2,400 research outputs found

    Cost-effective targeting of conservation investments to reduce the northern Gulf of Mexico hypoxic zone

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    A seasonally occurring summer hypoxic (low oxygen) zone in the northern Gulf of Mexico is the second largest in the world. Reductions in nutrients from agricultural cropland in its watershed are needed to reduce the hypoxic zone size to the national policy goal of 5,000 km2 (as a 5-y running average) set by the national Gulf of Mexico Task Force’s Action Plan. We develop an integrated assessment model linking the water quality effects of cropland conservation investment decisions on the more than 550 agricultural subwatersheds that deliver nutrients into the Gulf with a hypoxic zone model. We use this integrated assessment model to identify the most cost-effective subwatersheds to target for cropland conservation investments. We consider targeting of the location (which subwatersheds to treat) and the extent of conservation investment to undertake (how much cropland within a subwatershed to treat). We use process models to simulate the dynamics of the effects of cropland conservation investments on nutrient delivery to the Gulf and use an evolutionary algorithm to solve the optimization problem. Model results suggest that by targeting cropland conservation investments to the most cost-effective location and extent of coverage, the Action Plan goal of 5,000 km2 can be achieved at a cost of 2.7billionannually.Alargesetofcost−hypoxiatradeoffsisdeveloped,rangingfromthebaselinetothenontargetedadoptionofthemostaggressivecroplandconservationinvestmentsinallsubwatersheds(estimatedtoreducethehypoxiczonetolessthan3,000km2atacostof2.7 billion annually. A large set of cost-hypoxia tradeoffs is developed, ranging from the baseline to the nontargeted adoption of the most aggressive cropland conservation investments in all subwatersheds (estimated to reduce the hypoxic zone to less than 3,000 km2 at a cost of 5.6 billion annually)

    The driver landscape of sporadic chordoma.

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    Chordoma is a malignant, often incurable bone tumour showing notochordal differentiation. Here, we defined the somatic driver landscape of 104 cases of sporadic chordoma. We reveal somatic duplications of the notochordal transcription factor brachyury (T) in up to 27% of cases. These variants recapitulate the rearrangement architecture of the pathogenic germline duplications of T that underlie familial chordoma. In addition, we find potentially clinically actionable PI3K signalling mutations in 16% of cases. Intriguingly, one of the most frequently altered genes, mutated exclusively by inactivating mutation, was LYST (10%), which may represent a novel cancer gene in chordoma.Chordoma is a rare often incurable malignant bone tumour. Here, the authors investigate driver mutations of sporadic chordoma in 104 cases, revealing duplications in notochordal transcription factor brachyury (T), PI3K signalling mutations, and mutations in LYST, a potential novel cancer gene in chordoma

    Concert recording 2013-03-28

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    [Track 01]. Fanfares liturgiques. Procession du Vendredi-Saint / Henri Tomasi -- [Track 02]. The good soldier Schweik suite. Overture / Robert Kurka -- [Track 03]. The good soldier Schweik suite. Lament / Robert Kurka -- [Track 04]. The good soldier Schweik suite. March / Robert Kurka -- [Track 05]. The good soldier Schweik suite. War Dance / Robert Kurka -- [Track 06]. The good soldier Schweik suite. Pastoral / Robert Kurka -- [Track 07]. The good soldier Schweik suite. Finale / Robert Kurka -- [Track 08]. Serenade no. 11 in E flat major, KV 375. Allegro maestoso / Wolfgang Amadeus Mozart -- [Track 09]. Prelude, fugue and riffs / Leonard Bernstein

    Understanding Portfolio Efficiency with Conditioning Information *

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    Abstract I develop two new types of portfolio efficiency when returns are predictable. The first type maximizes the unconditional Sharpe ratio of excess returns and differs from unconditional efficiency unless the safe asset return is constant over time. The second type maximizes conditional mean-variance preferences and differs from unconditional efficiency unless, additionally, the maximum conditional Sharpe ratio is constant. Using stock data, I quantify and test their performance differences with respect to unconditionally and fixed-weight efficient returns. I also show the relevance of the two new portfolio strategies to test conditional asset pricing models

    Bigger, Better, Faster, More at the LHC

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    Multijet plus missing energy searches provide universal coverage for theories that have new colored particles that decay into a dark matter candidate and jets. These signals appear at the LHC further out on the missing energy tail than two-to-two scattering indicates. The simplicity of the searches at the LHC contrasts sharply with the Tevatron where more elaborate searches are necessary to separate signal from background. The searches presented in this article effectively distinguish signal from background for any theory where the LSP is a daughter or granddaughter of the pair-produced colored parent particle without ever having to consider missing energies less than 400 GeV.Comment: 26 pages, 8 Figures. Minor textual changes, typos fixed and references adde

    Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

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    Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts
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