ALBERT

Description: Circumpolar expansion of tall shrubs and trees into Arctic tundra is widely thought to be occurring as a result of recent climate warming, but little quantitative evidence exists for northern Siberia, which encompasses the world's largest forest-tundra ecotonal belt. We quantified changes in tall shrub and tree canopy cover in eleven, widely-distributed Siberian ecotonal landscapes by comparing very-high-resolution photography from the Cold War-era “Gambit” and “Corona” satellite surveillance systems (1965-1969) with modern imagery. We also analyzed within-landscape patterns of vegetation change to evaluate the susceptibility of different landscape components to tall shrub and tree increase. The total cover of tall shrubs and trees increased in nine of eleven ecotones. In northwest Siberia, alder ( Alnus ) shrubland cover increased 5.3 – 25.9% in five ecotones. In Taymyr and Yakutia, larch ( Larix ) cover increased 3.0 – 6.7% within three ecotones, but declined 16.8% at a fourth ecotone due to thaw of ice-rich permafrost. In Chukotka, the total cover of alder and dwarf pine ( Pinus ) increased 6.1% within one ecotone and was little-changed at a second ecotone. Within most landscapes, shrub and tree increase was linked to specific geomorphic settings, especially those with active disturbance regimes such as permafrost patterned-ground, floodplains, and colluvial hillslopes. Mean summer temperatures increased at most ecotones since the mid-1960s, but rates of shrub and tree canopy cover expansion were not strongly correlated with temperature trends and were better correlated with mean annual precipitation. We conclude that shrub and tree cover is increasing in tundra ecotones across most of northern Siberia, but rates of increase vary widely regionally and at the landscape-scale. Our results indicate that extensive changes can occur within decades in moist, shrub-dominated ecotones, as in northwest Siberia, while changes are likely to occur much more slowly in the highly continental, larch-dominated ecotones of central and eastern Siberia. This article is protected by copyright. All rights reserved.

Description: As the permafrost region warms, its large organic carbon pool will be increasingly vulnerable to decomposition, combustion, and hydrologic export. Models predict that some portion of this release will be offset by increased production of Arctic and boreal biomass; however, the lack of robust estimates of net carbon balance increases the risk of further overshooting international emissions targets. Precise empirical or model-based assessments of the critical factors driving carbon balance are unlikely in the near future, so to address this gap, we present estimates from 98 permafrost-region experts of the response of biomass, wildfire, and hydrologic carbon flux to climate change. Results suggest that contrary to model projections, total permafrost-region biomass could decrease due to water stress and disturbance, factors that are not adequately incorporated in current models. Assessments indicate that end-of-the-century organic carbon release from Arctic rivers and collapsing co...

Description: Growing season soil CO2 efflux is known to vary laterally by as much as seven fold within small subalpine watersheds (

Description: Northwestern Siberia has been undergoing a range of land cover and land use changes associated with climate change, animal husbandry and development of mineral resources, particularly oil and gas. The changes caused by climate and oil/gas development Southeast of the city of Nadym were investigated using multi-temporal and multi-spatial remotely sensed images. Comparison between high spatial resolution imagery acquired in 1968 and 2006 indicates that 8.9% of the study area experienced an increase in vegetation cover (e.g. establishment of new saplings, extent of vegetated cover) in response to climate warming while 10.8% of the area showed a decrease in vegetation cover due to oil and gas development and logging activities. Waterlogging along linear structures and vehicle tracks was found near the oil and gas development site, while in natural landscapes the drying of thermokarst lakes is evident due to warming caused permafrost degradation. A Landsat time series dataset was use...

Description: Permafrost and varying land surface properties greatly complicate modelling of the thermal response of Arctic soils to climate change. The forest-tundra transition near Nadym in west Siberia provides an excellent study area in which to examine the contrasting thermal properties of soils in a forested ecosystem without permafrost and peatlands with permafrost. We investigated the effects of forest shading, snow cover and variable organic soil horizons in three common ecosystems of the forest-tundra transition zone. Based on the year-round temperature profile data, the most informative annual parameters were: (1) the sum of positive average daily temperatures at depths of 10 and 20 cm; (2) the maximum penetration depth of temperatures above 10 °C; and (3) the number of days with temperatures below 0 °C at a depth of 20 cm. The insulative effect of snow cover in winter was at least twice that of the shading and cooling effect of vegetation in summer. In areas with shallow permafrost, the presence of a thick organic horizon, with an extremely low thermal diffusivity, creates a very steep temperature gradient that limits heat penetration to the top of the permafrost in summer. Copyright © 2015 John Wiley & Sons, Ltd.

Description: ABSTRACT Small patterned-ground features (PGFs) in the Arctic have unique soil properties that vary with latitude and may greatly affect tundra biogeochemistry. Because nitrogen availability can strongly limit arctic vegetation growth, we examined how soil nitrogen transformations differ between PGFs and the surrounding inter-PGF tundra along an arctic latitudinal gradient. We collected soils at eight sites from the Alaskan Low Arctic to the Canadian High Arctic. The soils were incubated for 21 days at 9 °C and 15 °C and analysed for changes in total inorganic nitrogen, nitrate and extractable organic nitrogen (EON). We found greater nitrogen immobilisation in the surrounding inter-PGF soils than in the PGF soils. Along the latitudinal gradient, differences in net nitrogen mineralisation and EON cycling between PGF and inter-PGF soils were strongly influenced by the presence of a pH boundary within the Low Arctic and the transition between the High and Low Arctic, with greater immobilisation in the nonacidic and Low Arctic sites, respectively. Incubation temperature affected EON flux but did not affect net nitrogen mineralisation or nitrification. These results show that spatial heterogeneity at several scales can influence soil nitrogen dynamics, and is therefore an important influence on arctic ecosystem function. Copyright © 2012 John Wiley & Sons, Ltd.

Description: Research on the terrestrial C balance focuses largely on measuring and predicting responses of ecosystem-scale production and respiration to changing temperatures and hydrologic regimes. However, landscape morphology can modify the availability of resources from year to year by imposing physical gradients that redistribute soil water and other biophysical variables within ecosystems. This paper demonstrates that the well-established biophysical relationship between soil respiration and soil moisture interacts with topographic structure to create bidirectional (i.e., opposite) responses of soil respiration to soil water availability within the landscape. Based on soil respiration measurements taken at a subalpine forest in central Montana, we found that locations with high drainage areas (i.e., lowlands and wet areas of the forest) had higher cumulative soil respiration in dry years, whereas locations with low drainage areas (i.e., uplands and dry areas of the forest) had higher cumulative soil respiration in wet years. Our results indicate that for 80.9% of the forest soil respiration is likely to increase during wet years, whereas for 19.1% of the forest soil respiration is likely to decrease under the same hydrologic conditions. This emergent, bidirectional behavior is generated from the interaction of three relatively simple elements (parabolic soil biophysics, the relative distribution of landscape positions, and inter-annual climate variability), indicating that terrain complexity is an important mediator of the landscape-scale soil C response to climate. These results highlight that evaluating and predicting ecosystem-scale soil C response to climate fluctuation requires detailed characterization of biophysical-topographic interactions in addition to biophysical-climate interactions.

Description: Myocardial infarction (MI), a leading cause of death around the world, displays a complex pattern of inheritance. When MI occurs early in life, genetic inheritance is a major component to risk. Previously, rare mutations in low-density lipoprotein (LDL) genes have been shown to contribute to MI risk in individual families, whereas common variants at more than 45 loci have been associated with MI risk in the population. Here we evaluate how rare mutations contribute to early-onset MI risk in the population. We sequenced the protein-coding regions of 9,793 genomes from patients with MI at an early age (〈/=50 years in males and 〈/=60 years in females) along with MI-free controls. We identified two genes in which rare coding-sequence mutations were more frequent in MI cases versus controls at exome-wide significance. At low-density lipoprotein receptor (LDLR), carriers of rare non-synonymous mutations were at 4.2-fold increased risk for MI; carriers of null alleles at LDLR were at even higher risk (13-fold difference). Approximately 2% of early MI cases harbour a rare, damaging mutation in LDLR; this estimate is similar to one made more than 40 years ago using an analysis of total cholesterol. Among controls, about 1 in 217 carried an LDLR coding-sequence mutation and had plasma LDL cholesterol 〉 190 mg dl(-1). At apolipoprotein A-V (APOA5), carriers of rare non-synonymous mutations were at 2.2-fold increased risk for MI. When compared with non-carriers, LDLR mutation carriers had higher plasma LDL cholesterol, whereas APOA5 mutation carriers had higher plasma triglycerides. Recent evidence has connected MI risk with coding-sequence mutations at two genes functionally related to APOA5, namely lipoprotein lipase and apolipoprotein C-III (refs 18, 19). Combined, these observations suggest that, as well as LDL cholesterol, disordered metabolism of triglyceride-rich lipoproteins contributes to MI risk.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4319990/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4319990/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Do, Ron -- Stitziel, Nathan O -- Won, Hong-Hee -- Jorgensen, Anders Berg -- Duga, Stefano -- Angelica Merlini, Pier -- Kiezun, Adam -- Farrall, Martin -- Goel, Anuj -- Zuk, Or -- Guella, Illaria -- Asselta, Rosanna -- Lange, Leslie A -- Peloso, Gina M -- Auer, Paul L -- NHLBI Exome Sequencing Project -- Girelli, Domenico -- Martinelli, Nicola -- Farlow, Deborah N -- DePristo, Mark A -- Roberts, Robert -- Stewart, Alexander F R -- Saleheen, Danish -- Danesh, John -- Epstein, Stephen E -- Sivapalaratnam, Suthesh -- Hovingh, G Kees -- Kastelein, John J -- Samani, Nilesh J -- Schunkert, Heribert -- Erdmann, Jeanette -- Shah, Svati H -- Kraus, William E -- Davies, Robert -- Nikpay, Majid -- Johansen, Christopher T -- Wang, Jian -- Hegele, Robert A -- Hechter, Eliana -- Marz, Winfried -- Kleber, Marcus E -- Huang, Jie -- Johnson, Andrew D -- Li, Mingyao -- Burke, Greg L -- Gross, Myron -- Liu, Yongmei -- Assimes, Themistocles L -- Heiss, Gerardo -- Lange, Ethan M -- Folsom, Aaron R -- Taylor, Herman A -- Olivieri, Oliviero -- Hamsten, Anders -- Clarke, Robert -- Reilly, Dermot F -- Yin, Wu -- Rivas, Manuel A -- Donnelly, Peter -- Rossouw, Jacques E -- Psaty, Bruce M -- Herrington, David M -- Wilson, James G -- Rich, Stephen S -- Bamshad, Michael J -- Tracy, Russell P -- Cupples, L Adrienne -- Rader, Daniel J -- Reilly, Muredach P -- Spertus, John A -- Cresci, Sharon -- Hartiala, Jaana -- Tang, W H Wilson -- Hazen, Stanley L -- Allayee, Hooman -- Reiner, Alex P -- Carlson, Christopher S -- Kooperberg, Charles -- Jackson, Rebecca D -- Boerwinkle, Eric -- Lander, Eric S -- Schwartz, Stephen M -- Siscovick, David S -- McPherson, Ruth -- Tybjaerg-Hansen, Anne -- Abecasis, Goncalo R -- Watkins, Hugh -- Nickerson, Deborah A -- Ardissino, Diego -- Sunyaev, Shamil R -- O'Donnell, Christopher J -- Altshuler, David -- Gabriel, Stacey -- Kathiresan, Sekar -- 090532/Wellcome Trust/United Kingdom -- 095552/Wellcome Trust/United Kingdom -- 5U54HG003067-11/HG/NHGRI NIH HHS/ -- G-0907/Parkinson's UK/United Kingdom -- K08 HL114642/HL/NHLBI NIH HHS/ -- K08HL114642/HL/NHLBI NIH HHS/ -- P01 HL076491/HL/NHLBI NIH HHS/ -- P01 HL098055/HL/NHLBI NIH HHS/ -- R01 HL107816/HL/NHLBI NIH HHS/ -- R01HL107816/HL/NHLBI NIH HHS/ -- RC2 HL-102923/HL/NHLBI NIH HHS/ -- RC2 HL-102924/HL/NHLBI NIH HHS/ -- RC2 HL-102925/HL/NHLBI NIH HHS/ -- RC2 HL-102926/HL/NHLBI NIH HHS/ -- RC2 HL-103010/HL/NHLBI NIH HHS/ -- T32 HL007208/HL/NHLBI NIH HHS/ -- T32HL00720/HL/NHLBI NIH HHS/ -- T32HL007604/HL/NHLBI NIH HHS/ -- UL1 TR000439/TR/NCATS NIH HHS/ -- Canadian Institutes of Health Research/Canada -- England -- Nature. 2015 Feb 5;518(7537):102-6. doi: 10.1038/nature13917. Epub 2014 Dec 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Center for Human Genetic Research, Massachusetts General Hospital, Boston, Massachusetts 02114, USA. [2] Cardiovascular Research Center, Massachusetts General Hospital, Boston, Massachusetts 02114, USA. [3] Department of Medicine, Harvard Medical School, Boston, Massachusetts 02114, USA. [4] Program in Medical and Population Genetics, Broad Institute, 7 Cambridge Center, Cambridge, Massachusetts 02142, USA. ; 1] Cardiovascular Division, Department of Medicine, Washington University School of Medicine, St Louis, Missouri 63110, USA. [2] Division of Statistical Genomics, Washington University School of Medicine, St Louis, Missouri 63110, USA. ; Department of Clinical Biochemistry KB3011, Section for Molecular Genetics, Rigshospitalet, Copenhagen University Hospitals and Faculty of Health Sciences, University of Copenhagen, Copenhagen 1165, Denmark. ; Dipartimento di Biotecnologie Mediche e Medicina Traslazionale, Universita degli Studi di Milano, Milano 20122, Italy. ; Division of Cardiology, Ospedale Niguarda, Milano 20162, Italy. ; Program in Medical and Population Genetics, Broad Institute, 7 Cambridge Center, Cambridge, Massachusetts 02142, USA. ; Department of Cardiovascular Medicine, The Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford OX1 2J, UK. ; Department of Genetics, University of North Carolina, Chapel Hill, North Carolina 27599, USA. ; Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA. ; University of Verona School of Medicine, Department of Medicine, Verona 37129, Italy. ; John &Jennifer Ruddy Canadian Cardiovascular Genetics Centre, University of Ottawa Heart Institute, Ottawa, Ontario K1Y 4W7, Canada. ; Department of Public Health and Primary Care, University of Cambridge, Cambridge CB2 1TN, UK. ; MedStar Health Research Institute, Cardiovascular Research Institute, Hyattsville, Maryland 20782, USA. ; Department of Vascular Medicine, Academic Medical Center, Amsterdam 1105 AZ, The Netherlands. ; Department of Cardiovascular Sciences, University of Leicester, and Leicester NIHR Biomedical Research Unit in Cardiovascular Disease, Glenfield Hospital, Leicester LE3 9QP, UK. ; DZHK (German Research Centre for Cardiovascular Research), Munich Heart Alliance, Deutsches Herzzentrum Munchen, Technische Universitat Munchen, Berlin 13347, Germany. ; Medizinische Klinik II, University of Lubeck, Lubeck 23562, Germany. ; 1] Center for Human Genetics, Duke University, Durham, North Carolina 27708, USA. [2] Department of Cardiology and Center for Genomic Medicine, Duke University School of Medicine, Durham, North Carolina 27708, USA. ; Department of Cardiology and Center for Genomic Medicine, Duke University School of Medicine, Durham, North Carolina 27708, USA. ; Division of Cardiology, University of Ottawa Heart Institute, Ottawa, Ontario K1Y 4W7, Canada. ; Department of Biochemistry, Schulich School of Medicine and Dentistry, Robarts Research Institute, University of Western Ontario, London, Ontario N6A 3K7, Canada. ; 1] Department of Biochemistry, Schulich School of Medicine and Dentistry, Robarts Research Institute, University of Western Ontario, London, Ontario N6A 3K7, Canada. [2] Department of Medicine, Schulich School of Medicine and Dentistry, Robarts Research Institute, University of Western Ontario, London, Ontario N6A 3K7, Canada. ; 1] Medical Faculty Mannheim, Mannheim Institute of Public Health, Social and Preventive Medicine, Heidelberg University, Ludolf Krehl Strasse 7-11, Mannheim D-68167, Germany. [2] Clinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University of Graz, Graz 8036, Austria. [3] Synlab Academy, Mannheim 68259, Germany. ; Medical Faculty Mannheim, Mannheim Institute of Public Health, Social and Preventive Medicine, Heidelberg University, Ludolf Krehl Strasse 7-11, Mannheim D-68167, Germany. ; The National Heart, Lung, Blood Institute's Framingham Heart Study, Framingham, Massachusetts 01702, USA. ; National Heart, Lung, and Blood Institute Center for Population Studies, The Framingham Heart Study, Framingham, Massachusetts 01702, USA. ; Department of Biostatistics and Epidemiology, School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. ; Department of Epidemiology, University of Alabama-Birmingham, Birmingham, Alabama 35233, USA. ; Department of Laboratory Medicine and Pathology, School of Medicine, University of Minnesota, Minneapolis, Minnesota 55455, USA. ; School of Medicine, Wake Forest University, Winston-Salem, North Carolina 27106, USA. ; Department of Medicine, Stanford University School of Medicine, Stanford, California 94305, USA. ; Department of Epidemiology, University of North Carolina, Chapel Hill, North Carolina 27599, USA. ; 1] Department of Genetics, University of North Carolina, Chapel Hill, North Carolina 27599, USA. [2] Carolina Center for Genome Sciences, University of North Carolina, Chapel Hill, North Carolina 27599, USA. ; Division of Epidemiology and Community Health, University of Minnesota School of Public Health, Minneapolis, Minnesota 55455, USA. ; University of Mississippi Medical Center, Jackson, Mississippi 39216, USA. ; Atherosclerosis Research Unit, Department of Medicine, and Center for Molecular Medicine, Karolinska Institutet, Stockholm 171 77, Sweden. ; Clinical Trial Service Unit and Epidemiological Studies Unit, University of Oxford, Oxford OX1 2JD, UK. ; Merck Sharp &Dohme Corporation, Rahway, New Jersey 08889, USA. ; The Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford OX1 2JD, UK. ; 1] The Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford OX1 2JD, UK. [2] Department of Statistics, University of Oxford, Oxford OX1 2JD, UK. ; National Heart, Lung, and Blood Institute, Bethesda, Maryland 20824, USA. ; 1] Cardiovascular Health Research Unit, Departments of Medicine, Epidemiology, and Health Services, University of Washington, Seattle, Washington 98195, USA. [2] Group Health Research Institute, Group Health Cooperative, Seattle, Washington 98101, USA. ; Section on Cardiology, and Public Health Sciences, Wake Forest School of Medicine, Winston-Salem, North Carolina 27106, USA. ; Jackson Heart Study, University of Mississippi Medical Center, Jackson State University, Jackson, Mississippi 39217, USA. ; Center for Public Health Genomics, University of Virginia, Charlottesville, Virginia 22904, USA. ; 1] Division of Genetic Medicine, Department of Pediatrics, University of Washington, Seattle, Washington 98195, USA. [2] Seattle Children's Hospital, Seattle, Washington 98105, USA. [3] Department of Genome Sciences, University of Washington, Seattle, Washington 98195, USA. ; Department of Biochemistry, University of Vermont, Burlington, Vermont 05405, USA. ; Department of Biostatistics, Boston University School of Public Health, Boston, Massachusetts 02118, USA. ; Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. ; Cardiovascular Institute, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. ; St Luke's Mid America Heart Institute, University of Missouri-Kansas City, Kansas City, Missouri 64111, USA. ; 1] Cardiovascular Division, Department of Medicine, Washington University School of Medicine, St Louis, Missouri 63110, USA. [2] Department of Genetics, Washington University in St Louis, Missouri 63130, USA. ; Department of Preventive Medicine and Institute for Genetic Medicine, University of Southern California Keck School of Medicine, Los Angeles, California 90033, USA. ; Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio 44195, USA. ; 1] Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA. [2] Department of Epidemiology, University of Washington, Seattle, Washington 98195, USA. ; Ohio State University, Columbus, Ohio 43210, USA. ; Human Genetics Center, The University of Texas Health Science Center at Houston, Houston, Texas 77030, USA. ; 1] Department of Epidemiology, University of Washington, Seattle, Washington 98195, USA. [2] Department of Medicine, School of Medicine, University of Washington, Seattle, Washington 98195, USA. ; 1] Department of Clinical Biochemistry KB3011, Section for Molecular Genetics, Rigshospitalet, Copenhagen University Hospitals and Faculty of Health Sciences, University of Copenhagen, Copenhagen 1165, Denmark. [2] Faculty of Health and Medical Sciences, University of Copenhagen, Blegdamsvej 3B, 2200 Kobenhavn N, Denmark. ; Center for Statistical Genetics, Department of Biostatistics, University of Michigan, Ann Arbor, Missouri 48109, USA. ; 1] Department of Cardiovascular Medicine, The Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford OX1 2J, UK. [2] The Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford OX1 2JD, UK. ; Department of Genome Sciences, University of Washington, Seattle, Washington 98195, USA. ; Department of Cardiology, Parma Hospital, Parma 43100, Italy. ; 1] Program in Medical and Population Genetics, Broad Institute, 7 Cambridge Center, Cambridge, Massachusetts 02142, USA. [2] Division of Genetics, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. ; 1] Center for Human Genetic Research, Massachusetts General Hospital, Boston, Massachusetts 02114, USA. [2] Program in Medical and Population Genetics, Broad Institute, 7 Cambridge Center, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25487149" target="_blank"〉PubMed〈/a〉

Description: Consistent, high-level, vaccine-induced protection against human malaria has only been achieved by inoculation of Plasmodium falciparum (Pf) sporozoites (SPZ) by mosquito bites. We report that the PfSPZ Vaccine--composed of attenuated, aseptic, purified, cryopreserved PfSPZ--was safe and well tolerated when administered four to six times intravenously (IV) to 40 adults. Zero of six subjects receiving five doses and three of nine subjects receiving four doses of 1.35 x 10(5) PfSPZ Vaccine and five of six nonvaccinated controls developed malaria after controlled human malaria infection (P = 0.015 in the five-dose group and P = 0.028 for overall, both versus controls). PfSPZ-specific antibody and T cell responses were dose-dependent. These data indicate that there is a dose-dependent immunological threshold for establishing high-level protection against malaria that can be achieved with IV administration of a vaccine that is safe and meets regulatory standards.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seder, Robert A -- Chang, Lee-Jah -- Enama, Mary E -- Zephir, Kathryn L -- Sarwar, Uzma N -- Gordon, Ingelise J -- Holman, LaSonji A -- James, Eric R -- Billingsley, Peter F -- Gunasekera, Anusha -- Richman, Adam -- Chakravarty, Sumana -- Manoj, Anita -- Velmurugan, Soundarapandian -- Li, MingLin -- Ruben, Adam J -- Li, Tao -- Eappen, Abraham G -- Stafford, Richard E -- Plummer, Sarah H -- Hendel, Cynthia S -- Novik, Laura -- Costner, Pamela J M -- Mendoza, Floreliz H -- Saunders, Jamie G -- Nason, Martha C -- Richardson, Jason H -- Murphy, Jittawadee -- Davidson, Silas A -- Richie, Thomas L -- Sedegah, Martha -- Sutamihardja, Awalludin -- Fahle, Gary A -- Lyke, Kirsten E -- Laurens, Matthew B -- Roederer, Mario -- Tewari, Kavita -- Epstein, Judith E -- Sim, B Kim Lee -- Ledgerwood, Julie E -- Graham, Barney S -- Hoffman, Stephen L -- VRC 312 Study Team -- 3R44AI055229-06S1/AI/NIAID NIH HHS/ -- 4R44AI055229-08/AI/NIAID NIH HHS/ -- 5R44AI058499-05/AI/NIAID NIH HHS/ -- N01-AI-40096/AI/NIAID NIH HHS/ -- Intramural NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Sep 20;341(6152):1359-65. doi: 10.1126/science.1241800. Epub 2013 Aug 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20852, USA. rseder@mail.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23929949" target="_blank"〉PubMed〈/a〉