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Objective@#To introduce Revised American Pain Society Patient Outcome Questionnaire for patients with cancer pain in China, and to test its reliability and validity.@*Methods@#Cross-cultural adjustment was conducted on the basis of the Revised American Pain Society Patient Outcome Questionnaire of the American Pain Association published on the official website through expert review and pre-experiment. A convenience sample of 153 hospital patients with cancer pain was recruited. And the data were analyzed for reliability and validity.@*Results@#The adjusted Revised American Pain Society Patient Outcome Questionnaire contains 18 core items, which are easy to understand and can be completed within 10 minutes. Reliability test: the Cronbach α coefficient of internal consistency for the total scale was 0.735. The Cronbach α coefficient of pain intensity dimension was 0.233, the Cronbach α coefficient of sleep interference dimension was 0.891, the Cronbach α coefficient of activity interference dimension was 0.830, the Cronbach α coefficient of emotion dimension was 0.846, the Cronbach α coefficient of pain management related side effects dimension was 0.591, and the Cronbach α coefficient of perception dimension of pain care was 0.633. Validity test: The total content validity of the scale was 0.98, and the content validity of each item ranged from 0.82 to 1.00.@*Conclusion@#The adjusted Revised American Pain Society Patient Outcome Questionnaire has good reliability and validity, providing an effective assessment tool for medical institutions to evaluate the quality of cancer pain management.
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Objective:To introduce Revised American Pain Society Patient Outcome Questionnaire for patients with cancer pain in China, and to test its reliability and validity.Methods:Cross-cultural adjustment was conducted on the basis of the Revised American Pain Society Patient Outcome Questionnaire of the American Pain Association published on the official website through expert review and pre-experiment. A convenience sample of 153 hospital patients with cancer pain was recruited. And the data were analyzed for reliability and validity.Results:The adjusted Revised American Pain Society Patient Outcome Questionnaire contains 18 core items, which are easy to understand and can be completed within 10 minutes. Reliability test: the Cronbach α coefficient of internal consistency for the total scale was 0.735. The Cronbach α coefficient of pain intensity dimension was 0.233, the Cronbach α coefficient of sleep interference dimension was 0.891, the Cronbach α coefficient of activity interference dimension was 0.830, the Cronbach α coefficient of emotion dimension was 0.846, the Cronbach α coefficient of pain management related side effects dimension was 0.591, and the Cronbach α coefficient of perception dimension of pain care was 0.633. Validity test: The total content validity of the scale was 0.98, and the content validity of each item ranged from 0.82 to 1.00.Conclusion:The adjusted Revised American Pain Society Patient Outcome Questionnaire has good reliability and validity, providing an effective assessment tool for medical institutions to evaluate the quality of cancer pain management.
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Objective:To design the small ubiquitin modification-fibroblast growth factor receptor 4 (SUMO-FGFR4) fusion gene and construct the expression vector pET22b-SUMO-FGFR4, to optimize the expression conditions. Methods:The SUMO-FGFR4 fusion gene was obtained by Overlap PCR and was connected to pET22b;the recombinant expression vector pET22b-SUMO-FGFR4 was obtained. The influence of lactose concentration, induction time,induction temperature,induction point and adding mode of lactose in the expression levels was observed,and the best induction condition was determined; then the solubility of recombinant protein was analyzed.Results:The SUMO-FGFR4 fusion protein was highly expressed,the molecular weight of the fusion protein was about 40 000 and it could bind with FGFR4 specific antibody.When the lactose concentration was 1.0 g·L-1 ,the induction time was 3 h,the induction temperature was 37℃,the value of A (600)was 0.8,the expression level was highest;but adding mode of lactose had no remarkable effect on the protein expression.The expression level of recombinant protein induced by lactose was higher than IPTG.SUMO-FGFR4 protein existed in a form of inclusion body.Conclusion:The SUMO-FGFR4 fusion protein is expressed successfully in this study while lactose is used as inducer and the best expression conditions are confirmed.
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OBJECTIVE To investigate the effect of mono-2-ethylhexyl phthalate(MEHP) on proliferation of primary neural stem cells(NSCs)of rats and NE-4C cells of mice and on the migration of NE-4C cells and the mechanism. METHODS NE-4C or NSCs were treated with MEHP 1,10,100 and 1000 μmol · L-1 for 72 h,respectively. The cytotoxicity was estimated with the cell counting kit-8 (CCK-8). Cell proliferation was analyzed by EdU assay. The mRNA expression levels of the glucocorticoid receptor(GR),signal transducer and activator of transcription 3(Stat3)and sex determining region Y (SRY)-box 2(Sox2) were detected by qRT-PCR. The protein expression levels of total GR,GRβ, Sox2,Stat3 and p-Stat3 were measured by Western blotting. RESULTS Cell viability of NE-4C cells and NSCs at MEHP 1000μmol·L-1 was significantly decreased,which was 70.3%and 40.0%of the control group, respectively. EdU assay showed that MEHP 100 μmol · L-1 decreased NE-4C cells and NSCs by 74.8%and 12.0%(P<0.05)compared with control. The effect of MEHP on the cell migration of NE-4C was evidenced by the fact that the migration was obviously reduced to (63.4±2.0)%(P<0.05)after treatment with MEHP 100μmol · L-1 for 72 h. The mRNA expression levels associated with proliferation and migration in NE-4C of GR,Stat3 and Sox2 in MEHP 100 μmol · L-1 group were down-regulated to 49.8%,26.0% and 14.0%of control(P<0.05). At MEHP 100μmol · L-1,mRNA of GR, Stat3 and Sox2 in NSCs declined to 10.0%,14.0% and 15.3% of normal control. Western blotting results revealed that protein expressions of GR,GRβ,Sox2 and p-Stat3 were remarkably inhibited by MEHP 100 μmol · L-1 in that the relative expression of NE-4C was 0.92 ± 0.17,0.87 ± 0.35,0.81 ± 0.22 and 0.62 ± 0.24(P<0.05). The corresponding protein expression in NSCs was 0.82 ± 0.20,0.56 ± 0.12,0.84 ± 0.36 and 0.53 ± 0.20(P<0.05)when the cells were treated with MEHP 100μmol · L-1 for 72 h. CONCLUSION MEHP can inhibit the proliferation and migration of NE-4C cells and NSCs possibly by decreasing Stat3 and Sox2 that are mediated by GRβ.
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Objective To evaluate the role of adenosine A1 receptors in hippocampal neurons in the cognitive dysfunction caused by isoflurane anesthesia in aged mice.Methods Sixteen male adenosine A1 receptor gene knockout homozygote mice (gene knockout mice) and 16 male wild-type mice,aged 18-22 months,weighing 27-32 g,were studied.Each type of mice was randomly divided into 2 groups (n=8 each) using a random number table:control group (group C) and isoflurane anesthesia group (group Ⅰ).Mice inhaled 1.4％ isoflurane in 100％ O2 for 2 h in group Ⅰ,and 100％ O2 for 2 h in group C.All the mice underwent Morris water maze test at 24 h after isoflurane or O2 inhalation.After the test,the mice were sacrificed and the hippocampal tissues were harvested to determine the number of β-amyloid1-42 (Aβ1-42) plaques (using immunohistochemistry) and expression of phosphorylated tau (p-tau) protein,and 2B subunit-containing N-methyl-D-aspartate receptors (NR2B) (by Western blot analysis).Results Compared with group C of wild type mice,the escape latency was significantly prolonged,the number of Aβ1-42 plaques was enlarged,the expression of p-tau protein was up-regulated,and the expression of N R2B was down-regulated in group Ⅰ of wild type mice.Compared with group Ⅰ of wild type mice,the escape latency was significantly shortened,the number of Aβ1-42 plaques was decreased,the expression of p-tau protein was down-regulated,and the expression of NR2B was up-regulated in group Ⅰ of gene knockout mice.There was no significant difference in the parameters mentioned above between group Ⅰ and group C of gene knockout mice.Conclusion Adenosine A1 receptors in hippocampal neurons mediate isoflurane anesthesia-induced cognitive dysfunction in aged mice,and the mechanism may be related to promotion of deposition of Aβ,phosphorylation of tau protein and inhibition of activities of NR2B.
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OBJECTIVE To investigate the effect of curcumin on proliferation of neural stem cells (NSCs) of rats and the mechanism. METHODS NSCs derived from the forebrain of rat E15 embryos were cultured in vitro and identified by neuroepithelial stem cell protein ( nestin and SOX2) staining. NSCs were treated with curcumin 0.1, 0.5, 2.5, 12.5 and 62.5 μmol.L-1 for 24 h, respectively. The cyto-toxicity was estimated by measuring the release of lactate dehydrogenase(LDH). Cell viability and prolif-eration were analyzed respectively by MTT and BrdU assay. The mRNA expression levels of glucocorti-coid receptor (GR), Stat3, Notch1 and p21 were detected by qRT-PCR. The protein expression levels of total GR, Stat3 and phosphorylated Stat3 were measured by Western blotting. RESULTS The primary neural stem cells were identified as NSCs. Curcumin 12.5 and 62.5 μmol.L-1 had cell cytotoxicity( P<0.05). Cell viability assay indicated that curcumin 0.5 and 2.5 μmol.L-1 enhanced NSCs viability( P <0.05), but in 62.5 μmol.L-1 group the cell cytotoxicity was inhibited(P<0.05). Curcumin 0.1, 0.5 and 2.5 μmol.L-1 increased NSCs proliferation ( P < 0. 05), whereas 12. 5 and 62. 5 μmol.L-1 caused a decrease in NSCs proliferation(P<0.05). The mRNA expression level of GR in 0.5 μmol.L-1 group was significantly reduced( P<0.05). Western blotting analysis revealed that the protein expression of GR, Stat3 and p-Stat3 was inhibited by curcumin in 0.5 μmol.L-1 group(P<0.05). CONCLUSION Curcumin stimulates NSCs proliferation, possibly by inhibiting GR mRNA and related protein expression.
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Objective To investigate the effect of fungus Aspergillus fumigatus and Candida albicans on the expression of endocellular interferon-γ (IFN-γ) and interleukin-4 (IL-4) in cytokineinduced natural killer (NK) cells.Methods NK cells were cultured with Aspergillusfumigatus or Candida albicans by non-contact or direct-contact methods with a ratio of NK cells to fungus of 10 ∶ 1.The expressions of IFN-γ and IL-4 in NK cells were evaluated by flow cytometry after co-cultured for 6 h.Analysis of variance or SNK-q test was used to compare the expressions of IFN-γ and IL-4 among different groups.Results The IFN-γexpression rates in NK cells with direct contacting to Aspergillus fumigatus hyphae,or to different morphotypes of Candida albicans were (20.12 ± 0.53) ％,(20.69 ± 0.34) ％ and (20.8 ±0.37)％ respectively,while IFN-γexpression in NK cells with indirect contacting to fumigatus hyphae,or to different morphotypes of Candida albicans were (21.40 ± 0.53) ％,(20.57 ± 1.09) ％ and (20.20 ±0.51) ％ respectively,and all were significantly higher than that in the blank group [(15.11 ± 2.60) ％,all P ＞ 0.05].The IFN-γ expression rates in the Aspergillus fumigatus spores direct and indirect contacting groups were (14.33 ± 0.98) ％ and (14.97 ± 1.53) ％,which were not of significant difference compared with the blank group (P ＞ 0.05).The IL-4 expression rates in NK cells with direct contacting to different morphotypes of Aspergillus fumigatus and Candida albicans were (1.25 ± 0.06) ％,(1.21 ± 0.03) ％,(1.22 ± 0.46) ％ and (1.26 ± 0.11) ％,while those in indirect contacting groups were (1.21 ± 0.06) ％,(1.25 ±0.04)％,(1.27 ±0.03)％ and (1.26 ±0.1)％,which were not of significant difference compared with the blank group [(1.23 ± 0.05) ％,all P ＞ 0.05].Conclusion Fungus stimuli can reduce the secretion of IFN-γ in NK cells,but have not significant influence on the secretion of IL-4.
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[ ABSTRACT] AIM: To study the autophagy of prostate cancer PC-3 cells induced by CD147 in vitro.ME-THODS:Themethod of amino acid starvation to induce autophagy was used.The expression of CD147 was detected by Western blotting.To study the functional effects of CD147 on autophagy in prostate cancer PC-3 cells, the down-regulation of CD147 expression was induced by the technique of RNAi.The conversion of autophagic marker protein LC3-I to LC3-II was determined by Western blotting.The cell death after starvation-induced autophagy was analyzed by trypan blue exclu-sion assay.RESULTS:The CD147 expression gradually increased in starvation-induced autophagy.The down-regulation of CD147 significantly increased the expression of autophagy-related protein LC3-II compared with control group.Mean-while, the cell death rates increased from (19.3 ±3.1)%and (22.3 ±3.5)%in control groups to (38.4 ±3.1)%in si-lencing the expression of CD147 in the PC-3 cells (P<0.05).CONCLUSION:CD147 inhibits starvation-induced auto-phgy and autophagy death in the prostate cancer PC-3 cells.