Objective To evaluate the surgical therapy on dislocated fracture of talus. Methods Retrospective analysis was mode in 21 patients with dislocated fracture of talus collected from Jan. 2004 to Jan.2010, which were treated with open reduction, cannulated screw fixation, and kept neutral position plaster fixation with no weight loading, to do functional exercise depending on the Ⅹ film demonstrations. Results All the patients were followed up from 6 months to 3.8 years post-operation, and according to the evaluation standard by American Foot-Ankle Surgery Society, good rate was 61.91%. Conclusion Treating dislocated fracture of talus with emergency operation, anatomical reduction, valid internal fixation and no weight loading plaster fixation post-operation, shows good effect with low rate of complication.

Objective To observe the effect of acanthopanax refined polysaccharide(ASPS)on nicotine-induced learning and memory impairment in mice.Methods A total of 48 male mice and 48 females at 6 weeks of age were selected and were divided into two batches for animal experiments:the Morris and the new object recognition batch.Each batch was randomly divided into 6 groups ac-cording to body weight:blank control group,model group,drug positive group,high-dose ASPS group,medium-dose ASPS group,and low-dose ASPS group.Except for the blank group,the remai-ning 5 groups were injected subcutaneously with 0.5mg/kg of nicotine every day for 7 days to prepare a nicotine memory disorder model.After 24 hours of injection of nicotine at the 7th day,the drug posi-tive group was gavaged piracetam for 800 mg/kg,and the high-dose,medium-dose and low-dose ASPS groups were gavaged for 270,90 and 30 mg/kg of ASPS respectively for 7 days.The learning and memory ability of mice was detected by water maze test and new object recognition test,respec-tively.After the two tests,superoxide dismutase(SOD)activity in serum and 5-Hydroxytryptamine(5-HT)content in hippocampal tissue were detected.Results The results of new object recognition experiment showed that the discrimination indexes of the high-,medium-and low-dose ASPS groups were significantly higher than that of the model group(P＜0.01 or P＜0.05).The results of water maze experiment showed that the time to find the platform in the spatial search experiment was signifi-cantly shorter in the high-and medium-dose ASPS groups than that in the model group(P＜0.05).In the positioning voyage test,the number of mouse platform entries in the high-dose ASPS group was significantly more than that in the model group(P＜0.05);the proportions of Ⅲ quadrant routes in the high-and medium-dose ASPS groups were higher than those in the model group(P＜0.05).The high-,medium-and low-dose ASPS groups were significantly higher than those in the model group(P＜0.01);the determination of hippocampal tissue content in mice showed that the content of 5-HT in the high-and medium-dose ASPS groups was significantly higher than that in the model group(P＜0.01 or P＜0.05).Conclusion ASPS can significantly improve the learning and memory ability of nicotine-quitting mice,relieve the damage of hippocampal neurotransmitters,and regulate oxidative stress in vivo.The mechanism may be related to improving the body's antioxidant capacity and regulating hippocampal neurotransmitter levels.

Objective To observe the effect of acanthopanax refined polysaccharide(ASPS)on nicotine-induced learning and memory impairment in mice.Methods A total of 48 male mice and 48 females at 6 weeks of age were selected and were divided into two batches for animal experiments:the Morris and the new object recognition batch.Each batch was randomly divided into 6 groups ac-cording to body weight:blank control group,model group,drug positive group,high-dose ASPS group,medium-dose ASPS group,and low-dose ASPS group.Except for the blank group,the remai-ning 5 groups were injected subcutaneously with 0.5mg/kg of nicotine every day for 7 days to prepare a nicotine memory disorder model.After 24 hours of injection of nicotine at the 7th day,the drug posi-tive group was gavaged piracetam for 800 mg/kg,and the high-dose,medium-dose and low-dose ASPS groups were gavaged for 270,90 and 30 mg/kg of ASPS respectively for 7 days.The learning and memory ability of mice was detected by water maze test and new object recognition test,respec-tively.After the two tests,superoxide dismutase(SOD)activity in serum and 5-Hydroxytryptamine(5-HT)content in hippocampal tissue were detected.Results The results of new object recognition experiment showed that the discrimination indexes of the high-,medium-and low-dose ASPS groups were significantly higher than that of the model group(P＜0.01 or P＜0.05).The results of water maze experiment showed that the time to find the platform in the spatial search experiment was signifi-cantly shorter in the high-and medium-dose ASPS groups than that in the model group(P＜0.05).In the positioning voyage test,the number of mouse platform entries in the high-dose ASPS group was significantly more than that in the model group(P＜0.05);the proportions of Ⅲ quadrant routes in the high-and medium-dose ASPS groups were higher than those in the model group(P＜0.05).The high-,medium-and low-dose ASPS groups were significantly higher than those in the model group(P＜0.01);the determination of hippocampal tissue content in mice showed that the content of 5-HT in the high-and medium-dose ASPS groups was significantly higher than that in the model group(P＜0.01 or P＜0.05).Conclusion ASPS can significantly improve the learning and memory ability of nicotine-quitting mice,relieve the damage of hippocampal neurotransmitters,and regulate oxidative stress in vivo.The mechanism may be related to improving the body's antioxidant capacity and regulating hippocampal neurotransmitter levels.

Objective To study the immunomodulatory effect of polysaccharides (CRPS25-Ⅱ) derived from Chroogomphus rutilus on mouse mononuclear macrophages, RAW264.7 cells. Methods RAW264.7 cells were resuspended and cultured, cell suspension was prepared. The blank control group and CRPS25-Ⅱ groups with different mass concentrations (1, 20, 40, 80 and 160 μg/ml) were set up. MTT assay was used to determine the cytotoxicity of CRPS25-Ⅱ on RAW264.7 cells. RT-PCR was used to detect the effects of CRPS25-Ⅱ on the secretion of immune regulatory factors IL-6 and TNF-α from RAW264.7 cells. Western blot was used to detect the effects of CRPS25-Ⅱ on the expression of p-P65 protein in NF-κB pathway of RAW264.7 cells. Results The results showed that CRPS25-Ⅱ (1−160 μg/ml) had no obvious cytotoxicity. CRPS25-Ⅱ (1−160 μg/ml) increased the secretion of cytokines, and thus promoted the mRNA expression of IL-6 and TNF-α. CRPS25-Ⅱ increased the phosphorylation of p-P65 protein and activated the NF-κB signaling pathway, and thus promoted the immune regulation of cells. CRPS25-Ⅱ (1−160 μg/ml) could increase the p-P65 protein, and the promoting effects of CRPS25-Ⅱshowed an upward trend in the concentration range of 1−40 μg/ml and gradually weakened in the concentration range of 40−160 μg/ml. Conclusion Polysaccharides derived from chroogomphus rutilus had no cytotoxicity to mouse macrophages, and could promote the secretion of inflammatory factors IL-6 and TNF-α and activate the NF-κB signaling pathway, thus playing an immunomodulatory role.

Hepatotoxicity is a common side effect for patients treated with gefitinib, but the related pathogenesis is unclear and lacks effective predictor and management strategies. A multi-omics approach integrating pharmacometabolomics, pharmacokinetics and pharmacogenomics was employed in non-small cell lung cancer patients to identify the effective predictor for gefitinib-induced hepatotoxicity and explore optional therapy substitution. Here, we found that patients with rs4946935 AA, located in Forkhead Box O3 (FOXO3) which is a well-known autophagic regulator, had a higher risk of hepatotoxicity than those with the GA or GG variant (OR = 18.020, 95%CI = 2.473 to 459.1784, P = 0.018) in a gefitinib-concentration dependent pattern. Furthermore, functional experiments identified that rs4946935_A impaired the expression of FOXO3 by inhibiting the promotor activity, increasing the threshold of autophagy initiation and inhibiting the autophagic activity which contributed to gefitinib-induced liver injury. In contrast, erlotinib-induced liver injury was independent on the variant and expression levels of FOXO3. This study reveals that FOXO3 mutation, leading to autophagic imbalance, plays important role in gefitinib-induced hepatotoxicity, especially for patients with high concentration of gefitinib. In conclusion, FOXO3 mutation is an effective predictor and erlotinib might be an appropriately and well-tolerated treatment option for patients carrying rs4946935 AA.