Tianjin Institute of Hepatobiliary Disease

Tianjin, China

Tianjin Institute of Hepatobiliary Disease

Tianjin, China
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Zeng X.,Third Central Hospital of Tianjin | Zeng X.,Tianjin Institute of Hepatobiliary Disease | Zeng X.,Tianjin Key Laboratory of Artificial Cell | Zeng X.,Artificial Cell Engineering Technology Research Center | And 25 more authors.
Bioscience Reports | Year: 2017

Ischemic stroke, a major cause of death, is caused by occlusion of a blood vessel, resulting in significant reduction in regional cerebral blood flow. MiRNAs are a family of short noncod-ing RNAs (18–22 nts) and bind the 3-UTR of their target genes to suppress the gene expression post-transcriptionally. In the present study, we report that miR-143 is down-regulated in rat neurones but highly expressed in astrocytes. In vivo middle cerebral artery occlusion (MCAO) and ex vivo oxygen-glucose deprivation (OGD) results showed that miR-143 was significantly induced by ischemia injury. Meanwhile, we observed suppression of glucose uptake and lactate product of rat brain and primary neurones after MCAO or OGD. The glycolysis enzymes hexokinase 2 (HK2), PKM2, and LDHA were inhibited by MCAO or OGD at protein and mRNA levels. In addition, overexpression of miR-143 significantly inhibited HK2 expression, glucose uptake, and lactate product. We report that HK2 is a direct target of miR-143. Importantly, restoration of HK2 in miR-143 overexpressing rat neurones recovered glucose uptake and lactate product. Our results demonstrated inhibition of miR-143 during OGD could protect rat neuronal cells from ischemic brain injury (IBI). In summary, the present study reveals a miRNA-mediated neuron protection during IBI, providing a new strategy for the development of therapeutic agents against IBI. © 2017 The Author(s). This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution


Lu H.,Tianjin Institute of Hepatobiliary Disease | Yu C.,Tianjin Institute of Hepatobiliary Disease | Li J.,Tianjin Institute of Hepatobiliary Disease | Wen D.,Tianjin Institute of Hepatobiliary Disease | And 2 more authors.
National Medical Journal of China | Year: 2017

Objective To explore the CT findings of the Takayasu' s arteritis ( TA) with pulmonary artery ( PA) involvement and its clinical significance. Methods A total of 35 patients with TA involving the PA in Xijing Hospital from November 2007 to November 2016, 6 male cases, 29 female cases, the age was 15 -52 (28 ±9) years old, were retrospectively collected and included in the study group (TA + P group) , meanwhile 40 patients with TA but not involving the pulmonary artery in this hospital from January 2015 to November 2016 were collected as control group, 5 male cases, 35 female cases, the age was 7 -67 (28 ± 12) years old. The clinical and laboratory data,the pulmonary artery and right heart measurement data of the two groups were compared by using t test, test , and rank sum test. The CT signs of pulmonary artery involvement in the TA + P group were analyzed. Results TA + P group patients had shortness of breath, wheezing(54. 3% vs 10. 0% ) , cough(31. 4% vs 12. 5% )and palpitations( 11. 4% vs 0)mostly, and there were statistical difference between TA + P group and TA group (all P < 0. 05 ) , However, there was no difference between the two groups in the activity and duration of disease (all P > 0. 05 ). In TA + P group, a total of 312 pulmonary artery segments were involved in 35 patients. The lumen stenosis of PA was more common(35 cases,211 segments) , followed by occlusion(14 cases,94 segments) , bilateral PA (23 cases, 217 segments) and multiple branches of PA involvement(34 cases,311 segments) were more common. The A systolic pressure, the diameter of main pulmonary artery, right atrium and right ventricular width of the TA + P group patients were significantly higher than those of the TA group (all P <0. 05). Conclusions There are some CT certain characteristics in TA pulmonary arterial involvement, and they are not related to the activity and duration of the disease. Most patients with PA involvement present pulmonary hypertension and a series of special clinical manifestations.


Zhang Q.,Tianjin Medical University | Zhang Q.,Tianjin Third Central Hospital | Han T.,Tianjin Medical University | Han T.,Tianjin Third Central Hospital | And 12 more authors.
Hepatology Research | Year: 2016

Aim: To compare the prognosis between the patients with progression into acute-on-chronic liver failure (ACLF) from acute deterioration of pre-existing chronic liver disease and patients without this progression, and to determine predictors of this disease progression. Methods: We retrospectively analyzed clinical data from 285 patients admitted with acute worsening of pre-existing chronic liver disease within 4 weeks characterized by total bilirubin (TBIL) of 51 μM/L or more and prothrombin activity (PTA) of more than 40% but less than 70%, which did not meet the Asia-Pacific Association for the Study of the Liver criteria for ACLF. Patient survival was estimated by Kaplan-Meier analysis and subsequently compared by log-rank test. Independent predictors of disease progression were determined using univariate analysis and multivariate Cox regression analysis. Results: The 90-day survival rates significantly worsened in patients with progression into ACLF compared with those without this progression. Baseline TBIL, baseline Model for End-Stage Liver Disease (MELD) score, and the maximum changing rates of PTA level and Child-Turcotte-Pugh (CTP) score were independently associated with progression into ACLF in patients with acute deterioration of pre-existing chronic liver disease. Conclusion: Patients with acute worsening of pre-existing chronic liver disease characterized by TBIL of 51 μM/L or more and PTA of more than 40% but less than 70% should receive aggressive prediction and prevention of ACLF development. Baseline TBIL, baseline MELD score, and the maximum changing rates of PTA level and CTP score may early predict the progression into ACLF. © 2016 The Japan Society of Hepatology.


Zhang Q.,Tianjin Medical University | Zhang Q.,Tianjin Third Central Hospital | Li Y.,Tianjin Third Central Hospital | Li Y.,Tianjin Institute of Hepatobiliary Disease | And 14 more authors.
PLoS ONE | Year: 2015

Background and Aims: Currently, acute-on-chronic liver failure (ACLF) has been defined differently by Asia-Pacific Association for the Study of the Liver (APASL) and Chinese Medical Association (CMA) in the East, as well as EASL-Chronic Liver Failure (EASL-CLIF) Consortium in the West. This study aimed to compare current different diagnostic criteria for ACLF and to determine predictors of the progression into post-enrollment EASL-CLIF ACLF from ACLF at enrollment defined by APASL alone or by both APASL and CMA but not by EASL-CLIF Consortium. Methods: We retrospectively analyzed clinical data from 394 eligible cirrhotic patients fulfilling at least APASL criteria for ACLF at enrollment. Patient survival was estimated by Kaplan-Meier analysis and subsequently compared by log-rank test. Independent predictors of disease progression were determined using univariate analysis and multivariate Cox regression analysis. Results: The 90-day mortality rate was 13.1% in patients with ACLF at enrollment defined by APASL alone, 25.3%in patients with ACLF at enrollment defined by both APASL and CMA but not EASL-CLIF Consortium, and 59.3% in patients with ACLF at enrollment defined by EASL-CLIF Consortium in addition to APASL. Baseline Chronic Liver Failure-Sequential Organ Failure Assessment (CLIF-SOFA) score, and the maximum rising rates of CLIF-SOFA score, Model for End-Stage Liver Disease-Sodium (MELD-Na) score and total bilirubin were independent predictors of progression into post-enrollment EASL-CLIF ACLF from ACLF at enrollment defined by APASL alone or by both APASL and CMA but not by EASL-CLIF Consortium. Conclusion: Different diagnostic criteria for ACLF caused different patient prognosis. So, it is imperative to formulate a unifying diagnostic criteria for ACLF worldwide, thus attaining early identification and treatment, and eventual improvement in survival of ACLF patients. Baseline CLIF-SOFA score, and the maximum rising rates of CLIF-SOFA score, MELD-Na score and total bilirubin may early predict post-enrollment development of EASL-CLIF ACLF. © 2015 Zhang et al.


Zhang Q.,Tianjin Medical University | Zhang Q.,Tianjin Third Central Hospital | Han T.,Tianjin Third Central Hospital | Han T.,Tianjin Institute of Hepatobiliary Disease | And 12 more authors.
Journal of Medical Virology | Year: 2015

In clinical practice, establishing a subsequent optimum treatment for chronic hepatitis B patients with a history of multiple NAs treatment failures, including a suboptimal response to a final therapy with combined ETV and ADV, is a complicated but crucial challenge. This study investigated the efficacy and safety of a tenofovir rescue regimen in these patients. A total of six eligible patients were enrolled and were switched to a tenofovir rescue regimen. At baseline, the genotypes and genotypic mutations of the reverse transcriptase and surface gene were determined by ultra-deep pyrosequencing, and further clonal analyses of the reverse transcriptase domain were performed to identify multidrug-resistant HBV strains. In addition, HBV DNA levels, serology, and biochemistry parameters were monitored at baseline and every 3 months, and abdominal ultrasonography was performed at baseline and every 6 months. All patients were confirmed to harbor LAM-related resistant HBV strains. After switching to the tenofovir rescue treatment, all patients had an undetectable level of HBV DNA within 6 months and achieved normalization of the ALT level within 9 months. These virological and biochemical responses persisted until the end of the observation period. None of the patients developed clinical deterioration or any adverse events related to the tenofovir therapy during the median 16.5-month follow-up. In conclusion, the tenofovir rescue regimen can be employed confidently as a highly effective and safe treatment choice following a suboptimal response to ETV plus ADV therapy for a subset of chronic hepatitis B patients with a history of multiple unsuccessful antiviral treatments. © 2015 Wiley Periodicals, Inc.


Ye Q.,Tianjin Medical University | Ye Q.,Tianjin Third Central Hospital | Ye Q.,Tianjin Institute of Hepatobiliary Disease | Ye Q.,Tianjin Key Laboratory of Artificial Cells | And 16 more authors.
PLoS ONE | Year: 2016

Background: Conflicting results have been obtained for the association between two common polymorphisms (C282Y, H63D) of human HFE (hereditary hemochromatosis) gene and the risks of the liver diseases, including non-alcoholic fatty liver disease (NAFLD), liver cirrhosis and hepatocellular carcinoma (HCC). Methods: An updated systematic review and meta-analysis was conducted to evaluate the potential role of HFE polymorphisms in the susceptibility to NAFLD, liver cirrhosis and HCC. After retrieving articles from online databases, eligible studies were enrolled according to the selection criteria. Stata/SE 12.0 software was utilized to perform the statistical analysis. Results: In total, 43 articles with 5,758 cases and 14,741 controls were selected. Compared with the control group, a significantly increased risk of NAFLD was observed for the C282Y polymorphism in the Caucasian population under all genetic models and for the H63D polymorphism under the allele, heterozygote and dominant models (all OR>1, Passociation<0.05). However, no significant difference between liver cirrhosis cases and the control group was observed for HFE C282Y and H63D (all Passociation>0.05). In addition, we found that HFE C282Y was statistically associated with increased HCC susceptibility in the overall population, while H63D increased the odds of developing non-cirrhotic HCC in the African population (all OR>1, Passociation<0.05). Moreover, a positive association between compound heterozygosity for C282Y/H63D and the risk of NAFLD and HCC, but not liver cirrhosis, was observed. Conclusion: Our meta-analysis provides evidence that the HFE C282Y and H63D polymorphisms confer increased genetic susceptibility to NAFLD and HCC but not liver cirrhosis. Additional well-powered studies are required to confirm our conclusion. © 2016 Ye 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.


Nie C.Y.,Tianjin Medical University | Han T.,Tianjin Medical University | Han T.,Tianjin Institute of Hepatobiliary Disease | Han T.,Tianjin Key Laboratory of Artificial Cells | And 12 more authors.
Journal of Viral Hepatitis | Year: 2014

Acute-on-chronic liver failure(ACLF) is an increasingly recognized entity encompassing an acute deterioration of liver function and results in the failure of one or more organs with high short-term mortality. The focus of this study was to discover noninvasive and reliable biomarkers for the diagnosis and prognosis of hepatitis B-related ACLF. Ultra-performance liquid chromatography-mass spectrometry (UPLC/MS) was used to analyse serum metabolites of 28 patients with hepatitis B-related ACLF, 35 patients with Child-Pugh A cirrhosis, 30 patients with chronic hepatitis B and 35 healthy volunteers (HS). Characteristic metabolites were screened, identified and dynamically tracked to investigate their value for diagnosis and prognosis. After comparing serum metabolic profile of hepatitis B-related ACLF and Child-Pugh A cirrhosis, 99 characteristic metabolites were selected, and 38 of them were identified. Dynamic tracking model demonstrated that 17 metabolites were related to prognosis of hepatitis B-related ACLF, and there were also 11 metabolites which improved with treatment in the survival group. The correlations between these characteristic metabolites and the model for end-stage liver disease score were strong. These observations contributed to the investigation of the mechanisms of hepatitis B-related ACLF manifestation and progression on the metabolic level, and they provided information for the identification of biomarkers for the diagnosis and prognosis of hepatitis B-related ACLF. © 2013 John Wiley & Sons Ltd.


Pei Y.Z.,Tianjin Institute of Hepatobiliary Disease
Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology | Year: 2011

To investigate the discrepancy of HBsAg titre and correlation of HBV DNA levels among patients with chronic hepatitis B (CHB), HBV-related liver cirrhosis (LC) and hepatocellular carcinoma (HCC). HBsAg titre and HBV DNA in serum samples were measured among 47 CHB, 72 LC and 54 HCC cases using Abbott chemiluminescence and fluorescence quantitative PCR, respectively. Statistical analyses among multiple groups, between two groups and about the correlation were performed using Kruskal-Wallis test, Mann-Whitney U test and Spearman test, respectively. The median HBsAg titre level in serum samples decreased from 2361.10 IU/ml in CHB cohort to 1001.64 IU/ml in LC cohort and 594.35 IU/ml in HCC cohort, suggesting a statistically significant difference (x2 = 24.394, P less than 0.05). Moreover, HBsAg titre in CHB group was significantly higher than that in LC group ( Z = -3.754, P less than 0.05). CHB patients had significantly higher HBsAg titre than HCC cases ( Z = -4.630, P less than 0.05). However, there was no statistically significant difference in HBsAg titre between LC and HCC group. Among HBeAg positive patients, HBsAg titre decreased from 3259.83 IU/ml in CHB group to 1077.30 IU/ml in LC group and 789.72 IU/ml in HCC group, indicating a significant difference (x2 = 15.643, P less than 0.01). Among HBeAg negative patients, HBsAg titre declined from 1669.00 IU/ml in CHB group to 1001.64 IU/ml in LC group and 582.05 IU/ml in HCC group, suggesting of a significant difference (x2 = 6.423, P less than 0.05). Positive correlation between HBsAg titre and HBV DNA was found in CHB ( r = 0.297, P less than 0.05), LC (r = 0.346, P less than 0.05) and HCC (r = 0.452, P less than 0.05), respectively. HBsAg titre level in serum decreased progressively from CHB to LC and HCC group. There were positive correlations between HBsAg titre and HBV DNA level in CHB, LC and HCC.


PubMed | Tianjin Institute of Hepatobiliary Disease
Type: Journal Article | Journal: Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology | Year: 2012

To investigate the discrepancy of HBsAg titre and correlation of HBV DNA levels among patients with chronic hepatitis B (CHB), HBV-related liver cirrhosis (LC) and hepatocellular carcinoma (HCC).HBsAg titre and HBV DNA in serum samples were measured among 47 CHB, 72 LC and 54 HCC cases using Abbott chemiluminescence and fluorescence quantitative PCR, respectively. Statistical analyses among multiple groups, between two groups and about the correlation were performed using Kruskal-Wallis test, Mann-Whitney U test and Spearman test, respectively.The median HBsAg titre level in serum samples decreased from 2361.10 IU/ml in CHB cohort to 1001.64 IU/ml in LC cohort and 594.35 IU/ml in HCC cohort, suggesting a statistically significant difference (x2 = 24.394, P less than 0.05). Moreover, HBsAg titre in CHB group was significantly higher than that in LC group ( Z = -3.754, P less than 0.05). CHB patients had significantly higher HBsAg titre than HCC cases ( Z = -4.630, P less than 0.05). However, there was no statistically significant difference in HBsAg titre between LC and HCC group. Among HBeAg positive patients, HBsAg titre decreased from 3259.83 IU/ml in CHB group to 1077.30 IU/ml in LC group and 789.72 IU/ml in HCC group, indicating a significant difference (x2 = 15.643, P less than 0.01). Among HBeAg negative patients, HBsAg titre declined from 1669.00 IU/ml in CHB group to 1001.64 IU/ml in LC group and 582.05 IU/ml in HCC group, suggesting of a significant difference (x2 = 6.423, P less than 0.05). Positive correlation between HBsAg titre and HBV DNA was found in CHB ( r = 0.297, P less than 0.05), LC (r = 0.346, P less than 0.05) and HCC (r = 0.452, P less than 0.05), respectively.HBsAg titre level in serum decreased progressively from CHB to LC and HCC group. There were positive correlations between HBsAg titre and HBV DNA level in CHB, LC and HCC.

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