No abstract

We demonstrate, via simulations of asymptotically reduced equations describing rotationally constrained Rayleigh-Bénard convection, that the efficiency of turbulent motion in the fluid bulk limits overall heat transport and determines the scaling of the nondimensional Nusselt number Nu with the Rayleigh number Ra, the Ekman number E, and the Prandtl number σ. For E << 1 inviscid scaling theory predicts and simulations confirm the large Ra scaling law Nu-1 ≈ C(1)σ(-1/2)Ra(3/2)E(2), where C(1) is a constant, estimated as C(1) ≈ 0.04 ± 0.0025. In contrast, the corresponding result for nonrotating convection, Nu-1 ≈ C(2)Ra(α), is determined by the efficiency of the thermal boundary layers (laminar: 0.28 ≤ α ≤ 0.31, turbulent: α ~ 0.38). The 3/2 scaling law breaks down at Rayleigh numbers at which the thermal boundary layer loses rotational constraint, i.e., when the local Rossby number ≈ 1. The breakdown takes place while the bulk Rossby number is still small and results in a gradual transition to the nonrotating scaling law. For low Ekman numbers the location of this transition is independent of the mechanical boundary conditions.

Notch signaling has been extensively implicated in cell-fate determination along the development of the immune system. However, a role for Notch signaling in fully differentiated immune cells has not been clearly defined. We have analyzed the expression of Notch protein family members during macrophage activation. Resting macrophages express Notch-1, -2, and -4, as well as the Notch ligands Jagged-1 and -2. After treatment with LPS and/or IFN-γ, we observed a p38 MAPK-dependent increase in Notch-1 and Jagged-1 mRNA and protein levels. To study the role of Notch signaling in macrophage activation, we forced the transient expression of truncated, active intracellular Notch-1 (Notch-IC) proteins in Raw 264.7 cells and analyzed their effects on the activity of transcription factors involved in macrophage activation. Notch-IC increased STAT-1-dependent transcription. Furthermore, Raw 264.7 Notch-IC stable transfectants increased STAT1-dependent transcription in response to IFN-γ, leading to higher expression of IFN regulatory factor-1, suppressor of cytokine signaling-1, ICAM-1, and MHC class II proteins. This effect was independent from an increase of STAT1 Tyr or Ser phosphorylation. However, inducible NO synthase expression and NO production decreased under the same conditions. Our results show that Notch up-regulation and subsequent signaling following macrophage activation modulate gene expression patterns known to affect the function of mature macrophages.