Objective To popularize preoperative "Time-out" procedure in order to strengthen safety management of surgical patient. Methods A feasible scheme was raised up by learning from the practical experience of Hongkong Mary Hospital and combining the medical system in Guangdong province and nursing model. Results No surgical accident happened after application of "Time-out" procedure in opera tion room of Hongkong Mary Hospital. Conclusions Preoperative "Time-out" procedure is one of the important measure to ensure the safety of surgical patients and prevent surgical accident. Managers in operation room should popularize this process according to actual situation in order to guarantee correct surgery on correct part of correct patients.

ObjectiveThe heroin-dependent animal model of rats was used to investigate the effects ofheroin on regulation of pain perception in the dorsal and ventral hippocampus of the heroin-dependent rats. Meth odsHeroin was injected subcutaneously twice a lay for 9 days according to the principle of daily increasing dose in the Sprague-Dawley rats. From the 10th day,rats were given heroin at dose of 27 mg · kg-1 once a day until the14th day, then the unit discharges of the dorsal and ventral hippocampus of rats were observed respectively afternoxious electric stimulation of the rat-tail by the extracellular single-unit recording with glass microelectrodes. ResultsWhen given noxious stimulation, most of the neurons in the dorsal hippocampus in the heroin-dependent ratswere unaffected(59.09％ ) ,whereas in the control rats ,the ratio of the neurons of the dorsal hippocampus affectedby noxious stimulation was about 66.67％, respectively(P ＜ 0.05 ). However,in the ventral hippocampus, the ratioof the neurons activated,inhibitory or unaffected was 20. 69％ ,41.38％ and 37.93％ from the control and was40.74％ ,33. 33％ and 25.93％ from the heroin group respectively with no significant difference between two groups (P ＞ 0.05 ) . ConclusionHeroin changed the regulation of pain perception in the hippocampus,primarily the dorsal hippocampus of rats.

0.05),the content ratio of glutamate to gamma-aminobutyric acid in the hippocampus of the dependent rats was lower than that in the control group(P

OBJECTIVE: To prepare Polylactic-co-glycolic acid)(PLGA) microspheres loaded with Chinese herbal extract cucurbitacin B.METHODS: Cucurbitacin B loaded by PLGA microspheres were prepared by modified emulsification-solvent evaporation method.Central composite design-response surface method was applied to optimize the formulation with PVA concentration and ratio of drug to polymer as independent variables,and with yield of microspheres(Y1),drug loading amount(Y2),encapsulation efficiency(Y3),mean particle diameter(Y4),and the cumulative percentage of the drug release in 24 hr(Y5) as indexes to conduct multiple linear regression and second-order polynomial equation fitting.In vitro release test was performed by modified immediate release method.RESULTS: The results showed that all response variables were greatly fitted by a second-order polynomial equation.The optimal formulation was proved to be as follows: PVA concentration was 0.014 and ratio of drug to polymer was 0.066 5.The microspheres prepared in the optimal formulation were spherical and had smooth surface.Y1,Y2,Y3,Y4,and Y5 were 79.9%,7.83%,80.5%,56.18 ?m and 6.98%,respectively.The cumulative release from microspheres within 35 days reached 86.73%.CONCLUSION: Cucurbitacin B-PLGA microspheres are characterized by prolonged action and sustained-release.Furthermore,the established model has satisfactory predictability.

Aim To investigate the effects of lentivirus mediated nerve growth factor ( NGF) gene silencing on pheochromocytoma cells ( PC12 ) and the possible mechanisms .Methods The NGF shRNA expression vector was constructed .PC12 cells were randomly divi-ded into five groups (n=3 each) as follows: negative control group ( NC ) , control lentivirus group ( LV CON) , lentivirus NGF shRNA1 group ( LV shNGF1 ) , lentivirus NGF shRNA2 group(LV shNGF2), lentivir-us NGF shRNA3 group(LV shNGF3).The cells in NC group were cultured in DMEM/HG and polybrene me-dium, while others were cultured in DMEM/HG, poly-brene and corresponding lentivirus medium .After the treatment, the infection efficiency was determined by fluorescent microscope .Relative expression of NGF , extracellular signal-regulated kinase ( ERK1/2 ) and p-ERK1/2 were assessed by Western blot .The expres-sion of NGF mRNA was analyzed by quantitative re-verse transcription polymerase chain reaction ( qRT-PCR) .The differentiation degree was valued according to the length of neuritis and max diameter of cells .The cell viability was detected by CCK-8.Results The in-fection efficiency in PC12 cells reached over 90%. Compared with NC group , the relative expression of NGF mRNA and NGF protein was significantly down-regulated ( P<0.05 ) .There was no difference in the expression of ERK1/2 protein and cell viability .The expression of p-ERK1/2 protein was markedly down-regulated in LV shNGF3 group ( P<0.01 ) .The cells morphology was changed , and the length of neuritis and max diameter of cells were strained in LV shNGF 3 group than those in NC group ( P<0.01 ) .Conclusion Lentivirus-mediated NGF gene silencing inhibits the differentiation of PC12 cells through suppressing the activation of ERK1/2.

Pure and drug hydrophilic matrix tablets were prepared by direct compression method with theophylline as a model drug. The characteristics of four hydrophilic matrix polymers, hydroxypropylmethylcellulose (HPMC), polyethylene oxide (PEO), sodium alginate (NaAlg) and xanthan gum (XG), were compared by investigating the water absorption, swelling, erosion and gel layer strength. The sequence of water absorption rate was XG >> NaAlg (H) > PEO > NaAlg (L) >> HPMC; The sequence of swelling index was XG >> PEO >> HPMC >> NaAlg; The sequence of erosion rate was NaAlg (L) > NaAlg (H) >> PEO80 > PEO200 > PEO300 > XG approximately PEO400 approximately K4M > K15M > PEO600 approximately K100M; The sequence of the gel layer strength was PEO > HPMC > XG >> NaAlg. For the PEO and HPMC matrix tablets, with the polymer molecular weight increased, the drug release mechanism was gradually transferred from mainly depending on the erosion to the diffusion; for SAL matrix tablets, the drug release mainly depends on erosion mechanism; and for XG matrix tablets, the drug release mainly depends on non-Fick diffusion mechanism. Comparison of the performance difference between the polymer materials will contribute to rational design and prediction of drug release behaviors from matrix tables and ultimately to achieve clinical needs.

AIM To investigate the anti oxidation activities of new systhesized nitroxides in liver, liver mitochondria and RBC from rats and in egg phospholipid. METHODS The homogenates of liver, liver mitochondria from rats and the suspensions of egg phospholipid were used to determine malondialdehyde (MDA) formation induced by Fe 2+ Vit C system using TBA colorimetric method. H 2O 2 caused hemolysis was measured spectrometrically. Superoxide anion was assayed spectrometrically. RESULTS Nitroxides A, B with one active group (NO?) could inhibit MDA generation caused by ?OH generation system significantly, antagonized hemolysis induced by H 2O 2, but did not affect O ? 2 formation; Nitroxide C with two active group (NO?) possessed similar potent anti lipoperoxidative activities,IC 50

Objective To investigate the mechanism underlying the WNK4 kinasemediated inhibitory effect on BK channel. Methods Cos-7 cells were cotransfected with BK in combination with either CD4 (control group) or wild type WNK4 (WNK4-WT).Immunostaining and confocal microscopy,chemiluminescence,Western blotting analysis were then employed to determine the BK localization in cells,BK surface expression and total protein level,respectively.To further investigate whether the reduction of BK protein expression is due to an increase in degradation through a lysosomal pathway,BK protein level was determined after treated with bafilomycin A1(Baf A1),a proton pump inhibitor affecting lysosomal degradation. Results Immunostaining and confocal microscopic study showed that BK was localized both in plasma membrane and cytosol in the control group.After cells transfected with WNK4-WT,BK expression was markedly reduced.Chemiluminescent assay found that BK surface expression level was 299.9±18.6 in the control group,whereas it was significantly reduced (148.4±13.7,P＜0.01) in the WNK4-WT group.Western blotting analysis showed that total BK protein level was markedly reduced in the presence of WNK4-WT compared to the control group.WNK4-WT was shown to significantly reduce the BK total protein level (42.3％±15.2％) compared to the control group (100％) (P＜0.01).When the cells was treated with Bafilomycin A1 (Baf A1,0.5 μmol/L),WNK4-mediated reduction in BK protein was reversed (82.2％±12.1％,P＜0.05). Conclusions WNK4 inhibits total and surface protein expression of BK in Cos-7 cells whick is likely due to an increase in BK degradation through a lysosomal pathway.

Background and purpose: Multidrug resistance (MDR) is the dominating obstacle to the chemotherapy. There is strong evidence that the phosphoinositide 3-kinases (PI3Ks) signaling pathway is involved in MDR phenotype, however, the mechanism of MDR occurrence is still unknown. This study tended to investigate the regulating effect of PI3K/Akt signaling pathway and its downstream target genes in P-glycoprotein (P-gp) (ABCB1 gene encoding)-mediated MDR in human colon carcinoma HCT-116/L-OHP cells. Methods:Pretreatment with PI3K selective inhibitor LY294002 (20μmol/L) for 2 h, the sensitivity of L-OHP was evaluated by the CCK-8 (cell counting kit-8) assay in HCT-116/L-OHP cells, and the expressions of P-gp, LRP, MRP-2, Akt, p-Akt, IκB and p-IκB were evaluated by Western blot. The activity of ABCB1 promoter was evaluated by chromatin immunoprecipitation analysis (CHIP). Results: After inhibiting the activity of PI3K/Akt signaling pathway, the IC50 value of L-OHP decreased from(157.48±16.73)μg/mL to (53.68±3.18)μg/mL in HCT-116/L-OHP cells, and the reversal index was 2.93 (P<0.01). The expressions of P-gp, p-Akt and p-IκB were down-regulation compared with the concrol group (P<0.01), but the expressions of LRP, MRP-2, Akt and IκB didn't change signiifcantly. CHIP result has conifrmed that NF-κB protein could bind to the region of ABCB1 gene promoter in HCT116/L-OHP cells. Conclusion:Blocking of PI3K/Akt/NF-kB signal pathway could increase the drug sensitivity to MDR cells, inhibit the phosphorylation of p-Akt and p-IκB, and reversing ABCB1/P-glycoprotein-mediated multidrug resistance in colon carcinoma cells.

Objective To investigate the effect of liver cirrhosis on the potency of propofol for sedation in rats. Methods Fifty-eight male SD rats, aged 10-12 weeks, weighing 180-220 g, were randomly divided into 3 groups: control group (group C, n = 18), mild liver cirrhosis group (group M1, n =20) and severe liver cirrhosis group (group M2, n = 20). The model of liver cirrhosis was established using four factors described by Chen et al. After successful establishment of the model, propofol was injected intravenously. The dose of propofol was determined by up-and-down sequential method for loss of righting reflex. The dose of propofol was 5.912 mg/kg in the first rat and the ratio of the doses between the two consecutive rats was 0.85. ED50 of propofol was calculated using up-and-down sequential method. Results ED50 of propofol was significantly lower in group M1 and M2 than in group C and in group M2 than in group M1 ( P ＜ 0.05 or 0.01 ). Conclusion The liver cirrhosis can enhance the potency of propofol for sedation in rats.