A theoretical description of the coexistence curves of binary and some ternary systems has been developed using methods of statistical geometry. It is based on the concept that macroscopically any molecular species in a solution is distributed at random and that every system composition on the binodal is a geometrically saturated solution of each solute in the presence of the other. The link between the model and thermodynamics is also established. The model has been applied to aqueous polydisperse polymer two-phase systems, and it is shown that when the molecular weights of the two phase-forming components are rather disparate, only one parameter, the effective excluded volume, is needed to reproduce experimental coexistence curves for polyethylene glycol-Dextran-water systems. The current model has been compared with some other approaches (lattice solution theories, treatments based on the Setschenow equation) and the deficiencies of the Setschenow equation and the current model have been commented on.

Edwardsiella piscicida is a leading fish pathogen that causes significant economic loses in the aquaculture industry. The pathogen depends on type III and type VI secretion systems (T3/T6SS) for growth and virulence in fish and the expression of both systems is controlled by the EsrB transcription activator. Here, we performed a Tn-seq-based screen to uncover factors that govern esrB expression. Unexpectedly, we discovered that RpoS antagonizes esrB expression and thereby inhibits production of E. piscicida’s T3/T6SS. Using in vitro transcription assays, we showed that RpoS can block RpoD-mediated transcription of esrB. ChIP-seq- and RNA-seq-based profiling, as well as mutational and biochemical analyses revealed that RpoS-repressed promoters contain a -6G in their respective discriminator sequences; moreover, this -6G proved critical for RpoS to inhibit esrB expression. Mutation of the RpoS R99 residue, an amino acid that molecular modeling predicts interacts with -6G in the esrB discriminator, abolished RpoS’ capacity for repression. In a turbot model, an rpoS deletion mutant was attenuated early but not late in infection, whereas a mutant expressing RpoSR99A exhibited elevated fitness throughout the infection period. Collectively, these findings deepen our understanding of how RpoS can inhibit gene expression and demonstrate the temporal variation in the requirement for this sigma factor during infection.

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Co–N–GA is synthesized and presents better HER activity in an acidic environment than almost all non-precious metal catalysts.