Objective To investigate the effects of changing the pancreatic stent number based on the last procedure on the prognosis of children and adolescents with recurrent chronic pancreatitis. Methods Data of 11 pediatric patients ( 3-16 years old) with chronic pancreatitis, undergoing ERCP for at least twice were retrospectively analyzed. Based on whether the number of stents changed in the second procedure, patients were divided into the control group( more than once and no change in the number) ,and the changing group ( more than once and change in the stent number in the second procedure ) . The hospitalization and surgery percentage and number of hospitalizations due to abdominal pain in follow-up period were compared to study whether number change of stents was efficient to cure pediatric patients with chronic pancreatitis. Results Eleven pediatric patients undergoing at least 2 ERCP procedures were recruited into our group. The hospitalization percentages were 140％( n=7) and 33. 3％( n=2) in the control group( n=5) and the changing group ( n=6) respectively( P<0. 001) . The number of hospitalizations due to abdominal pain was 1. 5 and 0. 8 in the control group and the changing group respectively ( P<0. 001) . The percentage of patient hospitalizations due to abdominal pain significantly reduced in the changing group ( P=0. 003) . Conclusion Increase in pancreatic stent number in the second procedure in pediatric patients can decrease hospital admissions related to the pancreatitis.

Objective To explore the effect of macrophages on the expression of vascular cell adhesion molecule 1 (VCAM1) in ovarian carcinoma cells and its mechanism. Methods Phorbol ester and lipopolysaccharide were used to activate the monocyte THP-1 that would become macrophages . Enzyme linked immunosorbent assay (ELISA) was used to detect the cytokines level in the supernatant of macrophages. The effect of macrophages ' supernatant on VCAM1 mRNA expression of ovarian HEY and IGROV1 carcinoma cells was detected by using quantitative real-time and polymerase chain reaction (qRT-PCR). Western blot was used to detect the effect of macrophages ' supernatant on VCAM1 protein expression of ovarian carcinoma cells with VCAM1 over expression (HEY-VCAM1 and IGROV1-VCAM1). Dual-luciferase report gene assay was used to detect the effect of macrophages' supernatant and the cytokines on promoter transcriptional activity in different truncations of human embryonic kidney cells HEK293T VCAM1 gene. Results Compared with the supernatant of THP-1 cells, the release number of tumor necrosis factor α (TNF-α), interleukin (IL)-6 and IL-12 in supernatant from macrophages was increased (all P< 0.05), and IL-10 was decreased (t=3.841, P=0.019). The levels of VCAM1 mRNA in HEY and IGROV1 cells were upregulated by macrophages' supernatant and 1 ng/ml TNF-α, and macrophages' supernatant could promote the expression levels of VCAM1 protein in HEY-VCAM1 cells and IGROV1-VCAM1 cells. Compared with the empty vector (pGV354) control group [(8.6 ±0.2) ×10-3 relative light unit (RLU)], the reporter gene luciferase activity of human embryonic kidney cells HEK293T VCAM1 gene promoter region were upregulated by supernatant from macrophages located at -1641 bp to +12 bp including the transcription binding site of AP-1 [(109.4±3.4)×10-3 RLU], and there was a significant difference (t=29.42, P<0.001). Compared with the negative control group untreated by cytokine [(21.0 ±0.5) ×10-3 RLU], 100 ng/ml TNF-α could promote the transcriptional activity of -1641 bp to +12 bp promoter of VCAM1 in HEK293T cells [(23.4±0.4)×10-3 RLU;t=4.134, P=0.001]. 150 ng/ml IL-6 had no effect on the transcriptional activity of the promoter [(21.4±1.0)× 10-3 RLU; t= 0.328, P= 0.708]. 5 ng/ml IL-12 inhibited the transcriptional activity of the promoter [(14.3 ± 1.0)×10-3 RLU;t= 6.390, P< 0.001]. Conclusion Macrophages can promote VCAM1 expression in ovarian carcinoma cells by secreting inflammatory factors like TNF-α to affect VCAM1 promoter region containing AP1 transcription binding site and can promote VCAM1 mRNA expression in ovarian cancer cells.