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This study identifies and summarizes potential risks to operations, regulatory compliance, supply chains, and infrastructure of the electric power industry from changing surface water conditions resulting from global climate change. The results help inform companies/utilities seeking to incorporate climate change risk in their planning and decision‐making processes by ranking risk severity and likelihood of occurrence on both a regional basis and by risk receptor. The assessment includes identification of potential risks to: (1) thermal generating, (2) hydroelectric, (3) land‐based renewable generating, and (4) transmission and distribution assets. These risks may result from such projected changes as reduced water availability (e.g., for hydroelectric or once‐through cooling), increased water temperatures (e.g., decrease in cooling efficiency, inability to meet discharge permit conditions), increased flood severity (e.g., increased streambank erosion and/or damage to river‐adjacent infrastructure), and decreased water quality (e.g., from increased transport of sediment and dissolved solids). The potential risks identified from this qualitative risk‐assessment are documented in a graphical format depicting both severity and likelihood. This approach allows for comparison of risks across a portfolio and for future prioritization of adaptation strategies. A total of 32 risks were identified in the study, including nine risks to infrastructure, six risks to operations, four risks to supply chain, and 13 environmental/regulatory risks. [ABSTRACT FROM AUTHOR]

Life span was measured by counting budding cycles in cohorts of yeast cells treated with erythromycin, paraquat, or geneticin. Paraquat treatment increases oxidative stress; geneticin treatment increases errors during cytoplasmic protein synthesis. Treating with either or both compounds resulted in shorter life spans. Saccharomyces cerevisiae strain K65-3D grown in 16 [micro]g/ml erythromycin, a treatment that results in more accurate protein synthesis by bacteria, had a mean life span that was significantly longer (27%) than that of untreated yeast cells. The life spans of petite variants with no detectable respiratory activity or extranuclear DNA were not affected by this dose of erythromycin, which appeared, therefore, to exert its effect on aging by means of mitochondria. Fitting the data to Weibull and Gompertz distributions allowed calculation of an accelerated life model that relates life span to dose of erythromycin.

Macrolide antibiotics bind to the large subunit of procaryotic ribosomes and perturb protein synthesis. There are two competing models to explain this perturbation: (1) shortly after initiation of the polypeptide chain, peptide bond formation and/or translocation is inhibited by the presence of macrolides that are bound in the ribosome ‘tunnel’ through which the nascent peptide travels; (2) bound macrolides loosen the interaction between the ribosome and peptidyl-tRNA, which therefore, dissociates with a higher probability. The former view cannot easily explain the observed enhancement by macrolides of the dissociation of peptidyl-tRNAs from ribosomes, while the latter view is consistent with the available data. Peptidyl-tRNAs are bound to ribosomes through non-specific and decoding-specific interactions. If macrolides preferentially weaken the non-specific interactions, a greater fraction of the binding energy will be due to decoding-specific interactions and better discrimination between erroneous and correct peptidyl-tRNAs should result. This idea has been tested with low doses of erythromycin, which was observed to counteract the error-inducing effects of streptomycin and of ethanol on the synthesis of β-galactosidase by Escherichia coli. A specific error near the C-terminus of the enzyme was also responsive to this effect of erythromycin, which therefore must have exerted its influence long after the initiation of the polypeptide synthesis. These results are more easily explained by the idea that the primary mechanism of inhibition of protein synthesis by macrolides is to stimulate the dissociation of peptidyl-tRNA from the ribosome. [ABSTRACT FROM PUBLISHER]