Search PubMed⌕ Search

Biomedical subjects

R J Lane

Publications and source records attributed to R J Lane.

At least 55 records · Page 3Linked to original sources
PubMed1993

Abnormal glycine metabolism in motor neurone disease: studies on plasma and cerebrospinal fluid.

Plasma amino acid levels were measured following oral glycine loading in 43 patients with motor neurone disease (MND), eight normal subjects and 18 neurological disease controls with wasting or spasticity from a variety of other causes. Levels at baseline and 1.5 h after loading did not differ, but at 4 h, plasma glycine levels in MND patients remained significantly higher than in normal and neurological controls (P < 0.013). Cerebrospinal fluid glycine levels, which were maximal at 2.5 h, were also significantly higher in MND patients than neurological controls (P < 0.04). These observations suggest a defect of glycine 'housekeeping' in the central nervous system in MND which may be relevant to the pathogenesis of the disease.

Amino Acids↗
PubMed1991

Wildervanck or cervico-oculo-acoustic syndrome and MRI findings.

In 1952, Wildervanck described the first case of what he styled the cervico-oculo-acoustic (COA) syndrome. This comprises Klippel Feil's (KF) anomaly (congenitally fused cervical vertebrae), congenital sensorineural deafness and Duane's retraction syndrome (deficient abduction with retraction on adduction). Since that original paper, there have been further reports describing this triad, either completely or incompletely. A further case of this syndrome is reported and the first report of MRI head scan findings in this condition is presented. In addition, the origin of mirror movements observed as part of the KF syndrome are discussed.

Abducens Nerve↗
PubMed1990

Persistence of enteroviral RNA in chronic fatigue syndrome is associated with the abnormal production of equal amounts of positive and negative strands of enteroviral RNA.

A subgenomic restriction fragment from cDNA prepared from Coxsackie B2 virus (CVB2) RNA was subcloned into a riboprobe vector allowing the production of enteroviral group-specific RNA probes complementary to either the positive (genomic) or negative (template) strand of enteroviral RNA. These riboprobes were used to follow productive infection of cultured cells by CVB2; as expected, positive strand RNA was synthesized in approximately 100-fold excess over negative strand. RNA was extracted from muscle biopsy samples from patients with chronic fatigue syndrome and probed for the presence of enteroviral RNA. In cases where enteroviral RNA was detected the amounts of positive and negative strands of enteroviral RNA were approximately equal, in contrast to the situation in lytic infection of cultured cells. This suggests that enterovirus persistence in muscle is due to a defect in control of viral RNA synthesis.

Animals↗
PubMed1989

Effects of tenotomy on muscle histology and energy metabolism in normal and dystrophic mice.

Creatine, phosphocreatine, ATP and phosphate concentrations were measured in extracts of tibialis anterior and gastrocnemius muscles from 42 normal and 39 dystrophic mice from 1 to 16 weeks of age. No differences were observed at 1 week, prior to the onset of histological abnormalities in dystrophic animals. Creatine and phosphocreatine concentrations were significantly reduced in older dystrophic mice, and phosphate levels were higher, while ATP levels generally did not differ. Tenotomy of gastrocnemius at 1 week prevented the development of dystrophy in this muscle but this was not associated with an increase in phosphogen concentrations. Serum creatine kinase levels were significantly higher in dystrophic mice than normal mice but only during the first two weeks of life; levels in older mice were not significantly different. This study shows that the reported deficits in phosphogen concentrations in dystrophic muscles are likely to reflect the results, rather than the cause, of the dystrophic process.

Age Factors↗
PubMed1989

Screening for mitochondrial cytopathies: the sub-anaerobic threshold exercise test (SATET).

A simple test is described for identifying patients with abnormalities of muscle energy metabolism secondary to mitochondrial dysfunction, based on the venous lactate response to exercise at 90% of predicted work rate at the anaerobic threshold. The test was standardised for age, weight and sex of subjects, and was abnormal in all cases of mitochondrial cytopathy tested, with a false positive rate of 7% in a control population. The test was abnormal in two cases of mitochondrial disease in which muscle biopsy was normal or showed only non-specific changes.

Adult↗
PubMed1989

Clinical, biochemical and histological responses to treatment in polymyositis: a prospective study.

Routine methods of monitoring treatment responses in polymyositis patients, such as clinical strength assessments and measurements of ESR and serum creatine kinase, have been compared with functional strength measurements and assay of serum myoglobin levels, in a prospective study of nine cases followed for up to five years. Seven patients also underwent serial muscle biopsies during the first year of treatment in order to document the nature and chronology of histological changes during therapy. Inflammatory and necrobiotic changes indicating active myositis resolved within six months in all cases and no patient developed histological evidence of steroid myopathy. Scores on functional muscle strength assessments improved more slowly than static manual muscle strength test results, reflecting morphometric and architectural abnormalities in the biopsies which persisted throughout the period of observation. Serum creatine kinase levels returned to normal more rapidly than serum myoglobin. No statistical relationship was found between muscle strength measurements and biochemical or histological changes within the patients as a group, but variations in these indices in individual subjects reflected changes in clinical state.

Adolescent↗
PubMed1988

Repair of incompetent venous valves: a new technique.

Current techniques for treating chronic venous disease caused by venous valve incompetence all have deficiencies. A need exists for a simple technique to restore competence to the diseased valves at multiple sites in the venous system. The Venocuff is an implantable device developed to restore venous valve competence by reducing the vein circumference. Two animal models are described that are useful in the study of venous valve incompetence; the device was tested in these two models in the jugular vein of sheep. The first model was of naturally incompetent valves. The device was implanted around 11 completely incompetent and seven partially incompetent valves in 18 veins of 11 sheep. After implantation competence was restored or improved in all valves. The second model made use of an arteriovenous fistula to produce incompetence in the jugular vein in four sheep. The implant increased the pressure difference across the valve from 16 to 68 mm Hg. The Venocuff implant was thus effective at restoring valvular competence in the two animal models studied. There is evidence that valvular incompetence in these models and the results observed may be applicable in some cases of chronic venous disease in humans.

Animals↗