1,431 research outputs found

    CONSUMER FOOD SAFETY BEHAVIOR: A CASE STUDY IN HAMBURGER COOKING AND ORDERING

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    More Americans are eating hamburgers more well-done than in the past, according to national surveys. This change reduced the risk of E. coli O157:H7 infection by an estimated 4.6 percent and reduced associated medical costs and productivity losses by an estimated $7.4 million annually. In a 1996 survey, respondents who were more concerned about the risk of foodborne illness cooked and ordered hamburgers more well-done than those who were less concerned. However, respondents who strongly preferred hamburgers less well-done cooked and ordered them that way, even after accounting for their concern about the risk of illness.hamburger doneness, ground beef, food safety, food safety education, E. coli O157:H7, consumer behavior, survey, risk, foodborne illness, risk perceptions, palatability, information, microbial pathogens, Food Consumption/Nutrition/Food Safety,

    FLIP (Flice-like inhibitory protein) suppresses cytoplasmic double-stranded-RNA-induced apoptosis and NF-κB and IRF3-mediated signaling

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    <p>Abstract</p> <p>Background</p> <p>Cytoplasmic viral double-stranded RNA (dsRNA) is detected by a class of ubiquitous cytoplasmic RNA helicases, retinoic acid inducible gene-I (RIG-I) and melanoma differentiation antigen-5 (MDA5), which initiate a signaling cascade via their common adaptor called interferon-β (IFN-β) promoter stimulator-1 (IPS-1). This leads to the production of proinflammatory and antiviral cytokines, the type I Interferons, via mainly nuclear factor kappa B (NF-κB) and interferon response factor-3 (IRF3) transcription factors. Fas-associated death domain (FADD) protein, receptor-interacting protein (RIP1), caspase-8 and tumor necrosis factor receptor (TNFR)-associated death domain (TRADD) protein, all traditionally associated with death receptor signaling, are also involved in RIG-I/MDA5 signaling pathway. We previously showed that FLIP (Flice-like inhibitory protein), also designated as <it>cflar </it>(CASP8 and FADD-like apoptosis regulator), negatively regulates lipopolysaccharide (LPS)-induced toll-like receptor 4 (TLR4) signaling in endothelial cells and mouse embryonic fibroblasts (MEFs) and protected against TLR4-mediated apoptosis.</p> <p>Results</p> <p>In this study, we investigated the role of FLIP in cellular response to cytoplasmic polyinosinic:polycytidylic acid, poly(I:C), a synthetic analog of dsRNA. <it>C</it>onsistent with the previously described role of FADD in RIG-I/MDA5-mediated apoptosis, we found that FLIP<sup>-/- </sup>MEFs were more susceptible to killing by cytoplasmic poly(I:C). However, FLIP<sup>-/- </sup>MEFs also exhibited markedly increased expression of NF-κB-and IRF3- dependent genes in response to cytoplasmic poly(I:C). Importantly, reconstitution of FLIP in FLIP<sup>-/-</sup>MEFs reversed the hyper-activation of IRF3- and NF-κB-mediated gene expression. Further, we found that caspase-8 catalytic activity was not required for cytoplasmic poly(I:C)-mediated NF-κB and IRF3 signaling.</p> <p>Conclusions</p> <p>These results provide evidence for a crucial dual role for FLIP in antiviral responses to cytoplasmic dsRNA: it protects from cytoplasmic dsRNA-mediated cell death while down-regulating IRF3-and NF-κB-mediated gene expression. Since the pathogenesis of several viral infections involves a heightened and dysregulated cytokine response, a possible therapy could involve modulating FLIP levels.</p

    Mapping resistance to the bird cherry-oat aphid and the greenbug in wheat using sequence-based genotyping

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    Citation: Crespo-Herrera, L. A., Akhunov, E., Garkava-Gustavsson, L., Jordan, K. W., Smith, C. M., Singh, R. P., & Åhman, I. (2014). Mapping resistance to the bird cherry-oat aphid and the greenbug in wheat using sequence-based genotyping. Theoretical and Applied Genetics, 127(9), 1963-1973.The aphids Rhopalosiphum padi and Schizaphis graminum are important pests of common wheat (Triticum aestivum L.). Characterization of the genetic bases of resistance sources is crucial to facilitate the development of resistant wheat cultivars to these insects. We examined 140 recombinant inbred lines (RILs) from the cross of the susceptible wheat Seri M82 with the synthetic hexaploid wheat CWI76364, resistant to both aphid species. The RILs were phenotyped for R. padi antibiosis and tolerance traits. Phenotyping of S. graminum resistance was based on leaf chlorosis in a greenhouse screening, and also on the number of S. graminum per tiller in a field trial. Seedling pubescence was scored in each RIL. Using a sequence-based genotyping method we located genomic regions associated to these resistance traits. One QTL for R. padi antibiosis was found in chromosome 4BL; it explained 10.2% of phenotypic variation and was located 14.6 cM apart from the pubescence locus. However, we did not find any association between plant pubescence and the other resistance traits. We found two QTLs for tolerance to R. padi in chromosomes 5AL and 5BL, with an epistatic interaction between a locus in chromosome 3AL and the tolerance QTL in 5AL. These genomic regions together explained about 35% of the phenotypic variation. We confirmed the location of a previously reported gene for S. graminum resistance (Gba) in 7DL and found an additional, novel QTL associated with the number of aphids per tiller in chromosome 2DL. This is the first report where resistance to R. padi in wheat is mapped and also where chromosome 2DL shown to be associated with S. graminum resistance

    Racial disparities in the SOFA score among patients hospitalized with COVID-19

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    BACKGROUND: Sequential Organ Failure Assessment (SOFA) score predicts probability of in-hospital mortality. Many crisis standards of care suggest the use of SOFA scores to allocate medical resources during the COVID-19 pandemic. RESEARCH QUESTION: Are SOFA scores elevated among Non-Hispanic Black and Hispanic patients hospitalized with COVID-19, compared to Non-Hispanic White patients? STUDY DESIGN AND METHODS: Retrospective cohort study conducted in Yale New Haven Health System, including 5 hospitals with total of 2681 beds. Study population drawn from consecutive patients aged ≥18 admitted with COVID-19 from March 29th to August 1st, 2020. Patients excluded from the analysis if not their first admission with COVID-19, if they did not have SOFA score recorded within 24 hours of admission, if race and ethnicity data were not Non-Hispanic Black, Non-Hispanic White, or Hispanic, or if they had other missing data. The primary outcome was SOFA score, with peak score within 24 hours of admission dichotomized as \u3c6 or ≥6. RESULTS: Of 2982 patients admitted with COVID-19, 2320 met inclusion criteria and were analyzed, of whom 1058 (45.6%) were Non-Hispanic White, 645 (27.8%) were Hispanic, and 617 (26.6%) were Non-Hispanic Black. Median age was 65.0 and 1226 (52.8%) were female. In univariate logistic screen and in full multivariate model, Non-Hispanic Black patients but not Hispanic patients had greater odds of an elevated SOFA score ≥6 when compared to Non-Hispanic White patients (OR 1.49, 95%CI 1.11-1.99). INTERPRETATION: Given current unequal patterns in social determinants of health, US crisis standards of care utilizing the SOFA score to allocate medical resources would be more likely to deny these resources to Non-Hispanic Black patients

    Retrotransposons Are the Major Contributors to the Expansion of the \u3ci\u3eDrosophila ananassae\u3c/i\u3e Muller F Element

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    The discordance between genome size and the complexity of eukaryotes can partly be attributed to differences in repeat density. The Muller F element (∼5.2 Mb) is the smallest chromosome in Drosophila melanogaster, but it is substantially larger (\u3e18.7 Mb) in D. ananassae. To identify the major contributors to the expansion of the F element and to assess their impact, we improved the genome sequence and annotated the genes in a 1.4-Mb region of the D. ananassae F element, and a 1.7-Mb region from the D element for comparison. We find that transposons (particularly LTR and LINE retrotransposons) are major contributors to this expansion (78.6%), while Wolbachia sequences integrated into the D. ananassae genome are minor contributors (0.02%). Both D. melanogaster and D. ananassae F-element genes exhibit distinct characteristics compared to D-element genes (e.g., larger coding spans, larger introns, more coding exons, and lower codon bias), but these differences are exaggerated in D. ananassae. Compared to D. melanogaster, the codon bias observed in D. ananassae F-element genes can primarily be attributed to mutational biases instead of selection. The 5′ ends of F-element genes in both species are enriched in dimethylation of lysine 4 on histone 3 (H3K4me2), while the coding spans are enriched in H3K9me2. Despite differences in repeat density and gene characteristics, D. ananassae F-element genes show a similar range of expression levels compared to genes in euchromatic domains. This study improves our understanding of how transposons can affect genome size and how genes can function within highly repetitive domains

    Genomic patterns of malignant peripheral nerve sheath tumor (MPNST) evolution correlate with clinical outcome and are detectable in cell-free DNA

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    Malignant peripheral nerve sheath tumor (MPNST), an aggressive soft-tissue sarcoma, occurs in people with neurofibromatosis type 1 (NF1) and sporadically. Whole-genome and multiregional exome sequencing, transcriptomic, and methylation profiling of 95 tumor samples revealed the order of genomic events in tumor evolution. Following biallelic inactivation of NF1, loss of CDKN2A or TP53 with or without inactivation of polycomb repressive complex 2 (PRC2) leads to extensive somatic copy-number aberrations (SCNA). Distinct pathways of tumor evolution are associated with inactivation of PRC2 genes and H3K27 trimethylation (H3K27me3) status. Tumors with H3K27me3 loss evolve through extensive chromosomal losses followed by whole-genome doubling and chromosome 8 amplification, and show lower levels of immune cell infiltration. Retention of H3K27me3 leads to extensive genomic instability, but an immune cell-rich phenotype. Specific SCNAs detected in both tumor samples and cell-free DNA (cfDNA) act as a surrogate for H3K27me3 loss and immune infiltration, and predict prognosis
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