Qiu X.,Hubei University |
Xu D.,Hubei University |
Ma L.,Wuhan University |
Wang Y.,HuangShi Central Hospital
International Journal of Electrochemical Science | Year: 2017
Electrochemical supercapacitors (ECs) with high energy density and power capability have demonstrated promising potential in various energy applications. In this study, 3D MnO2/rGO aerogels with excellent electrical conductivity was successfully prepared with a simple hydrothermal method. The as-prepared 3D aerogels could be applied for constructing the electrode of supercapacitor directly without the demand of other additives. Asymmetric supercapacitors were then constructed with Na2SO4 aqueous solution as electrolyte, MnO2/rGO aerogel and rGO aerogel as positive and negative electrode, respectively. The asymmetric supercapacitor demonstrated maximum energy density of 18.2 Wh/kg with power density of 400 W/kg and excellent cycle stability as well. © 2017 The Authors.
Cao Z.,Shanghai JiaoTong University |
Fu B.,Huangshi Central Hospital |
Deng B.,Shanghai JiaoTong University |
Zeng Y.,Shanghai JiaoTong University |
And 2 more authors.
Cancer Cell International | Year: 2014
Background: Many studies support that chemokine (C-X-C motif) ligand 1 (CXCL1) regulate tumor epithelial-stromal interactions involving in tumor growth and invasion. However, limited studies have been conducted on the expression and function of the CXCL1 gene in hepatocellular carcinoma (HCC).Methods: The mRNA and protein level expression of CXCL1 was examined in HCC tissues and cell lines. The expression of CXCL1 was correlated with clinicopathological features and follow-up data. Overexpression approaches were used to evaluate the biological functions of CXCL1 by MTT and matrigel invasion assays. Protein expression levels of CXCL1 and P65 were determined by western blot analysis.Results: In this study, we found that CXCL1 expression was markedly upregulated in HCC tissues. Ectopic expression of CXCL1 significantly promoted HCC cells proliferation and invasion. Furthermore, CXCL1 promote cell invasion through NF-kB-dependent pathway. CXCL1 expression in HCC associated with clinical stage (P = 0.034) and distant metastasis (P = 0.028). Moreover, Patients with high CXCL1 expression level had poorer overall survival (OS;P = 0.027) than those with low CXCL1 expression.Conclusions: These data indicated that the CXCL1 upregulation may contribute to both the development and progression of HCC and this effect may be associated with increased proliferation and invasiveness mainly via regulating P65 expression. © 2014 Cao et al.; licensee BioMed Central Ltd.
Luo P.,Vanderbilt University |
Luo P.,Huangshi Central Hospital |
Dematteo A.,Vanderbilt University |
Wang Z.,Vanderbilt University |
And 7 more authors.
Diabetologia | Year: 2013
Aims/hypothesis: Obesity is associated with aldosterone excess, hypertension and the metabolic syndrome, but the relative contribution of aldosterone to obesity-related complications is debated. We previously demonstrated that aldosterone impairs insulin secretion, and that genetic aldosterone deficiency increases glucose-stimulated insulin secretion in vivo. We hypothesised that elimination of endogenous aldosterone would prevent obesity-induced insulin resistance and hyperglycaemia. Methods: Wild-type and aldosterone synthase-deficient (As -/-) mice were fed a high-fat (HF) or normal chow diet for 12 weeks. We assessed insulin sensitivity and insulin secretion using clamp methodology and circulating plasma adipokines, and examined adipose tissue via histology. Results: HF diet induced weight gain similarly in the two groups, but As -/- mice were protected from blood glucose elevation. HF diet impaired insulin sensitivity similarly in As -/- and wild-type mice, assessed by hyperinsulinaemic-euglycaemic clamps. Fasting and glucose-stimulated insulin were higher in HF-fed As -/- mice than in wild-type controls. Although there was no difference in insulin sensitivity during HF feeding in As -/- mice compared with wild-type controls, fat mass, adipocyte size and adiponectin increased, while adipose macrophage infiltration decreased. HF feeding significantly increased hepatic steatosis and triacylglycerol content in wild-type mice, which was attenuated in aldosterone-deficient mice. Conclusions/interpretation: These studies demonstrate that obesity induces insulin resistance independently of aldosterone and adipose tissue inflammation, and suggest a novel role for aldosterone in promoting obesity-induced beta cell dysfunction, hepatic steatosis and adipose tissue inflammation. © 2013 Springer-Verlag Berlin Heidelberg.
Wang H.-L.,Huangshi Central Hospital |
Zhang H.-Y.,Wuhan University |
Zhai Z.-L.,Huangshi Central Hospital |
Zhou X.,Wuhan University
Bio-Medical Materials and Engineering | Year: 2012
Objective: To investigate the correlation between HBV infection and interleukin 27 (IL-27). Methods: Serum IL-27 levels in patients with HBV infection and in healthy individuals were measured by ELISA, regulation of IL-27 by HBV in vitro were analyzed by RT-PCR and ELISA. Results: IL-27 was significantly elevated in patients as compared to healthy individuals (P<0.001). IL-27 was also detected at higher levels in patients with liver cirrhosis or hepatocellular carcinoma than those with acute hepatitis B or chronic hepatitis B (P<0.05). We also found that IL-27 expression was influenced by HBV e antigen. In addition, our in vitro studies demonstrated that mRNA and protein expression were all stimulated in cells transfected with infectious HBV clone. Conclusions: IL-27 would be a novel cytokine for clinical management of HBV-infected patients, which may establish novel HBV therapeutic approaches. © 2012-IOS Press and the authors. All rights reserved.
Chen Z.,Renmin University of China |
Jiang H.,Renmin University of China |
Wan Y.,Huangshi Central Hospital |
Bi C.,Huangshi Central Hospital |
Yuan Y.,Huangshi Central Hospital
Cytotechnology | Year: 2012
P38 mitogen-activated protein kinases (p38 MAPK) and tumor necrosis factor-α (TNF-α) play important roles in oxidative stress-induced apoptosis in cardiac myocytes. However, the regulation and functional role of cross-talk between p38 MAPK and TNF-α pathways have not yet been fully characterized in cardiac myocytes. In this study, we found that inhibition of p38 MAPK with SB-203580 (SB) reduced H 2O 2-stimulated secretion of TNF-α, whereas pre-activation of p38 MAPK with sodium arsenite (SA) enhanced H 2O 2-stimulated secretion of TNF-α. In addition, pretreatment of cells with TNF-α increased basal and H 2O 2-stimulated p38 MAPK and apoptosis of cardiac myocytes, and p38 MAPK-associated apoptosis of cardiac myocytes induced by TNF-α was blocked by inhibition of p38 MAPK with SB. Finally, H 2O 2-induced apoptosis was attenuated by the inhibitors of p38 MAPK or reactive oxygen species (ROS), whereas it was enhanced by p38 MAPK agonist SA. These results suggest that H 2O 2-induced secretion of TNF-α increases apoptosis of cardiac myocytes through ROS-dependent activation of p38 MAPK. This may represent a novel mechanism that TNF-α partly interplays with p38 MAPK pathways during oxidative stress-modulated apoptosis in cardiac myocytes. © 2011 Springer Science+Business Media B.V.
Ao J.-E.,Jingmen Hubei Province First Peoples Hospital |
Kuang L.-H.,Huangshi Central Hospital |
Zhou Y.,Jingmen Hubei Province First Peoples Hospital |
Zhao R.,Huangshi Central Hospital |
Yang C.-M.,Jingmen Hubei Province First Peoples Hospital
Biochemical and Biophysical Research Communications | Year: 2012
Apoptosis repressor with caspase recruitment domain (ARC), an anti-apoptotic protein, plays an important role in the regulation of apoptosis by blocking both the extrinsic and intrinsic death pathways. However, its regulatory mechanism remains largely undefined. Here, we reported that hypoxia up-regulated the expression of ARC in p53 deficient human colon cancer cells. Moreover, ARC is a direct target of the . hypoxia-inducible factor 1 (HIF-1), a key transcriptional factor for the cellular response to hypoxia. Silencing the expression of HIF-1α in SW480 colon cancer cells by RNA interference abolished hypoxia induced ARC expression. Using luciferase reporter and ChIP assay, we showed that HIF-1α directly bound to hypoxia-responsive element located at -419 to -414 of ARC gene, which is essential for . HIF-1-induced expression. As a result of the increased ARC expression, TRAIL-induced apoptosis was reduced by hypoxia. These discoveries would shed novel insights on the mechanisms for ARC expression regulation and hypoxia induced inactivation of the intrinsic death pathway. © 2012 Elsevier Inc.
Kai L.,Jingmen No 1 Peoples Hospital |
Jia L.,Huangshi Central Hospital |
Zhi-Gang W.,Jingmen No 1 Peoples Hospital |
Lei Y.,Huangshi Central Hospital
Indian Journal of Cancer | Year: 2015
Objective: The aim of this retrospective study was to evaluate whether radiofrequency ablation (RFA) combined percutaneous ethanol injection (PEI) in the management of hepatocellular carcinoma (HCC) improves treatment outcomes. Patients and Methods: We retrospectively included 66 HCC patients who received RFA or RFA plus PEI from February 2011 to January 2014 in Jingmen No. 1 People's Hospital. Moreover, 31 cases received RFA plus PEI as the experiment group and 35 subjects treated with RFA aloe as the control group. The overall survival and treatment related complications were compared between the two groups. Results: For RFA group, the 1-year, 2-year, and 3-year survival rate were 82.0%, 69.3%, and 30.7%, respectively, with the median survival time of 27.1 months. For RFA plus PEI group, the 1-year, 2-year, and 3-year survival rate were 97.1%, 73.9%, and 37.5%, respectively, with the median survival time of 33.6 months. The overall survival of the two groups was not statistical different with the hazard ratio of 1.48 (P > 0.05); three cases of treatment associated complications were found in RFA group with 1 abscess, 1 pleural effusion, and 1 portal vein thrombosis. Moreover, 2 cases of complication were recorded in RFA plus PEI group with 1 pleural effusion and 1 portal vein thrombosis. The complicated incidence rate was not statistical different between the two groups (P < 0.05). Conclusion: The combination treatment of HCC was safe and had a slightly higher primary effectiveness rate than RFA alone.
Tian H.-Z.,Maternal and Child Health Care Hospital of Yuhang District |
Yu D.-L.,Huangshi Central Hospital
World Chinese Journal of Digestology | Year: 2016
AIM To explore the clinical effects of oral viable Bifidobacterium quadruple chip in children with persistent and chronic diarrhea, in order to provide a reference for future clinical treatment of this disease. METHODS One hundred and twenty children with persistent and chronic diarrhea treated from June 2013 to June 2015 were randomly divided into either an observation group or a conventional treatment group. The conventional group received conventional treatment, while the observation group r e c e ivedoralviable Bifidobacterium quadruple chip on the basis of conventional reatment. linical effectiveness, time to diarrhea disappearance, hospitalization time, and inflammatory cytokines were compared between the two groups. RESULTS The total effective rate was significantly higher in the observation group than in the conventional treatment group (93.3% vs 73.3%, P < 0.05). The times to fever remission, vomitingdisappearance, abdominal pain relief, diarrhea disappearance, and hospital stay were significantly lower in theobservation group than in the conventional treatment group (P < 0.05). After treatment, the levels of interleukin-4 and interferon-γ significantly improved compared with those before treatment in both groups, and the improvement was statistically better in the observation group (P < 0.05). CONCLUSION Oral administration of viable Bifidobacterium quadruple chip in children with persistent and chronic diarrhea can significantly improve clinical effectiveness, reduce the levels of inflammatory cytokines, and shorten the length of hospital stay. © 2016 Baishideng Publishing Group Inc. All rights reserved.
Shu C.,Huangshi Central Hospital |
Wang Y.,Huangshi Central Hospital |
Gong J.,Huangshi Central Hospital
International Journal of Clinical and Experimental Medicine | Year: 2016
Objective: To investigate the impact of Bay 11-7085, an inhibitor of nuclear factor kappa light chain enhancer of activated B cells (NF-κB), on the radiosensitivity of human pancreatic cancer cell line Sw1990, and to explore the possible mechanisms. Methods: The human pancreatic cancer cell line Sw1990 was cultured in vitro and then randomly assigned to one of five groups: The blank control group, the radiotherapy alone group, and the radiotherapy + Bay 11-7085 groups (2 μM, 6 μM and 10 μM). Annexin V-FITC/PI double staining was performed to detect cell apoptosis, and western blot analysis was performed to detect the expression of NF-κB, p65, IκB, B-cell lymphoma 2 (Bcl-2) and X-linked inhibitor of apoptosis protein (XIAP). Results: Bay 11-7085 significantly increased the rate of apoptosis in pancreatic cancer cells (P<0.05) in a dose-dependent manner. Compared with the blank control group, radiotherapy significantly increased the expression of the anti-apoptotic proteins Bcl-2, XIAP and p65 in the nucleus (P<0.05) and inhibited the expression of IκB protein (P<0.05). Compared with the radiotherapy alone group, radiotherapy + Bay 11-7085 significantly inhibited the expression of Bcl-2, XIAP and p65 in the nucleus (P<0.05) while increasing the expression of IκB protein (P<0.05). Conclusion: Bay 11-7085 inhibits NF-κB activity and regulates the expression of downstream anti-apoptotic proteins, thereby enhancing the radiosensitivity of pancreatic cancer cells. Thus, Bay 11-7085 may be used as a radiotherapy-sensitizing drug for the treatment of pancreatic cancer. © 2016, E-Century Publishing Corporation. All rights reserved.
Wang B.,Huazhong University of Science and Technology |
Li F.,Huazhong University of Science and Technology |
Zhang C.,Huazhong University of Science and Technology |
Wei G.,Huangshi Central Hospital |
And 2 more authors.
Journal of Thoracic and Cardiovascular Surgery | Year: 2016
Objectives Calcific aortic valve (AV) disease is known to be an inflammation-related process. High-mobility group box-1 (HMGB1) protein and Toll-like receptor 4 (TLR4) have been reported to participate in several inflammatory diseases. The purpose of the present study was to determine whether the HMGB1-TLR4 axis is involved in calcific AV disease, and to evaluate the effect of HMGB1, and its potential mechanisms, on the pro-osteogenic phenotype change of valvular interstitial cells (VICs). Methods Expression of HMGB1 and TLR4 in human calcific AVs was evaluated using immunohistochemical staining and immunoblotting. Cultured VICs were used as an in vitro model. The VICs were stimulated with HMGB1 for analysis, with versus without TLR4 small interfering ribonucleic acid (siRNA), c-Jun N-terminal kinase mitogen-activated protein kinase (JNK MAPK), and nuclear factor kappa-B (NF-κB) inhibitors. Results Enhanced accumulation of HMGB1 and TLR4 was observed in calcific valves. Moreover, we found that HMGB1 induced high levels of pro-inflammatory cytokine production and promoted the osteoblastic differentiation and calcification of VICs. In addition, HMGB1 induced phosphorylation of JNK MAPK and NF-κB. However, these effects were markedly suppressed by siRNA silencing of TLR4. In addition, blockade of JNK MAPK and NF-κB phosphorylation prohibited HMGB1-induced production of pro-osteogenic factors, and mineralization of VICs. Conclusions The HMGB1 protein may promote osteoblastic differentiation and calcification of VICs, through the TLR4-JNK-NF-κB signaling pathway. © 2016 The American Association for Thoracic Surgery.