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L W Bond

Publications and source records attributed to L W Bond.

11 recordsLinked to original sources
PubMed1990

Valproic acid-associated pancreatitis: report of three cases and a brief review.

We describe three patients with seizure disorders in whom pancreatitis or pancreatic injury was probably caused by valproic acid, a widely used anticonvulsant drug. Trivial or no increases of serum amylase (EC 3.2.1.1) but striking increases of serum lipase (EC 3.1.1.3) were common to all patients, as assayed in the Kodak Ektachem. In vitro, valproic acid does not cause any change in serum lipase. In patients with symptoms suggestive of pancreatitis and abnormal values for amylase and (or) lipase, treatment with valproic acid should be discontinued.

Adolescent↗
PubMed1977

Formation and properties of lactate dehydrogenase inhibitors in NADH.

We describe some characteristics of the mode of formation of inhibitors of lactate dehydrogenase from commercial NADH. Inhibitor formation is time- and concentration-dependent and also varies with the commercial source of NADH. At least two inhibitory components can form in concentrated NADH solutions. One of these can be separated from NADH by chromatography on either diethylaminoethyl-celluose or diethylaminoethyl-Sephadex; the second cannot. The NADH-associated inhibitor appeared to be present in each of the three commercial NADH preparations studied. The 260 nm/340 nm absorbance ratio was of no help in locating this inhibitor during chromatography.

Chromatography, Ion Exchange↗
PubMed1976

Partial purification and properties of the fatty acid elongation systems in the outer and inner membranes of beef liver mitochondria.

Purified outer membrane of beef liver mitochondria was found to elongate medium chain fatty acyl-CoA primer by the incorporation of [1-14C]acetyl-CoA. This enzymic activity, extracted by Triton X-100, was purified 8-fold by ammonium sulfate fractionation followed by chromatography on a Sephadex column. Purified inner membrane, when processed through an identical purification procedure, yielded a second enzyme system which incorporated [1-14C]acetyl-CoA into long chain fatty acids in the presence of medium chain fatty acyl-CoA primer. This enzyme preparation was about four times as active as the preparation from the outer membrane, and used NADH as the reductant for the synthesis. The molecular weights of the inner and the outer membrane enzyme systems, estimated by gel filtration as well as sucrose density gradient centrifugation, were approx. 57 000 and 126 000, respectively. The partially purified outer membrane enzyme system required NADH and a medium chain acyl-CoA primer for the incorporation of [1-14C]acetyl-CoA into long chain fatty acids. KNC stimulated the reaction. NADPH could substitute for NADH only to a limited extent. Malonyl-CoA was ineffective as a substrate in this reaction. The optimum pH of the reaction was 7.2-7.6 in 0.1 M potassium phosphate buffer. Dithiothreitol, beta-mercaptoethanol, N-ethylmaleimide and high concentrations of ATP and acyl-CoA primer inhibited the reaction. The specificity for the acyl-CoA primer in the reaction was very broad. All the primers tested, C8 to C16, incorporated acetyl-CoA significantly. However, maximum incorporation was observed with dodecanoyl-CoA. Decanoyl-CoA was the best primer for the enzyme system isolated from the inner membrane. About 42% of the radioactivity in the fatty acids synthesized by the outer membrane enzyme system, from myristoyl-CoA and [1-C14]acetyl-CoA, was in palmitic acid. Of the remaining activity, 41% was in stearic acid and about 38% in longer-chain acids. Hence, the elongation of the primer fatty acid by one C2 unit appeared to be the predominant process in this synthesis. In the elongation of myristoyl-C0A by the inner membrane enzyme system, palmitic acid which constituted nearly 78% of the fatty acids synthesized, was the primary product.

Animals↗
PubMed1976

Determination of the molar absorptivity of NADH.

The molar absorptivity of NADH at 340 nm has been determined by an indirect procedure in which high-purity glucose is phosphorylated by ATP in the presence of hexokinase, coupled to oxidation of the glucose-6-phosphate by NAD+ in the presence of glucose-6-phosphate dehydrogenase. The average value from 85 independent determinations is 6317 liter mol-1 cm-1 at 25 degrees C and pH 7.8. The overall uncertainty is -4.0 to +5.5 ppt (6292 to 6352 liter mol-1 cm-1), based on a standard error of the mean of 0.48 ppt and an estimate of systematic error of -2.6 to +4.1 ppt. Effects of pH, buffer, and temperature on the molar absorptivity are also reported.

Absorption↗
PubMedDate not supplied

Impact of cimetidine on the pharmacokinetics of theophylline.

The effect of cimetidine on the pharmacokinetics of theophylline was evaluated. Twelve healthy men volunteers participated in this two-way crossover study. Six subjects were initially treated with theophylline (control), and six were treated with cimetidine and theophylline (cimetidine). Sixteen days after the start of the first phase, the subjects were crossed over. Aminophylline equivalent to 2 mg/kg theophylline was dissolved in 100 ml 5% dextrose injection and infused into an antecubital or forearm vein over a 20-minute period. Cimetidine was ingested in 300-mg doses every six hours beginning 48 hours before the theophylline infusion and continued until 48 hours after the infusion. Blood samples were collected periodically for 48 hours, and serum theophylline concentrations were determined by liquid chromatography. Theophylline concentration versus time data were computer fitted to a biexponential equation. Total theophylline clearance (CLtot), apparent volume of distribution (V), and elimination half-life (t 1/2 beta) were calculated. Semilogarithmic plots of theophylline disappearance showed a decrease during cimetidine treatment. Mean theophylline t 1/2 beta increased significantly during cimetidine treatment from 5.9 +/- 1.0 to 7.3 +/- 1.5 hr, and CLtot decreased significantly from 0.065 +/- 0.010 to 0.049 +/- 0.012 liter/hr/kg. Mean V was unchanged. Two subjects failed to exhibit decreased theophylline clearances, and theophylline clearance increased in another subject. Cimetidine was found to slow the clearance of theophylline and to extend its half-life. Daily doses of theophylline may require adjustment in patients requiring the coadministration of cimetidine. Cimetidine should be added with caution, and serum theophylline concentrations should be monitored accordingly.

Adult↗