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Biomedical subjects

A M Lucas

Publications and source records attributed to A M Lucas.

12 recordsLinked to original sources
PubMed1992

Linkage studies in Charcot-Marie-Tooth disease type 2: evidence that CMT types 1 and 2 are distinct genetic entities.

Charcot-Marie-Tooth disease (CMT), the most common inherited peripheral neuropathy, is a progressive sensorimotor neuropathy divided into types 1 and 2 based upon electrophysiologic and neuropathologic differences. The more common autosomal dominant form of CMT type 1 (hereditary motor and sensory neuropathy type I) is genetically heterogeneous, with genes located on chromosomes 1 (type 1B) or 17 (type 1A). However, no locus for CMT type 2 is known. We have performed linkage studies on three large multigenerational CMT type 2 families using probes from chromosome 1 and chromosome 17, which span their respective linkage regions. Multipoint analysis of the chromosome 17 markers excluded linkage over an area of 45 cM--15 cM proximal and 30 cM distal to the region containing CMT type 1A. Multipoint analysis of the chromosome 1 markers exclude linkage 15 cM proximal and 20 cM distal to FC-gamma-RII in the region of CMT 1B. These data indicate that CMT type 2 is genetically distinct from CMT type 1.

Adolescent↗
PubMed1987

Role of protein kinase C in the pigment cell of the lizard (Anolis carolinensis).

The role of protein kinase C in melanosome dispersion was examined using the melanophores of the lizard Anolis carolinensis and an in-vitro rate method of bioassay. The phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate (TPA), which directly activates protein kinase C, was able to potentiate the melanophore response to alpha-MSH in a dose-dependent manner. Similarly, the stimulatory response to forskolin, which activates the adenylate cyclase catalytic subunit, was also potentiated by TPA. The response of the melanophore to cyclic AMP, however, remained unaltered by any dose of TPA. We thus propose that the potentiation of alpha-MSH potency by TPA is through an interaction of protein kinase C with adenylate cyclase and, more specifically, that this interaction may be at the level of the linkage of the nucleotide regulatory subunit Ns with the catalytic moiety C of adenylate cyclase.

Animals↗
PubMedDate not supplied

Alpha-MSH and coat color changes in the mouse.

The effect of alpha-MSH on coat color was examined in viable yellow mice (C3H/He-A*vy). These mice normally grow a coat of darkly pigmented hair at puberty. This darkening effect was also evident in hair that grew in a region that had been plucked at 13 days of age. Administration of alpha-MSH increased the darkness of this hair and the hair which grew naturally in an unplucked area. However, the natural coat darkening that occurred at puberty was not associated with an increase in plasma immunoreactive alpha-MSH levels. Moreover, although bromocryptine, a dopamine agonist that inhibits alpha-MSH release from the pituitary reduced the darkness of the coat that grew after plucking the reduction in coat darkening was unrelated to changes in plasma alpha-MSH. Nevertheless, this effect of bromocryptine was reversed when alpha-MSH was administered together with the drug. Apomorphine had no effect on coat darkening and produced only a slight decrease in plasma alpha-MSH. Melatonin reduced coat darkening slightly but, like apomorphine, had little effect on plasma alpha-MSH concentrations. Although alpha-MSH may have a physiological role in coat darkening in the C3H/He-A*vy mouse at puberty the response seems to be unrelated to an increase in circulating alpha-MSH. Thus, other factors, such as changes in melanocyte sensitivity to alpha-MSH or inhibitory mechanisms that prevent coat darkening during prepubertal and adult life may be involved in regulation of coat color in the viable yellow mouse.

Animals↗
PubMedDate not supplied

The role of calcium in MSH stimulated melanosome dispersion.

We have examined the role of the calcium ion in the response of the melanophores of the lizard, Anolis carolinensis to alpha-melanocyte stimulating hormone (alpha-MSH) by a rate method which allows kinetic analysis of melanosome dispersion. Dose-response curves to alpha-MSH were compared in the presence of different calcium concentrations, and Schild regression plots were constructed. An avidly binding analogue of alpha-MSH, Nle4-D-Phe7-alpha-MSH, was used to demonstrate kinetically the involvement of calcium in the melanophore response both for MSH receptor binding and the subsequent transduction of the MSH signal across the melanophore membrane.

Animals↗
PubMedDate not supplied

Sensitive method for the determination of phenytoin in plasma, and phenytoin and 5-(4-hydroxyphenyl)-5-phenylhydantoin in urine by high-performance liquid chromatography.

An isocratic high-performance liquid chromatographic method is described for the quantitative analysis of phenytoin (PHT) in plasma and both phenytoin and its main metabolite, 5-(4-hydroxyphenyl)-5-phenylhydantoin (p-HPPH) in urine. Following ethyl acetate (plasma) and Extrelut-1 (urine) extraction, samples are analysed by means of a reversed-phase column (Nova-Pak C18), using a mobile phase consisting of methanol-water-tetrahydrofuran (40:60:4, v/v/v) with UV detection at 230 nm. The chromatography is complete in 10 min and the results show good precision (RSD 1.23-4.49%) and sensitivity for a linear range of 0.4-4.0 micrograms ml-1 for PHT in plasma, 0.1-1.0 microgram ml-1 for PHT in urine and 0.1-1.2 microgram ml-1 for p-HPPH in urine. The results indicate the method to be suitable for pharmacokinetic studies.

Acetates↗