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  • 1
    Publication Date: 2008-08-30
    Description: It is thought that the Northern Hemisphere experienced only ephemeral glaciations from the Late Eocene to the Early Pliocene epochs (about 38 to 4 million years ago), and that the onset of extensive glaciations did not occur until about 3 million years ago. Several hypotheses have been proposed to explain this increase in Northern Hemisphere glaciation during the Late Pliocene. Here we use a fully coupled atmosphere-ocean general circulation model and an ice-sheet model to assess the impact of the proposed driving mechanisms for glaciation and the influence of orbital variations on the development of the Greenland ice sheet in particular. We find that Greenland glaciation is mainly controlled by a decrease in atmospheric carbon dioxide during the Late Pliocene. By contrast, our model results suggest that climatic shifts associated with the tectonically driven closure of the Panama seaway, with the termination of a permanent El Nino state or with tectonic uplift are not large enough to contribute significantly to the growth of the Greenland ice sheet; moreover, we find that none of these processes acted as a priming mechanism for glacial inception triggered by variations in the Earth's orbit.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lunt, Daniel J -- Foster, Gavin L -- Haywood, Alan M -- Stone, Emma J -- England -- Nature. 2008 Aug 28;454(7208):1102-5. doi: 10.1038/nature07223.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉BRIDGE, School of Geographical Sciences, University of Bristol, University Road, Bristol BS8 1SS, UK. d.j.lunt@bristol.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18756254" target="_blank"〉PubMed〈/a〉
    Keywords: Atmosphere/*chemistry ; Carbon Dioxide/analysis/*metabolism ; Climate ; Greenland ; History, Ancient ; *Ice Cover ; North America ; Rain ; Time Factors
    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: 2008-07-04
    Description: Voyager 2 crossed the solar wind termination shock at 83.7 au in the southern hemisphere, approximately 10 au closer to the Sun than found by Voyager 1 in the north. This asymmetry could indicate an asymmetric pressure from an interstellar magnetic field, from transient-induced shock motion, or from the solar wind dynamic pressure. Here we report that the intensity of 4-5 MeV protons accelerated by the shock near Voyager 2 was three times that observed concurrently by Voyager 1, indicating differences in the shock at the two locations. (Companion papers report on the plasma, magnetic field, plasma-wave and lower energy particle observations at the shock.) Voyager 2 did not find the source of anomalous cosmic rays at the shock, suggesting that the source is elsewhere on the shock or in the heliosheath. The small intensity gradient of Galactic cosmic ray helium indicates that either the gradient is further out in the heliosheath or the local interstellar Galactic cosmic ray intensity is lower than expected.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stone, Edward C -- Cummings, Alan C -- McDonald, Frank B -- Heikkila, Bryant C -- Lal, Nand -- Webber, William R -- England -- Nature. 2008 Jul 3;454(7200):71-4. doi: 10.1038/nature07022.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉California Institute of Technology, Pasadena, California 91125, USA. ecs@srl.caltech.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18596802" target="_blank"〉PubMed〈/a〉
    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: 2008-10-14
    Description: Susceptibility to Crohn's disease, a complex inflammatory disease involving the small intestine, is controlled by over 30 loci. One Crohn's disease risk allele is in ATG16L1, a gene homologous to the essential yeast autophagy gene ATG16 (ref. 2). It is not known how ATG16L1 or autophagy contributes to intestinal biology or Crohn's disease pathogenesis. To address these questions, we generated and characterized mice that are hypomorphic for ATG16L1 protein expression, and validated conclusions on the basis of studies in these mice by analysing intestinal tissues that we collected from Crohn's disease patients carrying the Crohn's disease risk allele of ATG16L1. Here we show that ATG16L1 is a bona fide autophagy protein. Within the ileal epithelium, both ATG16L1 and a second essential autophagy protein ATG5 are selectively important for the biology of the Paneth cell, a specialized epithelial cell that functions in part by secretion of granule contents containing antimicrobial peptides and other proteins that alter the intestinal environment. ATG16L1- and ATG5-deficient Paneth cells exhibited notable abnormalities in the granule exocytosis pathway. In addition, transcriptional analysis revealed an unexpected gain of function specific to ATG16L1-deficient Paneth cells including increased expression of genes involved in peroxisome proliferator-activated receptor (PPAR) signalling and lipid metabolism, of acute phase reactants and of two adipocytokines, leptin and adiponectin, known to directly influence intestinal injury responses. Importantly, Crohn's disease patients homozygous for the ATG16L1 Crohn's disease risk allele displayed Paneth cell granule abnormalities similar to those observed in autophagy-protein-deficient mice and expressed increased levels of leptin protein. Thus, ATG16L1, and probably the process of autophagy, have a role within the intestinal epithelium of mice and Crohn's disease patients by selective effects on the cell biology and specialized regulatory properties of Paneth cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2695978/" 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/PMC2695978/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cadwell, Ken -- Liu, John Y -- Brown, Sarah L -- Miyoshi, Hiroyuki -- Loh, Joy -- Lennerz, Jochen K -- Kishi, Chieko -- Kc, Wumesh -- Carrero, Javier A -- Hunt, Steven -- Stone, Christian D -- Brunt, Elizabeth M -- Xavier, Ramnik J -- Sleckman, Barry P -- Li, Ellen -- Mizushima, Noboru -- Stappenbeck, Thaddeus S -- Virgin, Herbert W 4th -- AI062773/AI/NIAID NIH HHS/ -- DK43351/DK/NIDDK NIH HHS/ -- P30 DK040561/DK/NIDDK NIH HHS/ -- P30 DK040561-13/DK/NIDDK NIH HHS/ -- P30 DK043351/DK/NIDDK NIH HHS/ -- P30 DK043351-18/DK/NIDDK NIH HHS/ -- P30 DK052574-09/DK/NIDDK NIH HHS/ -- P30 DK52574/DK/NIDDK NIH HHS/ -- R01 AI062773/AI/NIAID NIH HHS/ -- R01 AI062773-01A1/AI/NIAID NIH HHS/ -- R01 AI062832/AI/NIAID NIH HHS/ -- R01 AI062832-04/AI/NIAID NIH HHS/ -- T32 AR007279/AR/NIAMS NIH HHS/ -- T32 AR007279-30/AR/NIAMS NIH HHS/ -- T32 AR07279/AR/NIAMS NIH HHS/ -- U54 AI057160/AI/NIAID NIH HHS/ -- U54 AI057160-010005/AI/NIAID NIH HHS/ -- U54 AI057160-05S10018/AI/NIAID NIH HHS/ -- England -- Nature. 2008 Nov 13;456(7219):259-63. doi: 10.1038/nature07416. Epub 2008 Oct 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Immunology, Washington University School of Medicine, St Louis, Missouri 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18849966" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Autophagy/*genetics ; Carrier Proteins/genetics/*metabolism ; Cell Line ; Crohn Disease/genetics/pathology ; Exocytosis/genetics ; Homozygote ; Humans ; Mice ; Mice, Inbred C57BL ; Mutation ; Paneth Cells/*metabolism/pathology
    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: 2009-09-18
    Description: Electric fields induce motion in many fluid systems, including polymer melts, surfactant micelles and colloidal suspensions. Likewise, electric fields can be used to move liquid drops. Electrically induced droplet motion manifests itself in processes as diverse as storm cloud formation, commercial ink-jet printing, petroleum and vegetable oil dehydration, electrospray ionization for use in mass spectrometry, electrowetting and lab-on-a-chip manipulations. An important issue in practical applications is the tendency for adjacent drops to coalesce, and oppositely charged drops have long been assumed to experience an attractive force that favours their coalescence. Here we report the existence of a critical field strength above which oppositely charged drops do not coalesce. We observe that appropriately positioned and oppositely charged drops migrate towards one another in an applied electric field; but whereas the drops coalesce as expected at low field strengths, they are repelled from one another after contact at higher field strengths. Qualitatively, the drops appear to 'bounce' off one another. We directly image the transient formation of a meniscus bridge between the bouncing drops, and propose that this temporary bridge is unstable with respect to capillary pressure when it forms in an electric field exceeding a critical strength. The observation of oppositely charged drops bouncing rather than coalescing in strong electric fields should affect our understanding of any process involving charged liquid drops, including de-emulsification, electrospray ionization and atmospheric conduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ristenpart, W D -- Bird, J C -- Belmonte, A -- Dollar, F -- Stone, H A -- England -- Nature. 2009 Sep 17;461(7262):377-80. doi: 10.1038/nature08294.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemical Engineering and Materials Science, University of California at Davis, 1 Shields Drive, Davis, California 95616, USA. wdristenpart@ucdavis.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19759616" target="_blank"〉PubMed〈/a〉
    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: 2009-10-23
    Description: The tumour stroma is believed to contribute to some of the most malignant characteristics of epithelial tumours. However, signalling between stromal and tumour cells is complex and remains poorly understood. Here we show that the genetic inactivation of Pten in stromal fibroblasts of mouse mammary glands accelerated the initiation, progression and malignant transformation of mammary epithelial tumours. This was associated with the massive remodelling of the extracellular matrix (ECM), innate immune cell infiltration and increased angiogenesis. Loss of Pten in stromal fibroblasts led to increased expression, phosphorylation (T72) and recruitment of Ets2 to target promoters known to be involved in these processes. Remarkably, Ets2 inactivation in Pten stroma-deleted tumours ameliorated disruption of the tumour microenvironment and was sufficient to decrease tumour growth and progression. Global gene expression profiling of mammary stromal cells identified a Pten-specific signature that was highly represented in the tumour stroma of patients with breast cancer. These findings identify the Pten-Ets2 axis as a critical stroma-specific signalling pathway that suppresses mammary epithelial tumours.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2767301/" 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/PMC2767301/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Trimboli, Anthony J -- Cantemir-Stone, Carmen Z -- Li, Fu -- Wallace, Julie A -- Merchant, Anand -- Creasap, Nicholas -- Thompson, John C -- Caserta, Enrico -- Wang, Hui -- Chong, Jean-Leon -- Naidu, Shan -- Wei, Guo -- Sharma, Sudarshana M -- Stephens, Julie A -- Fernandez, Soledad A -- Gurcan, Metin N -- Weinstein, Michael B -- Barsky, Sanford H -- Yee, Lisa -- Rosol, Thomas J -- Stromberg, Paul C -- Robinson, Michael L -- Pepin, Francois -- Hallett, Michael -- Park, Morag -- Ostrowski, Michael C -- Leone, Gustavo -- P01 CA097189/CA/NCI NIH HHS/ -- P01 CA097189-050002/CA/NCI NIH HHS/ -- P01CA097189/CA/NCI NIH HHS/ -- R01 CA053271/CA/NCI NIH HHS/ -- R01 CA085619/CA/NCI NIH HHS/ -- R01 CA085619-05/CA/NCI NIH HHS/ -- R01 CA121275/CA/NCI NIH HHS/ -- R01 CA121275-02/CA/NCI NIH HHS/ -- R01 HD047470/HD/NICHD NIH HHS/ -- R01 HD047470-05/HD/NICHD NIH HHS/ -- R01CA053271/CA/NCI NIH HHS/ -- R01CA85619/CA/NCI NIH HHS/ -- R01HD47470/HD/NICHD NIH HHS/ -- England -- Nature. 2009 Oct 22;461(7267):1084-91. doi: 10.1038/nature08486.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, College of Biological Sciences, The Ohio State University, Columbus, Ohio 43210, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19847259" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/*metabolism/*pathology ; Cell Line, Tumor ; Cell Proliferation ; Cell Transformation, Neoplastic ; Extracellular Matrix/metabolism ; Fibroblasts/*metabolism ; Gene Deletion ; Gene Expression Regulation, Neoplastic ; Humans ; Immunity, Innate ; Mammary Neoplasms, Experimental/metabolism/pathology ; Mice ; Mice, Transgenic ; Neoplasms, Glandular and Epithelial/*metabolism/*pathology ; PTEN Phosphohydrolase/deficiency/genetics/*metabolism ; Proto-Oncogene Protein c-ets-2/deficiency/metabolism ; Stromal Cells/*metabolism
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  • 6
    Publication Date: 2009-08-21
    Description: A stochastic background of gravitational waves is expected to arise from a superposition of a large number of unresolved gravitational-wave sources of astrophysical and cosmological origin. It should carry unique signatures from the earliest epochs in the evolution of the Universe, inaccessible to standard astrophysical observations. Direct measurements of the amplitude of this background are therefore of fundamental importance for understanding the evolution of the Universe when it was younger than one minute. Here we report limits on the amplitude of the stochastic gravitational-wave background using the data from a two-year science run of the Laser Interferometer Gravitational-wave Observatory (LIGO). Our result constrains the energy density of the stochastic gravitational-wave background normalized by the critical energy density of the Universe, in the frequency band around 100 Hz, to be 〈6.9 x 10(-6) at 95% confidence. The data rule out models of early Universe evolution with relatively large equation-of-state parameter, as well as cosmic (super)string models with relatively small string tension that are favoured in some string theory models. This search for the stochastic background improves on the indirect limits from Big Bang nucleosynthesis and cosmic microwave background at 100 Hz.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉LIGO Scientific Collaboration & Virgo Collaboration -- Abbott, B P -- Abbott, R -- Acernese, F -- Adhikari, R -- Ajith, P -- Allen, B -- Allen, G -- Alshourbagy, M -- Amin, R S -- Anderson, S B -- Anderson, W G -- Antonucci, F -- Aoudia, S -- Arain, M A -- Araya, M -- Armandula, H -- Armor, P -- Arun, K G -- Aso, Y -- Aston, S -- Astone, P -- Aufmuth, P -- Aulbert, C -- Babak, S -- Baker, P -- Ballardin, G -- Ballmer, S -- Barker, C -- Barker, D -- Barone, F -- Barr, B -- Barriga, P -- Barsotti, L -- Barsuglia, M -- Barton, M A -- Bartos, I -- Bassiri, R -- Bastarrika, M -- Bauer, Th S -- Behnke, B -- Beker, M -- Benacquista, M -- Betzwieser, J -- Beyersdorf, P T -- Bigotta, S -- Bilenko, I A -- Billingsley, G -- Birindelli, S -- Biswas, R -- Bizouard, M A -- Black, E -- Blackburn, J K -- Blackburn, L -- Blair, D -- Bland, B -- Boccara, C -- Bodiya, T P -- Bogue, L -- Bondu, F -- Bonelli, L -- Bork, R -- Boschi, V -- Bose, S -- Bosi, L -- Braccini, S -- Bradaschia, C -- Brady, P R -- Braginsky, V B -- Brand, J F J van den -- Brau, J E -- Bridges, D O -- Brillet, A -- Brinkmann, M -- Brisson, V -- Van Den Broeck, C -- Brooks, A F -- Brown, D A -- Brummit, A -- Brunet, G -- Bullington, A -- Bulten, H J -- Buonanno, A -- Burmeister, O -- Buskulic, D -- Byer, R L -- Cadonati, L -- Cagnoli, G -- Calloni, E -- Camp, J B -- Campagna, E -- Cannizzo, J -- Cannon, K C -- Canuel, B -- Cao, J -- Carbognani, F -- Cardenas, L -- Caride, S -- Castaldi, G -- Caudill, S -- Cavaglia, M -- Cavalier, F -- Cavalieri, R -- Cella, G -- Cepeda, C -- Cesarini, E -- Chalermsongsak, T -- Chalkley, E -- Charlton, P -- Chassande-Mottin, E -- Chatterji, S -- Chelkowski, S -- Chen, Y -- Christensen, N -- Chung, C T Y -- Clark, D -- Clark, J -- Clayton, J H -- Cleva, F -- Coccia, E -- Cokelaer, T -- Colacino, C N -- Colas, J -- Colla, A -- Colombini, M -- Conte, R -- Cook, D -- Corbitt, T R C -- Corda, C -- Cornish, N -- Corsi, A -- Coulon, J-P -- Coward, D -- Coyne, D C -- Creighton, J D E -- Creighton, T D -- Cruise, A M -- Culter, R M -- Cumming, A -- Cunningham, L -- Cuoco, E -- Danilishin, S L -- D'Antonio, S -- Danzmann, K -- Dari, A -- Dattilo, V -- Daudert, B -- Davier, M -- Davies, G -- Daw, E J -- Day, R -- De Rosa, R -- Debra, D -- Degallaix, J -- Del Prete, M -- Dergachev, V -- Desai, S -- Desalvo, R -- Dhurandhar, S -- Di Fiore, L -- Di Lieto, A -- Di Paolo Emilio, M -- Di Virgilio, A -- Diaz, M -- Dietz, A -- Donovan, F -- Dooley, K L -- Doomes, E E -- Drago, M -- Drever, R W P -- Dueck, J -- Duke, I -- Dumas, J-C -- Dwyer, J G -- Echols, C -- Edgar, M -- Effler, A -- Ehrens, P -- Ely, G -- Espinoza, E -- Etzel, T -- Evans, M -- Evans, T -- Fafone, V -- Fairhurst, S -- Faltas, Y -- Fan, Y -- Fazi, D -- Fehrmann, H -- Ferrante, I -- Fidecaro, F -- Finn, L S -- Fiori, I -- Flaminio, R -- Flasch, K -- Foley, S -- Forrest, C -- Fotopoulos, N -- Fournier, J-D -- Franc, J -- Franzen, A -- Frasca, S -- Frasconi, F -- Frede, M -- Frei, M -- Frei, Z -- Freise, A -- Frey, R -- Fricke, T -- Fritschel, P -- Frolov, V V -- Fyffe, M -- Galdi, V -- Gammaitoni, L -- Garofoli, J A -- Garufi, F -- Genin, E -- Gennai, A -- Gholami, I -- Giaime, J A -- Giampanis, S -- Giardina, K D -- Giazotto, A -- Goda, K -- Goetz, E -- Goggin, L M -- Gonzalez, G -- Gorodetsky, M L -- Gobler, S -- Gouaty, R -- Granata, M -- Granata, V -- Grant, A -- Gras, S -- Gray, C -- Gray, M -- Greenhalgh, R J S -- Gretarsson, A M -- Greverie, C -- Grimaldi, F -- Grosso, R -- Grote, H -- Grunewald, S -- Guenther, M -- Guidi, G -- Gustafson, E K -- Gustafson, R -- Hage, B -- Hallam, J M -- Hammer, D -- Hammond, G D -- Hanna, C -- Hanson, J -- Harms, J -- Harry, G M -- Harry, I W -- Harstad, E D -- Haughian, K -- Hayama, K -- Heefner, J -- Heitmann, H -- Hello, P -- Heng, I S -- Heptonstall, A -- Hewitson, M -- Hild, S -- Hirose, E -- Hoak, D -- Hodge, K A -- Holt, K -- Hosken, D J -- Hough, J -- Hoyland, D -- Huet, D -- Hughey, B -- Huttner, S H -- Ingram, D R -- Isogai, T -- Ito, M -- Ivanov, A -- Johnson, B -- Johnson, W W -- Jones, D I -- Jones, G -- Jones, R -- Sancho de la Jordana, L -- Ju, L -- Kalmus, P -- Kalogera, V -- Kandhasamy, S -- Kanner, J -- Kasprzyk, D -- Katsavounidis, E -- Kawabe, K -- Kawamura, S -- Kawazoe, F -- Kells, W -- Keppel, D G -- Khalaidovski, A -- Khalili, F Y -- Khan, R -- Khazanov, E -- King, P -- Kissel, J S -- Klimenko, S -- Kokeyama, K -- Kondrashov, V -- Kopparapu, R -- Koranda, S -- Kozak, D -- Krishnan, B -- Kumar, R -- Kwee, P -- La Penna, P -- Lam, P K -- Landry, M -- Lantz, B -- Laval, M -- Lazzarini, A -- Lei, H -- Lei, M -- Leindecker, N -- Leonor, I -- Leroy, N -- Letendre, N -- Li, C -- Lin, H -- Lindquist, P E -- Littenberg, T B -- Lockerbie, N A -- Lodhia, D -- Longo, M -- Lorenzini, M -- Loriette, V -- Lormand, M -- Losurdo, G -- Lu, P -- Lubinski, M -- Lucianetti, A -- Luck, H -- Machenschalk, B -- Macinnis, M -- Mackowski, J-M -- Mageswaran, M -- Mailand, K -- Majorana, E -- Man, N -- Mandel, I -- Mandic, V -- Mantovani, M -- Marchesoni, F -- Marion, F -- Marka, S -- Marka, Z -- Markosyan, A -- Markowitz, J -- Maros, E -- Marque, J -- Martelli, F -- Martin, I W -- Martin, R M -- Marx, J N -- Mason, K -- Masserot, A -- Matichard, F -- Matone, L -- Matzner, R A -- Mavalvala, N -- McCarthy, R -- McClelland, D E -- McGuire, S C -- McHugh, M -- McIntyre, G -- McKechan, D J A -- McKenzie, K -- Mehmet, M -- Melatos, A -- Melissinos, A C -- Mendell, G -- Menendez, D F -- Menzinger, F -- Mercer, R A -- Meshkov, S -- Messenger, C -- Meyer, M S -- Michel, C -- Milano, L -- Miller, J -- Minelli, J -- Minenkov, Y -- Mino, Y -- Mitrofanov, V P -- Mitselmakher, G -- Mittleman, R -- Miyakawa, O -- Moe, B -- Mohan, M -- Mohanty, S D -- Mohapatra, S R P -- Moreau, J -- Moreno, G -- Morgado, N -- Morgia, A -- Morioka, T -- Mors, K -- Mosca, S -- Mossavi, K -- Mours, B -- Mowlowry, C -- Mueller, G -- Muhammad, D -- Muhlen, H Zur -- Mukherjee, S -- Mukhopadhyay, H -- Mullavey, A -- Muller-Ebhardt, H -- Munch, J -- Murray, P G -- Myers, E -- Myers, J -- Nash, T -- Nelson, J -- Neri, I -- Newton, G -- Nishizawa, A -- Nocera, F -- Numata, K -- Ochsner, E -- O'Dell, J -- Ogin, G H -- O'Reilly, B -- O'Shaughnessy, R -- Ottaway, D J -- Ottens, R S -- Overmier, H -- Owen, B J -- Pagliaroli, G -- Palomba, C -- Pan, Y -- Pankow, C -- Paoletti, F -- Papa, M A -- Parameshwaraiah, V -- Pardi, S -- Pasqualetti, A -- Passaquieti, R -- Passuello, D -- Patel, P -- Pedraza, M -- Penn, S -- Perreca, A -- Persichetti, G -- Pichot, M -- Piergiovanni, F -- Pierro, V -- Pinard, L -- Pinto, I M -- Pitkin, M -- Pletsch, H J -- Plissi, M V -- Poggiani, R -- Postiglione, F -- Principe, M -- Prix, R -- Prodi, G A -- Prokhorov, L -- Punken, O -- Punturo, M -- Puppo, P -- Putten, S van der -- Quetschke, V -- Raab, F J -- Rabaste, O -- Rabeling, D S -- Radkins, H -- Raffai, P -- Raics, Z -- Rainer, N -- Rakhmanov, M -- Rapagnani, P -- Raymond, V -- Re, V -- Reed, C M -- Reed, T -- Regimbau, T -- Rehbein, H -- Reid, S -- Reitze, D H -- Ricci, F -- Riesen, R -- Riles, K -- Rivera, B -- Roberts, P -- Robertson, N A -- Robinet, F -- Robinson, C -- Robinson, E L -- Rocchi, A -- Roddy, S -- Rolland, L -- Rollins, J -- Romano, J D -- Romano, R -- Romie, J H -- Rover, C -- Rowan, S -- Rudiger, A -- Ruggi, P -- Russell, P -- Ryan, K -- Sakata, S -- Salemi, F -- Sandberg, V -- Sannibale, V -- Santamaria, L -- Saraf, S -- Sarin, P -- Sassolas, B -- Sathyaprakash, B S -- Sato, S -- Satterthwaite, M -- Saulson, P R -- Savage, R -- Savov, P -- Scanlan, M -- Schilling, R -- Schnabel, R -- Schofield, R -- Schulz, B -- Schutz, B F -- Schwinberg, P -- Scott, J -- Scott, S M -- Searle, A C -- Sears, B -- Seifert, F -- Sellers, D -- Sengupta, A S -- Sentenac, D -- Sergeev, A -- Shapiro, B -- Shawhan, P -- Shoemaker, D H -- Sibley, A -- Siemens, X -- Sigg, D -- Sinha, S -- Sintes, A M -- Slagmolen, B J J -- Slutsky, J -- van der Sluys, M V -- Smith, J R -- Smith, M R -- Smith, N D -- Somiya, K -- Sorazu, B -- Stein, A -- Stein, L C -- Steplewski, S -- Stochino, A -- Stone, R -- Strain, K A -- Strigin, S -- Stroeer, A -- Sturani, R -- Stuver, A L -- Summerscales, T Z -- Sun, K-X -- Sung, M -- Sutton, P J -- Swinkels, B L -- Szokoly, G P -- Talukder, D -- Tang, L -- Tanner, D B -- Tarabrin, S P -- Taylor, J R -- Taylor, R -- Terenzi, R -- Thacker, J -- Thorne, K A -- Thorne, K S -- Thuring, A -- Tokmakov, K V -- Toncelli, A -- Tonelli, M -- Torres, C -- Torrie, C -- Tournefier, E -- Travasso, F -- Traylor, G -- Trias, M -- Trummer, J -- Ugolini, D -- Ulmen, J -- Urbanek, K -- Vahlbruch, H -- Vajente, G -- Vallisneri, M -- Vass, S -- Vaulin, R -- Vavoulidis, M -- Vecchio, A -- Vedovato, G -- van Veggel, A A -- Veitch, J -- Veitch, P -- Veltkamp, C -- Verkindt, D -- Vetrano, F -- Vicere, A -- Villar, A -- Vinet, J-Y -- Vocca, H -- Vorvick, C -- Vyachanin, S P -- Waldman, S J -- Wallace, L -- Ward, H -- Ward, R L -- Was, M -- Weidner, A -- Weinert, M -- Weinstein, A J -- Weiss, R -- Wen, L -- Wen, S -- Wette, K -- Whelan, J T -- Whitcomb, S E -- Whiting, B F -- Wilkinson, C -- Willems, P A -- Williams, H R -- Williams, L -- Willke, B -- Wilmut, I -- Winkelmann, L -- Winkler, W -- Wipf, C C -- Wiseman, A G -- Woan, G -- Wooley, R -- Worden, J -- Wu, W -- Yakushin, I -- Yamamoto, H -- Yan, Z -- Yoshida, S -- Yvert, M -- Zanolin, M -- Zhang, J -- Zhang, L -- Zhao, C -- Zotov, N -- Zucker, M E -- Zweizig, J -- England -- Nature. 2009 Aug 20;460(7258):990-4. doi: 10.1038/nature08278.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lists of participants and their affiliations appear at the end of the paper.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19693079" target="_blank"〉PubMed〈/a〉
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  • 7
    Publication Date: 2009-12-25
    Description: The ATP-dependent chromatin assembly and remodelling factor (ACF) functions to generate regularly spaced nucleosomes, which are required for heritable gene silencing. The mechanism by which ACF mobilizes nucleosomes remains poorly understood. Here we report a single-molecule FRET study that monitors the remodelling of individual nucleosomes by ACF in real time, revealing previously unknown remodelling intermediates and dynamics. In the presence of ACF and ATP, the nucleosomes exhibit gradual translocation along DNA interrupted by well-defined kinetic pauses that occurred after approximately seven or three to four base pairs of translocation. The binding of ACF, translocation of DNA and exiting of translocation pauses are all ATP-dependent, revealing three distinct functional roles of ATP during remodelling. At equilibrium, a continuously bound ACF complex can move the nucleosome back-and-forth many times before dissociation, indicating that ACF is a highly processive and bidirectional nucleosome translocase.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2835771/" 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/PMC2835771/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Blosser, Timothy R -- Yang, Janet G -- Stone, Michael D -- Narlikar, Geeta J -- Zhuang, Xiaowei -- GM073767/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Dec 24;462(7276):1022-7. doi: 10.1038/nature08627.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Massachusetts 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20033040" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; *Chromatin Assembly and Disassembly ; Fluorescence Resonance Energy Transfer ; Humans ; *Models, Molecular ; Nucleosomes/*chemistry ; Protein Structure, Tertiary ; Transcription Factors/*chemistry/*metabolism
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  • 8
    Publication Date: 2009-07-03
    Description: Schizophrenia is a severe mental disorder with a lifetime risk of about 1%, characterized by hallucinations, delusions and cognitive deficits, with heritability estimated at up to 80%. We performed a genome-wide association study of 3,322 European individuals with schizophrenia and 3,587 controls. Here we show, using two analytic approaches, the extent to which common genetic variation underlies the risk of schizophrenia. First, we implicate the major histocompatibility complex. Second, we provide molecular genetic evidence for a substantial polygenic component to the risk of schizophrenia involving thousands of common alleles of very small effect. We show that this component also contributes to the risk of bipolar disorder, but not to several non-psychiatric diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3912837/" 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/PMC3912837/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉International Schizophrenia Consortium -- Purcell, Shaun M -- Wray, Naomi R -- Stone, Jennifer L -- Visscher, Peter M -- O'Donovan, Michael C -- Sullivan, Patrick F -- Sklar, Pamela -- 066717/Wellcome Trust/United Kingdom -- G0500791/Medical Research Council/United Kingdom -- G0800509/Medical Research Council/United Kingdom -- R01 MH074027/MH/NIMH NIH HHS/ -- R01 MH077139/MH/NIMH NIH HHS/ -- R01 MH080403/MH/NIMH NIH HHS/ -- England -- Nature. 2009 Aug 6;460(7256):748-52. doi: 10.1038/nature08185. Epub 2009 Jul 1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19571811" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Bipolar Disorder/*genetics ; Case-Control Studies ; Europe ; Female ; Gene Frequency/genetics ; Genetic Predisposition to Disease/*genetics ; Genetic Variation/*genetics ; Genome, Human/genetics ; Genome-Wide Association Study ; Humans ; Major Histocompatibility Complex/genetics ; Male ; Models, Genetic ; Multifactorial Inheritance/*genetics ; Polymorphism, Single Nucleotide/genetics ; Schizophrenia/*genetics
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  • 9
    Publication Date: 2010-06-18
    Description: Sialic acid acetylesterase (SIAE) is an enzyme that negatively regulates B lymphocyte antigen receptor signalling and is required for the maintenance of immunological tolerance in mice. Heterozygous loss-of-function germline rare variants and a homozygous defective polymorphic variant of SIAE were identified in 24/923 subjects of European origin with relatively common autoimmune disorders and in 2/648 controls of European origin. All heterozygous loss-of-function SIAE mutations tested were capable of functioning in a dominant negative manner. A homozygous secretion-defective polymorphic variant of SIAE was catalytically active, lacked the ability to function in a dominant negative manner, and was seen in eight autoimmune subjects but in no control subjects. The odds ratio for inheriting defective SIAE alleles was 8.6 in all autoimmune subjects, 8.3 in subjects with rheumatoid arthritis, and 7.9 in subjects with type I diabetes. Functionally defective SIAE rare and polymorphic variants represent a strong genetic link to susceptibility in relatively common human autoimmune disorders.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2900412/" 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/PMC2900412/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Surolia, Ira -- Pirnie, Stephan P -- Chellappa, Vasant -- Taylor, Kendra N -- Cariappa, Annaiah -- Moya, Jesse -- Liu, Haoyuan -- Bell, Daphne W -- Driscoll, David R -- Diederichs, Sven -- Haider, Khaleda -- Netravali, Ilka -- Le, Sheila -- Elia, Roberto -- Dow, Ethan -- Lee, Annette -- Freudenberg, Jan -- De Jager, Philip L -- Chretien, Yves -- Varki, Ajit -- MacDonald, Marcy E -- Gillis, Tammy -- Behrens, Timothy W -- Bloch, Donald -- Collier, Deborah -- Korzenik, Joshua -- Podolsky, Daniel K -- Hafler, David -- Murali, Mandakolathur -- Sands, Bruce -- Stone, John H -- Gregersen, Peter K -- Pillai, Shiv -- AI 064930/AI/NIAID NIH HHS/ -- AI 068759/AI/NIAID NIH HHS/ -- AI 076505/AI/NIAID NIH HHS/ -- AR 022263/AR/NIAMS NIH HHS/ -- AR 044422/AR/NIAMS NIH HHS/ -- AR 058481/AR/NIAMS NIH HHS/ -- NS 32765/NS/NINDS NIH HHS/ -- P30 DK043351/DK/NIDDK NIH HHS/ -- R01 AI064930/AI/NIAID NIH HHS/ -- R01 AI064930-04/AI/NIAID NIH HHS/ -- R01 AI068759/AI/NIAID NIH HHS/ -- R01 AI068759-05/AI/NIAID NIH HHS/ -- R01 AI076505/AI/NIAID NIH HHS/ -- R01 AI076505-02/AI/NIAID NIH HHS/ -- R01 AR044422/AR/NIAMS NIH HHS/ -- R01 AR044422-13/AR/NIAMS NIH HHS/ -- RC1 AR058481/AR/NIAMS NIH HHS/ -- RC1 AR058481-01/AR/NIAMS NIH HHS/ -- England -- Nature. 2010 Jul 8;466(7303):243-7. doi: 10.1038/nature09115. Epub 2010 Jun 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Center, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20555325" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Acetylesterase/*genetics/metabolism/secretion ; Alleles ; Animals ; Antibodies, Antinuclear/blood ; Arthritis, Rheumatoid/enzymology/genetics ; Autoimmune Diseases/*enzymology/*genetics ; Autoimmunity/*genetics ; B-Lymphocytes/metabolism ; Biocatalysis ; Carboxylic Ester Hydrolases/*genetics/metabolism/secretion ; Case-Control Studies ; Cell Line ; Diabetes Mellitus, Type 1/enzymology/genetics ; Europe/ethnology ; Exons/genetics ; Genetic Predisposition to Disease/*genetics ; Germ-Line Mutation/*genetics ; Humans ; Mice ; N-Acetylneuraminic Acid/*metabolism ; Odds Ratio ; Polymorphism, Single Nucleotide/genetics ; Sample Size ; Sequence Analysis, DNA
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  • 10
    Publication Date: 2010-04-03
    Description: Copy number variants (CNVs) account for a major proportion of human genetic polymorphism and have been predicted to have an important role in genetic susceptibility to common disease. To address this we undertook a large, direct genome-wide study of association between CNVs and eight common human diseases. Using a purpose-designed array we typed approximately 19,000 individuals into distinct copy-number classes at 3,432 polymorphic CNVs, including an estimated approximately 50% of all common CNVs larger than 500 base pairs. We identified several biological artefacts that lead to false-positive associations, including systematic CNV differences between DNAs derived from blood and cell lines. Association testing and follow-up replication analyses confirmed three loci where CNVs were associated with disease-IRGM for Crohn's disease, HLA for Crohn's disease, rheumatoid arthritis and type 1 diabetes, and TSPAN8 for type 2 diabetes-although in each case the locus had previously been identified in single nucleotide polymorphism (SNP)-based studies, reflecting our observation that most common CNVs that are well-typed on our array are well tagged by SNPs and so have been indirectly explored through SNP studies. We conclude that common CNVs that can be typed on existing platforms are unlikely to contribute greatly to the genetic basis of common human diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2892339/" 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/PMC2892339/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wellcome Trust Case Control Consortium -- Craddock, Nick -- Hurles, Matthew E -- Cardin, Niall -- Pearson, Richard D -- Plagnol, Vincent -- Robson, Samuel -- Vukcevic, Damjan -- Barnes, Chris -- Conrad, Donald F -- Giannoulatou, Eleni -- Holmes, Chris -- Marchini, Jonathan L -- Stirrups, Kathy -- Tobin, Martin D -- Wain, Louise V -- Yau, Chris -- Aerts, Jan -- Ahmad, Tariq -- Andrews, T Daniel -- Arbury, Hazel -- Attwood, Anthony -- Auton, Adam -- Ball, Stephen G -- Balmforth, Anthony J -- Barrett, Jeffrey C -- Barroso, Ines -- Barton, Anne -- Bennett, Amanda J -- Bhaskar, Sanjeev -- Blaszczyk, Katarzyna -- Bowes, John -- Brand, Oliver J -- Braund, Peter S -- Bredin, Francesca -- Breen, Gerome -- Brown, Morris J -- Bruce, Ian N -- Bull, Jaswinder -- Burren, Oliver S -- Burton, John -- Byrnes, Jake -- Caesar, Sian -- Clee, Chris M -- Coffey, Alison J -- Connell, John M C -- Cooper, Jason D -- Dominiczak, Anna F -- Downes, Kate -- Drummond, Hazel E -- Dudakia, Darshna -- Dunham, Andrew -- Ebbs, Bernadette -- Eccles, Diana -- Edkins, Sarah -- Edwards, Cathryn -- Elliot, Anna -- Emery, Paul -- Evans, David M -- Evans, Gareth -- Eyre, Steve -- Farmer, Anne -- Ferrier, I Nicol -- Feuk, Lars -- Fitzgerald, Tomas -- Flynn, Edward -- Forbes, Alistair -- Forty, Liz -- Franklyn, Jayne A -- Freathy, Rachel M -- Gibbs, Polly -- Gilbert, Paul -- Gokumen, Omer -- Gordon-Smith, Katherine -- Gray, Emma -- Green, Elaine -- Groves, Chris J -- Grozeva, Detelina -- Gwilliam, Rhian -- Hall, Anita -- Hammond, Naomi -- Hardy, Matt -- Harrison, Pile -- Hassanali, Neelam -- Hebaishi, Husam -- Hines, Sarah -- Hinks, Anne -- Hitman, Graham A -- Hocking, Lynne -- Howard, Eleanor -- Howard, Philip -- Howson, Joanna M M -- Hughes, Debbie -- Hunt, Sarah -- Isaacs, John D -- Jain, Mahim -- Jewell, Derek P -- Johnson, Toby -- Jolley, Jennifer D -- Jones, Ian R -- Jones, Lisa A -- Kirov, George -- Langford, Cordelia F -- Lango-Allen, Hana -- Lathrop, G Mark -- Lee, James -- Lee, Kate L -- Lees, Charlie -- Lewis, Kevin -- Lindgren, Cecilia M -- Maisuria-Armer, Meeta -- Maller, Julian -- Mansfield, John -- Martin, Paul -- Massey, Dunecan C O -- McArdle, Wendy L -- McGuffin, Peter -- McLay, Kirsten E -- Mentzer, Alex -- Mimmack, Michael L -- Morgan, Ann E -- Morris, Andrew P -- Mowat, Craig -- Myers, Simon -- Newman, William -- Nimmo, Elaine R -- O'Donovan, Michael C -- Onipinla, Abiodun -- Onyiah, Ifejinelo -- Ovington, Nigel R -- Owen, Michael J -- Palin, Kimmo -- Parnell, Kirstie -- Pernet, David -- Perry, John R B -- Phillips, Anne -- Pinto, Dalila -- Prescott, Natalie J -- Prokopenko, Inga -- Quail, Michael A -- Rafelt, Suzanne -- Rayner, Nigel W -- Redon, Richard -- Reid, David M -- Renwick -- Ring, Susan M -- Robertson, Neil -- Russell, Ellie -- St Clair, David -- Sambrook, Jennifer G -- Sanderson, Jeremy D -- Schuilenburg, Helen -- Scott, Carol E -- Scott, Richard -- Seal, Sheila -- Shaw-Hawkins, Sue -- Shields, Beverley M -- Simmonds, Matthew J -- Smyth, Debbie J -- Somaskantharajah, Elilan -- Spanova, Katarina -- Steer, Sophia -- Stephens, Jonathan -- Stevens, Helen E -- Stone, Millicent A -- Su, Zhan -- Symmons, Deborah P M -- Thompson, John R -- Thomson, Wendy -- Travers, Mary E -- Turnbull, Clare -- Valsesia, Armand -- Walker, Mark -- Walker, Neil M -- Wallace, Chris -- Warren-Perry, Margaret -- Watkins, Nicholas A -- Webster, John -- Weedon, Michael N -- Wilson, Anthony G -- Woodburn, Matthew -- Wordsworth, B Paul -- Young, Allan H -- Zeggini, Eleftheria -- Carter, Nigel P -- Frayling, Timothy M -- Lee, Charles -- McVean, Gil -- Munroe, Patricia B -- Palotie, Aarno -- Sawcer, Stephen J -- Scherer, Stephen W -- Strachan, David P -- Tyler-Smith, Chris -- Brown, Matthew A -- Burton, Paul R -- Caulfield, Mark J -- Compston, Alastair -- Farrall, Martin -- Gough, Stephen C L -- Hall, Alistair S -- Hattersley, Andrew T -- Hill, Adrian V S -- Mathew, Christopher G -- Pembrey, Marcus -- Satsangi, Jack -- Stratton, Michael R -- Worthington, Jane -- Deloukas, Panos -- Duncanson, Audrey -- Kwiatkowski, Dominic P -- McCarthy, Mark I -- Ouwehand, Willem -- Parkes, Miles -- Rahman, Nazneen -- Todd, John A -- Samani, Nilesh J -- Donnelly, Peter -- 061858/Wellcome Trust/United Kingdom -- 083948/Wellcome Trust/United Kingdom -- 089989/Wellcome Trust/United Kingdom -- 090532/Wellcome Trust/United Kingdom -- 17552/Arthritis Research UK/United Kingdom -- CZB/4/540/Chief Scientist Office/United Kingdom -- ETM/137/Chief Scientist Office/United Kingdom -- ETM/75/Chief Scientist Office/United Kingdom -- G0000934/Medical Research Council/United Kingdom -- G0400874/Medical Research Council/United Kingdom -- G0500115/Medical Research Council/United Kingdom -- G0501942/Medical Research Council/United Kingdom -- G0600329/Medical Research Council/United Kingdom -- G0600705/Medical Research Council/United Kingdom -- G0700491/Medical Research Council/United Kingdom -- G0701003/Medical Research Council/United Kingdom -- G0701420/Medical Research Council/United Kingdom -- G0701810/Medical Research Council/United Kingdom -- G0701810(85517)/Medical Research Council/United Kingdom -- G0800383/Medical Research Council/United Kingdom -- G0800509/Medical Research Council/United Kingdom -- G0800759/Medical Research Council/United Kingdom -- G19/9/Medical Research Council/United Kingdom -- G90/106/Medical Research Council/United Kingdom -- G9521010/Medical Research Council/United Kingdom -- MC_UP_A390_1107/Medical Research Council/United Kingdom -- RG/09/012/28096/British Heart Foundation/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2010 Apr 1;464(7289):713-20. doi: 10.1038/nature08979.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20360734" target="_blank"〉PubMed〈/a〉
    Keywords: Arthritis, Rheumatoid/genetics ; Case-Control Studies ; Crohn Disease/genetics ; DNA Copy Number Variations/*genetics ; Diabetes Mellitus/genetics ; *Disease ; Gene Frequency/genetics ; Genetic Predisposition to Disease/*genetics ; *Genome-Wide Association Study ; Humans ; Nucleic Acid Hybridization ; Oligonucleotide Array Sequence Analysis ; Pilot Projects ; Polymorphism, Single Nucleotide/genetics ; Quality Control
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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