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S Rees

Publications and source records attributed to S Rees.

At least 127 records · Page 7Linked to original sources
PubMed1985

Activity dependent plasticity of postsynaptic density structure in the ventral cochlear nucleus of the rat.

Young adult male rats were anaesthetised with urethane and exposed to either 24 h of silence or 24 h of repetitive 77 dB tones in a sound-proofed anechoic chamber. The influence of these two conditions on the ultrastructure of the synaptic appositions made by auditory afferents in the anterior ventral cochlear nucleus (end bulbs of Held) was compared. Both the cross-sectional area and the mean thickness of the postsynaptic density (PSD) in the rats exposed to tones were significantly reduced when compared with rats maintained in silence. Similarly, the degree of curvature of the apposition was significantly reduced. The results of these experiments provide further evidence that the postsynaptic density material is a plastic structure significantly influenced by the amount of activity in the presynaptic element.

Acoustic Stimulation↗
PubMed1984

An evaluation of two-dimensional echocardiography in the diagnosis of hypertrophic cardiomyopathy.

Various anatomical and functional features of hypertrophic cardiomyopathy are analyzed in view of the data provided by two-dimensional echocardiography. Measurement of septal thickness is crucial, and is best done by a combination of M-Mode and 2-D echo. Two types of systolic anterior movement of the mitral valve (SAM) are observed and are related to the degree of subvalvular gradient. The specificity of these patterns of SAM is analyzed. The functional anatomy of the mitral valve in relation to the presence and degree of mitral regurgitation shows that although the presence and type of SAM are important, there are other causes of mitral regurgitation in hypertrophic cardiomyopathy unrelated to SAM. We emphasize the fact the 2-D echo cannot "diagnose" hypertrophic cardiomyopathy except when cardiac hypertrophy plus SAM involving the body of the mitral valve is seen; in the remaining cases, 2-D echo confirms/suggests the clinical diagnosis.

Cardiomyopathy, Hypertrophic↗
PubMed1984

Increased body:brain weight ratio in developing rats after low exposure to organic lead.

Tetramethyl lead in an oily vehicle was administered to rats at weekly intervals during gestation and early postnatal life, raising the total lead concentration in the brain to about 1 microgram/g. Birth weight was unaffected, but postnatal body growth was stimulated more than brain growth, resulting in a higher body:brain weight ratio. Histological measures of brain myelination, dendritic growth, granule cell production, and retinal receptor development showed no deficit. We conclude that the body:brain weight ratio is the most sensitive of the parameters measured for detecting the effect on development of exposure to a low concentration of tetramethyl lead. The latter is neurotoxic at higher concentrations, and the stimulating effect on body growth of a low concentration is an example of "hormesis," a phenomenon which has been noted with other toxins.

Animals↗
PubMed1983

The mechanism of mitral regurgitation in dilated left ventricle.

To assess the mechanism of mitral regurgitation in ventricular dilatation, 24 patients with dilated cardiomyopathy (13 with and 11 without mitral regurgitation) and 10 normal individuals were studied by two-dimensional echocardiography. Left ventricular dimensions and mitral ring diameters in systole and diastole were measured in the long-axis section, and systolic interpapillary muscle distance in the short-axis section. The results showed: Mitral ring diameter is increased in most patients with dilated cardiomyopathy. Neither increased ring diameter, reduced ring contraction, nor decreased interpapillary muscle distance determine the presence of mitral regurgitation. The only difference between those patients with and without mitral regurgitation was the degree of left ventricular dilatation (p less than 0.05).

Adult↗
PubMed1983

Is silica involved in neuritic (senile) plaque formation?

The agent responsible for inducing neuritic (senile) plaque formation in senile dementia of the Alzheimer's type and in the ageing non-demented brain is unknown. Other workers have detected a high concentration of silicon in the rims and cores of senile neuritic plaques. We have therefore looked at whether the reaction of brain tissue to silica particles resembles a neuritic plaque. In this study both fine (10 nm) and coarse (less than 5 microns) particles of silica have been introduced into the brains of rats and mice using a wide range of doses and several methods of administration. The reaction of the brain to the presence of the silica was examined by light and electronmicroscopy up to one year after the injection. The presence of silica particles in the brain resulted in the proliferation of fibrous astrocytes and macrophages and strongly stimulated the production of collagen fibres. Degeneration of some adjacent axons and axon terminals occurred, but there was no detectable deposition of amyloid which is characteristic of senile plaques. Coarse particles of silica invariably produced a more intense reaction than fine particles. The reaction of the brain did not diminish with time within one year of injection. The possible significance of the presence of silica in the plaque as a secondary phenomenon is discussed.

Alzheimer Disease↗
PubMed1983

Systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy. A cross-sectional echocardiographic study.

UNLABELLED: Different cross-sectional echocardiographic patterns of systolic anterior motion of the mitral valve (SAM) have been observed in patients with hypertrophic cardiomyopathy. chordae tendineae and/or the free edge of the mitral valve were seen to be involved in some: SAM(c). The body of the mitral valve encroached upon the left ventricular outflow tract in this movement in a second group: SAM(v). Other patients did not show SAM. A study of 27 patients was performed to investigate the relationship of these patterns of SAM to the subaortic gradient as well as the prevalence and degree of mitral regurgitation. The absence of SAM correlated with no obstruction and 29% prevalence of mitral regurgitation. In SAM(c), the mean gradient was 10 +/- 10 mmHg. (0-35 mmHg), and mitral regurgitation involved 36% of the patients. In SAM(v) the mean gradient found was 81 +/- 37 mmHg (20-150), and 67% had mitral regurgitation. In situations where mitral regurgitation was most prevalent its degree was greatest. IN CONCLUSION: (1) chordal or leaflet participation in SAM is relevant to the presence and degree of obstruction; (2) leaflet involvement usually implies severe obstruction; (3) distortion of the mitral valve apparatus may contribute to the genesis of mitral regurgitation.

Adolescent↗
PubMed1983

Different mechanisms of mitral regurgitation in acute and chronic forms of coronary heart disease.

Contradictory two-dimensional echocardiographic findings have been reported in relation to the role of prolapse of the mitral valve and lack of systolic leaflet coaptation in mitral regurgitation secondary to coronary heart disease. A prospective study of 22 patients with chronic coronary heart disease and mitral regurgitation showed the following: Inferior akinesia was detected in 14 (64%), fibrosis of the postero-medial papillary muscle in 10 (45%), and prolapse of the mitral valve in nine (41%). A combination of the three signs was seen in six patients (27%). Lack of systolic leaflet coaptation was seen in only two patients, both with anterior myocardial infarction. When these results are compared with those reported in the literature, it is apparent that in acute coronary heart disease, lack of leaflet coaptation is frequently visualized (P less than 0.01) and fibrosis of the postero-medial papillary muscle and prolapse of the mitral valve are lacking (P less than 0.01). A unitary explanation of all forms of mitral regurgitation in coronary heart disease is misleading; mechanisms of mitral regurgitation in coronary heart disease depend on the clinical presentation--acute or chronic, the site of infarction, and the presence of cardiac dilatation.

Adult↗
PubMed1982

Organomegaly and histopathology in an animal model of mucopolysaccharidosis induced by suramin.

The trypanocidal drug suramin causes glycosaminoglycan and sphingolipid accumulation in the rat, thus simulating a mucopolysaccharidosis (Constantopoulos et al. 1980). In this paper we report on the extent and nature of the morphological changes that occur in the liver, kidneys, spleen, heart, lung and brain as a result of short or long term suramin administration. The first group of rats received a single intravenous injection of suramin (500 mg/kg) and was sacrificed 3-9 days after the injection. The second group received low doses of suramin (50-90 mg/kg) at 2-3 weekly intervals over 3 months. Samples of the above mentioned organs were processed for light and electronmicroscopy and the remainder of the tissue weighed and assayed for total protein, DNA and RNA content. In both groups of rats, suramin caused an abnormal enlargement of the spleen, kidney, lung and liver, splenomegaly being the most pronounced. The total protein, and DNA content did not alter in the treated rats, however, the RNA content of the spleen increased 100%, 9 days after injection and there was a small but consistent increase in RNA content of the liver, kidney and lung. Significant pathological changes were observed in these organs and also in the brain and heart. The changes were similar in many respects to the pathology seen in the lysosomal storage disorder, mucopolysaccharidosis and further support the proposition that the suramin treated rat might be a useful experimental animal model of the disease. Several mechanisms by which suramin might produce organomegaly in the rat are discussed.

Animals↗
PubMed1982

Comparison of extracellular space in the mature and aging rat brain using a new technique.

A new technique for measuring extracellular space in the rat brain has been developed. It involves opening the blood-brain barrier with a bolus of hyperosmotic sucrose followed by a high-pressure perfusion of the cerebral vasculature with an isotonic solution containing an impermeant radioactive tracer, [3H]sucrose. After allowing the concentration of tracer in the brain to reach a plateau, the amount of radioactivity/mg of brain tissue is expressed as a percentage of the amount of radioactivity/mg of perfusate to obtain a value for extracellular space. The addition of glutaraldehyde to the perfusate results in the brain being fixed simultaneously for electron microscopy. Reproducible estimates of extracellular space were obtained similar to those obtained by other methods (e.g. Levin et al. 1970). As it is impossible to be sure of the validity of the absolute value of extracellular space obtained by any method using perfused solutions we have used our method for comparative purposes. Extracellular space was measured in mature (control) and ageing rats to test the claim that the volume of space in the cerebral cortex is substantially reduced with ageing (Bondareff and Narotsky 1972). We found a consistent tendency for the extracellular space to increase with age in the 6 regions of brain examined. This was not statistically significant except in the group of ageing rats on a food-restricted diet. Therefore, these results do not support a generalisation that the extracellular space decreases in the ageing brain. In both control and ageing rats, extracellular space was shown to be unevenly distributed in the brain, the largest space being present in the cerebellum, olfactory bulb, inferior and superior colliculi and the least space in the white matter. These are the first measurements of extracellular space in which assessment is possible by both electron microscopy and by the measurement of a chemical tracer.

Aging↗
PubMed1981

Effect of suramin on the activities of degradative enzymes of sphingolipids in rats.

Three to nine days after administration of suramin, 500 mg/kg intravenously in rats, a small amount of the drug (about 0.25 micromoles/g tissue) was retained by the liver and spleen, and a larger amount (about 1.2 micromoles/g tissue) was retained by the kidneys. The activities of the sphingolipid hydrolases beta-hexosaminidase and GM3-sialidase were strongly inhibited by suramin in vitro. The activity of beta-hexosaminidase was inhibited 70% by 10(-5M) and 85% by 10(-4M) suramin, and the activity of GM3-sialidase was inhibited 80% by 10(-4M) suramin. The activities of sphingomyelinase and beta-galactosidase were also inhibited by suramin but at higher concentrations of the drug. Suramin, in vitro is a weak inhibitor of glucocerebrosidase, galactocerebrosidase, alpha-galactosidase and arylsulfatase A (less than 50% inhibition at 10(-3M) concentration of the drug). The inhibition of beta-hexosaminidase by suramin was non-competitive. Inhibition of beta-hexosaminidase and GM3-sialidase may explain the accumulation of GM2 and GM3 gangliosides in the brains of rats treated intracerebrally with suramin (Constantopoulos et al, 1980).

Animals↗
PubMed1980

Experimental animal model for mucopolysaccharidosis: suramin-induced glycosaminoglycan and sphingolipid accumulation in the rat.

Intracerebral injection of the trypanocidal drug suramin in rats caused the formation of membranous neuronal and neuroglial inclusions. Here we show that intravenous administration suramin, 500 mg/kg, to 2-month-old rats causes a 5- to 8-fold increase of glycosaminoglycan concentration in the liver within 10 days and a 6-fold increase in urinary glycosaminoglycan excertion. The excess glycosaminoglycans consist of heparan sulfate and dermatan sulfate. Intracerebral injection of 250 micrograms of suramin results in a small increase of glycosaminoglycan and larger increase of ganglioside GM2, GM3, and GD3 concentrations in the treated region of the brain. The activities of the lysosomal enzymes iduronate sulfatase, beta-glucuronidase, and hyaluronidase in the liver of the suramin-treated mature rats were consistently decreased, whereas those of alpha-L-iduronidase, heparan N-sulfatase, arylsulfatase B, and others were considerably increased. The activity of iduronate sulfatase was completely inhibited in vitro by suramin at concentrations of 50 microM or higher. The activity of beta-glucuronidase was also strongly inhibited by low concentrations of suramin, but this inhibition was partially decreased at higher concentrations of the drug. The inhibition of both enzymes by suramin was noncompetitive. The suramin-treated rat may be a useful experimental animal model of mucopolysaccharidosis.

Age Factors↗
PubMed1980

Dual isotope stress testing in congenital atresia of left coronary ostium. Applications before and after surgical treatment.

A 38-year-old women presented with an 11-year history of angina pectoris. Coronary arteriography disclosed a large right coronary artery which filled the entire left coronary tree retrogradely. The left main coronary artery ended blindly and was not connected to the aortic root. There were no atherosclerotic lesions in any vessel. Exercise thallium-20l scintigrams showed a perfusion defect in the anterior region of the left ventricle and exercise first pass radionuclide ventriculography showed anterior hypokinesis of the left ventricle with an ejection fraction of 54 per cent, compared with 60 per cent at rest. An aortocoronary saphenous vein graft was constructed to the left coronary artery. Four months after operation the patient is free from symptoms. Repeat thallium scintigrams were normal. Exercise radionuclide ventriculography after operation disclosed no wall motion abnormality, and ejection fraction on exercise was 70 per cent. The mechanism of angina in this patient is unclear but may have been related to the abnormal timing of delivery of blood to the left ventricular myocardium. Dual radionuclide stress testing showed abnormalities after operation. This non-invasive approach may be useful in the assessment of the physiological significance of coronary anomalies and of the value of corrective surgery.

Adult↗
PubMed1978

Membranous neuronal and neuroglial inclusions produced by intracerebral injection of Suramin.

A single intracerebral injection of 5 micrometer of the trypanocidal drug Suramin, into the left hemisphere of young rats, resulted in the formation of membranous inclusion bodies within the perikarya and processes of neurones and neuroglia. These inclusion bodies were round or oval in shape and 0.5-3.0 micrometer in their longest diameter. They were bounded by a single trilaminar membrane and contained closely packed membranes in concentric, curved or parallel arrays. The inclusions were distributed throughout the cerebral cortex and underlying hippocampus at the injection site, and in reduced numbers up to 1 mm anteriorly and posteriorly from it. They formed within 22 hr of the injection and had increased in numbers and in the complexity of their arrays 3 days after injection. Within 14 days, the inclusions were markedly reduced in number. As Suramin is known to inhibit lysosomal hydrolases required for the degradation of proteins, glycolipids and mucopolysaccharides, the membranous inclusions could form as a result of the accumulation of these substances within lysosomes. These experiments indicate a possible experimental model for storage diseases. It is hoped that the extension of this paradigm to other enzyme inhibitors will provide a new means of identifying some of the unusual inclusions that can be found in neurones and neuroglia (Rees 1975).

Animals↗
PubMed1977

The incidence of ultrastructural abnormalities in the cortex of two retarded human brains (Down's syndrome).

In a quantitative electronmicroscopic study, autopsy samples from the frontal and temporal lobes of two severely defective mongoloid brains were examined for the presence of abnormalities in the ultrastructure of the cerebral cortex. Particular attention was paid to the occurrence of atypical neuronal and glial inclusions similar to those which occur in small numbers (1 in 5000 mu2 of cortex) in neurologically normal brain (Rees, 1975). An area of 3.6 x 10(5) mu2 of cortex was examined from each brain. Within the cortical parenchyma, there was no gliosis, neuronal death or areas of degeneration. Atypical neuronal and glial inclusions were observed in both of the retarded brains, but they did not occur in substantially different numbers from normal brains. There were no inclusions or structural abnormalities peculiar to the retarded brains. Thus, in these two defective brains, it has not been possible to demonstrate any specific abnormalities in the ultrastructure of the cortex.

Adolescent↗