Objective:A cell model of cardiac fibroblasts proliferation induced by aldosterone was established to observe the effect of aldosterone on the proliferation of rat cardiac fibroblasts.Methods:Primary cardiac fibroblas...Objective:A cell model of cardiac fibroblasts proliferation induced by aldosterone was established to observe the effect of aldosterone on the proliferation of rat cardiac fibroblasts.Methods:Primary cardiac fibroblasts were cultured by trypsin digestion method and differential adhesion method,primary cardiac fibroblasts were sub-cultured by conventional digestion method,and the immunocytochemical assay was used to identify cardiac fibroblasts.The second-generation cardiac fibroblasts were randomly divided into five groups:standard control group,10-9 mol/L aldosterone(ALD1)group,10-8 mol/L aldosterone(ALD2)group,10-7 mol/L aldosterone(ALD3)group,and 10-6 mol/L aldosterone(ALD4)group.The viability of fibroblast cells in each group was detected by the 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide method.Results:Vimentin staining assay showed that the cultured cells staining positive,and the purity of cultured mouse cardiac fibroblasts was 95%.The results of methyl thiazolyl tetrazolium showed that compared with the control group,the low concentration of aldosterone(10-9 mol/L)had no significant effect on the proliferation of normal cardiac fibroblasts.With the increase in the intensity of(10-8–10-6)mol/L,aldosterone could significantly promote the proliferation of cardiac fibroblasts.Moreover,there was no significant difference in absorbance value between the aldosterone group(10-6 mol/L)and the aldosterone group(10-7 mol/L)(P>0.05).The highest concentration of aldosterone group 10-7 mol/L promoted the proliferation of cardiac the optimum concentration was 10-7 mol/L.Conclusion:Aldosterone can promote the spread of cardiac fibroblasts in a specific concentration range.展开更多
In situ(TiC+SiC)particles(5 vol.%and 10 vol.%,respectively)-reinforced FeCrCoNi high entropy alloy matrix composites were fabricated via vacuum inductive melting method,with equal volume fractions of TiC and SiC parti...In situ(TiC+SiC)particles(5 vol.%and 10 vol.%,respectively)-reinforced FeCrCoNi high entropy alloy matrix composites were fabricated via vacuum inductive melting method,with equal volume fractions of TiC and SiC particles.X-ray diffraction,scanning electron microscope and energy diffraction spectrum were employed to analyze the microstructure and composi-tion of the samples.The results manifested that the FeCrCoNi matrix is composed of FCC phase,and the in situ particles are homogeneously scattered in the matrix.The presence of reinforcements augmented the ultimate tensile strength from 452 to 783 MPa,and raised the yield strength from 162 to 466 MPa at room temperature,whereas the elongation to fracture was reduced from 70.6%to 28.6%.All the tensile fracture surfaces consisted of numerous tiny dimples,indicating that the composites exhibited ductile fracture.Furthermore,the enhancement of strength ascribes to a combination of thermal mis-match strengthening,load-bearing effect,grain refinement,Orowan strengthening and solid solution strengthening effect,which contribute about 58.0%,2.4%,12.3%,11.1%and 16.2%to the improvement of yield tensile strength,respectively.展开更多
Trimethylated histone H3 lysine 27(H3 K27 me3)is a repressive histone marker that regulates a variety of developmental processes,including those that determine flowering time.However,relatively little is known about t...Trimethylated histone H3 lysine 27(H3 K27 me3)is a repressive histone marker that regulates a variety of developmental processes,including those that determine flowering time.However,relatively little is known about the mechanism of how H3 K27 me3 is recognized to regulate transcription.Here,we identified BAH domain-containing transcriptional regulator 1(BDT1)as an H3 K27 me3 reader.BDT1 is responsible for preventing flowering by suppressing the expression of flowering genes.Mutation of the H3 K27 me3 recognition sites in the BAH domain disrupted the binding of BDT1 to H3 K27 me3,leading to de-repression of H3 K27 me3-enriched flowering genes and an earlyflowering phenotype.We also found that BDT1 interacts with a family of PHD finger-containing proteins,which we named PHD1–6,and with CPL2,a Pol II carboxyl terminal domain(CTD)phosphatase responsible for transcriptional repression.Pull-down assays showed that the PHD finger-containing proteins can enhance the binding of BDT1 to the H3 K27 me3 peptide.Mutations in all of the PHD genes caused increased expression of flowering genes and an earlyflowering phenotype.This study suggests that the binding of BDT1 to the H3 K27 me3 peptide,which is enhanced by PHD proteins,is critical for preventing early flowering.展开更多
基金This study was supported by the project of Hebei Provincial Administration of traditional Chinese Medicine(No.2018161)the Hebei Health and Family Planning Commission(No.20170875)the Scientific Research Project of College students in Chengde Medical College(No.2019033).
文摘Objective:A cell model of cardiac fibroblasts proliferation induced by aldosterone was established to observe the effect of aldosterone on the proliferation of rat cardiac fibroblasts.Methods:Primary cardiac fibroblasts were cultured by trypsin digestion method and differential adhesion method,primary cardiac fibroblasts were sub-cultured by conventional digestion method,and the immunocytochemical assay was used to identify cardiac fibroblasts.The second-generation cardiac fibroblasts were randomly divided into five groups:standard control group,10-9 mol/L aldosterone(ALD1)group,10-8 mol/L aldosterone(ALD2)group,10-7 mol/L aldosterone(ALD3)group,and 10-6 mol/L aldosterone(ALD4)group.The viability of fibroblast cells in each group was detected by the 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide method.Results:Vimentin staining assay showed that the cultured cells staining positive,and the purity of cultured mouse cardiac fibroblasts was 95%.The results of methyl thiazolyl tetrazolium showed that compared with the control group,the low concentration of aldosterone(10-9 mol/L)had no significant effect on the proliferation of normal cardiac fibroblasts.With the increase in the intensity of(10-8–10-6)mol/L,aldosterone could significantly promote the proliferation of cardiac fibroblasts.Moreover,there was no significant difference in absorbance value between the aldosterone group(10-6 mol/L)and the aldosterone group(10-7 mol/L)(P>0.05).The highest concentration of aldosterone group 10-7 mol/L promoted the proliferation of cardiac the optimum concentration was 10-7 mol/L.Conclusion:Aldosterone can promote the spread of cardiac fibroblasts in a specific concentration range.
基金the National Undergraduate Training Program for Innovation and Entrepreneurship(No.201910288094Z)This work was also supported by the National Natural Science Foundation of China(51571118,51371098)Jiangsu Province Science and Technology Plan Project(BE2018753/KJ185629).
文摘In situ(TiC+SiC)particles(5 vol.%and 10 vol.%,respectively)-reinforced FeCrCoNi high entropy alloy matrix composites were fabricated via vacuum inductive melting method,with equal volume fractions of TiC and SiC particles.X-ray diffraction,scanning electron microscope and energy diffraction spectrum were employed to analyze the microstructure and composi-tion of the samples.The results manifested that the FeCrCoNi matrix is composed of FCC phase,and the in situ particles are homogeneously scattered in the matrix.The presence of reinforcements augmented the ultimate tensile strength from 452 to 783 MPa,and raised the yield strength from 162 to 466 MPa at room temperature,whereas the elongation to fracture was reduced from 70.6%to 28.6%.All the tensile fracture surfaces consisted of numerous tiny dimples,indicating that the composites exhibited ductile fracture.Furthermore,the enhancement of strength ascribes to a combination of thermal mis-match strengthening,load-bearing effect,grain refinement,Orowan strengthening and solid solution strengthening effect,which contribute about 58.0%,2.4%,12.3%,11.1%and 16.2%to the improvement of yield tensile strength,respectively.
基金supported by the National Natural Science Foundation of China(32025003)by the National Key Research and Development Program of China(2016YFA0500801)from the Chinese Ministry of Science and Technology。
文摘Trimethylated histone H3 lysine 27(H3 K27 me3)is a repressive histone marker that regulates a variety of developmental processes,including those that determine flowering time.However,relatively little is known about the mechanism of how H3 K27 me3 is recognized to regulate transcription.Here,we identified BAH domain-containing transcriptional regulator 1(BDT1)as an H3 K27 me3 reader.BDT1 is responsible for preventing flowering by suppressing the expression of flowering genes.Mutation of the H3 K27 me3 recognition sites in the BAH domain disrupted the binding of BDT1 to H3 K27 me3,leading to de-repression of H3 K27 me3-enriched flowering genes and an earlyflowering phenotype.We also found that BDT1 interacts with a family of PHD finger-containing proteins,which we named PHD1–6,and with CPL2,a Pol II carboxyl terminal domain(CTD)phosphatase responsible for transcriptional repression.Pull-down assays showed that the PHD finger-containing proteins can enhance the binding of BDT1 to the H3 K27 me3 peptide.Mutations in all of the PHD genes caused increased expression of flowering genes and an earlyflowering phenotype.This study suggests that the binding of BDT1 to the H3 K27 me3 peptide,which is enhanced by PHD proteins,is critical for preventing early flowering.
