Central scheduling: catalyst for change.
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Biomedical subjects
Publications and source records attributed to J Harvey.
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We report the results of our investigation using DNA markers, of the parental origin of 61 XXY males ascertained during cytogenetic studies of consecutive liveborn babies and compare our results with those obtained from a study of 50 XXY males ascertained through clinical referral or amniocentesis. In the former group 44% of newborn XXY males obtained the additional X chromosome from their father and 56% from their mother, while in the latter "referral" group the additional X chromosome was paternally derived in 54% and maternally derived in 46% of the cases. The precise maternal cell division at which nondisjunction occurred was determined in 39 cases of maternal origin. Twenty eight (72%) resulted from an error in the first meiotic division and 11 (28%) from an error in the second meiotic division. There was no evidence of an origin due to a postzygotic mitotic error. There was no significant difference in the parental age at birth between those patients who received the additional X from their father and those who received it from their mother. However, those patients who received the additional X chromosome as a result of a maternal meiotic I error had a higher maternal age than any other category, but the difference reached a level of formal significance only for the clinically referred patients.
A panel of monoclonal antibodies against major histocompatibility complex (MHC)- and monocyte/macrophage-associated antigens was used to compare human fetal and postnatal small intestinal macrophage subpopulations. Cryostat sections were stained using an indirect immunoperoxidase technique. Within the human fetal intestine from 12 weeks gestation, the antibody KiM8 identified a widespread population of type I accessory cells, which showed variable expression of HLA-DR. In contrast, the antibody 3.9 identified small clusters of HLA-DR- and HLA-DQ-positive lamina propria macrophages, presumably type II accessory cells. Comparison of fetal with postnatal small intestine revealed mainly quantitative changes, with an absolute increase in 3.9-, KiM8-, KiM6-, 10.1- and UCHMI-positive accessory cells in the postnatal intestine. The proportions of both UCHM1- and KiM6-positive cells relative to the KiM8-positive population was also increased postnatally. The villous population of 3.9- and KiM6-positive interdigitating type II macrophages characteristic of the postnatal lamina propria was largely absent from fetal small intestine. The monoclonal antibody 3.9 further reacted with the cytoplasm of ganglion cells and nerve fibres within the nerve plexuses of fetal and postnatal small intestine. The significance of this cross-reactivity remains unclear.
A retrospective study was undertaken to determine the incidence of secondary hemorrhage after traumatic hyphema in a medium-sized Canadian city. This was found to be 10%, which is similar to the incidence reported in other Canadian and northern European cities but much lower than that reported in some large American cities. The different racial mix of the sample populations is the most likely reason for these differences.
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Plasma and lipoprotein cholesterol and triglycerides, and plasma apolipoproteins AI, AII and B were compared in patients with chronic airflow limitation, and normal controls matched for body mass index. The controls were non-smokers, and free from respiratory disease. High-density lipoprotein (HDL) cholesterol concentration was significantly elevated in the patients, due mainly to a raised HDL2 cholesterol level. HDL triglyceride was significantly lower in the patients. All other lipids were not different from normal. Apolipoprotein AI levels were significantly raised in the patients but other apolipoproteins were unchanged. The changes found may account in part for the fact that patients with chronic airflow limitation have a lower incidence of atherosclerotic heart disease.
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The expression of the 220,000 MW (p220) glycoprotein component of the leucocyte common antigen (LCA) family by intestinal mucosal lymphocytes was studied using the CD45R monoclonal antibody WR16. In normal intestine, a proportion of CD3+ mucosal T cells were WR16+ and this population resided predominantly in the mid-villus and crypt region of lamina propria. In the inflammatory infiltrates of both coeliac disease and Crohn's disease the CD3+, WR16+ population was markedly reduced. The monoclonal antibody UCHL1 identifies the 180,000 MW member of the LCA family and is expressed on T cells and in macrophages. CD3+ lymphocytes expressing this marker were widespread in normal lamina propria and epithelium. In contrast with WR16, UCHL1+ cells remained at a high level in coeliac disease and Crohn's disease. Our results support the view that loss of the p220 molecule occurs upon T-cell activation in inflammation.
Eleven leukaemic patients and 43 potential unrelated marrow donors were typed serologically, tested in mixed lymphocyte reaction (MLR) and typed by restriction fragment length polymorphism (RFLP) analysis. RFLP typing data were compared with DR serology and MLR results. Eleven of the 54 individuals showed discrepancies between DR serology and RFLP DR assignment. RFLP DR/DQ mismatch always correlated with positive MLR, but RFLP identity was present in both MLR negative and MLR positive pairs. RFLP typing cannot reliably predict a negative MLR response, but we suggest that it should be used in the selection of unrelated marrow donors to exclude mismatched donors from testing in the MLR. This will facilitate donor searches by reducing the number of MLR performed.
A new method to reconstruct anterior lamellar pretarsal lid lesions is described. The cosmetic and functional results were excellent in all 12 patients. This method minimizes postoperative lid malposition.
Previous studies have suggested that the simple technique of minor salivary gland biopsy might be a useful method of diagnosing sarcoidosis. We have therefore investigated the success of this technique in 25 consecutive patients who were attending a chest clinic and in whom a diagnosis of sarcoid had been made. The histological appearances of the minor salivary glands were correlated with the degree of gallium uptake by the parotid glands after intravenous injection of gallium citrate. We also compared the histological appearances of the sarcoid patients with 40 patients suffering from a variety of mixed connective tissue disorders (systemic lupus erythematosis, systemic sclerosis, primary Sjogrens syndrome, rheumatoid arthritis and polymyositis). Five out of twenty-five (20%) of the sarcoid patients had classical non-caseating granulomata in their minor salivary glands, four of whom also had hilar lymphadenopathy and one had bone marrow involvement. All the patients with sarcoid histology in their minor salivary glands also had Gallium uptake in parotid tissue. None of the patients with mixed connective tissue disorders had granulomata in their minor salivary gland tissue although a continuum of changes were found, ranging from normal appearances through small foci of lymphocytic infiltrate to extensive inflammation and destruction of glandular tissue with fibrosis. Whilst minor salivary gland biopsy may be a simple and rapid method of diagnosing sarcoidosis it is most likely to be positive in patients with hilar lymphadenopathy.
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L-dopa 7 micrograms.kg-1.min-1 was given intravenously over 2 h to six healthy subjects, controlled by an infusion of saline on a separate occasion, with measurement of plasma renin activity (PRA), urinary sodium and potassium excretion, effective renal plasma flow (ERPF), glomerular filtration rate (GFR), blood pressure, and pulse rate. Mean PRA fell by 50% following L-dopa, which was significantly different from the slight rise which occurred after saline infusion. There was a significant increase in urinary sodium excretion and effective renal plasma flow on infusion of L-dopa. Mean diastolic blood pressure fell during L-dopa infusion, in contrast to the slight increase which occurred during the control study. These observations confirm the anticipated renal dopaminergic effects of L-dopa and also suggest a dopaminergic influence on renin release in man.