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Biomedical subjects

R Wilkinson

Publications and source records attributed to R Wilkinson.

At least 19 recordsLinked to original sources
PubMed1992

Serum triglyceride and insulin levels are associated with erythrocyte sodium-lithium counter-transport activity in normoglycaemic individuals.

The relationship between erythrocyte sodium-lithium counter-transport activity, serum insulin, lipids and demographic factors was examined in 93 normoglycaemic predominantly normotensive individuals with mild fasting hypercholesterolaemia (greater than 5.2 mmol/l). The major significant univariate correlates of sodium-lithium counter-transport activity were fasting serum triglycerides, HDL cholesterol, the ratio of fasting glucose: insulin, apo A1, alcohol consumption and apo B. Stepwise multiple regression analysis revealed 24% of the variability in sodium-lithium counter-transport activity could be accounted for by independent contributions of fasting serum triglycerides, alcohol consumption, the fasting glucose/insulin ratio and apo A1 and ANOVA confirmed a significant relationship with fasting insulin measures that was independent of serum triglycerides (P less than 0.05). The relationship between erythrocyte sodium-lithium counter-transport activity and concentrations of serum triglycerides, HDL components, insulin and additionally alcohol consumption, could reflect the influence of those variables on erythrocyte structure and function.

Alcohol Drinking↗
PubMed1992

Isolation of koala lymphoid cells and their in vitro responses to mitogens.

Baseline parameters have been established for the successful in vitro culture of mononuclear cells from the peripheral blood (PMC) of koalas. To minimise stress-related influences and allow repeated testing of cells from the same animals, most studies were performed using blood samples from captive koalas which had become accustomed to regular handling. Ficoll-Paque density gradient fractionation of whole blood was required to prepare cell suspensions which responded well to the T-lymphocyte mitogens phytohaemagglutinin, concanavalin A and pokeweed mitogen. In contrast, very low or negligible proliferative responses were induced by the B-lymphocyte mitogens lipopolysaccharide, jacalin and protein A, even when purified PMC were cultured with a wide range of concentrations of these molecules. Using the standard approaches established with T-lymphocytes of eutherian animals, it was shown that concanavalin A-stimulated PMC produced an interleukin 2-like growth factor. The significance of these findings is discussed in the context of current knowledge and understanding of similar studies carried out using the lymphoid cells of eutherian and other metatherian animals.

Animals↗
PubMed1992

Calcification and stress distribution in bovine pericardial heart valves.

There is a strong relationship between mechanical stress and calcification in biological prosthetic heart valves. A dynamic in vitro calcification test has been used to study the relationship between stress distributions in the leaflets of bovine pericardial valves and the deposition of calcium over the leaflet surfaces. Intuitive stress regions have been defined over the leaflet surfaces. Calcium uptake by the leaflets has been assayed directly by ashing of leaflet material and analysis of the ash by atomic absorption spectrophotometry. Calcium and phosphorus distribution over the leaflet surface has been analyzed using energy-dispersive x-ray analysis by scanning electron microscope and data points assigned to the appropriate stress region. The uptake of calcium is assessed by comparing stress regions, surfaces, and the degree of calcification of the valve. Differences between stress regions and surfaces are significant. Uptake of calcium in these valves appears to be strongly related to the degree and type of stress present in the valve leaflets.

Bioprosthesis↗
PubMed1992

Koala lymphoid cells: analysis of antigen-specific responses.

Bovine serum albumin (BSA) and ovine immunoglobulin (OvIgG) were used to induce humoral immune responses in two koalas which were also painted with 2-4-dinitrofluorobenzene (DNFB) and subsequently tested for local delayed-type hypersensitivity (DTH) reactions. The responses observed support the suggestion that the koala is 'immunologically lazy'. Antibody responses to BSA and OvIgG were not detected until 12 weeks after the initial antigen injection and antigen-specific in vitro proliferative responses by the mononuclear cells (PMC) of immunised animals could not be induced, although these cells did respond to concanavalin A and phytohaemagglutinin. Similarly, DTH responses to DNFB could be elicited in vivo, but took a relatively long time to develop and the PMC of the sensitised koalas were unresponsive to the sensitising antigen in vitro. The absence of proliferation when mixed suspensions of PMC from different koalas were cultured in vitro is consistent with these results.

Animals↗
PubMed1992

Kinetics of sodium-lithium countertransport activity in patients with uncomplicated type 1 diabetes.

1. Increased erythrocyte sodium-lithium countertransport activity has been reported to be associated with nephropathy in type 1 diabetes and linked to a family history of essential hypertension. 2. This study aimed to determine the mechanism of increased sodium-lithium countertransport activity. Sodium-lithium countertransport kinetics were measured in uncomplicated and hyperlipidaemic type 1 diabetic patients. 3. In the nine out of 31 uncomplicated type 1 diabetic patients who had high sodium-lithium countertransport activity, the sodium affinity (Km) was normal but the maximum velocity (Vmax) was increased. 4. Hyperlipidaemia, when present in diabetic patients, was associated with increased sodium-lithium countertransport activity, but could not explain the high activity in uncomplicated type 1 diabetic patients in whom plasma lipid concentrations were normal. 5. Sodium-lithium countertransport activity is increased in type 1 diabetes by a mechanism different to that in essential hypertension, where the mechanism is a low Km (increased sodium affinity). Hence familial hypertension cannot explain the raised sodium-lithium countertransport activity in type 1 diabetes.

Adult↗
PubMed1992

Changes in erythrocyte sodium-lithium countertransport kinetics in diabetic nephropathy.

1. It has been proposed that raised erythrocyte sodium-lithium countertransport activity in type 1 diabetic patients is associated with an increased risk of developing diabetic nephropathy. Diabetic patients with established nephropathy would therefore be expected to have high activity. 2. Standard sodium-lithium countertransport activity, sodium affinity (Km) and maximum velocity (Vmax) were measured in type 1 diabetic patients at different stages of diabetic nephropathy and in appropriately matched uncomplicated diabetic patients and normal control subjects. 3. A small proportion (15%) of patients with nephropathy had standard sodium-lithium countertransport activity higher than the control range. However, mean standard sodium-lithium countertransport activity in the diabetic patients with nephropathy [mean +/- SEM, 0.26 +/- 0.12 mmol of Li+ h-1 (l of cells)-1] was not significantly higher than in the uncomplicated diabetic patients [0.27 +/- 0.03 mmol of Li+ h-1 (l of cells)-1] or in the normal control subjects [0.25 +/- 0.02 mmol of Li+ h-1 (l of cells)-1]. 4. There were marked changes in the kinetic characteristics of the sodium-lithium countertransport in the diabetic patients with nephropathy so that there were decreases in both Km and Vmax. 5. These kinetic changes could not be attributed to an effect of either renal failure per se or the duration of diabetes. 6. The characteristic kinetic changes in sodium-lithium countertransport may indicate underlying alterations in membrane function with the onset of nephropathy in type 1 diabetes.

Antiporters↗
PubMed1992

Metabolic clearance rate of arginine vasopressin in severe chronic renal failure.

1. The metabolic clearance rate of arginine vasopressin was determined using a constant infusion technique in normal subjects and patients with chronic renal failure immediately before commencing dialysis. Endogenous arginine vasopressin was suppressed in all subjects before the infusion with a water load. 2. Plasma arginine vasopressin concentrations were determined using a sensitive and specific radioimmunoassay after Florisil extraction. The detection limit of the assay was 0.3 pmol/l, and intra- and inter-assay coefficients of variation at 2 pmol/l were 9.7% and 15.3%, respectively. 3. In normal subjects, the metabolic clearance rate was determined at two infusion rates producing steady-state concentrations of arginine vasopressin of 1.3 and 4.4 pmol/l. In the patients with renal failure, a single infusion rate was used, producing a steady-state concentration of 1.5 pmol/l. 4. At comparable plasma arginine vasopressin concentrations, metabolic clearance rate was significantly reduced in patients with renal failure (normal 1168 +/- 235 ml/min versus renal failure 584 +/- 169 ml/min; means +/- SD; P < 0.001). 5. Free water clearance was significantly reduced in normal subjects during the arginine vasopressin infusion from 8.19 +/- 2.61 to -1.41 +/- 0.51 ml/min (P < 0.001), but was unchanged in the patients with renal failure after attaining comparable plasma arginine vasopressin concentrations. 6. In normal subjects there was a small but significant fall in metabolic clearance rate at the higher steady-state arginine vasopressin concentration (1168 +/- 235 ml/min at 1.3 pmol/l versus 1059 +/- 269 ml/min at 4.4 pmol/l; P = 0.016).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1992

Rett syndrome: stimulation of endogenous biogenic amines.

Transient hypercapnic hyperoxemia was induced in two Rett syndrome children by the administration of a gaseous mixture of 80% O2 and 20% CO2. Time course studies of neurotransmitters and their metabolites showed an immediate and marked increase in central biogenic amine turnover following inhalation of the gas mixture. The increased turnover of biogenic amines was associated with improved clinical changes. This suggests a coupled relationship and provides further support for an etiological role of neurotransmitter dysfunction in Rett syndrome. In a complementary study, elevation of pulmonary CO2 by application of a simple rebreathing device resulted in improvement of abnormal blood gases and elimination of the Cheyne-Stokes-like respiratory pattern of the Rett syndrome. Near normalization of the EEG occurred when a normal respiratory pattern was imposed by means of a respirator. Taken together, these results lead to the preliminary conclusion that cerebral hypoxemia secondary to abnormal respiratory function may contribute to diminished production of biogenic amines in Rett syndrome.

Brain↗
PubMed1992

Reduced erythrocyte and leukocyte magnesium is associated with cyclosporin treatment and hypertension in renal transplant patients.

Plasma, urine, erythrocyte and leukocyte magnesium were measured in normotensive and hypertensive renal transplant patients who were being treated with either azathioprine or cyclosporin. These were compared with essential hypertensive patients and normal subjects. Erythrocyte and leukocyte magnesium were reduced in renal transplant patients in independent association (ANOVA) with both cyclosporin treatment (P = 0.03, P = 0.016 respectively) and hypertension (P less than 0.001 for both). Therefore, hypertensive transplant patients on cyclosporin had the lowest magnesium content of both erythrocytes (1.22 +/- 0.09 mmol/l cells) and leukocytes (2.68 +/- 0.2 nmol/10(6) cells) compared to normal subjects (1.96 +/- 0.17 and 4.11 +/- 0.58 respectively) whereas normotensive transplant patients on azathioprine had normal values (2.12 +/- 0.16 and 5.13 +/- 1.0 respectively). Plasma magnesium was also reduced with cyclosporin treatment. Urine magnesium was not significantly different between any of the groups. Therefore, magnesium depletion may have a role in hypertension in renal transplant patients. Since cyclosporin treatment is also associated with magnesium depletion, this could explain the increased occurrence of hypertension in these patients.

Adult↗
PubMed1992

Plasma lipids affect maximum velocity not sodium affinity of human sodium-lithium countertransport: distinction from essential hypertension.

Inheritance is a major determinant of increased sodium-lithium countertransport (SLC) activity in hypertension. However, hyperlipidaemia can also cause increased SLC activity in some individuals and it is difficult to distinguish this effect from the effect of hypertension. Erythrocyte SLC activity and its kinetic determinants sodium affinity (km) and maximum velocity (Vmax) were measured in 25 hyperlipidaemic patients and 15 normal controls (NC). Increased SLC activity (0.31 +/- SEM 0.03 mmol Li/(h x 1 cells) vs. NC 0.20 +/- 0.01, P < 0.01) in the hyperlipidaemic patients was associated with increased Vmax (0.59 +/- 0.07 vs. NC 0.41 +/- 0.03, P < 0.01) but normal km (median 120 range [40-324] mmol l-1 vs. 140 [108-260]. Lipid-lowering therapy resulted in decreased SLC activity secondary to a fall in Vmax. Km remained constant despite the changes in lipids and Vmax. The mechanism of increased SLC activity in hyperlipidaemia is different from that in essential hypertension where increased sodium affinity is found. Measurement of the kinetic characteristics of SLC may discriminate between the independent influences of hypertension and hyperlipidaemia on the sodium-lithium countertransporter.

Adult↗
PubMed1992

Sodium-lithium countertransport kinetics in normal and hypertensive human pregnancy.

Erythrocyte sodium-lithium countertransport activity is increased in a subgroup of patients with essential hypertension but activity also rises temporarily during normal pregnancy. It is not known if the mechanism of raised activity is the same in both of these situations. Standard sodium-lithium countertransport activity and its kinetic characteristics (sodium affinity and maximum velocity) were measured in 15 women with a normal pregnancy. The mechanism of raised sodium-lithium countertransport activity was an increase in maximum velocity. There was no change in sodium affinity. This contrasts with essential hypertension where the mechanism is increased sodium affinity. Sodium-lithium countertransport activity was also measured in 14 primigravidae whose pregnancies were complicated by hypertension, and mean activity was not significantly higher than in normal pregnancy. However, six women had increased sodium affinity suggestive of essential hypertension and a different underlying mechanism of hypertension to those with normal sodium affinity. Prospective measurement of sodium-lithium countertransport kinetics may lead to a better understanding of the pathophysiology of hypertension in pregnancy.

Adult↗
PubMed1992

Pregnancy induced hypertension and sodium pump function in erythrocytes.

OBJECTIVE: To determine if erythrocyte sodium pump function is altered with the onset of pregnancy induced hypertension. DESIGN: A prospective descriptive study. SUBJECTS: Thirty-two primigravid women with pregnancy-induced hypertension (17 had proteinuria) and 32 gestation-matched normotensive primigravid pregnant women were studied and measurements repeated 20 weeks after delivery. INTERVENTION: Erythrocyte sodium, ouabain-sensitive sodium flux and the sodium pump rate constant were measured in whole blood and the maximum velocity and sodium affinity of the sodium pump were measured in vitro. RESULTS: Blood pressure remained higher after delivery in the women who had been hypertensive during pregnancy. In normal pregnancy erythrocyte sodium was decreased, and ouabain-sensitive sodium flux, the sodium pump rate constant and maximum velocity (Vmax) were increased compared with 20 weeks after delivery. In pregnancy-induced hypertension erythrocyte sodium and sodium pump changes were the same as in normal pregnancy. The possibility of a positive association between changes in erythrocyte sodium and in blood pressure was excluded. The rate constant of the sodium pump in blood was related to its Vmax measured in vitro but the relation had greater variance in the hypertensives with 7 of the 32 women having rate constants greater than expected from their Vmax. CONCLUSION: There was no evidence of sodium pump inhibition or a rise in intracellular sodium associated with increased blood pressure in pregnancy. There may have been stimulation of the sodium pump by a plasma factor in some hypertensive women.

Adult↗