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To assess the effects of decreased erythrocyte production on the levels of serum erythropoietin in children, we measured simultaneous hemoglobin concentrations and erythropoietin in 18 children with iron deficiency anemia, 17 children with transient erythroblastopenia of childhood (TEC), and 7 children with aplastic anemia. In all but two patients (one with TEC; one with aplastic anemia), erythropoietin was measured at diagnosis, before institution of specific therapy for the anemia. There was a statistically significant inverse linear correlation between log10 erythropoietin and hemoglobin values for all patient groups (r = 0.904 to 0.912; p less than 0.005). A comparison of the slopes of the regressions for each patient group by analysis of covariance revealed a significantly steeper slope for the iron deficiency group (-0.553) versus the TEC (-0.287) and aplastic anemia (-0.256) groups (p = 0.0001). The difference in erythropoietin levels appeared greatest in patients whose presenting hemoglobin level was greater than 5 gm/dl. Decline in serum erythropoietin levels was more precipitous in the less severely anemic patients with iron deficiency anemia than in the patients with TEC or aplastic anemia. These data reveal quantitative and qualitative differences in the relationship between serum erythropoietin and hemoglobin levels when children with severe iron deficiency anemia versus those with TEC or aplastic anemia are considered, even though all three conditions are characterized by hypoproliferation of erythrocytes.

Over the past 10–15 yr, improvements in perinatal and neonatal care and in the laboratory diagnosis and monitoring of coagulation disorders have lead to significant reductions in morbidity and mortality from bleeding and thrombosis in sick and low birth-weight infants. Recent advances in our understanding of the normal developmental changes that occur in the coagulation mechanism of the fetus and newborn now allow for more intelligent and rational approaches to the treatment of disordered coagulation and fibrinolysis. This review will focus on current knowledge of the normal changes that occur in the coagulation mechanism during late fetal development and early infancy. Subsequent discussion will deal with how developmental aspects of the coagulation mechanism impact upon morbidity and mortality from common neonatal diseases. The diagnosis and management of specific bleeding and thrombotic syndromes of neonates will also be discussed. Finally, a brief overview of the indications for use of plasma products in neonatal medicine will be presented.

Materials and Methods: The use of plant extracts to alleviate inflammatory diseases is centuries old and continues to this day, therefore we screened thirty-four methanolic plant extracts for inhibition of constitutive NF-uB activity by a NF-uB-luciferase reporter gene assay. There was strong inhibition of NF-uB activity by Nuphar lutea L. SM. (Nuphar), leaf and rhizome extracts. An active fraction containing a mixture of dimeric sesquiterpene thioalkaloids was purified by solvent extraction, pH adjustment silica gel chromatography and HPLC. Oneand twodimensional NMR spectroscopy indicated the presence of nupharidine, 6-hydroxythionuphlutine as a major component. Results: Nupharidine showed a dose dependent inhibition of NF-uB activity by luciferase reporter gene assay as well as reduction of nuclear NF-uB subunits expression as tested by western blots and immunohistochemistry. Diminution of DNA binding was demonstrated by Electro Mobility Shift Assay (EMSA). Nupharidine inhibited both inducible and constitutive NF-uB activation and affected the canonical and alternative pathways. Suppression of NF-uB was not cell type specific. Conclusions: Induction of apoptosis by Nupharidine was demonstrated by time and dose dependent cleavage of procaspase-9 and PARP. Synergistic cytotoxicity of nupharidine with cisplatin and etoposide was demonstrated, therefore suggesting its possible use as a ‘sensitizer’ in anticancer treatment.