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Duan X.-Z.,Liver Failure Treatment and Research Center | Liu F.-F.,Liver Failure Treatment and Research Center | Tong J.-J.,Liver Failure Treatment and Research Center | Yang H.-Z.,Liver Failure Treatment and Research Center | And 5 more authors.
World Journal of Gastroenterology | Year: 2013

AIM: To evaluate the safety and efficacy of granulocyte-colony stimulating factor (G-CSF) therapy in patients with hepatitis B virus (HBV)-associated acuteon-chronic liver failure (ACLF). METHODS: Fifty-five patients with HBV-associated ACLF were randomized into two groups: the treatment group and the control group. Twenty-seven patients in the treatment group received G-CSF (5 μg/kg per day, six doses) treatment plus standard therapy, and 28 patients in the control group received standard therapy only. The peripheral CD34+ cell count was measured consecutively by flow cytometry. Circulating white blood cell count, biochemical parameters, and other clinical data of these patients were recorded and analyzed. All patients were followed up for a period of 3 mo to evaluate the changes in liver function and survival rate. RESULTS: The peripheral neutrophil and CD34+ cell counts in the G-CSF group increased on day 3 from the onset of therapy, continued to rise on day 7, and remained elevated on day 15 compared to those of the control group. Child-Turcotte-Pugh score of patients in the treatment group was improved on day 30 from the onset of G-CSF therapy, compared to that in the controls (P = 0.041). Model for End-Stage of Liver Disease score of patients in the treatment group was improved on day 7 (P = 0.004) and remained high on day 30 from the onset of G-CSF therapy (P < 0.001) compared to that in controls. After 3 mo of follow-up observation, the survival rate in the treatment group (48.1%) was significantly higher than that in the control group (21.4%) (P = 0.0181). CONCLUSION: G-CSF therapy promoted CD34+ cell mobilization in patients with HBV-associated ACLF, and improved the liver function and the survival rate of these patients. © 2013 Baishideng. All rights reserved.

Wang X.,Xian Jiaotong University | Zhao Y.-R.,Xian Jiaotong University | Liu H.-L.,Center for Clinical Laboratory | Ma X.-H.,Eighth Hospital of xiAn | And 2 more authors.
Journal of Clinical Gastroenterology | Year: 2016

Goals: To elucidate impact of insulin resistance (IR) on the response to interferon-α (IFN-α) therapy in chronic hepatitis B (CHB) patients. Background: Metabolic factors influencing the virological response of CHB patients on IFN-α treatment are still unexplored. Study: Eighty CHB patients were treated with IFN-α for 48 weeks. The IR was evaluated by homeostasis model assessment of IR (HOMA-IR) before treatment. Viral load and biochemical parameters were measured at 12, 24, and 48 weeks after starting treatment, and then 24 weeks after the end of treatment. IFN-γ and tumor necrosis factor-α were tested at baseline and 12 weeks of treatment. Results: Pretreatment HOMA-IR proved to be the only independent predictor of primary nonresponse, as well as the pretreatment HOMA-IR, viral load and primary nonresponse were independently associated with virological response at 24, 48 weeks of treatment and at the follow-up endpoint. The significant higher virological relapse rate in patients with IR was observed in patients with virological response at 48 weeks of treatment. The mean HOMA-IR was significantly lower in virological responders than in virological nonresponders. The secretion of IFN-γ and tumor necrosis factor-α was not induced in patients with IR at 12 weeks after IFN-α treatment. Conclusions: Our data suggest that IR is strongly associated with virological response, thus reflecting the important role played by metabolic factors in the viral kinetics during IFN-α treatment. These findings suggested clinical application of pretreatment HOMA-IR could enable treatment outcome to be predicted and treatment regimens to be determined. © 2015 Wolters Kluwer Health, Inc. All rights reserved.

Yang M.,Beijing 302 Hospital | Xu D.,Institute of Infectious Diseases | Liu Y.,Beijing 302 Hospital | Guo X.,Beijing 302 Hospital | And 6 more authors.
PLoS ONE | Year: 2015

Background: Non-alcoholic steatoheaptitis (NASH), the critical stage of non-alcoholic fatty liver disease (NAFLD), is of chronic progression and can develop cirrhosis even hepatocellular carcinoma (HCC). However, non-invasive biomarkers for NASH diagnosis remain poorly applied in clinical practice. Our study aims at testing the accuracy of the combination of cytokeratin-18 M30 fragment (CK-18-M30), fibroblast growth factor 21 (FGF-21), interleukin 1 receptor antagonist (IL-1Ra), pigment epithelium-derived factor (PEDF) and osteoprotegerin (OPG) in diagnosing NAFLD and NASH. Methods: 179 patients with biopsy-proven NAFLD were enrolled as training group, 91 age- and gender-matched healthy subjects were recruited at the same time as controls. 63 other NAFLD patients were separately collected as validation group. 45 alcoholic fatty liver disease (AFLD) patients, 50 hepatitis B virus (HBV) patients, 52 hepatitis C virus (HCV) patients were also included. Serum biomarker levels were measured by enzyme-linked immunosorbent assay. Results: Serum levels of CK-18-M30, FGF-21, IL-1Ra and PEDF increased, while OPG decreased in a stepwise fashion in controls, non-NASH NAFLD patients and NASH patients (P < 0.01). The area under receiver-operating characteristics curve to diagnose NASH was 0.86 for CK-18-M30, 0.89 for FGF-21, 0.89 for IL-1Ra, 0.89 for PEDF and 0.89 for OPG. CK-18-M30 had 70% negative predictive value (NPV) and 79% positive predictive value (PPV) to diagnose NASH. A 5-step approach measuring CK-18-M30 followed by FGF21, IL-1Ra, PEDF and OPG gradually improved the NPV to 76% and PPV to 85%, which reached 80% and 76% respectively in the validation cohort. Conclusion: Compared to single biomarker, stepwise combination of CK-18-M30, FGF-21, IL-1Ra, PEDF and OPG can further improve the accuracy in diagnosing NASH. © 2015 Yang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Wang F.,Shaannxi Provincial Peoples Hospital | Xie X.,Center for Clinical Laboratory | Hu J.,Central Laboratory | Chen L.,Shaannxi Provincial Peoples Hospital | And 3 more authors.
Neoplasma | Year: 2015

The therapeutic potential of cisplatin in ovarian cancer treatment is restricted by the occurrence of cellular resistance. We aimed to explore the role of SRPK1 in cisplatin resistance related to the long non-coding RNA UCA1 in ovarian cancer cell. Totally, 24 ovarian cancer tissues and 16 normal tissues were used to assess the expression of UCA1 RNA. UCA1 stable transfected SKOV3 cells were established and the ability of cell migration, invasion and cisplatin resistance was assessed. The expression of SRPK1 and apoptosis pathway proteins was then assessed to explore the mechanism. In addition, SRPK1 knockdown cell line was also established and the effects of SRPK1 on cell migration, invasion and cisplatin resistance was evaluated. Elevated expression of UCA1 RNA was identified in ovarian cancer tissues compared with normal tissues. Expression of UCA1 RNA in SKOV3 cells enhanced the cell migration, invasion and cisplatin resistance. Increased expression of SRPK1 and anti-apoptosis proteins were found in SKOV3/pcDNA-UCA1 cells. Knocking-down SRPK1 could partly rescue the effect of UCA1 expression on cell migration, invasion and cisplatin resistance in SKOV3 cells. Elevated expression of UCA1 RNA was found in ovarian cancer tissues. UCA1 can improve the cell migration, invasion and induce cisplatin resistance. SRPK1 and apoptosis pathway proteins may be involved in the effect of UCA1. © 2015, Cancer Research Institute Slovak Acad. of Sciences. All rights reserved.

Li X.,Institute of Infectious Diseases | Liu Y.,Institute of Infectious Diseases | Xu Z.,Institute of Infectious Diseases | Wan Z.,Institute of Infectious Diseases | And 5 more authors.
Journal of Medical Virology | Year: 2013

This study investigated features and clinical implications of HBV mutations in patients with different clinical manifestations. In total, 516 patients were enrolled in this study, including 131 patients with acute hepatitis B, 239 patients with chronic hepatitis B, and 146 patients with acute-on-chronic liver failure. HBV genotypes and mutations were analyzed by direct sequencing of complete viral genomes. Genotypes B2, C1, C2, and D1 accounted for 22.2%, 1.6%, 74.6%, and 1.6%, respectively. Genotype B was more frequently detected in patients with acute hepatitis B than those with chronic hepatitis B and acute-on-chronic liver failure. Deletion mutations were detected mostly in preS1 and preS2 regions and the detection rates were 3.8%, 19.7%, and 24.7% for acute hepatitis B, chronic hepatitis B and acute-on-chronic liver failure patients, respectively. Incidences of point mutation T53C (preS1F53L), G1613A (polR841K), G1775A and A1762T+G1764A in the basal core promoter region, G1896A and G1899A in precore region and A2189C (coreI97L) in core region increased along with acute hepatitis B, chronic hepatitis B, and acute-on-chronic liver failure. The mutation G1896A was independently associated with poor survival of patients with acute-on-chronic liver failure. The gradual increase of viral mutation incidences was also observed in three HLA-A2-restricted cytotoxic T lymphocyte epitopes from HLA-A2-positive patients, that is env188-196 (5.8%, 10.1%, 22.5%), core107-115 (4.3%, 4.6%, 19.7%), and x92-100 (1.4%, 20.2%, 33.8%). In conclusion, certain viral mutations in various regions of HBV genome are associated with disease progression of HBV infection. © 2013 Wiley Periodicals, Inc.

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