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  • Reproducibility of Results  (102)
  • Nature Publishing Group (NPG)  (102)
  • American Institute of Physics (AIP)
  • American Society of Hematology
  • 2010-2014  (102)
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  • 1
    Publication Date: 2012-07-27
    Description: The rapid disruption of tropical forests probably imperils global biodiversity more than any other contemporary phenomenon. With deforestation advancing quickly, protected areas are increasingly becoming final refuges for threatened species and natural ecosystem processes. However, many protected areas in the tropics are themselves vulnerable to human encroachment and other environmental stresses. As pressures mount, it is vital to know whether existing reserves can sustain their biodiversity. A critical constraint in addressing this question has been that data describing a broad array of biodiversity groups have been unavailable for a sufficiently large and representative sample of reserves. Here we present a uniquely comprehensive data set on changes over the past 20 to 30 years in 31 functional groups of species and 21 potential drivers of environmental change, for 60 protected areas stratified across the world's major tropical regions. Our analysis reveals great variation in reserve 'health': about half of all reserves have been effective or performed passably, but the rest are experiencing an erosion of biodiversity that is often alarmingly widespread taxonomically and functionally. Habitat disruption, hunting and forest-product exploitation were the strongest predictors of declining reserve health. Crucially, environmental changes immediately outside reserves seemed nearly as important as those inside in determining their ecological fate, with changes inside reserves strongly mirroring those occurring around them. These findings suggest that tropical protected areas are often intimately linked ecologically to their surrounding habitats, and that a failure to stem broad-scale loss and degradation of such habitats could sharply increase the likelihood of serious biodiversity declines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Laurance, William F -- Useche, D Carolina -- Rendeiro, Julio -- Kalka, Margareta -- Bradshaw, Corey J A -- Sloan, Sean P -- Laurance, Susan G -- Campbell, Mason -- Abernethy, Kate -- Alvarez, Patricia -- Arroyo-Rodriguez, Victor -- Ashton, Peter -- Benitez-Malvido, Julieta -- Blom, Allard -- Bobo, Kadiri S -- Cannon, Charles H -- Cao, Min -- Carroll, Richard -- Chapman, Colin -- Coates, Rosamond -- Cords, Marina -- Danielsen, Finn -- De Dijn, Bart -- Dinerstein, Eric -- Donnelly, Maureen A -- Edwards, David -- Edwards, Felicity -- Farwig, Nina -- Fashing, Peter -- Forget, Pierre-Michel -- Foster, Mercedes -- Gale, George -- Harris, David -- Harrison, Rhett -- Hart, John -- Karpanty, Sarah -- Kress, W John -- Krishnaswamy, Jagdish -- Logsdon, Willis -- Lovett, Jon -- Magnusson, William -- Maisels, Fiona -- Marshall, Andrew R -- McClearn, Deedra -- Mudappa, Divya -- Nielsen, Martin R -- Pearson, Richard -- Pitman, Nigel -- van der Ploeg, Jan -- Plumptre, Andrew -- Poulsen, John -- Quesada, Mauricio -- Rainey, Hugo -- Robinson, Douglas -- Roetgers, Christiane -- Rovero, Francesco -- Scatena, Frederick -- Schulze, Christian -- Sheil, Douglas -- Struhsaker, Thomas -- Terborgh, John -- Thomas, Duncan -- Timm, Robert -- Urbina-Cardona, J Nicolas -- Vasudevan, Karthikeyan -- Wright, S Joseph -- Arias-G, Juan Carlos -- Arroyo, Luzmila -- Ashton, Mark -- Auzel, Philippe -- Babaasa, Dennis -- Babweteera, Fred -- Baker, Patrick -- Banki, Olaf -- Bass, Margot -- Bila-Isia, Inogwabini -- Blake, Stephen -- Brockelman, Warren -- Brokaw, Nicholas -- Bruhl, Carsten A -- Bunyavejchewin, Sarayudh -- Chao, Jung-Tai -- Chave, Jerome -- Chellam, Ravi -- Clark, Connie J -- Clavijo, Jose -- Congdon, Robert -- Corlett, Richard -- Dattaraja, H S -- Dave, Chittaranjan -- Davies, Glyn -- Beisiegel, Beatriz de Mello -- da Silva, Rosa de Nazare Paes -- Di Fiore, Anthony -- Diesmos, Arvin -- Dirzo, Rodolfo -- Doran-Sheehy, Diane -- Eaton, Mitchell -- Emmons, Louise -- Estrada, Alejandro -- Ewango, Corneille -- Fedigan, Linda -- Feer, Francois -- Fruth, Barbara -- Willis, Jacalyn Giacalone -- Goodale, Uromi -- Goodman, Steven -- Guix, Juan C -- Guthiga, Paul -- Haber, William -- Hamer, Keith -- Herbinger, Ilka -- Hill, Jane -- Huang, Zhongliang -- Sun, I Fang -- Ickes, Kalan -- Itoh, Akira -- Ivanauskas, Natalia -- Jackes, Betsy -- Janovec, John -- Janzen, Daniel -- Jiangming, Mo -- Jin, Chen -- Jones, Trevor -- Justiniano, Hermes -- Kalko, Elisabeth -- Kasangaki, Aventino -- Killeen, Timothy -- King, Hen-biau -- Klop, Erik -- Knott, Cheryl -- Kone, Inza -- Kudavidanage, Enoka -- Ribeiro, Jose Lahoz da Silva -- Lattke, John -- Laval, Richard -- Lawton, Robert -- Leal, Miguel -- Leighton, Mark -- Lentino, Miguel -- Leonel, Cristiane -- Lindsell, Jeremy -- Ling-Ling, Lee -- Linsenmair, K Eduard -- Losos, Elizabeth -- Lugo, Ariel -- Lwanga, Jeremiah -- Mack, Andrew L -- Martins, Marlucia -- McGraw, W Scott -- McNab, Roan -- Montag, Luciano -- Thompson, Jo Myers -- Nabe-Nielsen, Jacob -- Nakagawa, Michiko -- Nepal, Sanjay -- Norconk, Marilyn -- Novotny, Vojtech -- O'Donnell, Sean -- Opiang, Muse -- Ouboter, Paul -- Parker, Kenneth -- Parthasarathy, N -- Pisciotta, Katia -- Prawiradilaga, Dewi -- Pringle, Catherine -- Rajathurai, Subaraj -- Reichard, Ulrich -- Reinartz, Gay -- Renton, Katherine -- Reynolds, Glen -- Reynolds, Vernon -- Riley, Erin -- Rodel, Mark-Oliver -- Rothman, Jessica -- Round, Philip -- Sakai, Shoko -- Sanaiotti, Tania -- Savini, Tommaso -- Schaab, Gertrud -- Seidensticker, John -- Siaka, Alhaji -- Silman, Miles R -- Smith, Thomas B -- de Almeida, Samuel Soares -- Sodhi, Navjot -- Stanford, Craig -- Stewart, Kristine -- Stokes, Emma -- Stoner, Kathryn E -- Sukumar, Raman -- Surbeck, Martin -- Tobler, Mathias -- Tscharntke, Teja -- Turkalo, Andrea -- Umapathy, Govindaswamy -- van Weerd, Merlijn -- Rivera, Jorge Vega -- Venkataraman, Meena -- Venn, Linda -- Verea, Carlos -- de Castilho, Carolina Volkmer -- Waltert, Matthias -- Wang, Benjamin -- Watts, David -- Weber, William -- West, Paige -- Whitacre, David -- Whitney, Ken -- Wilkie, David -- Williams, Stephen -- Wright, Debra D -- Wright, Patricia -- Xiankai, Lu -- Yonzon, Pralad -- Zamzani, Franky -- England -- Nature. 2012 Sep 13;489(7415):290-4. doi: 10.1038/nature11318.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Tropical Environmental and Sustainability Science and School of Marine and Tropical Biology, James Cook University, Cairns, Queensland 4878, Australia. bill.laurance@jcu.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22832582" target="_blank"〉PubMed〈/a〉
    Keywords: Agriculture/statistics & numerical data ; Animals ; *Biodiversity ; Conservation of Natural Resources/*statistics & numerical data ; Data Collection ; Ecology/statistics & numerical data ; Endangered Species/*statistics & numerical data ; Environmental Pollution/adverse effects/statistics & numerical data ; Fires/statistics & numerical data ; Forestry/statistics & numerical data ; Interviews as Topic ; Mining/statistics & numerical data ; Population Growth ; Rain ; Reproducibility of Results ; Research Personnel ; Surveys and Questionnaires ; Temperature ; Trees/*physiology ; *Tropical Climate
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2010-08-06
    Description: Plasma concentrations of total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol and triglycerides are among the most important risk factors for coronary artery disease (CAD) and are targets for therapeutic intervention. We screened the genome for common variants associated with plasma lipids in 〉100,000 individuals of European ancestry. Here we report 95 significantly associated loci (P 〈 5 x 10(-8)), with 59 showing genome-wide significant association with lipid traits for the first time. The newly reported associations include single nucleotide polymorphisms (SNPs) near known lipid regulators (for example, CYP7A1, NPC1L1 and SCARB1) as well as in scores of loci not previously implicated in lipoprotein metabolism. The 95 loci contribute not only to normal variation in lipid traits but also to extreme lipid phenotypes and have an impact on lipid traits in three non-European populations (East Asians, South Asians and African Americans). Our results identify several novel loci associated with plasma lipids that are also associated with CAD. Finally, we validated three of the novel genes-GALNT2, PPP1R3B and TTC39B-with experiments in mouse models. Taken together, our findings provide the foundation to develop a broader biological understanding of lipoprotein metabolism and to identify new therapeutic opportunities for the prevention of CAD.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3039276/" 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/PMC3039276/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Teslovich, Tanya M -- Musunuru, Kiran -- Smith, Albert V -- Edmondson, Andrew C -- Stylianou, Ioannis M -- Koseki, Masahiro -- Pirruccello, James P -- Ripatti, Samuli -- Chasman, Daniel I -- Willer, Cristen J -- Johansen, Christopher T -- Fouchier, Sigrid W -- Isaacs, Aaron -- Peloso, Gina M -- Barbalic, Maja -- Ricketts, Sally L -- Bis, Joshua C -- Aulchenko, Yurii S -- Thorleifsson, Gudmar -- Feitosa, Mary F -- Chambers, John -- Orho-Melander, Marju -- Melander, Olle -- Johnson, Toby -- Li, Xiaohui -- Guo, Xiuqing -- Li, Mingyao -- Shin Cho, Yoon -- Jin Go, Min -- Jin Kim, Young -- Lee, Jong-Young -- Park, Taesung -- Kim, Kyunga -- Sim, Xueling -- Twee-Hee Ong, Rick -- Croteau-Chonka, Damien C -- Lange, Leslie A -- Smith, Joshua D -- Song, Kijoung -- Hua Zhao, Jing -- Yuan, Xin -- Luan, Jian'an -- Lamina, Claudia -- Ziegler, Andreas -- Zhang, Weihua -- Zee, Robert Y L -- Wright, Alan F -- Witteman, Jacqueline C M -- Wilson, James F -- Willemsen, Gonneke -- Wichmann, H-Erich -- Whitfield, John B -- Waterworth, Dawn M -- Wareham, Nicholas J -- Waeber, Gerard -- Vollenweider, Peter -- Voight, Benjamin F -- Vitart, Veronique -- Uitterlinden, Andre G -- Uda, Manuela -- Tuomilehto, Jaakko -- Thompson, John R -- Tanaka, Toshiko -- Surakka, Ida -- Stringham, Heather M -- Spector, Tim D -- Soranzo, Nicole -- Smit, Johannes H -- Sinisalo, Juha -- Silander, Kaisa -- Sijbrands, Eric J G -- Scuteri, Angelo -- Scott, James -- Schlessinger, David -- Sanna, Serena -- Salomaa, Veikko -- Saharinen, Juha -- Sabatti, Chiara -- Ruokonen, Aimo -- Rudan, Igor -- Rose, Lynda M -- Roberts, Robert -- Rieder, Mark -- Psaty, Bruce M -- Pramstaller, Peter P -- Pichler, Irene -- Perola, Markus -- Penninx, Brenda W J H -- Pedersen, Nancy L -- Pattaro, Cristian -- Parker, Alex N -- Pare, Guillaume -- Oostra, Ben A -- O'Donnell, Christopher J -- Nieminen, Markku S -- Nickerson, Deborah A -- Montgomery, Grant W -- Meitinger, Thomas -- McPherson, Ruth -- McCarthy, Mark I -- McArdle, Wendy -- Masson, David -- Martin, Nicholas G -- Marroni, Fabio -- Mangino, Massimo -- Magnusson, Patrik K E -- Lucas, Gavin -- Luben, Robert -- Loos, Ruth J F -- Lokki, Marja-Liisa -- Lettre, Guillaume -- Langenberg, Claudia -- Launer, Lenore J -- Lakatta, Edward G -- Laaksonen, Reijo -- Kyvik, Kirsten O -- Kronenberg, Florian -- Konig, Inke R -- Khaw, Kay-Tee -- Kaprio, Jaakko -- Kaplan, Lee M -- Johansson, Asa -- Jarvelin, Marjo-Riitta -- Janssens, A Cecile J W -- Ingelsson, Erik -- Igl, Wilmar -- Kees Hovingh, G -- Hottenga, Jouke-Jan -- Hofman, Albert -- Hicks, Andrew A -- Hengstenberg, Christian -- Heid, Iris M -- Hayward, Caroline -- Havulinna, Aki S -- Hastie, Nicholas D -- Harris, Tamara B -- Haritunians, Talin -- Hall, Alistair S -- Gyllensten, Ulf -- Guiducci, Candace -- Groop, Leif C -- Gonzalez, Elena -- Gieger, Christian -- Freimer, Nelson B -- Ferrucci, Luigi -- Erdmann, Jeanette -- Elliott, Paul -- Ejebe, Kenechi G -- Doring, Angela -- Dominiczak, Anna F -- Demissie, Serkalem -- Deloukas, Panagiotis -- de Geus, Eco J C -- de Faire, Ulf -- Crawford, Gabriel -- Collins, Francis S -- Chen, Yii-der I -- Caulfield, Mark J -- Campbell, Harry -- Burtt, Noel P -- Bonnycastle, Lori L -- Boomsma, Dorret I -- Boekholdt, S Matthijs -- Bergman, Richard N -- Barroso, Ines -- Bandinelli, Stefania -- Ballantyne, Christie M -- Assimes, Themistocles L -- Quertermous, Thomas -- Altshuler, David -- Seielstad, Mark -- Wong, Tien Y -- Tai, E-Shyong -- Feranil, Alan B -- Kuzawa, Christopher W -- Adair, Linda S -- Taylor, Herman A Jr -- Borecki, Ingrid B -- Gabriel, Stacey B -- Wilson, James G -- Holm, Hilma -- Thorsteinsdottir, Unnur -- Gudnason, Vilmundur -- Krauss, Ronald M -- Mohlke, Karen L -- Ordovas, Jose M -- Munroe, Patricia B -- Kooner, Jaspal S -- Tall, Alan R -- Hegele, Robert A -- Kastelein, John J P -- Schadt, Eric E -- Rotter, Jerome I -- Boerwinkle, Eric -- Strachan, David P -- Mooser, Vincent -- Stefansson, Kari -- Reilly, Muredach P -- Samani, Nilesh J -- Schunkert, Heribert -- Cupples, L Adrienne -- Sandhu, Manjinder S -- Ridker, Paul M -- Rader, Daniel J -- van Duijn, Cornelia M -- Peltonen, Leena -- Abecasis, Goncalo R -- Boehnke, Michael -- Kathiresan, Sekar -- 068545/Z/02/Wellcome Trust/United Kingdom -- 076113/B/04/Z/Wellcome Trust/United Kingdom -- 077016/Z/05/Z/Wellcome Trust/United Kingdom -- 079895/Wellcome Trust/United Kingdom -- 1Z01 HG000024/HG/NHGRI NIH HHS/ -- 5R01DK06833603/DK/NIDDK NIH HHS/ -- 5R01DK07568102/DK/NIDDK NIH HHS/ -- 5R01HL087679-02/HL/NHLBI NIH HHS/ -- 5R01HL08770003/HL/NHLBI NIH HHS/ -- 5R01HL08821502/HL/NHLBI NIH HHS/ -- CA 047988/CA/NCI NIH HHS/ -- CZB/4/710/Chief Scientist Office/United Kingdom -- DK062370/DK/NIDDK NIH HHS/ -- DK063491/DK/NIDDK NIH HHS/ -- DK072193/DK/NIDDK NIH HHS/ -- DK078150/DK/NIDDK NIH HHS/ -- DK56350/DK/NIDDK NIH HHS/ -- ES10126/ES/NIEHS NIH HHS/ -- G0000934/Medical Research Council/United Kingdom -- G0401527/Medical Research Council/United Kingdom -- G0601966/Medical Research Council/United Kingdom -- G0700931/Medical Research Council/United Kingdom -- G0701863/Medical Research Council/United Kingdom -- G0801056/Medical Research Council/United Kingdom -- G0801566/Medical Research Council/United Kingdom -- G9521010/Medical Research Council/United Kingdom -- G9521010D/Medical Research Council/United Kingdom -- HHSN268200625226C/PHS HHS/ -- HL 04381/HL/NHLBI NIH HHS/ -- HL 080467/HL/NHLBI NIH HHS/ -- HL-54776/HL/NHLBI NIH HHS/ -- HL085144/HL/NHLBI NIH HHS/ -- K99 HL098364/HL/NHLBI NIH HHS/ -- K99 HL098364-01/HL/NHLBI NIH HHS/ -- K99HL094535/HL/NHLBI NIH HHS/ -- M01-RR00425/RR/NCRR NIH HHS/ -- MC_QA137934/Medical Research Council/United Kingdom -- MC_U106179471/Medical Research Council/United Kingdom -- MC_U106188470/Medical Research Council/United Kingdom -- MC_U127561128/Medical Research Council/United Kingdom -- N01 HC-15103/HC/NHLBI NIH HHS/ -- N01 HC-55222/HC/NHLBI NIH HHS/ -- N01-AG-12100/AG/NIA NIH HHS/ -- N01-HC-25195/HC/NHLBI NIH HHS/ -- N01-HC-35129/HC/NHLBI NIH HHS/ -- N01-HC-45133/HC/NHLBI NIH HHS/ -- N01-HC-55015/HC/NHLBI NIH HHS/ -- N01-HC-55016/HC/NHLBI NIH HHS/ -- N01-HC-55018/HC/NHLBI NIH HHS/ -- N01-HC-55019/HC/NHLBI NIH HHS/ -- N01-HC-55020/HC/NHLBI NIH HHS/ -- N01-HC-55021/HC/NHLBI NIH HHS/ -- N01-HC-55022/HC/NHLBI NIH HHS/ -- N01-HC-75150/HC/NHLBI NIH HHS/ -- N01-HC-85079/HC/NHLBI NIH HHS/ -- N01-HC-85080/HC/NHLBI NIH HHS/ -- N01-HC-85081/HC/NHLBI NIH HHS/ -- N01-HC-85082/HC/NHLBI NIH HHS/ -- N01-HC-85083/HC/NHLBI NIH HHS/ -- N01-HC-85084/HC/NHLBI NIH HHS/ -- N01-HC-85085/HC/NHLBI NIH HHS/ -- N01-HC-85086/HC/NHLBI NIH HHS/ -- N01-HG-65403/HG/NHGRI NIH HHS/ -- N02-HL-6-4278/HL/NHLBI NIH HHS/ -- PG/02/128/British Heart Foundation/United Kingdom -- PG/08/094/British Heart Foundation/United Kingdom -- PG/08/094/26019/British Heart Foundation/United Kingdom -- R01 DK072193/DK/NIDDK NIH HHS/ -- R01 DK078150/DK/NIDDK NIH HHS/ -- R01 HL087647/HL/NHLBI NIH HHS/ -- R01 HL087676/HL/NHLBI NIH HHS/ -- R01 HL089650/HL/NHLBI NIH HHS/ -- R01HL086694/HL/NHLBI NIH HHS/ -- R01HL087641/HL/NHLBI NIH HHS/ -- R01HL087652/HL/NHLBI NIH HHS/ -- R01HL59367/HL/NHLBI NIH HHS/ -- R24 HD050924/HD/NICHD NIH HHS/ -- RC1 HL099634/HL/NHLBI NIH HHS/ -- RC1 HL099634-02/HL/NHLBI NIH HHS/ -- RC1 HL099793/HL/NHLBI NIH HHS/ -- RC2 HL101864,/HL/NHLBI NIH HHS/ -- RC2 HL102419/HL/NHLBI NIH HHS/ -- RG/07/005/23633/British Heart Foundation/United Kingdom -- RR20649/RR/NCRR NIH HHS/ -- SP/08/005/25115/British Heart Foundation/United Kingdom -- T32 GM007092/GM/NIGMS NIH HHS/ -- T32 HG00040/HG/NHGRI NIH HHS/ -- T32HL007208/HL/NHLBI NIH HHS/ -- TW05596/TW/FIC NIH HHS/ -- U01 DK062370/DK/NIDDK NIH HHS/ -- U01 DK062418/DK/NIDDK NIH HHS/ -- U01 HL069757/HL/NHLBI NIH HHS/ -- U01 HL080295/HL/NHLBI NIH HHS/ -- U01HG004402/HG/NHGRI NIH HHS/ -- U54 RR020278/RR/NCRR NIH HHS/ -- UL1RR025005/RR/NCRR NIH HHS/ -- Intramural NIH HHS/ -- England -- Nature. 2010 Aug 5;466(7307):707-13. doi: 10.1038/nature09270.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Statistical Genetics, Department of Biostatistics, University of Michigan, Ann Arbor, Michigan 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20686565" target="_blank"〉PubMed〈/a〉
    Keywords: African Americans/genetics ; Animals ; Asian Continental Ancestry Group/genetics ; Cholesterol, HDL/blood ; Cholesterol, LDL/blood ; Coronary Artery Disease/blood/genetics/therapy ; Europe/ethnology ; European Continental Ancestry Group/genetics ; Female ; Genetic Loci/*genetics ; *Genome-Wide Association Study ; Genotype ; Humans ; Lipid Metabolism/*genetics ; Lipids/*blood ; Liver/metabolism ; Male ; Mice ; N-Acetylgalactosaminyltransferases/genetics/metabolism ; Phenotype ; Polymorphism, Single Nucleotide/genetics ; Protein Phosphatase 1/genetics/metabolism ; Reproducibility of Results ; Triglycerides/blood
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2011-03-25
    Description: Arising from M. A. Nowak, C. E. Tarnita & E. O. Wilson 466, 1057-1062 (2010); Nowak et al. reply. Nowak et al. argue that inclusive fitness theory has been of little value in explaining the natural world, and that it has led to negligible progress in explaining the evolution of eusociality. However, we believe that their arguments are based upon a misunderstanding of evolutionary theory and a misrepresentation of the empirical literature. We will focus our comments on three general issues.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3836173/" 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/PMC3836173/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abbot, Patrick -- Abe, Jun -- Alcock, John -- Alizon, Samuel -- Alpedrinha, Joao A C -- Andersson, Malte -- Andre, Jean-Baptiste -- van Baalen, Minus -- Balloux, Francois -- Balshine, Sigal -- Barton, Nick -- Beukeboom, Leo W -- Biernaskie, Jay M -- Bilde, Trine -- Borgia, Gerald -- Breed, Michael -- Brown, Sam -- Bshary, Redouan -- Buckling, Angus -- Burley, Nancy T -- Burton-Chellew, Max N -- Cant, Michael A -- Chapuisat, Michel -- Charnov, Eric L -- Clutton-Brock, Tim -- Cockburn, Andrew -- Cole, Blaine J -- Colegrave, Nick -- Cosmides, Leda -- Couzin, Iain D -- Coyne, Jerry A -- Creel, Scott -- Crespi, Bernard -- Curry, Robert L -- Dall, Sasha R X -- Day, Troy -- Dickinson, Janis L -- Dugatkin, Lee Alan -- El Mouden, Claire -- Emlen, Stephen T -- Evans, Jay -- Ferriere, Regis -- Field, Jeremy -- Foitzik, Susanne -- Foster, Kevin -- Foster, William A -- Fox, Charles W -- Gadau, Juergen -- Gandon, Sylvain -- Gardner, Andy -- Gardner, Michael G -- Getty, Thomas -- Goodisman, Michael A D -- Grafen, Alan -- Grosberg, Rick -- Grozinger, Christina M -- Gouyon, Pierre-Henri -- Gwynne, Darryl -- Harvey, Paul H -- Hatchwell, Ben J -- Heinze, Jurgen -- Helantera, Heikki -- Helms, Ken R -- Hill, Kim -- Jiricny, Natalie -- Johnstone, Rufus A -- Kacelnik, Alex -- Kiers, E Toby -- Kokko, Hanna -- Komdeur, Jan -- Korb, Judith -- Kronauer, Daniel -- Kummerli, Rolf -- Lehmann, Laurent -- Linksvayer, Timothy A -- Lion, Sebastien -- Lyon, Bruce -- Marshall, James A R -- McElreath, Richard -- Michalakis, Yannis -- Michod, Richard E -- Mock, Douglas -- Monnin, Thibaud -- Montgomerie, Robert -- Moore, Allen J -- Mueller, Ulrich G -- Noe, Ronald -- Okasha, Samir -- Pamilo, Pekka -- Parker, Geoff A -- Pedersen, Jes S -- Pen, Ido -- Pfennig, David -- Queller, David C -- Rankin, Daniel J -- Reece, Sarah E -- Reeve, Hudson K -- Reuter, Max -- Roberts, Gilbert -- Robson, Simon K A -- Roze, Denis -- Rousset, Francois -- Rueppell, Olav -- Sachs, Joel L -- Santorelli, Lorenzo -- Schmid-Hempel, Paul -- Schwarz, Michael P -- Scott-Phillips, Tom -- Shellmann-Sherman, Janet -- Sherman, Paul W -- Shuker, David M -- Smith, Jeff -- Spagna, Joseph C -- Strassmann, Beverly -- Suarez, Andrew V -- Sundstrom, Liselotte -- Taborsky, Michael -- Taylor, Peter -- Thompson, Graham -- Tooby, John -- Tsutsui, Neil D -- Tsuji, Kazuki -- Turillazzi, Stefano -- Ubeda, Francisco -- Vargo, Edward L -- Voelkl, Bernard -- Wenseleers, Tom -- West, Stuart A -- West-Eberhard, Mary Jane -- Westneat, David F -- Wiernasz, Diane C -- Wild, Geoff -- Wrangham, Richard -- Young, Andrew J -- Zeh, David W -- Zeh, Jeanne A -- Zink, Andrew -- BB/H022716/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- England -- Nature. 2011 Mar 24;471(7339):E1-4; author reply E9-10. doi: 10.1038/nature09831.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21430721" target="_blank"〉PubMed〈/a〉
    Keywords: *Altruism ; Animals ; *Biological Evolution ; Cooperative Behavior ; Female ; Game Theory ; *Genetic Fitness ; Genetics, Population ; Heredity ; Humans ; Male ; *Models, Biological ; Phenotype ; Reproducibility of Results ; *Selection, Genetic ; Sex Ratio
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2012-11-07
    Description: Crohn's disease and ulcerative colitis, the two common forms of inflammatory bowel disease (IBD), affect over 2.5 million people of European ancestry, with rising prevalence in other populations. Genome-wide association studies and subsequent meta-analyses of these two diseases as separate phenotypes have implicated previously unsuspected mechanisms, such as autophagy, in their pathogenesis and showed that some IBD loci are shared with other inflammatory diseases. Here we expand on the knowledge of relevant pathways by undertaking a meta-analysis of Crohn's disease and ulcerative colitis genome-wide association scans, followed by extensive validation of significant findings, with a combined total of more than 75,000 cases and controls. We identify 71 new associations, for a total of 163 IBD loci, that meet genome-wide significance thresholds. Most loci contribute to both phenotypes, and both directional (consistently favouring one allele over the course of human history) and balancing (favouring the retention of both alleles within populations) selection effects are evident. Many IBD loci are also implicated in other immune-mediated disorders, most notably with ankylosing spondylitis and psoriasis. We also observe considerable overlap between susceptibility loci for IBD and mycobacterial infection. Gene co-expression network analysis emphasizes this relationship, with pathways shared between host responses to mycobacteria and those predisposing to IBD.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3491803/" 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/PMC3491803/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jostins, Luke -- Ripke, Stephan -- Weersma, Rinse K -- Duerr, Richard H -- McGovern, Dermot P -- Hui, Ken Y -- Lee, James C -- Schumm, L Philip -- Sharma, Yashoda -- Anderson, Carl A -- Essers, Jonah -- Mitrovic, Mitja -- Ning, Kaida -- Cleynen, Isabelle -- Theatre, Emilie -- Spain, Sarah L -- Raychaudhuri, Soumya -- Goyette, Philippe -- Wei, Zhi -- Abraham, Clara -- Achkar, Jean-Paul -- Ahmad, Tariq -- Amininejad, Leila -- Ananthakrishnan, Ashwin N -- Andersen, Vibeke -- Andrews, Jane M -- Baidoo, Leonard -- Balschun, Tobias -- Bampton, Peter A -- Bitton, Alain -- Boucher, Gabrielle -- Brand, Stephan -- Buning, Carsten -- Cohain, Ariella -- Cichon, Sven -- D'Amato, Mauro -- De Jong, Dirk -- Devaney, Kathy L -- Dubinsky, Marla -- Edwards, Cathryn -- Ellinghaus, David -- Ferguson, Lynnette R -- Franchimont, Denis -- Fransen, Karin -- Gearry, Richard -- Georges, Michel -- Gieger, Christian -- Glas, Jurgen -- Haritunians, Talin -- Hart, Ailsa -- Hawkey, Chris -- Hedl, Matija -- Hu, Xinli -- Karlsen, Tom H -- Kupcinskas, Limas -- Kugathasan, Subra -- Latiano, Anna -- Laukens, Debby -- Lawrance, Ian C -- Lees, Charlie W -- Louis, Edouard -- Mahy, Gillian -- Mansfield, John -- Morgan, Angharad R -- Mowat, Craig -- Newman, William -- Palmieri, Orazio -- Ponsioen, Cyriel Y -- Potocnik, Uros -- Prescott, Natalie J -- Regueiro, Miguel -- Rotter, Jerome I -- Russell, Richard K -- Sanderson, Jeremy D -- Sans, Miquel -- Satsangi, Jack -- Schreiber, Stefan -- Simms, Lisa A -- Sventoraityte, Jurgita -- Targan, Stephan R -- Taylor, Kent D -- Tremelling, Mark -- Verspaget, Hein W -- De Vos, Martine -- Wijmenga, Cisca -- Wilson, David C -- Winkelmann, Juliane -- Xavier, Ramnik J -- Zeissig, Sebastian -- Zhang, Bin -- Zhang, Clarence K -- Zhao, Hongyu -- International IBD Genetics Consortium (IIBDGC) -- Silverberg, Mark S -- Annese, Vito -- Hakonarson, Hakon -- Brant, Steven R -- Radford-Smith, Graham -- Mathew, Christopher G -- Rioux, John D -- Schadt, Eric E -- Daly, Mark J -- Franke, Andre -- Parkes, Miles -- Vermeire, Severine -- Barrett, Jeffrey C -- Cho, Judy H -- 068545/Z/02/Wellcome Trust/United Kingdom -- 083948/Z/07/Z/Wellcome Trust/United Kingdom -- 085475/B/08/Z/Wellcome Trust/United Kingdom -- 085475/Z/08/Z/Wellcome Trust/United Kingdom -- 089120/Wellcome Trust/United Kingdom -- 090532/Wellcome Trust/United Kingdom -- 098051/Wellcome Trust/United Kingdom -- AI062773/AI/NIAID NIH HHS/ -- CA141743/CA/NCI NIH HHS/ -- CZB/4/540/Chief Scientist Office/United Kingdom -- DK043351/DK/NIDDK NIH HHS/ -- DK062413/DK/NIDDK NIH HHS/ -- DK062420/DK/NIDDK NIH HHS/ -- DK062422/DK/NIDDK NIH HHS/ -- DK062423/DK/NIDDK NIH HHS/ -- DK062429/DK/NIDDK NIH HHS/ -- DK062429-S1/DK/NIDDK NIH HHS/ -- DK062431/DK/NIDDK NIH HHS/ -- DK062432/DK/NIDDK NIH HHS/ -- DK063491/DK/NIDDK NIH HHS/ -- DK076984/DK/NIDDK NIH HHS/ -- DK084554/DK/NIDDK NIH HHS/ -- DK83756/DK/NIDDK NIH HHS/ -- ETM/137/Chief Scientist Office/United Kingdom -- ETM/75/Chief Scientist Office/United Kingdom -- G0000934/British Heart Foundation/United Kingdom -- G0600329/Medical Research Council/United Kingdom -- G0800675/Medical Research Council/United Kingdom -- G0800759/Medical Research Council/United Kingdom -- G1002033/Medical Research Council/United Kingdom -- K23 DK097142/DK/NIDDK NIH HHS/ -- M01-RR00425/RR/NCRR NIH HHS/ -- P01 DK046763/DK/NIDDK NIH HHS/ -- P01DK046763/DK/NIDDK NIH HHS/ -- P30 DK043351/DK/NIDDK NIH HHS/ -- R01 CA141743/CA/NCI NIH HHS/ -- R01 DK055731/DK/NIDDK NIH HHS/ -- T32 GM007205/GM/NIGMS NIH HHS/ -- T32GM07205/GM/NIGMS NIH HHS/ -- U01 DK062418/DK/NIDDK NIH HHS/ -- U01 DK062420/DK/NIDDK NIH HHS/ -- U01 DK062422/DK/NIDDK NIH HHS/ -- U01 DK062429/DK/NIDDK NIH HHS/ -- U01 DK062431/DK/NIDDK NIH HHS/ -- U01 DK062432/DK/NIDDK NIH HHS/ -- UL1 TR000005/TR/NCATS NIH HHS/ -- UL1 TR000124/TR/NCATS NIH HHS/ -- UL1 TR000124-01/TR/NCATS NIH HHS/ -- Medical Research Council/United Kingdom -- England -- Nature. 2012 Nov 1;491(7422):119-24. doi: 10.1038/nature11582.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1HH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23128233" target="_blank"〉PubMed〈/a〉
    Keywords: Colitis, Ulcerative/genetics/immunology/microbiology/physiopathology ; Crohn Disease/genetics/immunology/microbiology/physiopathology ; Genetic Predisposition to Disease/*genetics ; Genome, Human/genetics ; *Genome-Wide Association Study ; Haplotypes/genetics ; *Host-Pathogen Interactions/genetics/immunology ; Humans ; Inflammatory Bowel Diseases/*genetics/immunology/*microbiology/physiopathology ; Mycobacterium/*immunology/pathogenicity ; Mycobacterium Infections/genetics/microbiology ; Mycobacterium tuberculosis/immunology/pathogenicity ; Phenotype ; Polymorphism, Single Nucleotide/genetics ; Reproducibility of Results
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2012-01-13
    Description: Most patients with acute myeloid leukaemia (AML) die from progressive disease after relapse, which is associated with clonal evolution at the cytogenetic level. To determine the mutational spectrum associated with relapse, we sequenced the primary tumour and relapse genomes from eight AML patients, and validated hundreds of somatic mutations using deep sequencing; this allowed us to define clonality and clonal evolution patterns precisely at relapse. In addition to discovering novel, recurrently mutated genes (for example, WAC, SMC3, DIS3, DDX41 and DAXX) in AML, we also found two major clonal evolution patterns during AML relapse: (1) the founding clone in the primary tumour gained mutations and evolved into the relapse clone, or (2) a subclone of the founding clone survived initial therapy, gained additional mutations and expanded at relapse. In all cases, chemotherapy failed to eradicate the founding clone. The comparison of relapse-specific versus primary tumour mutations in all eight cases revealed an increase in transversions, probably due to DNA damage caused by cytotoxic chemotherapy. These data demonstrate that AML relapse is associated with the addition of new mutations and clonal evolution, which is shaped, in part, by the chemotherapy that the patients receive to establish and maintain remissions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3267864/" 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/PMC3267864/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ding, Li -- Ley, Timothy J -- Larson, David E -- Miller, Christopher A -- Koboldt, Daniel C -- Welch, John S -- Ritchey, Julie K -- Young, Margaret A -- Lamprecht, Tamara -- McLellan, Michael D -- McMichael, Joshua F -- Wallis, John W -- Lu, Charles -- Shen, Dong -- Harris, Christopher C -- Dooling, David J -- Fulton, Robert S -- Fulton, Lucinda L -- Chen, Ken -- Schmidt, Heather -- Kalicki-Veizer, Joelle -- Magrini, Vincent J -- Cook, Lisa -- McGrath, Sean D -- Vickery, Tammi L -- Wendl, Michael C -- Heath, Sharon -- Watson, Mark A -- Link, Daniel C -- Tomasson, Michael H -- Shannon, William D -- Payton, Jacqueline E -- Kulkarni, Shashikant -- Westervelt, Peter -- Walter, Matthew J -- Graubert, Timothy A -- Mardis, Elaine R -- Wilson, Richard K -- DiPersio, John F -- P01 CA101937/CA/NCI NIH HHS/ -- U54 HG003079/HG/NHGRI NIH HHS/ -- U54 HG003079-10/HG/NHGRI NIH HHS/ -- England -- Nature. 2012 Jan 11;481(7382):506-10. doi: 10.1038/nature10738.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Genome Institute, Washington University, St Louis, Missouri 63108, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22237025" target="_blank"〉PubMed〈/a〉
    Keywords: Antineoplastic Agents/adverse effects/therapeutic use ; Clonal Evolution/*genetics ; Clone Cells/drug effects/metabolism/pathology ; DNA Damage/drug effects ; DNA Mutational Analysis ; Genes, Neoplasm/genetics ; Genome, Human/drug effects/*genetics ; High-Throughput Nucleotide Sequencing ; Humans ; Leukemia, Myeloid, Acute/drug therapy/*genetics/*pathology ; Mutagenesis/drug effects/genetics ; Recurrence ; Reproducibility of Results
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2012-03-20
    Description: Targeted therapies have demonstrated efficacy against specific subsets of molecularly defined cancers. Although most patients with lung cancer are stratified according to a single oncogenic driver, cancers harbouring identical activating genetic mutations show large variations in their responses to the same targeted therapy. The biology underlying this heterogeneity is not well understood, and the impact of co-existing genetic mutations, especially the loss of tumour suppressors, has not been fully explored. Here we use genetically engineered mouse models to conduct a 'co-clinical' trial that mirrors an ongoing human clinical trial in patients with KRAS-mutant lung cancers. This trial aims to determine if the MEK inhibitor selumetinib (AZD6244) increases the efficacy of docetaxel, a standard of care chemotherapy. Our studies demonstrate that concomitant loss of either p53 (also known as Tp53) or Lkb1 (also known as Stk11), two clinically relevant tumour suppressors, markedly impaired the response of Kras-mutant cancers to docetaxel monotherapy. We observed that the addition of selumetinib provided substantial benefit for mice with lung cancer caused by Kras and Kras and p53 mutations, but mice with Kras and Lkb1 mutations had primary resistance to this combination therapy. Pharmacodynamic studies, including positron-emission tomography (PET) and computed tomography (CT), identified biological markers in mice and patients that provide a rationale for the differential efficacy of these therapies in the different genotypes. These co-clinical results identify predictive genetic biomarkers that should be validated by interrogating samples from patients enrolled on the concurrent clinical trial. These studies also highlight the rationale for synchronous co-clinical trials, not only to anticipate the results of ongoing human clinical trials, but also to generate clinically relevant hypotheses that can inform the analysis and design of human studies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3385933/" 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/PMC3385933/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Zhao -- Cheng, Katherine -- Walton, Zandra -- Wang, Yuchuan -- Ebi, Hiromichi -- Shimamura, Takeshi -- Liu, Yan -- Tupper, Tanya -- Ouyang, Jing -- Li, Jie -- Gao, Peng -- Woo, Michele S -- Xu, Chunxiao -- Yanagita, Masahiko -- Altabef, Abigail -- Wang, Shumei -- Lee, Charles -- Nakada, Yuji -- Pena, Christopher G -- Sun, Yanping -- Franchetti, Yoko -- Yao, Catherine -- Saur, Amy -- Cameron, Michael D -- Nishino, Mizuki -- Hayes, D Neil -- Wilkerson, Matthew D -- Roberts, Patrick J -- Lee, Carrie B -- Bardeesy, Nabeel -- Butaney, Mohit -- Chirieac, Lucian R -- Costa, Daniel B -- Jackman, David -- Sharpless, Norman E -- Castrillon, Diego H -- Demetri, George D -- Janne, Pasi A -- Pandolfi, Pier Paolo -- Cantley, Lewis C -- Kung, Andrew L -- Engelman, Jeffrey A -- Wong, Kwok-Kin -- 1U01CA141576/CA/NCI NIH HHS/ -- CA122794/CA/NCI NIH HHS/ -- CA137008/CA/NCI NIH HHS/ -- CA137008-01/CA/NCI NIH HHS/ -- CA137181/CA/NCI NIH HHS/ -- CA140594/CA/NCI NIH HHS/ -- CA147940/CA/NCI NIH HHS/ -- K23 CA157631/CA/NCI NIH HHS/ -- P01 CA120964/CA/NCI NIH HHS/ -- P30 CA016086/CA/NCI NIH HHS/ -- P50 CA090578/CA/NCI NIH HHS/ -- P50 CA090578-06/CA/NCI NIH HHS/ -- P50CA090578/CA/NCI NIH HHS/ -- R01 CA122794/CA/NCI NIH HHS/ -- R01 CA122794-01/CA/NCI NIH HHS/ -- R01 CA137008/CA/NCI NIH HHS/ -- R01 CA137008-01/CA/NCI NIH HHS/ -- R01 CA137181/CA/NCI NIH HHS/ -- R01 CA137181-01A2/CA/NCI NIH HHS/ -- R01 CA140594/CA/NCI NIH HHS/ -- R01 CA140594-01/CA/NCI NIH HHS/ -- R01 CA163896/CA/NCI NIH HHS/ -- RC2 CA147940/CA/NCI NIH HHS/ -- RC2 CA147940-01/CA/NCI NIH HHS/ -- U01 CA141576/CA/NCI NIH HHS/ -- U01 CA141576-01/CA/NCI NIH HHS/ -- England -- Nature. 2012 Mar 18;483(7391):613-7. doi: 10.1038/nature10937.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22425996" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Combined Chemotherapy Protocols ; Benzimidazoles/*pharmacology/therapeutic use ; Biomarkers, Tumor/genetics/metabolism ; *Clinical Trials, Phase II as Topic ; *Disease Models, Animal ; Drug Evaluation, Preclinical ; Fluorodeoxyglucose F18 ; Genes, p53/genetics ; Humans ; Lung Neoplasms/*drug therapy/enzymology/*genetics/metabolism ; MAP Kinase Signaling System/drug effects ; Mice ; Mitogen-Activated Protein Kinase Kinases/antagonists & inhibitors ; Mutation/genetics ; Pharmacogenetics/*methods ; Positron-Emission Tomography ; Protein-Serine-Threonine Kinases/deficiency/genetics ; Proto-Oncogene Proteins/genetics/metabolism ; Proto-Oncogene Proteins p21(ras)/genetics/metabolism ; Randomized Controlled Trials as Topic ; Reproducibility of Results ; Taxoids/*therapeutic use ; Tomography, X-Ray Computed ; Treatment Outcome ; ras Proteins/genetics/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2014-05-30
    Description: The availability of human genome sequence has transformed biomedical research over the past decade. However, an equivalent map for the human proteome with direct measurements of proteins and peptides does not exist yet. Here we present a draft map of the human proteome using high-resolution Fourier-transform mass spectrometry. In-depth proteomic profiling of 30 histologically normal human samples, including 17 adult tissues, 7 fetal tissues and 6 purified primary haematopoietic cells, resulted in identification of proteins encoded by 17,294 genes accounting for approximately 84% of the total annotated protein-coding genes in humans. A unique and comprehensive strategy for proteogenomic analysis enabled us to discover a number of novel protein-coding regions, which includes translated pseudogenes, non-coding RNAs and upstream open reading frames. This large human proteome catalogue (available as an interactive web-based resource at http://www.humanproteomemap.org) will complement available human genome and transcriptome data to accelerate biomedical research in health and disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4403737/" 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/PMC4403737/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Min-Sik -- Pinto, Sneha M -- Getnet, Derese -- Nirujogi, Raja Sekhar -- Manda, Srikanth S -- Chaerkady, Raghothama -- Madugundu, Anil K -- Kelkar, Dhanashree S -- Isserlin, Ruth -- Jain, Shobhit -- Thomas, Joji K -- Muthusamy, Babylakshmi -- Leal-Rojas, Pamela -- Kumar, Praveen -- Sahasrabuddhe, Nandini A -- Balakrishnan, Lavanya -- Advani, Jayshree -- George, Bijesh -- Renuse, Santosh -- Selvan, Lakshmi Dhevi N -- Patil, Arun H -- Nanjappa, Vishalakshi -- Radhakrishnan, Aneesha -- Prasad, Samarjeet -- Subbannayya, Tejaswini -- Raju, Rajesh -- Kumar, Manish -- Sreenivasamurthy, Sreelakshmi K -- Marimuthu, Arivusudar -- Sathe, Gajanan J -- Chavan, Sandip -- Datta, Keshava K -- Subbannayya, Yashwanth -- Sahu, Apeksha -- Yelamanchi, Soujanya D -- Jayaram, Savita -- Rajagopalan, Pavithra -- Sharma, Jyoti -- Murthy, Krishna R -- Syed, Nazia -- Goel, Renu -- Khan, Aafaque A -- Ahmad, Sartaj -- Dey, Gourav -- Mudgal, Keshav -- Chatterjee, Aditi -- Huang, Tai-Chung -- Zhong, Jun -- Wu, Xinyan -- Shaw, Patrick G -- Freed, Donald -- Zahari, Muhammad S -- Mukherjee, Kanchan K -- Shankar, Subramanian -- Mahadevan, Anita -- Lam, Henry -- Mitchell, Christopher J -- Shankar, Susarla Krishna -- Satishchandra, Parthasarathy -- Schroeder, John T -- Sirdeshmukh, Ravi -- Maitra, Anirban -- Leach, Steven D -- Drake, Charles G -- Halushka, Marc K -- Prasad, T S Keshava -- Hruban, Ralph H -- Kerr, Candace L -- Bader, Gary D -- Iacobuzio-Donahue, Christine A -- Gowda, Harsha -- Pandey, Akhilesh -- HHSN268201000032C/HL/NHLBI NIH HHS/ -- HHSN268201000032C/PHS HHS/ -- P41 GM103504/GM/NIGMS NIH HHS/ -- P41GM103504/GM/NIGMS NIH HHS/ -- T32 GM007814/GM/NIGMS NIH HHS/ -- U24 CA160036/CA/NCI NIH HHS/ -- U24CA160036/CA/NCI NIH HHS/ -- U54 GM103520/GM/NIGMS NIH HHS/ -- U54GM103520/GM/NIGMS NIH HHS/ -- England -- Nature. 2014 May 29;509(7502):575-81. doi: 10.1038/nature13302.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA [2] Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. ; Institute of Bioinformatics, International Tech Park, Bangalore 560066, India. ; 1] McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA [2] Adrienne Helis Malvin Medical Research Foundation, New Orleans, Louisiana 70130, USA. ; The Donnelly Centre, University of Toronto, Toronto, Ontario M5S 3E1, Canada. ; 1] McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA [2] Department of Pathology, Universidad de La Frontera, Center of Genetic and Immunological Studies-Scientific and Technological Bioresource Nucleus, Temuco 4811230, Chile. ; McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. ; School of Medicine, Imperial College London, South Kensington Campus, London SW7 2AZ, UK. ; Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. ; Department of Neurosurgery, Postgraduate Institute of Medical Education & Research, Chandigarh 160012, India. ; Department of Internal Medicine Armed Forces Medical College, Pune 411040, India. ; 1] Department of Neuropathology, National Institute of Mental Health and Neurosciences, Bangalore 560029, India [2] Human Brain Tissue Repository, Neurobiology Research Centre, National Institute of Mental Health and Neurosciences, Bangalore 560029, India. ; Department of Chemical and Biomolecular Engineering and Division of Biomedical Engineering, The Hong Kong University of Science and Technology, Clear Water Bay, Hong Kong. ; Department of Neurology, National Institute of Mental Health and Neurosciences, Bangalore 560029, India. ; Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21224, USA. ; 1] The Sol Goldman Pancreatic Cancer Research Center, Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA [2] Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA. ; 1] McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA [2] Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA. ; 1] Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA [2] Departments of Immunology and Urology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA. ; The Sol Goldman Pancreatic Cancer Research Center, Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA. ; 1] Department of Obstetrics and Gynecology, Johns Hopkins University School of Medicine Baltimore, Maryland 21205, USA [2] Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA. ; 1] The Sol Goldman Pancreatic Cancer Research Center, Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA [2] Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA [3] Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA. ; 1] McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA [2] Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA [3] Institute of Bioinformatics, International Tech Park, Bangalore 560066, India [4] Adrienne Helis Malvin Medical Research Foundation, New Orleans, Louisiana 70130, USA [5] The Sol Goldman Pancreatic Cancer Research Center, Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA [6] Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA [7] Diana Helis Henry Medical Research Foundation, New Orleans, Louisiana 70130, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24870542" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Cells, Cultured ; Databases, Protein ; Fetus/metabolism ; Fourier Analysis ; Gene Expression Profiling ; Genome, Human/genetics ; Hematopoietic Stem Cells/cytology/metabolism ; Humans ; Internet ; Mass Spectrometry ; Molecular Sequence Annotation ; Open Reading Frames/genetics ; Organ Specificity ; Protein Biosynthesis ; Protein Isoforms/analysis/genetics/metabolism ; Protein Sorting Signals ; Protein Transport ; Proteome/analysis/chemistry/genetics/*metabolism ; *Proteomics ; Pseudogenes/genetics ; RNA, Untranslated/genetics ; Reproducibility of Results ; Untranslated Regions/genetics
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    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2010-02-05
    Description: Obesity has become a major worldwide challenge to public health, owing to an interaction between the Western 'obesogenic' environment and a strong genetic contribution. Recent extensive genome-wide association studies (GWASs) have identified numerous single nucleotide polymorphisms associated with obesity, but these loci together account for only a small fraction of the known heritable component. Thus, the 'common disease, common variant' hypothesis is increasingly coming under challenge. Here we report a highly penetrant form of obesity, initially observed in 31 subjects who were heterozygous for deletions of at least 593 kilobases at 16p11.2 and whose ascertainment included cognitive deficits. Nineteen similar deletions were identified from GWAS data in 16,053 individuals from eight European cohorts. These deletions were absent from healthy non-obese controls and accounted for 0.7% of our morbid obesity cases (body mass index (BMI) 〉or= 40 kg m(-2) or BMI standard deviation score 〉or= 4; P = 6.4 x 10(-8), odds ratio 43.0), demonstrating the potential importance in common disease of rare variants with strong effects. This highlights a promising strategy for identifying missing heritability in obesity and other complex traits: cohorts with extreme phenotypes are likely to be enriched for rare variants, thereby improving power for their discovery. Subsequent analysis of the loci so identified may well reveal additional rare variants that further contribute to the missing heritability, as recently reported for SIM1 (ref. 3). The most productive approach may therefore be to combine the 'power of the extreme' in small, well-phenotyped cohorts, with targeted follow-up in case-control and population cohorts.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2880448/" 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/PMC2880448/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Walters, R G -- Jacquemont, S -- Valsesia, A -- de Smith, A J -- Martinet, D -- Andersson, J -- Falchi, M -- Chen, F -- Andrieux, J -- Lobbens, S -- Delobel, B -- Stutzmann, F -- El-Sayed Moustafa, J S -- Chevre, J-C -- Lecoeur, C -- Vatin, V -- Bouquillon, S -- Buxton, J L -- Boute, O -- Holder-Espinasse, M -- Cuisset, J-M -- Lemaitre, M-P -- Ambresin, A-E -- Brioschi, A -- Gaillard, M -- Giusti, V -- Fellmann, F -- Ferrarini, A -- Hadjikhani, N -- Campion, D -- Guilmatre, A -- Goldenberg, A -- Calmels, N -- Mandel, J-L -- Le Caignec, C -- David, A -- Isidor, B -- Cordier, M-P -- Dupuis-Girod, S -- Labalme, A -- Sanlaville, D -- Beri-Dexheimer, M -- Jonveaux, P -- Leheup, B -- Ounap, K -- Bochukova, E G -- Henning, E -- Keogh, J -- Ellis, R J -- Macdermot, K D -- van Haelst, M M -- Vincent-Delorme, C -- Plessis, G -- Touraine, R -- Philippe, A -- Malan, V -- Mathieu-Dramard, M -- Chiesa, J -- Blaumeiser, B -- Kooy, R F -- Caiazzo, R -- Pigeyre, M -- Balkau, B -- Sladek, R -- Bergmann, S -- Mooser, V -- Waterworth, D -- Reymond, A -- Vollenweider, P -- Waeber, G -- Kurg, A -- Palta, P -- Esko, T -- Metspalu, A -- Nelis, M -- Elliott, P -- Hartikainen, A-L -- McCarthy, M I -- Peltonen, L -- Carlsson, L -- Jacobson, P -- Sjostrom, L -- Huang, N -- Hurles, M E -- O'Rahilly, S -- Farooqi, I S -- Mannik, K -- Jarvelin, M-R -- Pattou, F -- Meyre, D -- Walley, A J -- Coin, L J M -- Blakemore, A I F -- Froguel, P -- Beckmann, J S -- 077014/Wellcome Trust/United Kingdom -- 079534/Wellcome Trust/United Kingdom -- 082390/Wellcome Trust/United Kingdom -- 089061/Wellcome Trust/United Kingdom -- 1RL1MH083268-01/MH/NIMH NIH HHS/ -- 5R01HL087679-02/HL/NHLBI NIH HHS/ -- 5R01MH63706:02/MH/NIMH NIH HHS/ -- G0500539/Medical Research Council/United Kingdom -- G0600331/Medical Research Council/United Kingdom -- G0600331(77796)/Medical Research Council/United Kingdom -- G0900554/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2010 Feb 4;463(7281):671-5. doi: 10.1038/nature08727.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Genomic Medicine, Imperial College London, London W12 0NN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20130649" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Age of Onset ; Aging ; Body Mass Index ; Case-Control Studies ; Child ; *Chromosome Deletion ; Chromosomes, Human, Pair 16/*genetics ; Cognition Disorders/complications/genetics ; Cohort Studies ; Europe ; Female ; Genome-Wide Association Study ; Heterozygote ; Humans ; Inheritance Patterns/genetics ; Male ; Mutation/genetics ; Obesity/complications/*genetics/*physiopathology ; *Penetrance ; Reproducibility of Results ; Sex Characteristics ; Young Adult
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2013-06-19
    Description: Major international projects are underway that are aimed at creating a comprehensive catalogue of all the genes responsible for the initiation and progression of cancer. These studies involve the sequencing of matched tumour-normal samples followed by mathematical analysis to identify those genes in which mutations occur more frequently than expected by random chance. Here we describe a fundamental problem with cancer genome studies: as the sample size increases, the list of putatively significant genes produced by current analytical methods burgeons into the hundreds. The list includes many implausible genes (such as those encoding olfactory receptors and the muscle protein titin), suggesting extensive false-positive findings that overshadow true driver events. We show that this problem stems largely from mutational heterogeneity and provide a novel analytical methodology, MutSigCV, for resolving the problem. We apply MutSigCV to exome sequences from 3,083 tumour-normal pairs and discover extraordinary variation in mutation frequency and spectrum within cancer types, which sheds light on mutational processes and disease aetiology, and in mutation frequency across the genome, which is strongly correlated with DNA replication timing and also with transcriptional activity. By incorporating mutational heterogeneity into the analyses, MutSigCV is able to eliminate most of the apparent artefactual findings and enable the identification of genes truly associated with cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3919509/" 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/PMC3919509/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lawrence, Michael S -- Stojanov, Petar -- Polak, Paz -- Kryukov, Gregory V -- Cibulskis, Kristian -- Sivachenko, Andrey -- Carter, Scott L -- Stewart, Chip -- Mermel, Craig H -- Roberts, Steven A -- Kiezun, Adam -- Hammerman, Peter S -- McKenna, Aaron -- Drier, Yotam -- Zou, Lihua -- Ramos, Alex H -- Pugh, Trevor J -- Stransky, Nicolas -- Helman, Elena -- Kim, Jaegil -- Sougnez, Carrie -- Ambrogio, Lauren -- Nickerson, Elizabeth -- Shefler, Erica -- Cortes, Maria L -- Auclair, Daniel -- Saksena, Gordon -- Voet, Douglas -- Noble, Michael -- DiCara, Daniel -- Lin, Pei -- Lichtenstein, Lee -- Heiman, David I -- Fennell, Timothy -- Imielinski, Marcin -- Hernandez, Bryan -- Hodis, Eran -- Baca, Sylvan -- Dulak, Austin M -- Lohr, Jens -- Landau, Dan-Avi -- Wu, Catherine J -- Melendez-Zajgla, Jorge -- Hidalgo-Miranda, Alfredo -- Koren, Amnon -- McCarroll, Steven A -- Mora, Jaume -- Lee, Ryan S -- Crompton, Brian -- Onofrio, Robert -- Parkin, Melissa -- Winckler, Wendy -- Ardlie, Kristin -- Gabriel, Stacey B -- Roberts, Charles W M -- Biegel, Jaclyn A -- Stegmaier, Kimberly -- Bass, Adam J -- Garraway, Levi A -- Meyerson, Matthew -- Golub, Todd R -- Gordenin, Dmitry A -- Sunyaev, Shamil -- Lander, Eric S -- Getz, Gad -- ES065073/ES/NIEHS NIH HHS/ -- T32 CA009172/CA/NCI NIH HHS/ -- T32 CA009216/CA/NCI NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- U24 CA143845/CA/NCI NIH HHS/ -- U54 HG003067/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- Intramural NIH HHS/ -- England -- Nature. 2013 Jul 11;499(7457):214-8. doi: 10.1038/nature12213. Epub 2013 Jun 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02141, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23770567" target="_blank"〉PubMed〈/a〉
    Keywords: Artifacts ; DNA Replication Timing ; Exome/genetics ; False Positive Reactions ; Gene Expression ; *Genetic Heterogeneity ; Genome, Human/genetics ; Humans ; Lung Neoplasms/genetics ; Mutation/*genetics ; Mutation Rate ; Neoplasms/classification/*genetics/pathology ; Neoplasms, Squamous Cell/genetics ; Oncogenes/*genetics ; Reproducibility of Results ; Sample Size
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2013-12-03
    Description: The increasing demands placed on natural resources for fuel and food production require that we explore the use of efficient, sustainable feedstocks such as brown macroalgae. The full potential of brown macroalgae as feedstocks for commercial-scale fuel ethanol production, however, requires extensive re-engineering of the alginate and mannitol catabolic pathways in the standard industrial microbe Saccharomyces cerevisiae. Here we present the discovery of an alginate monomer (4-deoxy-L-erythro-5-hexoseulose uronate, or DEHU) transporter from the alginolytic eukaryote Asteromyces cruciatus. The genomic integration and overexpression of the gene encoding this transporter, together with the necessary bacterial alginate and deregulated native mannitol catabolism genes, conferred the ability of an S. cerevisiae strain to efficiently metabolize DEHU and mannitol. When this platform was further adapted to grow on mannitol and DEHU under anaerobic conditions, it was capable of ethanol fermentation from mannitol and DEHU, achieving titres of 4.6% (v/v) (36.2 g l(-1)) and yields up to 83% of the maximum theoretical yield from consumed sugars. These results show that all major sugars in brown macroalgae can be used as feedstocks for biofuels and value-added renewable chemicals in a manner that is comparable to traditional arable-land-based feedstocks.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Enquist-Newman, Maria -- Faust, Ann Marie E -- Bravo, Daniel D -- Santos, Christine Nicole S -- Raisner, Ryan M -- Hanel, Arthur -- Sarvabhowman, Preethi -- Le, Chi -- Regitsky, Drew D -- Cooper, Susan R -- Peereboom, Lars -- Clark, Alana -- Martinez, Yessica -- Goldsmith, Joshua -- Cho, Min Y -- Donohoue, Paul D -- Luo, Lily -- Lamberson, Brigit -- Tamrakar, Pramila -- Kim, Edward J -- Villari, Jeffrey L -- Gill, Avinash -- Tripathi, Shital A -- Karamchedu, Padma -- Paredes, Carlos J -- Rajgarhia, Vineet -- Kotlar, Hans Kristian -- Bailey, Richard B -- Miller, Dennis J -- Ohler, Nicholas L -- Swimmer, Candace -- Yoshikuni, Yasuo -- England -- Nature. 2014 Jan 9;505(7482):239-43. doi: 10.1038/nature12771. Epub 2013 Dec 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Bio Architecture Lab Inc., 604 Bancroft Way, Suite A, Berkeley, California 94710, USA [2]. ; 1] Bio Architecture Lab Inc., 604 Bancroft Way, Suite A, Berkeley, California 94710, USA [2] Manus Biosynthesis Inc., 790 Memorial Drive, Suite 102, Cambridge, Massachusetts 02139 (C.N.S.S.); Calysta Energy, 1140 O'Brien Drive, Menlo Park, California 94025 (D.D.R.); Sutro Biopharma lnc., 310 Utah Avenue, Suite 150, South San Francisco, California 94080, USA (A.G.); Total New Energies USA, 5858 Horton Street, Emeryville, California 94560 (S.A.T.; V.R.). ; Bio Architecture Lab Inc., 604 Bancroft Way, Suite A, Berkeley, California 94710, USA. ; Department of Chemical Engineering and Materials Science, Michigan State University, 2527 Engineering Building, East Lansing, Michigan 48824-1226, USA. ; Statoil ASA, Statoil Research Centre, Arkitekt Ebbells vei 10, Rotvoll, 7005 Trondheim, Norway. ; 1] Bio Architecture Lab Inc., 604 Bancroft Way, Suite A, Berkeley, California 94710, USA [2] BALChile S.A., Badajoz 100, Oficina 1404, Las Condes, Santiago 7550000, Chile [3] BAL Biofuels S.A., Badajoz 100, Oficina 1404, Las Condes, Santiago 7550000, Chile.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24291791" target="_blank"〉PubMed〈/a〉
    Keywords: Alginates/metabolism ; Anaerobiosis ; Ascomycota/genetics/metabolism ; Biofuels/*supply & distribution ; Biotechnology ; *Carbohydrate Metabolism ; Carrier Proteins/genetics/metabolism ; Ethanol/*metabolism ; Evolution, Molecular ; Fermentation ; Genetic Complementation Test ; *Genetic Engineering ; Glucuronic Acid/metabolism ; Hexuronic Acids/metabolism ; Mannitol/metabolism ; Phaeophyta/genetics/*metabolism ; Quinic Acid/metabolism ; Reproducibility of Results ; Saccharomyces cerevisiae/genetics/*metabolism ; Seaweed/genetics/metabolism ; Uronic Acids/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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