Dynamics of seismogenic volcanic extrusion at Mount St Helens in 2004-05

The 2004-05 eruption of Mount St Helens exhibited sustained, near-equilibrium behaviour characterized by relatively steady extrusion of a solid dacite plug and nearly periodic shallow earthquakes. Here we present a diverse data set to support our hypothesis that these earthquakes resulted from stick-slip motion along the margins of the plug as it was forced incrementally upwards by ascending, solidifying, gas-poor magma. We formalize this hypothesis with a dynamical model that reveals a strong analogy between behaviour of the magma-plug system and that of a variably damped oscillator. Modelled stick-slip oscillations have properties that help constrain the balance of forces governing the earthquakes and eruption, and they imply that magma pressure never deviated much from the steady equilibrium pressure. We infer that the volcano was probably poised in a near-eruptive equilibrium state long before the onset of the 2004-05 eruption.     

WNT7b mediates macrophage-induced programmed cell death in patterning of the vasculature

Macrophages have a critical role in inflammatory and immune responses through their ability to recognize and engulf apoptotic cells. Here we show that macrophages initiate a cell-death programme in target cells by activating the canonical WNT pathway. We show in mice that macrophage WNT7b is a short-range paracrine signal required for WNT-pathway responses and programmed cell death in the vascular endothelial cells of the temporary hyaloid vessels of the developing eye. These findings indicate that macrophages can use WNT ligands to influence cell-fate decisions--including cell death--in adjacent cells, and raise the possibility that they do so in many different cellular contexts.     

Mutations in ENPP1 are associated with 'idiopathic' infantile arterial calcification

Idiopathic infantile arterial calcification (IIAC; OMIM 208000) is characterized by calcification of the internal elastic lamina of muscular arteries and stenosis due to myointimal proliferation. We analyzed affected individuals from 11 unrelated kindreds and found that IIAC was associated with mutations that inactivated ecto-nucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1). This cell surface enzyme generates inorganic pyrophosphate (PP(i)), a solute that regulates cell differentiation and serves as an essential physiologic inhibitor of calcification.