Objective To evaluate the effects of etomidate preconditioning on etomidate-induced toxicity to rat adrenal cortical cells in vitro.Methods After being primarily cultured for 7-9 days,the rat adrenal cortical cells at the exponential growth phase were seeded into 96-well culture plates (1 × 106 cells/ml) and cultured for 24 h.The cells were then randomly divided into 3 groups with 6 wells in each group:control group (group C),etomidate group (group E),and etomidate preconditioning group (group EP).In group E,the cells were incubated with 700 μmol/L etomidate for 24 h.In group EP,the cells were incubated with 1.25 μmol/L etomidate for 1 h,then washed out and incubated with 700 μmol/L eomidate for 24 h.The cell viability was determined by CCK-8 assay and the concentration of cortisol was determined by ELISA.Results Compared with group C,the cell viability and cortisol concentration were significantly decreased in E and EP groups.Compared with group E,the cell viability and cortisol concentration were significantly increased in group EP.Conclusion Etomidate preconditioning can reduce etomidate-induced toxicity to rat adrenal cortical cells in vitro.

This paper first analysis of hospital library in the present situation of the literature resources construction and utilization of the network environment that includes Literature resource management modernization,Extensive use of electronic resources,Information isolated island phenomenon seriously,inaccurate Localization of library self role et.Based on the above analysis,the author puts forwards some suggestions in Hospital library information resource integration and utilization.

OBJECTIVE: To investigate the clinical application and developing trend of narcotic analgesics in our hospital.METHODS: Analgesics used in our hospital during 2003～2007 were analyzed statistically.RESULTS: The consumption(amount of money and quantity) of narcotic analgesics especially that of morphine preparation witnessed an year-on-year increase while that of pethidine injection decreased year by year.CONCLUSION: The use of narcotic analgesics in our hospital was reasonable on the whole,but the dosage form and variety should be increased further.

Olfactory dysfunction is one of the common diseases in the Department of Otorhinolaryngology.Although the olfactory nerve has ability to regenerate in human central nervous system,if the damage involves nerve,only a few patients can restore the olfactory function.At present,there is no satisfactory treatment for sensorineural olfactory dysfunction.Therefore,it is urgent to explore new and effective method for treating sensorineural olfactory dysfunction.The progress of stem cells in the treatment of olfactory dysfunction is reviewed in this article.

Objective To establish an LC-MS/MS method for determination of S-071031 B, a novel antidepressant , in rat plasma and to study its pharmacokinetic profiles .Methods An LC-MS/MS method was established to determine S-071031B in rat plasma, and L-8021 was employed as the internal standard .The analytes were separated on a C18 column with a mobile phase consisting of water-acetonitrile containing 0.1%(v/v) formic acid at a flow rate of 0.3 ml/min.The mass spectrometer was operated in a selected reaction monitoring ( SRM ) mode with a positive electrospray ionization (ESI) interface.The plasma concentration-time curve was drawn and pharmacokinetic parameters were calculated by DAS 2.0.Results The linear range was from 2 to 1000 ng/ml with a sensitivity of 2 ng/ml as the lower limit of quantification . The intra-day and inter-day precisions , recoveries and matrix effects at three spiked levels were all suited to the determina-tion of biological samples.After oral administration of S-071031B, the Cmax of S-071031B was (287.2 ±50.8) μg/L and the Tmax was (0.8 ±0.3) h, with a t1/2of (2.9 ±0.6) h and an AUC(0-∞)of (1372.6 ±255.3) μg/L· h.Conclusion This method is sensitive and specific enough for determination of S-071031 B in rat plasma to facilitate the study of its phar-macokinetics .

Objective To investigate the pathological characteristics of lupus-like renal damages induced by double stranded DNA (dsDNA) derived from Trypanosoma Equiperdum (TE). Methods The TEs were propagated in normal rats and isolated from fresh rat blood by DEAE cellulose-chromatography. Their kinetoplast dsDNA (kDNA) was purified with Gibson's method. The emulsive mixture of kDNA and incomplete Freund's adjuvant (IFA) was injected into normal BALB/c mice subcutaneously. Eight weeks Later some parameters were examined, including sera titers of ANA and anti-dsDNA antibodies, 24h urine protein concentration, ESR, BUN, Scr and renal histological active index (AI). The pathological characteristics of renal tissues were observed under optical and electron microscopes, and then compared with that of BXSB mice and lupfis nephritis (LN) patients with positive anti-dsDNA antibodies in the sera. Results The results of all immunological parameters of TE kDNA-immunized mice corresponded with that of LN. Their renal damages mainly represented nephropathy syndrome. The pathological characteristics of these mice were similar to that of BXSB mice and LN patients, but Ⅱ (mesangial proliferative) and Ⅳ (diffuse proliferative) subtypes were more common in the former. Conclusion The pathological characteristics of renal damages in the mice immunized with TE dsDNA are similar to that of human LN induced by anti-dsDNA antibodies. This mice model could be used as a tool for invostigating the pathogenesis of LN.

Objective To evaluate the role of cyclooxygenase-2 (COX-2) in ventilator-induced lung injury in rats.Methods Thirty healthy adult male Sprague-Dawley rats,aged 3.0-3.5 months,weighing 300-350 g,were randomly divided into 3 groups (n =10 each) using a random number table:traditional tidal volume group (group T,VT =8 ml/kg),large tidal volume group (group L,VT =40 ml/kg) and NS398 (selective COX-2 inhibitor,VT =40 ml/kg) group (group N).In group N,8 mg/kg NS398 (in 2 ml of 10％ dimethyl sulfoxide) was injected intraperitoneally at 1 h before ventilation,while dimethyl sulfoxide 2 ml was administrated instead of NS398 in T and L groups.After 4 h of mechanical ventilation,arterial blood samples were obtained for blood gas analysis and PaO2 was recorded.The animals were sacrificed and lungs removed for microscopic examination and for determination of wet/dry lung weight ratio (W/D ratio) and concentrations of total protein,intercellular adhesion molecule-1 (ICAM-1),tumor necrosis factor-alpha (TNF-α),NO and 6-keto-prostaglandin F1alpha (6-keto-PGF1 α) in bronchoaveolar lavage fluid (BALF).Pulmonary permeability index (PPI) and TXB2/6-keto-PGF1 α ratio were calculated.Results Compared with group T,PaO2 was significantly decreased,W/D ratio and PPI were increased,the total protein,ICAM-1,TNF-α and NO levels and TXB2/6-keto-PGF1 α ratio in BALF were increased in group L(P ＜ 0.05).PaO2 was significantly higher,W/D ratio and PPI were lower,and total protein,ICAM-1,TNF-α and NO levels and TXB2/6-keto-PGF1 α ratio in BALF were lower in group NS than in group L (P ＜ 0.05).The damage to lung tissues was severe in group L,and obviously alleviated in group N.Conclusion COX-2 is involved in ventilator-induced lung injury in rats.

Objective To evaluate the effects of mild hypothermia performed at different times on the levels of glutamate, Bcl-2 and Bax during global cerebral ischemia-reperfsusion (I/R) in rats. Methods Twenty-four male SD rats weighing 230-270 g were randomly divided into 4 groups according to the time at which mild hypothermia was performed ( n =6 each): group A, B, C and D. Global cerebral ischemia was produced by occlusion of 4 vessels (cauterization of bilateral vertebral arteries and occlusion of bilateral common carotid arteries) in the 4 groups. In group B, C and D, the nasopharyngeal temperature was reduced to 32.5-33.5 ℃ and maintained for 1 h. Ischemia was performed after termination of cooling in group B. While ischemia was performed, cooling was started in group C. While reperfusion was performed, cooling was started in group D. Rewarming was started after termination of cooling in group B, C and D. Samples of dialysate in hippocampal CA1 area were collected every 10 min during 100 min reperfusion for determination of glutamate concentrations by high-performance capillary electrophoresis with laser-induced fluorescence detection ( HPCE-LIF). The brain tissues were taken at 3 h of reperfusion for determination of the expression of Bax and Bcl-2 in hippocampal CA1 area, and the ratio of Bcl-2/Bax was calculated. Results Compared with group A, the glutamate concentrations were significantly decreased, the Bcl-2 expression was up-regulated, the Bax expression was down-regulated and the ratio of Bcl-2/Bax was increased in the other thee groups ( P ＜ 0.05). Compared with group B, the Bcl-2 expression was significantly down-regulated, the Bax expression was up-regulated and the ratio of Bcl-2/Bax was decreased in group C ( P ＜0.05). The glutamate concentrations were significantly increased, the Bax expression was up-regulated and the ratio of Bcl-2/Bax was decreased in group D compared with group C ( P ＜ 0.05 ). Conclusion The earlier cooling is performed, the better the cerebral protective effect is during global cerebral I/R in rats.

Tumor radioresistance is the leading cause of clinical radiotherapy failure and disease progression.Researches show that the occurrence of radioresistance is related to the cell cycle arrest,relevant gene change,tumor microenvironment change,autophagy,tumor stem cells and other factors.Studying the mechanism of radioresistance and looking for an effective method to avoid it is the key to improve the effect of radiotherapy,which can provide the probability of the prognosis of radiosensitivity.

Aim To explore how MCP-1 induces neu-rodisorder by determing the effects of MCP-1 on excita-tory postsynaptic current(EPSCs) in the CA1 region of rat hippocampal brain slices .Methods EPSCs, the AMPA receptor-mediated EPSC (EPSCAMPAR ), NMDA receptor mediated EPSCs(EPSCNMDAR) and NR2BR re-ceptor-mediated EPSC ( EPSCNR2BR ) were recorded u-sing whole-cell patch recording techniques to observe the effects of 2.3 nmol· L-1 MCP-1 on pyramidal neu-rons in hippocampal CA1 region.Microtubule-associat-ed protein-2 ( MAP-2 ) staining was used to study whether MCP-1 induced dendritic injuries in hippocam-pal CA1 region and whether NMDAR , AMPAR or CCR2 receptor antagonists had protective effects a-gainst dendritic damage caused by MCP-1.Results ① Bath application of MCP-1 produced a significant enhancement of the amplitudes of EPSCs , EPSCAMPAR and EPSCNMDAR .②Further studies revealed that MCP-1 potentiated EPSC NR2BR; ③ The MCP-1-associated dendritic injuries were blocked by NMDAR , AMPAR and CCR2R antagonists respectively .Conclusions Our results suggest a potential role of MCP-1 which may play in neuroexcitotoxicity and neural injury via NMDA receptor(especially NMDAR subtype NR2BR) and CCR2 receptor .The antagonists of these receptors may have potential therapeutic effect for neurodegener-ation.