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Objective To investigate the role of TRIM65 on DSS induced colitis and the underlying molecular mechanisms. Methods Trim65+/+ and Trim65-/- mice were administered with 3% (w/v) DSS in their drinking water for 5 consecutive days and then were switched to sterile water for 2 days. DSS treated mice were monitored daily for the clinical symptoms (bodyweight, stool consistency and rectal bleeding score). Mice were sacrificed on day 7 to measure colon length. Colon homogenates were collected to measure MPO activity and detect cleaved caspase-1 and mature IL-1β by Enzyme linked immunosorbent assay (ELISA) and Western blot. Trim65-/- mice were intraperitoneally injected with NLRP3 inflammasome inhibitor MCC950, and were given the above treatment to determine the effect of MCC950 on colitis in Trim65-/- mice. Results The results showed that deletion of Trim65 significantly enhanced weight loss and colon shortening in DSS mice, increased disease activity index and histopathological score, induced the activity of MPO, and promoted the F4/80+ immune cell infiltration, the activation of caspase-1 and the secretion of mature IL-1 in the colon of DSS mice. The NLRP3 inflammasome inhibitor MCC950 alleviated DSS induced colitis symptoms and inflammation levels in trim65 deficient mice. Conclusion TRIM65 plays an anti-inflammatory role in DSS induced colitis mice by inhibiting the activation of NLRP3 inflammasome.
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Objective To analyze the incidence and risk factors of postoperative esophageal stenosis after endoscopic submucosal dissection(ESD)with mucosal defect of 1/2?<3/4 circumference. Methods A retrospective analysis was performed on the data of 301 patients with early esophageal cancer or precancerous lesions undergoing ESD at Drum Tower Hospital between January 2013 and August 2015. The incidence and risk factors for postoperative stenosis were analyzed. Results Esophageal stenosis was observed in 13 cases among the 113 cases of 1/2?<3/4 circumference mucosal defect. The rate of stenosis was 11.5%. There was no significant difference between stenosis group and non?stenosis group in regard of gender, age, family history, concomitant diseases, lesion type, operation time, invasion depth, lesion longitudinal length,pathological diagnosis or complications after ESD(P>0.05),while the rate of lesions in the upper esophagus in stenosis group was higher than that in the control group(P<0.05). Conclusion Mucosal defect of 1/2?<3/4 circumference has a lower esophageal stenosis rate after ESD,which is related to the location of lesion. The ratio of upper esophagus lesion in the stenosis group is significantly higher than that in the non?stenosis group.
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Background:Intrahepatic cholestasis is a commonly seen clinical manifestation, and often accompanied with jaundice.Study on clinical characteristics of patients with different degrees of jaundice is helpful for the acknowledge of intrahepatic cholestasis.Aims:To explore the clinical characteristics of intrahepatic cholestasis with jaundice.Methods:General data, biochemistry parameters, etiology and treatment of 703 patients with intrahepatic cholestasis were retrospectively analyzed.Results:Jaundice occurred in 168 patients (23.9%), including 149 mild jaundice, 15 moderate jaundice and 4 severe jaundice.Levels of ALT, AST, ALP, GGT, DBIL, TBIL, ratio of DBIL/TBIL, TBA were significantly increased in jaundice group than in non-jaundice group (P0.05).The main etiology of intrahepatic cholestasis were digestive system tumors, cardiovascular diseases, shock, hematologic diseases and primary biliary cholangitis.Ursodeoxycholic acid and S-ademetionine were the main drugs for treatment of intrahepatic cholestasis.Conclusions:For patients with intrahepatic cholestasis, levels of ALT, AST, ALP, GGT are increased with the development of jaundice, and attention on damage of hepatocytes should be paid.The etiology of intrahepatic cholestasis with jaundice involves diseases of different organs and systems, most of them are malignant tumor, cardiovascular diseases, shock and primary biliary cholangitis.