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Showing papers by "Boston University published in 2012"


Journal ArticleDOI
Rafael Lozano1, Mohsen Naghavi1, Kyle J Foreman2, Stephen S Lim1  +192 moreInstitutions (95)
TL;DR: The Global Burden of Diseases, Injuries, and Risk Factors Study 2010 aimed to estimate annual deaths for the world and 21 regions between 1980 and 2010 for 235 causes, with uncertainty intervals (UIs), separately by age and sex, using the Cause of Death Ensemble model.

11,809 citations


Journal ArticleDOI
Georges Aad1, T. Abajyan2, Brad Abbott3, Jalal Abdallah4  +2964 moreInstitutions (200)
TL;DR: In this article, a search for the Standard Model Higgs boson in proton-proton collisions with the ATLAS detector at the LHC is presented, which has a significance of 5.9 standard deviations, corresponding to a background fluctuation probability of 1.7×10−9.

9,282 citations


Journal ArticleDOI
TL;DR: In this paper, results from searches for the standard model Higgs boson in proton-proton collisions at 7 and 8 TeV in the CMS experiment at the LHC, using data samples corresponding to integrated luminosities of up to 5.8 standard deviations.

8,857 citations


Journal ArticleDOI
Theo Vos, Abraham D. Flaxman1, Mohsen Naghavi1, Rafael Lozano1  +360 moreInstitutions (143)
TL;DR: Prevalence and severity of health loss were weakly correlated and age-specific prevalence of YLDs increased with age in all regions and has decreased slightly from 1990 to 2010, but population growth and ageing have increased YLD numbers and crude rates over the past two decades.

7,021 citations


Journal ArticleDOI
Christopher J L Murray1, Theo Vos2, Rafael Lozano1, Mohsen Naghavi1  +366 moreInstitutions (141)
TL;DR: The results for 1990 and 2010 supersede all previously published Global Burden of Disease results and highlight the importance of understanding local burden of disease and setting goals and targets for the post-2015 agenda taking such patterns into account.

6,861 citations


Journal ArticleDOI
Kaoru Hagiwara, Ken Ichi Hikasa1, Koji Nakamura, Masaharu Tanabashi1, M. Aguilar-Benitez, Claude Amsler2, R. M. Barnett3, P. R. Burchat4, C. D. Carone5, C. Caso6, G. Conforto7, Olav Dahl3, Michael Doser8, Semen Eidelman9, Jonathan L. Feng10, L. K. Gibbons11, M. C. Goodman12, Christoph Grab13, D. E. Groom3, Atul Gurtu8, Atul Gurtu14, K. G. Hayes15, J.J. Hernández-Rey16, K. Honscheid17, Christopher Kolda18, Michelangelo L. Mangano8, D. M. Manley19, Aneesh V. Manohar20, John March-Russell8, Alberto Masoni, Ramon Miquel3, Klaus Mönig, Hitoshi Murayama3, Hitoshi Murayama21, S. Sánchez Navas13, Keith A. Olive22, Luc Pape8, C. Patrignani6, A. Piepke23, Matts Roos24, John Terning25, Nils A. Tornqvist24, T. G. Trippe3, Petr Vogel26, C. G. Wohl3, Ron L. Workman27, W-M. Yao3, B. Armstrong3, P. S. Gee3, K. S. Lugovsky, S. B. Lugovsky, V. S. Lugovsky, Marina Artuso28, D. Asner29, K. S. Babu30, E. L. Barberio8, Marco Battaglia8, H. Bichsel31, O. Biebel32, P. Bloch8, Robert N. Cahn3, Ariella Cattai8, R.S. Chivukula33, R. Cousins34, G. A. Cowan35, Thibault Damour36, K. Desler, R. J. Donahue3, D. A. Edwards, Victor Daniel Elvira37, Jens Erler38, V. V. Ezhela, A Fassò8, W. Fetscher13, Brian D. Fields39, B. Foster40, Daniel Froidevaux8, Masataka Fukugita41, Thomas K. Gaisser42, L. A. Garren37, H J Gerber13, Frederick J. Gilman43, Howard E. Haber44, C. A. Hagmann29, J.L. Hewett4, Ian Hinchliffe3, Craig J. Hogan31, G. Höhler45, P. Igo-Kemenes46, John David Jackson3, Kurtis F Johnson47, D. Karlen48, B. Kayser37, S. R. Klein3, Konrad Kleinknecht49, I.G. Knowles50, P. Kreitz4, Yu V. Kuyanov, R. Landua8, Paul Langacker38, L. S. Littenberg51, Alan D. Martin52, Tatsuya Nakada53, Tatsuya Nakada8, Meenakshi Narain33, Paolo Nason, John A. Peacock54, H. R. Quinn55, Stuart Raby17, Georg G. Raffelt32, E. A. Razuvaev, B. Renk49, L. Rolandi8, Michael T Ronan3, L.J. Rosenberg54, C.T. Sachrajda55, A. I. Sanda56, Subir Sarkar57, Michael Schmitt58, O. Schneider53, Douglas Scott59, W. G. Seligman60, M. H. Shaevitz60, Torbjörn Sjöstrand61, George F. Smoot3, Stefan M Spanier4, H. Spieler3, N. J. C. Spooner62, Mark Srednicki63, Achim Stahl, Todor Stanev42, M. Suzuki3, N. P. Tkachenko, German Valencia64, K. van Bibber29, Manuella Vincter65, D. R. Ward66, Bryan R. Webber66, M R Whalley52, Lincoln Wolfenstein43, J. Womersley37, C. L. Woody51, Oleg Zenin 
Tohoku University1, University of Zurich2, Lawrence Berkeley National Laboratory3, Stanford University4, College of William & Mary5, University of Genoa6, University of Urbino7, CERN8, Budker Institute of Nuclear Physics9, University of California, Irvine10, Cornell University11, Argonne National Laboratory12, ETH Zurich13, Tata Institute of Fundamental Research14, Hillsdale College15, Spanish National Research Council16, Ohio State University17, University of Notre Dame18, Kent State University19, University of California, San Diego20, University of California, Berkeley21, University of Minnesota22, University of Alabama23, University of Helsinki24, Los Alamos National Laboratory25, California Institute of Technology26, George Washington University27, Syracuse University28, Lawrence Livermore National Laboratory29, Oklahoma State University–Stillwater30, University of Washington31, Max Planck Society32, Boston University33, University of California, Los Angeles34, Royal Holloway, University of London35, Université Paris-Saclay36, Fermilab37, University of Pennsylvania38, University of Illinois at Urbana–Champaign39, University of Bristol40, University of Tokyo41, University of Delaware42, Carnegie Mellon University43, University of California, Santa Cruz44, Karlsruhe Institute of Technology45, Heidelberg University46, Florida State University47, Carleton University48, University of Mainz49, University of Edinburgh50, Brookhaven National Laboratory51, Durham University52, University of Lausanne53, Massachusetts Institute of Technology54, University of Southampton55, Nagoya University56, University of Oxford57, Northwestern University58, University of British Columbia59, Columbia University60, Lund University61, University of Sheffield62, University of California, Santa Barbara63, Iowa State University64, University of Alberta65, University of Cambridge66
TL;DR: The Particle Data Group's biennial review as mentioned in this paper summarizes much of particle physics, using data from previous editions, plus 2658 new measurements from 644 papers, and lists, evaluates, and average measured properties of gauge bosons, leptons, quarks, mesons, and baryons.
Abstract: This biennial Review summarizes much of particle physics. Using data from previous editions, plus 2658 new measurements from 644 papers, we list, evaluate, and average measured properties of gauge bosons, leptons, quarks, mesons, and baryons. We summarize searches for hypothetical particles such as Higgs bosons, heavy neutrinos, and supersymmetric particles. All the particle properties and search limits are listed in Summary Tables. We also give numerous tables, figures, formulae, and reviews of topics such as the Standard Model, particle detectors, probability, and statistics. Among the 112 reviews are many that are new or heavily revised including those on Heavy-Quark and Soft-Collinear Effective Theory, Neutrino Cross Section Measurements, Monte Carlo Event Generators, Lattice QCD, Heavy Quarkonium Spectroscopy, Top Quark, Dark Matter, V-cb & V-ub, Quantum Chromodynamics, High-Energy Collider Parameters, Astrophysical Constants, Cosmological Parameters, and Dark Matter. A booklet is available containing the Summary Tables and abbreviated versions of some of the other sections of this full Review. All tables, listings, and reviews (and errata) are also available on the Particle Data Group website: http://pdg.lbl.gov.

4,465 citations


Journal ArticleDOI
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Abstract: In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field.

4,316 citations


Journal ArticleDOI
TL;DR: The sva package is described, which supports surrogate variable estimation with the sva function, direct adjustment for known batch effects with the ComBat function and adjustment for batch and latent variables in prediction problems with the fsva function.
Abstract: Summary: Heterogeneity and latent variables are now widely recognized as major sources of bias and variability in high-throughput experiments. The most well-known source of latent variation in genomic experiments are batch effects—when samples are processed on different days, in different groups or by different people. However, there are also a large number of other variables that may have a major impact on high-throughput measurements. Here we describe the sva package for identifying, estimating and removing unwanted sources of variation in high-throughput experiments. The sva package supports surrogate variable estimation with the sva function, direct adjustment for known batch effects with the ComBat function and adjustment for batch and latent variables in prediction problems with the fsva function. Availability: The R package sva is freely available from http://www.bioconductor.org. Contact: jleek@jhsph.edu Supplementary information:Supplementary data are available at Bioinformatics online.

3,343 citations


Journal ArticleDOI
TL;DR: S spatially explicit probabilistic forecasts of global urban land-cover change are developed and the direct impacts on biodiversity hotspots and tropical carbon biomass are explored to minimize global biodiversity and vegetation carbon losses.
Abstract: Urban land-cover change threatens biodiversity and affects ecosystem productivity through loss of habitat, biomass, and carbon storage. However, despite projections that world urban populations will increase to nearly 5 billion by 2030, little is known about future locations, magnitudes, and rates of urban expansion. Here we develop spatially explicit probabilistic forecasts of global urban land-cover change and explore the direct impacts on biodiversity hotspots and tropical carbon biomass. If current trends in population density continue and all areas with high probabilities of urban expansion undergo change, then by 2030, urban land cover will increase by 1.2 million km2, nearly tripling the global urban land area circa 2000. This increase would result in considerable loss of habitats in key biodiversity hotspots, with the highest rates of forecasted urban growth to take place in regions that were relatively undisturbed by urban development in 2000: the Eastern Afromontane, the Guinean Forests of West Africa, and the Western Ghats and Sri Lanka hotspots. Within the pan-tropics, loss in vegetation biomass from areas with high probability of urban expansion is estimated to be 1.38 PgC (0.05 PgC yr−1), equal to ∼5% of emissions from tropical deforestation and land-use change. Although urbanization is often considered a local issue, the aggregate global impacts of projected urban expansion will require significant policy changes to affect future growth trajectories to minimize global biodiversity and vegetation carbon losses.

2,681 citations


Journal ArticleDOI
TL;DR: The evidence-base of CBT is very strong and the strongest support exists for CBT of anxiety disorders, somatoform disorders, bulimia, anger control problems, and general stress.
Abstract: Cognitive behavioral therapy (CBT) refers to a popular therapeutic approach that has been applied to a variety of problems. The goal of this review was to provide a comprehensive survey of meta-analyses examining the efficacy of CBT. We identified 269 meta-analytic studies and reviewed of those a representative sample of 106 meta-analyses examining CBT for the following problems: substance use disorder, schizophrenia and other psychotic disorders, depression and dysthymia, bipolar disorder, anxiety disorders, somatoform disorders, eating disorders, insomnia, personality disorders, anger and aggression, criminal behaviors, general stress, distress due to general medical conditions, chronic pain and fatigue, distress related to pregnancy complications and female hormonal conditions. Additional meta-analytic reviews examined the efficacy of CBT for various problems in children and elderly adults. The strongest support exists for CBT of anxiety disorders, somatoform disorders, bulimia, anger control problems, and general stress. Eleven studies compared response rates between CBT and other treatments or control conditions. CBT showed higher response rates than the comparison conditions in seven of these reviews and only one review reported that CBT had lower response rates than comparison treatments. In general, the evidence-base of CBT is very strong. However, additional research is needed to examine the efficacy of CBT for randomized-controlled studies. Moreover, except for children and elderly populations, no meta-analytic studies of CBT have been reported on specific subgroups, such as ethnic minorities and low income samples.

2,107 citations


01 Dec 2012
TL;DR: In this paper, the authors develop spatially explicit probabilistic forecasts of global urban land-cover change and explore the direct impacts on biodiversity hotspots and tropical carbon biomass, showing that urban land cover change threatens biodiversity and affects ecosystem productivity through loss of habitat, biomass, and carbon storage.
Abstract: Urban land-cover change threatens biodiversity and affects ecosystem productivity through loss of habitat, biomass, and carbon storage. However, despite projections that world urban populations will increase to nearly 5 billion by 2030, little is known about future locations, magnitudes, and rates of urban expansion. Here we develop spatially explicit probabilistic forecasts of global urban land-cover change and explore the direct impacts on biodiversity hotspots and tropical carbon biomass. If current trends in population density continue and all areas with high probabilities of urban expansion undergo change, then by 2030, urban land cover will increase by 1.2 million km2, nearly tripling the global urban land area circa 2000. This increase would result in considerable loss of habitats in key biodiversity hotspots, with the highest rates of forecasted urban growth to take place in regions that were relatively undisturbed by urban development in 2000: the Eastern Afromontane, the Guinean Forests of West Africa, and the Western Ghats and Sri Lanka hotspots. Within the pan-tropics, loss in vegetation biomass from areas with high probability of urban expansion is estimated to be 1.38 PgC (0.05 PgC yr−1), equal to ∼5% of emissions from tropical deforestation and land-use change. Although urbanization is often considered a local issue, the aggregate global impacts of projected urban expansion will require significant policy changes to affect future growth trajectories to minimize global biodiversity and vegetation carbon losses.

Journal ArticleDOI
TL;DR: This article conducted a meta-analysis of genetic variants on the Metabochip, including 34,840 cases and 114,981 controls, overwhelmingly of European descent, and identified ten previously unreported T2D susceptibility loci, including two showing sex-differentiated association.
Abstract: To extend understanding of the genetic architecture and molecular basis of type 2 diabetes (T2D), we conducted a meta-analysis of genetic variants on the Metabochip, including 34,840 cases and 114,981 controls, overwhelmingly of European descent. We identified ten previously unreported T2D susceptibility loci, including two showing sex-differentiated association. Genome-wide analyses of these data are consistent with a long tail of additional common variant loci explaining much of the variation in susceptibility to T2D. Exploration of the enlarged set of susceptibility loci implicates several processes, including CREBBP-related transcription, adipocytokine signaling and cell cycle regulation, in diabetes pathogenesis.

Journal ArticleDOI
Benjamin F. Voight1, Benjamin F. Voight2, Benjamin F. Voight3, Gina M. Peloso4, Gina M. Peloso5, Marju Orho-Melander6, Ruth Frikke-Schmidt7, Maja Barbalić8, Majken K. Jensen3, George Hindy6, Hilma Holm9, Eric L. Ding3, Toby Johnson10, Heribert Schunkert11, Nilesh J. Samani12, Nilesh J. Samani13, Robert Clarke14, Jemma C. Hopewell14, John F. Thompson12, Mingyao Li1, Gudmar Thorleifsson9, Christopher Newton-Cheh, Kiran Musunuru3, Kiran Musunuru2, James P. Pirruccello2, James P. Pirruccello3, Danish Saleheen15, Li Chen16, Alexandre F.R. Stewart16, Arne Schillert11, Unnur Thorsteinsdottir9, Unnur Thorsteinsdottir17, Gudmundur Thorgeirsson17, Sonia S. Anand18, James C. Engert19, Thomas M. Morgan20, John A. Spertus21, Monika Stoll22, Klaus Berger22, Nicola Martinelli23, Domenico Girelli23, Pascal P. McKeown24, Christopher Patterson24, Stephen E. Epstein25, Joseph M. Devaney25, Mary Susan Burnett25, Vincent Mooser26, Samuli Ripatti27, Ida Surakka27, Markku S. Nieminen27, Juha Sinisalo27, Marja-Liisa Lokki27, Markus Perola5, Aki S. Havulinna5, Ulf de Faire28, Bruna Gigante28, Erik Ingelsson28, Tanja Zeller29, Philipp S. Wild29, Paul I.W. de Bakker, Olaf H. Klungel30, Anke-Hilse Maitland-van der Zee30, Bas J M Peters30, Anthonius de Boer30, Diederick E. Grobbee30, Pieter Willem Kamphuisen31, Vera H.M. Deneer, Clara C. Elbers30, N. Charlotte Onland-Moret30, Marten H. Hofker31, Cisca Wijmenga31, W. M. Monique Verschuren, Jolanda M. A. Boer, Yvonne T. van der Schouw30, Asif Rasheed, Philippe M. Frossard, Serkalem Demissie4, Serkalem Demissie5, Cristen J. Willer32, Ron Do3, Jose M. Ordovas33, Jose M. Ordovas34, Gonçalo R. Abecasis32, Michael Boehnke32, Karen L. Mohlke35, Mark J. Daly3, Mark J. Daly2, Candace Guiducci2, Noël P. Burtt2, Aarti Surti2, Elena Gonzalez2, Shaun Purcell3, Shaun Purcell2, Stacey Gabriel2, Jaume Marrugat, John F. Peden14, Jeanette Erdmann11, Patrick Diemert11, Christina Willenborg11, Inke R. König11, Marcus Fischer36, Christian Hengstenberg36, Andreas Ziegler11, Ian Buysschaert37, Diether Lambrechts37, Frans Van de Werf37, Keith A.A. Fox38, Nour Eddine El Mokhtari39, Diana Rubin, Jürgen Schrezenmeir, Stefan Schreiber39, Arne Schäfer39, John Danesh15, Stefan Blankenberg29, Robert Roberts16, Ruth McPherson16, Hugh Watkins14, Alistair S. Hall40, Kim Overvad41, Eric B. Rimm3, Eric Boerwinkle8, Anne Tybjærg-Hansen7, L. Adrienne Cupples5, L. Adrienne Cupples4, Muredach P. Reilly1, Olle Melander6, Pier Mannuccio Mannucci42, Diego Ardissino, David S. Siscovick43, Roberto Elosua, Kari Stefansson9, Kari Stefansson17, Christopher J. O'Donnell5, Christopher J. O'Donnell3, Veikko Salomaa5, Daniel J. Rader1, Leena Peltonen44, Leena Peltonen27, Stephen M. Schwartz43, David Altshuler, Sekar Kathiresan 
11 Aug 2012
TL;DR: In this paper, a Mendelian randomisation analysis was performed to compare the effect of HDL cholesterol, LDL cholesterol, and genetic score on risk of myocardial infarction.
Abstract: Methods We performed two mendelian randomisation analyses. First, we used as an instrument a single nucleotide polymorphism (SNP) in the endothelial lipase gene (LIPG Asn396Ser) and tested this SNP in 20 studies (20 913 myocardial infarction cases, 95 407 controls). Second, we used as an instrument a genetic score consisting of 14 common SNPs that exclusively associate with HDL cholesterol and tested this score in up to 12 482 cases of myocardial infarction and 41 331 controls. As a positive control, we also tested a genetic score of 13 common SNPs exclusively associated with LDL cholesterol. – ¹³) but similar levels of other lipid and non-lipid risk factors for myocardial infarction compared with noncarriers. This diff erence in HDL cholesterol is expected to decrease risk of myocardial infarction by 13% (odds ratio [OR] 0·87, 95% CI 0·84–0·91). However, we noted that the 396Ser allele was not associated with risk of myocardial infarction (OR 0·99, 95% CI 0·88–1·11, p=0·85). From observational epidemiology, an increase of 1 SD in HDL cholesterol was associated with reduced risk of myocardial infarction (OR 0·62, 95% CI 0·58–0·66). However, a 1 SD increase in HDL cholesterol due to genetic score was not associated with risk of myocardial infarction (OR 0·93, 95% CI 0·68–1·26, p=0·63). For LDL cholesterol, the estimate from observational epidemiology (a 1 SD increase in LDL cholesterol associated with OR 1·54, 95% CI 1·45–1·63) was concordant with that from genetic score (OR 2·13, 95% CI 1·69–2·69, p=2×10

Journal ArticleDOI
05 Jul 2012-Nature
TL;DR: Using infrared nano-imaging, it is shown that common graphene/SiO2/Si back-gated structures support propagating surface plasmons and changes both the amplitude and the wavelength are altered by varying the gate voltage.
Abstract: Surface plasmons are collective oscillations of electrons in metals or semiconductors that enable confinement and control of electromagnetic energy at subwavelength scales. Rapid progress in plasmonics has largely relied on advances in device nano-fabrication, whereas less attention has been paid to the tunable properties of plasmonic media. One such medium--graphene--is amenable to convenient tuning of its electronic and optical properties by varying the applied voltage. Here, using infrared nano-imaging, we show that common graphene/SiO(2)/Si back-gated structures support propagating surface plasmons. The wavelength of graphene plasmons is of the order of 200 nanometres at technologically relevant infrared frequencies, and they can propagate several times this distance. We have succeeded in altering both the amplitude and the wavelength of these plasmons by varying the gate voltage. Using plasmon interferometry, we investigated losses in graphene by exploring real-space profiles of plasmon standing waves formed between the tip of our nano-probe and the edges of the samples. Plasmon dissipation quantified through this analysis is linked to the exotic electrodynamics of graphene. Standard plasmonic figures of merit of our tunable graphene devices surpass those of common metal-based structures.

Journal ArticleDOI
TL;DR: In this paper, the authors presented the first spectroscopic data from the Baryon Oscillation Spectroscopic Survey (BOSS) for the Sloan Digital Sky Survey III (SDSS-III) dataset.
Abstract: The Sloan Digital Sky Survey III (SDSS-III) presents the first spectroscopic data from the Baryon Oscillation Spectroscopic Survey (BOSS). This ninth data release (DR9) of the SDSS project includes 535,995 new galaxy spectra (median z ~ 0.52), 102,100 new quasar spectra (median z ~ 2.32), and 90,897 new stellar spectra, along with the data presented in previous data releases. These spectra were obtained with the new BOSS spectrograph and were taken between 2009 December and 2011 July. In addition, the stellar parameters pipeline, which determines radial velocities, surface temperatures, surface gravities, and metallicities of stars, has been updated and refined with improvements in temperature estimates for stars with T eff -0.5. DR9 includes new stellar parameters for all stars presented in DR8, including stars from SDSS-I and II, as well as those observed as part of the SEGUE-2. The astrometry error introduced in the DR8 imaging catalogs has been corrected in the DR9 data products. The next data release for SDSS-III will be in Summer 2013, which will present the first data from the APOGEE along with another year of data from BOSS, followed by the final SDSS-III data release in 2014 December.

Journal ArticleDOI
TL;DR: The goal is development of a cloud and cloud shadow detection algorithm suitable for routine usage with Landsat images and as high as 96.4%.

Journal ArticleDOI
TL;DR: Evidence from many independent research centers strongly supports the existence of a specific disease, as defined by the presence of A&bgr; plaques and neurofibrillary tangles.
Abstract: Clinicopathologic correlation studies are critically important for the field of Alzheimer disease (AD) research. Studies on human subjects with autopsy confirmation entail numerous potential biases that affect both their general applicability and the validity of the correlations. Many sources of data variability can weaken the apparent correlation between cognitive status and AD neuropathologic changes. Indeed, most persons in advanced old age have significant non-AD brain lesions that may alter cognition independently of AD. Worldwide research efforts have evaluated thousands of human subjects to assess the causes of cognitive impairment in the elderly, and these studies have been interpreted in different ways. We review the literature focusing on the correlation of AD neuropathologic changes (i.e. β-amyloid plaques and neurofibrillary tangles) with cognitive impairment. We discuss the various patterns of brain changes that have been observed in elderly individuals to provide a perspective for understanding AD clinicopathologic correlation and conclude that evidence from many independent research centers strongly supports the existence of a specific disease, as defined by the presence of Aβ plaques and neurofibrillary tangles. Although Aβ plaques may play a key role in AD pathogenesis, the severity of cognitive impairment correlates best with the burden of neocortical neurofibrillary tangles.

Journal ArticleDOI
TL;DR: In this paper, the authors examined the relationship between credit spreads and economic activity, by constructing a credit spread index based on an extensive data set of prices of outstanding corporate bonds trading in the secondary market and found that the predictive content of credit spreads for economic activity is due primarily to movements in the excess bond premium.
Abstract: We re-examine the evidence on the relationship between credit spreads and economic activity, by constructing a credit spread index based on an extensive data set of prices of outstanding corporate bonds trading in the secondary market. Compared with the standard default-risk indicators, our credit spread index is a robust predictor of economic activity at both the short- and longer-term horizons. Using an empirical framework, we decompose the index into a predictable component that captures the available firm-specific information on expected defaults and a residual component—the excess bond premium—which we argue likely reflects variation in the price of default risk rather than variation in the risk of default. Our results indicate that the predictive content of credit spreads for economic activity is due primarily to movements in the excess bond premium. Innovations in the excess bond premium that are orthogonal to the current state of the economy are shown to lead to significant declines in economic activity and equity prices. We also show that a deterioration in the creditworthiness of broker-dealers—key financial intermediaries in the corporate cash market—causes an increase in the excess bond premium. These findings support the notion that a rise in the excess bond premium represents a reduction in the e!ective risk-bearing capacity of the financial sector and, as a result, a contraction in the supply of credit with significant adverse consequences for the macroeconomy.

Journal ArticleDOI
TL;DR: Methods for preventing missing data and, failing that, dealing with data that are missing in clinical trials are reviewed.
Abstract: Missing data in clinical trials can have a major effect on the validity of the inferences that can be drawn from the trial. This article reviews methods for preventing missing data and, failing that, dealing with data that are missing.

Journal ArticleDOI
TL;DR: In this paper, the authors provided the most detailed estimate of the carbon density of vegetation and associated carbon dioxide emissions from deforestation for ecosystems across the tropics across the world, including tropical rainforests.
Abstract: Deforestation contributes 6–17% of anthropogenic carbon dioxide emissions. However, much uncertainty in the calculation of deforestation emissions stems from the inadequacy of forest carbon-density and deforestation data. Now an analysis provides the most-detailed estimate so far of the carbon density of vegetation and the associated carbon dioxide emissions from deforestation for ecosystems across the tropics.

Journal ArticleDOI
TL;DR: In this paper, the authors performed a comprehensive blind assessment of over 30 network inference methods on Escherichia coli, Staphylococcus aureus, Saccharomyces cerevisiae and in silico microarray data.
Abstract: Reconstructing gene regulatory networks from high-throughput data is a long-standing challenge. Through the Dialogue on Reverse Engineering Assessment and Methods (DREAM) project, we performed a comprehensive blind assessment of over 30 network inference methods on Escherichia coli, Staphylococcus aureus, Saccharomyces cerevisiae and in silico microarray data. We characterize the performance, data requirements and inherent biases of different inference approaches, and we provide guidelines for algorithm application and development. We observed that no single inference method performs optimally across all data sets. In contrast, integration of predictions from multiple inference methods shows robust and high performance across diverse data sets. We thereby constructed high-confidence networks for E. coli and S. aureus, each comprising ~1,700 transcriptional interactions at a precision of ~50%. We experimentally tested 53 previously unobserved regulatory interactions in E. coli, of which 23 (43%) were supported. Our results establish community-based methods as a powerful and robust tool for the inference of transcriptional gene regulatory networks.

Journal ArticleDOI
01 Feb 2012-Chest
TL;DR: There is a large amount of evidence on laboratory and clinical characteristics of vitamin K antagonists and a growing body of evidence is becoming available on the first new oral anticoagulant drugs available for clinical use, dabigatran and rivaroxaban.


Journal ArticleDOI
TL;DR: This Review attempts to present the current state of understanding of post-traumatic stress disorder on the basis of psychophysiological, structural and functional neuroimaging, and endocrinological, genetic and molecular biological studies in humans and in animal models.
Abstract: Post-traumatic stress disorder (PTSD) is the only major mental disorder for which a cause is considered to be known: that is, an event that involves threat to the physical integrity of oneself or others and induces a response of intense fear, helplessness or horror. Although PTSD is still largely regarded as a psychological phenomenon, over the past three decades the growth of the biological PTSD literature has been explosive, and thousands of references now exist. Ultimately, the impact of an environmental event, such as a psychological trauma, must be understood at organic, cellular and molecular levels. This Review attempts to present the current state of this understanding on the basis of psychophysiological, structural and functional neuroimaging, and endocrinological, genetic and molecular biological studies in humans and in animal models.

Journal ArticleDOI
23 Feb 2012-Neuron
TL;DR: A transgenic mouse model in which overexpression of human tau P301L is restricted to EC-II is described, suggesting that a sequence of progressive misfolding of tau proteins, circuit-based transfer to new cell populations, and deafferentation induced degeneration are part of a process of t Tau-induced neurodegeneration.

Journal ArticleDOI
TL;DR: The robust, consistent and inducible nature of the ChR2 mice represents a significant advance over previous lines, and the Arch-ER2 and eNpHR3.0 mice are to the authors' knowledge the first demonstration of successful conditional transgenic optogenetic silencing.
Abstract: Cell type-specific expression of optogenetic molecules allows temporally precise manipulation of targeted neuronal activity. Here we present a toolbox of four knock-in mouse lines engineered for strong, Cre-dependent expression of channelrhodopsins ChR2-tdTomato and ChR2-EYFP, halorhodopsin eNpHR3.0 and archaerhodopsin Arch-ER2. All four transgenes mediated Cre-dependent, robust activation or silencing of cortical pyramidal neurons in vitro and in vivo upon light stimulation, with ChR2-EYFP and Arch-ER2 demonstrating light sensitivity approaching that of in utero or virally transduced neurons. We further show specific photoactivation of parvalbumin-positive interneurons in behaving ChR2-EYFP reporter mice. The robust, consistent and inducible nature of our ChR2 mice represents a significant advance over previous lines, and the Arch-ER2 and eNpHR3.0 mice are to our knowledge the first demonstration of successful conditional transgenic optogenetic silencing. When combined with the hundreds of available Cre driver lines, this optimized toolbox of reporter mice will enable widespread investigations of neural circuit function with unprecedented reliability and accuracy.

Journal ArticleDOI
Joshua A. Salomon1, Theo Vos, Daniel R Hogan1, Michael L. Gagnon1, Mohsen Naghavi2, Ali Mokdad2, Nazma Begum3, Razibuzzaman Shah1, Muhammad Karyana, Soewarta Kosen, Mario Reyna Farje, Gilberto Moncada, Arup Dutta, Sunil Sazawal, Andrew Dyer4, Jason F. S. Seiler4, Victor Aboyans, Lesley Baker2, Amanda J Baxter5, Emelia J. Benjamin6, Kavi Bhalla1, Aref A. Bin Abdulhak, Fiona M. Blyth, Rupert R A Bourne, Tasanee Braithwaite7, Peter Brooks, Traolach S. Brugha8, Claire Bryan-Hancock, Rachelle Buchbinder, Peter Burney9, Bianca Calabria10, Honglei Chen11, Sumeet S. Chugh12, Rebecca Cooley2, Michael H. Criqui13, Marita Cross5, Kaustubh Dabhadkar, Nabila Dahodwala14, Adrian Davis15, Louisa Degenhardt16, Cesar Diaz-Torne17, E. Ray Dorsey3, Tim Driscoll, Karen Edmond18, Alexis Elbaz19, Majid Ezzati20, Valery L. Feigin21, Cleusa P. Ferri22, Abraham D. Flaxman2, Louise Flood8, Marlene Fransen, Kana Fuse, Belinda J. Gabbe23, Richard F. Gillum24, Juanita A. Haagsma25, James Harrison8, Rasmus Havmoeller16, Roderick J. Hay26, Abdullah Hel-Baqui, Hans W. Hoek27, Howard J. Hoffman28, Emily Hogeland29, Damian G Hoy5, Deborah Jarvis2, Ganesan Karthikeyan1, Lisa M. Knowlton30, Tim Lathlean8, Janet L Leasher31, Stephen S Lim2, Steven E. Lipshultz32, Alan D. Lopez, Rafael Lozano2, Ronan A Lyons33, Reza Malekzadeh, Wagner Marcenes, Lyn March6, David J. Margolis14, Neil McGill, John J. McGrath34, George A. Mensah35, Ana-Claire Meyer, Catherine Michaud36, Andrew E. Moran, Rintaro Mori37, Michele E. Murdoch38, Luigi Naldi39, Charles R. Newton12, Rosana E. Norman, Saad B. Omer40, Richard H. Osborne, Neil Pearce18, Fernando Perez-Ruiz, Norberto Perico41, Konrad Pesudovs8, David Phillips42, Farshad Pourmalek43, Martin Prince, Jürgen Rehm, G. Remuzzi41, Kathryn Richardson, Robin Room44, Sukanta Saha45, Uchechukwu Sampson, Lidia Sanchez-Riera46, Maria Segui-Gomez47, Saeid Shahraz48, Kenji Shibuya, David Singh49, Karen Sliwa50, Emma Smith50, Isabelle Soerjomataram51, Timothy J. Steiner, Wilma A. Stolk, Lars Jacob Stovner, Christopher R. Sudfeld1, Hugh R. Taylor, Imad M. Tleyjeh4, Marieke J. van der Werf52, Wendy L. Watson53, David J. Weatherall12, Robert G. Weintraub, Marc G. Weisskopf1, Harvey Whiteford, James D. Wilkinson32, Anthony D. Woolf52, Zhi-Jie Zheng54, Christopher J L Murray2 
Harvard University1, University of Queensland2, Johns Hopkins University3, ICF International4, Centre for Mental Health5, Boston University6, University of Sydney7, University of Melbourne8, Imperial College London9, University of New South Wales10, University of California, San Diego11, Emory University12, University of Pennsylvania13, Autonomous University of Barcelona14, University of London15, National Institutes of Health16, French Institute of Health and Medical Research17, Medical Research Council18, Auckland University of Technology19, Federal University of São Paulo20, National Institute of Population and Social Security Research21, Howard University22, Flinders University23, Erasmus University Rotterdam24, King's College London25, Karolinska Institutet26, University of California, San Francisco27, All India Institute of Medical Sciences28, Nova Southeastern University29, University of Miami30, Swansea University31, Tehran University of Medical Sciences32, Queen Mary University of London33, Allen Institute for Brain Science34, University of Cape Town35, Columbia University36, Watford General Hospital37, Centro Studi GISED38, University of Oxford39, Deakin University40, University of British Columbia41, University of Toronto42, Box Hill Hospital43, Vanderbilt University44, University of Washington45, Brandeis University46, University of Tokyo47, The Queen's Medical Center48, Norwegian University of Science and Technology49, China Medical Board50, University of Cambridge51, Royal Cornwall Hospital52, Cedars-Sinai Medical Center53, Shanghai Jiao Tong University54
TL;DR: In this paper, a comprehensive re-estimation of disability weights for the Global Burden of Disease Study 2010 through a large-scale empirical investigation in which judgments about health losses associated with many causes of disease and injury were elicited from the general public in diverse communities through a new, standardised approach.

Journal ArticleDOI
Kanchon K. Dasmahapatra1, James R. Walters2, Adriana D. Briscoe3, John W. Davey, Annabel Whibley, Nicola J. Nadeau2, Aleksey V. Zimin4, Daniel S.T. Hughes5, Laura Ferguson5, Simon H. Martin2, Camilo Salazar2, Camilo Salazar6, James J. Lewis3, Sebastian Adler7, Seung-Joon Ahn8, Dean A. Baker9, Simon W. Baxter2, Nicola Chamberlain10, Ritika Chauhan11, Brian A. Counterman12, Tamas Dalmay11, Lawrence E. Gilbert13, Karl H.J. Gordon14, David G. Heckel8, Heather M. Hines5, Katharina J. Hoff7, Peter W. H. Holland5, Emmanuelle Jacquin-Joly15, Francis M. Jiggins, Robert T. Jones, Durrell D. Kapan16, Durrell D. Kapan17, Paul J. Kersey, Gerardo Lamas, Daniel Lawson, Daniel Mapleson11, Luana S. Maroja18, Arnaud Martin3, Simon Moxon19, William J. Palmer2, Riccardo Papa20, Alexie Papanicolaou14, Yannick Pauchet8, David A. Ray12, Neil Rosser1, Steven L. Salzberg21, Megan A. Supple22, Alison K. Surridge2, Ayşe Tenger-Trolander10, Heiko Vogel8, Paul A. Wilkinson23, Derek Wilson, James A. Yorke4, Furong Yuan3, Alexi Balmuth24, Cathlene Eland, Karim Gharbi, Marian Thomson, Richard A. Gibbs25, Yi Han25, Joy Jayaseelan25, Christie Kovar25, Tittu Mathew25, Donna M. Muzny25, Fiona Ongeri25, Ling-Ling Pu25, Jiaxin Qu25, Rebecca Thornton25, Kim C. Worley25, Yuanqing Wu25, Mauricio Linares26, Mark Blaxter, Richard H. ffrench-Constant27, Mathieu Joron, Marcus R. Kronforst10, Sean P. Mullen28, Robert D. Reed3, Steven E. Scherer25, Stephen Richards25, James Mallet1, James Mallet10, W. Owen McMillan, Chris D. Jiggins6, Chris D. Jiggins2 
05 Jul 2012-Nature
TL;DR: It is inferred that closely related Heliconius species exchange protective colour-pattern genes promiscuously, implying that hybridization has an important role in adaptive radiation.
Abstract: Sequencing of the genome of the butterfly Heliconius melpomene shows that closely related Heliconius species exchange protective colour-pattern genes promiscuously.

Journal ArticleDOI
TL;DR: A model suggesting that Facebook use is motivated by two primary needs: (1) The need to belong and (2) the need for self-presentation is proposed.

Journal ArticleDOI
TL;DR: In this article, a general framework for modelling the percolation properties of interacting networks is presented, and the first results drawn from its study are drawn from their study are presented.
Abstract: Aspects concerning the structure and behaviours of individual networks have been studied intensely in the past decade, but the exploration of interdependent systems in the context of complex networks has started only recently. This article reviews a general framework for modelling the percolation properties of interacting networks and the first results drawn from its study.