A mathematical technique for integrating growth and thermal inactivation models of microorganisms into a smooth combined model that can be applied to circumstances under which the temperature gradually rises from growth to inactivation regions is described. For the death part of the model, a correction term is introduced to allow for additional resistance of the cells gained during slow heating. The model was validated with Brochothrix thermosphacta heated in broth at rising temperatures.

Escherichia coli is a well-studied bacterium that can be found in many niches, such as industrial wastewater, where the concentration of nickel can rise to low-millimolar levels. Recent studies show that nickel exposure can repress pyochelin or induce pyoverdine siderophore production in Pseudomonas aueroginosa. Understanding the molecular cross-talk between siderophore production, metal homeostasis, and metal toxicity in microorganisms is critical for designing bioremediation strategies for metal-contaminated sites. Here, we show that high-nickel exposure prolongs lag phase duration as a result of low-intracellular iron levels in E. coli. Although E. coli cells respond to low-intracellular iron during nickel stress by maintaining high expression of iron uptake systems such as fepA, the demand for iron is not met due to a lack of siderophores in the extracellular medium during nickel stress. Taken together, these results indicate that nickel inhibits iron accumulation in E. coli by reducing the presence of enterobactin in the extracellular medium.