Isolation of intact disks by concanavalin A columns.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to A J Adams.
Explore the source record for details and available documents.
Glycogen, in concentrations encountered in von Gierke's disease, has computed tomography (CT) attenuation coefficients in the 50 to 70 Hounsfield unit (HU: 1,000 scale) range and accounts for the increased density of the liver. However, in eight patients with Type I glycogen storage disease, simultaneous hepatic infiltration with fat and glycogen led to a range of liver CT densities from 13 to 80 HU. Fatty infiltration may facilitate the demonstration of hepatic tumors in older patients with this disease. Half the patients showed increased attenuation coefficients of the renal cortex, indicating glycogen deposition in the kidneys.
The initial stages of light and dark adaptation in the human visual system cannot be explained by a simple relation between sensitivity and pigment bleaching. We found changes in sensitivity in the goldfish ganglion cells similar to those seen in humans, and our results from experiments suggest that a change in gain, rather than an overloading of the ganglion cell activity, is responsible for the sensitivity loss. Furthermore, long wavelength background lights selected to stimulate only the long wavelength receptor mechanism produce only the early sensitivity changes in the medium wavelength cone mechanism being monitored at the ganglion cell. This suggests that the early gain changes occur due to neural interaction where different receptor signals merge.
Color vision loss can be an early sign of eye disease; in many retinal disorders the loss precedes any change in visual acuity. Noninvasive psychophysical methods allow factoring out of preretinal, receptoral, and postreceptoral (neural) components of the color vision change. A loss of chromatic but not achromatic sensitivity occurs for diabetics; the loss is selective for pathways subserving blue-sensitive photoreceptors. Both chromatic and achromatic pathways are altered in glaucoma and senile macular degeneration; the most marked change in central serous choroidopathy is loss of sensitivity somewhere in the blue-sensitive cone pathway. There is evidence that the pathways subserved by blue-sensitive cones have anatomically and physiologically different properties from those served by other receptor types, and they appear particularly vulnerable to disturbances of retinal integrity.
Color vision changes may occur early in the course of glaucoma and may precede visual field loss. Glaucoma suspects, having raised intraocular pressure and no diagnostic optic nerve head or visual field changes, may also have color vision loss. Unfortunately, the instruments used in the studies that have demonstrated these color vision changes were not feasible for routine clinical use; likewise, the studies did not carefully control for the effects of small pupil size and age or did not point to the underlying mechanisms responsible. We studied 19 glaucoma patients, 19 glaucoma suspects, and age-matched controls for each group by means of the Farnsworth D-15 panel test, a desaturated version of the D-15 test, and by measures of spectral increment threshold. Minor modifications of the Farnsworth D-15 panel test produce highly significant differentiation of glaucoma and glaucoma-suspect patients from age-matched normal groups. Further, spectral increment thresholds, with a two-degree spectral target flashed at either 1 or 25 Hz on a bright white background, show that both achromatic and chromatic sensitivity are significantly reduced when compared with their age-matched normals. Pupil size does not seem to be a significant factor. These results suggest that the function of two different ganglion cell populations is affected in glaucoma and that glaucoma may produce functional loss in the central foveal area earlier in the disease process than previously believed.
We have investigated the effects of an anticholinergic drug, benactyzine HCl on vision and vision function. Our experiments assess the time course and severity of benactyzine effects on visual acuity for static and moving targets, amplitude and dynamics of accommodation, pupil response to light and the spatial contrast sensitivity function. A single dose of the drug (4.14 mg/70 kg body weight, which is within the therapeutic range) and placebo were administered intramuscularly to 12 subjects. Large and significant decrements in visual function were demonstrated after the administration of benactyzine, particularly for those functions performed at near focus. The drug effect was rapid in onset, beginning 7-10 min after injection, peaked at approximately 30-40 min, and declined to baseline values over the next 2 h. The drug increased pulse rate and blood pressure, and induced an intoxicated state involving loss of concentration, attention, and short-term memory.
Benactyzine is an anticholinergic agent which has been used in past years in psychiatry, but is little used today. It has central and peripheral anticholinergic effects, and when administered intramuscularly, it has a rapid onset of action. This may make it useful as an antidote for organophosphate poisoning, in spite of side-effects such as deficits of short term memory, concentration, and attention. As an anticholinergic drug it could also be expected to produce vision changes by its action on the intraocular musculature controlling the pupil and lens accommodation. We tested the drug on six volunteer subjects to establish the visual side-effects of intramuscular administration. We found that it reduced static and dynamic visual acuity, increased pupil size, reduced amplitude of accommodation and contrast sensitivity, while having little or no effect on glare recovery, color vision, intraocular pressure, stereoacuity, oculomotor tracking, and distance heterophoria. Benactyzine produced reductions in visual performance for up to 3 h and had the greatest effects on functions which have significant cognitive components. The present results suggest that the drug is unsuitable for treatment for oganophosphate poisoning when continuous performance is required, although a definitive test of ths suggestion would require that performance should be tested when benactyzine and the organophosphate of interest were combined.
The measurement of 125I-insulin specific binding to erythrocytes obtained from seven infants and children with various hypoglycemic syndromes showed a significant increase in six patients with recurrent, documented, symptomatic hypoglycemia (percent specific 125I-insulin binding 9 to 14 versus 6.1 +/- 1.4% mean +/- 2 S.D. for 13 controls). The increase was due to an increased number of receptors sites per cell rather than to increased affinity for insulin. The patients included three children with nesidioblastosis, all after 90% pancreatectomy, two with leucine sensitivity, and two with glycogen storage disease type I. One of the patients with leucine sensitivity, who for 2 years before the study had no hypoglycemia, had normal insulin values (less than 10 microunits/ml). Thus, a symptomatic hypoglycemia correlated better with increased 125I-insulin binding than with plasma insulin values. Furthermore, Diazoxide therapy in two patients caused a mild but consistent decrease in the number of insulin receptor sites, and the institution of continuous nocturnal nasogastric feedings in a patient with glycogen storage disease type I was followed by amelioration of the hypoglycemia and a marked increase in 125I-insulin specific binding from 5.2 to 9.5%.
Explore the source record for details and available documents.
The time course of light adaptation after intense light exposure is significantly delayed by alcohol, marijuana, and a combined dose of alcohol and marijuana. These effects were found in a double blind experiment, using 10 subjects. The experimental treatments were placebo, 0.75 ml/kg of 95% ethanol, 8 and 15 mg of delta9 tetrahydrocannabinol (THC). and 0.75 ml/kg of 95% ethanol together with 15 mg of THC. The marijuana-induced delay in recovery is doserelated. Both drugs produce delayed recovery for at least 2 h after drug ingestion. The combined alcohol and marijuana treatment produces little more than the effect produced by either drug alone, suggesting some antagonism between the drugs--a suggestion supported by a significantly lower blood alcohol level for the alcohol dose when combined with marijuana than when taken alone.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
In an experiment using ten subjects, marijuana produced a dose-related constriction of the pupil at low photopic light levels; alcohol produced no effect on pupil size. The two drugs in combination produced no change in pupil size.
A simple, stable, and relatively calibration-free eye movement recording system for clinical application is described. This limbal sensing device makes use of a standard trial-lens clip that can be attached to the patient's spectacles, allowing easy and quick addition of lens or prism power. Horizontal eye movements or positions can be recorded with an accuracy of better than 1 degree over a 50-degree range; the linear range of the device is approximately 30 degrees.
Adrenocortical insufficiency was produced in rat fetuses by surgical decapitation. These animals show low plasma corticosterone levels compared to littermate controls. Lung slices from anencephalic fetuses were found to have reduced incorporation of [14C]choline into phosphatidylcholine, hence diminished choline pathway activity; this abnoramlity was present at 21 days of gestation but not at term. Cholinephosphotransferase (CPT), the terminal catalyst of the choline pathway, also showed diminished activity in lungs of anencephalic fetuses, with a mean of 120 pmol/min/mg protein compared to a control value of 190. Dexamethasone treatment of these animals for 6-12 hr led to enhanced choline incorporation rates. Corticosteroid administration also restored CPT activity and even elevated the enzyme to a mean level (340 pmol/min/mg protein) greater than that found in normal fetuses at 21-22 days of gestation. The early pulmonary biochemical effects of dexamethasone in this model were not accompanied by recognizable ultrastructural changes.
This study examines the effect of maternally injected glucocorticoid on the pattern of hypoglycemia exhibited by rat pups with intrauterine growth retardation (IUGR). The majority of surgical procedures designed to produce small-for-gestational age (SGA) newborns for biochemical studies were carried out on days 18 and 19 of gestation because of favorable vields of pups with IUGR at those operative days. At birth, normal controls showed a mean +/- SE plasma glucose value of 63 +/- 2 mg/dl; mean glucose for the group with IUGR was significantly lower at 43 +/- 2 mg/dl. There was a further decrease in the plasma glucose concentration of pups with IUGR at 2-4 hr of age, whereas values in the control littermates did not fall during this interval. Through the first 2 hr of neonatal life, 46% of the pups with IUGR exhibited plasma glucose values less than 40 mg/dl, whereas only 18% of the control littermates manifiested hypoglycemia. During the 2-4-hr interval, the incidence of hypoglycemia in animals with IUGR increased to 91%; however, the incidence in control remained at 18% from 2-4 hr and fell to 4% at 4-6 hr of age. At birth, the pups with IUGR had a lower mean liver weight compared to their control littermates, but glycogen concentration of liver was similar to the control mean +/- SE of 25.7 +/- 1.8 (IUGR = 22.2 +/- 1.3 mg/g wet weight). Total hepatic glycogen stores, however, were markedly lower in dysmature rat pups (IUGR = 2.96 +/- 0.17 mg; control = 7.23 +/- 0.43 mg). Concentrations of plasma glucose at birth of individual control and IUGR animals were found to correlate significantly (r = 0.64, p less than 0.001) with total liver glycogen content. The decline in plasma glucose values in pups with IUGR was not present in animals whose dams received glucocorticoid injection 24 and 48 hr before delivery. At 4-6 hr of age, for instance, the mean plasma glucose concentration in the corticoid-treated IUGR group (70.1 +/- 6.9 mg/dl) approximated that of the control group. Instead on the 91% incidence of hypoglycemia noted in the nontreated dysmature pups, an incidence of 55% was found at 2-4 hr of age in offspring of mothers given glucocorticoid. At 4-6 hr, the treated group showed an incidence of 18% compared to a 67% figure in the nontreated IUGR animals. The concentration of liver glycogen in these animals also differed in that the treated IUGR pups showed significantly higher values (26.9 +/- 1.7 mg/g wet weight, mean +/- SE) than nontreated progeny. It is concluded that antenatally administered corticosteroid influence the development of neonatal hypoglycemia in the dysmature rat pup and that the major effect is not at birth, but during the 2-4-hr period of neonatal life.
At threshold the eye is known to sum quanta as though the total catch were important and not the distribution on the retina. In humans, spatial summation is larger under dark adapted conditions. The extent of this spatial summation is studied in goldfish retinal ganglion cells which are known to receive both rod and cone inputs. The area of summation in single ganglion cells is found to be much larger for rod input compared to cone input. It seems that in single ganglion cells, the spatial summating properties increase markedly in the dark due largely to the neural organization of rod and cone input.
Experienced alcohol and marijuana users were instructed to track with their eyes a small spot that moved horizontally back and forth in pendular (sinusoidal) motion across a 7.5-degree field. The frequency of spot oscillation was gradually increased from 0.5 to 3.0 Hz in 40 sec. Eye movement recordings showed the frequency at which smooth tracking and, soon thereafter, saccadic tracking broke down. These smooth and saccadic cutoff frequencies were reduced after administration of alcohol, but not after marijuana or placebo. For low alcohol doses, smooth tracking was impaired and saccadic tracking was unaffected, much like an effect previously reported for barbiturates. Alcohol seems to affect smooth tracking by increasing the central processing time required to generate the appropriate eye movement. It affects saccadic tracking by slightly decreasing saccadic velocity and to a greater extent by increasing latency time, part of which may be devoted to central processing. The site of action of alcohol appears to be central to both the paramedian pontine reticular formation and the flocculus of the cerebellum.