[Comparison of risk factors for serrated polyps and conventional adenoma and the suitable age to start colorectal cancer screening].

OBJECTIVE: To compare the risk factors associated with serrated polyps (SPs) and conventional adenoma (CA). METHODS: One hundred and three healthy control subjects, 100 patients with pathologically confirmed SPs and 115 with CA were randomly selected from individuals undergoing colonoscopy in Nanfang Hospital from 2012 to 2015. The demographic and clinical data were collected from the subjects, including age, gender, height, weight, hypertension, diabetes, smoking status, alcohol use, family history of colorectal cancer (CRC) and blood lipids. RESULTS: Among the enrolled subjects, the mean onset age of SPs was 48.87 years (95%CI: 47.22-50.52 years), significantly younger than that of CA (P%0.038). The risk factors both for SPs and CA include an advanced age, a male gender (OR%2.75 [95%CI: 1.50-5.07] for SPs, and OR%2.19 [95%CI: 1.22-3.95] for CA), and a high body mass index (OR%1.18 [95%CI: 1.06-1.30] for SPs and OR%1.20 [95%CI: 1.09-1.32] for CA. Relative to the young individuals (below 45 years of age), the middle-aged individuals (45-60 years of age) had increased risks for SPs and CA by 2.31 [95% CI: 1.46-3.65] folds and 4.10 [95%CI: 2.50-6.72] folds, respectively, and in the elderly (beyond 60 years of age), the risks further increased by 2.77 [95%CI: 1.52-5.04] folds for SPs and by 6.00 [95%CI: 3.26-11.05] folds for CA. Age was more strongly associated with CA than with SPs (OR%2.14 [95%CI: 1.21-3.78], the elderly vs the young, P%0.009). CONCLUSION: SPs and CA have common risk factors, thus the screening strategy for CA may also be applicable to SPs. As the mean onset age of SPs is earlier than 50 years and SPs may rapidly progress to a carcinogenic state, an earlier screening age needs to be considered.

[Expressions of inflammatory cytokines in intestinal mucosa and their prognostic value in patients with ulcerative colitis].

OBJECTIVE: To detect the expressions of IL-17, IL-23, IL-22 and IL-11 in the intestinal mucosa of patients with ulcerative colitis (UC) and analyze their prognostic values. METHODS: Forty patients with active UC, 15 with UC in remission and 15 healthy subjects were examined for the expressions and distribution of IL-17, IL-23, IL-22, and IL-11 in the colorectal mucosausing immunohistochemistry. We further collected the data from 40 patients with routine therapy and regular follow-up and compared the expressions of those cytokines according to the condition of mucosal healing. RESULTS: The expressions of cytokines in patients with active UC were significantly higher than those in patients with remittent UC and healthy control subjects (IL-17: 0.0727∓0.0037 vs 0.0354∓0.0243 vs 0.0330∓0.0045; IL-23: 0.1407∓0.0068 vs 0.0865∓0.0051 vs 0.0442∓0.0137; IL-22: 0.0522∓0.0045 vs 0.0259∓0.0063 vs 0.0115∓0.0061; IL-11: 0.0479∓0.0022 vs 0.0365∓0.0024 vs 0.0232∓0.0009, P<0.05). The expression levels of IL-17, IL-23, and IL-22 increased significantly with the increase of the disease activity (IL-17: 0.0545∓0.0072 vs 0.0786∓ 0.0051 vs 0.0847∓0.0197; IL-23: 0.1112∓0.0046 vs 0.1480∓0.0089 vs 0.1644∓0.0190; IL-22: 0.0307∓0.0063 vs 0.0548∓ 0.0071 vs 0.0719∓0.0056, P<0.05). In patients with active UC, the expression levels of the 4 cytokines in the intestinal mucosa were positively correlated with the endoscopic activity grade (P<0.05), and IL-17 and IL-22 expression levels were also positively correlated with the histological grade (P<0.05). All the 4 cytokines were positively intercorrelated. The patients with low IL-17 expression (25.00%) showed a significantly lower rate of poor mucosal healing than those with high IL-17 expressions (25% vs 67%, P<0.05). CONCLUSION: The cytokines IL-17, IL-23, IL-22, and IL-11 all participate in the pathogenesis of UC and may serve as indicators for evaluating the inflammatory activity. The expression level of IL-17 can be a valuable indicator for predicting mucosal healing in UC patients after a short-term treatment.

GW4064, a farnesoid X receptor agonist, upregulates adipokine expression in preadipocytes and HepG2 cells.

AIM: To investigate the effect of GW4064 on the expression of adipokines and their receptors during differentiation of 3T3-L1 preadipocytes and in HepG2 cells. METHODS: The mRNA expression of farnesoid X receptor (FXR), peroxisome proliferator-activated receptor-gamma 2 (PPAR-γ2), adiponectin, leptin, resistin, adiponectin receptor 1 (AdipoR1), adiponectin receptor 2 (AdipoR2), and the long isoform of leptin receptor (OB-Rb) and protein levels of adiponectin, leptin, and resistin were determined using fluorescent real-time PCR and enzyme linked immunosorbent assay, respectively, on days 0, 2, 4, 6, and 8 during the differentiation of 3T3-L1 preadipocytes exposed to GW4064. Moreover, mRNA expression of AdipoR2 and OB-Rb was also examined using fluorescent real-time PCR at 0, 12, 24, and 48 h in HepG2 cells treated with GW4064. RESULTS: The mRNA expression of FXR, PPAR-γ2, adiponectin, leptin, resistin, AdipoR1, AdipoR2, and OB-Rb and protein levels of adiponectin, leptin, and resistin increased along with differentiation of 3T3-L1 preadipocytes (P < 0.05 for all). The mRNA expression of FXR, PPAR-γ2, adiponectin, leptin, and AdipoR2 in 3T3-L1 preadipocytes, and AdipoR2 and OB-Rb in HepG2 cells was significantly increased after treatment with GW4064, when compared with the control group (P < 0.05 for all). A similar trend was observed for protein levels of adipokines (including adiponectin, leptin and resistin). However, the expression of resistin, AdipoR1, and OB-Rb in 3T3-L1 cells did not change after treatment with GW4064. CONCLUSION: The FXR agonist through regulating, at least partially, the expression of adipokines and their receptors could offer an innovative way for counteracting the progress of metabolic diseases such as nonalcoholic fatty liver disease.