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Biomedical subjects

A M Moore

Publications and source records attributed to A M Moore.

At least 37 records · Page 2Linked to original sources
PubMed1990

Regional cerebral glucose metabolism is normal in young adults with Down syndrome.

Regional CMRglc (rCMRglc) values were measured with [18F]2-fluoro-2-deoxy-D-glucose (18FDG) and positron emission tomography (PET), using a Scanditronix PC-1024-7B scanner, in 14 healthy, noninstitutionalized subjects with trisomy 21 (Down syndrome; DS) (mean age 30.0 years, range 25-38 years) and in 13 sex-matched, healthy volunteers (mean age 29.5 years, range 22-38 years). In the DS group, mean mental age on the Peabody Picture Vocabulary Test was 7.8 years and dementia was not present. Resting rCMRglc was determined with eyes covered and ears occluded in a quiet, darkened room. Global gray CMRglc equaled 8.76 +/- 0.76 mg/100 g/min (mean +/- SD) in the DS group as compared with 8.74 +/- 1.19 mg/100 g/min in the control group (p greater than 0.05). Gray matter regional measurements also did not differ between groups. The ratio of rCMRglc to global CMRglc, calculated to reduce the variance associated with absolute rCMRglc, and right/left ratios did not show any consistent differences. These results show that healthy young DS adults do not have alterations in regional or global brain glucose metabolism, as measured with 18FDG and PET, prior to an age at which the neuropathological changes in Alzheimer disease are reported to occur.

Adult↗
PubMed1988

Determinants of anterior mitral leaflet fluttering in pure aortic regurgitation from pulsed Doppler study of the early diastolic interaction between the regurgitant jet and mitral inflow.

Fluttering of the anterior mitral leaflet may be absent in patients with moderate to severe aortic regurgitation (AR), suggesting that the volumetric severity of AR alone does not determine the presence or absence of abnormal diastolic mitral valve motion. Fifteen patients with moderate to severe AR and normal mitral valves, 9 of whom demonstrated anterior mitral leaflet fluttering, were studied to elucidate the determinants of abnormal anterior mitral leaflet motion in these patients. Pulsed Doppler mapping of the flow-velocity disturbance of AR demonstrated its presence in the third of the left ventricular outflow tract adjacent to the anterior mitral leaflet in 8 of 9 patients with anterior mitral leaflet fluttering and none of the 6 patients without anterior mitral leaflet fluttering (p less than 0.02). The impact of this regurgitant jet on early diastolic transmitral inflow was examined with pulsed Doppler in these 2 groups of patients with AR and in age-matched control subjects. Deceleration of early diastolic transmitral filling was slower in patients with AR and anterior mitral leaflet fluttering than in age-matched control subjects (283 +/- 107 vs 457 +/- 176 cm/s2, p less than 0.02), whereas it was not significantly different from controls in AR patients without anterior mitral leaflet fluttering. This resulted in significant prolongation of the duration of early diastolic transmitral filling in patients with AR and anterior mitral leaflet fluttering (297 +/- 93 vs 203 +/- 44 ms for age-matched control subjects, p less than 0.02), which was not observed in patients with AR who did not have anterior mitral leaflet fluttering.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Brain metabolism as measured with positron emission tomography: serial assessment in a patient with familial Alzheimer's disease.

This paper presents, for the first time, repeated assessments of cerebral metabolism and neuropsychological competence in early Alzheimer's disease. Regional cerebral metabolic rates for glucose were measured with positron emission tomography and 18F-fluoro-2-deoxy-D-glucose on three occasions at 8-month intervals, in a 57-year-old man with Alzheimer's disease of 2 1/2 years' duration and with a family history of neuropathologically confirmed Alzheimer's disease. Data were compared with mean cerebral metabolic rates from 12 healthy men. No differences in regional cerebral metabolic rates for glucose were found on the initial patient scan, whereas metabolism on the second and third scans was reduced significantly in the parietal lobes and bilaterally in some parietal lobe regions. Memory loss was demonstrable at the first scan, but then and at later scans, other aspects of cognitive performance remained within normal limits (Wechsler Adult Intelligence Scale, Boston Naming Test, Two-dimensional Block Construction). The results show that memory loss can precede a measurable reduction of cerebral metabolism in early Alzheimer's disease, but that later reductions in parietal lobe metabolism may not be accompanied by additional measurable neuropsychological deficits.

Aged↗
PubMed1983

Cerebral glucose utilization, as measured with positron emission tomography in 21 resting healthy men between the ages of 21 and 83 years.

Positron emission tomography (PET) scanning with 18F-2-deoxy-D-glucose was employed to examine hemispheric and regional rates of cerebral glucose utilization in 21 resting healthy men between the ages of 21 and 83 years. The eyes of the subjects were covered and the external auditory canals were plugged with cotton in the 45 minutes following injection of tracer. Mean hemispheric cerebral metabolic rates for glucose (CMRglc) averaged 4.3 to 4.4 mg x 100 g-1 X min-1, and mean hemispheric grey matter glucose utilization, (CMRglc)grey, averaged 5.2 to 5.3 mg x 100 g-1 X min-1. Neither parameter was correlated significantly with age, nor were their right/left ratios correlated with age (P greater than 0.05). The mean ratios, furthermore, did not differ significantly from 1. Regional cerebral metabolic rates for glucose, rCMRglc, at each of 31 identified midline and bilateral structures also were not correlated significantly with age. Mean rCMRglc ranged from 2.6 mg X 100 g-1 X min-1 at the centrum semiovale to 6.2 mg . 100 g-1 X min-1 at the precentral gyrus of the frontal lobe and precuneus of the parietal lobe. The results indicate that the cerebral metabolic rate for glucose is not correlated with age in healthy men.

Adult↗
PubMed1982

Reduced training duration effects on aerobic power, endurance, and cardiac growth.

Thirteen subjects participated in an exercise program of bicycling and running 40 min/day, 6 days/wk. After 10 wk they continued to train either 26 of 13 min/day for an additional 15 wk. Intensity and frequency for the additional 15 wk remained the same as the last 3 wk of training. This study was undertaken to gain further insights into whether the increases in maximum uptake (VO2 max), endurance, and cardiac size can be maintained with reduced training durations. The average increases in VO2 max in response to 10 wk training were between 10 and 20% during the bicycle and treadmill testing. After reduced training, VO2 max continued to remain at the training levels in both groups. Short-term endurance (approx 5 min) was also maintained by both groups. Long-term endurance (2 h or more) remained the same in the 26-min group but decreased significantly (10%, 139-123 min) in the 13-min group. Calculated left ventricular mass increased 15-20% after training and remained elevated after reduced training in both groups. We conclude that it is possible to maintain almost all of the performance increases with up to a two-thirds reduction of training duration. Nevertheless, the data provide initial evidence that all aspects of the endurance-trained state may not be regulated uniformly in reduced training, particularly since VO2 max and short-term endurance were maintained, but long-term endurance decreased in the 13-min group.

Adult↗
PubMed1979

Scopolamine-induced muscarinic supersensitivity in normal man: changes in sleep.

Scopolamine (6 microgram/kg) was administered on 3 consecutive mornings to normal human subjects. Sleep recordings obtained at night (when the central anticholinergic effect of the morning scopolamine was no longer present) indicated a significant reduction in latency to REM-sleep onset on the nights following the second and third injections. This effect is opposite to the direct pharmacological action of nighttime administration of scopolamine (i.e., prolongation of REM latency). In addition, total sleep time and sleep efficiency were reduced, and sleep latency was increased. Furthermore, scopolamine pretreatment on 2 consecutive mornings also potentiated the REM-inducing effect of arecoline, a central muscarinic agonist. These data are consistent with the development of cholinergic supersensitivity following cholinergic blockade.

Adult↗
PubMed1979

Review of 1,000 major facial fractures and associated injuries.

The records of 1,020 major facial fractures were reviewed, and it was found that the occurrence of life-threatening associated injuries was highly predictable on the basis of the pattern of facial fractures and the circumstances of the injury. Certain groups of patients have a high probability of associated serious injuries of the central nervous system, the trunk, or the extremities. Probably these patients should be primarily under the care of a surgeon who is capable of the diagnosis and emergency therapy of these associated injuries, as well as the facial injuries, so that appropriate priorities can be established and put in effect.

Abdominal Injuries↗
PubMed1978

The effect of physostigmine on normal human sleep and dreaming.

Physostigmine, an anticholinesterase that increases the action of brain acetylcholine, induces rapid eye movement (REM) sleep in normal humans. In this study we show that man dreams during physostigmine-induced REM sleep. Seventeen normal volunteers were pretreated with methscopolamine and received one intravenous infusion per night of either placebo or physostigmine either ten or 35 minutes after sleep onset. Subjects were awakened at specific times after infusion and interviewed regarding any sleep mentation prior to awakening. Results indicated that dreaming occurred during physostigmine-induced REM periods but that physostigmine did not alter mentation during non-REM sleep. These dreams were similar to spontaneous REM sleep dreams in content, vividness, unusualness, and emotionality.

Adult↗
PubMed1978

Induction and resetting of REM sleep rhythm in normal man by arecholine: blockade by scopolamine.

Arecholine, a cholinergic muscarinic agonist, was administered intravenously 35 min after sleep onset in eight normal volunteers who had been pretreated with either methscopolamine or scopolamine, muscarinic receptor blockers that do not and do cross the blood--brain barrier, respectively. Following pretreatment with methscopolamine, arecholine shortened the REM latency and increased the number of REM periods without altering the duration of individual REM periods or altering the REM--REM intervals. Pretreatment with scopolamine blocked the effects of arecholine. The results support the hypothesis that cholinergic muscarinic mechanisms are involved in the timing but not the duration of REM sleep.

Adult↗