Currently, the most common way to reduce blinking in quantum dots (QDs) is accomplished by using very thick and/or perfectly crystalline CdS shells on CdSe cores. Ideally, a nontoxic material such as ZnS is preferred to be the outer material in order to reduce environmental and cytotoxic effects. Blinking suppression with multishell configurations of CdS and ZnS has been reported only for "giant" QDs of 15 nm or more. One of the main reasons for the limited progress is that the role that interfacial trap states play in blinking in these systems is not very well understood. Here, we show a "Goldilocks" effect to reduce blinking in small (∼7 nm) QDs by carefully controlling the thicknesses of the shells in multishell QDs. Furthermore, by correlating the fluorescence lifetime components with the fraction of time that a QD spends in the on-state, both with and without applying a threshold, we found evidence for two types of blinking that separately affect the average fluorescence lifetime of a single QD. A thorough characterization of the time-resolved fluorescence at the ensemble and single-particle level allowed us to propose a detailed physical model involving both short-lived interfacial trap states and long-lived surface trap states that are coupled. This model highlights a strategy of reducing QD blinking in small QDs by balancing the magnitude of the induced lattice strain, which results in the formation of interfacial trap states between the inner shell and the outer shell, and the confinement potential that determines how accessible the interfacial trap states are. The combination of reducing blinking while maintaining a small overall QD size and using a Cd-free outer shell of ZnS will be useful in a wide array of applications, particularly for advanced bioimaging.

To investigate the mechanism of action by which farnesol functions as an antibacterial agent and inhibits Staphylococcus aureus growth, the growth rates of S. aureus cultured in farnesol versus S. aureus cultured in farnesol and supplemented with 3-hydroxy-3-methylglutaryl (HMG)-CoA or mevalonate were compared. The investigation was designed to observe whether farnesol affected on the mevalonate pathway by using the intermediate metabolites of the pathway. The resulting growth curves demonstrated that mevalonate reduced the antibacterial activity of farnesol, but HMG-CoA did not inhibit farnesol. These results suggest that farnesol affects the mevalonate pathway. Moreover, farnesol inhibited HMG-CoA reductase activity in an in vitro enzymatic assay.