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Biomedical subjects

J S Cameron

Publications and source records attributed to J S Cameron.

At least 307 records · Page 17Linked to original sources
PubMed1979

Liquid chromatographic demonstration of catecholamine release in fish heart.

High-pressure liquid chromatography (HPLC) was used to assay for catecholamines released into the heart of the goldfish (Carassius auratus L.) upon stimulation of vagal nerve fibers. Stimulation induced the release of norepinephrine, epinephrine and dopamine into the lumen of the perfused, isolated heart. The results suggest that heart activity in teleosts is directly modulated by functional adrenergic, cardioacceleratory nerve fibers.

Animals↗
PubMed1979

Complete deficiency of adenine phosphoribosyltransferase: a third case presenting as renal stones in a young child.

We report a third case of 2, 8-dihydroxyadenine stones in a child with a complete lack of the adenine salvage enzyme--adenine phosphoribosyltransferase (APRT). The propositus, a 20-month-old girl of consanguineous Arab parents, presented with multiple urinary tract infections and supposed 'uric acid' stones in the right renal pelvis and left ureter. Both parents and one brother were heterzygotes for the defect, in keeping with an autosomal recessive mode of inheritance. In contrast with the other purine salvage enzyme disorder of childhood with true uric acid stones (the Lesch-Nyhan syndrome), uric acid excretion was normal in all family members. As in our previous case, treatment with allopurinol, without alkali, has eliminated the urinary excretion of 2, 8-dihydroxyadenine: the stones were removed surgically. 2, 8-Dihydroxyadenine should be considered in any child thought to have uric acid stones and tests made to distinguish the two compounds.

Adenine↗
PubMed1979

An evaluation of the immunoperoxidase technique in renal biopsy diagnosis.

An evaluation of the use of horseradish peroxidase labelled antisera against IgG, IgM, IgA and C3 compared with corresponding antisera labelled with fluorescein isothiocyanate has been carried out on renal biopsy material from 200 patients with renal disease. A disparity between the two methods was observed in 10-19% of the readings according to the antigen being demonstrated. The majority of differences recorded would not have influenced the executive diagnosis. Where the immunological results could have influenced the executive diagnosis, 5 probable false results were obtained using innumofluorescence and 4 with immunoperoxidase. Immunoperoxidase has the advantage over immunofluorescence in that it provides a permanent preparation which can be reviewed months or years later. In addition it provides more accurate localization of the immune deposits since the section can be counterstained with Mayer's hemalum and viewed by conventional light microscopy. In view of these advantages we recommend that serious consideration should be given to using immunoperoxidase in place of immunofluorescence for the examination of renal biopsy material.

Biopsy↗
PubMed1979

The interaction of anti-glomerular basement membrane antibody deposition with immune elimination of bovine serum albumin in the rabbit.

We studied the interaction of two different forms of immune glomerular damage occurring simultaneously: anti-glomerular basement membrane (GBM) antibody fixation and immune elimination of bovine serum albumin (BSA). 125I-radiolabelled BSA anti-BSA immune complexes, formed in response to a single small intravenous dose (150 mg/kg) of 125I BSA, did not cause proteinuria in control animals within 15 days, despite evidence of immune elimination of the antigen. Similarly, a small dose of nephrotoxic globulin (NTG)(3.0 mg/kg) did not cause immediate proteinuria in controls. Test animals received the BSA injection followed by the NTG injection 5, 7 or 9 days later. In this way, antibody fixed to glomerular basement membrane antigens at various times after BSA anti-BSA complexes first appeared in the circulation. Animals were killed on day 15. Fifteen of the eighteen test animals developed moderate to severe clinical nephritis. The onset of the nephritis coincided with BSA elimination irrespective of when the NTG was given. Greatly increased amounts of nonlinear immunofluorescent deposits were demonstrated in the glomeruli of test animals. We concluded that there was a marked synergistic effect between two forms of immune glomerular damage (i.e. that mediated by anti-GBM antibody and immune complexes), which appeared to be due to the increased deposition of complex material in the presence of active fixation of anti-GBM antibody. The relevance of this finding to human glomerulonephritis is discussed.

Animals↗
PubMed1979

Immunosuppressive agents in the treatment of the nephrotic syndrome and glomerulonephritis in children.

There is good, controlled evidence which suggests that cyclophosphamide, and perhaps related drugs, have a definite role in the treatment of nephrotic children with the minimal change lesion. This role is one of secondary treatment, and the drugs should not be used as a first line of attack; they should be employed only when corticosteroid resistance or toxicity is a problem. In a few patients, azathioprine or 6-mercaptopurine may have a role in minimising corticosteroid toxicity, but the remission induced in relapsing children is no more durable than that after corticosteroids. Chlorambucil must be given in doses, and for periods long enough to run the risk of neoplasia, particularly leukaemia; there does not appear to be a place for its use in nephrotic children unless the duration of remission can be shown to be longer than that obtainable with cyclophosphamide. There is no evidence that any immunosuppressive agent has a place in the management of children with idiopathic glomerular disease showing structural alterations in the glomeruli. Children with systemic lupus erythematosus and nephritis may benefit from the addition of cytotoxic agents to their corticosteroid regime, although the indications for this are not clear, and controlled evidence is lacking.

Azathioprine↗
PubMed1979

Systemic lupus with nephritis: a long-term study.

Seventy-one patients with systemic lupus erythematosus and clinical evidence of nephritis were seen during a 15-year period, and followed for a mean of seven years. Survival was calculated to be 76 per cent at five years and 57 per cent at ten years from onset of clinical nephritis; and 80, 65, 55 and 55 per cent five, ten, fifteen and twenty years from onset of clinical lupus. Renal biopsies showed mild or focal lesions in 30 per cent of patients, membranous lesions in 14 per cent and diffuse proliferative lesions in 55 per cent. However, there was no difference in the long-term outcome of the different histological groups. Nineteen patients (27 per cent) died during follow up, eleven from renal failure, six from sepsis and two from cerebral lupus. Death in renal failure is now usually a late event in lupus, even in patients with clinical evidence of severe nephritis. The prognosis of even severe lupus nephritis is now better than formerly reported. Reducing the dose of corticosteroid drugs, by the use of cytotoxic drugs such as azathioprine may have diminished the mortality from cardiovascular complications. Side effects of treatment, however, remain an important cause of death and morbidity.

Adolescent↗
PubMed1978

Relapsing polychondritis with crescentic glomerulonephritis.

Relapsing polychondritis is rare and its cause is unknown. The tissues affected are those with a high glycosaminoglycan content, such as cartilage, the aorta, the sclera and cornea, and parts of the ear. Symptoms can usually be controlled with oral steroids, but when there is coexistent progressive crescentic glomerulonephritis quadruple chemotherapy may be used. Three cases of the clinical syndrome of relapsing polychondritis were studied in which rapidly progressive cresentic glomerulonephritis developed. In two the patients appeared to respond to aggressive treatment with immunosuppressive agents and anticoagulants. The multisystemic nature of the disease, the renal lesions, and the response to treatment all suggested that the condition might be related to periarteritis nodosa.

Adult↗