Measuring dietary intake in children enables the assessment of nutritional adequacy of individuals and groups and can provide information about nutrients, including energy, food, and eating habits. The aim of this review was to determine which dietary assessment method(s) provide a valid and accurate estimate of energy intake by comparison with the gold standard measure, doubly labeled water (DLW). English-language articles published between 1973 and 2009 and available from common nutrition databases were retrieved. Studies were included if the subjects were children birth to age 18 years and used the DLW technique to validate reported energy intake by any other dietary assessment method. The review identified 15 cross-sectional studies, with a variety of comparative dietary assessment methods. These included a total of 664 children, with the majority having <30 participants. The majority of dietary assessment method validation studies indicated a degree of misreporting, with only eight studies identifying this to a significant level (P<0.05) compared to DLW estimated energy intake. Under-reporting by food records varied from 19% to 41% (n=5 studies) with over-reporting most often associated with 24-hour recalls (7% to 11%, n=4), diet history (9% to 14%, n=3), and food frequency questionnaires (2% to 59%, n=2). This review suggested that the 24-hour multiple pass recall conducted over at least a 3-day period that includes weekdays and weekend days and uses parents as proxy reporters is the most accurate method to estimate total energy intake in children aged 4 to 11 years, compared to total energy expenditure measured by DLW. Weighed food records provided the best estimate for younger children aged 0.5 to 4 years, whereas the diet history provided better estimates for adolescents aged≥16 years. Further research is needed in this area to substantiate findings and improve estimates of total energy expenditure in children and adolescents.

IntroductionInflammation assumes many forms, such as the response to acute epithelial barrier injury, acute microbial infection, recurrent tissue nondestructive lesions as in psoriasis, chronic tissue destruction as seen in a myriad of autoimmune or innate inflammatory diseases, or chronic microbial/viral infestations and infections. Chronic inflammation with attendant microenvironmental alterations, resulting from growth factor, chemokine, cytokine secretion, and reactive oxygen species enrichment, also provides a fertile soil for de novo development of epithelial cancer. 1,2 Elucidation of the mechanisms of inflammatory modulation by epithelial cells is an emergent focus of investigation. Models of epithelial elaboration of specific inflammatory chemokines, cytokines, or growth factors have shed light on the roles of specific signaling networks in disease. In contrast, the concept that transcription factors regulate production of a repertoire of inflammatory chemokines and cytokines by epithelial cells is relatively new. 3,4 Here we demonstrate that gain of function of the transcription factor hypoxia inducible factor-1 (HIF-1), signaling indirectly through nuclear factor [kappa2]B (NFB), can "prime" and remodel the local stromal environment to affect an augmented, enhanced responsiveness "hyper-responsiveness" to an inflammatory stimulus. This may be yet another mechanism, broadcast from the epithelial cells themselves, by which both HIF-1 and NFB conspire to increase the severity of inflammatory diseases and carcinogenic progression.HIF-1 is a fundamental mediator of cellular adaptation to hypoxia, activating metabolic and signaling pathways promoting cell survival. HIF-1 consists of the oxygen-sensitive subunit HIF-1␣ and the constitutively expressed HIF-1␤ subunit. In normoxia, the alpha subunit is hydroxylated in position 402 and 564 by 3 prolyl hydroxylase enzymes (PHD) 1 to 3. These modifications allow interaction between HIF-1␣ and the von Hippel-Lindau protein, targeting HIF-1␣ for proteasomal degradation. In hypoxia, PHD activity is decreased, preventing HIF-1␣ degradation. 5,6 When HIF-1␣ levels increase, functional HIF-1 regulates transcription at hypoxia response elements of target gene enhancers, up-regulating genes involved in energy metabolism and angiogenesis. 7 HIF-1␣ protein synthesis can be regulated in an O 2 -independent manner by activation of the phosphatidylinositol 3-kinase and ERK mitogen-activated kinase pathways that are either physiologically stimulated by cognate growth factors or cytokines or activated by mutation. Thus, proinflammatory cytokines, interleukin-1␤ and tumor necrosis factor␣ (TNF␣) have each been shown to stabilize HIF-1␣ protein, suggesting that HIF-1␣ functions can be recruited by tissue inflammation. [8][9][10] The concept The online version of this article contains a data supplement.The publication costs of this article were defrayed in part by page charge payment. Therefore, and solely to indicate this fact, this article is hereby marked ''advertisement'' in a...

Hypoxia-inducible factor-1 is a known cancer progression factor, promoting growth, spread, and metastasis. However, in selected contexts HIF-1 is a tumor suppressor coordinating hypoxic cell cycle suppression and apoptosis. Prior studies focused on HIF-1 function in established malignancy, however little is known about its role during the entire process of carcinogenesis from neoplasia induction to malignancy. Here we tested HIF-1 gain of function during multistage murine skin chemical carcinogenesis in K14-HIF-1αPro402A564G (K14-HIF-1αDPM) transgenic mice. Transgenic papillomas appeared earlier and were more numerous, 6±3 transgenic versus 2±1.5 nontransgenic papillomas per mouse, yet they were more differentiated, their proliferation was lower, and their malignant conversion was profoundly inhibited, 7% in transgenic versus 40% in non transgenic mice. Moreover, transgenic cancers maintained squamous differentiation whereas epithelial mesenchymal transformation was frequent in nontransgenic malignancies. Transgenic basal keratinocytes upregulated the HIF-1 target N-myc downstream regulated gene-1, a known tumor suppressor gene in human malignancy, and its expression was maintained in transgenic papillomas and cancer. We also discovered a novel HIF-1 target gene, selenium binding protein-1 (selenbp1), a gene of unknown function whose expression is lost in human cancer. Thus, HIF-1 can function as a tumor suppressor through transactivation of genes that are themselves targets for negative selection in human cancers.

Learning strategies that create "desirable difficulties" by slowing or hindering improvement during learning often produce superior long-term retention and transfer (Bjork, 1994;Bjork, 1999). Despite the desirability of difficulties for learning, many learners choose not to use the learning strategies and/or disengage when they are implemented by a teacher. Knowledge of these learning strategies is necessary but insufficient for behavior change-learners must be motivated to embrace or, at minimum cope, with difficulties. To identify ways to help students engage with learning strategies that produce desirable difficulties, the present article briefly reviews five areas of psychological research on motivation that provide strategies for increasing engagement and persistence: finding value, reducing cost, reframing appraisals and attributions, creating appropriate challenges, and providing choice. Looking forward, there is a clear need for empirical work to investigate and theoretical frameworks to explain the interplay between motivation and learning strategies that create desirable difficulties.

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