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B Derby

Publications and source records attributed to B Derby.

6 recordsLinked to original sources

Novel collagen scaffolds with predefined internal morphology made by solid freeform fabrication.

Novel collagen scaffolds possessing predefined and reproducible internal channels with widths of 135 microm and greater have been produced. The process employed to make the collagen scaffold utilises a sacrificial mould, manufactured using solid freeform fabrication technology, and critical point drying technique. A computer aided design (CAD) file of the mould to be produced is created. This mould is manufactured using a phase change ink-jet printer. A dispersion of collagen is then cast into the mould and frozen. The mould is dissolved away with ethanol and the collagen scaffold is then critical point dried with liquid carbon dioxide. The effect of processing on the tertiary structure of collagen is assessed by monitoring the wavenumber of the N-H stretching vibration peak using Fourier transform infra-red spectroscopy and it is found that processing does not denature the collagen. Ultraviolet-visual spectroscopy was used to detect the presence of any contamination from the sacrificial mould on the collagen. The ability to use computer aided design and manufacture (CAD/CAM) provides a route to optimise scaffold designs using collagen in tissue engineering applications.

Animals↗

Manufacture of biomaterials by a novel printing process.

Tricalcium phosphate (TCP) scaffolds with controlled internal porosity were fabricated with a suspension of TCP in diacrylate cross-linking monomers using a mold prepared by ink-jet printing. Scaffolds were removed by selective dissolution of the mold. They were heat treated for removal of the acrylic binder followed by sintering. Despite a considerable linear shrinkage, scaffold porosity was retained after sintering. Composite scaffolds were fabricated from TCP in poly(ethylene glycol) diacrylate using an identical gel casting route.

Journal Article↗

Pathology of olivopontocerebellar atrophy with glutamate dehydrogenase deficiency.

We report the neuropathologic findings in the first patient with recognized glutamate dehydrogenase (GDH) deficiency to come to postmortem examination. He had progressive cerebellar ataxia beginning at age 21. He died at age 47 of pulmonary emboli. Postmortem examination revealed pancerebellar, olivary, and mild pontine atrophy, demyelination of the posterior columns, degeneration of anterior horn and dorsal root ganglion cells, and reduction of myelinated fibers in the sural nerve. In addition, there was neuronal storage of lipopigment diffusely throughout the CNS and the autonomic neurons, with cell distention, atrophy, and loss in selected areas.

Atrophy↗