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  • Clara cells  (2)
  • Drosophila melanogaster  (1)
  • Familial defective apolipoprotein B-100  (1)
  • 1
    ISSN: 1432-1440
    Keywords: Autoantibodies ; Pneumocytes type II ; Clara cells ; Pulmonary surfactant ; Pulmonary fibrosis ; Sarcoidosis ; Rheumatoid arthritis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Several experimental findings suggest an association between interstitial lung diseases and autoantibodies. Antibodies against lung tissue including pneumocytes type II in patients suffering from idiopathic pulmonary fibrosis (IPF) were reported in recent years. In this investigation the serum of 103 persons (10 with IPF, 23 with M. Boeck, 18 with rheumatoid arthritis (RA) and 52 healthy controls) was examined for autoantibodies against pneumocytes type II and Clara cells by indirect immunofluorescence on human lung tissue. These antibodies against both cell types are an additional proof for common antigens in pneumocytes type II and Clara cells. The autoantibodies were present in similar frequency in the 4 groups (IPF: 20%, M. Boeck: 26.1%, RA: 22.2% and 23.1% of the healthy controls). So no significant association was found between the antibodies and the interstitial lung diseases. A role of the antibodies in the pathogenesis of the diseases, however, can not be excluded by this study. A possible role as parameter of development of interstitial lung diseases should be subject to further investigations in form of a prospective follow up study.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1440
    Keywords: Familial hypercholesterolemia ; Familial defective apolipoprotein B-100 ; LDL ; LDL receptor ; Atherosclerosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Familial defective apolipoprotein B-100 (FDB) is a recently identified dominantly inherited genetic disorder, which leads to increased serum levels of low density lipoprotein (LDL) cholesterol with reduced affinity for the LDL receptor. This genetic disorder is characterized by defective binding of the apolipoprotein B-100 (apo B-100), which is virtually the sole protein constituent of LDL, to the LDL receptor. The defective binding results from a G to A mutation at amino acid 10708 in exon 26 of the apolipoprotein B (apo B) gene creating a substitution of glutamine for arginine in the codon for amino acid 3500. It is postulated that FDB can exhibit the same clinical features as familial hypercholesterolemia (FH) caused by a defective LDL receptor. The purpose of this paper is to report on an individual with a defective LDL and a defective LDL receptor. The clinical features of this individual were the same as in the family members with either defective LDL or a defective LDL receptor: premature arcus lipoides, tendon xanthomata, and premature atherosclerosis. Although the clinical features were present to the same degree as in individuals with either defect the prognosis and treatment of such an individual could be different.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1440
    Keywords: Relapsing polychondritis ; Immunology ; Pulmonary fibrosis ; Pneumocytes ; Clara cells ; Pulmonary surfactant ; Keratitis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A 62-year-old man with histological confirmed relapsing polychondritis showed chondritis of ears and nose, arthritis, keratitis and a hemolytic anemia. The bronchoalveolar lavage, computed tomography of the thorax and pulmonary function tests disclosed findings compatible with fibrosing alveolar disease. IgG antibodies to alveolar pneumocytes type II and bronchiolar Clara cells were detected by indirect immunofluorescense of human lung tissue. To our knowledge this is the first report of fibrosing alveolar disease in relapsing polychondritis and detection of antibodies to human pneumocytes type II and Clara cells.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Molecular genetics and genomics 202 (1986), S. 481-487 
    ISSN: 1617-4623
    Keywords: Position-effect variegation ; Suppressor mutations ; Chromosome 3 ; Heterochromatin ; Drosophila melanogaster
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary As a result of a genetic analysis of 63 third chromosome suppressor mutations of position-effect variegation 12 different loci showing dominant suppression have been identified and their map positions determined. A compilcation of the genetic data available for each suppressor locus is given. The strong suppressor effects of the mutations have been quantified by measurements of white variegation inw m4h /w m4h ,w m4h /Y andw m4h /O flies. Mutant alleles of three loci were found in these studies to dominate over the strong enhancer effect of complete loss of the Y chromosome. Most of the identified loci suppressing position-effect variegation represent essential genetic funtions; only three loci represent nonessential functions. Mutations of two loci display recessive butyrate sensitivity and lethal interaction with the heterochromatic Y chromosome suggesting that these genes affect chromosomal condensation. Studies with deficiencies and triploids revealed that most of the loci represent haplo-abnormal suppressor functions. The use of the isolated mutant material for genetic, developmental and molecular studies of processes connected with gene inactivation in position-effect variegation is discussed.
    Type of Medium: Electronic Resource
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