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Zhang D.-K.,China Military Institute of Chinese Medicine | Zhang D.-K.,Chengdu University of Traditional Chinese Medicine | Li R.-S.,Research Center for Clinical and Translational Medicine | Han X.,China Military Institute of Chinese Medicine | And 8 more authors.
Frontiers in Pharmacology | Year: 2016

Complex chemical composition is an important reason for restricting herbal quality evaluation. Despite the multi-components determination method significantly promoted the progress of herbal quality evaluation, however, which mainly concerned the total amount of multiple components and ignored the activity variation between each one, and did not accurately reflect the biological activity of botanical medicines. In this manuscript, we proposed a toxicity calibrated contents determination method for hyper toxic aconite, called toxic constituents index (TCI). Initially, we determined the minimum lethal dose value of mesaconitine (MA), aconitine (AC), and hypaconitine (HA), and established the equation TCI = 100 × (0.3387 ×XMA + 0.4778 ×XAC + 0.1835 ×XHA). Then, 10 batches of aconite were selected and their evaluation results of toxic potency (TP), diester diterpenoid alkaloids (DDAs), and TCI were compared. Linear regression analysis result suggested that the relevance between TCI and TP was the highest and the correlation coefficient R was 0.954. Prediction error values study also indicated that the evaluation results of TCI was highly consistent with that of TP. Moreover, TCI and DDAs were both applied to evaluate 14 batches of aconite samples oriented different origins; from the different evaluation results, we found when the proportion of HA was reached 25% in DDAs, the pharmacopeia method could generate false positive results. All these results testified the accuracy and universality of TCI method. We believe that this study method is rather accurate, simple, and easy operation and it will be of great utility in studies of other foods and herbs. © 2016 Zhang, Li, Han, Li, Zhao, Zhang, Yang, Wang and Xiao. Source


Li X.,Research Center for Clinical and Translational Medicine | Qin Y.,Research Center for Clinical and Translational Medicine | Liu Y.,Research Center for Clinical and Translational Medicine | Li F.,The Second Liver Cirrhosis Medical Center | And 5 more authors.
Journal of Clinical Virology | Year: 2016

Background The association of hepatitis B virus (HBV) preS1 and preS2 deletions with progressive liver diseases are not fully understood. Objective The study aimed to investigate characteristics of HBV preS deletion in HBV-infected patients with different illness categories. Study design Total of 539 HBV-infected patients were enrolled in the study, including 146 with chronic hepatitis B (CHB), 111 with HBV-related liver cirrhosis (LC), 146 with HBV-related acute-on-chronic liver failure (ACLF), and 136 with HBV-related hepatocellular carcinoma (HCC). PreS deletion was determined by sequencing. Replicons containing representative preS1 and preS2 deletion mutants and wild-type were respectively constructed and transfected into HepG2 cells for phenotypic analysis. Results The detection rates of overall preS deletion were 15.8%, 26.1%, 24.0%, and 34.6% in CHB, LC, ACLF, and HCC patients, respectively. PreS1 deletion was most frequently detected in LC patients while preS2 deletion was most frequently detected in HCC patients, both frequencies were significantly higher than that in CHB patients (17.1% vs. 4.8%, P < 0.01; 19.1% vs. 4.8%, P < 0.01). The deletion patterns across preS gene were different among the 4 illness categories. Compared with wild-type strain, the preS1 deletion mutant had defected preS1 expression, significantly decreased viral mRNA level and SP II promoter activity; while preS2 deletion mutant had defected preS2 expression, and significantly decreased viral mRNA level. Conclusions HBV preS deletion was associated with advancement of liver diseases not only presented in preS deletion incidence, but also in the deletion pattern. Patients with preS2 deletion might have a higher risk to develop HCC. © 2016 Elsevier B.V. Source


Lu S.-S.,Guilin Medical University | Li X.-D.,Research Center for Clinical and Translational Medicine | Luo S.-D.,Beijing Institute of Microbiology and Epidemiology | Qiao Y.,Guilin Medical University | And 5 more authors.
Medical Journal of Chinese People's Liberation Army | Year: 2016

Objective To analyze the characteristics of newly added N-glycosylation mutation in major hydrophilic region (MHR) of HBV S gene in patients with coexistence of HBsAg and antiHBs, and reveal the generation mechanism and clinical implications of the coexistence. Methods HBV S genes from 284 patients with HBsAg+antiHBs and 314 patients with single HBsAg were amplified respectively for sequence analysis. A chronic hepatitis B (CHB) patient with HBsAg+antiHBs in MHR was found to harbor a novel double N-glycosylation mutation and selected for further study. Recombinant vectors harboring the novel mutant or control PreS/S genes were constructed and transfected in HepG2 cells respectively for phenotypic analysis, and the effects of the mutations on HBV duplication and antigenicity were investigated. Results The detection rate of MHR N-glycosylation mutation was significantly higher in HBsAg+antiHBs group than in single HBsAg group (11.3% vs. 2.9%, P<0.01, respectively). In HBsAg+antiHBs cohort, the proportion of hepatocellular carcinoma (HCC) patients accounted for 46.9%(15/32) in patients with N-glycosylation mutation at the time of testing; by contrast, the number was 22.6%(57/252) in patients with non-N-glycosylation mutation (P<0.01). N-glycosylation mutational pattern of the novel strain was s116-118TST → NST+s131-133TSM → NST concomitant with sP120 deletion+G145D mutation. The novel mutants accounted for 98.0%, 2.0% and 2.5%, respectively, of viral clones in three sequential serum samples. Mutants with single N-glycosylation mutation s130-132GTS→NSS without sP120 deletion+G145D were detected in sample 2, accounting for 17.6% of viral clones. Compared to the wild-type, the novel mutant had an increase of 31% in replication capacity, but a decrease of 99% in HBsAg level. Immunofluorescence showed that elimination of the two additional N-glycosylation mutations only partly restored HBsAg detection by antiHBs, suggesting that sP120 deletion+G145D mutation also attenuated HBsAg antigenicity. Conclusions Additional N-glycosylation mutation in MHR of HBV S gene is associated with coexisting HBsAg+antiHBs, and the two parameters together might be a better risk factor for HCC occurrence. Combination of two additional N-glycosylation mutation, sP120 deletion and sG145D mutation may co-play a role in silence of HBsAg antigenicity. © 2016, People’s Military Medical Press. All rights reserved. Source


Wu S.,Research Center for Clinical and Translational Medicine | Hou J.,Research Center for Clinical and Translational Medicine | Ding Y.,Shanghai University | Wu F.,309th Hospital of PLA | And 3 more authors.
Medicine (United States) | Year: 2015

The aim of this study is to summarize and quantify the current evidence on the therapeutic efficacy of cryoablation compared with radiofrequency ablation (RFA) in patients with hepatic malignancies in a meta-analysis. Data were collected by searching PubMed, Scopus, and Cochrane databases for reports published up to May 26, 2015. Studies that reported data on comparisons of therapeutic efficacy of cryoablation and RFA were included. The random effects model was used to estimate the pooled relative risks of events comparing cryoablation to RFA for therapy of hepatic malignancies. Seven articles met the inclusion criteria and were included in the meta-analysis. The meta-analysis showed that there was no statistically significant difference in mortality of at least 6 months (odds ratio [OR]=1.00, 95% confidence interval [CI]: 0.68-1.49) and local tumor progression according to both patients (OR=1.64, 95% CI: 0.57-4.74) and tumors (OR=1.81, 95% CI: 0.74-4.38) between cryoablation group and RFA group. However, the risk of complications was significantly higher in the cryoablation group than that in the RFA group (OR=2.93, 95% CI: 1.15-7.46). When considering the specific complications, only thrombocytopenia (OR=51.13, 95% CI: 2.92-894.21) and renal impairment (OR=4.19, 95% CI: 1.34-13.11) but not other complications were significantly higher in the cryoablation group. In conclusion, the 2 methods had almost equal mortality and nonsignificant difference in local tumor progression, with higher risk of complications in cryoablation. Further large-scale, well-designed randomized controlled trials are needed to identify the current findings and investigate the long-term effects of cryoablation compared with RFA for therapy of hepatic malignancies. © 2015 Wolters Kluwer Health, Inc. All rights reserved. Source


Shi L.,Treatment and Research Center for Infectious Diseases | Qin E.,Treatment and Research Center for Infectious Diseases | Zhou J.,Beijing Institute of Transfusion Medicine | Zhao J.,Research Center for Clinical and Translational Medicine | And 10 more authors.
PLoS ONE | Year: 2016

Accelerated fibrosis in patients co-infected with hepatitis C virus (HCV) and human immunodeficiency virus (HIV) has been a major cause of mortality in the highly active anti-retroviral therapy (HAART) era. However, the role of co-infection in accelerating the progression of liver fibrosis, particularly with regard to the effects of co-infection on hepatic stellate cells (HSCs), remains unclear. We hypothesized that HIV and HCV induce liver fibrosis synergistically by altering the regulation of epimorphin production, and thereby indirectly alter HSC function. Here, we examined the effects of epimorphin on HSC proliferation and invasion, and the changes in fibrogenesis-related gene activity in HSCs (LX2) in the presence of inactivated CXCR4-tropic HIV and HCV (JFH1). The combination of HIV and HCV significantly increased epimorphin expression, which increased the proliferation and invasion capabilities of HSCs. Epimorphin also induced the expression of profibrogenic tissue inhibitor of metalloproteinase 1 (TIMP1) in an extracellular signal-regulated kinase (ERK)-dependent manner. These data indicated that the effects of HIV/HCV co-infection on hepatic fibrosis might be mediated in part by EPM. Strategies to limit the expression of EPM might represent a novel therapeutic approach to prevent the progression of hepatic fibrosis during HIV/HCV co-infection. © 2016 Shi 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. Source

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