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  • Bouchet, P., et al. (författare)
  • The Mid-Infrared Instrument for the James Webb Space Telescope, III: MIRIM, The MIRI Imager
  • 2015
  • Ingår i: Publications of the Astronomical Society of the Pacific. - : IOP Publishing. - 0004-6280 .- 1538-3873. ; 127:953, s. 612-622
  • Tidskriftsartikel (refereegranskat)abstract
    • In this article, we describe the Mid-Infrared Imager Module (MIRIM), which provides broadband imaging in the 5-27 mu m wavelength range for the James Webb Space Telescope. The imager has a 0 ''.11 pixel scale and a total unobstructed view of 74 '' x 113 '' The remainder of its nominal 113 '' x 113 '' field is occupied by the coronagraphs and the low-resolution spectrometer. We present the instrument optical and mechanical design. We show that the test data, as measured during the test campaigns undertaken at CEA-Saclay, at the Rutherford Appleton Laboratory, and at the NASA Goddard Space Flight Center, indicate that the instrument complies with its design requirements and goals. We also discuss the operational requirements (multiple dithers and exposures) needed for optimal scientific utilization of the MIRIM.
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  • Lee, Monica Y., et al. (författare)
  • Integrative genomics identifies DSCR1 (RCAN1) as a novel NFAT-dependent mediator of phenotypic modulation in vascular smooth muscle cells
  • 2010
  • Ingår i: Human Molecular Genetics. - : Oxford University Press (OUP). - 0964-6906 .- 1460-2083. ; 19:3, s. 468-479
  • Tidskriftsartikel (refereegranskat)abstract
    • Vascular smooth muscle cells (SMCs) display remarkable phenotypic plasticity in response to environmental cues. The nuclear factor of activated T-cells (NFAT) family of transcription factors plays a critical role in vascular pathology. However, known functional NFAT gene targets in vascular SMCs are currently limited. Publicly available whole-genome expression array data sets were analyzed to identify differentially expressed genes in human, mouse and rat SMCs. Comparison between vehicle and phenotypic modulatory stimuli identified 63 species-conserved, upregulated genes. Integration of the 63 upregulated genes with an in silico NFAT-ome (a species-conserved list of gene promoters containing at least one NFAT binding site) identified 18 putative NFAT-dependent genes. Further intersection of these 18 potential NFAT target genes with a mouse in vivo vascular injury microarray identified four putative NFAT-dependent, injury-responsive genes. In vitro validations substantiated the NFAT-dependent role of Cyclooxygenase 2 (COX2/PTGS2) in SMC phenotypic modulation and uncovered Down Syndrome Candidate Region 1 (DSCR1/RCAN1) as a novel NFAT target gene in SMCs. We show that induction of DSCR1 inhibits calcineurin/NFAT signaling through a negative feedback mechanism; DSCR1 overexpression attenuates NFAT transcriptional activity and COX2 protein expression, whereas knockdown of endogenous DSCR1 enhances NFAT transcriptional activity. Our integrative genomics approach illustrates how the combination of publicly available gene expression arrays, computational databases and empirical research methods can answer specific questions in any cell type for a transcriptional network of interest. Herein, we report DSCR1 as a novel NFAT-dependent, injury-inducible, early gene that may serve to negatively regulate SMC phenotypic switching.
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