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Biomedical subjects

M F Roberts

Publications and source records attributed to M F Roberts.

At least 127 records · Page 7Linked to original sources
PubMed1982

Kinetic model for surface-active enzymes based on the Langmuir adsorption isotherm: phospholipase C (Bacillus cereus) activity toward dimyristoyl phosphatidylcholine/detergent micelles.

A simple kinetic model for the enzymatic activity of surface-active proteins against mixed micelles has been developed. This model uses the Langmuir adsorption isotherm, the classic equation for the binding of gas molecules to metal surfaces, to characterize enzyme adsorption to micelles. The number of available enzyme binding sites is equated with the number of substrate and inhibitor molecules attached to micelles; enzyme molecules are attracted to the micelle due to the affinity of the enzyme active site for the molecules in the micelle. Phospholipase C (Bacillus cereus) kinetics in a wide variety of dimyristoyl phosphatidylcholine/detergent micelles are readily explained by this model and the assumption of competitive binding of the detergent at the enzyme active site. Binding of phospholipase C to pure detergent micelles is demonstrated by gel filtration chromatography. The experimentally determined enzyme-detergent micelle binding constants are used directly in the rate equation. The Langmuir adsorption model predicts a variety of the characteristics observed for phospholipase kinetics, such as differential inhibition by various charged, uncharged, and zwitterionic detergents and surface-dilution inhibition. The essential idea of this model, that proteins can be attracted and bound to bilayers or micelles by possessing a binding site for the molecules composing the surface, may have wider application in the study of water-soluble (extrinsic) protein-membrane interactions.

Bacillus cereus↗
PubMed1982

A three generation family study of cleft lip with or without cleft palate.

A family study of cleft lip, with or without cleft palate, was based on those treated by operation at The Hospital for Sick Children, London, between 1920 and 1939 in order to give information on the proportion affected of children and grandchildren. The probands were those who had survived, were successfully traced, and found to have had at least one child. Care was taken to exclude patients who were traced through a child, whether normal or affected, and not through the usual tracing procedure. Patients with recognised syndromes were also excluded. Because the series was based on patients who had survived and reproduced it was biased in favour of those with milder degrees of the malformation, and against those with any severe associated malformation. The proportion affected of children of probands was 3.15% (+/- 0.56), of sibs 2.79% (+/- 0.52), and of parents 1.18% (+/- 0.37), respectively. The lower proportion of parents affected is attributed to reduced reproductive fitness of patients born two generations ago. The proportion affected of nephews and nieces, aunts and uncles, and grandchildren was 0.47% (+/- 0.18), 0.59% (+/- 0.13), and 0.8% (+/- 0.6) respectively. The proportion affected of first cousins was 0.27% (+/- 0.08). The birth frequency of cleft lip (+/- cleft palate) is estimated to be about 0.1% in England. There were two first cousin and one second cousin marriages among the marriages of the parents. There was no increase of cleft palate among the relatives of the probands. The proportion of sibs affected increased with increasing severity of the malformation in the proband, where the proband was female, and where the proband had an affected parent or already had one affected sib. It was not, however, increased where a more remote relative was affected. The proportion of children affected was not increased when the proband had an affected parent or sib, but few families provided information. The most economical hypothesis to explain the findings is the multifactorial threshold model. The birth frequency of the malformation and the family patterns found make it improbable that one single mutant gene makes a major contribution to the liability to develop the condition.

Adult↗
PubMed1982

A family study of isolated cleft palate.

A family study was based on 245 boy and 329 girl patients treated surgically for non-syndromic cleft palate between 1920 and 1929; 86 and 81 respectively were traced and had had children. These 167 were the probands for the family study and were interviewed in their homes. None was born to a consanguineous marriage. Altogether they had had 384 children of whom 11 had cleft palate (2.9 +/- 0.9%). They had 398 sibs of whom five had cleft palate, 117 grandchildren of whom one was affected, and 517 nephews and nieces of whom one was affected. This is the largest series yet available on which to base an estimate of the risks to children of patients with non-syndromic cleft palate. The risk is probably increased where a parent or sib of the proband is affected and increased to a lesser degree where a second or third degree relative is affected. The family patterns in these and other studies suggest that the aetiology of cleft palate is heterogeneous, with some families showing modified dominant inheritance. This is in contrast to cleft lip (+/- cleft palate) where the data are consistent with a multifactorial threshold model.

Adult↗
PubMed1981

Cholesterol solubilization by short-chain lecithins: characterization of mixed micelles and cholesterol oxidase activity.

The synthetic short-chain lecithins diheptanoylphosphatidylcholine and dioctanoylphosphatidylcholine solubilize cholesterol up to 10 and 18 mol %, respectively. The half-time for diheptanoylphosphatidylcholine solubilization of solid cholesterol is 80 (+/- 30) min. This is much faster than Triton X-100 micelle or egg lecithin vesicle solubilization of solid cholesterol. Both the broadening of lecithin and [4-13C]cholesterol carbon resonances by Mn2+ and the observation of surface dilution kinetics for phospholipase A2 (Naja naja naja) and phospholipase C (Bacillus cereus) hydrolysis of the lecithins indicate that the cholesterol 3 beta-hydroxyl group resides at the particle surface exposed to solvent. Analysis of lecithin 13C chemical shifts suggests that cholesterol causes the short-chain lecithin acyl chains to become slightly more trans, although to a lesser extent than it affects egg lecithin chains in liposomes. Lecithin motion as characterized by 13C T1s and line widths is unaffected by the incorporation of cholesterol. [3,4-13C2]Cholesterol line widths are 5-10-fold narrower in these mixed micelles than in egg lecithin sonicated vesicles, while T1s in the two systems are comparable. These mixed micelles serve as substrates for cholesterol oxidase (Nocardia erythropolis) with a 40-fold rate increase over comparable cholesterol concentrations in egg lecithin vesicles. Part of this rate enhancement can be understood as an increase in interfacial area available to cholesterol oxidase in the micellar systems. These studies suggest that cholesterol oxidase has a weaker affinity for interfaces than other surface active enzymes.

3-Hydroxysteroid Dehydrogenases↗
PubMed1980

Control of forearm venous volume during exercise and body heating.

Subjects ate ice to cool sufficiently to constrict the superficial forearm veins. After ice-eating, esophageal temperature (Tes) recovered from local cooling in 10-15 min, and thereafter reflected body core temperature. Eight skin temperatures (Tsk) were measured, and a weighted mean (Tsk) computed. The left wrist was suspended 5-6 in. above shoulder level, and left forearm skin temperature was maintained at 35 degrees C with a controlled-temperature air stream. Forearm venous volume (FVV) w-s the volume difference between the forearm drained by gravity and the forearm congested by a pneumatic cuff inflated to 32 Torr. Subjects were warmed either by storage of resting metabolic heat or by cycle exercise at 40-45% of maximal O2 consumption. Exercise experiments were conducted in ambient temperatures of 15, 25, and 35 degrees C, and resting experiments in 25 and 35 degrees C. FVV rose linearly with Tes, but during exercise FVV was lower than at the same Tes and Tsk during rest, and the difference was greater at high Tsk and FVV. Our data fit the equation FVV-FVV0 = (a1 Tes + a2 Tsk - b).[1 - phi (W).(Tsk - T-sk0)], where phi (W) is a function of exercise, and phi (W) = 0 at rest.

Adult↗
PubMed1980

Control of skin blood flow during exercise by thermal reflexes and baroreflexes.

Four male subjects exercised on cycle ergometers at 40-51% of maximal aerobic power in the upright and supine positions at air temperatures of 15, 25, and 40 degrees C. Esophageal temperature (Tes) was measured at heart level, and mean skin temperature was computed from a weighted average of eight skin temperature measurements. Forearm blood flow (ABF) was measured by venous occlusion plethysmography, and cardiac output was measured by a CO2 rebreathing technique. At air temperatures of 15 and 25 degrees C, cardiac stroke volume was slightly lower during upright exercise than it was during supine exercise, as was ABF at a given Tes. At 40 degrees C, however, stroke volume was much lower and ABF at a given Tes was considerably lower during upright as opposed to supine exercise. The reduced stroke volume during upright exercise in the heat shows that gravity compounds the effect of cutaneous venodilation by allowing blood to pool in dependent limbs and thus impairing cardiac filling. The proportionality between reduced stroke volume and reduced forearm blood flow suggests that the reduction in blood flow may be mediated by cardiopulmonary baroreflexes that are activated by reduced cardiac filling pressure.

Adult↗
PubMed1979

Circulatory regulation during exercise in different ambient temperatures.

Three relatively fit subjects performed duplicate 20- to 25-min cycle ergometer exercise bouts at moderate and heavy intensities (40% and 70% Vo2 max) in ambient temperatures of 20, 26, and 36 degrees C. They approached a steady state in internal body temperature (Tes) in all but the heavy exercise in the heat, where Tes rose consistently, averaging 38.84 degrees C at the termination of exercise. Cardiac output (Q), estimated by a rebreathing technique, was proportional to Vo2 and independent of the body temperatures, except during the lower exercise intensity in the heart, where Q averaged 1.31 . min -1 higher throughout. In any environment, forearm blood flow was linearly related to Tes above the Tes threshold for vasodilation, but during heavy exercise in the heat this relationship was severely attenuated above a Tes around 38.0 degrees C, when forearm blood flow exceeded 15 ml.min -1 .100 ml -1. Plasma volume decreases during exercise were primarily a function of the intensity of exercise. During heavy exercise in the heat the relative vasconstriction contributes to the maintenance of an adequate stroke volume preventing a fall in Q. In this case, circulatory regulation has precedence over temperature regulation.

Adult↗
PubMed1979

Control of skin circulation during exercise and heat stress.

At any given environmental and mean skin temperature, exercise brings about an increase in internal body temperature and skin blood flow. At high environmental temperatures, when skin temperature is elevated, skin blood flow at any given internal temperature reaches higher levels than at cooler skin temperatures. Increased cutaneous blood flow serves to deliver metabolic heat from the core to the skin, where the heat is lost to the environment by convective, radiative, and evaporative mechanisms. However, at high levels of skin blood flow, peripheral vascular pooling and fluid losses by filtration lead to reduced central venous pressure. This lowers cardiac stroke volume, and requires a higher heart rate to maintain a given cardiac output. Mechanisms which alleviate some of the cardiovascular strain produced by exercise in the heat include the following: acutely, reflexes which arise from receptors in working muscles produce vasoconstriction in a number of central and peripheral vascular beds. Other reflexes, arising from cardiac baroreceptors, produce additional peripheral vasoconstriction when cardiac filling is impaired. In the long term, physical conditioning and heat acclimation lead to increases in sweat output during thermal stress, leading to cooler skin and core temperature during exercise, and decreasing the level of skin blood flow needed for regulation of body temperature.

Arm↗