Maprotiline effects in children with enuresis and behavioural disorders.
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Biomedical subjects
Publications and source records attributed to S Lawrence.
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The splenic component of mononuclear phagocytic cell function was investigated in rabbits using as a marker the clearance of N-ethylmaleimide-treated, technetium-labelled autologous erythrocytes. In 66 clearances performed in 23 normal rabbits, the clearance T1/2 was found to be between 5 and 16 min, the value for each rabbit remaining relatively constant. Clearance was proportional to incubation time or the dose of N-ethylmaleimide used. Clearance was delayed following injection of 20 to 65 mg of preformed complexes of BSA-anti-BSA made in 10-fold antigen excess. The degree and duration of this blockade was related to the dose of the complexes up to a critical value of 20 mg (antibody content after which no further decrease in clearance occurred although the duration of the blockade was longer at higher doses. Ultracentrifugation studies showed that these complexes were about 14S in size and sequential studies revealed that they were slowly cleared from the circulation. The experiments indicate that studies of splenic function may be of value in assessing immune complex disease, since circulating immune complexes of these characteristics are poorly detected by current methodology.
Thirty of the 39 patients treated at the Blacktown Dialysis Centre, the first "satellite" dialysis centre in the greater metropolitan Sydney, had been referred from four Sydney renal units for long-term dialysis therapy. The move save approximately 150 kilometres in travelling and eight hours time each week for each of these patients. The cost of running the unit was approximately $10,000 per patient per year in the first year--no greater than that of home dialysis, and less than that of dialysis in a teaching hospital. The advantages of establishing satellite dialysis centre, the method of operation, and the results of the first year of operation of the Blacktown Dialysis Centre are described.
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The complement system was investigated in 34 patients with infectious mononucleosis. Three had specific complications: one haemolytic anaemia, one severe arthralgia/myalgia and one proliferative glomerulonephritis. Complement changes consistent with classical pathway consumption were seen in ten of the uncomplicated group and the patients with haemolytic anaemia and arthralgia/myalgia. The patient with glomerulonephritis showed evidence of alternative pathway utilisation including C3 splitting activity and the deposition of properdin on renal biopsy. The complement findings suggest that circulating immune complexes are common in such patients and are likely to play a role in the pathogenesis of the complications. It is proposed that both complement pathways may be required for the effective clearance of viral material from the circulation.
Serial measurements of complement components were performed in fifty-nine patients with acute, uncomplicated hepatitis and twelve with alcoholic cirrhosis. Thirty-one of the former group had detectable hepatitis B antigen. Abnormal complement profiles were observed in nine patients with hepatitis B and seven with antigen-negative hepatitis. Low levels of C4, C3 and factor B were common in the subjects with cirrhosis and confined to those cases with severe reduction in serum albumin and/or prothrombin index. By contrast, the complement changes in the patients with hepatitis occurred without significant alteration in these parameters; certain subjects also had reduction in C1q and C5 and a significant number had C3d detectable in fresh plasma. The pattern of abnormality suggests predominant involvement of the classical pathway and it is concluded that this results, at least in part, from an immune process evident only in the early clinical phase of hepatitis. Such gross changes in complement are likely to reflect immune-complex activity and it is proposed that these complexes may be important in the clearance of virus material. The data supports a previous suggestion that recovery from acute hepatitis is primarily dependent on host immune competence rather than viral cytotoxicity or generation of immune complexes.
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A previous study demonstrated suppression of erythropoietin production in patients treated with long-term theophylline. This effect could exacerbate anemia of prematurity in neonates receiving this drug for apnea of prematurity. In this pilot project we evaluated the effect of short-term theophylline administration on serum erythropoietin in healthy adults. Six subjects were given a bolus followed by a continuous infusion of theophylline targeted to achieve a serum level of at least 10 micrograms/ml, followed by oral theophylline for 36 hours. Serum erythropoietin and theophylline levels were measured before, during, and after drug infusion. Complete hemograms were performed before and after completion of the infusion. No significant changes in serum erythropoietin levels were seen at any time (F = 1.57, p = 0.12). Hematologic values also remained unaltered. We conclude that short-term administration of theophylline is unlikely to have any effect on serum erythropoietin levels in healthy adults.
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Recent studies have suggested that there are three sites at which VLDL secretion by the liver may be controlled: (i) Newly synthesised apo-B either remains associated with the RER membrane and is degraded by the ubiquitin/proteasome system, or is translocated into the lumen and incorporated into lipid poor VLDL precursors; (ii) the lumenal apo-B is either degraded or moves on, and (iii) acquires the remaining VLDL lipids in the SER/cis-Golgi. Newly synthesised apo-B, at the cytosolic side of the RER, is stabilised and protected from degradation by the chaperone protein, hsp-70. Triacylglycerol, cholesterol ester and phospholipids have all been implicated in the translocation of apo-B and microsomal triglyceride protein plays a major role. If translocation does not occur then the apo-B is degraded. Dietary fish-oils, but not sunflower oil, inhibit movement of apo-B containing precursors from the RER and their assembly with lipids and target lumenal apo-B to degradation. This effect is reversed by inhibition of lumenal proteolysis, but not by inhibition of cytosolic proteolysis. Therefore lumenal degradation of apo-B and secretion appear to be in balance, so that if assembly of VLDL precursors is slowed, then degradation becomes predominant. If however, degradation is inhibited then VLDL assembly can proceed. These observations suggest that movement of VLDL precursors from the RER lumen to the second stage of assembly may be a further regulated step.