Objective To evaluate the clinical effect of restorative proctocolectomy with ileal pouch-anal anastomosis (IPAA) for refractory ulcerative colitis (UC).Methods In this study 60 refractory UC patients received IPAA operation during the period of 1990 to 2010.Data were collected regarding early and late postoperation complications,anal continence function,and characteristics of feces.The patients' quality of life was objectively accessed using the Clevend Global Quality of Life (CGQL)index.0ne-way analysis of variance was used.Results Mean follow-up period was 2 years.Early postoperative complication rate developed in 15％ (9/60),including abdominal or pelvic infection,anastomotic leak,pouch bleeding,pouch-vaginal fistula,and intestinal obstruction.Late postoperative complication rate was 12％ (7/60),including pouchitis,intestinal obstruction,and male sexual dysfunction.Stool frequency per 24 hours and that at night was 3.5 ± 1.3 and 1.4 ±0.6.93％ (56/60)patients differentiated gas and feces well and 3％ (2/60) needed daily pads.According to Kirwan Grading Scale,anal function outcomes were Grade Ⅰ:54 (90％),Grade Ⅱ:4 (7％),and Grade Ⅲ:2 (3％).According to Bristol Stool Form Scale,characteristics of feces were Grade Ⅳ:31 (52％),Grade Ⅴ:25(42％),and Grade Ⅵ:4 (6％).Postoperative CGQL result showed a much better quality of life than preoperative CGQL (F =12.368,P ＜ 0.05).Conclusions Refractory UC is surgically indicated and IPAA is the operation of choice with safety,satisfactory long-term outcome and improved quality of life.

Objective To investigate the effects of α7 nicotinic acetylcholine receptor(nAChR)agonist on β3-adrenoceptor agonist-induced impairment of white fat homeostasis and beige adipose formation and heat production in obese mice.Methods Forty obese C57BL/6J mice were randomized into high-fat feeding group,β3-adrenoceptor agonist-treated model group,α7 nAChR agonist group,and α7 nAChR inhibitor group(n=10),with another 10 mice with normal feeding as the blank control group.White adipose tissue from the epididymis of the mice were sampled for HE staining of the adipocytes.The expression levels of TNF-α,IL-1β,IL-10 and TGF-β in the white adipose tissue were determined by ELISA,and the mRNA levels of iNOS,Arg1,UCP-1,PRDM-16 and PGC-1α were detected using RT-qPCR.Western blotting was performed to detect the expression levels of NF-κB P65,p-JAK2,p-STAT3 in the white adipose tissue.Results Compared with those in the blank control group,the mice with high-fat feeding showed significantly increased body weight,more fat vacuoles in the white adipose tissue,increased volume of lipid droplets in the adipocytes,upregulated iNOS mRNA expression and protein expression of TNF-α and IL-1β,and lowered expression of Arg-1 mRNA and IL-10 and TGF-β proteins(P<0.01).Treatment with α7 nAChR significantly reduced mRNA levels of PRDM-16,PGC-1α and UCP-1,lowered TNF-α and IL-1β expressions,increased IL-10 and TGF-β expressions,and reduced M1/M2 macrophage ratio in the white adipose tissues(P<0.05 or 0.01).Conclusion Activation of α7 nAchR improves white adipose tissue homeostasis impairment induced by β3 agonist,promotes transformation of M1 to M2 macrophages,reduces inflammatory response in white adipose tissue,and promote beige adipogenesis and thermogenesis in obese mice.

Objective To investigate the effects of α7 nicotinic acetylcholine receptor(nAChR)agonist on β3-adrenoceptor agonist-induced impairment of white fat homeostasis and beige adipose formation and heat production in obese mice.Methods Forty obese C57BL/6J mice were randomized into high-fat feeding group,β3-adrenoceptor agonist-treated model group,α7 nAChR agonist group,and α7 nAChR inhibitor group(n=10),with another 10 mice with normal feeding as the blank control group.White adipose tissue from the epididymis of the mice were sampled for HE staining of the adipocytes.The expression levels of TNF-α,IL-1β,IL-10 and TGF-β in the white adipose tissue were determined by ELISA,and the mRNA levels of iNOS,Arg1,UCP-1,PRDM-16 and PGC-1α were detected using RT-qPCR.Western blotting was performed to detect the expression levels of NF-κB P65,p-JAK2,p-STAT3 in the white adipose tissue.Results Compared with those in the blank control group,the mice with high-fat feeding showed significantly increased body weight,more fat vacuoles in the white adipose tissue,increased volume of lipid droplets in the adipocytes,upregulated iNOS mRNA expression and protein expression of TNF-α and IL-1β,and lowered expression of Arg-1 mRNA and IL-10 and TGF-β proteins(P<0.01).Treatment with α7 nAChR significantly reduced mRNA levels of PRDM-16,PGC-1α and UCP-1,lowered TNF-α and IL-1β expressions,increased IL-10 and TGF-β expressions,and reduced M1/M2 macrophage ratio in the white adipose tissues(P<0.05 or 0.01).Conclusion Activation of α7 nAchR improves white adipose tissue homeostasis impairment induced by β3 agonist,promotes transformation of M1 to M2 macrophages,reduces inflammatory response in white adipose tissue,and promote beige adipogenesis and thermogenesis in obese mice.