ArticleVirchows Archiv : an international journal of pathology1995
Retarded bone formation in GM1-gangliosidosis: a study of the infantile form and comparison with two canine models.
Article in Virchows Archiv : an international journal of pathology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 15 citations in OpenAlex.
- Article
- Impaired elastic-fiber assembly by fibroblasts from patients with either Morquio B disease or infantile GM1-gangliosidosis is linked to deficiency in the 67-kD spliced variant of beta-galactosidase.American journal of human genetics · 2000Article
- An in vitro model for abnormal skeletal development in the lysosomal storage diseases.Virchows Archiv : an international journal of pathology · 1995Article
- Insights into post-translational processing of beta-galactosidase in an animal model resembling late infantile human G-gangliosidosis.Journal of cellular and molecular medicineArticle
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The development of skeletal lesions in two canine models of GM1-gangliosidosis, English springer spaniels and Portuguese water dogs, has been studied and compared to osseous abnormalities in a child with the infantile form of the disease. In the canine models, skeletal dysplasia was progressive. Lesions were noted at 2 months of age and characterized by retarded endochondral ossification and osteoporosis. Older puppies had focal cartilage necrosis within lumbar vertebral epiphyses. At the cellular level, lesions were characterized by chondrocytic hypertrohy and lysosomal accumulation of storage compounds. Our studies illustrate that the skeletal lesions in both canine models are similar to those in a child with GM1-gangliosidosis. Furthermore, we proposed that the abnormal storage of partially degraded compounds in affected chondrocytes might explain, at least in part, the retarded bone formation noted in patients with GM1-gangliosidosis.
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