Faulty fringes coming from an infrared spectrometer may creep into a spectrum. Because these come from one faulty interferogram out of many used to obtain the spectrum, these may pass unnoticed. However, they cause some problems in the data treatment of factor analysis and other spectral analysis. We present a method for detecting the faulty fringes and give a simple method to eliminate them at the interferogram accumulation level.
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http://dx.doi.org/10.1366/000370208786049132 | DOI Listing |
Organic farming has been hijacked by big business. Local food can have a larger carbon footprint than products shipped in from overseas. Fair trade doesn't address the real concerns of farmers in the global South.
View Article and Find Full Text PDFTransfusion
December 2010
Department of Pediatrics, Case Western Reserve University, Cleveland, Ohio 44106, USA.
Background: Modification of Notch receptors by O-linked fucose and its further elongation by the Fringe family of glycosyltransferase has been shown to be important for Notch signaling activation. Our recent studies disclose a myeloproliferative phenotype, hematopoietic stem cell (HSC) dysfunction, and abnormal Notch signaling in mice deficient in FX, which is required for fucosylation of a number of proteins including Notch. The purpose of this study was to assess the self-renewal and stem cell niche features of fucose-deficient HSCs.
View Article and Find Full Text PDFAppl Spectrosc
October 2008
ITF Labs, 400 Montpellier, Montréal, QC, Canada, H4N 2G7.
Faulty fringes coming from an infrared spectrometer may creep into a spectrum. Because these come from one faulty interferogram out of many used to obtain the spectrum, these may pass unnoticed. However, they cause some problems in the data treatment of factor analysis and other spectral analysis.
View Article and Find Full Text PDFJ Cell Biol
August 2002
Howard Hughes Medical Institute, The University of Michigan Medical School, 1150 W. Medical Center Drive, Ann Arbor, MI 48109, USA.
Glycoprotein fucosylation enables fringe-dependent modulation of signal transduction by Notch transmembrane receptors, contributes to selectin-dependent leukocyte trafficking, and is faulty in leukocyte adhesion deficiency (LAD) type II, also known as congenital disorder of glycosylation (CDG)-IIc, a rare human disorder characterized by psychomotor defects, developmental abnormalities, and leukocyte adhesion defects. We report here that mice with an induced null mutation in the FX locus, which encodes an enzyme in the de novo pathway for GDP-fucose synthesis, exhibit a virtually complete deficiency of cellular fucosylation, and variable frequency of intrauterine demise determined by parental FX genotype. Live-born FX(-/-) mice exhibit postnatal failure to thrive that is suppressed with a fucose-supplemented diet.
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