Objective: To build up rabbit models of hepatic cirrhosis in through common bile duct partial ligation (CBDPL). Methods: Male New Zealand rabbits were subjected to CBDPL to induce hepatic cirrhosis. The liver biopsies were performed during the surgery and after sacrifice to evaluate hepatic fibrosis. The serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TBIL), total protein (TP) and albumin (ALB) were determined at week 0, 1, 2, 4 and 11 following the occlusion. Results: There were two kinds of morphological and histological manifestations after CBDPL, the one was inconspicuous hepatic fibrosis coexisted with sacculation-like bile ductal dilation and muddy stone; the other is remarkable hepatic fibrosis and cirrhosis along with uneven bile ductal dilation. The serum levels of ALT, AST, TBIL and DBIL were significantly higher after one week of operation. The levels of ALT, AST, TP and ALB decreased after two-week of operation, and the levels of TBIL and DBIL were returned to the normal level after two-week of operation. Conclusion: The animal models of hepatic cirrhosis can be built up through CBDPL in rabbits.

Objective: To investigate the expression of long non-coding RNA (lncRNA) SNHG8 in EB virus related gastric cancer and their correlation prognosis. Methods: The expression of SNHG8 in 93 gastric cancers and 93 cancer-free controls, matched by age and sex, were determined by real-time PCR. EB virus expression was detected by EBER in situ hybridization. Results: Forty-one gastric cancers were EB virus associated. For all gastric cancers, SNHG8 expression was 14 times higher (P=0.001) than that in non-cancer controls; in the EB virus related gastric cancers, SNHG8 expression was increased 25 times (P<0.05) over EB virus negative gastric cancers. SNHG8 expression level was also significantly associated with TNM staging (P<0.05). Conclusions SNHG8 may act as a proto-oncogene, participating in gastric carcinogenesis.EB virus infection of gastric mucosa may promote SNHG8 expression.

Objective To explore the expression of circ_0006692 in NSCLC and its relation with clinicopathological characteristics and related mechanism. Methods We collected 50 pairs of NSCLC tissues and adjacent tissues. The expression of circ_0006692 was detected by qRT-PCR and its relation with clinicopathological features was analyzed. We constructed lung cancer A549 cell line with circ_0006692 overexpression and knockdown. Cell proliferation, migration and invasion were detected by MTS, colony forming, wound healing and Transwell invasion assays. qRT-PCR and Western blot were used to detect the effect of circ_0006692 expression change on EMT-related gene expression. Results The expression of circ_0006692 in NSCLC was significantly higher than that in adjacent tissues (P < 0.05). The expression level of circ_0006692 was closely related to tumor size, TNM stage and pulmonary membrane invasion (P < 0.05). circ_0006692 knockdown inhibited cell proliferation, invasion and metastasis, while its overexpression promoted cell proliferation, invasion and metastasis. circ_0006692 knockdown inhibited the expression of EMT-related genes CDH2 and MMP7 in A549 cells and promoted the expression of CDH1. Conclusion The upregulated expression of circ_0006692 in NSCLC is closely related to tumor size, TNM stage and pulmonary membrane invasion. circ_0006692 expression could regulate the proliferation, invasion, metastasis and EMT progression of lung cancer A549 cells.