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  • 2000-2004  (1)
  • 1995-1999  (2)
  • 1970-1974
  • Apocrine secretion  (1)
  • FBN1  (1)
  • Immune reaction  (1)
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  • 2000-2004  (1)
  • 1995-1999  (2)
  • 1970-1974
Year
  • 1
    ISSN: 1432-2307
    Keywords: Osteonecrosis ; Serum sickness ; Immune reaction ; Animal model
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Osteonecrosis (ON) was produced experimentally in rabbits by intravenous injection of horse serum. Eighty adult rabbits were used: 16 were injected twice with isotonic saline (Group A), 24 were injected once with saline and once with horse serum (Group B), and 40 were injected twice with horse serum (Group C). Both femurs of each rabbit were obtained from 2 h to 7 weeks after the final injection an were subjected to histological examination. No pathological changes were seen in Groups A and B. In Group C, 5 of 15 rabbits (33%) showed ON (necrosis of trabecula and bone marrow) in the femoral metaphysis. In Group C, the early major pathological findings in bone marrow are extravasation of erythrocytes in sinusoidal spaces and microthrombi in small arteries and arterioles near the lesion of extravasation. Immune complexes were demonstrated in the kidney within 24 h of the final injection of horse serum. The present study suggests that immunological reaction associated with serum sickness may play an important role in inducible ON and this model will contribute toward clarifying the pathogenesis of ON.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Cell & tissue research 285 (1996), S. 501-507 
    ISSN: 1432-0878
    Keywords: Key words: Harderian gland ; Apocrine secretion ; Myoepithelial cell ; NaF+AlCl3 ; Carbachol ; Papaverine ; Rat (Sprague Dawley)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. Harderian glands of male albino rats were stimulated with secretagogues and examined by transmission and scanning electron microscopy for the purpose of studying the apocrine secretory mechanism. Rats in the control group were perfused with standard HEPES-buffered Ringer’s solution. Their glandular endpieces showed wide lumina that contained few secretory materials; spontaneous exocytosis was sometimes observed. However, there were no features suggestive of an apocrine secretory mechanism or myoepithelial cell contractions. After stimulation with NaF+AlCl3 or carbachol in HEPES-buffered Ringer’s solution, the rats shed ”bloody tears” and the glandular lumina were jammed with apical protrusions, cytoplasmic material and secretory products. The basal surface of the glandular cells showed bulging caused by myoepithelial cell contraction. Perfusion with HEPES-buffered Ringer’s solution containing papaverine inhibited secretagogue-induced myoepithelial cell contraction but not the enhanced secretory activities of the glandular cells. The present results demonstrate that the Harderian gland of the rat can release secretory material not only by exocytosis, but also by an apocrine mechanism under stimulating conditions, and that myoepithelial cell contraction may not be involved in causing apical protrusion in the glandular cells.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1435-232X
    Keywords: Key words Marfan syndrome ; FBN1 ; Fibrillin-1 ; Japanese ; Mutation ; Gene
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Marfan syndrome (MFS; MIM #154700) is a connective tissue disorder characterized by cardiovascular, skeletal, and ocular abnormalities. The fibrillin-1 gene (FBN1; MIM no. 134797) on chromosome 15 was revealed to be the cause of Marfan syndrome. To date over 137 types of FBN1 mutations have been reported. In this study, two novel mutations and a recurrent de-novo mutation were identified in patients with MFS by means of single-strand conformational polymorphism (SSCP) analysis. The two novel mutations are a 4-bp deletion at nucleotide 2820-2823 and a G-to-T transversion at nucleotide 1421 (C474F), located on exon 23 and exon 11, respectively. A previously reported mutation at the splicing donor site of intron 2 (IVS2 G + 1A), which is predicted to cause exon skipping, was identified in a sporadic patient with classical MFS.
    Type of Medium: Electronic Resource
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