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Biomedical subjects

L A Melton

Publications and source records attributed to L A Melton.

5 recordsLinked to original sources
PubMed2001

Brn-3a activates the expression of Bcl-x(L) and promotes neuronal survival in vivo as well as in vitro.

The determination of cell fate plays a critical role during the later stages of embryogenesis and the early postnatal period-a time during which approximately half of neurons born during neurogenesis undergo programmed cell death. It has previously been reported that the type IV POU domain transcription factor Brn-3a plays a role in the maturation and survival of sensory neuronal populations. Indeed we have shown that the long form of Brn-3a is capable of activating expression of the antiapoptotic Bcl-2 gene and enhancing neuronal survival in cultures of sensory neurons. In this study, we report the identification of another antiapoptotic family member, Bcl-x(L), as a target gene of Brn-3a in sensory neurons, providing a further mechanism by which Brn-3a determines sensory neuronal fate during development. Bcl-x(L) gene expression is activated by Brn-3a in sensory but not in sympathetic neurons and its expression is reduced by antisense inhibition of Brn-3a expression in sensory neurons. Most importantly, both Bcl-x(L) expression and neuronal survival are enhanced by the overexpression of Brn-3a in dorsal root ganglion in vivo in a model of sciatic nerve injury in the intact animal.

Animals↗
PubMed1990

Lead concentrations in blood and milk from periparturient dairy heifers seven months after an episode of acute lead toxicosis.

In September 1988, 100 of 300 yearling dairy heifers developed blindness, tachypnea, foaming at the mouth, chewing, and facial fasciculations. Twenty-five animals died. Lead toxicosis was diagnosed based on the clinical signs and the presence of excessive concentrations of lead in whole blood, liver, kidney, and rumen contents of affected animals. The source of the lead was sudan grass silage that had been contaminated by soil that contained up to 77,000 mg/kg of lead. Lead concentrations were determined approximately 7 months after the acute episode of lead toxicosis. Whole blood and milk samples were obtained from heifers and a group of control cows 2 weeks prior to (blood only), at the time of, and 2 and 4 weeks after freshening. No lead was found in any of the milk samples (detection limit = 0.055 mg/liter). Animals that had been severely affected by lead toxicosis experienced a transient increase in whole blood lead concentrations at freshening that was not high enough to be considered toxic. No similar increases in blood lead were observed for control cows or heifers that had experienced milder toxicosis. These findings suggest that at parturition lead is mobilized into the blood of cattle previously exposed to excessive lead.

Animals↗
PubMed1990

Screening trace elements and electrolytes in serum by inductively-coupled plasma emission spectrometry.

This rapid, accurate procedure for trace elements and electrolytes in serum requires little sample preparation: to 1 mL of serum a single reagent is added that contains trichloroacetic and hydrochloric acids for protein precipitation, hydroxylamine sulfate for iron reduction, and yttrium as the internal standard. After centrifugation, the supernates are directly analyzed for Na, K, Mg, Ca, Pi, Fe, Cu, and Zn by inductively-coupled plasma emission spectrometry. The CVs were respectively 7.9%, 8.4%, 8.6%, 10.0%, 9.0%, 9.4%, 9.0%, and 9.0% for five assays of National Institute of Standards and Technology Standard Reference Material (SRM) no. 1598, Bovine Serum. Analytical recoveries ranged from 92% to 107% for both SRM 1598 and commercial control serum.

Blood Chemical Analysis↗