The protection of AC microgrids (MGs) is an issue of paramount importance to ensure their reliable and safe operation. Designing reliable protection mechanism, however, is not a trivial task, as many practical issues need to be considered. The operation mode of MGs, which can be grid-connected or islanded, employed control strategy and practical limitations of the power electronic converters that are utilized to interface renewable energy sources and the grid, are some of the practical constraints that make fault detection, classification, and coordination in MGs different from legacy grid protection. This article aims to present the state-of-the-art of the latest research and developments, including the challenges and issues in the field of AC MG protection. A broad overview of the available fault detection, fault classification, and fault location techniques for AC MG protection and coordination are presented. Moreover, the available methods are classified, and their advantages and disadvantages are discussed.

Escherichia coli transferred from pHo 7.0 to pHo 5.5 or 6.0 became alkali-sensitive by a rapidly induced phenotypic response. Alkali sensitization was reduced at pHo 5.0 and virtually abolished at pHo 6.5. The response was triggered by cytoplasmic rather than external or periplasmic acidification and de novo protein synthesis was needed. Alkali sensitivity failed to appear at pHo 5.5 plus DNA gyrase inhibitors and was markedly reduced by himA, himD, hns, ompC and nhaA lesions. A tonB deletion mutant showed alkali sensitivity at pHo 7.0. Alkali sensitivity induction was not subject to catabolite repression nor was it appreciably affected by a relA lesion. Acid-induced cells were more sensitive to alkali damage to both DNA and beta-galactosidase and to alkali inhibition of beta-galactosidase induction. Alkali sensitization induced at pHo 5.5 may involve NhaB loss.

become alkali sensitized on transfer from pH 7·0 to pH 5·5 but they also secrete extracellular agents which induce alkali sensitivity when added (in neutralized filtrates) to organisms growing at pH 7·0. In contrast, filtrates from cultures grown at pH 7·0 have no effect. Filtrates were inactivated by protease but not by heat treatment in a boiling water-bath, suggesting that a very heat-stable protein is involved in alkali sensitivity induction. A heatstable low molecular weight component (or components) may also be needed for induction, or the induction protein itself may be of low molecular weight. Strains with lesions in hns, fur or himA produced almost inactive filtrates and it therefore appears that H-NS, Fur and IHF are involved in synthesis of the induction components. As the presence of protease during incubation at pH 5·5 totally abolished alkali sensitization of strain 1829 while inhibition of sensitization induction occurred if the induction components were removed by filtration or dialysis during pH 5·5 incubation, it is proposed that the extracellular induction components (EICs) are essential for the original sensitization response. These results suggest that sensitization induction occurs by a different mechanism to that which is believed to occur for most bacterial inducible response systems; these are claimed to involve exclusively intracellular reactions and components whereas the present response involves functioning of extracellular components.

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