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Biomedical subjects

J MacLean

Publications and source records attributed to J MacLean.

34 records · Page 2Linked to original sources
PubMed1986

Ocular neuromyotonia. A clinical description of six patients.

We report the cases of six patients with ocular neuromyotonia, a disorder believed to result from episodic involuntary discharge of ocular motor nerves producing sustained and inappropriate contraction of their respective ocular muscles. Transient disturbances of ocular motility and diplopia result. Four patients had involvement of ocular muscles supplied by the third cranial nerve: one had presumed involvement of the superior oblique muscle, and one the lateral rectus muscle, suggesting abnormal discharge in the fourth and sixth cranial nerves, respectively. Four of six patients received prior radiation therapy for pituitary tumors, implying a possible pathogenic link. Three patients improved after treatment with membrane-stabilizing medication, suggesting that unstable membranes of injured ocular motor axons may generate spontaneous impulses, which produce involuntary sustained and inappropriate ocular muscle contraction.

Abducens Nerve↗
PubMed1986

Environmental control systems in chronic care hospitals and nursing homes.

Fifteen severely disabled people residing in institutions were provided with a simple environmental control system which performed five different functions. The disabled people used the equipment an average of ten times a day. Two hours of nursing care by nursing staff would have been required to perform these functions. The cost of the equipment was $1.35 a day. Both the residents and the nursing staff reacted favorably to this innovation. The main benefits which resulted were a heightened sense of independence on the part of the disabled people and a reduction of frustration levels of both the residents and the nursing staff. A considerable savings in nursing care was also achieved.

Attitude↗
PubMed1984

A thyrotropin radioimmunoassay kit evaluated vs two reference assays.

We evaluated a double-antibody radioimmunoassay kit for thyrotropin that includes calibrators prepared in a matrix of human serum and involves overnight nonequilibrium. Results were compared with those from two reference assays for thyrotropin. The range of within-assay CVs for the kit for thyrotropin values between 0.9 and 2.4 milli-int. units/L was 2.2 to 5.3%, that for between-assay CVs was 8.3 to 30%. The estimated minimum detectable concentration of thyrotropin was 0.6 milli-int. unit/L. We saw no cross reactivity with human choriogonadotropin by any of 48 sera from pregnant women. The original lot of serum specified as thyrotropin-free contained small but measurable amounts of thyrotropin; a second lot did not. Clinical data generated with the kit and the reference assays correlated well and were consistent with the clinical status of various categories of patients.

Chorionic Gonadotropin↗
PubMed1977

Aspartate-taurine imbalance in dominantly inherited olivopontocerebellar atrophy.

Amino acids were measured in autopsied brain from two patients who died with a dominantly inherited form of olivopontocerebellar atrophy. Neuropathologic changes found in the brain of these patients suggested a loss of cerebellar climbing fibers. The contents of aspartic acid, gamma-aminobutyric acid, and homocarnosine were reduced in the cerebellar cortex and the dentate nucleus, while taurine content was markedly elevated in the same brain regions. These findings are compatible with the possibility that aspartic acid is the excitatory synaptic transmitter of the climbing fibers and taurine is the inhibitory neurotransmitter of one or more types of interneurons in the cerebellum.

Adult↗
PubMed1976

Cerebrospinal fluid and plasma glutamine elevation by anticonvulsant drugs: a potential diagnostic and therapeutic trap.

Administration of phenobarbitone or primidone can produce an elevation of glutamine and ornithine concentrations, together with a reduction of urea concentrations, in the fasting plasma and CSF of some infants, and in the CSF of some older epileptic patients. These two anticonvulsant drugs may interfere with the metabolic conversion of ammonia to urea, possibly by enzyme inhibition at the step of carbomoyl phosphate synthesis. The elevation of glutamine in plasma and CSF can mimic values found in some hyperammonemias. Recognition of this drug reaction can prevent erroneous diagnoses of genetically-determined urea cycle disorders and subsequent inappropriate therapy.

Adolescent↗
PubMed1975

Nonketotic hyperglycinemia. Glycine accumulation due to absence of glycerine cleavage in brain.

Glycine concentrations were measured in plasma and cerebrospinal fluid of five patients in different types of hyperglycinemia to determine why severe neurologic deterioration is confined to the so-called nonketotic form of hyperglycinemia. Glycine content and glycine-cleavage enzyme activity were also determined in brain obtained in autopsy from three of these patients. Spinal-fluid glycine concentrations were 15 to 30 times above normal in patients with nonketotic hyperglycinemia, but were normal in those with hyperglycinemias of undetermined type who had comparable elevations of plasma glycine. Glycine content was two to four times above normal in several brain regions, and brain glycine cleavage enzyme activity was absent in two patients dying of nonketotic hyperglycinemia. By contrast, glycine content was normal and glycine cleavage activity present in the brain of an infant who died of hyperglycinemia of unknown cause. These results suggest that elevated glycine levels may be harmless in blood, but lethal in brain.

Adult↗