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Biomedical subjects

J P Moxham

Publications and source records attributed to J P Moxham.

3 recordsLinked to original sources

Chromosomal abnormalities in idiopathic congenital bilateral vocal cord paralysis.

Idiopathic congenital bilateral vocal cord paralysis (BVCP) can occur as an isolated abnormality or as part of a multisystem disorder. The chromosomal abnormalities found in 4 children who presented with idiopathic congenital BVCP in association with other congenital abnormalities between January 1991 and April 1999 are described. Three children had abductor paralysis, and tracheostomy was required in 1. The fourth child had adductor paralysis and required a feeding gastrostomy for management of aspiration. There was no clinically significant improvement in vocal cord function observed in any child. Idiopathic congenital BVCP, when associated with other congenital disorders, may occur as a consequence of an underlying chromosomal abnormality, and chromosome studies should be performed in this group of children. Similarly, the possibility of vocal cord dysfunction should be considered in children who are found to have chromosomal abnormalities. A chromosomal abnormality appears to preclude the possibility of early spontaneous improvement in vocal cord function.

Abnormalities, Multiple↗

Transforming growth factor-beta 1 in a guanidine-extracted demineralized bone matrix carrier rapidly closes a rabbit critical calvarial defect.

Transforming growth factor beta 1 (TGF-beta 1) is a polyfunctional regulatory cytokine that has been shown to have roles in extracellular matrix interactions, soft tissue healing, and osteogenesis. Twenty-five microL of recombinant human TGF-beta 1 was added to guanidine-extracted demineralized bone matrix carrier and the implants were used to fill a 14-mm osteoperiosteal critical calvarial defect in New Zealand white rabbit model. The defects were allowed to heal over 4 weeks and the degree of new bone formation was assess by radiodensitometry and undecalcified bone histomorphometry techniques. Implants with TGF-beta 1 showed complete bridging of the gap with new bone in all cases, while the controls showed fibrous tissue repair of the gap with little or no new bone formation. These results demonstrate the ability of TGF-beta 1 to induce new bone in a brief time period in an inactive carrier.

Animals↗

TGF-beta 1 forms functionally normal bone in a segmental sheep tibial diaphyseal defect.

OBJECTIVE: Transforming growth factor-beta 1 (TGF-beta 1) is a polyfunctional regulatory cytokine that has been shown to have roles in extracellular matrix interactions, soft tissue healing, and osteogenesis. This study was undertaken to determine the efficacy of TGF-beta 1 in the formation of functionally normal bone in tibial-diaphyseal defects. METHOD: Seven hundred fifty micrograms of recombinant human TGF-beta 1 was added to a guanidine-extracted demineralised bone matrix (Gu-DBM) carrier and the implants were used to fill a 2.5 cm tibial diaphyseal defect in skeletally mature female sheep. The defects were allowed to heal over a 12-week period. After sacrifice, they were analyzed using four-point bending mechanical testing. RESULTS: Implants with TGF-beta 1 showed complete bony bridging of the defect and stress-strain curves similar to the normal contralateral limb, while implants with the carrier alone failed to bridge the gap. CONCLUSIONS: These results demonstrate the ability of TGF-beta 1 to induce new bone which has structural and functional characteristics similar to normal bone.

Animals↗