ObjectiveTo screen differential expression of genes in hepatocellular carcinoma (HCC) by bioinformatics method, and analyze its clinical significance and its possible molecular mechanism in HCC.MethodsThe HCC gene expression profile GSE101728 was picked out to analyze the differential expression genes. The hub genes were identified by STRING and Cytoscape. GO and KEGG analysis were carried out by using DAVID and PPI network were constructed by STRING. The relationship among the hub genes were analyzed by using GEPIA.ResultsA total of 1 082 DEGs were captured (354 up-regulated genes and 728 down-regulated genes). Meantime, 10 hub genes ［cyclin dependent kinase 1 (CDK1), cyclin B1 (CCNB1), cyclin A2 (CCNA2), polo-like kinase 1 (PLK1), laser kinase B (AURKB), cyclin of cell division 20 (CDC20), centromere protein A (CENPA), mitotic arrest defective protein 2 (MAD2L1), cyclin B2 (CCNB2), and kinesin family 2C (KIF2C)］ were identified, and its expression and clinical significance were verified by GEPIA. GO and KEGG analysis showed 10 hub genes were mainly enriched in cell division and cell cycle. Expressions of AURKB, CCNB1, and MAD2L1 were obviously positively correlated (P<0.05).ConclusionThis study analyzes the hub genes in the development of HCC by bioinformatics methods and provides valuable information for further research on the mechanism of HCC.
Objective To study the anatomy and variations of hepatic veins draining into inferior vena cava （IVC）， and to classify the surgical techniques of piggyback liver transplantation （PBLT） based on the view of hepatic veins anatomy with IQQA liver image analysis system so as to provide the important basis for the perioperative clinical decision making. Methods Two hundred and forty-eight cases of PBLT were preformed in the Zhongnan Hospital of Wuhan University and the 3rd Xiangya Hospital of Central South University from May 2000 to August 2007， the types of hepatic veins were summarized according to the anatomy of hepatic veins and short hepatic veins draining into IVC at the second and third hepatic hilars. Forty cases of PBLT were preformed in the Zhongnan Hospital of Wuhan University from March 2010 to April 2013， and the anatomy of hepatic veins was reviewed with IQQA liver image analysis system. The anatomy of hepatic veins and technological type of liver transplantation were recorded respectively. Results Of these 248 livers studied in our center， type Ⅰ（the left and middle hepatic vein joined as one trunk ） was found in 142 cases （57.25%）， type Ⅱ （the right and middle hepatic vein joined as one trunk） was 54 cases （21.77%）， type Ⅲ （three hepatic veins joined as one trunk） in 14 cases （5.64%）， type Ⅳ （the left， middle， and right hepatic veins were all unique）in 34 cases （13.71%）， and type Ⅴ （no hepatic veins but short hepatic veins） in 4 cases （1.61%）. The data of 40 cases of PBLT from IQQA liver image analysis system showed that type Ⅰwere found in 24 cases （60.00%）， type Ⅱin 9 cases（22.50%）， type Ⅲ in 2 cases （5.00%）， type Ⅳ in 4 cases （10.00%）， and type Ⅴ in 1 case （2.50%）， which were matched with hepatic vein classification standard of the author. Conclusions Studying the anatomy and variations of hepatic veins draining into IVC with IQQA liver image analysis system and classifying the surgical techniques of PBLT （type Ⅰ，Ⅱ，Ⅲ，andⅣA patients can be performed classical PBLT；Type ⅣB and Ⅴ patients can only be performed ameliorative PBLT） could provide an important basis for clinical preoperative decision.
Objective To explore the protective effect and mechanism of Astragalus polysaccharides (APS) on liver injury in the state of brain death in New Zealand rabbits. Methods Twenty-four New Zealand rabbits were randomly divided into 3 groups (n=8): the blank control group, the brain death group, and the APS group. We obtained blood and liver tissue specimens from rabbits of three groups at 4 h and 8 h after treatment respectively (n=4). The rabbits of blank control group simulated the procedures of anesthesia and surgery of the brain death, without the Foley balloon catheter being pressurized, and maintained anesthesia. The brain death group: brain-dead models were established. The APS group: injection of APS (12 mg/kg) via the femoral vein bolus immediately after anesthesia, brain-dead models were established as same as rabbits of brain death group. The blood and liver tissue samples were taken at 4 h and 8 h after treatment to detect aminotrans-ferase (AST), alanine amino-transferase (ALT) and tumor necrosis factor α (TNF-α), and to observe the change of liver tissue by HE staining and immunohistochemical staining〔expression level of nuclear transcription factor p65 protein (NF-κB p65) could be detected by immunohistochemical staining〕. Results ① ALT and AST. Compare with the blank control group at the same time (4 h and 8 h), levels of ALT and AST in brain death group and APS group were significantly increased (P<0.05), and the levels of ALT and AST in brain death group were higher than those of APS group at each time point (P<0.05). In the same group, compared with 4 h, there was no significant difference in the levels of ALT and AST in blank control group at 8 h (P>0.05); the levels of ALT and AST in brain death group at 8 h were both higher than those of 4 h (P<0.05); the levels of ALT at 8 h in APS group was higher than that of 4 h, but there was no significant difference in the level of AST between 4 h and 8 h (P>0.05). ② TNF-α. Compare with the blank control groups at same time (4 h and 8 h), levels of TNF-α in brain death group and APS group were significantly increased(P<0.05), and level of TNF-α in brain death group was higher than that of APS group at 4 h and 8 h (P<0.05). ③ The HE results. The liver tissue structure of blank control group, brain death group, and APS group at 4 h had no obvious change. The liver tissue structure of brain death group at 8 h showed the evident tissue damage: liver cells showed the balloon samples, disordered arrangement, cytoplasmic loose light dye net-like, and inflammatory cells infiltrated in portal area. The liver tissue structure of APS group at 8 h showed that, liver cells showed mild edema, normal arrangement, and a small amount of inflammatory cells infiltrated in portal area. The liver tissue structure damage of APS group at 8 h was milder than that of brain death group. ④ Immunohistochemical staining results. There was no significant difference in expression levels of NF-κB p65 protein among blank control group, brain death group, and APS group at 4 h (P>0.05). But at 8 h, the expression levels of NF-κB p65 protein in brain death group and APS group were higher than that of blank control group (P<0.05), and the expression level of NF-κB p65 protein in brain death group was higher than that of APS group (P<0.05). The expression levels of NF-κB p65 protein in brain death group and APS group at 8 h was higher than that of 4 h in the same group (P<0.05), but there was no significant difference between 4 h and 8 h in blank control group (P>0.05). Conclusions Brain death will cause liver damage and the injury degree may be related to the continuous time. The damage at 8 h was more serious than that of 4 h. APS has a protective effect on liver of brain-dead rabbits' and its mechanism may be closely related to inhibit TNF-α and NF-κB by diverse ways to reduce the inflammation of the liver injury.