A new intrinsic thermal parameter for enzymes reveals true temperature optima

Two established thermal properties of enzymes are the Arrhenius activation energy and thermal stability. Arising from anomalies found in the variation of enzyme activity with temperature, a comparison has been made of experimental data for the activity and stability properties of five different enzymes with theoretical models. The results provide evidence for a new and fundamental third thermal parameter of enzymes, Teq, arising from a subsecond timescale-reversible temperature-dependent equilibrium between the active enzyme and an inactive (or less active) form. Thus, at temperatures above its optimum, the decrease in enzyme activity arising from the temperature-dependent shift in this equilibrium is up to two orders of magnitude greater than what occurs through thermal denaturation. This parameter has important implications for our understanding of the connection between catalytic activity and thermostability and of the effect of temperature on enzyme reactions within the cell. Unlike the Arrhenius activation energy, which is unaffected by the source (“evolved”) temperature of the enzyme, and enzyme stability, which is not necessarily related to activity, Teq is central to the physiological adaptation of an enzyme to its environmental temperature and links the molecular, physiological, and environmental aspects of the adaptation of life to temperature in a way that has not been described previously. We may therefore expect the effect of evolution on Teq with respect to enzyme temperature/activity effects to be more important than on thermal stability. Teq is also an important parameter to consider when engineering enzymes to modify their thermal properties by both rational design and by directed enzyme evolution

Enactment and retrieval

A number of memory phenomena are modulated by experimental design, with the effect (e.g. of bizarreness, generation, perceptual interference) occurring in recall for mixed-list but not pure-list designs. These effects have other similarities and have been treated in common theoretical frameworks, some focusing on encoding others on retrieval. The typical paradigm for examining design effects confounds encoding and retrieval contexts, making it difficult to compare these accounts. McDaniel et al. (2005), using a new paradigm, concluded that retrieval processes contribute to the bizarreness effect. This paradigm was applied to the related enactment effect. Participants were presented with two pure study lists, and later recalled the lists separately (inducing pure retrieval sets) or recalled the lists together in a single test (inducing a combined or mixed retrieval set). In three experiments, the combined recall condition consistently failed to enhance the size of the enactment effect. The results provide no support for the retrieval account of these two variables but are generally consistent with encoding accounts

More Tips: Communicating with Institutional Review Boards Over the Course of Your Project

This article focuses on the continuing review process required by Institutional Review Boards. It is a follow-up to a series of recent articles designed to help Extension Professionals navigate the university IRB process. The authors present general guidelines for the continuing review process and offer some issues and tips for success

What level of plasma homocyst(e)ine should be treated? Effects of vitamin therapy on progression of carotid atherosclerosis in patients with homocyst(e)ine levels above and below 14 μmol/L

High levels of plasma homocyst(e)ine (H[e]) are associated with increased vascular risk. Treatment is being contemplated, but the level at which patients should be treated is not known. We compared the response of carotid plaque to vitamin therapy in patients with H(e) above and below 14 μmol/L, a level commonly regarded as high enough to warrant treatment. Two-dimensional B-mode ultrasound measurement of carotid plaque was used to assess the response to vitamin therapy with folic acid 2.5 mg, pyridoxine 25 mg, and cyanocobalamin 250 μg daily, in 101 patients with vascular disease (51 with initial plasma levels above, and 50 below 14 μmol/L). Among patients with plasma H(e) \u3e14 μmol/L, the rate of progression of plaque area was 0.21 ± 0.41 cm2/year before vitamin therapy, and -0.049 ± 0.24 cm2/year after vitamin therapy (P2 = .0001; paired t test). Among patients with levels \u3c14 μmol/L, the rate of progression of plaque was 0.13 ± 0.24 cm2/ year before vitamin therapy and -0.024 ± 0.29 cm2/year after vitamin therapy (P2 = .022, paired t test). The change in rate of progression was -0.15 ± .44 cm2/year below 14 μmol/L, and -0.265 ± 0.46 cm2/year above 14 μmol/L (P = 0.20). Vitamin therapy regresses carotid plaque in patients with H(e) levels both above and below 14 μmol/L. These observations support a causal relationship between homocyst(e)ine and atherosclerosis and, taken with epidemiologic evidence, suggest that in patients with vascular disease, the level to treat may be \u3c9 μmol/L. © 2000 American Journal of Hypertension, Ltd