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Objective To explore clinical pathological characteristics and treatment changed with time in patients with colorectal laterally spreading tumors (LST) from 2001 to 2015.Methods The clinical data of 549 patients with colorectal LST who received endoscopic resection or surgical operation between 2001 and 2015 were retrospectively collected.According to the time of diagnosis,patients were divided into 2001 to 2005,2006 to 2010 and 2011 to 2015 groups.The gender,age,lesion size and lesion subtypes,clinical pathologic features and their therapeutic methods were analyzed.Chi-square test was used for statistical analysis.Results The detective rates of colorectal LST in 2001 to 2005 period,2006 to 2010 period and 2011 to 2015 period were 0.38％ (50/13 319),(0.60％ (144/23 912) and 0.79％ (355/ 44 715),respectively,and the differences were statistically significant (x2 =29.34,P ＜ 0.01).During these three period,the male to female ratio was about 1:1,mean age about 59 years old,and the mean maximum diameter of the LST lesions remained about 30 mm.The percentages of granular type laterally spreading tumor (LST-G) in 2001 to 2005 period,2006 to 2010 period and 2011 to 2015 period were 82.4％(42/51),67.7％ (105/155) and 78.2％(283/262),respectively;while those of non-granular type laterally spreading tumor (LST-NG) were 17.6 ％ (9/51),32.3 ％ (50/155) and 21.8 ％ (79/362),respectively;and the differences were statistically significant (x2 =7.77,P =0.02).The proportions of LST located at the proximal colon in the three periods were 21.6 ％ (11/51),34.2 ％ (53/155) and 41.4 ％ (150/362),respectively;while the percentages of LST at distal colon were 78.4％ (40/51),65.8％ (102/ 155) and 58.6 ％ (212/362),respectively;and the differnces were statistically significant (x2 =8.61,P=0.01).The percentages of high grade neoplasia (HGN) in the three periods were 13.7 ％ (7/51),21.9 ％(34/155) and 48.6％(176/362),respectively;while the percentages of invasive carcinoma were 2.0％(1/51),5.2％ (8/155) and 8.3％ (30/362),respectively;and the differnces were statistically significantly (x2 =58.89,P＜0.01).The percentages of endoscopic mucosal resection (EMR) in the three periods were 56.9％(29/51),58.7％ (91/155) and 32.0％ (116/362),respectively;the percentages of endoscopic piecemeal mucosal resection (EPMR) were 41.2 ％ (21/51),23.9 ％ (37/155) and 14.1％ (51/362),respectively;the percentages of endoscopic submucosal dissection (ESD) were 0,12.3％ (19/155) and 46.1 ％ (167/362),respectively;the percentages of surgical operation were 0,5.2 ％ (8/155) and 7.7 ％ (28/362),respectively;and the differences were statistically significant (x2 =112.46,P＜ 0.01).Conclusions From 2001 to 2015,the clinical pathological features and therapeutic methods of colorectal LST changed along with time.The proportion of colorectal LST located at proximal colon increased,and the percentage of LST-G decreased.ESD became the primary treatment,and the proportion of pathological diagnosis of HGN and invasive carcinomas increased after operation.
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<p><b>OBJECTIVE</b>To study the signaling pathways associated with lipopolysaccharide (LPS)-induced inflammation in islet micro-endothelial cells (IMECs) and the mechanism of pravastatin intervention.</p><p><b>METHODS</b>IMECs exposed to LPS, SB203580, pravastatin, or SB203580+pravastatin were examined for cell apoptosis with Hoechst staining and flow cytometry and for expression levels of total-p38, photophosphorylation-p38 (p-p38) and iNOS with Western blotting.</p><p><b>RESULTS</b>The apoptosis rate and expression levels of total-p38, p-p38, iNOS in IMECs all increased after LPS exposure. Pravastatin, SB203580, and their combination significantly attenuated LPS-induced enhancement of cell apoptosis and total-p38, p-p38, and iNOS expressions in IMECs.</p><p><b>CONCLUSION</b>LPS-induced inflammatory toxicity in IMECs is associated with the activation of P38MAPK and iNOS/NO signaling pathways. Pravastatin can inhibit these pathways and suppress the apoptosis and necrosis of IMECs to relieve the cell inflammatory injuries.</p>