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 Articles by B Li Total Records ( 12 ) for B Li
 Treatment of hepatitis C virus core-positive hepatocytes with the transfer of recombinant caspase-3 using the 2',5'-oligoadenylate synthetase gene promoter Y Wang , S Mao , B Li , P Tan , D Feng and J. Wen Hepatitis C virus (HCV) infection is a leading cause of liver-related morbidity and mortality throughout the world. There is no vaccine available and current therapy is only partially effective. Since HCV infects only a minority of hepatocytes, we hypothesized that induction of apoptosis might be a promising approach for the treatment of hepatitis C. In the present study, recombinant caspase-3 gene (re-caspase-3) was used because it has the ability to induce apoptosis that is independent of the initiator caspases. An HCV-specific promoter is required to regulate the cytotoxic caspase-3 expression in HCV-infected cells. It has been reported that HCV core protein can specifically activate the 2',5'-oligoadenylate synthetase (OAS) gene promoter in human hepatocytes. Therefore, we constructed an expression vector consisting of the re-caspase-3 under the OAS gene promoter (pGL3-OAS-re-caspase-3) and then investigated its effect on HCV core-positive liver cells. It was found that the pGL3-OAS-re-caspase-3 construct induced apoptosis in HCV core-positive liver cells, but not in normal liver cells. These results strongly suggested that the transfer of the re-caspase-3 gene under the OAS promoter was a novel targeting approach for the treatment of HCV infection.
 Apoptotic mechanism of MCF-7 breast cells in vivo and in vitro induced by photodynamic therapy with C-phycocyanin B Li , X Chu , M Gao and W. Li The aim of this study was to investigate the pro-apoptotic mechanism of C-phycocyanin (C-PC)-mediated photodynamic therapy (PDT) in a murine tumor model and cultured MCF-7 cells. The mice were divided into four groups: control, He–Ne laser radiation, C-PC treatment, and C-PC treatment + He–Ne laser radiation. The effects of C-PC and/or laser on immune organs, immunocyte proliferation, tumor genesis, and apoptosis-related proteins expressions were investigated by immunohistochemistry, in situ hybridization, MTT, electron microscope, western blot, and immunofluorescence assay. The results showed that He–Ne laser treatment alone showed marginal effects. In C-PC-treated mice, the weight of immune organs, proliferation of immunocytes, and expression of pro-apoptotic Fas protein were increased, whereas the tumor weight and the expressions of anti-apoptotic proteins (NF-B and P53) and CD44 mRNA were comparatively decreased. In vitro, C-PC was able to inhibit MCF-7 cell proliferation and cause ultrastructural changes including microvilli loss, formation of membrane blebs, and chromatin condensation. Moreover, C-PC treatment could activate caspase-9 expression, induce cytochrome c release, and downregulate Bcl-2 expression. When combined with He–Ne laser irradiation, the effects of C-PC treatment were further enhanced. Facilitating the apoptosis signals transduction and finally leading to the apoptosis of MCF-7 cells may be the mechanism of the anti-tumor activities of C-PC-mediated PDT.
 Tetra-glutamic acid residues adjacent to Lys248 in HMG-CoA reductase are critical for the ubiquitination mediated by gp78 and UBE2G2 H Miao , W Jiang , L Ge , B Li and B. Song Sterol-regulated degradation of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR) is a rapid feedback regulatory mechanism by which cells employ to control the cholesterol biosynthesis. This process is initiated by the sterol-induced interaction between HMGCR and Insig-1/gp78, a membrane-bound ubiquitin ligase complex. There are two Lys residues (Lys89 and Lys248) facing cytosol in the membrane domain of HMGCR, and Lys248 is the major ubiquitination site. In this study, we investigated the mechanism of ubiquitination site selection in HMGCR. We find that the distance of Lys248 to membrane is dispensable for its ubiquitination. However, the conserved tetra-glutamic acid residues adjacent to Lys248 in HMGCR are essential. Replacement of these negatively charged residues with tetra-arginine causes the resistance of HMGCR to sterol-induced ubiquitination and degradation, albeit this mutant HMGCR can still binds to Insig-1. We further find that the tetra-glutamic acid residues are necessary but not sufficient for the modification on their adjacent Lys, since they are not functional on Lys89 of HMGCR or in SCAP. UBE2G2, a previously known E2 of gp78, is demonstrated to be involved in the sterol-regulated ubiquitination and degradation of HMGCR. In summary, these results identify the tetra-glutamic acid residues as a critical motif in HMGCR for the ubiquitination reaction mediated by gp78 and UBE2G2.
 Development of retinol-binding protein 4 immunocolloidal gold fast test strip using high-sensitivity monoclonal antibodies generated by DNA immunization C Bian , F Zhang , F Wang , Z Ling , M Luo , H Wu , Y Sun , J Li , B Li , J Zhu , L Tang , Y Zhou , Q Shi , Y Ji , L Tian , G Lin , Y Fan , N Wang and B. Sun DNA immunization is an efficient method for high-affinity monoclonal antibody generation. Here, we describe the generation of several high-quality monoclonal antibodies (mAbs) against retinol-binding protein 4 (RBP4), an important marker for kidney abnormality and dysfunction, with a combination method of DNA priming and protein boost. The mAbs generated could bind to RBP4 with high sensitivity and using these mAbs, an immunocolloidal gold fast test strip was constructed. The strip can give a result in <5 min and is very sensitive with a detection limit of about 1 ng/ml. A small-scale clinical test revealed that the result of this strip was well in accordance with that of an enzyme-labeled immunosorbent assay kit currently available on the market. Consequently, it could be useful for more convenient and faster RBP4 determination in the clinic.
 Changes in Mitral Annular Geometry and Dynamics With {beta}-Blockade in Patients With Degenerative Mitral Valve Disease D. B Ennis , G. R Rudd Barnard , B Li , C. G Fonseca , A. A Young , B. R Cowan and R. A. H. Stewart Background— Remodeling of the mitral annulus contributes to progression of mitral regurgitation (MR). In patients with moderate-to-severe MR, short-term treatment with β-blockers has been shown to increase left ventricular (LV) end-diastolic and end-systolic volume, and this could deleteriously increase mitral valve annular dimensions. The objective of this study was to quantify the effects of a short duration of β-blocker treatment on mitral annular dimensions and dynamics in patients with MR due to primary degenerative valve disease. Methods and Results— Twenty-five patients with moderate-to-severe degenerative MR and normal LV systolic function were studied in a double-blind crossover experiment using a β1-selective adrenergic blocker and placebo administered for 14±3 days. Cardiac MRI images were acquired after each treatment period to quantify mitral annular dimensions. At end diastole, there was no change in annular area (1659±331 versus 1632±299 mm2; P<0.19), annular perimeter (154.3±16.4 versus 152±13.9 mm; P<0.13), septal-lateral (SL) dimension (38.0±5 versus 39.0±4.5 mm; P<0.15), or annular height (9.8±3.8 versus 9.5±2.5 mm; P<0.53). β-blockade resulted in significant end-diastole decreases in commissure-commissure dimension (48.9±4.6 versus 47.2±4.0 mm; P<0.01) and eccentricity (1.3±0.2 versus 1.2±0.1; P<0.01). At end systole (ES), β-blockade conferred a small, but significant decrease in annular perimeter (161.0±19.3 versus 156.8±16.9 mm; P<0.04) and eccentricity (1.2±0.1 versus 1.1±0.1; P<0.02), and the SL dimension significantly increased (41.5±5.7 versus 43.0±5.3 mm; P<0.03). Commissure-commissure dimension, annular area, and annular height at ES were not significantly different. Conclusions— Despite significant increases in LV end-diastolic and end-systolic volume, short-term β-blocker treatment of patients with moderate-to-severe MR reduced or preserved all mitral annular dimensions except SL at ES.
 Newton-Cotes rules for Hadamard finite-part integrals on an interval B Li and W. Sun The general (composite) Newton–Cotes rules are studied for Hadamard finite-part integrals. We prove that the error of the kth-order Newton–Cotes rule is O$$\left({h}^{k}\right|\mathrm{ln}h\left|\right)$$ for odd k and O$$\left({h}^{k+1}\right|\mathrm{ln}h\left|\right)$$ for even k when the singular point coincides with an element junction point. Two modified Newton–Cotes rules are proposed to remove the factor ln h from the error bound. The convergence rate (accuracy) of even-order Newton–Cotes rules at element junction points is the same as the superconvergence rate at certain Gaussian points as presented in Wu & Lü (2005, IMA J. Numer. Anal., 25, 253–263) and Wu & Sun (2008, Numer. Math., 109, 143–165). Based on the analysis, a class of collocation-type methods are proposed for solving integral equations with Hadamard finite-part kernels. The accuracy of the collocation method is the same as the accuracy of the proposed even-order Newton–Cotes rules. Several numerical examples are provided to illustrate the theoretical analysis.