Large Eddy Simulation of stratified flows over structures

We tested the ability of the LES model CLMM (Charles University Large-Eddy Microscale Model) to model the stratified flow around three dimensional hills. We compared the quantities, as the height of the dividing streamline, recirculation zone length or length of the lee waves with experiments by Hunt and Snyder[3] and numerical computations by Ding, Calhoun and Street[5]. The results mostly agreed with the references, but some important differences are present

Výzkum modelů pro šíření emisí znečišťujících látek:Výzkum modelů pro šíření emisí znečišťujících látek

Vznik, transport a rozptyl fotochemického smogu. Závislost na meteorologických podmínkách (modely). Porovnání lagrangeovského a eulerovského přístupu. Používané chemické mechanismy. Příklady fotochemických modelů

Výzkum modelů pro šíření emisí znečišťujících látek:Výzkum modelů pro šíření emisí znečišťujících látek

Chemickým transportním modelem vhodným pro každodenní rutinní provoz je model eulerovského typu, např. CTM CAMx. Lagrangeovský přístup (CTM SMOG) je vhodný např. pro případové studie o vysokém rozlišení nebo studie, v nichž se jedná o určení podílu jednotlivých zdrojů na tvorbě hodnoty koncentrace fotochemického smogu

Inhibition by Glucagon of the cGMP-inhibited Low-K, cAMP Phosphodiesterase in Heart Is Mediated by a Pertussis Toxin-sensitive G-protein"

International audienceWe have recently reported that glucagon activated the L-type Ca2+ channel current in frog ventricular myocytes and showed that this was linked to the inhibition of a membrane-bound low-Km cAMP phosphodiesterase (PDE) (Méry, P. F., Brechler, V., Pavoine, C., Pecker, F., and Fischmeister, R. (1990) Nature 345, 158-161). We show here that the inhibition of membrane-bound PDE activity by glucagon depends on guanine nucleotides, a reproducible inhibition of 40% being obtained with 0.1 microM glucagon in the presence of 10 microM GTP, with GTP greater than GTP gamma S, while GDP and ATP gamma S were without effect. Glucagon had no effect on the cytosolic low-Km cAMP PDE, assayed with or without 10 microM GTP. Glucagon inhibition of membrane-bound PDE activity was not affected by pretreatment of the ventricle particulate fraction with cholera toxin. However, it was abolished after pertussis toxin pretreatment. Mastoparan, a wasp venom peptide known to activate G(i)/G(o) proteins directly, mimicked the effect of glucagon. PDE inhibition by glucagon was additive with the inhibition induced by Ro 20-1724, but was prevented by milrinone. This was correlated with an increase by glucagon of cAMP levels in frog ventricular cells which was not additive with the increase in cAMP due to milrinone. We conclude that glucagon specifically inhibits the cGMP-inhibited, milrinone-sensitive PDE (CGI-PDE). Insensitivity of adenylylcyclase to glucagon and inhibition by the peptide of a low-Km cAMP PDE were not restricted to frog heart, but also occurred in mouse and guinea pig heart. These results confirm that two mechanisms mediate the action of glucagon in heart: one is the activation of adenylylcyclase through Gs, and the other relies on the inhibition of the membrane-bound low-Km CGI-PDE, via a pertussis toxin-sensitive G-protein