60 research outputs found

    Overestimating Resource Value and Its Effects on Fighting Decisions

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    Much work in behavioral ecology has shown that animals fight over resources such as food, and that they make strategic decisions about when to engage in such fights. Here, we examine the evolution of one, heretofore unexamined, component of that strategic decision about whether to fight for a resource. We present the results of a computer simulation that examined the evolution of over- or underestimating the value of a resource (food) as a function of an individual's current hunger level. In our model, animals fought for food when they perceived their current food level to be below the mean for the environment. We considered seven strategies for estimating food value: 1) always underestimate food value, 2) always overestimate food value, 3) never over- or underestimate food value, 4) overestimate food value when hungry, 5) underestimate food value when hungry, 6) overestimate food value when relatively satiated, and 7) underestimate food value when relatively satiated. We first competed all seven strategies against each other when they began at approximately equal frequencies. In such a competition, two strategies–“always overestimate food value,” and “overestimate food value when hungry”–were very successful. We next competed each of these strategies against the default strategy of “never over- or underestimate,” when the default strategy was set at 99% of the population. Again, the strategies of “always overestimate food value” and “overestimate food value when hungry” fared well. Our results suggest that overestimating food value when deciding whether to fight should be favored by natural selection

    Cheating on the Edge

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    We present the results of an individual agent-based model of antibiotic resistance in bacteria. Our model examines antibiotic resistance when two strategies exist: “producers”–who secrete a substance that breaks down antibiotics–and nonproducers (“cheats”) who do not secrete, or carry the machinery associated with secretion. The model allows for populations of up to 10,000, in which bacteria are affected by their nearest neighbors, and we assume cheaters die when there are no producers in their neighborhood. Each of 10,000 slots on our grid (a torus) could be occupied by a producer or a nonproducer, or could (temporarily) be unoccupied. The most surprising and dramatic result we uncovered is that when producers and nonproducers coexist at equilibrium, nonproducers are almost always found on the edges of clusters of producers

    Genetic variants in novel pathways influence blood pressure and cardiovascular disease risk.

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    Blood pressure is a heritable trait influenced by several biological pathways and responsive to environmental stimuli. Over one billion people worldwide have hypertension (≥140 mm Hg systolic blood pressure or  ≥90 mm Hg diastolic blood pressure). Even small increments in blood pressure are associated with an increased risk of cardiovascular events. This genome-wide association study of systolic and diastolic blood pressure, which used a multi-stage design in 200,000 individuals of European descent, identified sixteen novel loci: six of these loci contain genes previously known or suspected to regulate blood pressure (GUCY1A3-GUCY1B3, NPR3-C5orf23, ADM, FURIN-FES, GOSR2, GNAS-EDN3); the other ten provide new clues to blood pressure physiology. A genetic risk score based on 29 genome-wide significant variants was associated with hypertension, left ventricular wall thickness, stroke and coronary artery disease, but not kidney disease or kidney function. We also observed associations with blood pressure in East Asian, South Asian and African ancestry individuals. Our findings provide new insights into the genetics and biology of blood pressure, and suggest potential novel therapeutic pathways for cardiovascular disease prevention

    Genome-wide association study identifies six new loci influencing pulse pressure and mean arterial pressure.

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    Numerous genetic loci have been associated with systolic blood pressure (SBP) and diastolic blood pressure (DBP) in Europeans. We now report genome-wide association studies of pulse pressure (PP) and mean arterial pressure (MAP). In discovery (N = 74,064) and follow-up studies (N = 48,607), we identified at genome-wide significance (P = 2.7 × 10(-8) to P = 2.3 × 10(-13)) four new PP loci (at 4q12 near CHIC2, 7q22.3 near PIK3CG, 8q24.12 in NOV and 11q24.3 near ADAMTS8), two new MAP loci (3p21.31 in MAP4 and 10q25.3 near ADRB1) and one locus associated with both of these traits (2q24.3 near FIGN) that has also recently been associated with SBP in east Asians. For three of the new PP loci, the estimated effect for SBP was opposite of that for DBP, in contrast to the majority of common SBP- and DBP-associated variants, which show concordant effects on both traits. These findings suggest new genetic pathways underlying blood pressure variation, some of which may differentially influence SBP and DBP

    Genetic associations at 53 loci highlight cell types and biological pathways relevant for kidney function.

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    Reduced glomerular filtration rate defines chronic kidney disease and is associated with cardiovascular and all-cause mortality. We conducted a meta-analysis of genome-wide association studies for estimated glomerular filtration rate (eGFR), combining data across 133,413 individuals with replication in up to 42,166 individuals. We identify 24 new and confirm 29 previously identified loci. Of these 53 loci, 19 associate with eGFR among individuals with diabetes. Using bioinformatics, we show that identified genes at eGFR loci are enriched for expression in kidney tissues and in pathways relevant for kidney development and transmembrane transporter activity, kidney structure, and regulation of glucose metabolism. Chromatin state mapping and DNase I hypersensitivity analyses across adult tissues demonstrate preferential mapping of associated variants to regulatory regions in kidney but not extra-renal tissues. These findings suggest that genetic determinants of eGFR are mediated largely through direct effects within the kidney and highlight important cell types and biological pathways

    Health Reform: What Will It Take To Pass?

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