We hypothesized that 'quinine' taste sensitivity functions to regulate the intake of bitter-tasting, naturally occurring antimalarial substances of plant origin, and that this genetic trait has co-evolved with the G6PD locus. This hypothesis was tested by evaluating taste sensitivity to quinine sulphate and sodium chloride among 17 G6PD-deficient and 25 G6PD-normal African American subjects 14-40 years of age. There was no significant difference in mean 'quinine' taste sensitivity between the two groups, although there was a trend towards greater 'quinine' taste acuity among the G6PD-deficient subjects. A larger study sample would provide a fairer test of the hypothesis.
Seventy-one previously untreated patients with small cell lung cancer (SCLC) received a combination of VP-16, vincristine, doxorubicin (Adriamycin), and cyclophosphamide (EVAC) repeated every three weeks. Limited-disease (LD) patients and extensive-disease (ED) patients achieving a complete response (CR) or partial response (PR) after four to six cycles of EVAC received 4,000 rads over four weeks whole-brain radiotherapy (RT) and 5,000 rads over five weeks RT to the original pulmonary primary and mediastinum. ED patients with persisting disease outside the chest after six cycles of EVAC continued chemotherapy and did not receive RT. After RT was completed, EVAC was continued for a total treatment duration of 24 months. Of 65 patients evaluable for response 76% (25 of 33) of LD patients and 34% (11 of 32) of ED patients achieved a CR prior to RT; two additional ED patients achieved a CR after RT. Median survival for all 71 patients was 48 weeks (range, one to 207 weeks); median survival for 33 LD patients was 92 weeks and for 38 ED patients it was 36 weeks. Nine of 25 LD patients and 10 of 13 ED patients have relapsed from CR. The EVAC-RT protocol is promising in view of the high CR rate and long remission duration achieved, especially among patients with LD.
The in vitro spontaneous formation of sheep red blood cell (SRBC) (E) rosettes by peripheral blood lymphocytes is altered in vitro by the addition of micro-molar quantities of zinc chloride. Appropriate concentrations of zinc chloride cause marked enhancement of rosette formation, both in normal subjects and in cancer patients with low initial E rosette values. The effect is dependent upon zinc treatment of the lymphocyte and not the SRBC. Other zinc-induced effects on E rosettes include retardation of temperature-dependent spontaneous decay, increased mechanical stability due to enhanced of "capping." The formation of EAC rosettes is not altered by the presence of zinc.
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