275, P = 0.003) but not ulcers LBH589 purchase (RRR = 1.075, P = 0.444); with low MCV (RRR = 9.104, P = 0.036), low ferritin (RRR = 3.129, P = 0.016) and positive FOB (RRR = 2.7439, P = 0.007) individual predictors for carcinomas. Conclusion: Anaemic patients with a high total score, low MCV,

low ferritin and positive FOB are more likely to have carcinoma on endoscopy. Key Word(s): 1. anaemia; 2. lesion; 3. ulcer; 4. carcinoma; 5. endoscopy Presenting Author: JIN TAO Additional Authors: XIUQING WEI, YANPING LIANG, BIN WU Corresponding Author: JIN TAO Affiliations: 3rd Affiliated Hospital of Sun Yat-Sen University, 3rd Affiliated Hospital of Sun Yat-Sen University, 3rd Affiliated Hospital of Sun Yat-Sen University Objective: To study the effect of β-arrestin2 in radiation-induced progenitor/stem cells apoptosis by

mediating NF-B pathway. Methods: β-arrestin2 Knockout (KO) mice, stem cells marker Lgr5 knock-in (Lgr5-EGFP) and β-arrestin2 KO mice and their respective counterparts PD0325901 manufacturer were or were not injected with NF-B inhibitor of Bay117082 3 hour before exposure to radiation. Their small intestines were examined for histological and apoptosis and proliferation analysis. Intestinal epithelial cells were isolated for analyzing NF-B activity-related events. Moreover, β-arrestin2 and NF-B activity were down-regulated in vitro by RNA interference and chemical agent respectively following radiation. Cell apoptosis and NF-B activity-related events were investigated. Results: β-arrestin2 has a critical role in radio-sensitivity of intestinal injury and apoptosis. β-arrestin2 deficient mice exhibited decreased apoptosis in the intestinal progenitor/stem cells, promoted crypt proliferation and reproduction, and protracted survival following lethal doses of radiation. The intestinal radioprotection by β-arrestin2 deficiency depends on prolonged NF-B activation and

subsequent inhibition of PUMA mediated mitochondrial dysfunction. Unexpectedly, β-arrestin2 deficient selleck kinase inhibitor had little effect on radiation-induced intestinal vascular endothelial apoptosis. Consistently, β-arrestin2 knockdown also provided significant radio-protection through NF-B/PUMA in vitro. Conclusion: Our results suggest that β-arrestin2-mediated apoptosis in progenitor/stem cells compartments is crucial for radiation-stimulated intestinal injury and β-arrestin2 is a potential target for limiting the damaging effect of radiotherapy on the gastrointestinal system. Key Word(s): 1. ß-arrestin2; 2. progenitor/stem cells; 3. radiation-stimulated intestinal injury Presenting Author: JIN TAO Additional Authors: XIUQING WEI, YANPING LIANG, BIN WU Corresponding Author: JIN TAO Affiliations: 3rd Affiliated Hospital of Sun Yat-Sen University, 3rd Affiliated Hospital of Sun Yat-Sen University, 3rd Affiliated Hospital of Sun Yat-Sen University Objective: Intestinal mucositis is a common complication of chemotherapy.