Deterioration in diabetic control during calcitonin therapy.
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Biomedical subjects
Publications and source records attributed to D W Thomas.
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Nalidixic acid may cause severe acidosis and we report a fatal case of lactic acidosis assocaited with nalidixic acid therapy. Studies in normal volunteers showed drug related impairment of lactate metabolism. We question whether the drug should be used in patients who may accumulate the drug or be predisposed to lactic acidosis.
The addition of amino acid supplements to peritoneal dialysis fluid has been studied in 8 patients with compromised renal function requiring peritoneal dialysis. By the addition of 10 ml of Vamin-glucose solution to each one litre of peritoneal dialysate, amino acid losses were curtailed, no significant alterations occurred in the plasma amino acid concentrations, there were no local complications and no infections were seen. This procedure is recommended as a safe, simple way of keeping a patient in positive amino acid balance during peritoneal dialysis.
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X-ray equipment, used for radiation therapy at low voltages, is frequently operated in small hospitals which do not have full-time physics staff. Most of the X-ray units involved are not fitted with dose-rate monitors which would allow continuous control dose so that the output must be checked at frequent intervals by the radiographer using a suitable instrument. The design criteria for such an instrument are discussed and its construction described in detail together with the tests and field trials carried out. The instrument is designed to measure dose rates from 2500 rad min-1 at 10 kV to 50 rad min-1 at 250 kV. It has been possible by use of the instrument to determine the 'normal' behaviour of each X-ray unit and to establish criteria by which 'abnormal' behaviour can be determined.
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Nonimmune (2 x 13)F1 guinea pig T lymphocytes initially stimulated with trinitrophenyl- (TNP) modified macrophages from one parental strain and then treated with bromodeoxyuridrine (BUdR) and light are unable to be primed subsequently with TNP-modified macrophages of the same parental strain. In contrast, these BUdR and light treated F1 T cells can be primed with TNP-modified macrophages of the other parental strain. These results demonstrate that in a nonimmune F1 animal two T cell subpopulations exist before priming that are genetically predisposed to respond to antigen associated with macrophages derived from one or the other parent.
In the present study we examined the expression of I-region-associated (Ia) antigens by guinea pig T lymphocytes stimulated in vitro with antigen-pulsed macrophages. Treatment of lymph node (LNL) or peritoneal exudate (PEL) T cells taken directly from immune animals with anti-Ia serum and complement (C) dramatically reduced their proliferative response to antigen-pulsed macrophages when determined on the 4th day of culture. In contrast, the response of immune T cells that had been selected by culture for a week with antigen-pulsed macrophages and restimulated in a second culture was not affected by anti-Ia and C treatment. This same result occurred with selected LNL or PEL that were initially treated before the selection culture with either normal serum or anti-Ia serum and C. LNL became resistant to anti-Ia serum and C treatment by 3 days of culture whereas antigen-specific PEL were still sensitive at that time. These results indicate that in an immune animal two antigen-specific T cell subpopulations are generated based on their sensitivity to anti-Ia serum and C treatment, but that only the resistant population is selected by in vitro culture. In addition, we demonstrated that the Ig-negative T cell population can only be activated by histocompatible antigen-pulsed macrophages.
In this communication the effects of glutaraldehyde treatment of trinitrophenyl-(TNP) modified macrophages on their ability to stimulate TNP-specific guinea pig T lymphocyte proliferation were studied. TNP-modified macrophages briefly treated with glutaraldehyde retained much of their ability to stimulate TNP-primed T cells. In contrast, similar treatment of allogeneic macrophages or soluble protein antigen-pulsed syngeneic macrophages completely eliminated their ability to stimulate a mixed leukocyte reaction or protein antigen-specific proliferation, respectively. TNP-modification did not appear to interfere with glutaraldehyde reactivity since macrophages treated with glutaraldehyde before or after TNP-modification stimulated equivalent T cell responses. However, glutaraldehyde treatment of TNP-modified macrophages that had been cultured overnight dramatically reduced their ability to stimulate TNP-specific T cells. Glutaraldehyde-treated TNP-modified macrophages also expressed the same genetic restrictions of T cell activation as untreated stimulators. Thus, T cells primed with syngeneic TNP-modified macrophages were restimulated only by glutaraldehyde-treated TNP-modified syngeneic, but not by allogeneic, macrophages. These results are discussed with respect to the nature of the TNP-specific immunogen recognized by T cells.