BackgroundMulti-drug-resistant Escherichia coli poses a great threat to human health, especially resistant to ampicillin (AMP), but the mechanism of drug resistance is not very clear.PurposeTo understand the mechanism of resistance of E. coli to beta-lactam antibiotics by inducing drug resistance of sensitive bacteria in laboratory.MethodsClinical sensitive E. coli strain was induced into resistance strain by 1/2 minimum inhibitive concentration (MIC) induced trails of AMP. The drug resistance spectrum was measured by modified K-B susceptibility test. Whole-genome sequencing analysis was used to analyze primary sensitive strain, and resequencing was used to analyze induced strains. Protein tertiary structure encoded by the gene containing single nucleotide polymorphism (SNP) was analyzed by bioinformatics.ResultsAfter 315 hrs induced, the MIC value of E. coli 15743 reached to 256 µg/mL, 64 times higher than that of the sensitive bacteria. During the induction process, the bacterial resistance process is divided into two stages. The rate of drug resistance occurs rapidly before reaching the critical concentration of 32 µg/mL, and then the resistance rate slows down. Sequencing of the genome of resistant strain showed that E. coli 15743 drug-resistant strain with the MIC values of 32 and 256 µg/mL contained four and eight non-synonymous SNPs, respectively. These non-synonymous SNPs were distributed in the genes of frdD, ftsI, acrB, OmpD, marR, VgrG, and envZ.ConclusionThese studies will improve our understanding of the molecular mechanism of AMP resistance of E. coli, and may provide the basis for prevention and control of multi-drug-resistant bacteria and generation of new antibiotics to treat E. coli infection.

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With excellent damping capacity, growing interest has been focused on polymer concrete (PC) as a novel machine tool bed material in the field of ultraprecision machining. It is widely acknowledged that the fly ash (FA) is an essential component material in reducing the curing shrinkage of PC, which can significantly affect the curing characteristic of PC. However, the effect of FA on the curing characteristic of epoxy resin is not studied in detail. In this article, the effect of FA on the curing characteristic of epoxy resin was examined by differential scanning calorimetry. Experimental results show that the peak temperature and curing rates of epoxy resin/curing agent and epoxy resin/curing agent/FA increase with the increasing heating rates, and the peak temperature and curing rates of epoxy resin/curing agent are greater than that of the epoxy resin/curing agent/FA with the same heating rates. In addition, the difference between the maximum curing rates of epoxy resin/curing agent and epoxy resin/curing agent/FA decreased with the increasing heating rates. This article can provide technical reference for curing process of PC for machine tool beds and further improve the machining accuracy.

BackgroundBacterial dysentery is an intestinal infectious disease caused by Shigella. The resistance of Shigella species to ampicillin has increased rapidly. Besides resistance, bacteria in a state of tolerance to antibiotics can also lead to the failure of infectious diseases therapy.PurposeThe genetic mechanism of antibiotic tolerance remains largely unexplored. The current study aimed to investigate the mechanisms of antibiotic tolerance and to provide novel strategies for the prevention of drug resistance of Shigella.MethodsWe exposed Shigella to lethal doses of ampicillin to obtain tolerant strain. The tolerant strain was sequenced to screen non-single-nucleotide polymorphisms and Indels. We also quantitated the relative expression of gene by RT-PCR.ResultsThere was one nonsynonymous mutation in the 2252304 loci of the cfa gene (G to A/Val to Met) and 10 Indels in the noncoding regions of different genes. The expression of the cfa gene was 7.56-fold higher in the tolerant strain than in the wild-type strain.ConclusionOur results showed that Shigella could be tolerated to ampicillin, and the cfa gene might be associated with antibiotic tolerance by increasing its expression. Our data suggest that cfa gene might be a target for overcoming drug tolerance, delaying the occurrence of drug resistance to some extent.