63 research outputs found

    Spatially resolving polycyclic aromatic hydrocarbons in Herbig Ae disks with VISIR-NEAR at the VLT

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    We use the long-slit spectroscopy mode of the VISIR-NEAR experiment to perform diffraction-limited observations of eight nearby Herbig Ae protoplanetary disks. We extract spectra for various locations along the slit with a spectral resolution of R = 300 and perform a compositional fit at each spatial location using spectral templates of silicates and the four PAH bands. This yields the intensity vs. location profiles of each species. Results. We could obtain spatially-resolved intensity profiles of the PAH emission features in the N-band for five objects (AB Aurigae, HD 97048, HD 100546, HD 163296, and HD 169142). We observe two kinds of PAH emission geometry in our sample: centrally-peaked (HD 97048) and ring-like (AB Aurigae, HD 100546, HD 163296, and potentially HD 169142). Comparing the spatial PAH emission profiles with near-infrared scattered light images, we find a strong correlation in the disk sub-structure but a difference in radial intensity decay rate. The PAH emission shows a less steep decline with distance from the star. Finally, we find a correlation between the presence of (sub-) micron-sized silicate grains leading to the depletion of PAH emission within the inner regions of the disks. In this work, we find the following: (1) PAH emission traces the extent of Herbig Ae disks to a considerable radial distance. (2) The correlation between silicate emission within the inner regions of disks and the depletion of PAH emission can result from dust-mixing and PAH coagulation mechanisms and competition over UV photons. (3) For all objects in our sample, PAHs undergo stochastic heating across the entire spatial extent of the disk and are not saturated. (4) The difference in radial intensity decay rates between the PAHs and scattered-light profiles may be attributed to shadowing and dust-settling effects, which affect the scattering grains more than the PAHs

    Antagonists of Growth Hormone-Releasing Hormone Inhibit the Growth of U-87MG Human Glioblastoma in Nude Mice

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    Antagonists of growth hormone-releasing hormone(GH-RH) inhibit the growth of various cancers by mechanisms that involve the suppression of the insulin-like growth factor (IGF) -I and/or IGF-II. In view of the importance of the IGF system in glioma tumorigenesis, the effects of GH-RH antagonists MZ-5-156 and JV-1-36 were investigated in nude mice bearing subcutaneous and orthotopic xenografts of U-87MG human glioblastomas. After 4 weeks of therapy with MZ-5-156 or JV-1-36 at the dose of 20 µmg/day per animal, the final volume of subcutaneous U-87MG tumors was significantly (P < .01) decreased by 84% and 76%, respectively, as compared with controls. Treatment with GHRH antagonists also reduced tumor weight and the levels of mRNA for IGF receptor type I (IGFR-I). A reduction in the mRNA levels for IGF-II was found in tumors of mice treated with MZ-5-156. Treatment with MZ-5-156 or JV-1-36 also extended the survival of nude mice implanted orthotopically with U-87MG glioblastomas by 81% (P < .005) and 18%, respectively, as compared with the controls. Exposure in vitro to GH-RH antagonists MZ-5-156 or JV-1-36 at 1 MM concentration for 24 hours decreased the tumorigenicity of U-87MG cells in nude mice by 10% to 30% and extended the latency period for the development of subcutaneous palpable tumors by 31% to 56%, as compared with the controls. Exposure of U-87MG cells to GH-RH antagonists in vitro also resulted in a time-dependent increase in the mRNA levels of IGFR-II or a decrease in the mRNA levels of IGFR-I. mRNA for GH-RH was detected in U87MG cells and xenografts implying that GH-RH may play a role in the pathogenesis of this tumor. Our results suggest that GH-RH antagonists MZ-5-156 and JV-136 inhibit the growth of U-87MG human glioblastoma by mechanisms that involve the suppression of IGF system. Antagonistic analogs of GH-RH merit further development for the treatment of malignant glioblastoma

    GHRH antagonists reduce the invasive and metastatic potential of human cancer cell lines \u3ci\u3ein vitro\u3c/i\u3e

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    We investigated the effect of a GHRH antagonist, MIA-602 on the metastatic cascade in vitro of three human cancers, DBTRG-05 glioblastoma, MDA-MB-468 estrogen-independent breast, and ES-2 clear cell ovarian cancer. GHRH receptors and their main splice variant, SV1 were detected on all three cell lines. After treatment with MIA-602, the cell viability decreased significantly, significant inhibition of cell invasion was observed and the release of MMPs was significantly decreased. The attachment of cancer cells to fibronectin and matrigel was severely hindered. Wound-healing experiments demonstrated a reduced cellular motility in all three cell lines. The up regulation of caveolin-1 and E-cadherin, and the powerful down regulation of NF-ĸB and β-catenin was detected. Our study suggests that the clinical application of highly potent GHRH antagonists in cancer therapy would be desirable since they inhibit proliferation and metastasis development as well
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