First trimester fetal sexing in pregnancy at risk for Duchenne muscular dystrophy.
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Biomedical subjects
Publications and source records attributed to H Williams.
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We report here a case of polymyositis and toxoplasmosis, and review the previous examples of this association. We suggest that in most cases this relationship is due to reactivation of latent infection in an immunocompromised host. Gross immunological aberrations underline the pathogenesis of polymyositis and these predispose the patient to the development of toxoplasmosis. Anti-protozoal therapy is necessary and produces some clinical benefit, but it does not cure the polymyositis.
An investigation into the incidence of hydatid disease was carried out in the Hebridean islands of Lewis and Skye. The results showed that 20% of the sheep were infected and 10% of the dogs harboured Echinococcus granulosus. Sporadic human cases continue to occur but using serological tests we were unable to show evidence of subclinical infection in the population sampled.
A recently developed enzyme-linked immunosorbent assay for detection of immunoglobulin M (IgM) class antibodies to Toxoplasma gondii was evaluated with respect to specificity and sensitivity. By using an antibody capture principle and F(ab')2 conjugates, interference of rheumatoid factors was absent. No cross-reactions with anti-toxoplasma IgG occurred, and no interference with antinuclear antibodies was found. A large-scale study with about 1,500 clinical specimens revealed a 100% specificity. By testing 79 sera from patients with acute-phase acquired toxoplasmosis, sensitivity was found to be 97%. In routine clinical practice, the IgM-enzyme-linked immunosorbent assay proved to be a more sensitive tool for diagnosis than the immunofluorescent-antibody test. The course of IgM-enzyme-linked immunosorbent assay antibodies in acute patients was studied; IgM reached peak levels within 1 month after onset of illness, and could be demonstrated up to an average of 8 months after onset.
The effect of glucose polymer (GP) ingestion upon endurance performance during walking exercise at 45% VO2max was examined. Also, performance on a battery of psychomotor tests was assessed to determine if exhaustion from endurance exercise was related to central nervous system dysfunction. Ten trained male subjects ingested approximately 120 g of GP in four equally-divided dosages 60, 90, 120, and 150 min following the start of exercise. This treatment significantly increased time to exhaustion by 11.5% as compared to the control (C) group (GP=299.0 +/- 9.8 min; C=268.3 +/- 11.8 min). No difference in VO2 (1 X min-1) or perceived exertion was noted between treatments. As a result of the GP feedings the rate of carbohydrate utilization during the GP trial was 0.53 g X min-1 greater than during the C trial. However, during the GP trial plasma glucose did not fall below the pre-exercise level and was significantly higher than the C plasma glucose concentration at exhaustion. No differences in psychomotor performance between treatments or between rested and exhausted states for either the C or GP treatments were noted. These data suggest that exhaustion was not a result of hypoglycemia or central nervous system dysfunction and that glucose polymer supplements may enhance endurance capacity.
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We have isolated cDNA clones encoding human apolipoprotein (apo) A-I. Twenty putative apo A-I cDNA clones were selected by screening 10,000 clones of an adult human liver cDNA library with an oligonucleotide probe. The probe was a mixture of synthetic 14-base-long DNA oligomers constructed to correspond to the codons for apo A-I amino acids 105-109. Four of these clones were examined further and showed 600- to 800-base-pair (bp) inserts. Preliminary restriction mapping and partial DNA sequence analysis indicated that the shorter inserts were a subset of the longer DNA inserts. DNA sequence analysis of the clone with an insert of approximately equal to 600 bp, designated pAI-113, revealed that it contained a DNA sequence corresponding to apo A-I amino acids 94-243. The DNA base sequence of this clone also contained a standard termination codon, polyadenylylation signal, and poly(A) tail. Partial DNA sequence of a second clone that contained an 800-bp insert, designated pAI-107, showed that it corresponded to apo A-I amino acids 18-243 and also included the 3' untranslated region. Isolation of these cDNA clones will facilitate molecular analyses of apolipoproteins in normal and disease states.
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A strain of the cattle piroplasm Babesia divergens isolated from a fatal human infection was propagated in the Mongolian gerbil through 150 semi-continuous intraperitoneal passages. The infection was normally fatal; death, accompanied by profuse haemoglobinuria and debilitation, occurred as early as 44 h after intraperitoneal inoculation of heavily parasitized blood with precipitous drops in red blood cell and platelet counts. The average maximum parasitaemia achieved increased on continuous passage reaching 80% by the 150th stage. Twenty-four hours after infection erythrophagocytosis and splenic congestion were apparent by light and electron-microscopical examination and by 48 h hepatic necrosis, renal tubular damage with haemoglobin cast accumulation and ischaemic necrosis of ileal mucosa had developed. Gerbils were highly susceptible to small numbers of parasites when the inoculum was either fresh parasitized blood in high dilution or erythrocytes concentrated from animals showing minimal parasitaemia. Animals inoculated with parasites preserved in dimethyl sulphoxide at low temperatures usually developed fatal infections. However, occasionally animals suffered at most a low grade parasitaemia subsequent to recovery with parasite elimination. These animals were immune to further challenge, and no chronic infections developed. A field strain of B. divergens isolated locally from a case of bovine redwater behaved similarly to the human strain on continuous passage in gerbils.
Hemodynamic and humoral effects of lofexidine were assessed in 11 patients with essential hypertension after a total of 1.5 mg were given orally over 24 hr. Heart rate (bpm) slowed (-12 +/- 6 [SEM], p less than 0.05) and cardiac output (liters per minute) was reduced (-0.78 +/-0.18, p less than 0.01) irrespective of blood pressure response; the latter was related to changes in systemic resistance (TPR) (r = 0.72, p less than 0.01). Cardiac performance judged from ejection fraction (0.61 +/- 0.03 to 0.59 +/- 0.03, NS) and mean transit time (8.73 +/- 0.53 sec to 9.20 +/- 0.35, NS) were not altered. Plasma volume was expanded more than 10% in two patients but not changed in the others. Supine plasma catecholamines determined in five patients were reduced in all but one with no correlation to changes in either TPR or diastolic blood pressure. On the other hand, there was an increase in plasma catecholamines during head-up tilt in four of five patients, indicating normal catecholamines release. Orthostatic hypotension occurred de novo in three patients; two of them had simultaneous slowing of heart rate (vasovagal attack). Results suggested that reduction of blood pressure by lofexidine depended on lack of increase in TPR in response to reduction of cardiac output; the hemodynamic pattern of this centrally acting adrenergic blocker closely resembled that reported for beta blockers.
Rats were fed on diets containing methyl mercury dicyandiamide (MMD) at concentrations of 1.5, 7.5 or 75 ppm, and observations made of their social and exploratory behaviour and of gross neurotoxicity (ataxia). Mercury concentration in the blood was monitored. MMD at 75 ppm (50 ppm Hg) for 24 days caused ataxia with a sudden onset at 21-27 days. Social behaviour was reduced at 16-17 days. In two experiments at 7.5 ppm MMD, activity was increased in observations of social behaviour after 2 to 17 days, and treated rats found water in an unfamiliar cage sooner than controls. No difference from controls was apparent from then until increased activity re-appeared after 9 mon of the diet (exp. 1) or after 7 days recovery from 31 or 45 days diet (exp. 2). Ataxia was not observed after 7.5 ppm MMD for up to 47 weeks or in 14 weeks recovery. No consistent effect was observed at 1.5 ppm MMD for 31-45 days. MMD, therefore, had a behavioural effect in rats, independent of gross neurotoxicity; its details were consistent with a hyperresponsiveness to stimuli. Tolerance occurred to this effect at a time when blood-mercury concentration was still rising, but the tolerance appeared to be subject to overload.
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