Arrhythmias during venous cannulation prior to pulmonary artery catheter insertion.
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Biomedical subjects
Publications and source records attributed to S Brauer.
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The results of treating 143 patients with trigeminal neuralgia with carbamazepine (CBZ) over a 16-year period have been reviewed. The drug was effective initially with few mild side effects in 99 patients (69%). Of these, 19 developed resistance later, i.e. between 2 months and 10 years after commencing treatment, and required alternative measures. Of the remaining 80 (56%), the drug was effective in 49 for 1-4 years and in 31 for 5-16 years. Thirty-six patients (25%) failed to respond to CBZ initially and required alternative measures, as did 8 (6%) who were intolerant of the drug. One patient developed CBZ-induced water intoxication with hyponatraemia. Subsequently hyponatraemia was excluded in 17 patients who had been taking CBZ for between 4 months and 7 years. This study has thus confirmed the efficacy of CBZ in the treatment of trigeminal neuralgia and shown that it may continue to be effective for many years.
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Immunologic escape includes the loss of Fas-receptor and the gain of Fas-ligand expression. Normal adrenal glands express the Fas-receptor and MHC class II molecules in inner cortical zones. A distinctive feature of adrenocortical tumors is the loss of MHC class II expression. Here we demonstrate loss of Fas and gain of Fas-ligand expression in the adrenocortical carcinoma cell line NCI-H295 by immunohistochemistry and RT-PCR. In a co-culture system of tumor cells and HLA-matched leukocytes, CD 8-positive or CD 4-positive lymphocytes, we examined the immunologic escape and the ability to induce apoptosis in the immune cells. The direct co-culture with either leukocytes, CD 8-positive or CD 4-positive lymphocytes reduced spontaneous apoptosis in immune cells from 49.9% to 13.0%, 8.6% and 15.3%, respectively, as determined by FACS analysis of Annexin V binding and LDH release in the medium. In co-culture, cortisol secretion increased up to 200%. Cellular communication does not induce apoptosis in immune cells, but promotes their survival. This may be due to partial HLA class I mismatches contributing to immunologic activity. The viability of the tumor cells was not affected, and these cells were stimulated to secrete cortisol. In summary, immune escape of adrenocortical carcinomas may occur because of altered Fas/Fas-L system expression and loss of MHC class H expression.