Search PubMed⌕ Search

Biomedical subjects

E M Williams

Publications and source records attributed to E M Williams.

At least 55 records · Page 3Linked to original sources
PubMed1990

Anti-Sc1 in pregnancy.

Anti-Sc1 was detected in a gravida-2 patient at 12 weeks' gestation. At 29 weeks, the antibody was found to be of the IgG3 subclass with a titer of 16, score 36, by the indirect antiglobulin test, and it produced 7 percent lysis by antibody-dependent cellular cytotoxicity (ADCC) assay, a finding that suggested an unaffected fetus. The titer remained constant throughout the pregnancy, as did the IgG subclass and activity in the ADCC assay. At delivery of the full-term infant, the cord hemoglobin was 13.5 g per dL and the direct antiglobulin test was positive (3+) with anti-IgG. The infant did not require transfusion. A sample taken 9 weeks after delivery showed 44 percent lysis in the ADCC assay. The anti-Sc1 titer was 32, score 65.

Adult↗
PubMed1990

Compliance with breast cancer screening achieved by the Aylesbury Vale mobile service (1984-1988).

The uptake of breast cancer screening in women aged 45-64 years, living in Aylesbury Vale district, was determined between 1984 and 1988. During this period, self-referral gave way to invitation as the method of gaining access to the service. In the initial period of open access the estimated uptake was 27.9 per cent. A pilot study of response to invitation (and reminder) in two general practices resulted in a compliance of 80.6 per cent. Extended to 20 general practices in Aylesbury Vale, overall compliance with invitation was 73.7 per cent. The response amongst previously screened volunteers was higher (91.5 per cent) than amongst unscreened women (67.6 per cent). There was no significant trend in compliance with age although the oldest women had the lowest uptake. Second round compliance in the two pilot practices reduced to 77 per cent, with 86.1 per cent of a cohort of screened women responding to a second offer of screening. The implications of these results for the national breast cancer screening programme are discussed together with the difficulties associated with the routine derivation of uptake. It is concluded that not only must the accuracy of population registers be improved, but also standard definitions of uptake measurements should be agreed and adopted.

England↗
PubMed1989

Phenotypical features of an unique Irish family with severe autosomal recessive osteogenesis imperfecta.

Severe Sillence type II/III Osteogenesis imperfecta (OI) is a lethal or severely crippling disease with either autosomal dominant or recessively inherited type I collagen mutations. Here we describe the detailed clinical features of a thin-ribbed OI variant with deformed limbs. The three consecutively affected children showed no genetic linkage with either of the two type I collagen genes, which implies that a novel mechanism causes this clinical phenotype. It can be prevented using ultrasound to diagnose affected foetuses.

Collagen↗
PubMed1987

Some effects of adrenaline on anion transport and nitrite-induced methaemoglobin formation in the rainbow trout (Salmo gairdneri Richardson).

The effects of adrenaline on branchial anion transport and nitrite-induced methaemoglobinaemia have been investigated in rainbow trout. Nitrite uptake and efflux results suggest that adrenaline effects a net anion efflux principally by stimulation of the unidirectional branchial anion efflux. In oxygenated whole blood nitrite-induced methaemogloblin was significantly reduced in the presence of adrenaline. The physiological and environmental consequences of nitrite-induced stress are discussed.

Animals↗
PubMed1986

Further studies of alinidine induced bradycardia in the presence of caesium.

Alinidine, the N-allyl derivative of clonidine, reduces heart rate in animals and man by a selective action on the sinoatrial node. In this study, in the presence of caesium, which blocks the time dependent inward current activated by hyperpolarisation (ih or if), alinidine still caused a concentration related bradycardia in the rabbit sinoatrial node. Within the clinical range of concentrations of alinidine the curve relating heart rate to alinidine concentration in the presence of caesium was parallel to that observed in its absence. It is concluded that the alinidine induced bradycardia cannot be attributed to blockade of ih.

Animals↗
PubMed1984

Contribution of isolated general practitioner maternity units.

A postal survey of isolated general practitioner maternity units in England and Wales showed that just under 4% of deliveries take place in them. Eight per cent of general practitioners are on the staffs, and in 87% of units midwives are integrated with the community midwifery service. Sixty two per cent of units have visiting consultant cover. Fifty seven per cent of patients are booked and delivered in the unit, 28% are booked and deliberately delivered elsewhere, 5% are transferred in the antenatal period, and 10% transferred as emergencies. The perinatal mortality rate for cases booked and delivered in the units is 1.1 per 1000. The number of emergency transfers was appreciably less for those units that were prepared to do their own operations. Thirty five per cent of these units are liable to be cut off in bad weather, and they will continue to fulfil an essential role in the midwifery services.

Delivery, Obstetric↗
PubMed1983

The absence of effect of chemical sympathectomy on ventricular hypertrophy induced by hypoxia in young rabbits.

Young rabbits, eight at a time, were exposed to 203 and 208 h (groups I and II) and 283 and 298 h (groups III and IV) of hypoxia (O2 at 70 to 80 mmHg), at atmospheric pressure. The animals were injected ip with 25 mg X kg-1 on the first day, and with 50 mg X kg-1 on the second day and every 48 h thereafter of guanethidine (G) or 6-hydroxydopamine (6-OHDA) (O), or an equivalent volume of saline (H = hypoxic controls, or N = normoxic controls). This regime of treatment abolished, in normoxic and hypoxic animals alike, the effect of sympathetic nerve stimulation on the pupil at voltages which produced maximum dilatation in control animals. Injection of atenolol reduced heart rate by 32% in control animals, but had no effect in the guanethidine treated animals, and a very small effect in the 6-OHDA treated group. The animals in each group were litter mates of those in the other groups. In the first series the dry weight of the hypoxic right ventricles increased, relative to the normoxic controls, by 38.8% (H), 40.5% (G) and 40.9% (O). There was no left ventricular hypertrophy in the hypoxic animals, but there was a small, but not statistically significant, rise in the haematocrit (Hct). In the second series the right ventricular hypertrophy was greater (+98% (H), +89% (G) and +102% (O]. There was also a significant left ventricular hypertrophy (+38% (H), +40.3% (G) and +41% (O] and a highly significant increase in haematocrit in all the hypoxic groups. The right atria were only slightly hypertrophied in the first series, but greatly hypertrophied in the second series (+103%, H), an effect attenuated by the treatment (+34%, G, and +39%, O). When each treated hypoxic animal was compared with its untreated hypoxic littermate (n = 12), the mean treated/untreated ratio for the right ventricular dry weight was 0.991 +/- 0.022 for the guanethidine group (n = 11) and 1.023 +/- 0.043 for the 6-hydroxydopamine (n = 11). Such identity of the extent of the hypertrophy in all the hypoxic groups, irrespective of the duration of hypoxia, implies that the hypertrophy was not conditional upon sympathetic activity.

Animals↗
PubMed1982

The effects of nadolol on various cardiac tissues in normoxia, and on atrial muscle in simulated ischaemia.

Nadolol, a non-selective beta-blocker with a long duration of action, reportedly is devoid of membrane stabilizing action. Since such action is augmented by ischaemic conditions, it was of interest to investigate whether, in simulated ischaemia, a direct membrane effect of nadolol might be revealed. We have confirmed that in normoxia nadolol had no effects on intracellulary recorded potentials in isolated rabbit atrial or ventricular muscle at a concentration of 4.84 microM, but significantly reduced action potential amplitude and maximum rate of depolarisation at 14.5 microM. In Purkinje cells a small reduction of action potential amplitude was produced by 1.61 microM nadolol, but the effect was not increased by nadolol 4.84 microM. There were no drug-induced changes in action potential duration (APD), spontaneous frequency, conduction velocity, contractions, electrical threshold, effective refractory period or the maximum frequency at which a stimulus could be followed. Nadolol 14.5 microM did not reduce the positive inotropic effect of increasing extracellular calcium concentrations. Nadolol was 25 times less potent than procaine as a local anaesthetic on desheathed frog nerve. In a solution simulating ischaemia (8 mM KCl, 10 mM NaHCO3, gassed with 20% O2, pH 7.0) nadolol had a significant class 1 action on atrial muscle, however, even at 4.84 microM and reduced the shortening of APD caused by the solution. It is concluded that nadolol has no class 1, 3 or 4 antiarrhythmic activity in normoxia, but could have an additional protective effect in ischaemic myocardium against the arrhythmogenic factor of shortened APD.

Adrenergic beta-Antagonists↗
PubMed1982

Parasympathetic rebound following EMG biofeedback training: a case study.

The self-regulation literature contains very few reports of negative side-effects stemming from biofeedback training. Nevertheless, the case reported here is unique in that immediately following each of several early EMG feedback sessions, an otherwise headache-free patient reported an acute attack of headache and nausea. These attacks, the conditions under which they appeared, and the conditions leading to their remission will be described. Discussion will focus on the possible physiological mechanisms involved.

Adult↗
PubMed1981

Pacemaker selectivity: influence on rabbit atria of ionic environment and of alinidine, a possible anion antagonist.

Alinidine, a new compound which reduces heart rate in man and animals, has a selective action on the sinus node. The dose-response relation between alinidine and frequency is not altered by atropine, and alinidine does not block the positive chronotropic action of isoprenaline. Alinidine has no negative inotropic action and has no effect on the linear relation between extracellular Ca and force of myocardial contraction. Alinidine did not alter the slope of the relation between frequency and external calcium concentration. Intracellular recordings showed that alinidine had no effect on the maximum rate of depolarisation or overshoot potential of rabbit atrial muscle, nor was conduction velocity, electrical threshold or maximum follow frequency affected. It was concluded that alinidine did not restrict current through fast inward channels. Alinidine did not increase resting potential or accelerate repolarisation, suggesting that potassium conductance was not increased. The effect of alinidine on frequency was not increased in 14 mmol . litre-1 KCl, or decreased in 2.24 mmol . litre-1 KCl, suggesting that the attachment of alinidine to receptors was not voltage-dependent. Spontaneous frequency was higher when NaCl was replaced by NaBr, and the bradycardic effect of alinidine was increased. Conversely, frequency was lower in NaCH3SO4 and the slope of the dose-response curve decreased. Intracellular recordings from sinus node cells showed that alinidine decreased the slope of the slow diastolic depolarisation and increased action potential duration, without altering the overshoot, the maximum diastolic potential, or the "take-off" potential. A possible explanation for these results is that alinidine restricts current through anion-selective channels. If so, the high potency of alinidine suggests that anionic current normally carries a substantial fraction of the current causing slow diastolic depolarisation.

Animals↗
PubMed1981

The effect of prolonged propranolol administration on myocardial transmural capillary density in young rabbits.

1. As a sequel to previous evidence that prolonged beta-adrenoceptor blockade in young rabbits led to a relative increase in the capillarity of ventricular muscle, an attempt has been made to localize and quantify the capillary density from epicardium to endocardium in 12-week old rabbits treated for 6 weeks with propranolol (3 mg kg-1) S.C. twice daily and in litter-mates treated with saline (controls). 2. Full-thickness 0.5 micrometers sections of the left ventricular wall were point-counted in 200 micrometers steps. In the controls the capillary 'volume density' decreased progressively below the epicardial surface from a value of 9% to reach a minimum of 7.1% at a depth of 2.5 mm. Capillary density then increased again towards the endocardium, reaching a maximum of 11.5% in the trabeculae carnae (depth 3.5 mm). 3. In the treated animals the capillary density was increased in the mid wall at 2.3 and 2.5 mm, but significantly decreased in the trabeculae at 3.7 mm (P less than 0.05). 4. A more detailed analysis was undertaken at depths of 0.7 (Epi), 2.3 (Endo) and 3.5 mm (Trab), comprising estimates of capillary number, capillary diameter and intercapillary distance, via the stereological parameters of mean intercept length and mean free distance. 5. In the controls the order was Epi greater than Trab greater than Endo for number, Trab greater than Endo greater than Epi for diameter and Endo greater than Epi greater than Trab for intercapillary distance. 6. In the treated rabbits the mean intercapillary distance was significantly reduced in the epicardial (by 17.5%, P less than 0.05) and endocardial zones (by 32%, P less than 0.005), but was not significantly altered (+3.7%, P greater than 0.05) in the trabeculae. 7. The non-uniform distribution of capillaries in the controls illustrates that detection of changes in transmural capillary density requires that the depth of samples be measured from the epicardial surface and not, owing to the presence of trabeculae carnae, from the endocardium. 8. If similar treatment effects were to occur in man, they would suggest that prolonged beta-blockade could induce an increase in capillary density which would render the ventricular mid wall less susceptible to ischaemia.

Animals↗