The

novel findings of this study help to dissect out the role of the complex cellular interactions C646 chemical structure occurring in I/R, with the potential to develop therapeutic interventions to abrogate the sterile inflammatory response. The authors thank Nicole Hays and Junda Chen for their technical assistance in preparing this manuscript. Additional Supporting Information may be found in the online version of this article. “
“Background and Aims:  Non-steroidal anti-inflammatory drugs (NSAIDs) are among the most significant causative factors of gastroduodenal ulcers. Recent reports have demonstrated that NSAIDs can also frequently induce ulceration and erosions of the small intestine. The aim of this study was to examine whether or not roxatidine (an H2 receptor antagonist), which is known to increase gastric mucus in addition to inhibiting gastric acid, might suppress indomethacin-induced small intestinal mucosal injury, through an increase SAHA HDAC molecular weight in mucus in rats. Methods:  Rats were given two p.o. doses of roxatidine, famotidine or cimetidine before and after the s.c. indomethacin injection. The injured area of the small intestine was analyzed. To examine effects of drugs on small intestinal mucus, rats were also given two p.o. doses of roxatidine, famotidine or cimetidine, and the ratio of the periodic

acid Schiff (PAS)-positive

area to the area of the mucosa in the small intestine was analyzed. In addition, we evaluated the involvement of nitric oxide (NO) and prostaglandins (PG) in the effect of roxatidine on small intestinal cAMP mucus. Results:  Roxatidine significantly ameliorated indomethacin-induced small intestinal injury and increased the PAS-stained areas in the small intestinal mucosa, while cimetidine and famotidine had no significant effect. Pretreatment with N-nitro-L-arginine methyl ester but not with indomethacin, suppressed the effect of roxatidine on small intestinal mucus, suggesting that the effect is mediated by endogenous NO but not by PG. Conclusion:  Roxatidine suppressed indomethacin-induced small intestinal injury in rats. One possible mechanism is an increase of small intestinal mucus, mediated by NO. “
“Surgery remains an important treatment modality for many aspects of gastrointestinal cancer. In particular, it is the only definitive treatment for esophageal, gastric, and colorectal cancer, although the outcomes in esophegeal and gastric cancer remain modest. Recent developments in surgery for colorectal cancer, however, have resulted in improved outcomes, particularly with the introduction of mesorectal excision for rectal cancer. Surgery is also indicated for cancers of the liver, biliary tract, and pancreas.