Jie-pin Wang

Fourth Military Medical University, Xi’an, Liaoning, China

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Publications (4)3.54 Total impact

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    ABSTRACT: BACKGROUND/AIM: There is very limited experience in the management of telbivudine (LdT)-associated virological breakthrough (VBT) and resistance in the treatment of chronic hepatitis B (CHB) patients, and the guideline recommendations are primitively based on the general principles of rescue therapy to nucleos(t)ide analog resistance. The aim of this study is to determine the effect of the addition of adefovir (ADV) in hepatitis B e antigen (HBeAg)-positive CHB patients with VBT or resistance to LdT. METHODS: Thirty-seven CHB patients with confirmed VBT and 31 patients with genotypic resistance to LdT were enrolled and thereafter treated with a combination of LdT and ADV for 12 months. RESULTS: Combination therapy was safe and the majority of patients tolerated the therapy. LdT+ADV led to rapid decreases in viral loads, and viral replications were persistently suppressed, with 2.17 (VBT) and 2.31 (resistance) log10 copies/ml reductions 12 months after rescue therapy, respectively. The rates corresponding to virological and biochemical responses were similar between the two groups at the end of observations (70.3 vs. 74.2% for virological response, P=0.720; 64.0 vs. 65.5% for biochemical response, P=0.907). The cumulative rates of serological responses were higher in patients with VBT than in those with resistance (35.1 vs. 9.67% for HBeAg loss, P=0.014; 10.8 vs. 3.23% for HBeAg/anti-HBe seroconversion, P=0.233). CONCLUSION: LdT and ADV combination therapy led to significant decreases in serum hepatitis B virus DNA levels and normalization of alanine aminotransferase levels in patients with VBT or genotypic resistance to LdT. This rescue strategy was also associated with a higher rate of HBeAg serological outcomes in patients with confirmed LdT-related VBT.
    European journal of gastroenterology & hepatology 02/2013; · 1.66 Impact Factor
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    ABSTRACT: Omentin-1, an adipokine secreted from visceral adipose tissue, has been reported to be associated with coronary artery disease (CAD) and metabolic disorders. To clarify the relationship between serum omentin-1 levels and the presence and severity of CAD in patients with metabolic syndrome (MetS). We measured serum omentin-1 levels in 175 consecutive patients with MetS and in 46 controls. Serum omentin-1 levels are inversely associated with the presence and angiographic severity of CAD in MetS patients. Serum omentin-1 might be a potential biomarker to predict the development and progression of CAD in MetS patients.
    Biomarkers 12/2011; 16(8):657-62. · 1.88 Impact Factor
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    ABSTRACT: To investigate the role of p38 mitogen-activated protein kinase(MAPK) in lipopolysaccharide (LPS)-induced tumor necrosis factor-α (TNF-α) expression in neonatal rat cardiomyocytes and to determine the relationship between reactive oxygen species (ROS) and p38 MAPK activation. Cardiomyocytes were isolated from neonatal Sprague-Dawley rats and cultured by differential adhesion. Expression of TNF-α was determined in culture medium by ELISA. Activation of p38 MAPK was determined by Western blot analysis with phospho-specific antibody. ROS generation in cardiomyocytes was determined by peroxide specific probe 2', 7'-dichlorofluorescin diacetate (DCF-DA). In cardiomyocytes stimulated with LPS, the content of TNF-α in culture medium correlated with the activity of p38 MAPK in a time-dependent manner. The activation of p38 was observed after stimulation of 1 mg/L LPS for 1 h. TNF-α accumulated significantly in culture medium at 3 h after stimulation of LPS (P<0.05), which was remarkably attenuated by pretreatment with p38 MAPK specific inhibitor SB203580 (P<0.01). Furthermore, the production of ROS in cardiomyocytes stimulated with LPS was also increased at 1 h after stimulation of LPS, consistent with p38 MAPK activity. Pretreatment with antioxidants such as N-acetylcysteine and diphenyleneiodonium significantly inhibited the activation of p38 MAPK compared with LPS control (P<0.05). There was no significance in the activity of p38 MAPK among antioxidants pretreatment and non-LPS control groups. The activation of p38 MAPK plays an important role in TNF-α expression in LPS-stimulated cardiomyocytes and the increase of ROS production is prerequisite for the activation of p38 MAPK.
    Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 01/2011; 27(1):7-10.
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    ABSTRACT: To investigate the effects of cyclosporin A (CsA) on growth and collagen synthesis of cardiac fibroblasts (CFs) induced by arginine vasopressin (AVP). CFs of neonatal Sprague-Dawley rats were isolated by trypsinization and cultured; growth-arrested CFs were stimulated with 1 x 10(-7) mol x L(-1) AVP in the presence or absence of CsA (0.05, 0.5 and 5 micromol x L(-1)). MTT and flow cytometry techniques were adopted to measure cell number and analyze cell cycle respectively. Collagen synthesis was determined by measurement of hydroxyproline content in culture supernatant with colorimetry. Calcineurin activity was estimated by chemiluminescence. Trypan blue staining to test the viability of CFs. 0.05, 0.5 and 5 micromol x L(-1) CsA inhibited the increase of CFs number induced by 1 x 10(-7) mol x L(-1) AVP in a dose-dependent manner, with the inhibitory rates by 12%, 24% and 29%, respectively (P < 0.05). Furthermore, cell cycle analysis showed 0.5 micromol x L(-1) CsA decreased the S stage percentage and proliferation index of CFs stimulated by AVP (P < 0.05). In culture medium, the hydroxyproline content induced by AVP decreased by 0.5 and 5 micromol x L(-1) CsA (P < 0.05), with the inhibitory rates of 29% and 33%, respectively. CsA completely inhibited the increment of calcineurin activity induced by AVP (P < 0.01), but CsA itself had no effect on the baseline of calcineurin activity and CFs viability. CsA inhibits proliferation and collagen synthesis of CFs by virtue of blocking calcineurin signaling pathway and might provide a novel target for prevention and treatment to cardiac fibrosis.
    Yao xue xue bao = Acta pharmaceutica Sinica 11/2006; 41(11):1044-9.