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Avycaz combines an older cephalosporin antibiotic, ceftazidime, and the β-lactamase inhibitor avibactam. Ceftazidime targets penicillin-binding proteins (PBPs) in the bacterial periplasm that are required for cell wall synthesis. Avibactam blocks β-lactamases (β-L) in the periplasm, which would otherwise inactivate the antibiotics resulting in drug resistance.
How do antibiotics actually work? Although the primary cellular targets of many antimicrobial agents have been identified, the downstream events leading to bacterial cell death remain unclear. In this issue, Kohanski et al. (2007) provide evidence that the production of reactive oxygen species is a shared mechanism of cell death initiated by bactericidal antibiotics.
Increased leukocyte elastase activity in mice lacking secretory leukocyte protease inhibitor (SLPI) leads to impaired wound healing due to enhanced activity of TGFβ and perhaps additional mechanisms. Proepithelin (PEPI), an epithelial growth factor, can be converted to epithelins (EPIs) in vivo by unknown mechanisms with unknown consequences. We found that PEPI and EPIs exert opposing activities....
Bacterial resistance to aminoglycoside antibiotics is almost exclusively accomplished through either phosphorylation, adenylylation, or acetylation of the antibacterial agent. The aminoglycoside kinase, APH(3')-III a, catalyzes the phosphorylation of a broad spectrum of aminoglycoside antibiotics. The crystal structure of this enzyme complexed with ADP was determined at 2.2 Å resolution. The three-dimensional...
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