Biomedical subjects
Publications and source records attributed to R J Adams.
We describe the first case of Miller Fisher syndrome, a Guillain Barré variant, complicating systemic lupus erythematosus. The symptoms and signs mimicked a brainstem syndrome. Despite treatment with high dose gamma globulin, our patient worsened and required mechanical ventilation. After plasma exchange, the patient improved.
The single-headed myosins called myosin-I were first isolated from the protozoan Acanthamoeba and subsequently identified in other cells. We previously reported evidence that myosin-I is responsible for the movement of membranes, extracted from Acanthamoeba, along actin filaments in vitro. Here we show for the first time that myosin-I can bind directly to NaOH-extracted membranes isolated from Acanthamoeba and to vesicles of pure lipids with an affinity sufficient for extensive binding in the cell. Membrane-bound myosin-I may provide a mechanism for many cellular movements previously thought to involve filamentous myosin-II.
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Recent anatomical and behavioral evidence suggests that important visual functions like color vision may be severely limited at birth. Therefore, we examined human newborns' ability to discriminate among stimuli of different wavelength by habituating them to a 16 degrees chromatic square of widely varying luminance (as wide as 1.1 log cd/m2) and then testing for recovery of habituation to a different chromatic square of the same size. In the first experiment, newborns showed evidence of recovery to a 650-nm (peak wavelength) red square after habituating to 545-nm green squares, but they did not recover to the red or the green after habituating to 585-nm yellow squares. In a second experiment using the same procedure, newborns did not show evidence of discriminating the 650-nm red from the 545-nm green when the stimulus size was reduced to 8 degrees. These data suggest that human newborns are capable of making a chromatic discrimination within the spectral region above 540 nm (the Rayleigh region) but their ability is limited to chromatic stimuli of very wide spectral separation and of very large size. Possible neurological bases underlying this immaturity are discussed.
The effects of scopolamine (anticholinergic) and methysergide (antiserotonergic) on memory and long-latency auditory cognitive evoked potentials (EPs) were tested in 16 normal adults. Recent memory was impaired by both drugs. In contrast, scopolamine, but not methysergide, significantly delayed P3 latency and decreased P3 amplitude. Immediate memory and the earlier EP components (i.e., N1 and P2) were unaffected. The findings support the hypothesis that cholinergic neurons are important in the neuronal networks generating the P3 potential. Serotonergic neurons do not appear to play a major role in the networks that generate the P3.
The electrophysiologic effects of high concentrations of the opioid agonists, fentanyl and sufentanil, on isolated canine cardiac Purkinje fibers were studied. Changes in action potential parameters were examined at the following concentrations: fentanyl 94.6 nM, 0.19 microM, and 0.95 microM; sufentanil 8.6 nM, 86.4 nM, 0.17 microM, and 0.26 microM. Naloxone 5.5 microM was administered after maximal changes were induced by fentanyl in order to explore the possibility of an opioid receptor interaction. Action potential parameters measured were Vmax of phase 0, amplitude, overshoot, maximum diastolic potential, action potential duration at 50%, and 90% repolarization and membrane responsiveness. Fentanyl 0.19 microM and sufentanil-0.17 microM caused a significant lengthening of action potential duration at 50 and 90% repolarization, 6.4% and 7.3%, and 10.2% and 12.4%, respectively, P less than 0.05. Other action potential parameters were not significantly affected by the opioids. Naloxone 5.5 microM alone did not alter action potential characteristics and failed to reverse action potential prolongation produced by fentanyl. The authors suggest that fentanyl and sufentanil prolong action potential duration in canine cardiac Purkinje fibers via direct membrane actions.
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The visual habituation of two groups of newborn infants was tested at a mean age of 2.9 days with large achromatic squares of varying luminance. Mothers of the infants in one group received no medication during labour; mothers in the second group received a single dose of the synthetic narcotic alphaprodine hydrochloride. The two groups did not differ in the number of trials to reach the criterion, but newborns in the no-medication group fixated the stimuli for much longer periods than did infants in the alphaprodine group. First-fixation times of babies in the alphaprodine group were shorter when drug-to-delivery intervals were longer. These results, although tentative, imply that babies of medicated and unmedicated mothers differ in the manner in which they respond to visual stimuli.
We investigated the relation of plasma lipids to the risk for ischemic stroke by comparing clinical and biochemical characteristics of survivors of cortical (n = 48) and lacunar (n = 36) brain infarction. By analysis of variance, no differences were observed in the concentrations of total cholesterol, triglycerides, low density lipoprotein cholesterol, very low density lipoprotein cholesterol, or apoproteins A1 and B. Patients with lacunar infarction, however, had higher concentrations of high density lipoprotein (HDL)-cholesterol than patients with cortical stroke. This HDL-cholesterol difference was due primarily to a strikingly low HDL-cholesterol content in white patients with cortical stroke. These data suggest that previously demonstrated differences in HDL-cholesterol concentrations between patients with ischemic stroke and control subjects without stroke may apply to patients with cortical but not lacunar infarction. Separation of cerebral infarction into subtypes based on mechanism may help clarify lipid-related risk factors in cerebrovascular disease.
We examined 3-mo.-old human infants' ability to detect flicker in 454-nm blue and 627-nm red lights at 1.5 log cd/m2. Infants showed the same critical flicker frequency (CFF) to both wavelengths, suggesting that retinal cones mediate the detection of flicker at this luminance level. Infants' CFFs for chromatic stimuli were much lower than those reported for achromatic stimuli and also much lower than adults' CFFs tested under the same conditions.
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As a neurotransmitter involved in modulating central nervous system nociception and awareness, 5-hydroxytryptamine (5-HT) may play an important role in the clinical sequelae of certain anesthetic compounds. Anesthetic agents are known to affect peripheral, non-neuronal 5-HT uptake but little is known about their effects on 5-HT metabolism in the central nervous system. The effects of several anesthetic compounds on 5-HT uptake were examined in synaptosomes isolated from rat brain cortex. Inhibition of this uptake process was observed by exposure to clinically relevant concentrations of the volatile anesthetics halothane, isoflurane, and enflurane. The non-volatile agent, ketamine also inhibited uptake while the narcotic fentanyl had an effect only at the highest concentrations tested. Non-volatile agents which had neither a consistent nor significant effect on synaptosomal 5-HT uptake included pentobarbital, sufentanil, and etomidate. These alterations of 5-HT metabolism could represent a mechanism that contributes to anesthetic action.
Two women with a presumptive diagnosis of Hallervorden-Spatz syndrome had a combination of dystonia and parkinsonism. One had retinitis pigmentosa. Neuropsychological testing revealed decreased verbal fluency and visuoconstructional and motor deficits. Magnetic resonance imaging performed with a high-field-strength unit (1.5 Tesla) showed striking abnormalities in the globus pallidus bilaterally ("eye-of-the-tiger" sign). Magnetic resonance imaging may prove useful in the diagnosis of Hallervorden-Spatz syndrome.
Virgil Sydenstricker was a member of a notable American family which included authoress Pearl S. Buck and the eminent epidemiologist Edgar Sydenstricker. Dr. Sydenstricker's contributions in the fields of hematology and nutritional disease are legion. His landmark work in sickle cell anemia characterized a definite symptom complex with specific hematologic findings and inheritance pattern. He wrote on the complications of malnutrition and attempted to delineate the specific effects of individual nutritional factors. Dr. Sydenstricker and his associate H. M. Cleckley first described the syndrome of niacin deficiency encephalopathy. Today, the syndrome is still occasionally reported. Niacin deficiency should be considered when unexplained acute confusional states or neurologic deficits occur in the setting of malnutrition, antituberculous drug use, or chronic partial nutritional deficiency with acute increase in metabolic demand.
We describe a case of homozygous sickle cell anemia in which noninvasive transcranial Doppler ultrasonography and magnetic resonance imaging were used to detect angiographically documented occlusive lesions of intracranial arteries.
We studied 25 patients with sickle cell anemia and cerebral infarction. We classified lesions as to probable mechanism (large versus small vessel disease) based on the CT/MRI appearance of established infarction. Most patients had CT/MRI patterns of major cerebral vessel occlusion (41%) or border-zone (distal insufficiency) infarcts (31%) best explained by large cerebral vessel vasculopathy. Seven of 25 (28%) had either isolated subcortical (12%) or small cortical branch occlusion (16%) consistent with other mechanisms such as small vessel occlusion or embolism. These results suggest that most clinically recognized cerebral infarctions in sickle cell anemia are caused by large vessel disease, but this mechanism may not account for symptoms of cerebral ischemia in all cases.
The effects of the clinical preparation of ketamine, Ketalar and its preservative, benzethonium chloride on [3H]5-hydroxytryptamine uptake were studied using rat brain synaptosomes. Ketalar caused a concentration-dependent inhibition of substrate uptake by the high affinity transport site (I50 = 20.2 +/- 2.75 microM) while benzethonium chloride had no effect. Kinetic analysis indicated the inhibition to be competitive with serotonin; the apparent km (54 nM) was increased nearly two-fold at 10 microM ketamine. This action may represent a mechanism involved in ketamine anesthesia.
Two different methods which minimize achromatic cues were used to test the ability of 1-month-olds to discriminate gray from broadband blue (lambda peak = 475-480 nm). Unlike the newborns we tested previously, 1-month-olds demonstrated the discrimination with both methods. In Experiment 1 they showed preferences for each of four blue-and-gray checkerboards over gray squares of the same mean luminance, even though the luminance of the gray checks was varied in small steps over a wide range. In Experiment 2 they looked longer at a blue square than at a gray square, after they had been habituated to five other gray squares of varying luminance. Compared to previous results, these data imply an improvement between birth and 1 month of age in the discrimination of gray from broadband blue. Possible physiological changes underlying this improvement are discussed.