835 research outputs found

    Water Ice and Dust in the Innermost Coma of Comet 103P/Hartley 2

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    On November 4th, 2010, the Deep Impact eXtended Investigation (DIXI) successfully encountered comet 103P/Hartley 2, when it was at a heliocentric distance of 1.06 AU. Spatially resolved near-IR spectra of comet Hartley 2 were acquired in the 1.05-4.83 micron wavelength range using the HRI-IR spectrometer. We present spectral maps of the inner ~10 kilometers of the coma collected 7 minutes and 23 minutes after closest approach. The extracted reflectance spectra include well-defined absorption bands near 1.5, 2.0, and 3.0 micron consistent in position, bandwidth, and shape with the presence of water ice grains. Using Hapke's radiative transfer model, we characterize the type of mixing (areal vs. intimate), relative abundance, grain size, and spatial distribution of water ice and refractories. Our modeling suggests that the dust, which dominates the innermost coma of Hartley 2 and is at a temperature of 300K, is thermally and physically decoupled from the fine-grained water ice particles, which are on the order of 1 micron in size. The strong correlation between the water ice, dust, and CO2 spatial distribution supports the concept that CO2 gas drags the water ice and dust grains from the nucleus. Once in the coma, the water ice begins subliming while the dust is in a constant outflow. The derived water ice scale-length is compatible with the lifetimes expected for 1-micron pure water ice grains at 1 AU, if velocities are near 0.5 m/s. Such velocities, about three order of magnitudes lower than the expansion velocities expected for isolated 1-micron water ice particles [Hanner, 1981; Whipple, 1951], suggest that the observed water ice grains are likely aggregates.Comment: 51 pages, 12 figures, accepted for publication in Icaru

    Uncorrelated Volatile Behavior during the 2011 Apparition of Comet C/2009 P1 Garradd

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    The High Resolution Instrument Infrared Spectrometer (HRI-IR) on board the Deep Impact Flyby spacecraft detected H2O, CO2, and CO in the coma of the dynamically young Oort Cloud comet C/2009 P1 (Garradd) post-perihelion at a heliocentric distance of 2 AU. Production rates were derived for the parent volatiles, Q_(H2O) = 4.6 ± 0.8 × 10^(28), Q_(CO2) = 3.9 ± 0.7 × 10^(27), and Q_(CO) = 2.9 ± 0.8 × 10^(28) molecules s^(–1), and are consistent with the trends seen by other observers and within the error bars of measurements acquired during a similar time period. When compiled with other observations of Garradd's dominant volatiles, unexpected behavior was seen in the release of CO. Garradd's H_2O outgassing, increasing and peaking pre-perihelion and then steadily decreasing, is more typical than that of CO, which monotonically increased throughout the entire apparition. Due to the temporal asymmetry in volatile release, Garradd exhibited the highest CO to H_2O abundance ratio ever observed for any comet inside the water snow line at ~60% during the HRI-IR observations. Also, the HRI-IR made the only direct measurement of CO_2, giving a typical cometary abundance ratio of CO_2 to H_2O of 8% but, with only one measurement, no sense of how it varied with orbital position

    YAP/TAZ Activation Drives Uveal Melanoma Initiation and Progression

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    Uveal melanoma (UM), the most common ocular malignancy, is characterized by GNAQ/11 mutations. Hippo/YAP and Ras/mitogen-activated protein kinase (MAPK) emerge as two important signaling pathways downstream of G protein alpha subunits of the Q class (GalphaQ/11)-mediated transformation, although whether and how they contribute to UM genesis in vivo remain unclear. Here, we adapt an adeno-associated virus (AAV)-based ocular injection method to directly deliver Cre recombinase into the mouse uveal tract and demonstrate that Lats1/2 kinases suppress UM formation specifically in uveal melanocytes. We find that genetic activation of YAP, but not Kras, is sufficient to initiate UM. We show that YAP/TAZ activation induced by Lats1/2 deletion cooperates with Kras to promote UM progression via downstream transcriptional reinforcement. Furthermore, dual inhibition of YAP/TAZ and Ras/MAPK synergizes to suppress oncogenic growth of human UM cells. Our data highlight the functional significance of Lats-YAP/TAZ in UM initiation and progression in vivo and suggest combination inhibition of YAP/TAZ and Ras/MAPK as a new therapeutic strategy for UM
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