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Biomedical subjects

J Patrick

Publications and source records attributed to J Patrick.

At least 235 records · Page 13Linked to original sources

Death during recovery from severe malnutrition and its possible relationship to sodium pump activity in the leucocyte.

The leucocyte data on four malnourished children who died suddenly when high-energy feeding was started were retrospectively analysed. The pretreatment rate constant for sodium efflux in leucocytes was higher and the intracellular sodium concentration lower in this group than in 13 malnourished children who recovered uneventfully with feeding. Two other children with unusual leucocyte electrolyte values and sodium pump activity were identified and closely monitored when high-energy treatment was begun. They rapidly developed the syndrome of extracellular fluid overload but were successfully treated with diuretics and digoxin. Though the precise relation between the findings in the leucocytes and the development of this overload syndrome is not clear, the pretreatment leucocyte values are nevertheless valuable in predicting which malnourished children are at risk of sudden death when refeeding is started.

Child, Preschool↗

Definition of sleep state in the newborn infant by heart rate analysis.

The relationship of heart rate variability to sleep state was examined in 9 term newborn infants at one to three days of age. Spectral density plots of rhythmic variations in heart rate during active sleep and quiet sleep were characteristic and always distinct from each other. Heart rate and heart rate variability were significantly higher during active sleep than during quiet sleep. It was always possible to identify quiet sleep and active sleep during sleep periods by inspecting spectral density plots of the variations in heart rate. Similar relationships between heart rate variability and sleep states may exist in utero. Spectral analysis of heart rate variations may provide an indirect measurement of fetal sleep states, and such measurements might become useful in assessing fetal brain maturity and fetal well-being.

Female↗

Acetylcholine receptor metabolism in a nonfusing muscle cell line.

The development and turnover of acetylcholine receptors in a nonfusing muscle cell line has been investigated using iodinated alpha-bungarotoxin as a probe for acetylcholine receptor. logarithmically growing cells do not bind toxin, while cells that have ceased cell division bind toxin at a site which has the pharmacological characteristics of an acetylcholine receptor. These binding sites are removed from the cell surface at a rate equal to 8.9 +/- 0.5% of the total surface binding sites/h and appear at a rate equal to 8.3 +/- 1.5% of the total surface binding sites/h. Appearance of new binding sites can occur for a period of 1 1/2 h in the presence of cycloheximide, during which time 15% of the surface receptors can be replaced. There is a hidden population of receptors which is not accessible to toxin without disrupting the cell. This population amounts to 35% of the Triton-extractable receptors in the cell and is composed of two classes. One class, termed a precursor receptor, appears to move from the hidden population to the cell surface, and composes about 40% of the total hidden receptor population. The second class of hidden receptors does not appear to function as a surface precursor and is neither depleted nor enriched by any of the procedures we employed. Surface receptors and hidden receptors are distinguishable on the basis of their sedimentation coefficient about 0.5 to 0.6 S lower than surface receptors. We were unable to distinguish between precursor and non-precursor hidden receptors on the basis of cursor and nonprecursor hidden receptors on the basis of their sedimentation coefficients.

Acetylcholine↗

Immunological distinction between acetylcholine receptor and the alpha-bungarotoxin-binding component on sympathetic neurons.

Clone PC12 of a rat sympathetic neuron cell line binds alpha-bungarotoxin and exhibits carbamoylcholine-stimulated uptake of sodium ions. Concentrations of alpha-bungarotoxin that saturate the alpha-bungarotoxin-binding site have no effect on agonist-stimulated sodium uptake. Conversely, antibodies against eel acetylcholine receptor block the agonist-induced sodium flux but fail to recognize the alpha-bungarotoxin-binding component. Detergent extracts of the PC12 clone inhibit the ability of antibody to eel acetylcholine receptor to recognize 125I-alpha-bungarotoxin-acetylcholine receptor complexes derived from muscle. These results distinguish between a ganglionic nicotinic acetylcholine receptor and an alpha-bungarotoxin-binding component on these cells, and provide evidence for antigenic similarities between muscle acetylcholine receptor and ganglionic acetylcholine receptor.

Acetylcholine↗

Leukocyte electrolytes and sodium transport in protein energy malnutrition.

Intracellular electrolytes and sodium transport were measured in leukocytes obtained from malnourished children. In the presence of edema, leukocyte sodium and potassium were raised. The total flux and the glycoside-sensitive portion were increased. Loss of edema was associated with reductions in all these measurements. In marasmus, glycoside-sensitive sodium efflux was reduced compared to recovered values. Sodium was increased and potassium reduced. It is concluded that at least two defects in sodium transport may occur in protein energy malnutrition, an increased passive permeability in kwashiorkor and a reduced active transport for sodium in marasmus.

Biological Transport↗

The prediction of postoperative potassium excretion after cardiopulmonary bypass.

Potassium excretion following cardiopulmonary bypass has been studied in 11 patients. After an initial period of 4 to 5 hours, potassium excretion was found to be directly related to urine flow provided diuretics had not been administered. Triamterene altered the slope of the regression line so that, for any given urine flow rate, less potassium was excreted. A simple program for postoperative potassium therapy is described.

Cardiopulmonary Bypass↗

Effect of triamterene on leucocyte sodium and potassium levels in heart disease.

Sodium and potassium levels in plasma and leucocytes and the sodium efflux rate constants of leucocytes were measured in patients with congenital heart disease not on treatment, patients with valvular heart disease being treated with digoxin and conventional diuretics, and patients with valvular heart disease receiving digoxin and either conventional diuretics or triamterene or both. The group being treated with digoxin and conventional diuretics showed low cellular potassium levels, low sodium efflux rate constants, and a rise in cellular sodium levels. Patients given triamterene showed a rise in potassium levels in plasma and cells and in the sodium efflux rate constant.

Digoxin↗

Cellular immunity in myasthenia gravis. Response to purified acetylcholine receptor and autologous thymocytes.

To determine the potential importance of an immune response directed against the acetylcholine receptor in myasthenia gravis, we studied cell-mediated immunity to receptor as measured by lymphocyte stimulation in 21 myasthenic patients and 21 controls, including five with amyotrophic lateral sclerosis. The mean (+/- S.E.M.) stimulation index was 5.3 +/- 1.3 for patients and 1.2 +/- 0.3 for controls (P less than 0.005). Fourteen patients had indexes greater than 2.0 (nine of 11 males, five of 10 females, 10 of 11 elderly patients, and five of six with thymoma). Stimulation index correlated with disease activity (rs = 0.71, P less than 0.01). Peripheral blood lymphocytes from one of three young female myasthenic patients responded to autologous thymocytes but not to receptor; peripheral blood lymphocytes from the other two responded to receptor but not to autologous thymocytes. Our findings are further evidence that autoimmunity to the acetylcholine receptor plays a central part in myasthenia gravis.

Acetylcholine↗

Abnormal leucocyte composition and sodium transport in essential hypertension.

Cation transport and electrolyte composition were studied in leucocytes from 17 patients with uncomplicated essential hypertension. Significant increases in cell sodium and water contents, associated with a depression of the rate-constant for active sodium efflux, were found in the hypertensive patients. These abnormalities in cell sodium transport may possibly be related to mechanisms of hypertension.

Adolescent↗

Leucocyte sodium transport in uraemia.

1. In sixteen patients with severe chronic renal failure the rate constant for total sodium efflux from leucocytes was significantly reduced compared with that in thirty control subjects. This difference lay chiefly in the glycoside-sensitive ('active') moiety of sodium efflux. 2. In sixteen patients receiving regular haemodialysis, the rate constant for total sodium efflux from the leucocyte was significantly greater than in the undialysed uraemic patients though still subnormal. 3. In individual patients, an increase in sodium efflux could be detected as early as 1 week after regular haemodialysis was started. 4. These results are compatible with the existence of a dialysable molecule in uraemic plasma affecting leucocyte sodium transport.

Adult↗

The effect of external potassium concentration on leucocyte cation transport in vitro.

1. Sodium and potassium transport rates in human leucocytes were measured in vitro at different external potassium concentrations. 2. At nominally zero external potassium concentrations, the ouabain-sensitive sodium efflux was reduced to less than 20% of its maximum value. There was evidence that under these conditions a ouabain-sensitive sodium-sodium exchange occurs. 3. Both total and ouabain-insensitive potassium influx increased with increasing external potassium concentration. The ouabain-sensitive potassium influx showed saturation. 4. Ouabain-insensitive potassium efflux was also stimulated by increasing the external potassium concentration, suggesting significant potassium-potassium exchange at physiological external potassium concentrations.

Biological Transport, Active↗