An orthodontic-prosthetic solution to complex malocclusions.
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Biomedical subjects
Publications and source records attributed to L M Smart.
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Human blood leucocytes were tested for their capacity to bind histamine coupled as a rabbit serum albumin conjugate (H-RSA) to formalized ox red cells. The percentage of rosette-forming target cells was directly related to the concentration of erythrocyte-bound H-RSA. Under optimal experimental conditions the average number of rosettes was 52% for monocytes, 3 for lymphocytes, 25% for neutrophils and 59% for eosinophils. Free histamine partially inhibited rosette formation by blood monocytes in a dose-dependent fashion from 10-3 to 10-5 mol/l, and complete inhibition was achieved by the H-RSA conjugate. In contrast, three amines chemically related to histamine, L-histidine, imidazoleacetic acid and N-acetylhistamine, had no inhibitory effect. The histamine H1 antagonists, mepyramine and chlorpheniramine, and the H1 receptor agonist, 2-(2-aminoethyl)-thiazole, all inhibited rosette formation by blood monocytes in a dose-dependent fashion. However, the H2 receptor antagonists, burimamide and metiamide, and the H2 receptor agonists, Dimaprit and 4-methyl-histamine, were inactive. There was no statistical difference in the percentage of histamine rosettes for monocytes. lymphocytes, neutrophils or eosinophils between atopic and non-atopic individuals.
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The toxicity of cyclosporin A (CsA) formulated in either olive oil (OO) or fish muscle oil (FO) was investigated in groups of normal Sprague-Dawley rats or in animals which had undergone laparotomy or unilateral nephrectomy. CsA (25 mg/kg/day for 14 days) was administered by gavage from the time of operation, and indices of renal and hepatic function were determined at regular intervals. Urinary thromboxane B2 (TxB2) excretion and whole blood CsA concentrations were determined on day 14, when renal histology was also examined. Compared to CsA/OO treatment, and observed only in normal animals, body weight was significantly increased following administration of CsA/FO, to values similar to those observed following treatment with FO alone. Although there was evidence of renal dysfunction in all CsA-treated animals, irrespective of drug vehicle, elevations in plasma urea and urinary N-acetyl-beta-D-glucosaminidase activity were significantly more pronounced in rats given CsA/OO compared with CsA/FO. Indeed, compared with pretreatment values, no significant changes in these parameters were observed in CsA/FO-treated nephrectomized animals. Whilst there were no great differences in plasma creatinine or creatinine clearance rates between CsA/OO- and CsA/FO-treated groups, animals given CsA/FO showed less evidence of renal structural change as assessed by proximal tubular cell vacuolation, basophilia and microcalcification. The extent of hepatic impairment was also significantly less pronounced when FO was used as drug vehicle. Groups of CsA/FO-treated animals also demonstrated significantly lower whole blood CsA levels compared with CsA/OO groups; moreover, TxB2 excretion was significantly lower in the former group.(ABSTRACT TRUNCATED AT 250 WORDS)