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Biomedical subjects

S J Pearson

Publications and source records attributed to S J Pearson.

At least 19 recordsLinked to original sources
PubMed2004

Power output of the lower limb during variable inertial loading: a comparison between methods using single and repeated contractions.

The power-inertial load relationship of the lower limb muscles was studied during a single leg thrust using the Modified Nottingham Power Rig (mNPR) and during cycling exercise in nine young male subjects. The relationship between peak power and inertial load showed a parabolic-like relationship for mNPR exertions, with a peak [937 (SD 246) W] at 0.158 kg m(2), this being significantly (P <0.05) different from the power generated at both the lowest [723 (162) W] and highest [756 (206) W] inertial loads. In contrast, for cycling exercise power output did not differ significantly between inertial loads, except at the lowest inertia where power output was significantly ( P<0.05) less compared with all other inertial loads. Maximum peak power output during cycling was 1,620 (336) W, which was significantly (P <0.05) greater than that recorded on the mNPR. However, a close association was observed between the mean power generated by each method (r=0.84, P<0.05). The results suggest that during a single contraction a range of inertial loads is required to allow peak power to be expressed. Above a certain critical value, this is unnecessary during cycling movements where the load can be repeatedly accelerated.

Adaptation, Physiological↗
PubMed2001

A variable inertial system for measuring the contractile properties of human muscle.

PURPOSE: A flywheel system of variable inertia is described for inferring the mechanical properties of human muscle during a single explosive movement. METHODS: The system consists of a lightweight aluminum disk mounted on a shaft onto which a driving cog is mounted. The inertia of the system can be varied from 0.024 to 0.69 kg.m(2) by attaching semicircular steel plates to the disk. A rotary encoder detects displacement of the wheel with a resolution of 1 degrees. Digital signals from the encoder are collected using an A/D converter interfaced to a PC. The data are then processed for the calculation of torque, velocity, power, work done, and acceleration. The mechanical properties of the muscles employed are inferred from calculations of flywheel displacement, time, and force. In addition, a pretension release mechanism can be incorporated into the system to allow isometric force to be developed before movement. This can increase power generation at the low inertias where the time of contraction is typically less than 200 ms. Seven subjects were test-retested using the device. Measures of both average and peak power were made. RESULTS: When mounted in the apparatus described by Bassey and Short, the maximum values for peak and average power were on average 965 +/- 103 and 448 +/- 47 W, respectively. Upon retesting, these results were found to be reliable (cv = 3.3% and 3.0%, respectively). CONCLUSIONS: The inertial system described has been shown to have validity in reproducibility and provided a suitable method of determining a number of muscle output properties during short-term single exertions. This tool could prove useful in a research or clinical setting and may also prove useful as a training device as it negates the need for a strain gauge or goniometer attachment.

Acceleration↗
PubMed1996

Imidazoline binding sites in Huntington's and Parkinson's disease putamen.

Binding of [3H]2-(2-benzofuranyl)-2-imidazoline ([3H]BFI) to the imidazoline I2 receptor was determined in putamen taken post mortem from patients with two extrapyramidal motor disorders, Parkinson's and Huntington's diseases, and age-matched control subjects. No deficit of binding was apparent in Parkinson's disease, indicating that the receptors are not present on nigrostriatal terminals. A significant loss (by 56%) in imidazoline I2 receptor binding was observed in Huntington's disease, consistent with the receptors being sited on degenerating neurons.

Adrenergic alpha-Antagonists↗
PubMed1995

An investigation of the activities of 3-hydroxykynureninase and kynurenine aminotransferase in the brain in Huntington's disease.

Previous reports have indicated abnormalities in the concentrations of metabolites of the tryptophan/kynurenine pathway in the brain in Huntington's disease. These have included an increase in 3-hydroxykynurenine and both increases and decreases in kynurenic acid. The activities of two enzymes involved in the metabolism of these compounds, 3-hydroxykynureninase and kynurenine aminotransferase, have been determined in post mortem brain tissue taken from Huntington's disease patients and control subjects.

Aged↗
PubMed1994

Neocortical neurotransmitter markers in Huntington's disease.

Several neurotransmitter markers were determined in post mortem tissue from temporal and frontal cortex in Huntington's disease in order to identify and understand the specific neuronal losses that occur in the neocortex in this disease. Decreases in GABA and glutamate concentrations were identified, together with increases in metabolites of dopamine and 5-hydroxytryptamine, indicative of regulatory changes presumably induced by the neuronal deficits. There is also evidence for abnormal cortical tryptophan metabolism. These changes may well contribute to some of the behavioural symptoms of the disease.

Adult↗
PubMed1994

Deficit of [3H]L-689,560 binding to the glycine site of the glutamate/NMDA receptor in the brain in Huntington's disease.

Binding of [3H]L-689,560 to the glycine site of the glutamate/NMDA receptor was carried out using post-mortem brain tissue from patients with Huntington's disease (HD) and from matched controls. Decreased binding site density (by 62% in the caudate nucleus, 20% in the frontal cortex) was identified in HD. The deficit found in the caudate nucleus in HD correlated with deficits of GABA and glutamate concentrations and thus may reflect the ongoing disease process.

Adult↗
PubMed1993

Neurochemical-clinical correlates in Huntington's disease--applications of brain banking techniques.

Our present understanding of the neuronal abnormalities of Huntington's disease (HD) owes everything to the post mortem study of brain tissue from patients with this disorder. HD was one of the first brain disorders to be studied after systematic brain banking, and it is now well defined in terms of its histological and neurotransmitter pathology. Having established the neurotransmitter systems that are particularly affected in HD (and which include striatal and pallidal GABAergic pathways), it has proven possible to assess post-mortem neurochemistry in the light of pre-mortem clinical information to identify some of the neurotransmitter correlates of the individual motor, behavioural and cognitive symptoms seen in the disease. Thus a further loss of pallidal GABA is associated with a diminution of chorea in HD, while the dementia that occurs in the great majority of cases is related to amino acid transmitter losses in the caudate, but not the cortex. The neurochemical pattern of neuronal loss in the brain in HD has also indicated the possible mechanism for the pathogenesis of the disease: excitotoxic damage via the glutamate/NMDA receptor. Banked brain tissue has also provided the means for the search for abnormal concentrations of biochemical toxins that might bring about this damage. One such endogenous neurotoxin, the tryptophan metabolite quinolinic acid, was found to be unchanged in HD, although another little-studied, but toxic, tryptophan metabolite, 3-hydroxykynurenine, was found to be increased in HD brain samples.(ABSTRACT TRUNCATED AT 250 WORDS)

Brain Chemistry↗
PubMed1992

Increased brain concentrations of a neurotoxin, 3-hydroxykynurenine, in Huntington's disease.

Concentrations of the neurotoxic tryptophan metabolite, 3-hydroxykynurenine, were determined in brain tissue taken post-mortem from patients with Huntington's disease and Alzheimer's disease. 3-Hydroxykynurenine was substantially and significantly increased in all three brain areas studied in Huntington's disease, but not significantly increased in the cortex in Alzheimer's disease, when compared to matched controls. These results demonstrate a possible dysfunction of tryptophan metabolism, via the kynurenine pathway, in Huntington's disease.

Aged↗
PubMed1991

Determination of 3-hydroxykynurenine in human brain and plasma by high-performance liquid chromatography with electrochemical detection. Increased concentrations in hepatic encephalopathy.

A simple and specific method was developed for the determination of 3-hydroxykynurenine in brain tissue and blood plasma using high-performance liquid chromatography with electrochemical detection. This involved an extraction procedure using strong cation-exchange columns and also permitted the determination of 3-hydroxyanthranilic acid in brain tissue. The method was applied to the investigation of post mortem brain tissue from patients with hepatic encephalopathy. Cortical 3-hydroxykynurenine concentrations were substantially increased in such patients above control values, providing evidence for a dysfunction of tryptophan metabolism in this disease.

Brain↗
PubMed1991

Electrochemical detection of human brain transmitter amino acids by high-performance liquid chromatography of stable o-phthalaldehyde-sulphite derivatives.

A simple, sensitive, reliable and reproducible isocratic HPLC technique for the measurement of OPA/sulphite derivatives of human brain amino acid neurotransmitters is described. This employs a sample preparation that is also compatible with the concurrent determination of monoamines and their metabolites on a separate HPLC system. The method has been applied to the determination of GABA and glutamate in brain tissue taken post-mortem from patients with Huntington's disease and control subjects.

Amino Acids↗
PubMed1990

Dementia in Huntington's disease is associated with neurochemical deficits in the caudate nucleus, not the cerebral cortex.

Choline acetyltransferase (ChAT) and the neurotransmitter amino acids gamma-aminobutyric acid (GABA) and glutamic acid were measured in brain tissue taken post-mortem from control subjects and from patients with Huntington's disease (HD). Two subgroups of HD patients were defined with either severe dementia or no dementia. It was found that ChAT exhibited no greater decrease in cortical tissue from severely demented patients. While there were also no significant deficits associated with dementia in cortical concentrations of the amino acids, a substantial and regionally-specific decrease in both GABA and glutamate was observed in the caudate nucleus of severely demented HD patients.

Adult↗
PubMed1990

Pallidal GABA and chorea in Huntington's disease.

Neurochemical correlates of chorea in Huntington's disease were studied using striatal and pallidal tissue taken post mortem from patients with mild and severe chorea. While GABA was decreased in all these areas in Huntington's disease, patients with mild chorea had significantly less GABA in the medial pallidum than did those with severe chorea. There was no relationship between the degree of chorea and concentrations of dopamine or its metabolite. Thus the chorea of Huntington's disease may relate to the balance of residual GABAergic innervation between specific areas of the basal ganglia, consistent with primate models of dyskinesias.

Adult↗
PubMed1988

Depletion of monoamine transmitters by tetrabenazine in brain tissue in Huntington's disease.

The neurochemical effect of tetrabenazine was assessed by determining the levels of dopamine, noradrenaline and 5-hydroxytryptamine and their metabolites in post-mortem brain from Huntington's disease patients with or without a history of tetrabenazine treatment. The tetrabenazine-treated group showed a general description of monoamines in all regions studied, the greatest reduction being dopamine in the caudate. This provides the basis for the effect of tetrabenzine on chorea, while monoamine losses in limbic regions may mediate the production of side effects, such as depression.

Brain Chemistry↗