The immuno‐reactivity of C57BL mouse spleen cells previously sensitized in vitro against syngeneic fibroblasts or syngeneic 3LL Lewis tumor cells was investigated. The sensitized spleen cells were assayed in vitro to test their cytotoxicity against the 3LL tumor cells. In addition, spleen cells autosensitized against syngeneic fibroblasts were mixed with 3LL tumor cells and injected into syngeneic recipient mice in order to ascertain their influence on tumor growth. The in vitro assay indicated that lymphoid cells specifically sensitized against either fibroblasts or tumor cells were equally cytotoxic against the 3LL target cells. On the other hand, in the in vivo experiments lymphoid cells sensitized against syngeneic fibroblasts promoted the growth of the 3LL tumor. An attempt to explain the underlying mechanisms involved in the paradoxical behavior of autosensitized lymphocytes is reported herein.
The effect of nifedipine, 10 mg po q.i.d. for 2 weeks, was studied in a randomized, double-blind, crossover trial in nine patients with asthma receiving theophylline. Nifedipine did not significantly affect the mean (+/- SD) morning peak expiratory flow rate (PEFR; 336 +/- 130 L/min for drug vs. 349 +/- 92 L/min for placebo), evening PEFR (393 +/- 69 L/min for drug vs. 367 +/- 66 L/min for placebo), symptom score (27.4% +/- 22.9% for drug vs. 33.8% +/- 26.4% for placebo), or the number of albuterol inhalations per day (5.8 +/- 3.5 for drug vs. 6.2 +/- 4.1 for placebo). Furthermore, there was no change in PEFR 30, 60, or 120 minutes after nifedipine dosing. Nifedipine did not significantly affect the steady-state serum theophylline trough levels (9.1 +/- 2.2 mg/ml for drug vs. 10.2 +/- 1.9 micrograms/ml for placebo) or the theophylline pharmacokinetic parameters, such as the elimination t1/2, peak serum concentration, time to peak, and AUC(0-24). We conclude that nifedipine has little, if any, effect on the clinical status, PEFR, or theophylline serum levels in patients with asthma who receive theophylline.
We tested the clinical and immunoregulatory effects of peritoneal dialysis and hemodialysis on a patient with familial Mediterranean fever (FMF), amyloidosis, and chronic renal failure. His frequency of FMF attacks during maintenance hemodialysis (no attacks in 21 months) was significantly less than during conservative medical therapy (10 attacks in 14 months, P < 0.00002) or during intermittent peritoneal dialysis (3 attacks in 4 months, P < 0.004). His mean (kSE) percentage suppressor cell function was significantly (P
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