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Biomedical subjects

R C Ward

Publications and source records attributed to R C Ward.

12 recordsLinked to original sources
PubMed1993

Dystrophic calcification of silicone scleral buckling implant materials.

In six patients, removal of solid silicone scleral buckling implant materials that had been in place between eight and 21 years disclosed gray-white deposits firmly adherent to the silicone. Four of the six patients had culture-proven infections, whereas two had no evidence of infection and had negative cultures. One of these two patients, however, had intermittent pain, which was the indication for removal of the implant. Analysis of the deposits disclosed that they were calcium phosphate. The exact mechanism responsible for the calcification on the silicone material is unknown. Dystrophic calcification can occur without infection in injured tissue wherein extracellular deposits of devitalized cells, blood cells, and lipids may act as a nidus for calcification. In the presence of infection, bacteria may serve as such a nidus. Additionally, it is possible that biofilm produced by the bacteria had a role in the deposition of calcium phosphate, as well as in its firm adhesion to the silicone materials. We considered the possibility of similar deposits developing on intraocular silicone lenses.

Adolescent↗
PubMed1990

Interspecies extrapolation of pharmacokinetics.

The purpose of this paper is to use physiologically based pharmacokinetic models to demonstrate that if toxic response is a function of the time profile in physiological time of the concentration of the toxic moiety in the target tissue, then the appropriate interspecies scaling law for toxic compounds which are metabolically deactivated is mg kg-1 per unit of physiological time (mg kg-1 pt-1). At low dose rates this metric is approximately equivalent to mg kg-0.75 day-1. For reactive metabolites which are spontaneously deactivated, an approximate interspecies scaling law is mg kg-1 day-1.

Animals↗
PubMed1988

Abnormal scleral findings in uveal effusion syndrome.

We successfully treated a patient with uveal effusion syndrome and abnormal sclera with a partial-thickness sclerectomy. Part of the sclera was immediately cultured, and the excised sclera and the cultured cells were examined by electron microscopy. The sclera demonstrated increased glycosaminoglycan-like deposits between the scleral fibers. The cultured scleral cells showed large intracellular glycogen-like deposits, which were not seen in cells cultured from two control scleras. These findings may be the result of a metabolic defect, which causes a thick, impermeable sclera in some cases of uveal effusion.

Body Fluids↗
PubMed1988

Pharmacokinetics of tetrachloroethylene.

A physiological pharmacokinetic model is developed to describe the pharmacokinetics of tetrachloroethylene (PCE) in mice, rats, and humans. The body is divided into four tissue compartments (vessel-rich, muscle, slowly perfused fat, and liver) connected by the arterial and venous blood flow pathways. The physiological parameters of the model are blood flow rates, cardiac output, tissue volumes, ventilation rate, and tissue/air and blood/air partition coefficients. Metabolism is assumed to occur only in the liver compartment and is described by a combination of a linear metabolic component and a Michaelis-Menten component. The metabolic parameters for PCE were determined by fitting model predictions to species-specific empirical data. Comparison of model results with independent empirical data on inhalation and gavage exposures in mice, rats, and humans demonstrates that the physiological pharmacokinetic model can be used to determine the time course of PCE in these species. We show that human metabolic parameters can be predicted by scaling rat metabolic parameters as a function of body weight, whereas scaling of the metabolic parameters of mice overestimates human metabolism.

Animals↗
PubMed1987

Sensitivity and uncertainty studies of the CRAC2 computer code.

We have studied the sensitivity of health impacts from nuclear reactor accidents, as predicted by the CRAC2 computer code, to the following sources of uncertainty: (1) the model for plume rise, (2) the model for wet deposition, (3) the meteorological bin-sampling procedure for selecting weather sequences with rain, (4) the dose conversion factors for inhalation as affected by uncertainties in the particle size of the carrier aerosol and the clearance rates of radionuclides from the respiratory tract, (5) the weathering half-time for external ground-surface exposure, and (6) the transfer coefficients for terrestrial foodchain pathways. Predicted health impacts usually showed little sensitivity to use of an alternative plume-rise model or a modified rain-bin structure in bin-sampling. Health impacts often were quite sensitive to use of an alternative wet-deposition model in single-trial runs with rain during plume passage, but were less sensitive to the model in bin-sampling runs. Uncertainties in the inhalation dose conversion factors had important effects on early injuries in single-trial runs. Latent cancer fatalities were moderately sensitive to uncertainties in the weathering half-time for ground-surface exposure, but showed little sensitivity to the transfer coefficients for terrestrial foodchain pathways. Sensitivities of CRAC2 predictions to uncertainties in the models and parameters also depended on the magnitude of the source term, and some of the effects on early health effects were comparable to those that were due only to selection of different sets of weather sequences in bin-sampling.

Accidents↗