Endoscopically, ulcerating pattern was Staurosporine more common than hypertrophic and ulcerohypertrophic. The typical histologic findings of chronic granulomatous colitis with Langhan’s giant cells was noted in only 1/3 of cases. The presence of tissue positive TB-PCR complimented the diagnosis. Key Word(s): 1. Tuberculosis; 2. GI tract; 3. TB PCR; Presenting Author: JIN TAO Additional Authors: QI YANG, BIN WU Corresponding Author: JIN TAO Affiliations: The Third Affiliated Hospital of Sun Yat-Sen University Objective: To determine 1) whether inhibition of TNF-α ameliorated I/R-induced intestinal mucosal injury by suppressing cell apoptosis, 2) whether

TNF-α involves in caspase-dependent apoptotic signaling in intestinal I/R injury, 3) whether JNK signaling pathways activated by TNF-α response to cell apoptosis in intestinal I/R injury. Methods: In this study, the intestinal I/R was induced by 60-min occlusion of the superior mesenteric artery followed by 60-min reperfusion, and the rats were pretreated with PF-562271 chemical structure a TNF-α inhibitor pentoxifylline or a TNF-α antibody infliximab. After the animal surgery,

part of the intestine was collected for histological analysis. The mucosal layer was harvested for RNA and protein extraction, which were used for further real-time PCR, ELISA and Western blot analysis. The TNF-α expression, intestinal mucosal injury, cell apoptosis, the activation of apoptotic protein and JNK signaling pathway were analyzed. Results: I/R significantly enhanced expression of mucosal TNF-α in both mRNA and protein levels, induced severe mucosal injury and cell apoptosis, activated caspase-9/caspase-3, and initiated JNK signaling pathway. Pretreated with pentoxifylline markedly downregulated TNF-α in both mRNA and protein levels, whereas infliximab pretreatment did not affected the

expression of TNF-α induced by I/R. However, pretreatment with pentoxifylline medchemexpress or infliximab dramatically suppressed I/R-induced mucosal injury and cell apoptosis, and significantly inhibited the activation of caspase-9/3 and JNK signaling (P < 0.05). Conclusion: Our data suggested that TNF-α played a pivotal role in intestinal I/R injury; and pretreatment of both pentoxifylline and infliximab remarkably attenuated I/R-induced injury partly by inhibiting the TNF-α mediated apoptosis. Further, the results indicated that TNF-α mediated JNK activation response to intestinal I/R injury. Key Word(s): 1. TNF-α; 2. small intestine; 3. mucosa; 4. JNK; Presenting Author: GAIUS LONGCROFT-WHEATON Additional Authors: PRADEEP BHANDARI Corresponding Author: GAIUS LONGCROFT-WHEATON Affiliations: University of Portsmouth Objective: Endoscopic management of early colonic neoplasia or polyp cancer remains unclear. There are no national guidelines or good quality data to guide clinicians with these difficult lesions.