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Biomedical subjects

J D Fewings

Publications and source records attributed to J D Fewings.

15 recordsLinked to original sources
PubMed1985

Tomaculous neuropathy: hereditary predisposition to pressure palsies.

A family is described in which six members in three generations have been affected by a remittent and pressure-sensitive mononeuritis or mononeuritis multiplex. In addition, nerve conduction studies have demonstrated the presence of peripheral neuropathy in clinically unaffected as well as affected family members, thus providing evidence of an autosomal dominant inheritance pattern. A sural nerve biopsy from one of of an autosomal dominant inheritance pattern. A sural nerve biopsy from one of the clinically affected members of this family showed 'sausage-shaped' swellings of myelin sheaths characteristic of tomaculous neuropathy. This rare condition, which is briefly reviewed, appears to be a distinctive clinicopathological entity and usually follows a benign course.

Adolescent↗
PubMed1981

The progression of Duchenne muscular dystrophy: clinical trial of allopurinol therapy.

A 12-month clinical study of Duchenne muscular dystrophy was carried out during a double-blind trial of allopurinol therapy. The disease was monitored by assessment of muscle power and function, pulmonary function tests, and electrocardiography. Biochemical assessments were made of plasma creatine kinase, pyruvate kinase, uric acid, and urinary excretion of 3-methylhistidine and creatinine. Allopurinol did not alter the progression of the disease.

Adolescent↗
PubMed1976

Emetine myopathy in the rat.

1 (-)Emetine (0.25-2.0 mg/kg i.p.) was administered to rats for up to 220 days. 2 At doses of 1.0 mg/kg or less, the animals continued to gain weight but more slowly than the untreated control animals. The physiological changes in the muscles from these animals were minimal; there was a small reduction in both the resting membrane potential and in the maximum rate of rise of the action potential. There was no atrophy or loss of muscle fibres although in the occasional muscle, hyaline fibres, necrotic fibres and split fibres were observed. There was a focal loss of myofibrillar adenosine triphosphatase (ATPase) and nicotinamide adenine dinucleotide tetrazolium reductase (NADH-TR) in Type II and Type III fibres, but no such loss in Type I fibres. 3 The animals receiving 2.0 mg/kg of (-)emetine gained weight slowly for up to 20 days but then rapidly lost weight and by 30 days they were weak and emaciated. The muscles from these animals were severly atrophied and the total muscle wet weight was reduced by almost 20%. 4 The strength of the muscles from these animals was measured in vitro using direct stimulation. They were weaker than normal both in absolute terms and when expressed in terms of tension developed/unit wet weight. 5 There was no evidence of either functional or structural denervation but surgically denervated muscles from animals in this group were indistinguishable from denervated muscles from normal rats. 6 Severe structural damage was obvious in the fibres of both extensor digitorum longus and soleus. Necrotic, hyaline and splitting fibres were common and the focal loss of myofibrillar ATPase and NADH-TR activity was extensive and occurred in Type I fibres as well as in Type II and Type II fibres. 7 It is concluded that the muscular weakness induced by (-)-emetine is due to a direct effect on the muscle fibres and that this occurs at a subcellular level. There is no evidence that functional or structural denervation plays any role in the aetiology of emetine myopathy in the rat.

Animals↗
PubMedDate not supplied

Delayed myeloradiculopathy produced by spinal X-irradiation in the rat.

Rats were subjected to 3,500 r of X-irradiation in a single dose while breathing oxygen at 1 ATM pressure. Comparison was made between the delayed effects of irradiating thoracic, lumbar, and the cauda equina fields. The lumbar field involved the alpha-motoneurons and spinal roots supplying the sciatic nerve, while the cauda equina field involved these spinal roots but spared the alpha-motoneurons in the spinal cord. Thoracic irradiation produced paraplegia after an interval of 127-150 days. In the irradiated zone, the spinal cord was severely damaged, but the thoracic spinal roots were spared. Lumbar irradiation produced paraplegia after an interval of 83-211 days. In the irradiated zone, the alpha-motoneurons were largely spared, the spinal cord showed mild to moderate white matter damage, but the most severe damage was of the lumbosacral spinal roots. The posterior roots were more affected than the anterior. In longer interval cases the degeneration of the roots appeared to be due to focal devitalization. Evidence is advanced that root degeneration had been progressing for at least 4 weeks before the onset of paraplegia. In the cauda equina series the lumbosacral spinal root changes were similar to those in the lumbar series. This study indicates that different levels of the neuraxis have different degrees of susceptibility to X-irradiation. The thoracic cord appears more susceptible than the lumbosacral; the lumbosacral roots appear more susceptible than the thoracic; the posterior roots are more susceptible than the anterior. These findings may have relevance to the study of radiation damage in man, even though the dose schedule used in this experimental study differs greatly from that used for radiotherapy.

Animals↗