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Table of Content

    31 August 2019, Volume 24 Issue 8
    Original Articles
    Analysis of risk factors for 30-day death of cirrhosis-associated acute kidney injury
    XU Qiang, MA Yan, GUO Feng, WANG Xiao-bo, WANG Xiao-zhong
    2019, 24(8):  857-860. 
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    Objective To analyze the risk factors for death within 30 days in patients with cirrhosis-associated acute kidney injury (AKI) according to the latest diagnostic criteria for AKI.Methods A total of 131 patients who met the 2015 International Club of Ascites-AKI diagnostic criteria were retrospectively analyzed. They were followed up for 30 days, and divided into the death and survival groups. Univariate and multivariate analyses were performed to identify important factors affecting 30-day mortality of cirrhosis-associated AKI patients. Results (1) During 30 days of follow-up, 29 (22.14%) patients died. Among all the patients, 64 with stage I AKI had a mortality rate of 20.69%, 44 with stage II AKI had a mortality rate of 34.48%, and 23 with stage III AKI had a mortality rate of 44.83%. (2) Univariate analysis showed that mean arterial pressure, hepatopulmonary syndrome, primary liver cancer, white blood cell (WBC) count, aspartate aminotransferase, total bilirubin, serum cholinesterase, the international normalized ratio (INR), blood urea nitrogen, creatinine, noradrenaline (NA) and end-stage liver disease score were correlated with 30-day death of cirrhosis-associated AKI, and the odds ratio (OR) values were 1.05, 3.54, 6.15, 0.83, 0.99, 1.00, 1.00, 0.32, 0.94, 0.53, 1.11 and 0.87, respectively (P<0.05). (3) Multivariate analysis showed that primary liver cancer, WBC count, INR and NA were important factors for 30-day death of cirrhosis-associated AKI, and the OR values were 6.21, 0.83, 0.28 and 1.05, respectively (P<0.05). (4) Both univariate and multivariate analyses indicated that patients with stage III cirrhosis-associated AKI had a higher 30-day mortality than those with stage I (OR: 0.08, 0.16, P<0.05).Conclusion For patients with cirrhosis, the higher the AKI stage, the higher the 30-day mortality.
    Evaluation the hemodynamics of middle cerebral artery in patients with liver cirrhosis by transcranial Doppler ultrasound combined with breath-holding test
    QIAN Rong, YANG Wei-zhong
    2019, 24(8):  861-863. 
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    Objective To detect the hemodynamic changes of middle cerebral artery (MCA) in patients with different degrees of cirrhosis by transcranial Doppler ultrasound (TCD) combined with breath-holding test.Methods In the study, 20 healthy volunteers were enrolled as control group, 48 patients with cirrhosis were divided into 3 groups according to Child-Pugh grade. The mean blood flow velocity (Vm), resistance index (RI), pulsatility index (PI) and blood flow volume (BFV) of MCA were measured by TCD before and after breath-holding test, and the cerebrovascular reserve (CVR) was calculated. Results Compared with the control and group A, the PI and RI of group B and C were significantly increased (P<0.05), the Vm and BFV in group B and C were significantly decreased (P<0.05). After holding the breath, the Vm and BFV of the MCA increased, the PI and RI decreased in all groups. The CVR of group A, B and C were 39.65±12.76, 31.49±15 and 24.52±14.58, respectively, which were significantly lower than those of the control group (P<0.05), and CVR differences were significant between the 3 groups (P<0.05).Conclusion The MCA in patients with cirrhosis has different degrees of hemodynamic changes. CVR can effectively reflect the variation of MCA vascular function in patients with early cirrhosis.
    Effects of prohibitin 1 on cell proliferation of human hepatocellular carcinoma cells and its mechanism
    SHI Juan-juan, ZHANG Xin, WU Feng-ping, WANG Mu-qi, LI Ya-ping, WANG Wen-jun, GAO Ning, DANG Shuang-suo
    2019, 24(8):  864-870. 
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    Objective To investigat the effects of prohibitin1 (PHB1) on cell proliferation of human hepatocellular? carcinoma (HCC) cells, and to elucidate the mechanism of PHB1 in the occurrence and development of HCC.Methods HepG2 and SMMC-7721 cells were transfected with enhanced green fluorescent protein plasmid-PHB1 and PHB1-specific short hairpin ribonucleic acid (RNA) to induce the up-regulation and down-regulation of PHB1 expression. The cell proliferation, cell cycle and key regulators of cell cycle were investigated by MTT assay, flow cytometry, real-time polymerase chain reaction and western blot. Results Overexpression of PHB1 arrested the HepG2 and SMMC-7721 cell cycle in G0/G1 phase (67.28%±2.94 vs 56.71% ± 2.56, t=6.64, P=0.00; 69.48%±3.82 vs 60.43%±2.59, t=4.80, P=0.00), decreased the proportion of cells in S phase (14.74%±1.45 vs 24.13%±1.92, t=9.54, P=0.00; 13.73%±1.26 vs 25.50% ± 2.30, t=10.99, P=0.00), and inhibited cell proliferation. Furthermore, as PHB1 overexpressed, the messenger RNA and protein levels of p53 and p21CIP1 were increased, while those of cyclin A2, cyclin E1 and cyclin-dependent kinase 2 were decreased in the HepG2 and SMMC-7721cells (P<0.01). Conversely, these results were reversed when the expression of PHB1 was inhibited.Conclusion Overexpression of PHB1 arrested the HCC cell cycle in G0/G1 phase, thus inhibit cell proliferation, which might be related to p53-mediated G0/G1 phase-related cell cycle protein.
    The study of immortalized hepatocyte-derived liver progenitor-like cells used in bioartificial liver therapy
    LI Wei-jian, WANG Zhen-yu, YUAN Tian-jie, JING Hong-shu, DAI Meng-jun, PENG Yuan, YAN He-xin, ZHAI Bo
    2019, 24(8):  871-874. 
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    Objective To verify the function of hepatocyte-derived liver progenitor-like cells (HepLPCs), and to find new seed cells for bioartificial liver application.Methods Human primary hepatocytes were isolated by 2-step separation method, and hepatocytes were purified by fluorescence activated cell sorting to exclude HepLPCs from cluster of differentiation 24 + or epithelial cell adhesion molecule + progenitor cells. HepLPCs were immortalized by large T antigen. Then, cell morphology, proliferation states, functional gene levels, detoxification and synthesis levels, and responses to acute hepatic failure (AHF) toxic plasma of immortalized HepLPCs (iHepLPCs) were comprehensively evaluated. Results After immortalization, iHepLPCs could proliferate rapidly and stably in different passages. There was no significant difference in the proliferation rates of passage 0, passage 10 and passage 20 at the same time point (P>0.05), and the cell morphology remained unchanged. The cell detoxification and synthesis functions were stable during the proliferation process, and there was no significant difference among passages (P>0.05). Besides, the differentiation of iHepLPCs cells significantly enhanced expression of the functional genes. The urea production of differentiated iHepLPCs cells was higher than that of undifferentiated ones (13.683±1.238 vs 7.769±0.323, P<0.005). Also, albumin synthesis of differentiated iHepLPCs cells was higher than that of undifferentiated ones (11.270±0.63 vs 5.565±0.025, P<0.005). Furthermore, differentiated iHepLPCs cells had certain tolerance to AHF plasma with detoxification and synthesis abilities. After 6-hour culture in AHF plasma, urea synthesis reached 8.25±0.31, and albumin synthesis reached 12±0.41.Conclusion The iHepLPCs have certain tolerance to AHF plasma, whose cell morphology, detoxification and synthesis functions maintain stable in the process of rapid proliferation. Therefore, iHepLPCs could be a new source of bioartificial hepatocytes.