Thirdly, some reports suggest that patients with tumours in the left side of the colon generally have a higher incidence of increased S-CEA than those with malignancies on the right side of the colon [33,34]. Fourthly, Sugarbaker [35] showed that bowel obstruction may give rise to S-CEA in patients with CRC and decompression alone can reduce serum CEA values. Fifthly, this S-CEA values can be almost doubled by smoking [36]. Finally, patients with aneuploid CRC have been shown to produce higher S-CEA than those with tumours with a near diploid pattern [37]. All these findings make the S-CEA and T-CEA unparallel. The results of this series suggest that the prognostic value of T-CEA concentration may be superior to that of preoperative S-CEA level.

The disease-free survival time after surgery for patients with a high T-CEA concentration was significantly shorter in univariate analysis than those with a low T-CEA. Multivariate analysis also revealed that T-CEA status (high or low) was an independent prognostic factor in CRC. The hazard of recurrence and metastasis postoperatively in the high T-CEA group is 1.587 times compared with the low T-CEA group. It is coincident with the study of Nakagoe et al.[38]. We think that the prognostic value of T-CEA concentration may be more reliable than preoperative S-CEA levels. However, strict statistical process in a large number of patients is needed to clarify the issue. In conclusion, our study suggests that a high T-CEA concentration may be a useful and independent predictor for poor outcome after surgery in CRC patients, and it may be stronger than a high preoperative serum CEA level.

Acknowledgments We thank Drs Yu Wang, Yun-Tao Xie, Yan-Hua Yuan, Yan Han, Zhen-Dong Gu and Zhen-Yuan Sun for their help and excellent technical support. Grant support This work was supported by the Research fund of the Beijing Municipal Science & Technology Commission (grant H020920030390) and New Star Program of Science and Technology of the Beijing Science and Technology Committee (grant 2006B55).
Acute pancreatitis (AP) is an inflammatory condition that its severe form involves systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndromes (MODS) [1], [2].

The severity of AP depends Entinostat largely upon the balance between two forms of cell death-apoptosis and necrosis, the former presumed to be predominantly protective with mild or no inflammatory response, while necrosis, cell membrane integrity is lost, associated with the release of the digestive enzymes and inflammatory mediators, which can ultimately escalate local and systemic damage [3], [4]. A therapeutic agent that could induce apoptosis of injured pancreatic acinar cells by regulating the apoptosis/necrosis switch is likely to reduce necrosis and provide a new effective treatment [3], [5].