Taking control.

The wet bulb globe temperature (WBGT) is the de facto standard to assess environmental contributions to heat stress. A practical problem emerges when the heat stress conditions vary over many locations or during the day. To address this problem, investigators have suggested empirical relationships and thermodynamic models. The purpose of this effort was to examine a thermodynamic model in the laboratory and to predict WBGTs in an aluminum smelter by both the empirical and thermodynamic models. In the laboratory, there was no real difference between the experimental data and the thermodynamic model. In the application to an aluminum smelter, there was a small overall tendency for the predicted values to be greater than the actual values, but there was no practical difference between the models. The empirical model provided a good match with a slight over-prediction by 0.5 degree C with a standard deviation of 3.0 degrees C. For the same data, the thermodynamic model had an average over-prediction of 0.7 degree C with a standard deviation of 2.8 degrees C. Either method of predicting WBGT was effective. The empirical method required less computation and was conceptually simpler.

Heat Stress Disorders↗

PubMed1999

Analysis of phosphorylated sphingolipid long-chain bases reveals potential roles in heat stress and growth control in Saccharomyces.

Sphingolipid long-chain bases and their phosphorylated derivatives, for example, sphingosine-1-phosphate in mammals, have been implicated as signaling molecules. The possibility that Saccharomyces cerevisiae cells also use long-chain-base phosphates to regulate cellular processes has only recently begun to be examined. Here we present a simple and sensitive procedure for analyzing and quantifying long-chain-base phosphates in S. cerevisiae cells. Our data show for the first time that phytosphingosine-1-phosphate (PHS-1-P) is present at a low but detectable level in cells grown on a fermentable carbon source at 25 degreesC, while dihydrosphingosine-1-phosphate (DHS-1-P) is only barely detectable. Shifting cells to 37 degreesC causes transient eight- and fivefold increases in levels of PHS-1-P and DHS-1-P, respectively, which peak after about 10 min. The amounts of both compounds return to the unstressed levels by 20 min after the temperature shift. These data are consistent with PHS-1-P and DHS-1-P being signaling molecules. Cells unable to break down long-chain-base phosphates, due to deletion of DPL1 and LCB3, show a 500-fold increase in PHS-1-P and DHS-1-P levels, grow slowly, and survive a 44 degreesC heat stress 10-fold better than parental cells. These and other data for dpl1 or lcb3 single-mutant strains suggest that DHS-1-P and/or PHS-1-P act as signals for resistance to heat stress. Our procedure should expedite experiments to determine how the synthesis and breakdown of these compounds is regulated and how the compounds mediate resistance to elevated temperature.

Heat Stress Disorders↗