Diet quality is positively associated with 100% fruit juice consumption in children and adults in the United States: NHANES 2003-2006

<p>Abstract</p> <p>Background</p> <p>One hundred percent fruit juice (100% FJ) has been viewed by some as a sweetened beverage with concerns about its effect on weight. Little regard has been given to the contribution of 100% FJ to diet quality.</p> <p>Methods</p> <p>In this study data from the 2003-2006 National Health and Nutrition Examination Survey were used to examine the association of 100% FJ consumption with diet quality in participants 2-5 years of age (y) (n = 1665), 6-12 y (n = 2446), 13-18 y (n = 3139), and 19+y (n = 8861). Two 24-hour dietary recalls were used to determine usual intake using the National Cancer Institute method. Usual intake, standard errors, and regression analyses (juice independent variable and Healthy Eating Index-2005 [HEI-2005] components were dependent variables), using appropriate covariates, were determined using sample weights.</p> <p>Results</p> <p>The percentage of participants 2-5 y, 6-12 y, 13-18 y, and 19+y that consumed 100% FJ was 71%, 57%, 45%, and 62%, respectively. Usual intake of 100% FJ (ounce [oz]/day) among the four age groups was: 5.8 ± 0.6, 2.6 ± 0.4, 3.7 ± 0.4, and 2.4 ± 0.2 for those in age groups 2-5 y, 6-12 y, 13-18 y, and 19+y, respectively. Consumption of 100% FJ was associated with higher energy intake in 6-12 y, 13-18 y, and 19+y; and higher total, saturated, and discretionary fats in 13-18 y participants. Consumption of 100% FJ was associated with higher total HEI-2005 scores in all age groups (< 0.0001). In 100% FJ consumers, total and whole fruit consumption was higher and intake of added sugars was lower in all age groups.</p> <p>Conclusions</p> <p>Usual intake of 100% FJ consumption exceeded MyPyramid recommendations for children 2-5 y, but was associated with better diet quality in all age groups and should be encouraged in moderation as part of a healthy diet.</p

Two Genes on A/J Chromosome 18 Are Associated with Susceptibility to Staphylococcus aureus Infection by Combined Microarray and QTL Analyses

Although it has recently been shown that A/J mice are highly susceptible to Staphylococcus aureus sepsis as compared to C57BL/6J, the specific genes responsible for this differential phenotype are unknown. Using chromosome substitution strains (CSS), we found that loci on chromosomes 8, 11, and 18 influence susceptibility to S. aureus sepsis in A/J mice. We then used two candidate gene selection strategies to identify genes on these three chromosomes associated with S. aureus susceptibility, and targeted genes identified by both gene selection strategies. First, we used whole genome transcription profiling to identify 191 (56 on chr. 8, 100 on chr. 11, and 35 on chr. 18) genes on our three chromosomes of interest that are differentially expressed between S. aureus-infected A/J and C57BL/6J. Second, we identified two significant quantitative trait loci (QTL) for survival post-infection on chr. 18 using N2 backcross mice (F1 [C18A]×C57BL/6J). Ten genes on chr. 18 (March3, Cep120, Chmp1b, Dcp2, Dtwd2, Isoc1, Lman1, Spire1, Tnfaip8, and Seh1l) mapped to the two significant QTL regions and were also identified by the expression array selection strategy. Using real-time PCR, 6 of these 10 genes (Chmp1b, Dtwd2, Isoc1, Lman1, Tnfaip8, and Seh1l) showed significantly different expression levels between S. aureus-infected A/J and C57BL/6J. For two (Tnfaip8 and Seh1l) of these 6 genes, siRNA-mediated knockdown of gene expression in S. aureus–challenged RAW264.7 macrophages induced significant changes in the cytokine response (IL-1 β and GM-CSF) compared to negative controls. These cytokine response changes were consistent with those seen in S. aureus-challenged peritoneal macrophages from CSS 18 mice (which contain A/J chromosome 18 but are otherwise C57BL/6J), but not C57BL/6J mice. These findings suggest that two genes, Tnfaip8 and Seh1l, may contribute to susceptibility to S. aureus in A/J mice, and represent promising candidates for human genetic susceptibility studies

Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.

Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field