Using the 1.26 m National Astronomical Observatory-Guangzhou University Infrared/Optical Telescope(NGT),we monitor one BL Lac object,OJ 287.For this source,we obtain 15094 gri observations(4900 at g band,5184 at r ban...Using the 1.26 m National Astronomical Observatory-Guangzhou University Infrared/Optical Telescope(NGT),we monitor one BL Lac object,OJ 287.For this source,we obtain 15094 gri observations(4900 at g band,5184 at r band and 5010 at i band)in 155 nights from 2014 December 13 to 2019 March15.Based on the upper observations,we obtain the following results.(1)The total variation amplitude is~2.3 mag.(2)There are intra-day variabilities(IDVs).The IDV timescales(△T)are in the range from 7.69 min(Δm=0.06±0.02 mag)to 371.09 min(Δm=0.26±0.04 mag).(3)There are strong correlations betweenΔT andΔm,△m=(2.91±0.66)×10^(-4)ΔT+(0.08±0.009),with r=0.52,p=5.33×10^(-5).(4)There are intra-day periods in this source,with the period P≈94 min on 2017 December 10.When we supplement the observations from the literature,we can obtain that the long-term period is about 12.02±0.41 yr.(5)The spectral properties of OJ 287 show the bluer-when-brighter behavior,whatever state the source is at.展开更多
Background and Aims:Although activation of hepatic stellate cells(HSCs)plays a central role in the development of liver fibrosis,the mechanism underlying the activation of HSCs remains unclear.Keratin 17(KRT17),a memb...Background and Aims:Although activation of hepatic stellate cells(HSCs)plays a central role in the development of liver fibrosis,the mechanism underlying the activation of HSCs remains unclear.Keratin 17(KRT17),a member of the intermediate filament family,can regulate tumor cell proliferation and migration.The current study aimed to elucidate the role of KRT17 in the activation of HSCs and the mechanisms underlying liver fibrosis.Methods:The expression of KRT17 was determined using immunohistochemistry in tissue microarray.Western blotting and qRT-PCR assays were used to determine the KRT17 expression in fibrotic liver tissues obtained from human subjects and mice.LX-2 cells were treated with TGF-β1 recombinant protein and adipocyte differentiation mixture(MDI)mix to induce and reverse LX-2 cell activation,respectively,in order to explore the correlation between KRT17 and HSC activation.Additionally,cell proliferation and migration abilities of LX-2 cells transfected with KRT17-overexpressing plasmid or small interfering RNA were determined using CCK-8,flow cytometry,Transwell,and wound healing assays.Finally,rescue assay was used to explore the role of KRT17 in HSC activation and epithelial-mesenchymal transition(EMT).Results:The expression of KRT17 was higher in the hu-man and mouse fibrotic liver tissues than in healthy liver tissues,and it was positively correlated with HSC activa-tion.Upregulated KRT17 enhanced proliferation,migration,HSC activation and EMT in LX-2 cells,while knockdown of KRT17 reversed these effects.TGF-β1 recombinant protein accelerated KRT17-mediated EMT,HSC activation and proliferation,while TGF-β1 inhibitor counteracted the effect of KRT17 in vitro.Conclusions:KRT17 promoted HSC activation,proliferation and EMT in hepatic fibrosis probably via TGF-β1 signaling,and KRT17 might serve as a therapeutic target for the treatment of liver fibrosis.展开更多
基金partially supported by the National Natural Science Foundation of China(Grant Nos.U1831119,U1531245,U1431112,11733006,11503004 and 11403006)Science and Technology Program of Guangzhou(201707010401)。
文摘Using the 1.26 m National Astronomical Observatory-Guangzhou University Infrared/Optical Telescope(NGT),we monitor one BL Lac object,OJ 287.For this source,we obtain 15094 gri observations(4900 at g band,5184 at r band and 5010 at i band)in 155 nights from 2014 December 13 to 2019 March15.Based on the upper observations,we obtain the following results.(1)The total variation amplitude is~2.3 mag.(2)There are intra-day variabilities(IDVs).The IDV timescales(△T)are in the range from 7.69 min(Δm=0.06±0.02 mag)to 371.09 min(Δm=0.26±0.04 mag).(3)There are strong correlations betweenΔT andΔm,△m=(2.91±0.66)×10^(-4)ΔT+(0.08±0.009),with r=0.52,p=5.33×10^(-5).(4)There are intra-day periods in this source,with the period P≈94 min on 2017 December 10.When we supplement the observations from the literature,we can obtain that the long-term period is about 12.02±0.41 yr.(5)The spectral properties of OJ 287 show the bluer-when-brighter behavior,whatever state the source is at.
基金supported by the National Natural Science Foundation of China,General Project(No.82070624)Health Commission of Jiangsu Province,Key Project(No.ZDB2020006)+1 种基金Tianqing Liver Disease Research Foundation of China Hepatitis Prevention Foundation(No.TQGB20210029)Social Development Foundation of Nantong City(No.JC2019032).
文摘Background and Aims:Although activation of hepatic stellate cells(HSCs)plays a central role in the development of liver fibrosis,the mechanism underlying the activation of HSCs remains unclear.Keratin 17(KRT17),a member of the intermediate filament family,can regulate tumor cell proliferation and migration.The current study aimed to elucidate the role of KRT17 in the activation of HSCs and the mechanisms underlying liver fibrosis.Methods:The expression of KRT17 was determined using immunohistochemistry in tissue microarray.Western blotting and qRT-PCR assays were used to determine the KRT17 expression in fibrotic liver tissues obtained from human subjects and mice.LX-2 cells were treated with TGF-β1 recombinant protein and adipocyte differentiation mixture(MDI)mix to induce and reverse LX-2 cell activation,respectively,in order to explore the correlation between KRT17 and HSC activation.Additionally,cell proliferation and migration abilities of LX-2 cells transfected with KRT17-overexpressing plasmid or small interfering RNA were determined using CCK-8,flow cytometry,Transwell,and wound healing assays.Finally,rescue assay was used to explore the role of KRT17 in HSC activation and epithelial-mesenchymal transition(EMT).Results:The expression of KRT17 was higher in the hu-man and mouse fibrotic liver tissues than in healthy liver tissues,and it was positively correlated with HSC activa-tion.Upregulated KRT17 enhanced proliferation,migration,HSC activation and EMT in LX-2 cells,while knockdown of KRT17 reversed these effects.TGF-β1 recombinant protein accelerated KRT17-mediated EMT,HSC activation and proliferation,while TGF-β1 inhibitor counteracted the effect of KRT17 in vitro.Conclusions:KRT17 promoted HSC activation,proliferation and EMT in hepatic fibrosis probably via TGF-β1 signaling,and KRT17 might serve as a therapeutic target for the treatment of liver fibrosis.
