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Biomedical subjects

D McHale

Publications and source records attributed to D McHale.

15 recordsLinked to original sources
PubMed1996

Further evidence of genetic heterogeneity in hereditary hydronephrosis.

Hereditary hydronephrosis is a rare condition but several families are described in the literature. The inheritance pattern is autosomal dominant (McKusick number 143400) but the exact aetiology of the hydronephrosis is not clear. However, linkage with the HLA region on chromosome six has been shown previously. We report a family not showing linkage to this region, giving further evidence of genetic heterogeneity in this condition.

Adolescent↗
PubMed1993

Persistent movement disorders induced by buspirone.

Buspirone, an azospirone compound, is a nonsedative anxiolytic that has achieved wide usage since its introduction in 1987. Although relatively free of side-effects, there have been several instances of dyskinesia and dystonia associated with the use of buspirone. We report two patients with persistent movement disorders that developed after prolonged treatment with the drug. One patient developed a lasting problem of cervical-cranial dystonia and tremors after treatment with buspirone at a dosage of 40 mg/day for several weeks. Another, receiving 30 mg/day for 6 weeks, experienced an exacerbation of preexisting spasmodic torticollis and tardive dyskinesia as well as the onset of involuntary phonations. As shown by these and other examples, buspirone poses the risk for inducing or exacerbating several types of movement disorders.

Antipsychotic Agents↗
PubMed1990

A blinded study of the suppressibility of involuntary movements in Huntington's chorea, tardive dyskinesia, and L-dopa-induced chorea.

Videotapes of patients with Huntington's chorea, tardive dyskinesia (TD), and L-DOPA-induced chorea in Parkinson's disease were taken while the patients were seated with their legs dangling. The videotapes were scored in a blinded fashion for suppressibility of dyskinesias. Most patients with TD or L-DOPA-induced chorea substantially suppressed their involuntary movements, whereas most patients with Huntington's chorea did not. There was a small overlap between the TD and Huntington's chorea groups and suppressibility therefore could not absolutely distinguish between them. Suppressibility testing may nonetheless be a valuable clinical tool since a good, excellent, or complete suppressibility rating was highly suggestive of TD but not Huntington's chorea. TD and L-DOPA-induced chorea may be more pathophysiologically similar to each other than either is to Huntington's chorea.

Chorea↗
PubMed1986

The presence of free D-aspartic acid in rodents and man.

Free D-aspartic acid is present in appreciable quantities in the brain and other tissues of rodents and in human blood. In the newborn rat, the highest concentration of D-aspartic acid was found in cerebral hemispheres, where, at 164 nmol/g (8.4% of the total aspartic acid), the level of D-aspartic acid exceeds that of many essential L-amino acids. The highest ratio of D- to total aspartic acid (38%) occurred in neonatal blood cells. In the adult rat, the highest concentration was present in the pituitary gland (127 nmol/g, 3.8%). Within the central nervous system marked regional differences are present and characteristic changes with development take place. In general, the levels of D-aspartic acid fall rapidly with increasing age. In cerebral hemispheres adult values (13 nmol/g, 0.43%) are approached within one week. D-aspartic acid concentrations may also be higher in young humans since fetal blood, taken from placental cord, contains 2.6 nmol/g (4.9%) of D-aspartic acid, a value five times that of adult human blood. These distributional patterns and developmental changes may be the result of differences in the ability of various tissues to dispose of an extraneous metabolite, or, reflect alterations in a specific functional requirement for D-aspartic acid.

Age Factors↗
PubMed1966

Vitamin K and oxidative phosphorylation.

1. Oxidative phosphorylation was studied in a cell-free preparation of Mycobacterium phlei and in rat-liver mitochondria. Phosphorylation was destroyed in both systems by long-wave ultraviolet radiation and restored by the addition of small amounts of [2-Me-(14)C,(3)H]phylloquinone. When the radioactive quinones were recovered from the phosphorylating system and chromatographed with carrier phylloquinone and menaquinone-4 in adsorption and partition systems, only the phylloquinone band was labelled, and its isotopic ratio was identical with that of the original [2-Me-(14)C,(3)H]phylloquinone. This result does not support the contention that the role of vitamin K in oxidative phosphorylation involves a cyclic mechanism with intermediate formation of a quinone methide. 2. When the [2-Me-(14)C,(3)H]phylloquinone was given intravenously to rats and radioactive phylloquinone isolated from their liver mitochondria and microsomes 20hr. later, its isotopic ratio was unchanged. There was thus no evidence for quinone methide formation in vivo. No measurable conversion of phylloquinone into menaquinone-4 was observed. 3. When [(14)C]menadione was given intraperitoneally to rats whose alimentary tract had been treated with neomycin, conversion into menaquinone-4 was found in the liver mitochondria and microsomes, but there was also some indication that there had been synthesis of phylloquinone.

Animals↗