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  • Articles: DFG German National Licenses  (3)
  • Child  (1)
  • Complement deficiency  (1)
  • Drosophila  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Giant cell tumor of bone in a child (1999)
    Springer
    International journal of clinical oncology 4 (1999), S. 403-406 
    Details
    ISSN: 1437-7772
    Keywords: Key words Giant cell tumor ; Child ; Bone tumor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Giant cell tumor (GCT) of bone was first established as a distinct clinicopathological radiographic entity in 1940 when Jaffe distinguished it from other lesions containing giant cells. GCT is rare in patients under 15 years of age. We report a case of GCT in a 10-year-old boy whose X-ray films showed osteolysis suggesting a malignant bone tumor. We believe this to be the youngest patient with giant cell bone tumor ever reported in the Japanese literature.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s101470050093
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Meiotic mutations from natural populations ofDrosophila melanogaster (1993)
    Springer
    Genetica 88 (1993), S. 165-173 
    Details
    ISSN: 1573-6857
    Keywords: Drosophila ; meiosis ; recombination ; spermatogenesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract Two meiotic genes from natural populations are described. A female meiotic mutation,mei(1)g13, mapped to 17.4 on the X chromosome, causes nondisjunction of all homologs except for the fourth chromosomes. In addition, it reduces recombination by 10% in the homozygotes and causes 18% increased recombination in the heterozygotes. A male meiotic mutation,mei-1223 m144 , is located on the third chromosome. Although this mutation causes nondisjunction of all chromosomes, each chromosome pair exhibits a different nondisjunction frequency. Large variations in the sizes of the premature sperm heads observed in the homozygotes may reflect irregular meiotic pairing and the subsequent abnormal segregation, resulting in aneuploid chromosome complements.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02424473
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Behçet's disease associated with complement component 9 (C9) deficiency (2000)
    Springer
    Modern rheumatology 10 (2000), S. 276-278 
    Details
    ISSN: 1439-7609
    Keywords: Key words Behçet's disease ; Complement component 9 (C9) ; Complement deficiency
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Behçet's disease is a multisystem inflammatory disorder with unknown etiology. It has been shown that the titer of plasma complement component 9 (C9) is a good indicator of the disease activity. Therefore, the involvement of C9 in the pathogenesis of Behçet's disease has been suggested. We report a case of Behçet's disease associated with complete C9 deficiency (C9D) carrying the homozygous nonsense mutation at Arg-95 of C9 (R95X). The patient presented the typical characteristics of Behçet's disease, such as uveitis, recurrent oral aphthae and genital ulcers, and arthritis, suggesting that C9 does not play an essential role in the pathogenesis of Behçet's disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s101650070017
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    Paper (German National Licenses)
    Fulltext
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