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Biomedical subjects

J Hunter

Publications and source records attributed to J Hunter.

At least 163 records · Page 9Linked to original sources
PubMed1987

Laser catheter ablation of simulated ventricular tachycardia.

Catheter-directed laser injury of the left ventricular endocardium for ablation of ventricular tachycardia was studied in a canine model of simulated ventricular tachycardia. Bipolar plunge electrodes were placed at thoracotomy into the left ventricular endocardium in nine anesthetized dogs. Ventricular tachycardia was simulated by pacing at 200 beats per minute. After four days of recovery, catheter-directed neodymium:yttrium-aluminum-garnet laser injury was produced at the site of earliest recorded electrical activation during pacing tachycardia as detected by endocardial catheter mapping. Immediately after laser injury and again five days after injury, pacing tachycardia was attempted. Failure to pace after laser injury was defined as successful arrhythmia ablation. In 3/9 (33%) experiments, the laser-injured tissue surrounded the tachycardia source (pacing wires), and pacing-simulated ventricular tachycardia was prevented. When the laser injury did not involve the tachycardia source, 6/9 animals, due to limitations of the mapping system, pacing was not prevented. One animal developed sustained ventricular tachycardia during laser injury, with conversion to sinus rhythm by lidocaine. One animal, without recognized ventricular arrhythmia, died five days after laser injury. No unusual findings were noted at autopsy. These preliminary data suggest that catheter-directed laser-induced injury can ablate arrhythmia sources. Further studies are indicated in a more physiologic model, and the safety and risks of the procedure need further evaluation.

Animals↗
PubMed1987

The evaluation of "spasticity".

Lesions of the upper motor neuron cause: 1. Alterations in segmental reflex activity. For example increased tendon jerks and velocity dependent stretch reflexes ("spasticity"), clonus, the clasp knife response, release of flexion reflexes and extensor plantar reflexes. 2. Impaired ability to activate motoneurons rapidly and selectively. Voluntary movements may also be restrained by co-contraction of antagonists muscles, by segmental reflexes (enhanced during voluntary effort) or by contractures. A combination of these factors may impair overall functional ability. Segmental reflexes, voluntary power and overall functional abilities can be assessed using clinical scoring systems. Recordings of muscle length, tension and EMG offer more objective measures of reflex and voluntary activity and of overall functions such as locomotion, and can separate weakness from co-contraction, spasticity from contracture. Methods are now available for exploring individual (transmitter specific) segmental reflex pathways and descending pathways in man. Lesions of the upper motor neuron are complicated by secondary changes in segmental neurons. Segmental reflex activity and muscle mechanics depend on the immediate past history of events. These factors must be taken into account.

Electromyography↗
PubMed1987

The relative roles of genetic and environmental factors in the regulation of erythrocyte C3b receptor (ECR1) numbers in normal individuals.

Erythrocyte C3b receptors (ECR1) have been measured in 122 pairs of twins (60 monozygotic, 62 dizygotic) using an [125I]-labelled monoclonal antibody (E11). The range of ECR1 numbers was wide, 99-4179 sites/cell, with a log-normal distribution around a geometric mean of 837 sites/cell. The intra-pair variance in dizygotic twins was no greater than that in monozygotic twins. These data indicate that ECR1 numerical expression is governed by environmental rather than genetic factors.

Adolescent↗
PubMed1986

Antenatal ultrasonographic findings in tuberous sclerosis. Report of 2 cases.

Tuberous sclerosis is an autosomal dominant disease with variable expression. The initial manifestations have been reported at varying stages postnatally, but little is known about the fetal age at which the disease may be detected. The antenatal ultrasonographic features in 2 affected fetuses, at 40 and 26 weeks respectively, are reported. The second case appears unique because of the early fetal involvement and the abnormally large brain tumour.

Adult↗
PubMed1986

Recurrent myocardial infarctions secondary to luetic coronary arteritis in hypertrophic cardiomyopathy. A case report.

A 43-year-old coloured man had no risk factors for atheromatous coronary artery disease but suffered two acute myocardial infarctions (MIs) in rapid succession. Serological reactions for previous syphilitic (luetic) infection were positive. Hypertrophic cardiomyopathy (HCM) without obstruction was verified, although right ventricular endomyocardial biopsy specimens did not demonstrate histological features of this disease. Extensive MI was verified on left ventricular cine angiography. Selective coronary arteriography showed that the coronary arterial tree was diffusely aneurysmal in the absence of any obstruction. We postulate that syphilitic coronary arteritis, in the absence of the more pathognomonic coronary ostial stenotic lesions, was present and may have predisposed to coronary thrombus formation and repeated acute MI. Recurrent coronary vasospasm, associated with the HCM, cannot be excluded with certainty.

Adult↗
PubMed1986

Carcase damage.

Explore the source record for details and available documents.

Abscess↗
PubMed1986

The relationship between blood-lead concentrations, intelligence, attainment and behaviour in a school population: the second London study.

This study replicates an earlier one carried out in London in which an association was found between lead and intelligence, reading and spelling. In the present study 194 children living near an urban motorway were given the same battery of tests as well as an extensive family interview to determine background variables. Before social factors were taken into account there were no significant associations between lead and outcome variable. Possible reasons for the negative results from this study are discussed.

Achievement↗
PubMed1986

An inhibitor of complement-mediated prevention of immune precipitation in rheumatoid arthritis--relationship to disease activity and systemic manifestations.

In normal serum complement prevents precipitation of antigen-antibody complexes (PIP). However rheumatoid arthritis (RA) serum contains an inhibitor of this complement-mediated function. We have undertaken two prospective studies in order to look for any relationship between the presence and levels of inhibitory activity in sera and synovial fluids (SF) of patients with RA and disease activity (study A), and the presence of systemic manifestations (nodules and vasculitis) of RA (study B). In study A, levels of inhibitory activity were highest in the sera and synovial fluids of patients with seropositive RA. However there was no correlation between the inhibitory levels and indices of generalised disease activity (articular index, erythrocyte sedimentation rate (ESR), haemoglobin, white cell and platelet counts). Local joint tenderness score correlated weakly with the inhibitory level in SF (P less than 0.05). There was no correlation, however, with either the SF protein concentration or white cell count. In study B, PIP was shown to be lower in patients with the systemic manifestations of RA than in those with purely articular manifestations. PIP was particularly low in those patients with vasculitis compared to those with subcutaneous nodules. Serum levels of inhibitory activity were highest in patients with vasculitis and lowest in those with articular disease only, whereas patients with nodules had intermediate levels. Our conclusion is that inhibition of immune precipitation is not associated with disease activity, but is associated with the extra-articular manifestations of RA. The inhibitory factor may play a role in the pathogenesis of RA.

Antigen-Antibody Complex↗
PubMed1986

Secondary amyloidosis in association with Aspergillus lung disease.

Three patients with amyloidosis secondary to bronchiectasis are described: in two patients bronchiectasis was secondary to allergic bronchopulmonary aspergillosis and in the third, post-tuberculous bronchiectasis was complicated by asthma and allergy to Aspergillus. We suggest that chronic Aspergillus allergy may cause amyloidosis and that some cases of amyloidosis ascribed to tuberculosis in the past may in fact have been secondary to Aspergillus allergy.

Amyloidosis↗
PubMed1986

Tonsil flora in the very young tonsillectomy patient.

The tonsil flora of 20 children below the age of 4 years undergoing tonsillectomy, and a control group of 18 children were studied using tonsil swabs and core specimens. The study group had a significantly higher culture rate of anaerobic organisms, whereas there was no significant difference between the groups in respect of aerobic pathogens. Since most anaerobic organisms are relatively resistant to the antibiotics usually prescribed for recurring tonsillitis, the use of more appropriate antimicrobial therapy may be helpful in the prevention of early tonsillectomy.

Age Factors↗
PubMed1986

Decreased C3b receptors (CR1) on erythrocytes from patients with systemic lupus erythematosus.

Using 125I-F(ab')2 anti-CR1 we have measured C3b receptors (CR1) on the erythrocytes of 56 normal individuals 26 patients with systemic lupus erythematosus (SLE) and 24 with rheumatoid arthritis (RA). The mean number of CR1 sites in SLE (1150/cell) but not RA (1460/cell) was significantly lower (P less than 0.01) than normal (2200/cell). Although the cumulative frequency curve for normals showed minor inflections at frequencies of 18% and 64%, these were not sufficiently marked to permit us to conclude that they distinguished subpopulations of different CR1 phenotypes. Measurement of CR1 numbers of two normal families and four families of SLE patients indicated that low CR1 numbers aggregated in families as did high CR1 numbers, a finding which suggests that CR1 numbers are under genetic control. However, certain observations in SLE patients indicated that low CR1 numbers could be an acquired abnormality. These included, (a) absent CR1 phenotype in a patient whose family had moderate and high CR1 numbers, (b) increasing CR1 numbers as SLE patients went into remission, (c) CR1 numbers were lower in patients with active compared with inactive disease and (d) CR1 numbers were different in each of two sets of identical twins (Fig. 4A). Our conclusions are that, (a) genetic factors probably influence CR1 numbers in normal individuals, (b) that our findings were not inconsistent with the two codominant allele models (Wilson et al., 1982), and (c) the low CR1 phenotype of SLE patients may be secondary to the disease process.

Arthritis, Rheumatoid↗