[Ambulatory nursing conference. 9. At Life Planning Center Clinic. Communication with patients via telephone: conversations to solve patients' problems].
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Biomedical subjects
Publications and source records attributed to N Matsui.
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Forty-five patients with uncomplicated rheumatoid arthritis and 45 control individuals were subjected to immunochemical investigation of the urinary excretion of renal tubular basement membrane antigen (TBM), renal tubular epithelial antigen (RTE), and beta-2-microglobulin. Tubular proteinuria occurred significantly more frequently in patients treated with gold salts than in those not treated (P less than 0.05). Large amounts of RTE and TBM were detected only in the urine of patients who received gold salt therapy. However, the amounts of these proteins in urine did no correlate with the total dose of gold. These results indicate that renal tubular damage frequently occurs in patients with rheumatoid arthritis who are treated with gold salts; the tests outlined are useful in detecting renal tubular disorders developing during gold salt therapy and have certain advantages over routine urinalysis.
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Thymocytotoxic autoantibodies were demonstrated in sera of C3H/HeJms, C57BL/6J, and ddY mice infected with 50 cercariae of Schistosoma japonicum, using C57BL/6J thymocytes as target cells in the trypan blue dye exclusion test. Kinetic study revealed that thymocytotoxic activity began to increase at week 6 of infection, reached a maximum at 8 weeks, and thereafter decreased gradually. Thymocytotoxic antibodies had an optimal reactivity at 4 degrees C and were sensitive to 2-mercaptoethanol treatment, suggesting that they were immunoglobulin M in nature. The cytotoxicity was completely abolished by absorption with C57BL/6J thymocytes but not with S. japonicum parasites or eggs. The antigen reacting with thymocytotoxic antibodies was found in the thymus, brain, spleen, and, to a lesser extent, kidney and liver. In parallel with the appearance of thymocytotoxic antibodies, the increase of background plaque-forming cells to trinitrophenyl, polyvinyl pyrrolidone, and sheep erythrocytes in the spleen of S. japonicum-infected mice suggested that te induction of thymocytotoxic antibodies may be the consequence of polyclonal B-lymphocyte stimulation by the infection.
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Prostaglandin D2 (PGD2), a potent antiplatelet agent, was evaluated as an antithrombotic agent for haemodialysis in comparison with prostaglandin E1 (PGE1) and prostaglandin I2 (PGI2). When antiplatelet action was evaluated, taking the degree of associated hypotension into consideration, PGD2 was found to be superior to PGE1 and PGI2 as the latter two had the negative effect of inducing hypotension, while PGD2 had a less hypotensive effect. The suppression of the platelet function by PGD2 was observed to have only a slight influence on platelet function in systemic blood.
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To elucidate the contributory role of heparin to abnormal lipid metabolism in patients on regular haemodialysis (RDT), six week haemodialysis without heparin was performed using gabexate mesilate in combination with low dose aspirin. Total cholesterol and beta-lipoprotein were significantly increased at the fourth week after the start of the study. No significant changes were observed in high density lipoprotein cholesterol, phospholipid, triglyceride, lipoprotein phenotype and post heparin lipolytic activity. Routine dose heparin in RDT might have a favourable effect on abnormal lipid metabolism by inducing post heparin lipolytic activity in circulating blood, not by reducing the lipid removing activity in peripheral tissues.