Human gene for physical performance.
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Biomedical subjects
Publications and source records attributed to M Hayward.
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Auditory and visual event-related potentials (ERPs) generated by digit-probe identification and matching in a modified Sternberg paradigm have been recorded in 37 healthy subjects with the aim of identifying the potentials which best reflect the memory processes associated with this task. We analysed the effects of memory load (one, three or five digits to memorise), probe type (probe digit present or absent from the preceding memory set) and recording site, on the ERPs. With conventional methods of determining component amplitudes and latencies, the main effects of increasing memory load on the major positive wave varied according to stimulus modality-there was an amplitude decrease for the auditory ERPs and a latency increase for the visual ERPs. However, subjective component identification methods may be prone to errors when comparing responses recorded under different stimulus conditions. Waveform changes with increasing memory load may be misinterpreted as latency (or amplitude) effects if non-analogous potentials are compared. Further, component analysis may provide only partial information, because of its relative insensitivity to sustained amplitude shifts. For these reasons, an objective computer method was used to determine the mean amplitudes for multiple '50 ms' epochs. This showed, for both auditory and visual stimuli, that the main effect of increasing memory load was a 'negative amplitude shift'. It was seen between 315 and 525 ms for auditory stimuli and between 210 and 472 ms for visual stimuli and could be distinguished from other ERP features that were sensitive to stimulus modality. These changes are either specific to the memory processes involved in carrying out this task or reflect other parallel processing which covaries with memory processing.
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BACKGROUND: Parkinson's disease (PD) patients frequently report a family history of PD and this may provide etiological clues to PD. It has also been suggested that a report of a negative family history is reliable. We studied the prevalence of PD in relatives of PD patients to assess the reliability of family history and to evaluate possible explanations of "familial PD" (fPD). METHODS: 81 of 650 (12.5%) PD probands (all PD patients seen at clinic in 4 years) reported a positive family history of PD. Each fPD proband was matched with non-familial PD (nfPD) proband by gender and year of birth. Screening and follow-up questionnaires were mailed to relatives to obtain information concerning pedigree and presence of neurodegenerative disease. Available family members (regardless of disease status) were examined. RESULTS: On examination, 8 persons, said to be "normal" by probands, relatives and themselves, had definite or possible PD (5 fPD, 3 nfPD). The prevalence rate of PD among first and second degree living relatives of probands varied significantly between fPD and nfPD groups (6269/100,000 versus 1190/100,000; p < 0.001). The weighted prevalence (taking into account the proportions of fPD and nfPD within the clinic) was 1822/100,000, a value more than 5 times higher than reported prevalence rates of PD in the general population (p < 0.001). The prevalence rate was greater in first degree relatives than second degree. CONCLUSIONS: "Familial parkinsonism" cannot be explained merely by size of or advanced age within families. Significant numbers of previously unrecognized PD patients may be identified despite a "negative" family history. That is, the patient's report of an absence of familial parkinsonism is frequently inaccurate. The prevalence rate in relatives of PD patients appears to be higher than the general population-regardless of the family history reported by a PD patient. We believe our study suggests that genetic influences or early life environmental exposures are likely to be of etiological importance in PD.
Auditory and visual event-related potentials were recorded during a short-term memory task in 24 patients who had recently presented with symptomatically and clinically isolated spinal cord syndromes suspected to be due to multiple sclerosis, and in 24 matched control subjects. Event-related potentials (ERPs) were recorded during two sequential components of the working memory task, first the temporary active memorizing of sets of digits and secondly, their subsequent manipulation, namely digit-probe recognition and matching. The patients' reaction times were slower and showed larger increments than those of the control subjects as the number of items to be memorized was increased. The patients' ERPs during both memorizing and probe matching/recognition phases differed significantly from control subjects for both auditory and visual presentations. The more marked changes were seen in a subgroup of eight patients who had the lowest levels of performance on a battery of general tests of memory and who also made significantly more errors in the working memory task as the memory load increased. In this subgroup, the abnormalities of the ERPs during recognition and matching tests occurred in the component of the response that has been shown to be sensitive to memory loading in healthy control subjects. This study provides objective evidence of subclinical working memory dysfunction in patients at an early stage of demyelinating disease, i.e. when they first present with clinically isolated spinal cord lesions and before they have developed symptoms of cognitive or memory dysfunction. The defect at this early stage is either restricted to processes involved in the formation of a memory trace or, more probably, involves both trace formation and the mechanisms that underly recognition ('retrieval') and matching of memory traces in working memory.
An in vitro study was designed to evaluate the uptake of sestamibi (MIBI) in P-glycoprotein (Pgp) and glutathione-associated (GSH) multidrug-resistant (MDR) cell lines. MIBI uptake was studied in various human breast carcinoma cell lines, i.e. in wild-type (MCF7/wt) cells, in adriamycin-resistant (MCF7/adr) cells which express Pgp and in melphalan-resistant (MCF7/mph) cells with increased levels of GSH. The effects of buthiomine sulphoximine (BSO) and verapamil on MIBI uptake were also studied in the MCF7/mph and MCF7/adr cells respectively. The cells were incubated for 1 h with a dose of 0.1 MBq thallium-201 and technetium-99m MIBI. Both MIBI and 201Tl uptakes were higher for MCF7/mph cells than for the other cells studied. The mean MIBI uptake in MCF7/adr cells was significantly lower than that in MCF7/wt cells (1.9%+/-0.5% vs 3. 1%.0.6%; P <0.01). Verapamil treatment increased the MIBI uptake in MCF7/adr cells (to 2.6%.0.3%; P <0.05). Treatment of MCF7/mph cells with BSO resulted in a significant reduction in GSH content (from 243.2+/-81.1 nmol/mg protein to 17.6+/-4.4 nmol/mg protein; P <0. 001). However, MIBI uptake in BSO-treated and untreated MCF7/mph cells was similar (4.43%+/-0.5% and 5.93%+/-1.7%, respectively; P >0. 1). This study suggests that the uptake of MIBI is not diminished by glutathione-associated drug resistance and that MIBI uptake in a tumour sample does not necessarily indicate that a cancer is sensitive to drugs.
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This article examines the theoretical connection between health capital and financial capital in an economic life-cycle model, exploring possible explanations for racial differences in capital accumulation behavior. Using data from the Health and Retirement Survey, detailed descriptive analysis and a comparison of regression models for health and financial capital are presented. The results, although preliminary and based on cross-section data, suggest possible racial differences in the connection between health and wealth and deserve further study.
Enlargement of the peroneus longus muscle is a common occurrence in patients with forefoot pes cavus, and may contribute to the cavus deformity. The present study compares the morphology of up to five lower leg muscles from 17 patients with forefoot pes cavus with those of normal muscles. Eight cases had an identifiable neurogenic cause for the cavus. In four cases of hereditary motor-sensory neuropathy, the tibialis anterior showed more severe damage than the peroneus longus. In two cases of cerebral palsy, fibre atrophy and increased oxidative enzyme activity were observed. In nine clinically idiopathic cases, the histological appearances ranged from normal to generalised fibre atrophy or hypertrophy in individual muscles. There was a trend for the mean fibre area to be greater in peroneus longus than in tibialis anterior in six of the idiopathic group of patients. The muscle cross-sectional area on magnetic resonance imaging was correlated closely with the mean fibre area measured on tissue sections. In idiopathic forefoot pes cavus, fibre hypertrophy in peroneus longus (relative to tibialis anterior) may contribute to the cavus deformity. Muscle fibre hyperplasia may contribute to the peroneal muscle enlargement in Friedreich's ataxia. In none of the cases was peroneus longus enlargement due to fat or fibrous tissue replacement.
The time taken to scan short term memory for a target (probe) digit in the Sternberg paradigm is thought to be reflected in the latency of a major positive wave in the associated event-related potentials. In the present study we have recorded and analysed reaction time and event-related potentials to a digit probe identification task in 37 healthy subjects. Using methods similar to those of earlier studies, we have confirmed the previously reported relationship between memory set size and the apparent latency of the major positive wave. However, analysis of the responses of individual subjects showed that increasing set size had no consistent effects on this wave. One-third of the subjects showed no latency change with increasing set size. In the other subjects, possible latency changes were invariably associated with wave form changes, suggesting that impression of latency shifts may arise from a comparison of non-analogous waves. We suggest that the most significant effect of increasing set size, in the majority of subjects, is a negative amplitude shift which overlaps and distorts a variable section of the major positive wave. In these subjects, an apparent shift in the latency of the major positive wave could be attributed to a combination of attenuation of earlier contributions and relative preservation of later subpeaks, with the result that the dominant positive waves at different levels of memory load are not analogous. By contrast, reaction time increased with set size in all subjects, irrespective of the presence or absence of associated wave form changes. Whereas the reaction time changes with increasing memory load in our study support the original concept of memory scanning, we found no consistent relationship between the latency of event-related potentials generated by this digit probe identification task and memory load. While the presence or absence of a latency shift in some subjects may be open to interpretation, our findings do not support the hypothesis that the latency of the major positive waves is an index of the time involved in memory scanning.
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OBJECTIVE: The present study evaluated whether chronic stress levels moderated the impact of laboratory stressors on subjective and behavioral responses to alcohol. METHOD: Healthy volunteers (N = 60; 30 male) completed measures of background stress levels (e.g., major life events). In addition, subjects were exposed to two laboratory stressors (i.e., cold pressor or film stressor task) or a control condition after consuming a 0.7 g/kg dose of alcohol. RESULTS: Regression analyses showed that the combination of high background stress levels and exposure to a lab stressor reduced two measures of perceived intoxication (i.e., Sensation Scale, Visual Analog Intoxication Scale). CONCLUSIONS: These data are consistent with a biobehavioral model of alcohol use where acute and chronic stressors are associated with a diminished response to alcohol. The possible mechanisms that may underlie this sobering effect include stress-related cognitive deficits and situation specific tolerance associated with high chronic stress levels.
We report the first description of a patient with parkinsonism induced by solvent abuse. Our patient developed parkinsonism acutely, following heavy abuse of lacquer thinner. Her clinical deficits were indistinguishable from idiopathic parkinsonism (Parkinson's disease) and she responded to levodopa. Parkinsonism has persisted for more than 3 months. Brain computed tomography was normal. Positron emission tomographic studies showed normal fluorodopa uptake and reduced raclopride binding, indicating an unusual disturbance of striatal dopaminergic function. This patient suggests that organic solvents may cause parkinsonism in susceptible individuals.
The health care environment across the country is undergoing unprecedented uncertainty and change, so it is imperative that hospital leaders develop processes that enhance their organization's ability to adapt to new realities and directions. The key factors in maximizing the utilization of resources to meet community demand involve corporate changes and active support from medical, nursing, professional and support staff. This article describes the methods adopted by one community hospital to improve the utilization of surgical resources, with particular emphasis on the process developed for allocating Operating Room time to support corporate priorities.
To determine the influence of stress on intoxication and blood alcohol concentration (BAC) 60 healthy male and female volunteers were exposed to a cold pressor test, distressing film, or control condition after consuming a moderate dose of alcohol. Two measures of perceived intoxication suggested a sobering effect of acute stressors. In addition, Ss viewing the distressing film showed longer latency to peak BAC than Ss in the control condition. As BAC began to fall, the cold pressor test initially increased rate of alcohol elimination. These stress-induced changes in intoxication and the BAC curve support a biobehavioral model in which stress may increase alcohol use partly because it attenuates alcohol's psychopharmacological impact.
There is a widely held belief that most patients presenting with senile chorea have late-onset Huntington's disease (HD) with an unknown family history. We measured CAG trinucleotide repeat expansion in the HD gene in four patients with a clinical presentation of senile chorea and found that CAG repetition lengths were normal. These findings support senile chorea as being a distinct clinical entity that is nosologically separate from late-onset HD.
The development of a multicellular organism involves a delicate balance among the processes of proliferation, differentiation and death. Naturally occurring cell death aids tissue remodelling, eliminates supernumerary cell populations and provides structural elements such as hair and skin. In the nervous system, selective cell death contributes to the formation and organization of the spinal cord and sympathetic ganglia, retina and corpus callosum. But cell death also occurs in several neuropathological conditions, such as amyelotrophic lateral sclerosis and Alzheimer's disease. Therefore an elucidation of the mechanisms responsible for cell death is critical for an appreciation of both normal development and neuropathological disorders. Using a fos-lacZ transgenic mouse, we provide evidence showing that the continuous expression of Fos, beginning hours or days before the morphological demise of the cell, appears to be a hallmark of terminal differentiation and a harbinger of death.
OBJECTIVE: To assess whether transdermal nicotine patches combined with low-intensity support can help outpatients in a general hospital stop smoking. DESIGN: Randomized, double-blind, placebo-controlled trial with 12 weeks of follow-up. SETTING: Department of Thoracic Medicine in an inner-city public general hospital, London, England. SUBJECTS: Two hundred forty-eight outpatients in a general hospital, who smoked at least 10 cigarettes per day (the majority were being treated for smoking-related diseases), referred by clinicians at the hospital. INTERVENTION: Brief advice to stop smoking and daily application of transdermal nicotine patches (delivering 15 mg over 16 hours) or placebo, with follow-up appointments at 1, 3, 6, and 12 weeks, with a doubling of the dosage for continuing smokers at week 1. MAIN OUTCOME MEASURE: Sustained abstinence from tobacco from week 3 to week 12 validated with measurement of expired-air carbon monoxide concentration at weeks 3, 6, and 12. RESULTS: Twenty-nine (23.4%) of 124 subjects assigned to the nicotine group were validated as having abstained from smoking at both weeks 3 and 6, compared with 16 (12.9%) of 124 subjects receiving placebo (P = .008). At week 12, 22 (17.7%) of the subjects in the nicotine group were validated as having abstained at all three points as were 15 (12.1%) of the subjects in the placebo group (P = .058). CONCLUSION: Transdermal nicotine patches combined with low-intensity support are effective in helping outpatients in a general hospital stop smoking but do not prevent relapse after 6 weeks.