殖,且改变细胞周期;(3)模拟失重条件或CDK12低表达抑制了RNAPⅡ磷酸化水平,并下调了DNA复制相关基因表达;(4)模拟失重条件下,CDK12高表达促进成骨细胞增殖、增加RNAPⅡ磷酸化水平,并上调DNA复制相关基因表达,对模拟失重条件抑制成骨细胞增殖具有挽救作用。结论CDK12在模拟失重条件抑制成骨细胞增殖中起重要作用。模拟失重条件下,CDK12表达受到抑制,RNAPⅡ磷酸化水平降低,进而抑制CDC6等DNA复制相关基因表达,改变细胞周期,导致成骨细胞增殖能力下降,而CDK12高表达对模拟失重抑制成骨细胞增殖具有挽救作用。展开更多
基金supported by the Army Laboratory Animal Foundation of China,No.SYDW[2020]22(to TC)the Shaanxi Provincial Key R&D Plan General Project of China,No.2022SF-236(to YM)the National Natural Science Foundation of China,No.82202070(to TC)。
文摘A microgravity environment has been shown to cause ocular damage and affect visual acuity,but the underlying mechanisms remain unclear.Therefore,we established an animal model of weightlessness via tail suspension to examine the pathological changes and molecular mechanisms of retinal damage under microgravity.After 4 weeks of tail suspension,there were no notable alterations in retinal function and morphology,while after 8 weeks of tail suspension,significant reductions in retinal function were observed,and the outer nuclear layer was thinner,with abundant apoptotic cells.To investigate the mechanism underlying the degenerative changes that occurred in the outer nuclear layer of the retina,proteomics was used to analyze differentially expressed proteins in rat retinas after 8 weeks of tail suspension.The results showed that the expression levels of fibroblast growth factor 2(also known as basic fibroblast growth factor)and glial fibrillary acidic protein,which are closely related to Müller cell activation,were significantly upregulated.In addition,Müller cell regeneration and Müller cell gliosis were observed after 4 and 8 weeks,respectively,of simulated weightlessness.These findings indicate that Müller cells play an important regulatory role in retinal outer nuclear layer degeneration during weightlessness.
文摘目的本研究拟通过视频头脉冲试验(video head impulse test,vHIT)建立军事飞行学员动态前庭眼反射功能的生理参考值范围,为优化军事飞行学员前庭功能评估及选拔标准提供客观依据。方法2023年选取276名男性军事飞行学员作为受试者,年龄17~22岁,平均年龄(19.09±1.09)岁。分别测试其头脉冲试验(head impulse paradigm,HIMP)和头脉冲抑制试验(suppression head impulse paradigm,SHIMP)两种vHIT模式的前庭眼动参数。在HIMP模式下检测左前、右前、左水平、右水平、左后和右后半规管功能;在SHIMP模式下检测左水平和右水平功能。结果HIMP模式下测试增益值分别为左前0.85(0.79,0.92)、右前(0.90±0.09)、左水平0.92(0.88,0.96)、右水平0.98(0.93,1.02)、左后0.77(0.72,0.82)、右后半规管0.91(0.84,0.98)。增益不对称值分别为右水平/左水平3%(2%~4%)、左前/右后半规管3%(1%~6%)、右前/左后7%(5%~11%)。SHIMP模式下,增益值分别为左水平0.84(0.81,0.88)和右水平0.86(0.82,0.93);增益不对称值为2%(1%~4%)。右侧增益高于左侧(P<0.05),水平半规管增益高于垂直半规管增益(P<0.05),HIMP模式下水平半规管增益值高于SHIMP模式(P<0.05)。结论本研究建立了两种测试模式的军事飞行学员vHIT生理参考值范围,为下一步有关标准制定提供参考。
文摘目的失重环境下成骨细胞增殖能力下降是引起失重性骨丢失的重要原因之一,然而其具体机制仍不清楚。本文在前期研究基础上,研究CDK12参与模拟失重抑制成骨细胞增殖的作用及机制。方法采用RPM模拟失重条件,以CDK12高/低表达成骨细胞与对照组成骨细胞为研究对象,分别采用Ed U染色、流式细胞术、细胞免疫荧光染色、Real time PCR和Western Blot检测成骨细胞增殖、细胞周期、CDK12分布,以及CDK12介导的信号转导的变化,并检测CDK12高表达对失重抑制成骨细胞增殖的挽救作用。结果(1)模拟失重条件抑制成骨细胞增殖,改变细胞周期,下调成骨细胞中CDK12表达;(2)CDK12低表达抑制成骨细胞增殖,且改变细胞周期;(3)模拟失重条件或CDK12低表达抑制了RNAPⅡ磷酸化水平,并下调了DNA复制相关基因表达;(4)模拟失重条件下,CDK12高表达促进成骨细胞增殖、增加RNAPⅡ磷酸化水平,并上调DNA复制相关基因表达,对模拟失重条件抑制成骨细胞增殖具有挽救作用。结论CDK12在模拟失重条件抑制成骨细胞增殖中起重要作用。模拟失重条件下,CDK12表达受到抑制,RNAPⅡ磷酸化水平降低,进而抑制CDC6等DNA复制相关基因表达,改变细胞周期,导致成骨细胞增殖能力下降,而CDK12高表达对模拟失重抑制成骨细胞增殖具有挽救作用。
