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  • 1980-1984  (2)
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Material
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Year
  • 1
    Electronic Resource
    Electronic Resource
    An increase in Sendai virus-induced cell fusion of erythrocytes infected withPlasmodium chabaudi (1982)
    Springer
    Cellular and molecular life sciences 38 (1982), S. 342-344 
    Details
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The extent of cell fusion induced by Sendai virus was examined in erythrocytes infected withPlasmodium chabaudi. An increase in cell fusion of erythrocytes with Ehrlich tumor cells and of erythrocytes with erythrocytes was observed wit the infected erythrocytes. However, agglutination by the virus was not changed between erythrocytes of normal and malarial mice. These results indicate that the increase in cell fusion occurred in the process of membrane fusion, suggesting that some membrane property ofPlasmodium-parasitized erythrocytes is changed in terms of Sendai virus-induced cell fusion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01949381
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    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Immunofluorescence staining and immunological studies of arylsulphatase a of multiple sulphatase deficiency (MSD) and metachromatic leukodystrophy (MLD) fibroblasts (1983)
    Springer
    Journal of inherited metabolic disease 6 (1983), S. 21-26 
    Details
    ISSN: 1573-2665
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Multiple sulphatase deficiency (MSD) and metachromatic leukodystrophy (MLD) are both characterized by a deficiency of arylsulphatase A (ARS A) activity, although they are inherited as separate autosomal recessive traits. However, it has been found that the immunologically active substance with anti-ARS A antibody is present in quite normal levels in MLD and in smaller quantities in MSD fibroblasts (Fiddler, 1979). Indirect immunofluorescence staining with anti-ARS A antibody displayed a coarse granular and diffuse distribution of ARS A or cross-reacting material (CRM) in the normal control and MLD fibroblasts, whereas very weak fluorescence staining was observed in MSD fibroblasts proportional to the decrease in the ARS A activity observed in the lysate enzyme assay. These results suggest that ARS A deficiency in MLD cells is due to an enzymatically deficient ARS A molecule, which is immunologically cross-reactive with anti-normal ARS A antibody. ARS A deficiency in MSD cells appears to be due to a reduced amount of normal ARS A.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02391188
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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