ObjectiveTo investigate the effects of propofol and etomidate on apoptosis in hippocampal neurons in rats.MethodsOne hundred and forty male 4 weeks old SD rats were randomly divided into 7 groups (n =20 each):control group (group C) ; groups P1,2,3 received intraperitoneal (IP) propofol 50,100 and 200mg/kg and groups E1,2,3 received IP etomidate 10,30 and 60 mg/kg respectively.Arterial blood samples were obtained at 2 h after the animals were fully awake for blood gas analysis.The animals were then sacrificed and their brains removed for microscopic examination of the ultrastructure of neurons in hippocampal CA1 area and detection of Survivin and Caspase-3 mRNA and protein expression in hippocampus by RT-PCR and Western blot analysis.ResultsThere was no significant difference in PaO2,PaCO2,SaO2,HCO3-,BE and pH value among the 7 groups.The neurons in CA1 area were basically normal in groups C,P1 and E1 while condensation of the chromatin of the nucleus and apoptotic bodies were observed in groups P3 and E3.Caspase-3 mRNA and protein expression was significantly up-regulated while Survivin mRNA and protein down-regulated in groups P3 and E3.Conclusion High dose of propofol and etomidate may induce apoptosis in hippocampal neurons in rats by up-regulation of Caspase-3 expression and down-regulation of Survivin expression.

Objective To investigate the effects of different doses of propofol anesthesia on the long-term cognitive function in neonatal rats.Methods One hundred 7-day-old male Sprague-Dawley rats,weighing 9-18 g,were randomly divided into 5 groups (n =20 each) ∶ control group (C group) and propofol 25,50,100 and 200mg/kg groups (groups P1-4,respectively).Groups P1 and P2 received intraperitoneal propofol 25 and 50 mg/kg,respectively.Groups P3 and P4 received intraperitoneal propofol 100 and 200 mg/kg,respectively,and after righting reflex completely recovered,an increment of propofol 50 mg/kg was given until the total amount was finished.Five animals in each were chosen and arterial blood samples were obtained immediately after the animals were fully awake for blood gas analysis.The rats were then continuously fed.When the rats were 9 weeks old,the spatial learning and memory function was tested by Morris water maze.The animals were then sacrificed and their brains were removed for detection of the expression of nerve growth factor (NGF) and Caspase-9 protein and mRNA in hippocampal tissues (by Western blot analysis and RT-PCR) and for microscopic examination of the ultrastructure of hippocampal neurons.Results There was no significant difference in blood gas analysis index between the 5 groups (P ＞ 0.05).Compared with group C,no significant change was found in the escape latency and frequency of crossing the original platform in group P1,the escape latency was prolonged and the frequency of crossing the original platform was decreased in groups P2-4,the expression of NGF protein and mRNA was down-regulated and the expression of Caspase-9 protein and mRNA was up-regulated in groups P1-4 (P ＜ 0.05).The escape latency was gradually prolonged,the expression of NGF protein and mRNA was gradually down-regulated and the expression of Caspase-9 protein and mRNA was gradually up-regulated in groups P1-4.The frequency of crossing the original platform was decreased in groups P2-4 compared with group P1 (P ＜ 0.05).There was no significant difference in the frequency of crossing the original platform between groups P2-4 (P ＞ 0.05).Nucleus condensation,chromatin condensation,nuclear fragmentation and apoptotic bodies were observed in groups P2-4.Conclusion Propofol anesthesia can impair the long-term cognitive function in neonatal rats,the effect is related to the dose,and inhibition of NGF expression and increase in the activity of Caspase-9 may be involved in the mechanism.

Objective To investigate the effect of morphine on the expression of p53 mRNA and E2F-1 mRNA in human gastric carcinoma cell line MGC-803 .Methods The human gastric cancer cell line MGC-803 was purchased from Cell Biology Research Institute, Chinese Academy of Sciences, and cultured in DMEM liquid culture mediun. The cells were seeded in 6-well plates (1 × 103/ml or 2 × 105/ml, 1 ml/well) and divided into 2 groups (n = 18 wells each):group Ⅰ normal control (group C); group Ⅱ was exposed to 10 μmol/L morphine (group M). The proliferation of the cells was determined by colony formation assay at 7 day of incubation with morphine. The expression of p53 mRNA and E2F-1 mRNA was detected and the ulrastructure of the cells examined with transmission electron microscope after being incubated with morphine for 24 h. Results The proliferation of the cells and E2F-1 mRNA expression were significantly lower and p53 mRNA expression was significantly higher in group M than in group C (P ＜ 0.05). The nuclear evelope was intact and the nucleolus and chromosomes were clearly visible in group C, while in group M fragmentation of nuclear envelope and nucleolus and apoptotic bodies were observed. Conclusion Morphine can inhibit the proliferation of the cells and accelerate the cell apoptosis through up-regulating the expression of p53 gene and down-regulating the expression of E2F-1gene in human gastric carcinoma cell line MGC-803.

Objective To analyze the outcome and the prognostic factors of hepatic veno-occlusive disease (HVOD) after hematopoietic stem cell transplantation (HSCT). Methods A total of 797 patients receiving HSCT were analyzed retrospectively. The prophylaxis regimen of HVOD in the First Affiliated Hospital of Guangxi Medical University consisted of low molecular weight heparin and lipoprostaglandin E1 (PGE1). Results Fifty-nine patients (7.4%) developed HVOD at 3-49 days after HSCT (median 12 days). Age younger than 15 years at transplant( HR=6.47, P<0.001), busulphan conditioning ( HR=6.40, P<0.001), thalassemia major ( HR=6.35,P<0.001), allogeneic transplantation ( HR=7.74, P=0.005) were univariate risk factors for HVOD. Multivariate analyses suggested that thalassemia major and busulphan conditioning were independently correlated with the development of HVOD. Conclusion Thalassemia major and busulphan conditioning are independent risk factors for HVOD after HSCT.