First trimester multivitamin/mineral use is associated with reduced risk of pre‐eclampsia among overweight and obese women

The use of pregnancy‐specific multivitamin supplements is widely recommended to support maternal homeostasis during pregnancy. Our objective was to investigate whether multivitamin use during pregnancy is associated with a reduced risk of pre‐eclampsia. The effect of multivitamin use on incidence of pre‐eclampsia in lean and overweight/obese women was analysed using data collected between 2006 and 2011 as part of the Environments for Healthy Living Project, Griffith University, Australia. A total of 2261 pregnancies were included in the analysis with pre‐eclampsia reported in 1.95% of subjects. Body mass index (BMI) ≥ 25 was associated with a 1.97‐fold [95% confidence interval (CI): 0.93, 4.16] increase in pre‐eclampsia risk. First trimester multivitamin use was reported by 31.8% of women and after adjustment, was associated with a 67% reduction in pre‐eclampsia risk (95%CI: 0.14, 0.75). Stratification by BMI demonstrated a 55% reduction in pre‐eclampsia risk (95%CI: 0.30, 0.86) in overweight (BMI: 25–29.9) and 62% risk reduction (95%CI: 0.16, 0.92) in obese (BMI: ≥30) cohorts that supplemented with multivitamins in the first trimester of pregnancy. This finding may be particular to the Australian population and reflect inherent nutritional deficits. First trimester folate supplementation was found to reduce pre‐eclampsia incidence [adjusted odds ratios (AOR) 0.42 95%CI: 0.13, 0.98] and demonstrated significance upon stratification by overweight status for women with BMI >25 (AOR 0.55 95%CI: 0.31, 0.96). These results support the hypothesis that multivitamin supplementation may be beneficial in reducing the incidence of pre‐eclampsia during pregnancy and be of particular importance for those with a BMI ≥25.     

Maternal administration of granulocyte colony-stimulating factor improves neonatal rat survival after a lethal group B streptococcal infection

Maternally administered recombinant human granulocyte colony- stimulating factor (rhG-CSF) has been shown to cross the placenta and induce a peripheral neutrophilia and increases in the marrow and spleen neutrophil storage pools in fetal and newborn rats. In the present study, we have used this model system to investigate the efficacy of prenatally administered rhG-CSF on neonatal defense to a lethal challenge with Group B-beta hemolytic Streptococcus (GBS). Pregnant rats were injected with rhG-CSF twice daily beginning 6 days before parturition. At birth, all pups were infected with a dose of GBS that is lethal for 90% of infected pups (LD90). Survival was monitored daily for 5 days. Survival of infected pups from saline-treated mothers beyond 60 hours after infection was 10%. No difference in survival was observed among pups from mothers treated 2 and 4 days before parturition. In contrast, we determined that survival was 82.5% among infected pups from mothers treated for 6 days before parturition with rhG-CSF. Our results demonstrate that maternal administration of rhG- CSF augments neonatal defenses against a lethal bacterial challenge.     

Heterogeneity of B cell involvement in acute nonlymphocytic leukemia

In order to study the pattern of B cell involvement in acute nonlymphocytic leukemia (ANLL), multiple B lymphoid cell lines were established by Epstein-Barr virus transformation of peripheral blood mononuclear cells from two patients with the disease who were heterozygous for the X chromosome-linked glucose-6-phosphate dehydrogenase (G6PD). In one patient, the progenitor cells involved by the leukemia exhibited multipotent differentiative expression, whereas in the other patient the cells showed differentiative expression restricted to the granulocytic pathway. In the patient whose abnormal clone showed multipotent expression, the ratio of B-A G6PD in B lymphoid cell lines was skewed in the direction of type B (the enzyme characteristic of the leukemia clone) and significantly different from the 1:1 ratio expected. It is, therefore, likely that the neoplastic event occurred in a stem cell common to the lymphoid series as well as to the myeloid series. In contrast, evidence for B cell involvement was not detected in the patient whose ANLL progenitor cells exhibited restricted differentiative expression. These findings underscore the heterogeneity of ANLL. Clinically and morphologically similar malignancies in these two patients originated in progenitors with different patterns of stem cell differentiative expression. This difference may reflect differences in cause and pathogenesis.