130 research outputs found

    Offspring of parents with chronic pain: A systematic review and meta-analysis of pain, health, psychological, and family outcomes

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    Offspring of parents with chronic pain may be at risk for poorer outcomes than offspring of healthy parents. The objective of this research was to provide a comprehensive mixed-methods systematic synthesis of all available research on outcomes in offspring of parents with chronic pain. A systematic search was conducted for published articles in English examining pain, health, psychological, or family outcomes in offspring of parents with chronic pain. Fifty-nine eligible articles were identified (31 population-based, 25 clinical, 3 qualitative), including offspring from birth to adulthood and parents with varying chronic pain diagnoses (eg, mixed pain samples, arthritis). Meta-analysis was used to synthesize the results from population-based and clinical studies, while meta-ethnography was used to synthesize the results of qualitative studies. Increased pain complaints were found in offspring of mothers and of fathers with chronic pain and when both parents had chronic pain. Newborns of mothers with chronic pain were more likely to have adverse birth outcomes, including low birthweight, preterm delivery, caesarian section, intensive care admission, and mortality. Offspring of parents with chronic pain had greater externalizing and internalizing problems and poorer social competence and family outcomes. No significant differences were found on teacher-reported externalizing problems. The meta-ethnography identified 6 key concepts (developing independence, developing compassion, learning about health and coping, missing out, emotional health, and struggles communicating with parents). Across study designs, offspring of parents with chronic pain had poorer outcomes than other offspring, although the meta-ethnography noted some constructive impact of having a parent with chronic pain. © 2015 International Association for the Study of Pain

    The Iowa Homemaker vol.20, no.1

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    Recreation that Recreates, Editor, page 1 Dual Personalities, Catherine Raymond, page 2 Married Right Out of College, Mary Ellen Lynch Brown, page 3 Sally Bows to Summer’s Sun, Kathryn Cooley, page 4 Selling Yourself, Kathryn Monson, page 6 I Want a Cotton Dress, Marcia E. Turner, page 7 Playtime Pays Dividends, Jane Wiley, page 8 Behind Closed Doors, Margaret Kumlien, page 9 Sunshine Sports, Jeanette Woodward, page 10 Packing the Convention Bag, Shirley Ambrose, page 11 What’s New in Home Economics, page 12 Veishea Presents, Adelaide Richardson, page 14 Picnic Basket, Dorothy Jo Weber, page 16 Alums in the News, Bette Simpson, page 17 Make Room for Music, Nancy Mason, page 18 Behind Bright Jackets, Betty Bice, page 20 Journalistic Spindles, Dorothy Anne Roost, page 23 Biography of a Home Economist, Eleanor White, page 2

    Genome-wide analysis of YY2 versus YY1 target genes

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    Yin Yang 1 (YY1) is a critical transcription factor controlling cell proliferation, development and DNA damage responses. Retrotranspositions have independently generated additional YY family members in multiple species. Although Drosophila YY1 [pleiohomeotic (Pho)] and its homolog [pleiohomeotic-like (Phol)] redundantly control homeotic gene expression, the regulatory contributions of YY1-homologs have not yet been examined in other species. Indeed, targets for the mammalian YY1 homolog YY2 are completely unknown. Using gene set enrichment analysis, we found that lentiviral constructs containing short hairpin loop inhibitory RNAs for human YY1 (shYY1) and its homolog YY2 (shYY2) caused significant changes in both shared and distinguishable gene sets in human cells. Ribosomal protein genes were the most significant gene set upregulated by both shYY1 and shYY2, although combined shYY1/2 knock downs were not additive. In contrast, shYY2 reversed the anti-proliferative effects of shYY1, and shYY2 particularly altered UV damage response, platelet-specific and mitochondrial function genes. We found that decreases in YY1 or YY2 caused inverse changes in UV sensitivity, and that their combined loss reversed their respective individual effects. Our studies show that human YY2 is not redundant to YY1, and YY2 is a significant regulator of genes previously identified as uniquely responding to YY1

    Prioritization of knowledge-needs to achieve best practices for bottom trawling in relation to seabed habitats

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    Management and technical approaches that achieve a sustainable level of fish production while at the same time minimizing or limiting the wider ecological effects caused through fishing gear contact with the seabed might be considered to be ‘best practice’. To identify future knowledge-needs that would help to support a transition towards the adoption of best practices for trawling, a prioritization exercise was undertaken with a group of 39 practitioners from the seafood industry and management, and 13 research scientists who have an active research interest in bottom-trawl and dredge fisheries. A list of 108 knowledge-needs related to trawl and dredge fisheries was developed in conjunction with an ‘expert task force’. The long list was further refined through a three stage process of voting and scoring, including discussions of each knowledge-need. The top 25 knowledge-needs are presented, as scored separately by practitioners and scientists. There was considerable consistency in the priorities identified by these two groups. The top priority knowledge-need to improve current understanding on the distribution and extent of different habitat types also reinforced the concomitant need for the provision and access to data on the spatial and temporal distribution of all forms of towed bottom-fishing activities. Many of the other top 25 knowledge-needs concerned the evaluation of different management approaches or implementation of different fishing practices, particularly those that explore trade-offs between effects of bottom trawling on biodiversity and ecosystem services and the benefits of fish production as food.Fil: Kaiser, Michel J.. Bangor University; Reino UnidoFil: Hilborn, Ray. University of Washington; Estados UnidosFil: Jennings, Simon. Fisheries and Aquaculture Science; Reino UnidoFil: Amaroso, Ricky. University of Washington; Estados UnidosFil: Andersen, Michael. Danish Fishermen; DinamarcaFil: Balliet, Kris. Sustainable Fisheries Partnership; Estados UnidosFil: Barratt, Eric. Sanford Limited; Nueva ZelandaFil: Bergstad, Odd A. Institute of Marine Research; NoruegaFil: Bishop, Stephen. Independent Fisheries Ltd; Nueva ZelandaFil: Bostrom, Jodi L. Marine Stewardship Council; Reino UnidoFil: Boyd, Catherine. Clearwater Seafoods; CanadáFil: Bruce, Eduardo A. Friosur S.A.; ChileFil: Burden, Merrick. Marine Conservation Alliance; Estados UnidosFil: Carey, Chris. Independent Fisheries Ltd.; Estados UnidosFil: Clermont, Jason. New England Aquarium; Estados UnidosFil: Collie, Jeremy S. University of Rhode Island,; Estados UnidosFil: Delahunty, Antony. National Federation of Fishermen; Reino UnidoFil: Dixon, Jacqui. Pacific Andes International Holdings Limited; ChinaFil: Eayrs, Steve. Gulf of Maine Research Institute; Estados UnidosFil: Edwards, Nigel. Seachill Ltd.; Reino UnidoFil: Fujita, Rod. Environmental Defense Fund; Reino UnidoFil: Gauvin, John. Alaska Seafood Cooperative; Estados UnidosFil: Gleason, Mary. The Nature Conservancy; Estados UnidosFil: Harris, Brad. Alaska Pacific University; Estados UnidosFil: He, Pingguo. University of Massachusetts Dartmouth; Estados UnidosFil: Hiddink, Jan G. Bangor University; Reino UnidoFil: Hughes, Kathryn M. Bangor University; Reino UnidoFil: Inostroza, Mario. EMDEPES; ChileFil: Kenny, Andrew. Fisheries and Aquaculture Science; Reino UnidoFil: Kritzer, Jake. Environmental Defense Fund; Estados UnidosFil: Kuntzsch, Volker. Sanford Limited; Estados UnidosFil: Lasta, Mario. Diag. Montegrande N° 7078. Mar del Plata; ArgentinaFil: Lopez, Ivan. Confederacion Española de Pesca; EspañaFil: Loveridge, Craig. South Pacific Regional Fisheries Management Organisation; Nueva ZelandaFil: Lynch, Don. Gorton; Estados UnidosFil: Masters, Jim. Marine Conservation Society; Reino UnidoFil: Mazor, Tessa. CSIRO Marine and Atmospheric Research; AustraliaFil: McConnaughey, Robert A. US National Marine Fisheries Service; Estados UnidosFil: Moenne, Marcel. Pacificblu; ChileFil: Francis. Marine Scotland Science; Reino UnidoFil: Nimick, Aileen M. Alaska Pacific University; Estados UnidosFil: Olsen, Alex. A. Espersen; DinamarcaFil: Parker, David. Young; Reino UnidoFil: Parma, Ana María. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Nacional Patagónico; ArgentinaFil: Penney, Christine. Clearwater Seafoods; CanadáFil: Pierce, David. Massachusetts Division of Marine Fisheries; Estados UnidosFil: Pitcher, Roland. CSIRO Marine and Atmospheric Research; AustraliaFil: Pol, Michael. Massachusetts Division of Marine Fisheries; Estados UnidosFil: Richardson, Ed. Pollock Conservation Cooperative; Estados UnidosFil: Rijnsdorp, Adriaan D. Wageningen IMARES; Países BajosFil: Rilatt, Simon. A. Espersen; DinamarcaFil: Rodmell, Dale P. National Federation of Fishermen's Organisations; Reino UnidoFil: Rose, Craig. FishNext Research; Estados UnidosFil: Sethi, Suresh A. Alaska Pacific University; Estados UnidosFil: Short, Katherine. F.L.O.W. Collaborative; Nueva ZelandaFil: Suuronen, Petri. Fisheries and Aquaculture Department; ItaliaFil: Taylor, Erin. New England Aquarium; Estados UnidosFil: Wallace, Scott. The David Suzuki Foundation; CanadáFil: Webb, Lisa. Gorton's Inc.; Estados UnidosFil: Wickham, Eric. Unit four –1957 McNicoll Avenue; CanadáFil: Wilding, Sam R. Monterey Bay Aquarium; Estados UnidosFil: Wilson, Ashley. Department for Environment; Reino UnidoFil: Winger, Paul. Memorial University Of Newfoundland; CanadáFil: Sutherland, William J. University of Cambridge; Reino Unid

    Identification of a BRCA2-Specific modifier locus at 6p24 related to breast cancer risk

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    Common genetic variants contribute to the observed variation in breast cancer risk for BRCA2 mutation carriers; those known to date have all been found through population-based genome-wide association studies (GWAS). To comprehensively identify breast cancer risk modifying loci for BRCA2 mutation carriers, we conducted a deep replication of an ongoing GWAS discovery study. Using the ranked P-values of the breast cancer associations with the imputed genotype of 1.4 M SNPs, 19,029 SNPs were selected and designed for inclusion on a custom Illumina array that included a total of 211,155 SNPs as part of a multi-consortial project. DNA samples from 3,881 breast cancer affected and 4,330 unaffected BRCA2 mutation carriers from 47 studies belonging to the Consortium of Investigators of Modifiers of BRCA1/2 were genotyped and available for analysis. We replicated previously reported breast cancer susceptibility alleles in these BRCA2 mutation carriers and for several regions (including FGFR2, MAP3K1, CDKN2A/B, and PTHLH) identified SNPs that have stronger evidence of association than those previously published. We also identified a novel susceptibility allele at 6p24 that was inversely associated with risk in BRCA2 mutation carriers (rs9348512; per allele HR = 0.85, 95% CI 0.80-0.90, P = 3.9×10−8). This SNP was not associated with breast cancer risk either in the general population or in BRCA1 mutation carriers. The locus lies within a region containing TFAP2A, which encodes a transcriptional activation protein that interacts with several tumor suppressor genes. This report identifies the first breast cancer risk locus specific to a BRCA2 mutation background. This comprehensive update of novel and previously reported breast cancer susceptibility loci contributes to the establishment of a panel of SNPs that modify breast cancer risk in BRCA2 mutation carriers. This panel may have clinical utility for women with BRCA2 mutations weighing options for medical prevention of breast cancer
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