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  • 1
    Electronic Resource
    Electronic Resource
    Non-Diabetogenic Insulitis in NOD↔BIO. GD Allophenic Mice in Spite of Permissive Class I MHC Antigens (1994)
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 40 (1994), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Allophenic mice (embryo aggregation mouse chimeras) enable us to dissect the process of spontaneous autoimmunity under physiological conditions. Our previous experiments showed that the autoimmune process in allophenic mice of the NOD↔C57Bl/6 strain combination does not progress from insulitis to diabetes. One possible explanation for this protection is that H-2 Kd-restricted CD8+ T cells kill only NOD ß cells (Kd, Db) in the chimeric islets, while the B6ß cells (Kb, Db) are spared from destruction. To test this hypothesis we analysed 22 NOD↔B10. GD chimeras in which the class I MHC are shared by both parental strains. Therefore all the ß cells in these chimeras express H-2 Kd molecules. Ten allophenic mice were killed at 7 weeks and studied for early pathology. No evidence for intra-islet infiltration was obtained at this age, suggesting that the autoimmune process in NOD↔B10. GD chimeras is slower than in NOD mice. Twelve chimeras were followed up for 1 year for disease development and all failed to progress to full-blown diabetes, despite the occurrence of intra-insulitis in six out of 12 mice. The lack of disease in NOD↔B10. GD chimeras demonstrates that class I MHC chimerism does not account for diabetes resistance in NOD-allophenic mice.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3083.1994.tb03520.x
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  • 2
    Electronic Resource
    Electronic Resource
    Apoptosis and autoimmune disease (1999)
    Springer
    Inflammation research 48 (1999), S. 5-21 
    Details
    ISSN: 1420-908X
    Keywords: Key words: Cell death — Apoptosis — Autoimmunity — Bcl-2 — Fas (Apo-1, CD95)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. The process of programmed cell death or apoptosis was already noted in 1842 by Vogt [1], but it was not until the more recent studies of Kerr et al. 1972 [2] that an explosion of interest in apoptosis research occurred. Genetic, biochemical and cellular analysis in certain mammals, in the nematode Caenorhabditis elegans and in the fruitfly Drosophila melanogaster have identified several apoptosis regulating genes. This indicates that programmed cell death is an active, genetically controlled process. Many of the known cell death regulators are homologous in mammals, nematodes and insects, indicating that apoptosis is an evolutionarily conserved process. Apoptosis can be induced via multiple independent signalling pathways which converge upon a common final effector machinery. This stimulates activation of latent cysteine proteases (caspases), which cleave vital cellular substrates and thereby lead to the death of cells. The regulatory pathways of apoptosis are becoming clear with the discovery of specific signalling molecules. It has become evident that many disease processes including autoimmunity and cancer can be caused by deregulation of the apoptotic process. With the discovery of novel cell surface-bound death receptors, their ligands and further insight into the apoptotic machinery within the cell, research may ultimately lead to the design of therapies that allow intervention in the apoptotic process. The aims of such strategies would be to turn on apoptosis in neoplastic cells or in lymphocytes that are causing autoimmune disease or to prevent cell death in degenerative disorders. This review describes current understanding of the molecular regulation of apoptosis, and focuses on issues relating to possible roles of defective cell death control in autoimmunity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s000110050369
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  • 3
    Electronic Resource
    Electronic Resource
    An X-Ray Topographic Analysis of the Crystal Quality of Globally Available SiC Wafers (2007)
    s.l. ; Stafa-Zurich, Switzerland
    Materials science forum Vol. 556-557 (Sept. 2007), p. 227-230 
    Details
    ISSN: 1662-9752
    Source: Scientific.Net: Materials Science & Technology / Trans Tech Publications Archiv 1984-2008
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics
    Notes: We present herein a first comparative analysis of the quality of 50 mm and 75 mmdiameter SiC wafers, purchased directly from vendors across the world, types including the mostwidely available configurations. Large Area White Beam Synchrotron Back Reflection X-RayTopography was used to analyse selected ~1cm2 regions at various locations on up to 10 differentbulk SiC wafers. The study concentrated particularly on the density and distribution of threadingscrew dislocations (TSDs). We also examined all wafers for basal plane dislocation (BPDs)densities and distributions. Alarmingly large variation in wafer quality was observed. TSD densitiesvary from a minimum of 0 cm-2 (in a-plane material) to values as large as over 2,000 cm-2 on somen-type 4H-SiC wafers. TSD densities on individual wafers can also vary by similar magnitudes, e.g.500cm-2 to 2,500 cm-2 on two regions only 2 cm apart on a 50 mm diameter wafer. Computer-basedimage process analysis was used to present a statistical analysis of the distributions of defects. Forexample algorithms created in MATLAB®, Image Processing Toolbox, isolated possible TSDlocations allowing rapid counting to be performed. These counts were confirmed by manualcounting of selected unmodified images
    Type of Medium: Electronic Resource
    URL: http://www.tib-hannover.de/fulltexts/2011/0528/02/17/transtech_doi~10.4028%252Fwww.scientific.net%252FMSF.556-557.227.pdf
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