SummaryIn 781 female college students, there were 41 cases of iron deficiency anemia, 209 of latent iron deficiency, 3 of other anemias, and 528 normal cases. Fifty-four volunteers recruited from the iron deficiency anemia and severe latent iron deficiency groups were randomly divided into 4 study groups. Groups I and III received 500 mg of vitamin C daily, and groups II and IV received ferric ammonium citrate (FeAC; equiva lent to 6 mg iron) in addition to vitamin C for 9 weeks. Groups I and II were loaded by aerobic exercise at 50% V02 max. Significant differences between groups were noted in serum ferritin (SF) in III/IV, hematocrit (Ht) in II/III and III/IV, and reticulocytes (RET) in I/II, I/IV, and III/IV. Hemoglobin (Hb) and other iron-related blood indices tended to nor malize in groups II and IV when compared with the pre-values. VO2 max was elevated in groups I and II regardless of iron treatment, but was augmented more in group II than group I.
Low concentrations of exogenously added recombinant interleukin 2 (rIL-2) were able to augment OK-432-induced natural killer (NK) cell activity. This kind of augmenting effect depended on the dose of rIL-2 and manifested itself only in PBMC stimulated with OK-432 (OK-MC) followed by rIL-2; augmentation did not happen in the reverse order. The existence of CD16+ /CD25+ (IL-2 receptor positive; IL-2R+) and CD57-VCD25+ double positive cells which possess NK cell surface markers in OK-MC markedly increased in a long-term culture (12 days). A strong positive correlation was observed between the IL-2-dependent augmentation of NK activity and the quantitative changes in cell populations that possessed NK cell phenotypes. Treatment of the day-12-OK-MC with monoclonal anti-CD56 antibody plus complement could almost completely abrogate the augmented NK cytotoxicity. Furthermore, this augmenting effect was detectable within 4 hr after addition of rIL-2 at single cell level, suggesting that the effect did not require NK cell's DNA synthesis. Thus it was suggested that OK-432 could promote and upregulate the expression of IL-2 receptor (CD25) on CD56+ NK cell populations. Moreover, it was considered that the interaction of low concentration rIL-2 with IL-2 receptors on OK-432-activated NK cells could augment their lytic function.
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