A P-value of less than 0.05 was considered to be significant. The follow-up time was calculated as the interval between the date of surgery and intervention of the medical treatment, last follow up or recognition of HCC. Survival rates or failure rates were analyzed with the Kaplan–Meier method using the log–rank test to assess differences between curves. A P-value of less than 0.05 was check details considered to be significant. Statistical calculations were performed using the

JMP software package (release 10, SAS Institute, Cary, NC, USA). IN THE SEVEN follow-up liver biopsy sections (Table 2) available for histological examination, liver fibrosis in the hepatic lobules improved from F4 to F3 in four cases (cases 4–7: average, 268.5 ± 168.6 days; range, 42–431 days) (Fig. 2a). Improvements were not observed in the remaining three cases (cases 1–3: average, 312 ± 279.1 days; range, 24–581 days) (Fig. 2b). There were no statistical differences in the duration between the improvement cases and non-improvement

cases (P = 0.80). Conducting an evaluation was difficult because only a few specimens were available; however, no significant differences in clinical profiles were observed selleck screening library among the seven patients. In four of these cases (cases 4–7), the ratio significantly decreased from 19.5% to 8.2% (P < 0.05) (Fig. 2b), while the average AF in the remaining three cases (cases 1–3) increased from 8.0% to 13.1% (P = 0.15). The four cases of improved fibrosis were all Child–Pugh A, and one of the three cases that selleck kinase inhibitor showed no improvement was Child–Pugh B. In addition, AF before splenectomy was slightly higher in the improvement cases than in the non-improvement cases, while the CD4+/CD8+ ratio before splenectomy was lower in the improvement cases than in the non-improvement cases (P < 0.05). Histopathologically, CD4+ and CD8+ lymphocytes were mainly seen in the periportal area, and CD4+ lymphocytes were rarely seen in the hepatic lobules. The

epithelial cells, fibroblasts, monocytes and macrophages also produced TGF-β1.[4, 21, 26] However, we picked up and counted the TGF-β1 positive cells that were seen in the lymphocytes and found that these cells were distributed diffusely in the hepatic lobules and periportal area. The distribution pattern of Treg and granzyme B was the same as that of CD4+ and CD8+ lymphocytes, respectively. No significant differences were observed in the CD4+/CD8+ ratio (P = 0.21) in liver specimens, regardless of the association of HCC. The CD4+/CD8+ ratio (P < 0.05) and FOXP3/CD4+ ratio (P < 0.001) significantly increased with the progression of liver fibrosis (from F0 to F4). However, the granzyme B/CD8+ ratio was approximately constant, and was unrelated to the progression of liver fibrosis (P = 0.32). The number of TGF-β1 positive cells in livers with HCC was slightly higher than that in livers without (P = 0.