Objective To investigate the effects of thymosin ?1 on the proliferation of human umbilical veinssel endothelial cells(HUVECs) and synthesis of vascular endothelial growth factor(VEGF).Methods HUVECs(ECV-304) were cultured with the treatment of 100 ?l thymosin ?1 at 0,5 or 2.5 ?g/ml for 1 d in vitro.The proliferation of HUVECs were measured with MTT assay,cell cycle was tested with flow cytometry and the synthesis of VEGF was detected with Western blot analysis.Results Thymosinal promoted the proliferation of HUVECs,and the cells in S-phase was increased,and obviously promoted the synthesis of VEGF.Conclusion Thymosin ?1 promotes the proliferation of HUVECs and increases the synthesis of VEGF in HUVECs,and may have the effect of increasing the angiogenesis in the process of wound tissue.

Objective To determine the relationship between early postoperative delirium (EPD) and prognosis in patients undergoing non-cardiac surgery. Methods This was a prospective cohort study consisted of 698 patients admitted to postanesthesia care unit, undergoing non-cardiac surgery under general anesthesia, between June and December 2009. The risk factors affecting prognosis were collected. All the patients were assessed for the development of delirium by experienced research staff using Confusion Assessment Method for Intensive Care Unit. The patients were divided into 2 groups according to the occurrence of EPD: EPD group and no EPD (NEPD) group. The postoperative hospital length of stay was made as a major prognostic indicator. Cox proportional hazard regression model was used to analyze the risk factors affecting prognosis. Results Of the 698 patients, 197 (28.2%) developed EPD. The postoperative hospital length of stay was prolonged in group EPD compared with group NEPD. The Cox proportional hazard regression model analysis indicated that EPD was an independent risk factor affecting prognosis. Conclusion EPD is an independent risk factor affecting prognosis in patients undergoing non-cardiac surgery.

Objective Pulmonary fibrosis is a progressive chronic lung disease with a high incidence.Although the path of the disease has not been fully elucidated,the pathogenesis of the disease is roughly similar.Tyrosine kinases are involved in a series of signaling pathways that are critical for cell homeostasis.Substantial evidence from in vitro studies and experimental animal models suggests that tyrosine kinases play a role in promoting the development and progression of pulmonary fibrosis,and tyrosine kinase inhibitors have shown good anti-fibrosis and anti-inflammatory effect in animal models of pulmonary fibrosis.

OBJECTIVE: To observe the effects of nilotinib on silicon dioxide(SiO_2)-induced cell proliferation and collagen synthesis in human fetal lung fibroblast-1(HFL-1) cells and to explore the related mechanism. METHODS: ⅰ) HFL-1 cells were induced with different doses of SiO_2 suspension(0, 5,10, 25, 50 and 100 mg/L) for 24.0 hours. The expression of transforming growth factor-β1(TGF-β1), C-Abl, and platelet-derived growth factor receptor(PDGFR) was detected by Western blot, and the dose of SiO_2 in subsequent experiments was screened. ⅱ) HFL-1 cells were randomly divided into 6 groups: 1) the control group: no treatment; 2) the solvent control group: cells were treated with 0.10% dimethyl sulfoxide; 3) the SiO_2 stimulation group: cells were induced with SiO_2 suspension at a dose of 50 mg/L for 24.0 hours; 4)-6) the nilotinib groups: cells were induced with SiO_2 suspension at a dose of 50 mg/L for 24.0 hours and treated with nilotinib at the concentration of 5, 10, or 15 mmol/L for 24.0 hours. Cell proliferation was detected by MTS assay. The TGF-β1 protein secreted by cells was measured using enzyme linked immunosorbent assay. The expression of TGF-β1, C-Abl, platelet derived growth factor(PDGF), PDGFR and collagen typeⅠproteins was measured by Western blot. RESULTS: ⅰ) The dose of the SiO_2 in the experiments was set to 50 mg/L. ⅱ) The cell proliferation rate of HFL-1 cells in the SiO_2 stimulation group and the 3 nilotinib groups was higher than that in control group and solvent control group(P<0.05). The proliferation rates of HFL-1 cells in 10 and 15 mmol/L nilotinib groups were lower than that in SiO_2 stimulation group(P<0.05). The level of TGF-β1 and the protein relative expression levels of TGF-β1, collagen typeⅠ, C-Abl, PDGFR and PDGF in HFL-1 cells of SiO_2 stimulation group were higher than those in control group and solvent control group(P<0.05). The above indexes of HFL-1 cells in 15 mmol/L nilotinib group were lower than that in SiO_2 stimulation group(P<0.05); the above indexes of HFL-1 cells in 5 mmol/L nilotinib group were not significantly different from those in SiO_2 stimulation group(P>0.05). The level of TGF-β1 and the relative expression level of C-Abl protein in HFL-1 cells of 10 mmol/L nilotinib group were lower than those in SiO_2 stimulation group(P<0.05). CONCLUSION: Nilotinib can inhibit the proliferation of HFL-1 cells and reduce the expression of collagen typeⅠprotein induced by SiO_2. This process may be achieved by inhibiting tyrosine kinase-mediated signaling pathway.