Production of intermediate-mass dileptons in relativistic heavy ion collisions

The production of intermediate mass dileptons in ultrarelativistic nuclear collisions at SPS energies is studied. The acceptance and detector resolution inherent to measurements by the NA50 experimental collaboration are accurately modeled. The measured centrality dependence of the intermediate mass lepton pair excess is also addressed.Comment: 9 pages, 8 figures, ReVTe

Integrating Omic Technologies into Aquatic Ecological Risk Assessment and Environmental Monitoring: Hurdles, Achievements, and Future Outlook

Background: In this commentary we present the findings from an international consortium on fish toxicogenomics sponsored by the U.K. Natural Environment Research Council (Fish Toxicogenomics—Moving into Regulation and Monitoring, held 21–23 April 2008 at the Pacific Environmental Science Centre, Vancouver, BC, Canada). Objectives: The consortium from government agencies, academia, and industry addressed three topics: progress in ecotoxicogenomics, regulatory perspectives on roadblocks for practical implementation of toxicogenomics into risk assessment, and dealing with variability in data sets. Discussion: Participants noted that examples of successful application of omic technologies have been identified, but critical studies are needed to relate molecular changes to ecological adverse outcome. Participants made recommendations for the management of technical and biological variation. They also stressed the need for enhanced interdisciplinary training and communication as well as considerable investment into the generation and curation of appropriate reference omic data. Conclusions: The participants concluded that, although there are hurdles to pass on the road to regulatory acceptance, omics technologies are already useful for elucidating modes of action of toxicants and can contribute to the risk assessment process as part of a weight-of-evidence approach

Measurement of prompt hadron production ratios in pppp collisions at s=\sqrt{s} = 0.9 and 7 TeV

The charged-particle production ratios $\bar{p}/p$, $K^-/K^+$, $\pi^-/\pi^+$, $(p + \bar{p})/(\pi^+ + \pi^-)$, $(K^+ + K^-)/(\pi^+ + \pi^-)$ and $(p + \bar{p})/(K^+ + K^-)$ are measured with the LHCb detector using $0.3 {\rm nb^{-1}}$ of $pp$ collisions delivered by the LHC at $\sqrt{s} = 0.9$ TeV and $1.8 {\rm nb^{-1}}$ at $\sqrt{s} = 7$ TeV. The measurements are performed as a function of transverse momentum $p_{\rm T}$ and pseudorapidity $\eta$. The production ratios are compared to the predictions of several Monte Carlo generator settings, none of which are able to describe adequately all observables. The ratio $\bar{p}/p$ is also considered as a function of rapidity loss, $\Delta y \equiv y_{\rm beam} - y$, and is used to constrain models of baryon transport.Comment: Incorrect entries in Table 2 corrected. No consequences for rest of pape

A Nondegenerate Code of Deleterious Variants in Mendelian Loci Contributes to Complex Disease Risk

SummaryAlthough countless highly penetrant variants have been associated with Mendelian disorders, the genetic etiologies underlying complex diseases remain largely unresolved. By mining the medical records of over 110 million patients, we examine the extent to which Mendelian variation contributes to complex disease risk. We detect thousands of associations between Mendelian and complex diseases, revealing a nondegenerate, phenotypic code that links each complex disorder to a unique collection of Mendelian loci. Using genome-wide association results, we demonstrate that common variants associated with complex diseases are enriched in the genes indicated by this “Mendelian code.” Finally, we detect hundreds of comorbidity associations among Mendelian disorders, and we use probabilistic genetic modeling to demonstrate that Mendelian variants likely contribute nonadditively to the risk for a subset of complex diseases. Overall, this study illustrates a complementary approach for mapping complex disease loci and provides unique predictions concerning the etiologies of specific diseases