Objective: The accuracy of the AMPM was evaluated by comparing reported energy intake (EI) with total energy expenditure (TEE) by using the doubly labeled water (DLW) technique. Design: The 524 volunteers, aged 30 -69 y, included an equal number of men and women recruited from the Washington, DC, area. Each subject was dosed with DLW on the first day of the 2-wk study period; three 24-h recalls were collected during the 2-wk period by using the AMPM. The first recall was conducted in person, and subsequent recalls were over the telephone. Results: Overall, the subjects underreported EI by 11% compared with TEE. Normal-weight subjects [body mass index (in kg/m 2 ) 25] underreported EI by 3%. By using a linear mixed model, 95% CIs were determined for the ratio of EI to TEE. Approximately 78% of men and 74% of women were classified as acceptable energy reporters (within 95% CI of EI:TEE). Both the percentage by which energy was underreported and the percentage of subjects classified as low energy reporters (95% CI of EI:TEE) were highest for subjects classified as obese (body mass index 30). Conclusions: Although the AMPM accurately reported EIs in normal-weight subjects, research is warranted to enhance its accuracy in overweight and obese persons.Am J Clin Nutr 2008;88: 324 -32.

Children and teens in the United States follow eating patterns that do not meet national recommendations. Nutrition education and intervention are needed among US children.

Poly (ADP-ribose) polymerase (PARP) inhibitor (PARPi) olaparib has been approved for treatment of advanced ovarian cancer associated with BRCA1 and BRCA2 mutations. BRCA1- and BRCA2-mutated cells, which are homologous recombination (HR) deficient, are hypersensitive to PARPi through the mechanism of synthetic lethality. Here we examine the effect of PARPi on HR-proficient cells. Olaparib pretreatment, PARP1 knockdown or Parp1 heterozygosity of Brca2cko/ko mouse embryonic stem cells (mESCs), carrying a null (ko) and a conditional (cko) allele of Brca2, results in viable Brca2ko/ko cells. PARP1 deficiency does not restore HR in Brca2ko/ko cells, but protects stalled replication forks from MRE11-mediated degradation through its impaired recruitment. The functional consequence of Parp1 heterozygosity on BRCA2 loss is demonstrated by a significant increase in tumorigenesis in Brca2cko/cko mice. Thus, while olaparib efficiently kills BRCA2-deficient cells, we demonstrate that it can also contribute to the synthetic viability if PARP is inhibited before BRCA2 loss.