Objective To estimate the pharmacoeconomics of two remedy scheme in curing acute cerebral infarction. Method In 212 cases with acute cerebral infarction patients, 206 cases were adopted, and randomly divided into two group. Group A was 102 cases and Group B was 104 cases. Group A was administered with 18 ml cattle encephalon glycoside which was added into 250 ml 5%glucose injection, ivgtt, qd. After 7 days it was administered compound Butylphthalide Soft Capsules, 0.2 g qid, combined Xiaoshuantongluo capsule, 2.1 g tid until 14 days later. Group B was administered with cattle encephalon glycoside and ignotin injection 18 ml which was added into 250 ml 5%glucose injection, ivgtt, qd until 14 days. The basic therapy of two groups were same. After therapy compared the safety and clinic curative effect from European Stroke Scale(ESS) and activities of daily living(ADL).Then outcome-effectiveness was assayed in pharmacoeconomics. Results The total effective rate were 92.2 and 95.2%,and ccurrence of adverse react were 4.7 and 7.5, respectively,in the two group.The clinic total effective rate counting C/E was respectively 129.1 and 178.5;ΔC/ΔE was 1697.7. Conclusion The clinic curative effect of two group was intimate, but the cost had signiifcant difference. The sequential antimicrobial therapy in curing acute cerebral infarction had excellent advantage in outcome-effectiveness.

Objective To observe the phosphorylation of extraceUular signal-regulated kinase (p-ERK1/2) and its nuclear translocation at different time points after the hippocampal neurons were cul-tured in the magnesium-free medium, and discuss the changes of ERK1/2 signal pathway after epileptic injury of hippocampal neurons. Methods Hippocampal neurons from newly-born Wistar rats were cul-tured with NB medium and B-27 for 9 days, and then were transferred to the magnesium-free medium to induce epileptic injury to the hippocampal neurons. The distribution of p-ERK1/2 in the hippocampal neurons before and after the epileptic injury was observed under laser scanning confocal microscope, and the expression of p-ERK1/2 at different time points after culturing the hippocampal neurons in the magne-sium-free medium was detected by Western blot. Results Before the epileptic injury of hippocampal neurons, p-ERK1/2 mainly expressed in the cytoplasm and axoplasm of the neurons. While after the epi-leptic injury, the expression of p-ERK1/2 was detected in the cytoplasm, axoplasm and nucleus of the neurons. The expression of p-ERK1/2 was increased one hour after the epileptic injury, and peaked at hour 3 (p-ERK1:2.2838±0.1 186; p-ERK2:4.1 273±0.0 927). There was significant difference in the expression of p-ERK1/2 between the hippocampal neurons cultured with or without magnesium-free medium (P < 0.05). Conclusion Epileptic injury may induce increased expression of p-ERK1/2 in hippocampal neurons, and the activated ERK1/2 signal pathway may be associated with the epileptic dis-charge in neurons.