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Objective To understand the drug resistance and changes of Pseudomonas aeruginosa in Tianjin Medical University Eye Hospita and to explore the relationship between the drug resistance and the dosage of antimicrobial agents, so as to provide the basis for clinical rational drug use.MethodsUsage of antibiotics in our hospital during 2012 to 2016 were analyzed retrospectively, and the drug resistance of pseudomonas aeruginosa were calculated respectively.SPSS 22.0 software was used to analyze the drug resistance and the frequency of use of antimicrobial agents (DDDs).ResultsResistance rate of pseudomonas aeruginosa to aztreonam, ceftazidime and meropenem were decreased gradually.Resistance rate of pseudomonas aeruginosa to gentamicin increased gradually.The resistance of pseudomonas aeruginosa to piperacillin, imipenem, cefepime, evil ciprofloxacin, piperacillin/tazobactam tazobactam and cefempidone/sulbactam is in a state of fluctuation.Piperacillin DDDs were significantly negatively correlated with gentamicin resistance.There was a significant positive correlation between imipenem DDDs and gentamicin resistance and there was a significant negative correlation between imipenem DDDs and drug resistance rates of piperacillin, imipenem, ceftazidime, meropenem, levofloxacin and cefoperazone/sulbactam.There was a significant positive correlation between aztreonam DDDs and ceftazidime, meropenem, ciprofloxacin and cefoperazone/sulbactam, There was a significant negative correlation between cephalosporin DDDs and gentamicin resistance rates.There was a significant positive correlation between the DDDs of piperacillin/tazobactam and the resistance rate of piperacillin/tazobactam;the resistance rates of cefoperazone/sulbactam DDDs to aztreonam and meropenem were Significant negative correlation.ConclusionDrug resistance of pseudomonas aeruginosa and the dosage of clinical antibacterial drug is closely related, suggesting that clinicians should use antibiotics for clinical rationally, in order to reduce the number of drug resistance of pseudomonas aeruginosa.
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Objective To explore the inhibitory effect of harmine on melanoma A375 cells and its mechanism thereof.Methods (1) Melanoma A375 cells were treated with harmine at 0,0.5,1,2,5,10,20,50 and 100 mg/L for 48 h in vitro.CCK-8 method was used to detect the cell viability and confirm the experimental concentrations.(2) After the cells were treated with 0,1,2 mg/L harmine,the scratch and transwell assays were used to detect the cell migration and invasion ability.Western blot assay was used to detect the expression levels of epithelial mesenchymal transition (EMT)-related protein E-cadherin,N-cadherin,Snail and p53.(3) Three groups of ceils were set up.The control group was transfected with empty vector ordy.The empty vector group was transfected with empty vector after treated with 2 mg/L harmine for 24 h.The Snail transfection group was transfected with Snail cDNA after treated with 2 mg/L harmine for 24 h.The cell migration and invasion ability were detected after the transfection.Results (1) When the concentration of harmine was above 2 mg/L,the survival rate of A375 cells was significantly lower than that of the control group with the increase of harmine concentrations (P ＜ 0.05).Then,the concentrations of 0,1 and 2 mg/L of harmine were used in the following experiments.(2) With the increase of the harmine concentrations,the number of cells in the scratched area and the number of trans-membrane cells in each group were significantly decreased.The migration and invasion ability of the ceils were decreased gradually.The expression levels of E-cadherin and p53 were increased,while the expression levels of N-cadherin and Snail were decreased.(3) Cell transfection experiments showed that the migration and invasion ability of the cells were increased compared with those of empty vector group after transfection with Snail.Conclusion Harmine can inhibit the proliferation of A375 cells and decrease the abilities of metastasis and invasion,which may be achieved by decreasing the expression of Snail after activating the p53,thereby increasing E-cadherin and down-regulating N-cadherin to inhibit the EMT process.
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Chemotherapy is one of the main treatments for gastric cancer, but its drug resistance often limits the effectiveness of chemotherapy, leading to treatment failure. Drug resistance can be divided into primary drug resistance and secondary resistance. It has showed that several factors were involved in the multidrug resistance of gastric cancer, including the expression of drug resistance-related proteins, abnormalities of apoptosis-related genes, dysfunction of DNA damage repair, epithelial-mesenchymal transition and non-coding RNA. The solution to improve the efficacy of chemotherapy is to overcome drug resistance or delay drug resistance. This article will explore the progress in multi-drug resistance of gastric cancer.