Rice false smut has become an increasingly serious disease in rice （Oryza sativa L.） production worldwide. The typical feature of this disease is that the fungal pathogen Ustilaginoidea virens （Uv） specifical y in...Rice false smut has become an increasingly serious disease in rice （Oryza sativa L.） production worldwide. The typical feature of this disease is that the fungal pathogen Ustilaginoidea virens （Uv） specifical y infects rice flower and forms false smut bal , the ustiloxin-containing bal-like fungal colony, of which the size is usual y several times larger than that of a mature rice seed. However, the underlying mechanisms of Uv-rice interac-tion are poorly understood. Here, we applied time-course microscopic and transcriptional approaches to investigate rice responses to Uv infection. The results demonstrated that the flower-opening process and expression of associated transcription factors, including ARF6 and ARF8, were inhibited in Uv-infected spikelets. The ovaries in infected spikelets were interrupted in fertilization and thus were unable to set seeds. However, a number of grain-fil ing-related genes, including seed storage protein genes, starch anabolism genes and endosperm-specific transcription factors （RISBZ1 and RPBF）, were highly transcribed as if the ovaries were fertilized. In addition, critical defense-related genes like NPR1 and PR1 were downregulated by;Uv infection. Our data imply that Uv may hijack host nutrient reservoir by activation of the grain-fil ing network because of growth and formation of false smut bal s.展开更多
目的:探查基于"治趣"移动信息化平台的CBL(case based learning)教学方案对内科学教学的效率及质量的影响。方法:选取安康职业技术学院医学院2020届临床医学专业学生100例,按照随机数字表法分为对照组(50例),给予传统教学,观...目的:探查基于"治趣"移动信息化平台的CBL(case based learning)教学方案对内科学教学的效率及质量的影响。方法:选取安康职业技术学院医学院2020届临床医学专业学生100例,按照随机数字表法分为对照组(50例),给予传统教学,观察组(50例),给予基于"治趣"移动信息化平台的CBL教学,观察两组学生学习三个月后内科基础知识、案例分析、临床操作技能以及对基于"治趣"移动信息化平台的CBL教学方案的评价。结果:观察组基础知识、案例分析、临床操作评分显著高于对照组,差异具有统计学意义(P<0.05);观察组学生对基于"治趣"移动信息化平台的CBL教学方案的评价整体优于传统教学。结论:基于"治趣"移动信息化平台的CBL教育模式可加强学生学习的主动性,提高分析问题及解决问题能力,有利于改善学习质量,提高学习效率,值得应用。展开更多
Background Urotensin Ⅱ （UⅡ） is a new vasoconstrictive peptide that may activate the adventitial fibroblasts.Transforming growth factor-β1 （TGF-β1） is an important factor that could induce the phenotypical tran...Background Urotensin Ⅱ （UⅡ） is a new vasoconstrictive peptide that may activate the adventitial fibroblasts.Transforming growth factor-β1 （TGF-β1） is an important factor that could induce the phenotypical transdifferentiation of adventitial fibroblasts. This study aimed to explore whether TGF-β1 is involved in UⅡ-induced phenotypic differentiation of adventitial fibroblasts from rat aorta.Methods Adventitial fibroblasts were prepared by the explant culture method. TGF-β1 protein secretion from the cells was determined by enzyme-linked immunosorbent assay （ELISA）. The mRNA and protein expression of α-smooth nuscle actin （α-SM-actin）, the marker of phenotypic differentiation from fibroblasts to myofibroblasts, were determined using real-time quantitative RT-PCR （real-time RT-PCR） and Western blotting, respectively.Results UⅡ stimulated the secretion of TGF-β1 in cultured adventitial fibroblasts in a time-dependent manner. The secretion reached a peak at 24 hours, was higher by 69.8% （P ＜0.01）, than the control group. This effect was also concentration dependent. Maximal stimulation was reached at 10-8 mol/L of UⅡ （P ＜0.01）, which was increased by 59.9%,compared with in the control group （P ＜0.01）. The secretion of TGF-β1 induced by UⅡ was significantly blocked by SB-710411 （10-7 mol/L）, a specific antagonist of UⅡ receptor. In addition, both UⅡ （10-8 mol/L） and TGF-β1 significantly stimulated α-SM-actin mRNA and protein expression. Moreover, the α-SM-actin induced by UⅡ was inhibited by the specific neutralizing antibody （20 μg/ml） of TGF-β1, while the α-SM-actin expression stimulated by TGF-β1 （20 ng/ml）was inhibited by SB-710411 （10-7 mol/L）, the UⅡ receptor antagonist.Conclusion This study suggests that UⅡ could induce TGF-β1 secretion in adventitial fibroblasts via UT activation, and TGF-β1 might be involved in phenotypic differentiation from adventitial fibroblasts into myofibroblasts induced by UⅡ, and TGF-β1 s展开更多
基金supported by Sichuan Agricultural University start-up packages awarded to W.-M.W.and J.F.grants from the China Postdoctoral Science Foundation (2012M521679 to J.F.)grants from the Special Fund for Agro-Scientific Research in the Public Interest (200903039 to F.H.and W.-X.S.)
文摘Rice false smut has become an increasingly serious disease in rice （Oryza sativa L.） production worldwide. The typical feature of this disease is that the fungal pathogen Ustilaginoidea virens （Uv） specifical y infects rice flower and forms false smut bal , the ustiloxin-containing bal-like fungal colony, of which the size is usual y several times larger than that of a mature rice seed. However, the underlying mechanisms of Uv-rice interac-tion are poorly understood. Here, we applied time-course microscopic and transcriptional approaches to investigate rice responses to Uv infection. The results demonstrated that the flower-opening process and expression of associated transcription factors, including ARF6 and ARF8, were inhibited in Uv-infected spikelets. The ovaries in infected spikelets were interrupted in fertilization and thus were unable to set seeds. However, a number of grain-fil ing-related genes, including seed storage protein genes, starch anabolism genes and endosperm-specific transcription factors （RISBZ1 and RPBF）, were highly transcribed as if the ovaries were fertilized. In addition, critical defense-related genes like NPR1 and PR1 were downregulated by;Uv infection. Our data imply that Uv may hijack host nutrient reservoir by activation of the grain-fil ing network because of growth and formation of false smut bal s.
文摘目的:探查基于"治趣"移动信息化平台的CBL(case based learning)教学方案对内科学教学的效率及质量的影响。方法:选取安康职业技术学院医学院2020届临床医学专业学生100例,按照随机数字表法分为对照组(50例),给予传统教学,观察组(50例),给予基于"治趣"移动信息化平台的CBL教学,观察两组学生学习三个月后内科基础知识、案例分析、临床操作技能以及对基于"治趣"移动信息化平台的CBL教学方案的评价。结果:观察组基础知识、案例分析、临床操作评分显著高于对照组,差异具有统计学意义(P<0.05);观察组学生对基于"治趣"移动信息化平台的CBL教学方案的评价整体优于传统教学。结论:基于"治趣"移动信息化平台的CBL教育模式可加强学生学习的主动性,提高分析问题及解决问题能力,有利于改善学习质量,提高学习效率,值得应用。
基金This project was supported by grants from the National Natural Science Foundation of China （No. 30470730, No. 30971273）, the Natural Science Foundation of Guangdong Province （No. 9151051501000016）, and the Medical Scientific Research Foundation of Guangdong Province, China （No. A2007425）.
文摘Background Urotensin Ⅱ （UⅡ） is a new vasoconstrictive peptide that may activate the adventitial fibroblasts.Transforming growth factor-β1 （TGF-β1） is an important factor that could induce the phenotypical transdifferentiation of adventitial fibroblasts. This study aimed to explore whether TGF-β1 is involved in UⅡ-induced phenotypic differentiation of adventitial fibroblasts from rat aorta.Methods Adventitial fibroblasts were prepared by the explant culture method. TGF-β1 protein secretion from the cells was determined by enzyme-linked immunosorbent assay （ELISA）. The mRNA and protein expression of α-smooth nuscle actin （α-SM-actin）, the marker of phenotypic differentiation from fibroblasts to myofibroblasts, were determined using real-time quantitative RT-PCR （real-time RT-PCR） and Western blotting, respectively.Results UⅡ stimulated the secretion of TGF-β1 in cultured adventitial fibroblasts in a time-dependent manner. The secretion reached a peak at 24 hours, was higher by 69.8% （P ＜0.01）, than the control group. This effect was also concentration dependent. Maximal stimulation was reached at 10-8 mol/L of UⅡ （P ＜0.01）, which was increased by 59.9%,compared with in the control group （P ＜0.01）. The secretion of TGF-β1 induced by UⅡ was significantly blocked by SB-710411 （10-7 mol/L）, a specific antagonist of UⅡ receptor. In addition, both UⅡ （10-8 mol/L） and TGF-β1 significantly stimulated α-SM-actin mRNA and protein expression. Moreover, the α-SM-actin induced by UⅡ was inhibited by the specific neutralizing antibody （20 μg/ml） of TGF-β1, while the α-SM-actin expression stimulated by TGF-β1 （20 ng/ml）was inhibited by SB-710411 （10-7 mol/L）, the UⅡ receptor antagonist.Conclusion This study suggests that UⅡ could induce TGF-β1 secretion in adventitial fibroblasts via UT activation, and TGF-β1 might be involved in phenotypic differentiation from adventitial fibroblasts into myofibroblasts induced by UⅡ, and TGF-β1 s
