OBJECTIVE To investigate the effects of peiminine B （PEI） on Streptococcus pneumoniae （SP）-induced alveolar epithelial cell injury by regulating the Ras-related C3 botulinum toxin substrate 1 in nucleus accumbens （Rac1）/protein kinase B （Akt）/nuclear factor κB （NF-κB） signaling pathway. METHODS Human alveolar epithelial cells （HPAEpiC） were taken and randomly divided into the Control group， SP group （1×108 cfu/mL SP bacterial solution）， low-， medium-， and high-concentration PEI groups （1×108 cfu/mL SP bacterial solution+0.05， 0.10， 0.20 mmol/L PEI）， and high-concentration PEI+Akt activator group （P-H+SC79 group， 1×108 cfu/mL SP bacterial solution+0.20 mmol/L PEI+10 μmol/L SC79）. Except for the Control group， the other groups of cells were treated with SP bacterial solution and/or corresponding drug solution. After 24 h of treatment， the levels of inflammatory factors （interleukin-6， -18， -1β） in the supernatant solution， the contents of oxidative stress indexes [lactate dehydrogenase （LDH）， reactive oxygen species （ROS） and superoxide dismutase （SOD）]， apoptosis rate， as well as the expressions of proliferation/apoptosis-related proteins [cyclin-dependent kinase 1 （CDK1）， B cell lymphoma-2 related X protein （Bax）] and pathway-related proteins （Rac1， Akt， phosphorylated Akt， NF-κB and phosphorylated NF-κB） were detected in each group. RESULTS Compared with the Control group， the levels of inflammatory factors in supernatant solution， LDH and ROS contents， apoptosis rate， the protein expressions of Bax and Rac1 and the phosphorylation levels of Akt and NF-κB in the SP group were significantly increased or up-regulated， while SOD content and the protein expression of CDK1 were significantly decreased or down-regulated （P＜0.05）. Compared with the SP group， the above indexes in PEI groups were significantly improved in a concentration-dependent manner （P＜0.05）. SC79 could significantly reverse the improvement effect of the high concentration of PEI （P＜0.05）. CONCLUSIONS PEI can alleviate SP-induced inflammation and oxidative stress damage of alveolar epithelial cells and inhibit apoptosis， which may be achieved by inhibiting Rac1/Akt/NF-κB signaling pathway.

Objective To investigate the effects and mechanisms of valproic acid on brain edema,neurobehavioral outcome and inflammatory response after traumatic brain injury (TBI) in rats.Methods TBI animal models were established using Feeney's method.Fifty-four SD male rats,weighting 220-250 g,were randomly divided into 3 groups (n =18):sham operation group (group sham),traumatic brain injury group (group TBI) and valproic acid treatment group (group TBI + VPA).Experimental rats were treated with valproic acid (300 mg/kg,twice daily) by intraperitoneal injection.Rat behavioral outcomes were measured by modified neurologic severity score (mNSS) tests at day 1,3,and 7 after TBI.Brain water content was measured with wet-dry weight method.The blood cells infiltration into cerebral cortex were tested with immunohistochemistry staining against ED-1 for macrophage.Inflammatory cytokines (INF-γ,tumor necrosis factor-α,interleukin-6) were measured by Western blotting.The statistical analysis were performed by ANOVA and chi-square tests using the statistical software program SPSS 13.0.Results Compared with the Sham group,the levels of brain edema,mNSS and macrophage cell infiltration were significantly increased after TBI (all P =0.00).The expressions of inflammatory cytokines were also increased significantly (all P =0.00).Compared with the TBI group,TBI + VAP group had significantly lower brain water content[3day:(80.12 ±0.59)％ vs.(82.14 ±0.67)％,P=0.04;7day:(74.74 ±0.72)％ vs.(77.93 ±0.48)％,P=0.01],and mNSS scores [3 day:(10.53 ±0.32) vs.(11.74 ±0.48),P =0.02;7 day:(7.97 ± 0.32) vs.(10.73 ± 0.42),P =0.01].VPA suppressed macrophage cell infiltration into cerebral cortex [(36.44 ± 0.72) ％ vs.(25.93 ± 0.48) ％ P =0.00].Meanwhile,VPA inhibited the expressions of inflammatory cytokines (INF-γ,TNF-α,IL-6) (P ＜ 0.05).Conclusions Treatment with VPA markedly reduced brain edema and improved neurological outcomes after TBI,possibly mediated by inhibited TBI-induced cerebral inflammatory responses and macrophage cell infiltrating into cerebral cortex.

ObjectiveTo investigate the best pattern of the discussion on nursing cases of severe cardiac patients and improve the quality of the clinical nursing activity.Methods90 nurses from six cardiac units were divided into the control group and the experimental group with 45 nurses in each group. The experimental group adopted PBL teaching method, the control group adopted conventional teaching method. The discussion of severe cardiac patients was proceeded twice every month for one year.Results The experimental group was better than the control group in master and application of the basic cardiac knowledge, nursing quality of serious patients and effectiveness of nurse-patient communication.ConclusionsDiscussion with PBL teaching method is superior to the conventional method. This method can widen the nurses'thread, improve the nurses' ability to solve problem, so it is worthy of wide application.