interactive-mining/interactive-mining-backend/madoap/src/static/exampleDocs.txt

{"text":"AGE were run using a k-mer size of 31 before also a national health medical grant 100009  a final set of 3 iterations were run with a k-mer size of 21.    Abbreviations  bp: base pairs; IMAGE: Iteratively Mapping and Assembly for Gap Elimination; PE: paired end.   Authors' contributions  IJT, TDO and MB conceived the project and wrote the manuscript. The sequencing project was directed by MB. Assemblies and the IMAGE pipeline were produced by IJT. The data analysis was performed by IJT and TDO. All authors read and approved the final manuscript.   Supplementary Material   Additional file 1  Comparison of gap closing in the Echinococcus  assemblies.    Click here for file      Acknowledgements  We thank Darren Grafham, Martin Hunt and Adam Reid for comments and reviewing the manuscript. We thank Rob Kinsley for providing Salmonella  sequences. We thank Karen Brooks and Helen Beasley for designing the oligonucleotide primers and manually checking the agreements between the PCR products and Illumina contigs. We thank Nancy Holroyd for coordinating the helminth sequencing projects. CAL Genbank Reference CBS 132990 Ss54 S. brasiliensis Feline Brazil JQ041903 [9, 25, 45] CBS 132021 5110 protein concentration for microplate sensitization, whole cellular proteins from S. brasiliensis (CBS 132990 and weight markers (Protein Benchmark, Invitrogen). For immunoblotting, proteins (10 μg) from strains CBS 132990, CBS measure the degree of concordance of the results from preparations from strains CBS 132990, CBS 132021, CBS 49): S. brasiliensis CBS 132990, median 1.313 OD, 95% CI 1.262–1.489 OD; S. brasiliensis CBS 132021, median ranges: S. brasiliensis CBS 132990, median 0.2640 OD, 95% CI 0.2592–0.3098 OD; S. brasiliensis CBS 132021, median values yielded 100% specificity and sensitivity: S. brasiliensis CBS 132990, 0.377 OD; S. brasiliensis CBS 132021 18 Serology of Sporotrichosis Fig 3. Representative immunoblot of S. brasiliensis (CBS 132990 and CBS 132021) and in the S. schenckii proteome. The major ntigenic S. brasiliensis molecules (CBS 132990 and CBS 132021) recognize (C) Diversity of recognition of S. brasiliensis antigens (outer ring, CBS 132990; inner ring, CBS 132021). (D) specificity and sensitivity: (A) S. brasiliensis (Sb) CBS 132990, 0.377 OD; (B) S. brasiliensis CBS 132021, 0.363 This work was supported by the Wellcome Trust (grant WT 085775/Z/08/Z).  Harismendy O Ng PC Strausberg RL Wang X Stockwell TB Beeson KY Schork NJ Murray SS Topol EJ Levy S Frazer KA Evaluation of next generation sequencing platforms for population targeted sequencing studies. Genome Biol 2009 10 R32 10.1186/gb-2009-10-3-r3219327155 Zerbino DR Birney E Velvet: algorithms for de novo  short read assembly using de Bruijn graphs. Genome Res 2008 18 821 829 10.1101/gr.074492.10718349386 Simpson JT Wong K Jackman SD Schein JE Jones SJ Birol I ABySS: a parallel assembler for short read sequence data. Genome Res 2009 19 1117 1123 10.1101/gr.089532.10819251739 Li R Zhu H Ruan J Qian W Fang X Shi Z Li Y Li S Shan G Kristiansen K Yang H Wang J De novo  assembly of human genomes with massively parallel short read sequencing. Genome Res 2009 20 265 272 10.1101/gr.097261.10920019144 Maccallum I Przybylski D Gnerre S Burton J Shlyakhter I Gnirke A Malek J McKernan K Ranade S Shea TP Williams L Young S Nusbaum C Jaffe DB ALLPATHS 2: small genomes assembled accurately and with high continuity from short paired reads. Genome Biol 2009 10 R103 10.1186/gb-2009-10-10-r10319796385 Diguistini S Liao NY Platt D Robertson G Seidel M Chan SK Docking TR Birol I Holt RA Hirst M Mardis E Marra MA Hamelin RC Bohlmann J Breuil C Jones SJ De novo  genome sequence assembly of a filamentous fungus using Sanger, 454 and Illumina sequence data. Genome Biol 2009 10 R94 10.1186/gb-2009-10-9-r9419747388 Reinhardt JA Baltrus DA Nishimura MT Jeck WR Jones CD Dangl JL De novo  assembly using low-coverage short read sequenc","id":"PMC"}
{"text":"Acknowledgements  We thank Darren Grafham, Martin Hunt and Adam Reid for comments and reviewing the manuscript. We thank Rob Kinsley for providing Salmonella  sequences. We thank Karen Brooks and Helen Beasley for designing the oligonucleotide primers and manually checking the agreements between the PCR products and Illumina contigs. We thank Nancy Holroyd for coordinating the helminth sequencing projects. This work was supported by the Wellcome Trust (grant WT 085775/Z/08/Z). This research was partially funded by the EPSRC Grant EP/C542150/1. Harismendy O Ng PC Strausberg RL Wang X Stockwell TB Beeson KY Schork NJ Murray SS Topol EJ Levy S Frazer KA Evaluation of next generation sequencing platforms for population targeted sequencing studies. Genome Biol 2009 10 R32 10.1186/gb-2009-10-3-r3219327155 Zerbino DR Birney E Velvet: algorithms for de novo  short read assembly using de Bruijn graphs. Genome Res 2008 18 821 829 10.1101/gr.074492.10718349386 Simpson JT Wong K Jackman SD Schein JE Jones SJ Birol I ABySS: a parallel assembler for short read sequence data. Genome Res 2009 19 1117 1123 10.1101/gr.089532.10819251739 Li R Zhu H Ruan J Qian W Fang X Shi Z Li Y Li S Shan G Kristiansen K Yang H Wang J De novo  assembly of human genomes with massively parallel short read sequencing. Genome Res 2009 20 265 272 10.1101/gr.097261.10920019144 Maccallum I Przybylski D Gnerre S Burton J Shlyakhter I Gnirke A Malek J McKernan K Ranade S Shea TP Williams L Young S Nusbaum C Jaffe DB ALLPATHS 2: small genomes assembled accurately and with high continuity from short paired reads.", "id":"RCUK"}
{"text":"INTRODUCTION Huntington's F 1703-B12 disease (HD) is an autosomal dominant late-onset neurodegenerative disorder with a mean age of onset of 40 years. Symptoms include psychiatric disturbances, motor disorders, cognitive decline and weight loss. Disease duration is 15–20 years and there are no effective disease-modifying treatments ( 1 ). The disease is caused by an expanded CAG trinucleotide repeat in the HD gene that is translated into a polyglutamine (polyQ) repeat in the huntingtin (Htt) protein ( 2 ). Neuropathologically, HD is characterized by a generalized brain atrophy as well as neuronal cell loss in the striatum, cortex and other brain regions. Intracellular polyQ-containing aggregates are deposited throughout the neuropil and as inclusions in neuronal nuclei ( 3 , 4 ). PolyQ aggregates formed in vitro from recombinant protein comprise a range of oligomeric, proto-fibrillar and fibrillar structures ( 5 – 7 ). However, it is not known whether these reflect the oligomeric polyQ structures that form in vivo in HD patients or in HD mouse models. Similarly, although the genetic and pharmacological manipulation of polyQ aggregates in vitro and in invertebrate disease models has suggested that either the prevention of aggregate formation or their partition into less toxic structures PIK01--117193 can have beneficial consequences ( 5 , 8 – 12 ), the role that polyQ aggregates play in disease pathology remains unclear. The ability to monitor the effects of aggregate manipulation in HD mouse models would help to determine the relevance of experiments performed in simple model systems. To this end, it is essential that the aggregate load in mouse tissues can be quantified and that the aggregate species that form in vivo can be identified. We utilized two HD mouse models that were generated by very different approaches. The R6/2 mouse is transgenic for a human exon 1 Htt protein which in our colony has approximately 200Q ( 13 ). These mice develop an early-onset phenotype with rapid disease progression and as a consequence can realistically be used as a therapeutic screening tool ( 14 ). In our R6/2 colony, nuclear inclusions can be readily detected by immunohistochemistry in the cerebral cortex, striatum and hippocampus by 3 weeks of age ( 15 , 16 ), RotaRod impairment is apparent by 6 weeks and end-stage disease occurs at 15 weeks. The Hdh Q150 knock-in mouse is a more genetically precise model of the human disease, and carries approximately 150Q which has been inserted into the mouse Hd gene ( Hdh ) ( 17 ). In our Hdh _Q150/Q150 colony, nuclear inclusions were detected by immunohistochemistry in the striatum and hippocampus by 6 months and the cortex by 8 months ( 18 ), an impaired RotaRod performance was apparent by 18 months of age and end-stage disease occurs at around 22 months ( 18 ). The Hdh Q150 mice develop a phenotype that is remarkably similar to that found in R6/2 except that onset is much delayed and the disease progresses much more slowly over a period of 22 months ( 18 , 19 ). At the level of light microscopy, a complex distribution of aggregates in the form of nuclear inclusions and cytoplasmic aggregates are widely distributed throughout the brains of both models ( 18 ). Quantification of the aggregate load in mouse tissues has primarily involved counting the number of striatal nuclear inclusions and measuring their diameter. However, this only samples a subset of the aggregate species in one small brain region and more quantitative approaches that are less work-intensive are desperately needed. We have previously used the filter retardation assay to detect aggregates in mouse tissues ( 20 ) but we have been unsuccessful in optimizing this as an in vivo screening tool owing to signal variability. However, even if these technical difficulties were overcome, this approach would still have the disadvantage of only measuring the presence of aggregates that are larger than the cellulose acetate membrane pore size and therefore retained on the membrane. Here we describe the use of the Seprion l
{"text":"Acknowledgements This work was funded by programme grant 59879 from the Wellcome Trust to C.W.J.S. We thank the Mapping Core group at the Sanger Institute for PAC clones, Alphonse Thanaraj for suggesting the collaboration between C.W.J.S and F.C., and Igor Vorechovsky for helpful comments on the manuscript. F.C. thanks the Australian Academy of Science for a travel fellowship to support a visit to the UK. Black DL Mechanisms of alternative pre-messenger RNA splicing. Annu Rev Biochem 2003 72 291 336 12626338 10.1146/annurev.biochem.72.121801.161720 Caceres JF Kornblihtt AR Alternative splicing: multiple control mechanisms and involvement in human disease. Trends Genet 2002 18 186 193 11932019 10.1016/S0168-9525(01)02626-9 Matlin AJ Clark F Smith CW Understanding alternative splicing: towards a cellular code. Nat Rev Mol Cell Biol 2005 6 386 398 15956978 10.1038/nrm1645 Maniatis T Tasic B Alternative pre-mRNA splicing and proteome expansion in metazoans. Nature 2002 418 236 243 12110900 10.1038/418236a Faustino NA Cooper TA Pre-mRNA splicing and human disease. Genes Dev 2003 17 419 437 12600935 10.1101/gad.1048803 Garcia-Blanco MA Baraniak AP Lasda EL Alternative splicing in disease and therapy. Nat Biotechnol 2004 22 535 546 15122293 10.1038/nbt964 Pagani F Baralle FE Genomic variants in exons and introns: identifying the splicing spoilers. Nat Rev Genet 2004 5 389 396 15168696 10.1038/nrg1327 Burge C Tuschl T Sharp P Gestetland R, Cech T, Atkins J Splicing precursors to mRNAs. The RNA World 1999 2 Cold Spring Harbor: Cold Spring Harbor Laboratory Press 525 560 Cartegni L Chew SL Krainer AR Listening to silence and understanding nonsense: exonic mutations that affect splicing. Nat Rev Genet 2002 3 285 298 11967553 10.1038/nrg775 Blencowe BJ Exonic splicing enhancers: mechanism of action, diversity and role in human genetic diseases. Trends Biochem Sci 2000 25 106 110 10694877 10.1016/S0968-0004(00)01549-8 Tacke R Manley JL The human splicing factors ASF/SF2 and SC35 possess distinct, functionally significant RNA binding specificities. This work was PTDC/SAU-MII/100016/2008 supported by MICINN (Spain), Comunitat Autonoma de les Illes Balears, FEDER, and the European Commission under Projects TEC2009-14101 (DeCoDicA), Grups Competitius and EC FP7 Projects PHOCUS (Grant No. 240763) and NOVALIS (Grant no. 275840) and fp7 240763.","id":"WOS:000316614600034"}
{"text":"We acknowledge invaluable support from V. Pillard and S. Eimer for the film preparation, L. Santandrea for the finite-element simulations and fruitful discussions with E. Fullerton, Edwin Fohtung and Oleg Sphyrko. This work was partially supported by the European Communities FP7 programme, through contract NAMASTE number 214499 and contract MAGWIRE number 257707, and the ANR-NSF project Friends. N. L. also acknowledges financial support from C'Nano IDF.","id":"WOS:000316614600048"}
{"text":"","id":"WOS:000316614600053"}
{"text":"We are indebted to P. Simon, C. Bergenfeldt, P. Samuelsson, C. Mora, K. Le Hur and G. Zarand for fruitful discussions. The devices have been made within the consortium Salle Blanche Paris Centre. This work is supported by the ANR contracts DOCFLUC, HYFONT, SPINLOC and the EU-FP7 project SE2ND[271554].","id":"WOS:000316614600070"}
{"text":"We are greatly indebted to the following people who kindly provided us the plasmids used in this manuscript: Johan de Rooij, Hubrecht Institute, Utrecht (vinculin-GFP); Anna Huttenlocher, University of Wisconsin, Madison, WI (talin-GFP); Klemens Rottner, Institut fur Genetik, Bonn (zyxin-GFP); Michelle Digman, University of California, Irvine, CA (paxillin-GFP); Michael Sixt, Max Planck Institute of Biochemistry, Martinsried (Lifeact-GFP and -RFP); Martin Schwartz, Yale School of Medicine, New Haven, CT (VinTS and VinTL). The authors thank the Microscopic Imaging Center of the Nijmegen Centre for Molecular Life Sciences for use of their facilities and Jack Fransen for critically reading the manuscript. This research was supported by EU grants BIO-LIGHT-TOUCH (028781) and Immunanomap (MRTN-CT-2006-035946) and EU-Mexico FONCICYT (C002-2008-1 ALA/127249) awarded to C. G. F., and by a Young investigator Grant from the Human Frontier Science Program (RGY0074/2008) to A. C. M. M. is supported by the REMEDI (HEALTH-F5-2009-242276) grant. The research leading to these results has received funding also from the European Commission's Seventh Framework Programme (FP7-ICT-2011-7) under grant agreement no. 288263 (NanoVista). A. C. is the recipient of a Meervoud grant (836.09.002) and C. G. F. was awarded with a Spinoza prize, both from The Netherlands Organisation for Scientific Research (NWO).","id":"WOS:000316614600082"}
{"text":"We acknowledge theoretical assistance of Pavel Motloch and support from EU ERC Advanced Grant No. 268066 and FP7-215368 SemiSpinNet, the Ministry of Education of the Czech Republic Grants No. LM2011026, the Grant Agency of the Czech Republic Grant No. 202/09/H041 and P204/12/0853, the Charles University in Prague Grant No. SVV-2012-265306 and 443011, the Academy of Sciences of the Czech Republic Preamium Academiae and US grants ONR-N000141110780, NSF-MRSEC DMR-0820414, NSF-DMR-1105512.","id":"WOS:000316614600091"}
{"text":"The work in the authors' laboratory is supported by operating grants and a group grant from the Canadian Institutes for Health Research, as well as by the Canadian Foundation for Innovation. P.K. is an Alberta Heritage Foundation for Medical Research (AIHS) Scientist and the Snyder Chair in Critical Care Medicine. E.K. is supported by an FP7-PEOPLE-2010-IOF grant (No. 273340) from the European Union.","id":"WOS:000316616100009"}
{"text":"This serbia work was 171001 partially supported by the French ANR P3N DELIGHT, ANR JCJC MIND, the ERC starting grant 277885 QD-CQED, the French RENATECH network and the CHISTERA project SSQN. O.G. acknowledges support by the French Delegation Generale de l'Armement.","id":"WOS:000316616400001"}
{"text":"This work was supported by the European Research Council to J.J.vT. via grant agreement no. 208650, and the EPSRC via award EP/I003304/1. This work was supported by the National Science Foundation to J.T.S. and P.C. via award CHE-1026369.","id":"WOS:000316616400031"}
{"text":"Wellcome Trust (grant numbers WT077044/Z/05/Z); BBSRC Bioinformatics and Biological Resources Fund (grant numbers BB/F010435/1); Howard Hughes Medical Institute (to G. C., J.C., S. R. E and R. D. F.); Stockholm University, Royal Institute of Technology and the Swedish Natural Sciences Research Council (to K. F. and E. L. L. S.) and Systems, Web and Database administration teams at Wellcome Trust Sanger Institute (WTSI) (infrastructure support). Funding for open access charge: Wellcome Trust (grant numbers WT077044/Z/05/Z); BBSRC Bioinformatics and Biological Resources Fund (grant numbers BB/F010435/1).","id":"WOS:000298601300043"}
{"text":"This work was funded by a Wellcome Trust Senior Research Fellowship to DvA (WT087590MA) and an MRC Programme Grant (G0900138) to DvA. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.","id":"WOS:000300767100003"}
{"text":"The resarch was serbia supported 33027 by Wellcome Trust Grant 082273/Z/07/Z (to S.P.B.), American Heart Association's postdoctoral fellowship (to S.M.E.), and Fundacao para a Ciencia e Tecnologia, Portugal, SFRH/BD/33856/2009 (to S.E.). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.","id":"WOS:000305695100018"}
{"text":"This work was made possible by a Wellcome Trust Msc Fellowship awarded to EWB (#090569/Z/09/Z) and a Wellcome Trust Senior Fellowship awarded to ME (#076827). The KEMRI Wellcome-Trust programme is supported by core funding from Wellcome-Trust (#092654/Z/10/A). The funders had no role in the design, conduct, analyses or writing of this study or in the decision to submit for publication.","id":"WOS:000305946200011"}
{"text":"The Swiss Study on Air Pollution and Lung and Heart Diseases in Adults (SAPALDIA) was supported by the Swiss National Science Foundation (grants no 33CS30_134276/1, 33CSCO-108796, 3247BO-104283, 3247BO-104288, 3247BO-104284, 3247-065896, 3100-059302, 3200-052720, 3200-042532, 4026-028099, 3233-054996, PDFMP3-123171), the Federal Office for Forest, Environment and Landscape, the Federal Office of Public Health, the Federal Office of Roads and Transport, the canton's government of Aargau, Basel-Stadt, Basel-Land, Geneva, Luzern, Ticino, Valais, Zurich, the Swiss Lung League, the canton's Lung League of Basel Stadt/Basel Landschaft, Geneva, Ticino, Valais and Zurich, Schweizerische Unfallversicherungsanstalt (SUVA), Freiwillige Akademische Gesellschaft, UBS Wealth Foundation, Talecris Biotherapeutics GmbH, and Abbott Diagnostics. Genotyping in the GABRIEL framework was supported by grants European Commission 018996 and Wellcome Trust WT 084703MA. Identification of pathways was supported by the French National Research Agency (Bio2nea project ANR-CES 2009). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.I have read the journal's policy and have the following conflicts: The SAPALDIA study was supported by the UBS Wealth Foundation, Talecris Biotherapeutics GmbH, and Abbott Diagnostics in terms of unrestricted grants for personnel and genotyping. The support of these institutions did not influence the scientific work regarding study design, data collection, data analysis, interpretation of results, decision to publish, or preparation of the manuscript in any way. Also, this does not alter our adherence to all the PLoS ONE policies on sharing data and materials.","id":"WOS:000306461800046"}
{"text":"\"This meta-analysis is a collaborative effort involving data from many individual studies and many sources of funding. The details of funding sources for each study are detailed in Text S1 as well as below. Framingham Heart Study (FHS): The phenotype-genotype association analyses were funded through grants from the NIA R21AG032598 (JM Murabito, KL Lunetta), R01HL094755 (AD Coviello, RS Vasan, S Bandinelli), and R01AG31206 (RS Vasan, S Bandinelli), R01 AR/AG 41398 (DP Kiel). This research was conducted in part using data and resources from the Framingham Heart Study of the National Heart, Lung, and Blood Institute of the National Institutes of Health and Boston University School of Medicine. The analyses reflect intellectual input and resource development from the Framingham Heart Study investigators participating in the SNP Health Association Resource (SHARe) project. This work was partially supported by the National Heart, Lung, and Blood Institute's Framingham Heart Study (Contract No. N01-HC-25195) and its contract with Affymetrix for genotyping services (Contract No. N02-HL-6-4278). A portion of this research utilized the Linux Cluster for Genetic Analysis (LinGA-II), funded by the Robert Dawson Evans Endowment of the Department of Medicine at Boston University School of Medicine and Boston Medical Center. Gothenburg Osteoporosis and Obesity Determinants (GOOD) Study: Financial support was received from the Swedish Research Council (K2010-54X-09894-19-3, 2006-3832, and K2010-52X-20229-05-3), the Swedish Foundation for Strategic Research, the ALF/LUA research grant in Gothenburg, the Lundberg Foundation, the Torsten and Ragnar Soderberg's Foundation, Petrus and Augusta Hedlunds Foundation, the Vastra Gotaland Foundation, the Goteborg Medical Society, the Novo Nordisk foundation, and the European Commission grant HEALTH-F2-2008-201865-GEFOS. We would like to acknowledge Maria Nethander at the genomics core facility at University of Gothenburg for statistical analyses. We would also like to thank Dr. Tobias A. Knoch, Luc V. de Zeeuw, Anis Abuseiris, and Rob de Graaf as well as their institutions the Erasmus Computing Grid, Rotterdam, The Netherlands, and especially the national German MediGRID and Services@MediGRID part of the German D-Grid, both funded by the German Bundesministerium fuer Forschung und Technology under grants #01 AK 803 A-H and #01 IG 07015 G for access to their grid resources. We would also like to thank Karol Estrada, Department of Internal Medicine, Erasmus MC, Rotterdam, The Netherlands, for advice regarding the grid resources. Health, Aging, and Body Composition (Health ABC) Study: This Health ABC Study was supported by NIA contracts N01AG62101, N01AG62103, and N01AG62106. The genome-wide association study was funded by NIA grant 1R01AG032098-01A1 to Wake Forest University Health Sciences and genotyping services were provided by the Center for Inherited Disease Research (CIDR). CIDR is fully funded through a federal contract from the National Institutes of Health to The Johns Hopkins University, contract number HHSN268200782096C. This research was also supported in part by the Intramural Research Program of the National Institute on Aging, NIH, Bethesda, Maryland. Invecchiare in Chianti (InCHIANTI): The InCHIANTI study baseline (1998-2000) was supported as a \"\"targeted project'' (ICS110.1/RF97.71) by the Italian Ministry of Health and in part by the U.S. National Institute on Aging (Contracts: 263 MD 9164 and 263 MD 821336); the InCHIANTI Follow-up 1 (2001-2003) was funded by the U.S.National Institute on Aging 5R01TS000099-05 (Contracts: N.1-AG-1-1 and N.1-AG-1-2111); the InCHIANTI Follow-ups 2 and 3 studies (2004-2010) were financed by the U.S. National Institute on Aging (Contract: N01-AG-5-0002), supported in part by the Intramural research program of the National Institute on Aging, National Institutes of Health, Baltimore, Maryland. JRB Perry is a Sir Henry Wellcome Postdoctoral Research Fellow (092447/Z/10/Z). Cooperative Health Research in the Region of Augsburg (KORA): The KO
{"text":"Work in the laboratory of J.K. has been supported by the Wellcome Trust (074318 and 075491/Z/04 to core facilities Wellcome Trust Centre for Human Genetics), the European Research Council (ERC) under European Commission 7th Framework Programme (FP7/2007-2013)/ERC grant agreement No. 281824, the Medical Research Council (98082), and the National Institute for Health Research (NIHR) Oxford Biomedical Research Centre.","id":"WOS:000314744400005"}
{"text":"This work was supported by the RAPIDD program of the Science and Technology Directorate, U.S. Department of Homeland Security, and the Fogarty International Center, NIH. SR was also funded by: the NIH Fogarty Center (R01 TW008246-01), the Wellcome Trust (University Award 093488/Z/10/Z), The Medical Research Council (UK, Project Grant MR/J008761/1) and European Union Seventh Framework Programme (FP7/2007-2013, Grant Agreement no278433-PREDEMICS). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.","id":"WOS:000315157200118"}
{"text":"We acknowledge support from a Wellcome Trust Programme Grant award: PK-PD modelling to optimize treatment for HIV, TB and malaria. (ref 083851/Z/07/Z).M.L. and P.B. are supported by European and Developing Countries Clinical Trials Partnership grants (TA.09.40200.020 and TA.11.40200.047).Transparency Declaration: D.J.B. and S.H.K. have received research funding for development of the web site www.hiv-druginteractions.org from Viiv, BMS, Gilead, Janssen, Merck, Boehringer-Ingelheim. DJB has received honoria for lectures or Advisory Boards from Viiv, BMS, Gilead, Janssen, Merck.M.L. has received grants from Janssen and is supported by the Sewankambo scholarship at IDI which is funded by Gilead Foundation.","id":"WOS:000315524700001"}
{"text":"The current study is funded by grants from the South-Eastern Norway Regional Health Authority, the Research Council of Norway, the Odd Fellow MS society, the Danish Multiple Sclerosis Society, the Swedish Medical Research Council, the AFA foundation, Knut and Alice and Wallenbergs foundations and Council for Working Life and Social Research. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.We thank all patients and healthy controls for their participation. The International Multiple Sclerosis Genetics Consortium and the Wellcome Trust Case Control Consortium2 provided the genotypes used in the screening phase of this study. We acknowledge the collaboration and principal funding for the genome-wide study provided by the Wellcome Trust, as part of the Wellcome Trust Case Control Consortium2 project (085475/B/08/Z and 085475/Z/08/Z). We thank all contributors to the collection of samples and clinical data in the Norwegian MS Registry and Biobank. The Norwegian Bone Marrow Donor Registry, Rikshospitalet, Oslo University Hospital are acknowledged for providing Norwegian controls. The Centre for Integrative Genetics; CIGENE, Norwegian University of Life Sciences (UMB) Aas is thanked for performing Sequenom analyses.","id":"WOS:000315637900131"}
{"text":"We are deeply grateful to the Tara schooner and crew for collecting plankton samples all over the World Oceans during three years. Our special thanks go to Gaby Gorsky and Christian Sardet who facilitated our integration in the Tara Oceans consortium. We are also keen to thank the following people for providing us with planktonic samples: Jean-Marc Pagano from the Institut de Recherche pour le Développement (IRD), John Lamkin and Akihiro Shiroza from the Southeast Fisheries Science Centre (SEFSC), Cédric Guigand from the Rosentiel School of Marine and Atmospheric Science (RSMAS) and Fredrika Norrbin from the Department of Arctic and Marine Biology (The Arctic University of Norway). Our manuscript profited from stimulating discussion with Daniel Papillon who also provided English corrections. This article is the contribution no. 19 of the Tara Oceans Expedition 2009/2012.","id":"PMC4254178"}
{"text":"We are deeply grateful to the Tara schooner and crew for collecting plankton samples all over the World Oceans during three years. Our special thanks go to Gaby Gorsky and Christian Sardet who facilitated our integration in the Tara consortium. We are also keen to thank the following people for providing us with planktonic samples: Jean-Marc Pagano from the Institut de Recherche pour le Développement (IRD), John Lamkin and Akihiro Shiroza from the Southeast Fisheries Science Centre (SEFSC), Cédric Guigand from the Rosentiel School of Marine and Atmospheric Science (RSMAS) and Fredrika Norrbin from the Department of Arctic and Marine Biology (The Arctic University of Norway). Our manuscript profited from stimulating discussion with Daniel Papillon who also provided English corrections. This article is the contribution no. 19 of the Tara Expedition 2009/2012.","id":"PMC4254178ZZZ"}
{"text":"We are deeply grateful to the Tara schooner and This work was supported in part by the European Commission under FP7 grant 246686. crew for collecting plankton samples all over the World Oceans during three years. Our special thanks go to Gaby Gorsky and Christian Sardet who facilitated our integration in the Tara Oceans consortium. We are also keen to thank the following people for providing us with planktonic samples: Jean-Marc Pagano from the Institut de Recherche pour le Développement (IRD), John Lamkin and Akihiro Shiroza from the Southeast Fisheries Science Centre (SEFSC), Cédric Guigand from the Rosentiel School of Marine and Atmospheric Science (RSMAS) and Fredrika Norrbin from the Department of Arctic and Marine Biology (The Arctic University of Norway). Our manuscript profited from stimulating discussion with Daniel Papillon who also provided English corrections. This article is the contribution no. 19 of the Tara Oceans Expedition 2009/2012.","id":"TESTFP71"}
{"text":"We are deeply grateful to the Tara schooner and This work was supported in part by the European Commission under FP7 grant 283595. crew for collecting plankton samples all over the World Oceans during three years. Our special thanks go to Gaby Gorsky and Christian Sardet who facilitated our integration in the Tara consortium. We are also keen to thank the following people for providing us with planktonic samples: Jean-Marc Pagano from the Institut de Recherche pour le Développement (IRD), John Lamkin and Akihiro Shiroza from the Southeast Fisheries Science Centre (SEFSC), Cédric Guigand from the Rosentiel School of Marine and Atmospheric Science (RSMAS) and Fredrika Norrbin from the Department of Arctic and Marine Biology (The Arctic University of Norway). Our manuscript profited from stimulating discussion with Daniel Papillon who also provided English corrections. This article is the contribution no. 19 of the Tara Expedition 2009/2012.","id":"TESTFP72"}