基于COLEC和LOCNESS语料库,对比分析了中国非英语专业大学生和美国大学生在the government +情态动词上的使用差异及成因。结果显示,在the government +情态动词的数量和选词偏好上,中美大学生存在显著差异,体现在中国学生过多地将the g...基于COLEC和LOCNESS语料库,对比分析了中国非英语专业大学生和美国大学生在the government +情态动词上的使用差异及成因。结果显示,在the government +情态动词的数量和选词偏好上,中美大学生存在显著差异,体现在中国学生过多地将the government当作施事格,且对should和must的过度使用。产生这种差异的原因有:写作文体差异、文化差异和习得重点差异。这些差异造成中国学生文体单一、文章教化性严重及对情态动词运用不当等问题。最后,就这一现象为英语教学提出了两点建议。展开更多
Background:Renalfibrosis is an important process in the development of chronic kidney disease.Understanding the pathogenesis andfinding effective treatments for renalfibrosis is crucial.This study aims to investigate whe...Background:Renalfibrosis is an important process in the development of chronic kidney disease.Understanding the pathogenesis andfinding effective treatments for renalfibrosis is crucial.This study aims to investigate whether a newly discovered long non-coding RNA(lncRNA)called LOC103694972 could be a potential target for treatingfibrosis of NRK-49F cells.Methods:LncRNA Chip was used to identify differentially expressed lncRNAs between TGF-β1-induced NRK-49F cells and normal cells.The dual-luciferase assay confirmed the binding between miR-29c-3p and signal transducer and activator of transcription(STAT3),as well as between miR-29c-3p and lncRNA LOC103694972.Si-LOC103694972 and miR-29c-3p mimic were then transfected into TGF-β1-induced NRK-49F cells.Results:The study found that LOC103694972 was highly expressed in TGF-β1-induced NRK-49F cells.These cells exhibited increased cell length and activity compared to the control group.The expression levels of Collagen I,α-Smooth muscle actin(α-SMA),and tissue inhibitor of metalloproteinase(TIMP-1)were increased,while matrix Metalloproteinase 2(MMP2)and matrix Metalloproteinase 9(MMP9)expression was decreased.However,transfection with si-LOC103694972 and miR-29c-3p mimics restored cell morphology and reduced cell viability.This led to a decrease in the levels of Collagen I,α-SMA,and TIMP-1,as well as an increase in MMP2 and MMP9 expression.Additionally,TGF-β1-induced NRK-49F cells transfected with miR-29c-3p mimics activated the STAT3-Smad3/CTGF pathway.Conclusion:Based on thesefindings,lncRNA LOC103694972 shows promise as a target for treating renalfibrosis.It negatively regulates miR-29c-3p and activates the STAT3-Smad3/CTGF pathway.展开更多
文摘基于COLEC和LOCNESS语料库,对比分析了中国非英语专业大学生和美国大学生在the government +情态动词上的使用差异及成因。结果显示,在the government +情态动词的数量和选词偏好上,中美大学生存在显著差异,体现在中国学生过多地将the government当作施事格,且对should和must的过度使用。产生这种差异的原因有:写作文体差异、文化差异和习得重点差异。这些差异造成中国学生文体单一、文章教化性严重及对情态动词运用不当等问题。最后,就这一现象为英语教学提出了两点建议。
基金This work was supported by the Hunan Provincial Education Department General Project Research Fund(No.20C1412)the Hunan Graduate Scientific Research Innovation Project(No.CX2018B474)the National Famous Elderly Chinese Medicine Experts Xinyu Chen Inheritance Workshop Construction Project(No.[2022]75).
文摘Background:Renalfibrosis is an important process in the development of chronic kidney disease.Understanding the pathogenesis andfinding effective treatments for renalfibrosis is crucial.This study aims to investigate whether a newly discovered long non-coding RNA(lncRNA)called LOC103694972 could be a potential target for treatingfibrosis of NRK-49F cells.Methods:LncRNA Chip was used to identify differentially expressed lncRNAs between TGF-β1-induced NRK-49F cells and normal cells.The dual-luciferase assay confirmed the binding between miR-29c-3p and signal transducer and activator of transcription(STAT3),as well as between miR-29c-3p and lncRNA LOC103694972.Si-LOC103694972 and miR-29c-3p mimic were then transfected into TGF-β1-induced NRK-49F cells.Results:The study found that LOC103694972 was highly expressed in TGF-β1-induced NRK-49F cells.These cells exhibited increased cell length and activity compared to the control group.The expression levels of Collagen I,α-Smooth muscle actin(α-SMA),and tissue inhibitor of metalloproteinase(TIMP-1)were increased,while matrix Metalloproteinase 2(MMP2)and matrix Metalloproteinase 9(MMP9)expression was decreased.However,transfection with si-LOC103694972 and miR-29c-3p mimics restored cell morphology and reduced cell viability.This led to a decrease in the levels of Collagen I,α-SMA,and TIMP-1,as well as an increase in MMP2 and MMP9 expression.Additionally,TGF-β1-induced NRK-49F cells transfected with miR-29c-3p mimics activated the STAT3-Smad3/CTGF pathway.Conclusion:Based on thesefindings,lncRNA LOC103694972 shows promise as a target for treating renalfibrosis.It negatively regulates miR-29c-3p and activates the STAT3-Smad3/CTGF pathway.
