29 research outputs found

    Construction of the Galapagos platform by large submarine volcanic terraces

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    Author Posting. © American Geophysical Union, 2008. This article is posted here by permission of American Geophysical Union for personal use, not for redistribution. The definitive version was published in Geochemistry Geophysics Geosystems 9 (2008): Q03015, doi:10.1029/2007GC001795.New multibeam bathymetric and side-scan sonar data from the southwestern edge of the Galápagos platform reveal the presence of ∼60 large, stepped submarine terraces between depths of 800 m and 3500 m. These terraces are unique features, as none are known from any other archipelago that share this geomorphic form or size. The terraces slope seaward at 3000 m) lava flow fields west of Fernandina and Isabela Islands. The terraces are formed of thick sequences of lava flows that coalesce to form the foundation of the Galápagos platform, on which the subaerial central volcanoes are built. The compositions of basalts dredged from the submarine terraces indicate that most lavas are chemically similar to subaerial lavas erupted from Sierra Negra volcano on southern Isabela Island. There are no regular major element, trace element, or isotopic variations in the submarine lavas as a function of depth, relative stratigraphic position, or geographic location along the southwest margin of the platform. We hypothesize that magma supply at the western edge of the Galápagos hot spot, which is influenced by both plume and mid-ocean ridge magmatic processes, leads to episodic eruption of large lava flows. These large lava flows coalesce to form the archipelagic apron upon which the island volcanoes are built.This work was supported by the National Science Foundation grants OCE0002818 and EAR0207605 (D.G.), OCE0002461 (D.J.F. and M.K.), OCE05-25864 (M.K.), and EAR0207425 (K.H.)

    Hard Two-Photon Contribution to Elastic Lepton-Proton Scattering: Determined by the OLYMPUS Experiment

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    The OLYMPUS collaboration reports on a precision measurement of the positron-proton to electron-proton elastic cross section ratio, R2γR_{2\gamma}, a direct measure of the contribution of hard two-photon exchange to the elastic cross section. In the OLYMPUS measurement, 2.01~GeV electron and positron beams were directed through a hydrogen gas target internal to the DORIS storage ring at DESY. A toroidal magnetic spectrometer instrumented with drift chambers and time-of-flight scintillators detected elastically scattered leptons in coincidence with recoiling protons over a scattering angle range of 20°\approx 20\degree to 80°80\degree. The relative luminosity between the two beam species was monitored using tracking telescopes of interleaved GEM and MWPC detectors at 12°12\degree, as well as symmetric M{\o}ller/Bhabha calorimeters at 1.29°1.29\degree. A total integrated luminosity of 4.5~fb1^{-1} was collected. In the extraction of R2γR_{2\gamma}, radiative effects were taken into account using a Monte Carlo generator to simulate the convolutions of internal bremsstrahlung with experiment-specific conditions such as detector acceptance and reconstruction efficiency. The resulting values of R2γR_{2\gamma}, presented here for a wide range of virtual photon polarization 0.456<ϵ<0.9780.456<\epsilon<0.978, are smaller than some hadronic two-photon exchange calculations predict, but are in reasonable agreement with a subtracted dispersion model and a phenomenological fit to the form factor data.Comment: 5 pages, 3 figures, 2 table

    Vesicular Stomatitis Virus Infection Promotes Immune Evasion by Preventing NKG2D-Ligand Surface Expression

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    Vesicular stomatitis virus (VSV) has recently gained attention for its oncolytic ability in cancer treatment. Initially, we hypothesized that VSV infection could increase immune recognition of cancer cells through induction of the immune stimulatory NKG2D-ligands. Here we show that VSV infection leads to a robust induction of MICA mRNA expression, however the subsequent surface expression is potently hindered. Thus, VSV lines up with human cytomegalovirus (HCMV) and adenovirus, which actively subvert the immune system by negatively affecting NKG2D-ligand surface expression. VSV infection caused an active suppression of NKG2D-ligand surface expression, affecting both endogenous and histone deacetylase (HDAC)-inhibitor induced MICA, MICB and ULBP-2 expression. The classical immune escape mechanism of VSV (i.e., the M protein blockade of nucleocytoplasmic mRNA transport) was not involved, as the VSV mutant strain, VSVΔM51, which possess a defective M protein, prevented MICA surface expression similarly to wild-type VSV. The VSV mediated down modulation of NKG2D-ligand expression did not involve apoptosis. Constitutive expression of MICA bypassed the escape mechanism, suggesting that VSV affect NKG2D-ligand expression at an early post-transcriptional level. Our results show that VSV possess an escape mechanism, which could affect the immune recognition of VSV infected cancer cells. This may also have implications for immune recognition of cancer cells after combined treatment with VSV and chemotherapeutic drugs

    Impact on Patient Care of a Multidisciplinary Center Specializing in Colorectal and Pelvic Reconstruction

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    Aim of the study: Many patients with an anorectal malformation (ARM) or pelvic anomaly have associated urologic or gynecologic problems. We hypothesized that our multidisciplinary center, which integrates pediatric colorectal, urologic, gynecologic and GI motility services, could impact a patient's anesthetic exposures and hospital visits.Methods: We tabulated during 2015 anesthetic/surgical events, endotracheal intubations, and clinic/hospital visits for all patients having a combined procedure.Main results: Eighty two patients underwent 132 combined procedures (Table 1). The median age at intervention was 3 years [0.2-17], and length of follow up was 25 months [7-31]. The number of procedures in patients who underwent combined surgery was lower as compared to if they had been done independently [1(1-5) vs. 3(2-7) (p &lt; 0.001)]. Intubations were also lower [1[1-3] vs. 2[1-6]; p &lt; 0.001]. Hospital length of stay was significantly lower for the combined procedures vs. the theoretical individual procedures [8 days [3-20] vs. 10 days [4-16]] p &lt; 0.05. Post-operative clinic visits were fewer when combined visits were coordinated as compared to the theoretical individual clinic visits (urology, gynecology, and colorectal) [1[1-4] vs. 2[1-6]; p = &lt; 0.001].Conclusions: Patients with anorectal and pelvic malformations are likely to have many medical or surgical interventions during their lifetime. A multidisciplinary approach can reduce surgical interventions, anesthetic procedures, endotracheal intubations, and hospital/outpatient visits

    Entry of Herpes Simplex Virus Type 1 (HSV-1) into the Distal Axons of Trigeminal Neurons Favors the Onset of Nonproductive, Silent Infection

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    Following productive, lytic infection in epithelia, herpes simplex virus type 1 (HSV-1) establishes a lifelong latent infection in sensory neurons that is interrupted by episodes of reactivation. In order to better understand what triggers this lytic/latent decision in neurons, we set up an organotypic model based on chicken embryonic trigeminal ganglia explants (TGEs) in a double chamber system. Adding HSV-1 to the ganglion compartment (GC) resulted in a productive infection in the explants. By contrast, selective application of the virus to distal axons led to a largely nonproductive infection that was characterized by the poor expression of lytic genes and the presence of high levels of the 2.0-kb major latency-associated transcript (LAT) RNA. Treatment of the explants with the immediate-early (IE) gene transcriptional inducer hexamethylene bisacetamide, and simultaneous co-infection of the GC with HSV-1, herpes simplex virus type 2 (HSV-2) or pseudorabies virus (PrV) helper virus significantly enhanced the ability of HSV-1 to productively infect sensory neurons upon axonal entry. Helper-virus-induced transactivation of HSV-1 IE gene expression in axonally-infected TGEs in the absence of de novo protein synthesis was dependent on the presence of functional tegument protein VP16 in HSV-1 helper virus particles. After the establishment of a LAT-positive silent infection in TGEs, HSV-1 was refractory to transactivation by superinfection of the GC with HSV-1 but not with HSV-2 and PrV helper virus. In conclusion, the site of entry appears to be a critical determinant in the lytic/latent decision in sensory neurons. HSV-1 entry into distal axons results in an insufficient transactivation of IE gene expression and favors the establishment of a nonproductive, silent infection in trigeminal neurons

    Pediatric inflammatory bowel disease

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