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      Very rapid flow cytometric assessment of antimicrobial susceptibility during the apparent lag phase of microbial (re)growth

      1 , 2 , 3 , 2 , 4 , 5 , 2 , 3 , 1

      Microbiology

      Microbiology Society

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          A common mechanism of cellular death induced by bactericidal antibiotics.

          Antibiotic mode-of-action classification is based upon drug-target interaction and whether the resultant inhibition of cellular function is lethal to bacteria. Here we show that the three major classes of bactericidal antibiotics, regardless of drug-target interaction, stimulate the production of highly deleterious hydroxyl radicals in Gram-negative and Gram-positive bacteria, which ultimately contribute to cell death. We also show, in contrast, that bacteriostatic drugs do not produce hydroxyl radicals. We demonstrate that the mechanism of hydroxyl radical formation induced by bactericidal antibiotics is the end product of an oxidative damage cellular death pathway involving the tricarboxylic acid cycle, a transient depletion of NADH, destabilization of iron-sulfur clusters, and stimulation of the Fenton reaction. Our results suggest that all three major classes of bactericidal drugs can be potentiated by targeting bacterial systems that remediate hydroxyl radical damage, including proteins involved in triggering the DNA damage response, e.g., RecA.
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            A Simple Statistical Parameter for Use in Evaluation and Validation of High Throughput Screening Assays

             J-H Zhang (1999)
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              A dynamic approach to predicting bacterial growth in food.

              A new member of the family of growth models described by Baranyi et al. (1993a) is introduced in which the physiological state of the cells is represented by a single variable. The duration of lag is determined by the value of that variable at inoculation and by the post-inoculation environment. When the subculturing procedure is standardized, as occurs in laboratory experiments leading to models, the physiological state of the inoculum is relatively constant and independent of subsequent growth conditions. It is shown that, with cells with the same pre-inoculation history, the product of the lag parameter and the maximum specific growth rate is a simple transformation of the initial physiological state. An important consequence is that it is sufficient to estimate this constant product and to determine how the environmental factors define the specific growth rate without modelling the environment dependence of the lag separately. Assuming that the specific growth rate follows the environmental changes instantaneously, the new model can also describe the bacterial growth in an environment where the factors, such as temperature, pH and aw, change with time.
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                Author and article information

                Journal
                Microbiology
                Microbiology Society
                1350-0872
                1465-2080
                April 01 2019
                April 01 2019
                : 165
                : 4
                : 439-454
                Affiliations
                [1 ] 1​School of Chemistry, The University of Manchester, 131 Princess St, Manchester M1 7DN, UK
                [2 ] 2​Manchester Institute of Biotechnology, The University of Manchester, 131 Princess St, Manchester M1 7DN, UK
                [3 ] 3​Firsway Health Centre, 121 Firs Way, Sale, Manchester M33 4BR, UK
                [4 ] 4​Faculty of Faculty of Biology, Medicine and Health, The University of Manchester, Manchester M13 9PT, UK
                [5 ] †​Present address: Department of Biochemistry, Institute of Integrative Biology, Faculty of Health and Life Sciences, University of Liverpool, Crown St, Liverpool L69 7ZB, UK.
                Article
                10.1099/mic.0.000777
                © 2019

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