Objective To explore how to treat open neck trauma in time and with reason in the primary hospital.Methods 57 cases of neck open injury were hospitalized from Aug.1997 to Jan.2()07,and injury cause,mechanism,diagnosis and treatment of them are analyzed retrospectively.Results There were 29 incisal wounds and 23 penetrating wounds and 5 contusing wounds.Among 57 patients there were 12 significant injuries and 55 minor injuries cases.53 patients had been treated with operative exploration and 10 patients had therapeutic exploration.The result of treatment showed that 50 patients were cured,and 4 patients died of head injury,cervical spinal injury and respiratory failure,anoxic encephalopathy from airway obstruction and hemorrhagic shock from combined injuries of common carotid artery and internal jugular vein.Conclusion The mainstay of choice of treatment is the injury mechanism and clinical signs and symptoms of patient.

AIM:To explore the changes of L-selectin expression and F-actin distribution of leukocytes from pancreatic circulation in the experimental acute necrotizing pancreatitis (ANP) rats and impact of Chinese herbs west China pancreatitis yi hao (WPY) on them in vivo. METHODS:Forty-four Wistar rats were randomized into control group,ANP group and ANP WPY treated group. The leukocytes from blood of splenic vein were incubated with PE-anti-CD62L for L-selectin and TRTIC-Phalloidin for F-actin,then the ratio of CD62L positive granulocytes was measured by flow cytometry and leukocytes were taken images with confocal laser scanning microscope. The distribution of F-actin at the border or central part of leukocyte was analyzed by using Mias system. RESULTS:The ratio of CD62L positive granulocytes increased in ANP rats,but those increases at 6 h (31.78%?12.37%) and 12 h (29.83%?13.73%) were significant [vs control group(11.96%?5.32%),P

AIM: To investigate the effect of cobalt chloride (CoCl2) on the apoptosis of neural stem cells (NSCs) and the expression of microRNA-26a (miR-26a) in vitro, and to explore the mechanisms of NSC apoptosis in-duced by CoCl 2 .METHODS:NSCs were exposed to CoCl 2 at different doses (200~600μmol/L) for 24 h.The cell via-bility and apoptosis were measured by CCK-8 assay and TUNEL method.The expression of miR-26a-3p, miR-26a-5p, GSK-3β, caspase-3, Bcl-2 and Bax was examined by real-time PCR.The protein levels of Bcl-2 and Bax were detected by Western blotting .RESULTS: The cell viability was inhibited and the apoptosis of NSCs was increased significantly by CoCl2 in a dose-dependent manner (P<0.05).CoCl2 at concentration of 400μmol/L for 24 h was used to induce apopto-sis and the expression of miR-26a was down-regulated compared with control (P<0.05).Exposure to CoCl2 at concentra-tion of 400μmol/L up-regulated the expression of GSK-3β, caspase-3 and Bax , down-regulated the expression of Bcl-2 and Bcl-2/Bax (P<0.05).CONCLUSION:CoCl2 at concentration of 400μmol/L induces the apoptosis of NSCs obviously . CoCl2 may induce the NSC apoptosis by mitochondrial apoptotic pathway .Declining miR-26a may be related to NSC apopto-sis.