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M E Barker

Publications and source records attributed to M E Barker.

41 records · Page 3Linked to original sources
PubMedDate not supplied

The effect of concentration on hepatic transport of exogenous epidermal growth factor.

Epidermal growth factor (EGF), taken up by rat liver hepatocytes, is primarily transported to the lysosomes and degraded. However, a small but significant percentage of endocytosed EGF is transported by a nonlysosomal pathway and is secreted intact into bile. There is no information as to the mechanisms that regulate the selection of transport pathway and thereby determine the different metabolic fates for EGF. The experiments reported here were undertaken to determine whether the amount of exogenous EGF administered to the liver (the transport load) might affect the selection of the transport pathway. If "excess" EGF, exceeding some as yet undetermined threshold, is preferentially transported by the lysosomal pathway, then the proportion of degraded EGF secreted into bile should increase as a function of the amount of EGF administered. 125I-EGF (3 to 175 ng) was injected into rat portal veins, and bile samples were collected via cannula. The radioactivity secreted into bile was measured, and the bile samples were immunoprecipitated with anti-EGF antiserum. The proportion of intact vs. degraded EGF in bile was determined by the percentage of immunoprecipitable radioactivity. Regardless of the amount of EGF injected, the pattern of its secretion was unaltered. The percentage of immunoprecipitable EGF in bile was the same for all doses. Therefore, the amount of EGF that was degraded did not change as a function of EGF concentration, implying that the lysosomal pathway was not preferentially utilized as the transport load increased. In conclusion, transport load does not appear to be a regulatory mechanism in the selection of transport pathway utilized by EGF.

Animals↗
PubMedDate not supplied

Thermal effects of acrylic cementation at bone tumour sites.

The use of acrylic bone cement as an adjunct to surgical excision of giant cell tumour of bone appears to reduce the incidence of tumour recurrence. Possible mechanisms for this apparent tumour inhibition include cytotoxic effects from the methylmethacrylate monomer and tissue hyperthermia from the heat of polymerization of the cement. This work presents a method for the prediction of temperature fields and resulting tissue necrosis arising from the implantation of polymethylmethacrylate (PMMA) at the site of a curretted giant cell tumour of bone. This is accomplished using a two-dimensional model based on geometry obtained from digitized MRI images of the distal femur. A general-coordinate, non-orthogonal grid generation technique is used and solutions are obtained with an alternating-direction implicit (ADI) finite-difference scheme. The nodal temperature histories are then used to evaluate the effect of variable defect size on the zone of thermally induced cell necrosis. The results suggest the depth of the necrotic region is quite sensitive to the size of the implant. In at least some cases, the heating effect is sufficient to cause significant necrosis of tumorigenic cells. Implanting a large mass of acrylic may risk overkill, damaging substantial amounts of healthy tissue.

Bone Cements↗