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Search Results: 1 - 10 of 81005 matches for " Mingli Liu "
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p38 and STAT3 activation by vGPCR in KSHV-infected cells
Mingli Liu, Shanchun Guo
Virus Adaptation and Treatment , 2010, DOI: http://dx.doi.org/10.2147/VAAT.S13434
Abstract: nd STAT3 activation by vGPCR in KSHV-infected cells Original Research (4701) Total Article Views Authors: Mingli Liu, Shanchun Guo Published Date September 2010 Volume 2010:2 Pages 103 - 113 DOI: http://dx.doi.org/10.2147/VAAT.S13434 Mingli Liu, Shanchun Guo Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, FL, USA Abstract: The molecular mechanism whereby viral G protein-coupled receptor (vGPCR) signaling regulates vascular endothelial growth factor (VEGF) expression in Kaposi sarcoma (KS) formation remains incompletely defined. mECK36 cells, generated by transfection of mouse bone marrow endothelial cells with Kaposi’s sarcoma-associated herpesviruses (KSHV) bacterial artificial chromosome (KSHVBac36), have been reported to be angiogenic, tumorigenic, and suitable for demonstrating a nonredundant role for vGPCR in KSHV-mediated tumorigenesis.1 In this report we used mECK36 and the cells composed of wild-type KSHVBac36 or the cells without vGPCR, namely vGPCR-null KSHVBac36 mutant, to dissect the molecular mechanisms of VEGF secretion induced by vGPCR in the context of KSHV infection. We found that vGPCR activates VEGF transcription via p38 MAPK and STAT3 in mECK36 and mECK36-derived cell models. We also found that in cells containing KSHV genome, STAT3 is tyrosine-phosphorylated and translocated into the nucleus, transactivating the target VEGF gene by binding to the specific DNA element TT (N4–5) AA in a strictly vGPCR-dependent manner. Moreover, treatment of mECK36-derived cells with AG490 or a dominant negative STAT3 DNA vector showed strong inhibitory effects on vGPCR-induced VEGF promoter activity. In addition, vGPCR can upregulate STAT3 mRNA levels. Taken together, our findings show that vGPCR plays a nonredundant role in STAT3 activation in KSHV infected cells and that this activation plays an important role in the connection of the viral oncogene vGPCR and VEGF upregulation. Our results indicate the broad signaling activating capacity of vGPCR in the context of KSHV infection and suggest that the STAT3 pathway could be targeted for preventing KSHV-mediated angiogenesis in KS.
p38 and STAT3 activation by vGPCR in KSHV-infected cells
Mingli Liu,Shanchun Guo
Virus Adaptation and Treatment , 2010,
Abstract: Mingli Liu, Shanchun GuoSylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, FL, USAAbstract: The molecular mechanism whereby viral G protein-coupled receptor (vGPCR) signaling regulates vascular endothelial growth factor (VEGF) expression in Kaposi sarcoma (KS) formation remains incompletely defined. mECK36 cells, generated by transfection of mouse bone marrow endothelial cells with Kaposi’s sarcoma-associated herpesviruses (KSHV) bacterial artificial chromosome (KSHVBac36), have been reported to be angiogenic, tumorigenic, and suitable for demonstrating a nonredundant role for vGPCR in KSHV-mediated tumorigenesis.1 In this report we used mECK36 and the cells composed of wild-type KSHVBac36 or the cells without vGPCR, namely vGPCR-null KSHVBac36 mutant, to dissect the molecular mechanisms of VEGF secretion induced by vGPCR in the context of KSHV infection. We found that vGPCR activates VEGF transcription via p38 MAPK and STAT3 in mECK36 and mECK36-derived cell models. We also found that in cells containing KSHV genome, STAT3 is tyrosine-phosphorylated and translocated into the nucleus, transactivating the target VEGF gene by binding to the specific DNA element TT (N4–5) AA in a strictly vGPCR-dependent manner. Moreover, treatment of mECK36-derived cells with AG490 or a dominant negative STAT3 DNA vector showed strong inhibitory effects on vGPCR-induced VEGF promoter activity. In addition, vGPCR can upregulate STAT3 mRNA levels. Taken together, our findings show that vGPCR plays a nonredundant role in STAT3 activation in KSHV infected cells and that this activation plays an important role in the connection of the viral oncogene vGPCR and VEGF upregulation. Our results indicate the broad signaling activating capacity of vGPCR in the context of KSHV infection and suggest that the STAT3 pathway could be targeted for preventing KSHV-mediated angiogenesis in KS.Keywords: Kaposi’s sarcoma, vGPCR, p38, STAT3, KSHV
Dynamic Game Research on Multiple Subjects in the Real Estate Market of China  [PDF]
Mingli Gong
Open Journal of Applied Sciences (OJAppS) , 2017, DOI: 10.4236/ojapps.2017.74016
Abstract: In order to analyze the deep-routed reason for the failure of the real estate market regulation policy, this paper established an incomplete information tri-game model in which central government, local government and the real estate developer were chosen as three main research objects. Based on the analysis of their interest appeals under the assumption of rational economic man, we found that it was the difference of interest appeals of central and local governments as well as the real estate developers that caused the game among the three participants. This, however, led to the failure of the macro-control at last. Strengthening the supervision of central government and reducing its cost at the same time, what’s more, improving the efficiency of the supervision and increasing the punishment of the rent-seeking behavior between local government and the real estate developers will contribute to improve the implementation status of the regulation and control policy. We suggest the authorities improve the government political achievement appraisal system and reform the current system of benefits distribution; moreover, reform the existing regulatory system and strength the regulatory role of media and the third-party so as to promote the healthy development of the real estate market.
Transcriptional Regulation of hTREX84 in Human Cancer Cells
Shanchun Guo, Mingli Liu, Andrew K. Godwin
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0043610
Abstract: TREX (transcription/export) is a multiprotein complex that plays a key role in the transcriptional elongation and transport of mRNA from the nucleus to the cytoplasm. We previously reported the purification of the human TREX protein and found that expression of a member of this complex, p84N5 (referred to as hTREX84 or hHPR1), a RB binding protein, correlated with breast tumor size and metastasis. Here we examine the mechanisms of aberrant expression of hTREX84 in breast and ovarian cancer cells and evaluate its role in tumorigenesis. We show that ovarian tumor cells over-express hTREX84 4-fold and 10-fold compared to immortal, non-tumorigenic and primary ovarian surface epithelial cells, respectively. Reduction of hTREX84 levels by small interfering RNA result in inhibition of cellular proliferation and G2/M arrest. Even though we observed that hTREX84 expression was induced by treatment with a demethylation agent, 5-aza-2′-deoxycytidine (5-aza-dC), sodium bisulfite DNA sequencing and methylation specific PCR found no evidence of changes in DNA methylation in the CpG islands in the regulator region of hTREX84. We subsequently identify several transcriptional factors, including NF-κB binding sites in the hTREX84 gene promoter and demonstrate by chromatin immunoprecipation (ChIP) and site directed mutagenesis that RelA/p65 binds the NF-kB binding sites and induces hTREX84 expression. Finally, we show by immunohistochemistry (IHC) that RelA/p65 is abundantly expressed in malignant cells that aberrantly express hTREX84 indicating that RelA/p65 might play a pivotal role in regulating hTREX84 expression in cancer. Our results indicate that overexpression of hTREX84 is associated with cancer cell transformation, proliferation and may be regulated by RelA/p65.
Cultivating of Service-Oriented Pharmaceutical Talents in China  [PDF]
Rong Xu, Mingli Shao
Creative Education (CE) , 2013, DOI: 10.4236/ce.2013.412A1002
Abstract: Health Care System Reform of Chinaputs forward new requirements for service-oriented pharmaceutical talents. Traditional mode of higher pharmaceutical education in China could not meet the social demand because of its “drug-centered” teaching system and shortage of service-oriented pharmaceutical talents. So it is urgent to transform the traditional mode and cultivate application-oriented pharmaceutical talents. This paper will give some suggestions, including establishing uniform standards for cultivating service-oriented pharmaceutical talents and transiting traditional curriculum and teaching methods. Moreover, it is feasible to establish effective linkup between professional degree and license examination.
A General Approach for Orthogonal 4-Tap Integer Multiwavelet Transforms
Mingli Jing,Hua Huang,Wuling Liu,Chun Qi
Mathematical Problems in Engineering , 2010, DOI: 10.1155/2010/163758
Abstract: An algorithm for orthogonal 4-tap integer multiwavelet transforms is proposed. We compute the singular value decomposition (SVD) of block recursive matrices of transform matrix, and then transform matrix can be rewritten in a product of two block diagonal matrices and a permutation matrix. Furthermore, we factorize the block matrix of block diagonal matrices into triangular elementary reversible matrices (TERMs), which map integers to integers by rounding arithmetic. The cost of factorizing block matrix into TERMs does not increase with the increase of the dimension of transform matrix, and the proposed algorithm is in-place calculation and without allocating auxiliary memory. Examples of integer multiwavelet transform using DGHM and CL are given, which verify that the proposed algorithm is an executable algorithm and outperforms the existing algorithm for orthogonal 4-tap integer multiwavelet transform.
Gene promoter hypermethylation in leukoplakia of the oral mucosa
Mingli Liu, Lei Feng, Ximing Tang, et al
Pathology and Laboratory Medicine International , 2010, DOI: http://dx.doi.org/10.2147/PLMI.S10916
Abstract: e promoter hypermethylation in leukoplakia of the oral mucosa Original Research (3394) Total Article Views Authors: Mingli Liu, Lei Feng, Ximing Tang, et al Published Date July 2010 Volume 2010:2 Pages 71 - 77 DOI: http://dx.doi.org/10.2147/PLMI.S10916 Mingli Liu1, Lei Feng2, Ximing Tang3, Shanchun Guo4 1Department of Physics, Tufts University School of Medicine, Boston, Massachussetts; 2Department of Thoracic/Head and Neck Medical Oncology, 3Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, Texas; 4Sylvester Cancer Center, University of Miami School of Medicine, Florida, USA Abstract: To examine whether aberrant DNA methylation in the promoter region might occur earlier in tumorigenesis, particularly in premalignant lesions, we examined biopsies from 111 participants in a chemoprevention trial aimed at reversal of oral leukoplakia, using methylation-specific polymerase chain reaction for the promoter regions of the tumor suppressor gene CDKN2A (p16), the putative metastasis suppressor gene for death-associated protein kinase (DAP-K), the DNA repair gene O6-methyguanine-DNA-methyltransferase (MGMT), and the detoxification gene glutathione S-transferase p1(GSTP1). p16 promoter hypermethylation was detected in 21 of 82 (25.6%), DAP-K hypermethylation in 28 of 87 (32.2%), and MGMT hypermethylation in 32 of 106 (30.2%) oral leukoplakia lesions analyzed. No aberrant methylation was found at the GSTP1 gene in 110 lesions examined. Among 68 biopsies analyzed for all three genes (p16, DAP-K, MGMT), 17 biopsies were detected with an abnormal methylation pattern at only one gene, 15 at two genes, and 8 at all three genes. Among clinical characteristics and their correlation with methylation, only alcohol consumption was correlated with DAP-K methylation (P = 0.027), while MGMT methylation was more frequent in females (P = 0.003) and nonsmokers (P = 0.0005). A significant correlation was found between p16 and DAP-K hypermethylation; p16 promoter was methylated in 14 (56%) of 25 lesions with DAP-K methylation, and only 5 (11.1%) of 45 DAP-K methylation-negative lesions (P = 0.0001). DAP-K aberrant methylation was also significantly correlated with MGMT methylation (16 of 31 in MGMT methylation-positive lesions versus 12 of 52 MGMT methylation-negative lesions, P = 0.0016). Our results suggest that epigenetic mechanisms of inactivation, such as aberrant methylation of p16, DAP-K, and MGMT genes, occur early in head and neck tumorigenesis, and might play a role in the progression of these lesions.
Gene promoter hypermethylation in leukoplakia of the oral mucosa
Mingli Liu,Lei Feng,Ximing Tang,et al
Pathology and Laboratory Medicine International , 2010,
Abstract: Mingli Liu1, Lei Feng2, Ximing Tang3, Shanchun Guo41Department of Physics, Tufts University School of Medicine, Boston, Massachussetts; 2Department of Thoracic/Head and Neck Medical Oncology, 3Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, Texas; 4Sylvester Cancer Center, University of Miami School of Medicine, Florida, USAAbstract: To examine whether aberrant DNA methylation in the promoter region might occur earlier in tumorigenesis, particularly in premalignant lesions, we examined biopsies from 111 participants in a chemoprevention trial aimed at reversal of oral leukoplakia, using methylation-specific polymerase chain reaction for the promoter regions of the tumor suppressor gene CDKN2A (p16), the putative metastasis suppressor gene for death-associated protein kinase (DAP-K), the DNA repair gene O6-methyguanine-DNA-methyltransferase (MGMT), and the detoxification gene glutathione S-transferase p1(GSTP1). p16 promoter hypermethylation was detected in 21 of 82 (25.6%), DAP-K hypermethylation in 28 of 87 (32.2%), and MGMT hypermethylation in 32 of 106 (30.2%) oral leukoplakia lesions analyzed. No aberrant methylation was found at the GSTP1 gene in 110 lesions examined. Among 68 biopsies analyzed for all three genes (p16, DAP-K, MGMT), 17 biopsies were detected with an abnormal methylation pattern at only one gene, 15 at two genes, and 8 at all three genes. Among clinical characteristics and their correlation with methylation, only alcohol consumption was correlated with DAP-K methylation (P = 0.027), while MGMT methylation was more frequent in females (P = 0.003) and nonsmokers (P = 0.0005). A significant correlation was found between p16 and DAP-K hypermethylation; p16 promoter was methylated in 14 (56%) of 25 lesions with DAP-K methylation, and only 5 (11.1%) of 45 DAP-K methylation-negative lesions (P = 0.0001). DAP-K aberrant methylation was also significantly correlated with MGMT methylation (16 of 31 in MGMT methylation-positive lesions versus 12 of 52 MGMT methylation-negative lesions, P = 0.0016). Our results suggest that epigenetic mechanisms of inactivation, such as aberrant methylation of p16, DAP-K, and MGMT genes, occur early in head and neck tumorigenesis, and might play a role in the progression of these lesions.Keywords: p16, DAP-K, MGMT, GSTP1 genes, methylation, leukoplakia
Do Major Roads Reduce Gene Flow in Urban Bird Populations?
Shuping Zhang, Mingli Suo, Shenglin Liu, Wei Liang
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0077026
Abstract: Background Although the negative effects of roads on the genetics of animal populations have been extensively reported, the question of whether roads reduce gene flow in volant, urban bird populations has so far not been addressed. In this study, we assess whether highways decreased gene flow and genetic variation in a small passerine bird, the tree sparrow (Passer montanus). Methodology We assessed genetic differences among tree sparrows (Passer montanus) sampled at 19 sites within Beijing Municipality, China, using 7 DNA microsatellites as genetic markers. Results AMOVA showed that genetic variation between sites, between urban and rural populations, and between opposite sides of the same highway, were very weak. Mantel tests on all samples, and on urban samples only, indicated that the age and number of highways, and the number of ordinary roads, were uncorrelated with genetic differences (FST) among tree sparrows from different urban sites. Birds sampled at urban sites had similar levels of genetic diversity to those at rural sites. There was, however, evidence of some weak genetic structure between urban sites. Firstly, there were significant genetic differences (FST) between birds from opposite sides of the same highway, but no significant FST values between those from sites that were not separated by highways. Secondly, birds from eleven urban sites had loci that significantly deviated from the Hardy–Weinberg equilibrium but no such deviation was found in birds from rural sites. Conclusion We cannot, therefore, conclusively reject the hypothesis that highways have no effect on the gene flow of tree sparrow populations. Furthermore, since the significance of these results may increase with time, we suggested that research on the influence of highways on gene flow in urban bird populations needs to be conducted over several decades.
First-principles investigation of effect of pressure on BaFe$_2$As$_2$
Wenhui Xie,Mingli Bao,Zhenjie Zhao,Bang-Gui Liu
Physics , 2008, DOI: 10.1103/PhysRevB.79.115128
Abstract: On experimental side, BaFe$_2$As$_2$ without doping has been made superconducting by applying appropriate pressure (2-6 GPa). Here, we use a full-potential linearized augmented plane wave method within the density-functional theory to investigate the effect of pressure on its crystal structure, magnetic order, and electronic structure. Our calculations show that the striped antiferromagnetic order observed in experiment is stable against pressure up to 13 GPa. Calculated antiferromagnetic lattice parameters are in good agreements with experimental data, while calculations with nonmagnetic state underestimate Fe-As bond length and c-axis lattice constant. The effects of pressure on crystal structure and electronic structure are investigated for both the antiferromagnetic state and the nonmagnetic one. We find that the compressibility of the antiferromagnetic state is quite isotropic up to about 6.4 GPa. With increasing pressure, the FeAs$_4$ tetrahedra is hardly distorted. We observe a transition of Fermi surface topology in the striped antiferromagnetic state when the compression of volume is beyond 8% (or pressure 6 GPa), which corresponds to a large change of $c/a$ ratio. These first-principles results should be useful to understanding the antiferromagnetism and electronic states in the FeAs-based materials, and may have some useful implications to the superconductivity.
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