Objective To explore the risk factors affecting T-tube sinus tract formation after common bile duct exploration and T-tube drainage by spiral computed tomography (SCT)examination.Methods The clinical data of 465 patients undergoing common bile duct exploration and T-tube drainage at the Affiliated Hospital of Youjiang Medical College for Nationalities from May 2011 to December 2013 were retrospectively analyzed.The residual stones and biliary stricture were detected by T-tube cholangiography,and the T-tube sinus tract formation in all the patients was detected by SCT examination at postoperative week 2.The factors affecting sinus tract formation were analyzed,including gender,age,albumin (Alb),C-reactive protein,alanine transaminase (ALT),total bilirubin (TBil),hemoglobin (Hb),surgical method,effusion around T tube,reoperation,diabetes.Univariate analysis was done using the chi-square test.Multivariate analysis was done using the Logistic regression.Results T-tubes of 465 patients were clear without residual stones.T-tube in the 397 patients was removed when the sinus tract formation was confirmed by CT examination at postoperative week 2.T-tubes in other patients were removed when the sinus tract formation was detected by CT reexamination at postoperative week 4.In univariate analysis,Alb,surgery method,effusion around T-tube and diabetes were important factors affecting T-tube sinus tract formation (x2 =50.750,7.671,19.022,15.373,P ＜ 0.05).Alb ＜ 30 g/L,laparoscopic surgery,effusion around T-tube and diabetes were independent risk factors affecting T-tube sinus tract formation in multivariate analysis [Odds ratio =1.135,0.493,0.262,0.363; 95％ confidence interval:1.061-1.214,0.280-0.865,0.104-0.658,0.156-0.843,P ＜ 0.05].Conclusions The T-tube removal is determined according to the sinus tract formation by CT examination at week 2 after common bile duct exploration and T-tube drainage.Alb ＜ 30 g/L,laparoscopic surgery,effusion around T-tube and diabetes are independent risk factors affecting T-tube sinus tract formation.

Background and purpose:The previous research has found that the prostate stromal cells derived from different prostate zones have distinct effect on prostate epithelial cells. We also revealed that LMO2 protein was highly expressed in PZ stromal cells (PZSCs) and prostate cancer associated fibroblasts (CAFs) compared with TZ stromal cells. This study investigated the effect of LMO2 protein in prostate stromal cells on proliferation and invasion of prostate cancer PC-3 cells and its mechanisms. Methods:Lentivirus overexpression vectors were used to establish LMO2-overexpressed prostate WPMY-1 stromal cell line. shRNA plasmids were used to suppress LMO2 in CAFs. LMO2 mRNA and protein level of both WPMY-1 and CAFs were evaluated by real-time fluorescent quantitative polymerase chain reaction (RTFQ-PCR) and Western blot. Then, PC-3 cells were co-cultured with different prostate stromal cells and the in vitro proliferation and invasion of PC-3 were measured by CCK-8 and matrigel invasion assays respectively. Results:When co-cultured with LMO2-overexpressed prostate stromal cells, both proliferation and in-vasion of PC-3 were improved. However, when co-cultured with CAFs which have inhibited expression of LMO2, the proliferation and invasion of PC-3 were reduced. The protein array proifling found that both interleukin-11 (IL-11) and ifbroblast growth factor-9 (FGF-9) were enhanced extensively in the supernatant collected from LMO2-overexpressed WPMY-1 cells. Conclusion:The expression of LMO2 in prostate stromal cells could be responsible for development of prostate cancer. Paracrine of cytokines, such as IL-11 and FGF-9, from LMO2-overexpressed stromal cells had effects on the proliferation and invasion of prostate cancer cells.

Objective:To investigate the effects of hyperuricemia on the prognosis of IgA nephropathy (IgAN) using propensity score matching (PSM) method.Methods:IgAN patients proven by biopsy were included. PSM was used to match patients. Kaplan-Meier method was used for survival analysis, and Cox regression analysis was used to analyze the effects of hyperuricemia on IgAN prognosis. Primary outcome events were defined as death, or end-stage renal disease (dialysis, transplantation), or a decrease in estimated glomerular filtration rate (eGFR) greater than 40%. Renal outcome was defined as end-stage renal disease (dialysis, transplantation), or a decrease in eGFR greater than 40%.Results:A total of 1 454 IgAN patients were included in this study, including 850 females and 604 males. Uric acid level was (368.26±92.87) μmol/L in the males, and (277.23±92.71) μmol/L in the females. The median follow-up time was 85.00(56.10, 106.33) months. During the follow-up period, a total of 134 patients reached the primary outcome events, including 5 deaths, 24 dialysis patients, 5 kidney transplant patients, and 100 patients with eGFR decreased by more than 40%. After 1∶1 matching, 131 males and 159 females in the hyperuricemia group were successfully matched with 131 males and 159 females in the normal uric acid group, and there was no significant statistical difference in each parameter in baseline between the hyperuricemia group and normal uric acid group after matching. Kaplan-Meier survival analysis showed that either before or after matching, the incidence of primary outcome events in male or female patients with hyperuricemia was higher than those with normal uric acid, but there was no statistically significant difference in incidence of primary outcome events between female hyperuricemia group and female normal uric acid group after matching (Log-rank test, χ2=3.586, P=0.058). Cox proportional hazard regression model showed that, in the pre-match fully adjusted model, the hazard ratio ( HR) of entering primary outcome events was 2.29-fold (95% CI 1.27-4.11, P=0.006) for men with hyperuricemia and 1.85-fold (95% CI 1.01-3.37, P=0.045) for women with hyperuricemia compared with those with normal uric acid. In the post-match fully adjusted model, the HR of entering primary outcome events was 2.41-fold (95% CI 1.18-4.93, P=0.016) for men with hyperuricemia and 1.83-fold (95% CI 0.91-3.67, P=0.091) for women with hyperuricemia compared with those with normal uric acid. In the pre-match fully adjusted model, the HR of entering renal outcome events was 2.68-fold (95% CI 1.47-4.88, P=0.001) for men with hyperuricemia and 1.81-fold (95% CI 0.99-3.33, P=0.056) for women with hyperuricemia compared with those with normal uric acid. In the post-match fully adjusted model, the HR of entering renal outcome events was 2.89-fold (95% CI 1.36-6.15, P=0.006) for men with hyperuricemia and 1.81-fold (95% CI 0.88-3.72, P=0.106) for women with hyperuricemia compared with those with normal uric acid. Conclusion:Hyperuricemia may be associated with IgAN progression, and it has a more significant effect on male IgAN patients.