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  • 1
    ISSN: 1432-0533
    Keywords: Major histocompatibility complex class II ; Wallerian degeneration ; Microglia ; Autoimmune disease ; Experimental allergic encephalitis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To clarify the implication of the major histocompatibility complex class II (Ia) antigen induction in microglia following Wallerian degeneration in the central nervous system (CNS), experimental allergic encephalitis (EAE) was adoptively transferred to Lewis rats in which Ia antigens had been induced in microglia at the sites of Wallerian degeneration. In addition to randomly distributed typical EAE lesions, the recipient rats developed distinct inflammatory lesions in accord with the distribution of Ia-positive microglia; i.e., in the ipsilateral thalamus after cortical cryoinjury, and in the ipsilateral optic nerve, the contralateral optic tract and superior colliculus after unilateral eye ball enucleation. Thus, the EAE locus may be targeted by this approach. The inflammatory response was inducible by transfer of myelin basic protein-stimulated lymphocytes but not by transfer of phytohemagglutinin-stimulated or non-stimulated lymphocytes. When examined using monoclonal antibody surface markers; OX-6 for Ia antigen, W3/13 for pan T lymphocyte and OX-8 for cytotoxic/suppresser T lymphocyte, the types of lymphocytes in these lesions did not differ from those in ordinary EAE lesions in the spinal cord. The potential role of non-immunologically induced Ia-positive cell clusters that serve as a target for autoimmune CNS diseases was discussed.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 30 (1989), S. 0 
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The DNA–anti-DNA antibody immune complexes were isolated from plasma of systemic lupus crythematosus (SLE) patients and DNA fragments separated from immune complexes were subjected to molecular cloning. The resulting recombinant DNA clones showed a molecular size of 37–79 base pairs, a high guanine and cytosine content, high frequencies of CpG dinucleotides, and palindromic sequences, and also clusters of G+C- and A+T-rich segments. These clones hybridized randomly to total human DNA. The reactivity of dsDNA antibodies, both monoclonal and polyclonal, from SLE was examined with a cloned SLE antigen DNA. A competitive inhibition assay showed that human monoclonal antibodies had at least one magnitude higher affinity to the cloned DNA than to the native DNA fragments. In order to characterize the factors that were recognized by antibodies, human G+C-rich and also A+T-rich 100 bp DNA fragments were cloned, and their base sequences determined. The antibody showed a higher affinity to the G+C-rich DNA fragment (71% G+C) than to the A+T-rich DNA fragment (46% G+C). When cytosines in CpG doublets in G+C-rich fragments were methylated (mCpG), the reactivity increased up to 100-fold. The native anti-DNA antibodies from SLE patients also showed preferential binding to G+C-rich fragments. These observations suggested that human anti-dsDNA antibodies may recognize some unique structures around the G+C regions or G+C clusters of DNA.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Metabolic brain disease 8 (1993), S. 45-59 
    ISSN: 1573-7365
    Keywords: thiamine content ; thiamine deficiency ; HPLC analysis ; Wernicke-Korsakoff syndrome
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The regional distribution of thiamine and its phosphate esters was measured in the central nervous system (CNS) of normal and thiamine-deficient mice. Twelve small areas were punched out from frozen sections and they were individually analyzed by high performance liquid chromatography (HPLC). Regional difference was noted in both the content and ratio of thiamine and its phosphate esters in the normal CNS. In pyrithiamine-induced thiamine deficiency, thiamine pyrophosphate (TPP) content in all the areas was reduced to less than 13% of the control values on day 10, when the neurological signs developed. Although there were considerable regional variations in the reduction rate of thiamine and its phosphate esters, no correlation was established between the severity of tissue damage and the magnitude of thiamine reduction in individual areas. These results indicate that a derangement in TPP-dependent processes, either alone or in combination with other factors, plays a more critical role in the neuronal damage under thiamine deficiency than depletion of thiamine compoundsper se.
    Type of Medium: Electronic Resource
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