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L A Meyer

Publications and source records attributed to L A Meyer.

8 recordsLinked to original sources
PubMed2001

Copper transport and metabolism are normal in aceruloplasminemic mice.

Ceruloplasmin is an abundant serum glycoprotein containing greater than 95% of the copper found in the plasma of vertebrate species. Although this protein is known to function as an essential ferroxidase, the role of ceruloplasmin in copper transport and metabolism remains unclear. To elucidate the role of ceruloplasmin in copper metabolism, the kinetics of copper absorption, transport, distribution, and excretion were examined utilizing (64)Cu in wild-type and aceruloplasminemic mice. No differences in gastrointestinal absorption, hepatic uptake, or biliary excretion were observed in these animals. Furthermore, steady state measurements of tissue copper content utilizing (64)Cu and atomic absorption spectroscopy revealed no differences in the copper content of the brain, heart, spleen, and kidney. Consistent with these findings, the activity of copper-zinc superoxide dismutase in these tissues was equivalent in wild-type and ceruloplasmin-deficient mice. Hepatic iron was elevated 3.5-fold in aceruloplasminemic mice because of the loss of ferroxidase function. Hepatic copper content was markedly increased in aceruloplasminemic mice. As no differences were observed in copper absorption or biliary copper excretion, these data suggest that in these animals, hepatocyte copper intended for ceruloplasmin incorporation is trafficked into a compartment that is less available for biliary copper excretion. Taken together, these data reveal no essential role for ceruloplasmin in copper metabolism and suggest a previously unappreciated complexity to the subcellular distribution of this metal within the hepatocyte secretory pathway.

Animals↗
PubMed1988

Corneal endothelial morphology in the rat. Effects of aging, diabetes, and topical aldose reductase inhibitor treatment.

Increases in corneal endothelial cell polymegathism and pleomorphism are characteristic of diabetic human and dog corneas. This study investigated the rat as a model for age- and diabetes-related changes in endothelial cell morphology. As in most mammals, aging of the normal rat results in a progressive decrease in cell density as well as reduced numbers of hexagonal endothelial cells and increased coefficient of variation of cell size after age 34 weeks. Streptozotocin-induced diabetes produced an early progressive increase in the coefficient of variation of cell size and decrease in percentage of hexagonal cells so that diabetic rats were significantly different from age-matched normal rats by 24 weeks of age. Topical treatment with the aldose reductase inhibitor, AL 1576, begun immediately after diabetes induction, prevents endothelial cell changes and cataract formation. Topical aldose reductase inhibition also reverses endothelial cell changes when treatment is begun 8 weeks after streptozotocin injection. These results indicate that the rat is a good model for studying diabetes-induced corneal endothelial changes and that topical aldose reductase inhibitors may be effective in preventing or reversing diabetic corneal endothelial cell changes.

Aging↗
PubMed1986

The role of the polymorphonuclear leukocyte in the induction of corneal edema.

Corneal inflammation is frequently associated with the development of corneal edema. It has been suggested the development of corneal edema might in some way be related to the presence of polymorphonuclear leukocytes (PMNLs) within inflamed corneas. In the present studies, it was found that corneal thickness markedly increased after experimental infection with Pseudomonas aeruginosa, but in guinea pigs made neutropenic by whole body irradiation, significantly less of an increase in corneal thickness occurred. Furthermore, corneas from non-neutropenic animals experimentally infected with P. aeruginosa consistently showed a greater increase in water content than did infected corneas from neutropenic animals. Over the first 48 hr of infection, the increase in corneal water was directly proportional to the corneal ingress of radiolabelled PMNLs. Corneal inflammation induced by intracorneal injection of the PMNL chemotactic agents phorbol myristate acetate (PMA) or endotoxin was also associated with a significant increase in corneal water compared with neutropenic animals. These data strongly suggest that activated PMNLs in the cornea are responsible for the induction of corneal edema in infected corneas.

Animals↗
PubMed1985

Correlation of corneal endothelial pump site density, barrier function, and morphology in wound repair.

After transcorneal freezing, physiologic function (pump and barrier) of the regenerating rabbit corneal endothelium was evaluated and compared with the morphologic differentiation that occurs during wound healing. Endothelial pump function was investigated utilizing the specific binding of tritiated ouabain to endothelial Na+/K+ ATPase (pump sites); the permeabilities of isolated de-epithelialized corneas to labeled inulin and dextran were measured to determine endothelial barrier function. Endothelial recovery after transcorneal freezing can be described as a three-stage process. Stage one is characterized by the establishment of an initial coverage of the wound by pleomorphic spindle-shaped cells which form a functional but incomplete barrier and minimal pump site density. In stage two, the cells assume a flattened configuration consisting of irregular polygons and establish nearly normal pump capacity. In stage three, a significant remodeling of the monolayer continues despite the layer's early physiologic recovery.

Animals↗