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Objective: To determine the effectiveness and cost of antibiotic chemoprophylaxis in reducing infectious morbidity in low-risk women undergoing elective cesarean delivery.Methods: A prospective randomized clinical trial was performed at a single tertiary care center in Jinan, China between November 2012 and December 2013. Women were randomized to receive either antibiotic prophylaxis or no antibiotics prior to elective cesarean delivery at term. The infectious morbidity (fever, surgical site infection - SSI, endometritis and urinary tract infection), routine blood tests and hospital costs were measured.Results: Total of 414 women were enrolled into the study; and 202 women received antibiotic chemoprophylaxis and 212 women received no antibiotics. Demographic and clinical characteristics were similar between the two groups. Total of one case in the treatment group and four case in the non-treatment group developed endometritis, giving the postoperative infection rate of 1.2%, which was not statistically significant between the two groups (χ(2) = 1.679, p = 0.195). The secondary outcomes were also not different between the two groups, except the costs of hospitalization, which was significantly higher in the treatment group (p < 0.001).Conclusions: In low-risk women undergoing elective cesarean delivery at term, prophylactic antibiotics did not reduce the risk of postoperative infection, but significantly increased the cost of hospitalization. [ABSTRACT FROM AUTHOR]

Background: Tumor necrosis factor-alpha (TNF-α), a key player in cancer-related inflammation, was recently demonstrated to be involved in the lymphatic metastasis of gallbladder cancer (GBC). Vascular endothelial growth factor D (VEGF-D) is a key lymphangiogenic factor that is associated with lymphangiogenesis and lymph node metastasis in GBC. However, whether VEGF-D is involved in TNF-α-induced lymphatic metastasis of GBC remains undetermined.Methods: The expression of VEGF-D in patient specimens was detected by immunohistochemistry and the relationship between VEGF-D in the tissue and TNF-α in the bile of the matching patients was analyzed. The VEGF-D mRNA and protein levels after treatment with exogenous TNF-α in NOZ, GBC-SD and SGC-996 cell lines were measured by real-time PCR and ELISA. The promoter activity and transcriptional regulation of VEGF-D were analyzed with the relative luciferase reporter assay, mutant constructs, electrophoretic mobility shift assay (EMSA), chromatin immunoprecipitation (ChIP) assay, RNA interference and Western blotting. Inhibitors of JNK, p38 MAPK and ERK1/2 were used to explore the upstream signaling effector of AP-1. We used lentiviral vector expressing a VEGF-D shRNA construct to knockdown VEGF-D gene in NOZ and GBC-SD cells. The role of the TNF-α-VEGF-D axis in the tube formation of human dermal lymphatic endothelial cells (HDLECs) was determined using a three-dimensional coculture system. The role of the TNF-α - VEGF-D axis in lymphangiogenesis and lymph node metastasis was studied via animal experiment.Results: TNF-α levels in the bile of GBC patients were positively correlated with VEGF-D expression in the clinical specimens. TNF-α can upregulate the protein expression and promoter activity of VEGF-D through the ERK1/2 - AP-1 pathway. Moreover, TNF-α can promote tube formation of HDLECs, lymphangiogenesis and lymph node metastasis of GBC by upregulation of VEGF-D in vitro and in vivo.Conclusion: Taken together, our data suggest that TNF-α can promote lymphangiogenesis and lymphatic metastasis of GBC through the ERK1/2/AP-1/VEGF-D pathway. [ABSTRACT FROM AUTHOR]