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001, one-way ANOVA with Tukey HSD post hoc test), indicating that the cell lines carrying ABCG2 wt and ABCG2 34G A actively transports erlotinib out of the cells. The ABCG2 34G A cell line had a higher transport capacity compared with ABCG2 wt after adjusting for ABCG2 expression (P = .024, t test). No differences were observed between K562/ve and K562 ABCG2 421 C A. Genetic polymorphism in the ABCG2 gene has an influence on the transport of erlotinib which can contribute to the observed variation in erlotinib pharmacokine

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0%), and AIDS (6.7%); 12% of causes were unknown. These clinical diagnoses were further grouped into AIDS-related infections (22%) and non-infections (5.8%), and non-AIDS-related infections (47%) and non-infections (11%); with 12% unknown, 2.2% not reviewed. Higher CD4 count and better weight-for-age z-score were protective against death. Conclusions Our standardized cause of death assessment provides robust data to inform regional resource allocation for pediatric diagnostic evaluations and prioritization of clinical inte