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  • 1
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Biochemistry 9 (1970), S. 3837-3846 
    ISSN: 1520-4995
    Source: ACS Legacy Archives
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1211
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Three unrelated individuals with, respectively, lupus erythematosus, polyarteritis, and membranoproliferative glomerulonephritis and totally deficient in the second component of complement are demonstrated to be mutually poorly reactive in mixed lymphocyte culture and homozygous for the mixed lymphocyte reaction determinant (MLR-S or LD) short 7a (7a*). The gene controlling the elaboration of C2 in man is shown to be separate from, and probably to map outside of, the second locus ofHL-A and theMLR-S locus. Genetic linkage disequilibrium is strongly suggested between HL-A 10, W18, 7a*, and C2 deficiency.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Pediatric nephrology 4 (1990), S. 523-532 
    ISSN: 1432-198X
    Keywords: Alport syndrome ; Hereditary nephritis ; Basement membranes ; Collagen IV ; X-linkage ; Post-transplant anti-glomerular basement membrane nephritis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Alport syndrome, an inherited disorder of the kidney, eye and ear, has fascinated nephrologists, pathologists, and geneticists for nearly a century. With the recent application of molecular biochemical and genetic techniques, this mysterious disease has begun to yield some of its secrets. Alport syndrome can now be viewed as a generalized disorder of basement membranes that appears to result from mutations in an X-chromosome-encoded basement membrane collagen chain. This chain, along with two other novel collagen chains, is absent from Alport basement membranes, in contrast to the classical chains of collagen IV. Phenotypic heterogeneity in Alport syndrome probably arises from allelic mutations at a single genetic locus. The phenomenon of post-transplant anti-glomerular basement membrane nephritis may be a manifestation of specific mutations at the Alport locus that prevent synthesis of the gene's protein product and the establishment of immunological tolerance.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Springer seminars in immunopathology 9 (1987), S. 317-339 
    ISSN: 1432-2196
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Conclusion The intent of the previous discussion has been to acquaint the reader with the recent expanding knowledge in matrix biochemistry and immunopathology as it pertains to the human GBM. However, it must be emphasized that the GBM antigens, which have yet to be characterized, may outnumber those that are currently defined. SDS-PAGE analysis of GBM isolated by detergent solubilization or sonication reveals at least fifteen different polypeptide components [39]. Of a panel of nine monoclonal antibodies developed following immunization of mice with human GBM, eight stain mature and/or fetal GBM by immunofluorescence microscopy, but only two react by ELISA with currently defined components of basement membrane [98]. Furthermore, current understanding of the mechanisms by which matrix macromolecules participate in such human pathological states as diabetic nephropathy, nephrotic syndrome, sclerosis, and immune complex glomerulonephritis is still quite limited. It is obvious that much is yet to be learned and considerably more is to be gained from continued research in this area.
    Type of Medium: Electronic Resource
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