Increased bacterial growth efficiency with environmental variability: results from DOC degradation by bacteria in pure culture experiments.

This paper assesses how considering variation in DOC availability and cell maintenance in bacterial models affects Bacterial Growth Efficiency (BGE) estimations. For this purpose, we conducted two biodegradation experiments simultaneously. In experiment one, a given amount of substrate was added to the culture at the start of the experiment whilst in experiment two, the same amount of substrate was added, but using periodic pulses over the time course of the experiment. Three bacterial models, with different levels of complexity, (the Monod, Marr-Pirt and the dynamic energy budget – DEB – models), were used and calibrated using the above experiments. BGE has been estimated using the experimental values obtained from discrete samples and from model generated data. Cell maintenance was derived experimentally, from respiration rate measurements. The results showed that the Monod model did not reproduce the experimental data accurately, whereas the Marr-Pirt and DEB models demonstrated a good level of reproducibility, probably because cell maintenance was built into their formula. Whatever estimation method was used, the BGE value was always higher in experiment two (the periodically pulsed substrate) as compared to the initially one-pulsed-substrate experiment. Moreover, BGE values estimated without considering cell maintenance (Monod model and empirical formula) were always smaller than BGE values obtained from models taking cell maintenance into account. Since BGE is commonly estimated using constant experimental systems and ignore maintenance, we conclude that these typical methods underestimate BGE values. On a larger scale, and for biogeochemical cycles, this would lead to the conclusion that, for a given DOC supply rate and a given DOC consumption rate, these BGE estimation methods overestimate the role of bacterioplankton as CO<sub>2</sub> producers

Maintenance of GLUT4 expression in smooth muscle prevents hypertension‐induced changes in vascular reactivity

Previous studies have shown that expression of GLUT4 is decreased in arterial smooth muscle of hypertensive rats and mice and that total body overexpression of GLUT4 in mice prevents enhanced arterial reactivity in hypertension. To demonstrate that the effect of GLUT4 overexpression on vascular responses is dependent on vascular smooth muscle GLUT4 rather than on some systemic effect we developed and tested smooth‐muscle‐specific GLUT4 transgenic mice (SMG4). When made hypertensive with angiotensin II, both wild‐type and SMG4 mice exhibited similarly increased systolic blood pressure. Responsiveness to phenylephrine, serotonin, and prostaglandin F2α was significantly increased in endothelium‐intact aortic rings from hypertensive wild‐type mice but not in aortae of SMG4 mice. Inhibition of Rho‐kinase equally reduced serotonin‐stimulated contractility in aortae of hypertensive wild‐type and SMG4‐mice. In addition, acetylcholine‐stimulated relaxation was significantly decreased in aortic rings of hypertensive wild‐type mice, but not in rings of SMG4 mice. Inhibition of either prostacylin receptors or cyclooxygenase‐2 reduced relaxation in rings of hypertensive SMG4 mice. Inhibition of cyclooxygenase‐2 had no effect on relaxation in rings of hypertensive wild‐type mice. Cyclooxygenase‐2 protein expression was decreased in hypertensive wild‐type aortae but not in hypertensive SMG4 aortae compared to nonhypertensive controls. Our results demonstrate that smooth muscle expression of GLUT4 exerts a major effect on smooth muscle contractile responses and endothelium‐dependent vasorelaxation and that normal expression of GLUT4 in vascular smooth muscle is required for appropriate smooth muscle and endothelial responses.e12299In the smooth muscle of aortae of hypertensive mice, expression of GLUT4 is decreased. Maintenance of aortic smooth muscle GLUT4 expression prevents hypertension‐mediated changes in vasomotor response. These effects include decreasing/preventing endothelial dysfunction.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/110755/1/phy212299.pd