As a fundamental principle of medical ethics,informed consent shares a critical role in medical ethics research,while its specific enforcement is not optimistic at present.Possible reasons are analyzed as follows: the impact of traditional culture,the limited health resources,the imperfect health system and legislation,drawbacks of the education system and professional barriers.The principle of informed consent can be implemented well only by tackling all the above problems.

Objective To explore the protective effect of thyroxin on severe traumatic brain injury of brain tissue by observing the effect of thyroxin on neuronal apoptosis,serum neuronal specific enolase(NSE),interleukin-6 (IL-6) and serum FT3 and FT4.Methods A total of 90 SD rats was randomly divided into control group,model group,low dosage of levothyroxine sodium tablets group,moderate dosage of levothyroxine sodium tablets group and high dosage of levothyroxine sodium tablets group,18 rats in each group.The animal model was reproduced by referring to Feeney's free fall impact modeling.Intragastric administration was performed at 6 h after injury.The levels of neuronal apoptosis and serum NSE,IL-6,FT3 and FT4 were detected by TUNEL method,ELISA method and radioimmunoassay at 24,72,168 h after intragastric administration.Results (1) After severe traumatic brain injury,the levels of serum FT3 and FT4 were under the normal and the level of FT4 was decreased to the lowest at 168 h.Thyroxine could increase the levels of FT3 and FT4.(2) Significant neuronal apoptosis was observed in rats with severe craniocerebral injury,and the apoptosis continued until 168 h.Moderate and high dose of thyroxine could improve neuronal apoptosis within 24 h,while low dose of thyroxine changed within 168 h.(3) The levels of serum NSE and IL-6 were increased significantly in rats after severe traumatic brain injury until 168 h,and they could be decreased by moderate and high dose of thyroxine within 72 h.Conclusion Exogenous thyroxine can protect brain tissue in rats with severe traumatic brain injury.

To investigate the effect of Toxoplasma gondii infection upon the expression of brain-derived neurotrophic factor (BDNF) mRNA and N-methyl-D-aspirate receptor (NMDA) subunits NR2A and NR2B,Wistar rats of 4 weeks old were randomly divided into 3 groups with 10 rats in each group in which 2 mL suspensions of T.gondii tachyzoits in the concentrations of 2×10~7/mL and 2×10~5/mL were injected intra-peritoneally to rats in group A and group B respectively, serving as the experimental groups, while 2 mL of sterile physiologic saline was injected intra-peritoneally in group C serving as the control group. Four weeks after injection, the expressions of BDNF mRNA and BDNF protein in the brain tissues were detected by in situ hybridization and immunohistochemical assay and the expressions of NR2A and NR2B immune activity in the hippocampal CA1,CA3 and DG were investigated by using computer-assisted image analysis system. Compared with the control group, the expression of BDNF protein in the hippocampus of the experimental groups was significantly enhanced [(64.27±23.18), (50.39±19.34) vs (44.68±22.74)/mm~2,P＜0.05]. In addition, the increased expressions of BDNF mRNA in the hippocampus of the experimental groups were also demonstrated [(0.13±0.02), (0.12±0.02) vs (0.09±0.01); P＜0.05]. In the expression of the NR2A protein, their expressions in group A and B of rats were significantly lower than that of group C in CA3 (P＜0.05),but there was no significant change in CA1 and DG. In the expression of NR2B protein, the expressions in group A and B were also lower than that of group C in CA1 and CA3, and had no significant change in DG. It is evident that the expressions of BDNF mRNA and BDNF protein in hippocampal tissues were significantly increased following chronic infection with T.gondii, supporting the hypothesis that BDNF may be involved in the intrinsic neuro-protective mechanism.