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  • Articles  (2)
  • Blister injury  (1)
  • Developmental genes  (1)
  • Springer  (2)
  • National Academy of Sciences
  • 2000-2004
  • 1985-1989  (2)
  • Biology  (2)
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  • Articles  (2)
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Keywords
Publisher
  • Springer  (2)
  • National Academy of Sciences
Years
  • 2000-2004
  • 1985-1989  (2)
Year
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  • 1
    Electronic Resource
    Electronic Resource
    Developmental genetics (1986)
    Springer
    Cellular and molecular life sciences 42 (1986), S. 1117-1128 
    Details
    ISSN: 1420-9071
    Keywords: Developmental genes ; developmental disorders ; chromosome abnormalities ; animal models
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Of particular concern to the human geneticist are the effects of genetic abnormalities on development. To gain an understanding of these effects it is necessary to engage in a reciprocal process of using knowledge of normal developmental events to elucidate the mechanisms operative in abnormal situations and then of using what is learned about these abnormal situations to expand our understanding of the normal. True developmental genes have not been described in man, although it is likely that they exist, but many developmental abnormalities are ascribable to mutations in genes coding for enzymes and structural proteins. Some of these even produce multiple malformation syndromes with dysmorphic features. These situations provide a precedent for asserting that not only monogenic developmental abnormalities, but also abnormalities resulting from chromosome imbalance must ultimately be explicable in molecular terms. However, the major problem confronted by the investigator interested in the pathogenesis of any of the chromosome anomaly syndromes is to understand how the presence of an extra set of normal genes or the loss of one of two sets of genes has an adverse effect on development. Several molecular mechanisms for which limited precedents exist may be considered on theoretical grounds. Because of the difficulties in studying developmental disorders in man, a variety of experimental systems have been employed. Particularly useful has been the mouse, which provides models for both monogenic and aneuploidy produced abnormalities of development. An example of the former is the mutation oligosyndactylism which in the heterozygous state causes oligosyndactyly and in the homozygous state causes early embryonic mitotic arrest. All whole arm trisomies and monosomies of the mouse can be produced experimentally, and of special interest is mouse trisomy 16 which has been developed as an animal model of human trisomy 21 (Down syndrome). In the long run, the most direct approach to elucidating the genetic problems of human development will involve not only the study of man himself but also of the appropriate experimental models in other species.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01941286
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  • 2
    Electronic Resource
    Electronic Resource
    Dynamic changes of cell-surface glycoconjugates in human palmar epidermis following friction-blisters (1989)
    Springer
    Cell & tissue research 258 (1989), S. 403-408 
    Details
    ISSN: 1432-0878
    Keywords: Epidermis ; Blister injury ; Lectin histochemistry ; Cell-surface ; Glycoconjugates ; Oligosaccharides ; Man
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Damage and repair of cell-surface glycoconjugates were examined in human palmar skin following friction-blister injury, using biotinylated lectins and the avidinbiotin complex method. In normal skin, concanavalin A, Ricinus communis, and Triticum vulgaris bound to the surface of cells from the basal layer to the granular layer. After injury, binding of concanavalin A was absent in the plasma membrane, but appeared in the cytoplasm at perinuclear sites. The surface reaction was recovered in basal and spinous cells, but not in granular cells, when cell maturation began at 5 days after injury. In contrast, binding of Ricinus communis and Triticum vulgaris was, in general, much more resistant to tissue damage. Even in some cells, where the surface staining became obscure at an early period, a normal staining pattern reappeared by 6 h after injury. Staining of Ulex europeus I and Glycine max, detected on the surface of upper spinous and granular cells in normal skin, disappeared immediately after the injury, but recovered quickly on the surfaces of the differentiated cells. These findings suggest that at least 2 oligosaccharide sequences, one binding with concanavalin A, and the other with Ricinus communis and Triticum vulgaris, may exist on epidermal cells. Addition of terminal carbohydrates, detectable with binding of Ulex europeus I and Glycine max, appears to occur on the Ricinus communis I and Triticum vulgaris-bound oligosaccharide chain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00239461
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    Paper (German National Licenses)
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