AIM: To investigate the role of TIP30 in apoptotic signal pathway in hepatoblastoma cells and to provide a basis for TIP30 as a gene therapy candidate in the regression of hepatoblastoma cells. METHODS: Apoptosis of h...AIM: To investigate the role of TIP30 in apoptotic signal pathway in hepatoblastoma cells and to provide a basis for TIP30 as a gene therapy candidate in the regression of hepatoblastoma cells. METHODS: Apoptosis of human hepatoblastoma cell lines HepG2 (p53 wild), Hep3B (p53 null) and PLC/RPF/5 (p53 mutant) infected with Ad-TIP30 (bearing a wild type human Tip30 gene) were analyzed and p53, Bax and Bcl-xl expression levels were compared among these cells. MTT assay, DNA fragmentation, in situ 3' end labeling of DNA, annexin-V FITC staining were used to detect cell death and apoptosis in cells at various time intervals subsequent to infection, and to determine whether TIP30 had an effect on the expression levels of some apoptosis-related gene products such as Bax, p53 and Bcl-xl. A similar time course experiment was performed by Western blotting. RESULTS: In MTT assay, the viability of HepG2 cells decreased significantly from 99.7% to 10% and displayed more massive cell death within 5-8 d than Hep3B and PLC/ RPF/5 cells, with their viability decreased from 97.8% to 44.3% and 98.1% to 50.4%, respectively. In annexin-V FITC assay, the percentage of apoptosis cells in HepG2 cells was two to three-fold higher than that in control cells (infected with Ad-GFP), two-fold higher than that in Hep3B cells and 1.4-fold higher than that in PLC/RPF/5 cells 36 h after infection, respectively. Moreover, in HepG2 cells, the p53 began to increase 6-8 h after infection, reaching a maximum level between 8 and 12 h after infection and then dropped. Bax showed a similar increase in the cells as p53 reached the maximum at 8-12 h and subsequently decreased. Interestingly, Bcl-xl protein levels were down regulated during 24 to 36 h after Ad-TIP30 infection. In contrast, ectopic expression of TIP30 in Hep3B and PLC/ RPF/5 cells had no effect on the regulation of Bax expression, but had an effect on Bcl-xl levels. In comparison with HepG2 cells, these data suggested that up-regulation of p53 levels by TIP30 might be a pre-requisite for Ba展开更多
AIM: To investigate the role of Gadd45a in hepatic fibrosis and the transforming growth factor (TGF)-beta/ Smad signaling pathway. METHODS: Wild-type male BALB/c mice were treated with CCl4 to induce a model of chroni...AIM: To investigate the role of Gadd45a in hepatic fibrosis and the transforming growth factor (TGF)-beta/ Smad signaling pathway. METHODS: Wild-type male BALB/c mice were treated with CCl4 to induce a model of chronic liver injury. Hepatic stellate cells (HSCs) were isolated from the liver of BALB/c mice and were treated with small interfering RNAs (siRNAs) targeting Gadd45a or the pcDNA3.1-Gadd45a recombinant plasmid. Cellular alpha-smooth muscle actin (alpha-SMA), beta-actin, type I collagen, phospho-Smad2, phospho-Smad3, Smad2, Smad3, and Smad4 were detected by Western blots. The mRNA levels of alpha-SMA, beta-actin, and type I collagen were determined by quantitative real-time (qRT)-PCR analyses. Reactive oxygen species production was monitored by flow cytometry using 2,7-dichlorodihydrofluorescein diacetate. Gadd45a, Gadd45b, anti-Gadd45g, type I collagen, and SMA local expression in liver tissue were measured by histologic and immunohistochemical analyses. RESULTS: Significant downregulation of Gadd45a, but not Gadd45b or Gadd45g, accompanied by activation of the TGF-beta/Smad signaling pathways was detected in fibrotic liver tissues of mice and isolated HSCs with chronic liver injury induced by CCl4 treatment. Overexpression of Gadd45a reduced the expression of extracellular matrix proteins and alpha-SMA in HSCs, whereas transient knockdown of Gadd45a with siRNA reversed this process. Gadd45a inhibited the activity of a plasminogen activator inhibitor-1 promoter construct and (CAGA)(9) MLP-Luc, an artificial Smad3/4-specific reporter, as well as reduced the phosphorylation and nuclear translocation of Smad3. Gadd45a showed protective effects by scavenging reactive oxygen species and upregulating antioxidant enzymes. CONCLUSION: Gadd45a may counteract hepatic fibrosis by regulating the activation of HSCs via the inhibition of TGF-beta/Smad signaling.展开更多
The problem of approximate joint diagonalization of a set of matrices is instrumental in numerous statistical signal processing applications. This paper describes a relative gradient non-orthogonal approximate joint d...The problem of approximate joint diagonalization of a set of matrices is instrumental in numerous statistical signal processing applications. This paper describes a relative gradient non-orthogonal approximate joint diagonalization （AJD） algorithm based on a non-least squares AJD criterion and a special AJD using a non-square diagonalizing matrix and an AJD method for ill-conditioned matrices. Simulation results demonstrate the better performance of the relative gradient AJD algorithm compared with the conventional least squares （LS） criteria based gradient-type AJD algorithms. The algorithm is attractive for practical applications since it is simple and efficient.展开更多
The structures of three new eremophilanolides isolated from the roots of Ligularia Veitchiana were shown,by the spectral and chemical evidences,to be 1β,10β-epoxy-6β- hydrox-y-8β-methoxy-eremophil-7(11)-en-12,8α-...The structures of three new eremophilanolides isolated from the roots of Ligularia Veitchiana were shown,by the spectral and chemical evidences,to be 1β,10β-epoxy-6β- hydrox-y-8β-methoxy-eremophil-7(11)-en-12,8α-olide(3),1β,10β-epoxy-6β- (2'-hydroxymethylacryloyloxy)-8β-methoxy-eremophil-7(11)-en-12,8α-olide (4)and 1β,10β-epoxy-6β-(2'-methoxymethylacryloyloxy)-8β-hydroxy-eremophil -7(11)-en-12,8α-olide(5).展开更多
Some scientists say that animals in the ocean are increasinglythreatened by noise pollution caused by humans.The issue of noisepollution in the oceans was dissussed at a conference this month ofthe Acoustical Society ...Some scientists say that animals in the ocean are increasinglythreatened by noise pollution caused by humans.The issue of noisepollution in the oceans was dissussed at a conference this month ofthe Acoustical Society of America.The noise that affects sea creatuescomes from a number of human activities.It is caused mainly byindustrial under-water explosions,ocean drilling,ship engines andsubmarines.Such noises are addded to natural sounds.These soundsinclude the breaking of ice-fields,under-water earthquakes andvolcanoes,storms and sounds made by animals themselves.展开更多
文摘AIM: To investigate the role of TIP30 in apoptotic signal pathway in hepatoblastoma cells and to provide a basis for TIP30 as a gene therapy candidate in the regression of hepatoblastoma cells. METHODS: Apoptosis of human hepatoblastoma cell lines HepG2 (p53 wild), Hep3B (p53 null) and PLC/RPF/5 (p53 mutant) infected with Ad-TIP30 (bearing a wild type human Tip30 gene) were analyzed and p53, Bax and Bcl-xl expression levels were compared among these cells. MTT assay, DNA fragmentation, in situ 3' end labeling of DNA, annexin-V FITC staining were used to detect cell death and apoptosis in cells at various time intervals subsequent to infection, and to determine whether TIP30 had an effect on the expression levels of some apoptosis-related gene products such as Bax, p53 and Bcl-xl. A similar time course experiment was performed by Western blotting. RESULTS: In MTT assay, the viability of HepG2 cells decreased significantly from 99.7% to 10% and displayed more massive cell death within 5-8 d than Hep3B and PLC/ RPF/5 cells, with their viability decreased from 97.8% to 44.3% and 98.1% to 50.4%, respectively. In annexin-V FITC assay, the percentage of apoptosis cells in HepG2 cells was two to three-fold higher than that in control cells (infected with Ad-GFP), two-fold higher than that in Hep3B cells and 1.4-fold higher than that in PLC/RPF/5 cells 36 h after infection, respectively. Moreover, in HepG2 cells, the p53 began to increase 6-8 h after infection, reaching a maximum level between 8 and 12 h after infection and then dropped. Bax showed a similar increase in the cells as p53 reached the maximum at 8-12 h and subsequently decreased. Interestingly, Bcl-xl protein levels were down regulated during 24 to 36 h after Ad-TIP30 infection. In contrast, ectopic expression of TIP30 in Hep3B and PLC/ RPF/5 cells had no effect on the regulation of Bax expression, but had an effect on Bcl-xl levels. In comparison with HepG2 cells, these data suggested that up-regulation of p53 levels by TIP30 might be a pre-requisite for Ba
基金Supported by Medicine and Health Research Programs of Zhejiang Province,No.2013KYB252the Science Foundation of the Science and Technology Commission of Ruian City,No.201302012
文摘AIM: To investigate the role of Gadd45a in hepatic fibrosis and the transforming growth factor (TGF)-beta/ Smad signaling pathway. METHODS: Wild-type male BALB/c mice were treated with CCl4 to induce a model of chronic liver injury. Hepatic stellate cells (HSCs) were isolated from the liver of BALB/c mice and were treated with small interfering RNAs (siRNAs) targeting Gadd45a or the pcDNA3.1-Gadd45a recombinant plasmid. Cellular alpha-smooth muscle actin (alpha-SMA), beta-actin, type I collagen, phospho-Smad2, phospho-Smad3, Smad2, Smad3, and Smad4 were detected by Western blots. The mRNA levels of alpha-SMA, beta-actin, and type I collagen were determined by quantitative real-time (qRT)-PCR analyses. Reactive oxygen species production was monitored by flow cytometry using 2,7-dichlorodihydrofluorescein diacetate. Gadd45a, Gadd45b, anti-Gadd45g, type I collagen, and SMA local expression in liver tissue were measured by histologic and immunohistochemical analyses. RESULTS: Significant downregulation of Gadd45a, but not Gadd45b or Gadd45g, accompanied by activation of the TGF-beta/Smad signaling pathways was detected in fibrotic liver tissues of mice and isolated HSCs with chronic liver injury induced by CCl4 treatment. Overexpression of Gadd45a reduced the expression of extracellular matrix proteins and alpha-SMA in HSCs, whereas transient knockdown of Gadd45a with siRNA reversed this process. Gadd45a inhibited the activity of a plasminogen activator inhibitor-1 promoter construct and (CAGA)(9) MLP-Luc, an artificial Smad3/4-specific reporter, as well as reduced the phosphorylation and nuclear translocation of Smad3. Gadd45a showed protective effects by scavenging reactive oxygen species and upregulating antioxidant enzymes. CONCLUSION: Gadd45a may counteract hepatic fibrosis by regulating the activation of HSCs via the inhibition of TGF-beta/Smad signaling.
基金Supported by the Basic Research Foundation of Tsinghua National Laboratory for Information Science and Technology (TNList) the National Natural Science Foundation of China (No. 60675002)
文摘The problem of approximate joint diagonalization of a set of matrices is instrumental in numerous statistical signal processing applications. This paper describes a relative gradient non-orthogonal approximate joint diagonalization （AJD） algorithm based on a non-least squares AJD criterion and a special AJD using a non-square diagonalizing matrix and an AJD method for ill-conditioned matrices. Simulation results demonstrate the better performance of the relative gradient AJD algorithm compared with the conventional least squares （LS） criteria based gradient-type AJD algorithms. The algorithm is attractive for practical applications since it is simple and efficient.
基金The Natural Science Foundation of China and the doctoral programme from State Education Commission of China.
文摘The structures of three new eremophilanolides isolated from the roots of Ligularia Veitchiana were shown,by the spectral and chemical evidences,to be 1β,10β-epoxy-6β- hydrox-y-8β-methoxy-eremophil-7(11)-en-12,8α-olide(3),1β,10β-epoxy-6β- (2'-hydroxymethylacryloyloxy)-8β-methoxy-eremophil-7(11)-en-12,8α-olide (4)and 1β,10β-epoxy-6β-(2'-methoxymethylacryloyloxy)-8β-hydroxy-eremophil -7(11)-en-12,8α-olide(5).
文摘Some scientists say that animals in the ocean are increasinglythreatened by noise pollution caused by humans.The issue of noisepollution in the oceans was dissussed at a conference this month ofthe Acoustical Society of America.The noise that affects sea creatuescomes from a number of human activities.It is caused mainly byindustrial under-water explosions,ocean drilling,ship engines andsubmarines.Such noises are addded to natural sounds.These soundsinclude the breaking of ice-fields,under-water earthquakes andvolcanoes,storms and sounds made by animals themselves.
