The aim of this study was to evaluate the efficiency of sonication in releasing protein from a widespread lipase-producing yeast, Yarrowia lipolytica KKP 379, and to examine the impact of ultrasound waves generated in a horn-type sonicator on the lipolytic activity of Y. lipolytica in the hydrolysis of p-nitrophenyl laurate. In this paper, we focused on a few parameters of ultrasound cell disruption, such as the time of sonication, acoustic power, storage time of the frozen yeast biomass used in sonication and the solvent used to suspend the yeast cells which were considered as the most important part in the process of obtaining a biocatalyst from Y. lipolytica for organic synthesis. The most effective additive in protein release proved to be 2% Tween 80; other ideal parameters of the process were ultrasonic power at 150 W for 15 min and 9 weeks of frozen biomass storage time. The sonication parameters, which were the best for protein release, did not seem to be the most effective for obtaining high lipolytic activity due to denaturation as an effect of cavitation.
Vancomycin is a glycopeptide antibiotic that inhibits transpeptidation during cell wall synthesis by binding to the D-Ala-D-Ala termini of lipid II. For long, it has been used as a last resort antibiotic. However, since the emergence of the first vancomycin-resistant enterococci in 1987, vancomycin resistance has become widespread, especially in hospitals. We have synthesized and evaluated 110 vancomycin analogs modified at the C-terminal carboxyl group of the heptapeptide moiety with R2NHR1NH2 substituents. Through iterative optimizations of the substituents, we identified vancomycin analogs that fully restore (or even exceed) the original inhibitory activity against vancomycin-resistant enterococci (VRE), vancomycin-intermediate (VISA) and vancomycin-resistant Staphylococcus aureus (VRSA) strains. The best analogs have improved growth inhibitory activity and in vitro therapeutic indices against a broad set of VRE and methicillin-resistant S. aureus (MRSA) isolates. They also exceed the activity of vancomycin against Clostridium difficile ribotypes. Vanc-39 and Vanc-42 have a low probability to provoke antibiotic resistance, and overcome different vancomycin resistance mechanisms (VanA, VanB, and VanC1).
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