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Biomedical subjects

W A Roy

Publications and source records attributed to W A Roy.

6 recordsLinked to original sources
PubMed1981

Craniosynostosis in vitamin D-resistant rickets. A mouse model.

Craniosynostosis and associated craniofacial deformities, such as frontal bossing, often occur as symptoms of vitamin D-resistant rickets in children. Similar skull deformities develop in mice with X-linked dominant hypophosphatemia, the most common form of vitamin D-resistant rickets. These mice have a short, wide, high neurocranium, which suggested an inhibition of coronal suture growth. To study this question, we compared histologically the postnatal development of the coronal sutures in normal and hypophosphatemic mice between 1 and 13 weeks of age. Premature fusion of the coronal suture occurred in hypophosphatemic mice by 4 weeks of age. The proportion of the suture obliterated by bone varied among individual animals, but craniosynostosis was present in all animals studied at 4 weeks and older. Fusion of the coronal suture did not occur through 13 weeks of age in any of the normal mice studied. The x-linked hypophosphatemic mouse is an animal model that can be used to study the role of vitamin D-resistant rickets in the development of craniosynostosis, to relate craniosynostosis to the development of associated skull deformities, and to test new treatment procedures.

Animals↗
PubMed1979

Craniofacial growth following experimental craniosynostosis and craniectomy in rabbits.

Premature fusion of the coronal suture was produced in 9-day-old rabbits by immobilization of the suture area bilaterally with methyl-cyanoacrylate adhesive. The effects of suture fusion and its surgical release on suture growth and on skull morphology were evaluated by radiographic cephalometry. Immobilization resulted in significant changes in the angular dimensions in the vault toward an anteroposterior shortening. No permanent deformity was observed in the angular relationship between the cranial base and the facial skeleton. Craniectomy at 30 days, when a skull deformity had been established, resulted in rapid separation of the bones at the suture site which returned the deformed skull to a normal configuration by 90 days of age. Surgical removal of a normal suture in a control group also resulted in accelerated separation of the bones at the excised suture site, but it was less than after removal of an immobilized suture. The experimental data indicate that premature fusion of rapidly growing sutures results in consistent skull deformity. Early release of the fusion, when this is the primary abnormality, will result in spontaneous correction of the deformity.

Age Factors↗
PubMed1976

Ascorbate inhibition of 6-aminonicotinamide teratogenesis in chicken embryos.

Chicken eggs of 4 or 6 days of incubation were injected with 10 mug 6-aminonicotinamide (6-AN) or 6-AN plus various doses of sodium ascorbate, calcium ascorbate, or ascorbic acid; 11-day embryos were examined grossly and histologically. 6-AN-treated embryos had various degrees of micromelia and were reduced in overall size. All three ascorbates inhibited 6-AN teratogenesis but not completely. The extent of inhibition was dose related. Increased amounts of intercellular matrix and decreased necrosis of chondrocytes in the limb cartilage of protected embryos correlated with the gross findings.

6-Aminonicotinamide↗