| 1. |
- Aaltonen, T., et al.
(författare)
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Combination of Tevatron Searches for the Standard Model Higgs Boson in the W+W- Decay Mode
- 2010
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Ingår i: Physical Review Letters. - 0031-9007 .- 1079-7114. ; 104:6, s. 061802-
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Tidskriftsartikel (refereegranskat)abstract
- We combine searches by the CDF and D0 Collaborations for a Higgs boson decaying to W+W-. The data correspond to an integrated total luminosity of 4.8 (CDF) and 5.4 (D0) fb(-1) of p (p) over bar collisions at root s = 1.96 TeV at the Fermilab Tevatron collider. No excess is observed above background expectation, and resulting limits on Higgs boson production exclude a standard model Higgs boson in the mass range 162-166 GeV at the 95% C.L.
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| 2. |
- Aaltonen, T., et al.
(författare)
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Combination of CDF and D0 measurements of the W boson helicity in top quark decays
- 2012
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Ingår i: Physical Review D. - 1550-7998 .- 1550-2368. ; 85:7, s. 071106-
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Tidskriftsartikel (refereegranskat)abstract
- We report the combination of recent measurements of the helicity of the W boson from top quark decay by the CDF and D0 collaborations, based on data samples corresponding to integrated luminosities of 2.7-5.4 fb(-1) of p (p) over bar collisions collected during Run II of the Fermilab Tevatron collider. Combining measurements that simultaneously determine the fractions of W bosons with longitudinal (f(0)) and right-handed (f(+)) helicities, we find f(0) = 0.722 +/- 0.081[+/- 0.062(stat) +/- 0.052(syst)] and f(+) = -0.033 +/- 0.046[+/- 0.034(stat) +/- 0.031(syst)]. Combining measurements where one of the helicity fractions is fixed to the value expected in the standard model, we find f(0) = 0.682 +/- 0.057[+/- 0.035(stat) +/- 0.046(syst)] for fixed f(+) and f(+) = -0.015 +/- 0.035[+/- 0.018(stat) +/- 0.030(syst)] for fixed f(0). The results are consistent with standard model expectations.
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| 3. |
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| 4. |
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| 5. |
- Gaulton, Kyle J, et al.
(författare)
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Genetic fine mapping and genomic annotation defines causal mechanisms at type 2 diabetes susceptibility loci.
- 2015
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Ingår i: Nature Genetics. - : Springer Science and Business Media LLC. - 1546-1718 .- 1061-4036. ; 47:12, s. 1415-1415
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Tidskriftsartikel (refereegranskat)abstract
- We performed fine mapping of 39 established type 2 diabetes (T2D) loci in 27,206 cases and 57,574 controls of European ancestry. We identified 49 distinct association signals at these loci, including five mapping in or near KCNQ1. 'Credible sets' of the variants most likely to drive each distinct signal mapped predominantly to noncoding sequence, implying that association with T2D is mediated through gene regulation. Credible set variants were enriched for overlap with FOXA2 chromatin immunoprecipitation binding sites in human islet and liver cells, including at MTNR1B, where fine mapping implicated rs10830963 as driving T2D association. We confirmed that the T2D risk allele for this SNP increases FOXA2-bound enhancer activity in islet- and liver-derived cells. We observed allele-specific differences in NEUROD1 binding in islet-derived cells, consistent with evidence that the T2D risk allele increases islet MTNR1B expression. Our study demonstrates how integration of genetic and genomic information can define molecular mechanisms through which variants underlying association signals exert their effects on disease.
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| 6. |
- Evangelou, Evangelos, et al.
(författare)
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Genetic analysis of over 1 million people identifies 535 new loci associated with blood pressure traits.
- 2018
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Ingår i: Nature Genetics. - : Springer Science and Business Media LLC. - 1061-4036 .- 1546-1718. ; 50:10, s. 1412-1425
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Tidskriftsartikel (refereegranskat)abstract
- High blood pressure is a highly heritable and modifiable risk factor for cardiovascular disease. We report the largest genetic association study of blood pressure traits (systolic, diastolic and pulse pressure) to date in over 1 million people of European ancestry. We identify 535 novel blood pressure loci that not only offer new biological insights into blood pressure regulation but also highlight shared genetic architecture between blood pressure and lifestyle exposures. Our findings identify new biological pathways for blood pressure regulation with potential for improved cardiovascular disease prevention in the future.
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| 7. |
- Scott, Robert A., et al.
(författare)
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An Expanded Genome-Wide Association Study of Type 2 Diabetes in Europeans
- 2017
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Ingår i: Diabetes. - : American Diabetes Association. - 0012-1797 .- 1939-327X. ; 66:11, s. 2888-2902
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Tidskriftsartikel (refereegranskat)abstract
- To characterize type 2 diabetes (T2D)-associated variation across the allele frequency spectrum, we conducted a meta-analysis of genome-wide association data from 26,676 T2D case and 132,532 control subjects of European ancestry after imputation using the 1000 Genomes multiethnic reference panel. Promising association signals were followed up in additional data sets (of 14,545 or 7,397 T2D case and 38,994 or 71,604 control subjects). We identified 13 novel T2D-associated loci (P < 5 x 10(-8)), including variants near the GLP2R, GIP, and HLA-DQA1 genes. Our analysis brought the total number of independent T2D associations to 128 distinct signals at 113 loci. Despite substantially increased sample size and more complete coverage of low-frequency variation, all novel associations were driven by common single nucleotide variants. Credible sets of potentially causal variants were generally larger than those based on imputation with earlier reference panels, consistent with resolution of causal signals to common risk haplotypes. Stratification of T2D-associated loci based on T2D-related quantitative trait associations revealed tissue-specific enrichment of regulatory annotations in pancreatic islet enhancers for loci influencing insulin secretion and in adipocytes, monocytes, and hepatocytes for insulin action-associated loci. These findings highlight the predominant role played by common variants of modest effect and the diversity of biological mechanisms influencing T2D pathophysiology.
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| 8. |
- Dalerum, Fredrik, et al.
(författare)
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Exploring the diet of arctic wolves (Canis lupus arctos) at their northern range limit
- 2018
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Ingår i: Canadian Journal of Zoology. - : Canadian Science Publishing. - 0008-4301 .- 1480-3283. ; 96:3, s. 277-281
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Tidskriftsartikel (refereegranskat)abstract
- The grey wolf (Canis lupus Linnaeus, 1758) is one of the most widespread large carnivores on Earth, and occurs throughout the Arctic. Although wolf diet is well studied, we have scant information from high Arctic areas. Global warming is expected to increase the importance of predation for ecosystem regulation in Arctic environments. To improve our ability to manage Arctic ecosystems under environmental change, we therefore need knowledge about Arctic predator diets. Prey remains in 54 wolf scats collected at three sites in the high Arctic region surrounding the Hall Basin (Judge Daly Promontory, Ellesmere Island, Canada, and Washington Land and Hall Land, both in northwestern Greenland) pointed to a dietary importance of arctic hare (Lepus arcticus Ross, 1819; 55% frequency of occurrence) and muskoxen (Ovibos moschatus (Zimmermann, 1780); 39% frequency of occurrence), although we observed diet variation among the sites. A literature compilation suggested that arctic wolves (Canis lupus arctos Pocock, 1935) preferentially feed on caribou (Rangifer tarandus (Linnaeus, 1758)) and muskoxen, but can sustain themselves on arctic hares and Greenland collared lemmings (Dicrostonyx groenlandicus (Traill, 1823)) in areas with limited or no ungulate populations. We suggest that climate change may alter the dynamics among wolves, arctic hare, muskoxen, and caribou, and we encourage further studies evaluating how climate change influences predator-prey interactions in high Arctic environments.
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| 9. |
- Elmqvist, Thomas, et al.
(författare)
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Urban tinkering
- 2018
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Ingår i: Sustainability Science. - : Springer Science and Business Media LLC. - 1862-4065 .- 1862-4057. ; 13:6, s. 1549-1564
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Tidskriftsartikel (refereegranskat)abstract
- Cities are currently experiencing serious, multifaceted impacts from global environmental change, especially climate change, and the degree to which they will need to cope with and adapt to such challenges will continue to increase. A complex systems approach inspired by evolutionary theory can inform strategies for policies and interventions to deal with growing urban vulnerabilities. Such an approach would guide the design of new (and redesign of existing) urban structures, while promoting innovative integration of grey, green and blue infrastructure in service of environmental and health objectives. Moreover, it would contribute to more flexible, effective policies for urban management and the use of urban space. Four decades ago, in a seminal paper in Science, the French evolutionary biologist and philosopher Francois Jacob noted that evolution differs significantly in its characteristic modes of action from processes that are designed and engineered de novo (Jacob in Science 196(4295):1161-1166, 1977). He labeled the evolutionary process tinkering, recognizing its foundation in the modification and molding of existing traits and forms, with occasional dramatic shifts in function in the context of changing conditions. This contrasts greatly with conventional engineering and design approaches that apply tailor-made materials and tools to achieve well-defined functions that are specified a priori. We here propose that urban tinkering is the application of evolutionary thinking to urban design, engineering, ecological restoration, management and governance. We define urban tinkering as:A mode of operation, encompassing policy, planning and management processes, that seeks to transform the use of existing and design of new urban systems in ways that diversify their functions, anticipate new uses and enhance adaptability, to better meet the social, economic and ecological needs of cities under conditions of deep uncertainty about the future.This approach has the potential to substantially complement and augment conventional urban development, replacing predictability, linearity and monofunctional design with anticipation of uncertainty and non-linearity and design for multiple, potentially shifting functions. Urban tinkering can function by promoting a diversity of small-scale urban experiments that, in aggregate, lead to large-scale often playful innovative solutions to the problems of sustainable development. Moreover, the tinkering approach is naturally suited to exploring multi-functional uses and approaches (e.g., bricolage) for new and existing urban structures and policies through collaborative engagement and analysis. It is thus well worth exploring as a means of delivering co-benefits for environment and human health and wellbeing. Indeed, urban tinkering has close ties to systems approaches, which often are recognized as critical to sustainable development. We believe this concept can help forge much-closer, much-needed ties among engineers, architects, evolutionary ecologists, health specialists, and numerous other urban stakeholders in developing innovative, widely beneficial solutions for society and contribute to successful implementation of SDG11 and the New Urban Agenda.
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| 10. |
- Waara, Erik R., et al.
(författare)
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Entrapping Digestive Enzymes with Engineered Mesoporous Silica Particles Reduces Metabolic Risk Factors in Humans
- 2020
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Ingår i: Advanced Healthcare Materials. - : Wiley. - 2192-2640 .- 2192-2659. ; 9:11
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Tidskriftsartikel (refereegranskat)abstract
- Engineered mesoporous silica particles (MSP) are thermally and chemically stable porous materials composed of pure silica and have attracted attention for their potential biomedical applications. Oral intake of engineered MSP is shown to reduce body weight and adipose tissue in mice. Here, clinical data from a first-in-humans study in ten healthy individuals with obesity are reported, demonstrating a reduction in glycated hemoglobin (HbA1c) and low-density lipoprotein cholesterol, which are well-established metabolic and cardiovascular risk factors. In vitro investigations demonstrate sequestration of pancreatic alpha-amylase and lipase in an MSP pore-size dependent manner. Subsequent ex vivo experiments in conditions mimicking intestinal conditions and in vivo experiments in mice show a decrease in enzyme activity upon exposure to the engineered MSP, presumably by the same mechanism. Therefore, it is suggested that tailored MSP act by lowering the digestive enzyme availability in the small intestine, resulting in decreased digestion of macronutrient and leading to reduced caloric uptake. This novel MSP based mechanism-of-action, combined with its excellent safety in man, makes it a promising future agent for prevention and treatment of metabolic diseases.
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