Objective　To investigate changes in intestinal microflora in patients with chronic severe hepatitis (CSH), and their role in this life-threatening disease. Methods　We classified nineteen patients with chronic severe hepatitis as the CSH group, thirty patients with chronic hepatitis (CH) as the CH group and thirty-one healthy volunteer as the control group. Fecal flora from all subjects were analyzed. Concentrations of plasma endotoxin, serum cytokines tumor necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1β) and liver function were assessed. Results　The number of fecal bifidobacterium (P<0.001, P<0.05 respectively), as well as bacteroidaceae (P<0.001, P<0.01 respectively) were significantly deceased in patients with chronic severe hepatitis compared with the CH and control groups, while the number of enterobacteriaceae (P<0.001, P<0.05 respectively) and yeasts (P<0.01, P<0.05 respectively) were significantly increased. Levels of plasma endotoxin, serum TNF-α, IL-1β and total bilirubin (TBiL) were significantly increased in the CSH group. The concentration of endotoxin positively correlated with levels of both TNF-α, IL-1β and TBiL (P<0.001, respectively). Levels of plasma endotoxin were positively correlated with the number of fecal enterobacteriaceae and negatively correlated with bifidobacterium (P<0.05, P<0.001, respectively). Conclusion　Intestinal flora in patients with chronic severe hepatitis were severely disturbed and gut mircobiological colonization resistance was impaired. Changes in intestinal flora may have a pivotal role in both the elevation of plasma endotoxin and further hepatic lesions resulting in liver failure.

Objective To study the interaction between telomerase activity and abnormalities of the p16 gene in liver metastases of colorectal carcinoma. Methods Telomerase activity was detected by a non-isotopic PCR-based telomeric repeat amplification protocol (TRAP) assay, and homozygous deletions of the p16 gene were detected by a semiquantitative multiplex polymerase chain reaction in tissue samples from 24 liver metastases of colorectal carcinoma and 5 primary colorectal carcinomas. Results Telomerase activity was observed in 19 (79.2%) of 24 liver metastases of colorectal carcinoma. Telomerase activity was also observed in all 5 primary colorectal carcinomas and in 3 of their liver metastatic samples. The incidence of telomerase activity in liver metastases of colorectal carcinoma was not significantly correlated to tumor diameter, number of tumors, cirrhosis, and HBsAg. Homozygous deletions of the p16 gene were found in 9 of 24 (37.5%) liver metastases of colorectal carcinoma. Homozygous deletions of the p16 gene were observed in 2 of the 5 primary colorectal carcinomas and in 1 of the matching liver metastatic cancers. There was a correlation between telomerase activity and homozygous deletions of the p16 gene. Conclusions There is a correlation between telomerase activity and homozygous deletions of the p16 gene in liver metastases of colorectal carcinoma, suggesting its crucial role in liver metastases. However, telomerase activation and homozygous deletions of the p16 gene might not be the initiating event in liver metastases of colorectal carcinoma.