Ethnic differences in postpartum weight retention: a Norwegian cohort study.

OBJECTIVE: To explore ethnic differences in weight retention 14 weeks postpartum. DESIGN: Population-based cohort study. SETTING: The STORK Groruddalen Study. POPULATION: A multi-ethnic cohort of healthy pregnant women attending primary antenatal care at three public Child Health Clinics, in Oslo, Norway (n = 642). METHODS: An explanatory linear regression was performed to model the relationship between ethnicity and postpartum weight retention. Forward selection of 12 explanatory factors was used to adjust for potential confounding factors, based on univariate analysis and adjusted R(2) . MAIN OUTCOME MEASURE: Postpartum weight retention. RESULTS: Unadjusted mean postpartum weight retention was 2.3 (4.9) kg for women from Western Europe and varied from 3.7 (3.5) to 6.3 (4.7) kg among the five ethnic minority groups. The proportion of women in the highest quintile (postpartum weight retention >8.5-24.4 kg) significantly differed by ethnicity (P < 0.01 for the proportion of women from South Asia, the Middle East and Africa compared with Western Europeans). Women from all ethnic minority groups had a higher relative increase in weight from pre-pregnancy to postpartum (P < 0.01) compared with Western Europeans. After adjustments for significant exposures, women from the Middle East retained 2.0 kg (95% CI: 1.0-3.0), South Asia 2.8 kg (91.9-3.6), and Africa 4.4 kg (3.1-5.8) more than Western Europeans (P < 0.01). CONCLUSIONS: Significantly more women with an ethnic origin from South Asia, the Middle East and Africa had high postpartum weight retention compared with Western European women.

The effects of selective complement and CD14 inhibition on the E. coli-induced tissue factor mRNA upregulation, monocyte tissue factor expression, and tissue factor functional activity in human whole blood.

BACKGROUND: The complement pathway and CD14 play essential roles in inflammation, but little is known about the relative roles of complement and CD14 in E. coli-induced tissue factor (TF) mRNA upregulation, expression by monocytes, and functional activity in human whole blood. METHODS: Whole E. coli bacteria were incubated for up to 4 h in human whole blood containing the anticoagulant lepirudin, which does not affect complement activation. TF mRNA levels were analyzed using reverse transcription, quantitative real-time PCR (RT-qPCR), and the expression of TF on the cell surface was analyzed using flow cytometry. Complement was selectively inhibited using the C3 convertase inhibitor compstatin or a C5a receptor antagonist (C5aRa), while CD14 was blocked by an anti-CD14 F(ab')2 monoclonal antibody. RESULTS: The E. coli-induced TF mRNA upregulation was reduced to virtually background levels by compstatin, whereas anti-CD14 had no effect. Monocyte TF expression and TF activity in plasma microparticles were significantly reduced by C5aRa. Anti-CD14 alone only slightly reduced E. coli-induced monocyte TF expression but showed a modest additive effect when combined with the complement inhibitors. Inhibiting complement and CD14 efficiently reduced the expression of the E. coli-induced cytokines IL-1beta, IL-6, IL-8, and platelet-derived growth factor bb. CONCLUSION: Our results indicate that E. coli-induced TF mRNA upregulation is mainly dependent on complement activation, while CDI4 plays a modest role in monocyte TF expression and the plasma TF activity in human whole blood.