Triangular flow in event-by-event ideal hydrodynamics in Au+Au collisions at √SNN = 200A GeV

The first calculation of triangular flow ν3 in Au+Au collisions at √sNN = 200A GeV from an event-by-event (3 + 1) d transport+hydrodynamics hybrid approach is presented. As a response to the initial triangularity Ie{cyrillic, ukrainian}3 of the collision zone, ν3 is computed in a similar way to the standard event-plane analysis for elliptic flow ν2. It is found that the triangular flow exhibits weak centrality dependence and is roughly equal to elliptic flow in most central collisions. We also explore the transverse momentum and rapidity dependence of ν2 and ν3 for charged particles as well as identified particles. We conclude that an event-by-event treatment of the ideal hydrodynamic evolution startingwith realistic initial conditions generates the main features expected for triangular flow. © 2010 The American Physical Society.

Regulation of DLK-1 kinase activity by calcium-mediated dissociation from an inhibitory isoform.

MAPKKK dual leucine zipper-bearing kinases (DLKs) are regulators of synaptic development and axon regeneration. The mechanisms underlying their activation are not fully understood. Here, we show that C. elegans DLK-1 is activated by a Ca(2+)-dependent switch from inactive heteromeric to active homomeric protein complexes. We identify a DLK-1 isoform, DLK-1S, that shares identical kinase and leucine zipper domains with the previously described long isoform DLK-1L but acts to inhibit DLK-1 function by binding to DLK-1L. The switch between homo- or heteromeric DLK-1 complexes is influenced by Ca(2+) concentration. A conserved hexapeptide in the DLK-1L C terminus is essential for DLK-1 activity and is required for Ca(2+) regulation. The mammalian DLK-1 homolog MAP3K13 contains an identical C-terminal hexapeptide and can functionally complement dlk-1 mutants, suggesting that the DLK activation mechanism is conserved. The DLK activation mechanism is ideally suited for rapid and spatially controlled signal transduction in response to axonal injury and synaptic activity.