Routine ultrasound scanning in pregnancy. The benefits are clinical ... and psychological.
Explore the source record for details and available documents.
Female↗
Biomedical subjects
D J Taylor
Publications and source records attributed to D J Taylor.
Habitat-dependent hybrid parentage and differential introgression between neighboringly sympatric Daphnia species.
Allozyme, morphological, and PCR-generated mtDNA markers were used to analyze hybrid parentage and introgression between the neighboringly sympatric crustaceans Daphnia galeata mendotae and Daphnia rosea. mtDNA analysis of D. galeata mendotae from 15 lakes and of D. rosea from 8 lakes revealed species-specific fragment patterns resulting from TaqI and RsaI digestion. No individuals of one parent species possessed the typical mtDNA of the other parent species, suggesting that mtDNA introgression is rare or nonexistent. Hybrids from 18 lakes possessed either the mtDNA patterns of D. rosea or of D. galeata mendotae, indicating that reciprocal hybridization occurs. The mtDNA genome of the dominant parent species in a lake was overrepresented in the hybrids, suggesting that hybridization most often involves females of the common species and males of the rare species. Such a pattern is consistent with the differing importance of density to the environmental induction of males and sexual eggs in Daphnia. For the assessment of nuclear gene flow, eight sympatric populations of each parental taxon and seven allopatric populations of D. galeata were analyzed for allozyme variation at nine polymorphic loci. Our results provided evidence for asymmetric interspecific gene flow involving alleles at six loci that are unlikely to be convergent or symplesiomorphic. This reticulate evolution accounted for much of the genetic divergence between European and North American populations of D. galeata.
Animals↗
An outbreak of strangles in young ponies.
A natural outbreak of strangles occurred in a group of 19 young experimental ponies. The disease was diagnosed in 11 of them within two days of their arrival at Glasgow University veterinary school and five others developed clinical signs within a further four days, a morbidity rate of 84 per cent. All of the affected ponies had typical signs of strangles including dullness, anorexia, pyrexia, regional lymphadenitis, occasionally with rupture of the lymph node, conjunctivitis and a mucopurulent nasal discharge. Nine of the affected ponies were destroyed during the clinical phase of the disease for post mortem studies. The clinical disease in the remaining animals lasted approximately 21 days although one pony had to be destroyed 10 days after the onset of clinical signs because of the development of septic arthritis. All 16 affected animals exhibited peripheral blood neutrophilia and high plasma fibrinogen levels. beta haemolytic streptococci were isolated by nasopharyngeal swabbing from 18 of the 19 ponies. Streptococcus equi was confirmed only in three animals within the first four days of the outbreak. The majority of the other isolates identified to species were S zooepidemicus. beta haemolytic streptococci were still present in six ponies 40 days after they had clinically recovered and were isolated regularly from three ponies which did not develop clinical strangles but remained in contract with affected animals throughout the study.
Animals↗
ACE inhibitors after myocardial infarction.
Explore the source record for details and available documents.
Aged↗
Studies on the expression of the TNF alpha receptors (p55 and p75) and their relative contributions to prostanoid production and glycolytic rate by rheumatoid synovial fibroblasts in vitro.
The effect of monoclonal antibodies against the 55- and 75-kDa (p55 and p75) tumour necrosis factor (TNF) receptors on two tumour necrosis factor alpha (TNF alpha) induced responses was studied in rheumatoid synovial fibroblasts (RSF) in vitro. This provided functional evidence for the expression of both receptor types, which was confirmed by substantial inhibition of 125I-TNF alpha binding to RSF by both antibodies. TNF alpha stimulation of prostanoid production was found to be a function of ligand binding to both receptor types, whereas the stimulation of cellular glycolysis was largely mediated via the p55 receptor. Thus, we showed that RSF express both types of TNF receptor and functional studies showed that stimulation of each receptor results in both similar and dissimilar cellular responses.
Antibodies, Monoclonal↗
Skeletal muscle bioenergetics in myotonic dystrophy.
Skeletal muscle function of 15 patients with myotonic dystrophy (dystrophia myotonica, DM) was investigated using 31P magnetic resonance spectroscopy to evaluate bioenergetics and intracellular pH at rest and during exercise and recovery. Results from DM patients, normal controls and mitochondrial myopathy patients were compared in order to assess the possible contribution of abnormal mitochondrial metabolism to muscle dysfunction in DM. In resting DM muscle, intracellular pH (pHi) was normal, but there were significant elevations in the concentration ratios of Pi/ATP, phosphomonoesters/ATP and phosphodiesters/ATP. In patients with the most severe exercise intolerance the phosphocreatine/ATP ratio was also reduced. Resting muscle of 11 mitochondrial myopathy patients showed similar changes to those of the most exercise-intolerant DM patients. In exercising DM muscle, energy stores were rapidly depleted as in mitochondrial myopathy. Muscle acidified in all subjects, but in DM the decrease in pHi was less than in normal muscle. Recovery half-times for phosphocreatine, Pi and ADP were normal in DM but slow in mitochondrial myopathy. The initial rate of phosphocreatine repletion after exercise was rapid in DM, consistent with high [ADP], but slow in mitochondrial myopathy in spite of elevated [ADP]. Because recovery is an oxidative process, we conclude that there was no decrease in the oxidative capacity of the muscles in this group of DM patients. In the subjects in whom it could be measured, the rate of recovery of intracellular pH was greater in the 3 DM patients (0.14, 0.15 and 0.16 U/min) than in the 7 normal controls (0.08-0.12 U/min, mean 0.10). The results do not rule out a minor abnormality in glycogenolysis, but they suggest that the failure to acidify normally during exercise is probably due to rapid proton efflux.
Adenosine Diphosphate↗
Cellular energetics of dystrophic muscle.
Cytosolic pH and phosphorus metabolite ratios in skeletal muscle were measured by 31P magnetic resonance spectroscopy in patients with Duchenne muscular dystrophy (DMD) and Becker's muscular dystrophy (BMD) and in Duchenne/Becker carriers. In resting dystrophin-deficient muscle, there was a decrease in phosphocreatine (PCr) and increase in orthophosphate (Pi) relative to ATP, and an increase in calculated free [ADP]. Phosphomonester and phosphodiester were also increased relative to ATP. These changes were largest in DMD, smaller in BMD and small or absent in carriers. Cytosolic pH was increased substantially in DMD, moderately in BMD and slightly but significantly in gastrocnemius of carriers. Raised intracellular pH thus appears to be the most characteristic abnormality in dystrophin-deficient muscle. Responses to erobic exercise were studied in the forearm muscle flexor digitorum superficialis of carriers. PCr depletion during exercise was greater than normal but the fall in pH was disproportionately small, resulting in increased [ADP]. This is likely to result either from reduced anaerobic glycogenolysis to lactic acid or from increased proton efflux (as is seen in mitochondrial myopathy). Detailed analysis suggests: (1) at the start of exercise, calculated lactic acid production was increased, as was the rate of PCr depletion, suggesting that there was no absolute defect of glycogenolysis. (2) At the start of recovery, calculated proton efflux was not increased, although as the pH at the end of exercise was higher than in controls and proton efflux is normally pH-dependent, an up-regulation of proton efflux cannot be excluded. (3) Recovery of PCr, Pi and ADP after exercise were not impaired, suggesting that mitochondrial function is normal.
Adenosine Diphosphate↗
Oral phosphate supplements reverse skeletal muscle abnormalities in a case of chronic fatigue with idiopathic renal hypophosphatemia.
A 57-yr-old man presented with a long history of undiagnosed fatigue but no evidence of bone disease. He was noted to have hypophosphatemia due to an idiopathic phosphaturia. Marked abnormalities of exercising skeletal muscle detected by phosphorus magnetic resonance spectroscopy and by plasma metabolite measurements were consistent with mitochondrial dysfunction. Oral phosphate supplements restored plasma phosphate concentration and muscle biochemistry to normal and produced considerable improvement in symptoms and exercise tolerance, although the phosphate concentration in muscle was only marginally low and increased little by treatment. We conclude that hypophosphatemia should be excluded in unexplained fatigue.
Adenosine Diphosphate↗
Control of oxidative phosphorylation in muscle.
Explore the source record for details and available documents.
Adenosine Triphosphate↗
Quantitative analysis of defects of mitochondrial oxidation during recovery from exercise.
Explore the source record for details and available documents.
Adenosine Diphosphate↗
Abnormalities in skeletal muscle metabolism in cyanotic patients with congenital heart disease: a 31P nuclear magnetic resonance spectroscopy study.
1. Exercise tolerance is impaired in congenital heart disease. To examine the possible contribution of abnormalities in skeletal muscle bioenergetics, we used 31P nuclear magnetic resonance spectroscopy to investigate muscle metabolism in 10 subjects with congenital heart disease with cyanosis (median age 17.3 years) and in eight healthy age-matched control subjects. Spectra were collected from the gastrocnemius muscle at rest and during exercise and recovery. 2. In resting muscle there were significant elevations in cytosolic pH and in the cytosolic concentration of inorganic phosphate in the patients, and a strong positive correlation between cytosolic pH and blood haemoglobin concentration in all subjects. 3. During plantar flexion exercise the patients showed increased phosphocreatine depletion and cytosolic acidification over a shorter duration of exercise. The rise in calculated cytosolic ADP concentration was similar in both groups. 4. After cessation of exercise, the recovery half-times of phosphocreatine, ADP and phosphate were two to three times longer in the patients, and the initial rate of phosphocreatine resynthesis (a measure of the rate of mitochondrial ATP synthesis) was half the control value, consistent with a reduction in the effective maximum rate of oxidative ATP synthesis (expressed per volume of muscle). Also, recovery was faster in the young control subjects than in our earlier studies of older healthy control subjects. 5. The high phosphate concentration in resting muscle and the abnormalities found in exercise and recovery are consistent with a decrease in oxidative ATP synthesis due to reduced oxygen delivery by the blood in chronic hypoxaemia. The correlation between cytosolic pH and haemoglobin concentration remains to be explained.
Adolescent↗
Imaging of ear deformities in Treacher Collins syndrome.
Conductive deafness is a common feature of the Treacher Collins syndrome. The bilateral, essentially symmetrical hypoplastic deformities of middle and external ears, are characteristic. Improved imaging of the deformities using high resolution computed tomography (HRCT) has accompanied a present reluctance to explore surgically these middle ears because of poor results and the increasing success of bone anchored hearing aids. We describe the results of HRCT in 13 patients with Treacher Collins syndrome. An unpneumatized mastoid and a greatly reduced attico-antral region are almost constant findings, but a proportion of patients have a patent external auditory meatus, and, only in these is exploratory surgery feasible. Correction of ossicular deformities may be possible. Patients with atresia of the external auditory meatus are not suitable for exploration and need bone anchored hearing aids. Imaging for these children should be limited with regard to radiation dose and sedation.
Adolescent↗
No evidence of mitochondrial abnormality in skeletal muscle of patients with iron-deficient anaemia.
OBJECTIVES: Patients with iron deficiency anaemia complain of decreased exercise capacity. We asked whether this is due to defective oxidative ATP synthesis in skeletal muscle as a consequence of reduced blood oxygen content and/or intrinsic mitochondrial abnormalities. DESIGN: We used 31P magnetic resonance spectroscopy to examine skeletal muscle bioenergetics in iron-deficient patients and in age- and sex-matched controls. SETTING: The patients were recruited from the primary care population. SUBJECTS: We studied seven symptomatic female iron-deficient patients (aged 32-70 years) with haemoglobin (Hb) concentration, [Hb], 8.0 g dl-1. Six had menorrhagia, the cause in the seventh patient remained undiagnosed. Results were compared with those of 8 healthy female controls (aged 25-48 years) with mean [Hb] 13.7 g dl-1. RESULTS: The right calf muscle was by studied 31P magnetic resonance spectroscopy in a 1.9 T super-conducting magnet. We measured the intracellular concentrations of phosphocreatine (PCr), inorganic phosphate (Pi), adenosine triphosphate (ATP) and the intracellular pH at rest, during plantar flexion exercise and during recovery from exercise. Exercise duration was reduced in the patients, yet end-exercise PCr/(PCr+Pi) was higher and adenosine diphosphate (ADP) lower than in controls. After exercise, initial PCr recovery was slowed but this was probably because of the lower cytosolic ADP concentration. CONCLUSIONS: Mitochondrial ATP synthesis was not limited by oxygen supply or an intrinsic mitochondrial defect. Therefore, the reduced exercise capacity seen in iron deficiency could be due to central causes and not to skeletal muscle metabolic abnormalities.
Adenosine Triphosphate↗
Neurodevelopmental disability--a sibling-control study.
The antecedents of a population of children with neurodevelopmental disability were examined in a sibling-control study: siblings were used to control for the effect of the family environment on development. Of 294 children with neurodevelopmental disability, 228 who had normally developing siblings were matched with the sibling of nearest ordinal position in the family. There was a significantly higher incidence of prenatal complications among disabled children than among their matched siblings, even after correction for gestational age at birth. Prenatal complications and delayed onset of regular respiration were predictive of disability. These data confirm the authors' observation that the relation between prenatal complications and neurodevelopmental disability is independent of social class and gestational age at birth.
Anesthesia, Obstetrical↗
The assessment of clinical competence in obstetrics and gynaecology in two medical schools by an objective structured clinical examination.
OBJECTIVE: To compare and assess clinical competence among final year students in two British medical schools using a standardised objective structured clinical examination (OSCE) in obstetrics and gynaecology. DESIGN: A comparative study of an OSCE with stations designed to test student abilities in history-taking, physical examination, interpretation of data or results, interpersonal skills, practical procedures, as well as factual knowledge. SUBJECTS: Two groups of final year medical students from two British medical schools. METHODS: An OSCE of 26 stations. RESULTS: The standardised OSCE was simple to organise and conduct once the content had been decided. Analysis of the results revealed significant differences in mean marks between the two sets of students in six stations, and in eight stations the mean score was less than five for one or other sets of students. The reasons for the differences between the medical schools and the poor performance of the students at some stations were investigated and possible causative factors identified. CONCLUSIONS: We have shown that an OSCE is suitable for testing clinical competence of students within and across medical schools, is able to highlight differences in standards between institutions, and can identify areas where teaching methods and/or course content are deficient.
Attitude↗
Skeletal muscle bioenergetics in the chronic fatigue syndrome.
Skeletal muscle bioenergetics and control of intracellular pH have been investigated in 46 patients with chronic fatigue syndrome by phosphorus magnetic resonance spectroscopy. The results have been compared with those from healthy controls and from a group of patients with mitochondrial cytopathies affecting skeletal muscle. No consistent abnormalities of glycolysis, mitochondrial metabolism or pH regulation were identified in the group when taken as a whole, although in 12 of the 46 patients the relationship between pH and phosphocreatine utilisation during exercise fell outside the normal range. Of these, 6 patients showed increased acidification relative to phosphocreatine depletion while 6 showed reduced acidification. These findings do not support the hypothesis that any specific metabolic abnormality underlies fatigue in this syndrome although abnormalities may be present in a minority of patients.
Adolescent↗
Skeletal muscle metabolism during exercise and recovery in patients with respiratory failure.
BACKGROUND: Patients with respiratory failure have early fatiguability which may be due to limitation of oxygen supply for oxidative (mitochondrial) ATP synthesis. Skeletal muscle in exercise and recovery was studied to examine the effect of chronic hypoxia on mitochondrial activity in vivo. METHODS: The skeletal muscle of five patients with respiratory failure (PaO2 < 9 kPa) was studied by phosphorus-31 magnetic resonance spectroscopy and compared with 10 age and sex matched controls. Patients lay in a 1.9 Tesla superconducting magnet with the gastrocnemius muscle overlying a six cm surface coil. Spectra were acquired at rest, during plantar flexion exercise, and during recovery from exercise. Relative concentrations of inorganic phosphate (Pi), phosphocreatine (PCr) and ATP were measured from peak areas, and pH and free ADP concentration were calculated. For the start of exercise, the rates of PCr depletion and estimated lactic acid production were calculated. For the post exercise recovery period, the initial rate of PCr recovery (a quantitative measure of mitochondrial ATP synthesis), the apparent Vmax for mitochondrial ATP synthesis (calculated from initial PCr resynthesis and the end exercise ADP concentration which drives this process), and the recovery half times of PCr, Pi, and ADP (also measures of mitochondrial function) were determined. RESULTS: Considerably greater and faster PCr depletion and intracellular acidosis were found during exercise. This is consistent with limitation of oxygen supply to the muscle and might explain the early fatiguability of these patients. There was no abnormality in recovery from exercise, however, suggesting that mitochondria function normally after exercise. CONCLUSIONS: These results are consistent with one or more of the following: (a) decreased level of activity of these patients; (b) changes in the fibre type of the muscle; (c) decreased oxygen supply to the muscle during exercise but not during recovery. They are not consistent with an intrinsic defect of mitochondrial ATP synthesis in skeletal muscle in respiratory failure.
Adenosine Triphosphate↗
Protein turnover in the human fetus studied at term using stable isotope tracer amino acids.
Before elective cesarean delivery (4 h), we infused L-[1-13C]leucine and L-[15N]phenylalanine into the maternal circulation and measured enrichment and concentration of amino acids and carbon dioxide in cord blood of six normal human fetuses at delivery. There were net fetal uptakes of leucine (2.22 +/- 0.29 mumol.kg-1.min-1) and phenylalanine (0.80 +/- 0.11 mumol.kg-1.min-1) with net outputs of CO2 (6.11 +/- 1.12 ml.kg-1.min-1) and the transamination product of leucine, alpha-ketoisocaproate (1.04 +/- 0.32 mumol.kg-1.min-1). Fetal amino acid oxidation accounted for a substantial proportion of the flux from the mother (leucine, 0.36 +/- 0.09 mumol.kg-1.min-1 and phenylalanine, 0.18 +/- 0.04 mumol.kg-1.min-1). Fetal whole body accretion of leucine carbon (0.82 +/- 0.21 mumol.kg-1.min-1) was 69% of the umbilical uptake, and that of phenylalanine (0.62 +/- 0.08 mumol.kg-1.min-1) was 78%. Fetal whole body protein synthesis was approximately 13 g.kg-1.day-1, i.e., much faster than in adults but similar to that in the newborn. Net protein accretion was 2-4 g.kg-1.day-1. The placental supply of leucine and phenylalanine exceeds the fetal demand for protein synthesis by only a small amount, suggesting that the safety margin of placental transfer may be small for these amino acids. The results suggest that the method could be applied safely to studies of fetal growth retardation.
Adult↗