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Biomedical subjects

M E Gilman

Publications and source records attributed to M E Gilman.

7 recordsLinked to original sources

Genetic mapping of bovine mitochondrial DNA from a single animal.

Using a physical map of bovine mitochondrial DNA derived from the liver of a single Holstein cow, we have determined the location of the genes specifying the large and small ribosomal RNAs by hybridization analysis and electron microscopic observations of R-loop forms. Also, the position of the origin of DNA replication (D-loop) has been located by electron microscopy. Additionally, the direction of D-loop expansion and the polarity of the large and small ribosomal RNA genes were determined.

Animals↗

Rapid modulation of gill Na+ + K+-dependent ATPase activity during acclimation of the killifish Fundulus heteroclitus to salinity change.

The enzymatic properties of membrane-bound Na+ + K+-ATPase from gills of killifish acclimated to fresh water, to 16% sea water, or to 30% sea water appear to be identical, indicating that the same enzyme may function to absorb Na+ in low salinities and excrete Na+ at the gills in high salinities. Ammonium ion is an effective substitute for K+: in the ATPase reaction itself, in blocking phosphorylation of the ATPase protein, and in inhibiting the binding of ouabain to the enzyme. The specific activities of the Na+ + K+-ATPase in the three different salinities are consistent with the expected Na+ pumping rates: higher in fresh water and 30% sea water than in 16% sea water. Within one-half hour after transfer of killifish from one salinity to another, gill Na+ + K+-ATPase activities reach equilibrium levels. The rapid increase in Na+ + K+-ATPase activity in gill microsomes of fish acclimating from fresh water to 30% sea water is accompanied by a slow decrease in the number of binding sites for ouabain, supporting the idea that acclimation to short-term salinity changes may involve modifications in the catalytic rate rather than the number of Na+ + K+-ATPase molecules.

Acclimatization↗

Individualizing phenobarbital dosing in neonates.

A method was developed for estimating elimination rate constants for phenobarbital in neonates on the basis of two serum samples drawn at any interval. Phenobarbital serum concentrations were obtained for 16 neonates being treated for fetal asphyxia, intraventricular hemorrhage, narcotic withdrawal, or seizure activity. The mean birth weight was 2.18 kg, mean gestational age was 34.8 weeks, and mean postnatal age was 12.1 days. The first blood sample was drawn two hours after an i.v. loading dose of phenobarbital sodium 7-15 mg/kg; maintenance doses ranging from 1.3 to 7.5 mg/kg/day were given by single i.v. injection. On the third day of therapy, trough concentration was determined; elimination rate constants were calculated using the two concentrations and the total dosage administered. Maintenance doses were adjusted to achieve desired serum concentrations, and predicted concentrations were compared with actual concentrations on the seventh day of therapy. Measured and predicted serum concentrations on day 7 were not significantly different. Only one patient exhibited phenobarbital toxicity. Phenobarbital serum half-life did not show a correlation with either gestational age or postnatal age. This method is clinically useful for individualizing phenobarbital dosing in neonates because it allows for integration of therapeutic drug monitoring with maintenance dosing based on the patient's metabolic capacity for the drug.

Dose-Response Relationship, Drug↗