The Kelvin-Helmholtz instability in Orion: a source of turbulence and chemical mixing

Hydrodynamical instabilities are believed to power some of the small scale (0.1-10 pc) turbulence and chemical mixing in the interstellar medium. Identifying such instabilities has always been difficult but recent observations of a wavelike structure (the Ripples) in the Orion nebula have been interpreted as a signature of the Kelvin-Helmholtz instability (KHI), occurring at the interface between the HII region and the molecular cloud. However, this has not been verified theoretically. In this letter, we investigate theoretically the stability of this interface using observational constraints for the local physical conditions. A linear analysis shows that the HII/molecular cloud interface is indeed KH unstable for a certain range of magnetic field orientation. We find that the maximal growth-rates correspond to typical timescales of a few 1e4 years and instability wavelengths of 0.06 to 0.6 pc. We predict that after 2e5 years the KHI saturates and forms a turbulent layer of thickness ~0.5 pc. The KHI can remain in linear phase over a maximum distance of 0.75 pc. These spatial and time scales are compatible with the Ripples representing the linear phase of the KHI. These results suggest that the KHI may be crucial to generate turbulence and to bring heavy elements injected by the winds of massive stars in HII regions to colder regions where planetary systems around low mass stars are being formed. This could apply to the transport of 26Al injected by a massive star in an HII region to the nascent solar-system.Comment: Accepted for publication in ApJ Letter

<ORIGINAL ARTICLE>Inhibitory effects of extracellular ATP on the Ca^<2+> mobilization evoked by muscarinic stimulation in rat parotid acinar cells

In rat parotid acinar cells, extracellular ATP reduced the increase in cytosolic Ca^ concentration ([Ca^]_i) induced by the muscarinic receptor agonist carbachol (CCh) dose-dependently. This inhibitory effect was also observed in the absence of extracellular Ca^, indicating that the Ca^ release from intracellular Ca^ stores was prevented by ATP. Formation of inositol trisphosphate induced by CCh stimulation was strongly attenuated in the presence of extracellular ATP, suggesting that the effect of ATP on the CCh-induced [Ca^]_i response was the result of a decreased phosphoinositide hydrolysis. Extracellular ATP had no effect on the CCh-induced increase in [Ca^] j in rat lacrimal acinar cells that lack the purinergic receptors. This result supports the view that the inhibitory effect of ATP on the CCh-induced [Ca^]_i response in parotid acinar cells is mediated through activation of the purinergic receptros. In rat parotid acinar cells, the purinergic receptors may play a role in modulating the activity of muscarinic receptors