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Träfflista för sökning "WFRF:(Lauren A) srt2:(2005-2009)"

Search: WFRF:(Lauren A) > (2005-2009)

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  • Willer, Cristen J., et al. (author)
  • Six new loci associated with body mass index highlight a neuronal influence on body weight regulation
  • 2009
  • In: Nature Genetics. - : Springer Science and Business Media LLC. - 1546-1718 .- 1061-4036. ; 41:1, s. 25-34
  • Journal article (peer-reviewed)abstract
    • Common variants at only two loci, FTO and MC4R, have been reproducibly associated with body mass index (BMI) in humans. To identify additional loci, we conducted meta-analysis of 15 genome-wide association studies for BMI (n > 32,000) and followed up top signals in 14 additional cohorts (n > 59,000). We strongly confirm FTO and MC4R and identify six additional loci (P < 5 x 10(-8)): TMEM18, KCTD15, GNPDA2, SH2B1, MTCH2 and NEGR1 (where a 45-kb deletion polymorphism is a candidate causal variant). Several of the likely causal genes are highly expressed or known to act in the central nervous system (CNS), emphasizing, as in rare monogenic forms of obesity, the role of the CNS in predisposition to obesity.
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3.
  • Zeggini, Eleftheria, et al. (author)
  • Meta-analysis of genome-wide association data and large-scale replication identifies additional susceptibility loci for type 2 diabetes
  • 2008
  • In: Nature Genetics. - : Springer Science and Business Media LLC. - 1546-1718 .- 1061-4036. ; 40:5, s. 638-645
  • Journal article (peer-reviewed)abstract
    • Genome-wide association (GWA) studies have identified multiple loci at which common variants modestly but reproducibly influence risk of type 2 diabetes (T2D)(1-11). Established associations to common and rare variants explain only a small proportion of the heritability of T2D. As previously published analyses had limited power to identify variants with modest effects, we carried out meta-analysis of three T2D GWA scans comprising 10,128 individuals of European descent and similar to 2.2 million SNPs (directly genotyped and imputed), followed by replication testing in an independent sample with an effective sample size of up to 53,975. We detected at least six previously unknown loci with robust evidence for association, including the JAZF1 (P=5.0 x 10(-14)), CDC123-CAMK1D (P=1.2 x 10(-10)), TSPAN8-LGR5 (P=1.1 x 10(-9)), THADA (P=1.1 x 10(-9)), ADAMTS9 (P=1.2 x 10(-8)) and NOTCH2 (P=4.1 x 10(-8)) gene regions. Our results illustrate the value of large discovery and follow-up samples for gaining further insights into the inherited basis of T2D.
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4.
  • Haas, Brian J., et al. (author)
  • Genome sequence and analysis of the Irish potato famine pathogen Phytophthora infestans
  • 2009
  • In: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 461:7262, s. 393-398
  • Journal article (peer-reviewed)abstract
    • Phytophthora infestans is the most destructive pathogen of potato and a model organism for the oomycetes, a distinct lineage of fungus-like eukaryotes that are related to organisms such as brown algae and diatoms. As the agent of the Irish potato famine in the mid-nineteenth century, P. infestans has had a tremendous effect on human history, resulting in famine and population displacement(1). To this day, it affects world agriculture by causing the most destructive disease of potato, the fourth largest food crop and a critical alternative to the major cereal crops for feeding the world's population(1). Current annual worldwide potato crop losses due to late blight are conservatively estimated at $6.7 billion(2). Management of this devastating pathogen is challenged by its remarkable speed of adaptation to control strategies such as genetically resistant cultivars(3,4). Here we report the sequence of the P. infestans genome, which at similar to 240 megabases (Mb) is by far the largest and most complex genome sequenced so far in the chromalveolates. Its expansion results from a proliferation of repetitive DNA accounting for similar to 74% of the genome. Comparison with two other Phytophthora genomes showed rapid turnover and extensive expansion of specific families of secreted disease effector proteins, including many genes that are induced during infection or are predicted to have activities that alter host physiology. These fast-evolving effector genes are localized to highly dynamic and expanded regions of the P. infestans genome. This probably plays a crucial part in the rapid adaptability of the pathogen to host plants and underpins its evolutionary potential.
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5.
  • Lissner, Lauren, 1956, et al. (author)
  • Statement by Members of the Task Force on Prevention and Public Health of the European Association for the Study of Obesity (EASO)
  • 2009
  • In: Obesity Facts. - 1662-4025. ; 2:1, s. 54-55
  • Journal article (peer-reviewed)abstract
    • This document is signed by all members of the task force, who will contribute knowledge on the problem of obesity in the various regions of Europe. It is apparent from the wide range of available prevalence estimates that the magnitude of the obesity epidemic varies across Europe. However certain similarities are present, including consistent but varying increases in prevalence in all countries from the end of the 20th century to the present, together with clear inverse socioeconomic gradients. The lack of harmonized surveillance efforts across Europe makes international monitoring and comparative assessments imprecise at best. A particularly worrisome aspect of this epidemic is the recently observed increase in the proportion of European children with overweight and obesity. The Task Force is in agreement that the epidemic reflects changing lifestyles and environments and that prevention can only be achieved by identifying and arresting these trends, a statement that has been repeated by many groups advocating obesity prevention over the years. For instance, in 1999 the Milan Declaration was made on behalf of all members of the EASO, resolving to support the development of coherent national and Europe-wide strategies for the prevention and management of overweight and obesity. Since then, there have been recent steps to develop a public health strategy for obesity prevention across Europe, including most notably the 2006 European Ministerial Conference on Counteracting Obesity in the European Region. At that time, all member states of WHO Europe met in Istanbul and explicitly agreed on an ecological approach to fighting the obesity epidemic, with a charter recognizing that counteracting obesity requires a multidisciplinary effort with a timeline for improvements (www.euro.who.int/ document/E89567.pdf). In this context, the vision of our Task Force is to provide guidance and leadership to researchers, governments, and agencies that are trying to fulfill the charter developed in Istanbul and other recent initiatives. Specifically, we will support and strengthen research and interventions to improve prevention of obesity across Europe, within the framework of the EASO.
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6.
  • Verhertbruggen, Y, et al. (author)
  • Developmental complexity of arabinan polysaccharides and their processing in plant cell walls
  • 2009
  • In: The Plant Journal. - : Wiley-Blackwell. - 0960-7412 .- 1365-313X. ; 59:3
  • Journal article (peer-reviewed)abstract
    • Plant cell walls are constructed from a diversity of polysaccharide components. Molecular probes directed to structural elements of these polymers are required to assay polysaccharide structures in situ, and to determine polymer roles in the context of cell wall biology. Here, we report on the isolation and the characterization of three rat monoclonal antibodies that are directed to 1,5-linked arabinans and related polymers. LM13, LM16 and LM17, together with LM6, constitute a set of antibodies that can detect differing aspects of arabinan structures within cell walls. Each of these antibodies binds strongly to isolated sugar beet arabinan samples in ELISAs. Competitive-inhibition ELISAs indicate the antibodies bind differentially to arabinans with the binding of LM6 and LM17 being effectively inhibited by short oligoarabinosides. LM13 binds preferentially to longer oligoarabinosides, and its binding is highly sensitive to arabinanase action, indicating the recognition of a longer linearized arabinan epitope. In contrast, the binding of LM16 to branched arabinan and to cell walls is increased by arabinofuranosidase action. The presence of all epitopes can be differentially modulated in vitro using glycoside hydrolase family 43 and family 51 arabinofuranosidases. In addition, the LM16 epitope is sensitive to the action of β-galactosidase. Immunofluorescence microscopy indicates that the antibodies can be used to detect epitopes in cell walls, and that the four antibodies reveal complex patterns of epitope occurrence that vary between organs and species, and relate both to the probable processing of arabinan structural elements and the differing mechanical properties of cell walls.
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  • Kaput, J, et al. (author)
  • The case for strategic international alliances to harness nutritional genomics for public and personal health
  • 2005
  • In: The British journal of nutrition. - : Cambridge University Press (CUP). - 0007-1145 .- 1475-2662. ; 94:5, s. 623-632
  • Journal article (peer-reviewed)abstract
    • Nutrigenomics is the study of how constituents of the diet interact with genes, and their products, to alter phenotype and, conversely, how genes and their products metabolise these constituents into nutrients, antinutrients, and bioactive compounds. Results from molecular and genetic epidemiological studies indicate that dietary unbalance can alter gene–nutrient interactions in ways that increase the risk of developing chronic disease. The interplay of human genetic variation and environmental factors will make identifying causative genes and nutrients a formidable, but not intractable, challenge. We provide specific recommendations for how to best meet this challenge and discuss the need for new methodologies and the use of comprehensive analyses of nutrient–genotype interactions involving large and diverse populations. The objective of the present paper is to stimulate discourse and collaboration among nutrigenomic researchers and stakeholders, a process that will lead to an increase in global health and wellness by reducing health disparities in developed and developing countries.
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