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Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Wednesday, 2015 January 21
Search: (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))

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Items 1 - 6 of 6

1.	Science. 2015 Jan 2;347(6217):1258524. doi: 10.1126/science.1258524. Epub 2014 Nov 27. Mosquito genomics. Extensive introgression in a malaria vector species complex revealed by phylogenomics. Fontaine MC1, Pease JB2, Steele A3, Waterhouse RM4, Neafsey DE5, Sharakhov IV6, Jiang X7, Hall AB7, Catteruccia F8, Kakani E8, Mitchell SN9, Wu YC10, Smith HA1, Love RR1, Lawniczak MK11, Slotman MA12, Emrich SJ13, Hahn MW14, Besansky NJ15. Comment in Evolutionary genomics. Conundrum of jumbled mosquito genomes. [Science. 2015] Evolutionary genomics. Conundrum of jumbled mosquito genomes.Clark AG, Messer PW. Science. 2015 Jan 2; 347(6217):27-8. Abstract Introgressive hybridization is now recognized as a widespread phenomenon, but its role in evolution remains contested. Here, we use newly available reference genome assemblies to investigate phylogenetic relationships and introgression in a medically important group of Afrotropical mosquito sibling species. We have identified the correct species branching order to resolve a contentious phylogeny and show that lineages leading to the principal vectors of human malaria were among the first to split. Pervasive autosomal introgression between these malaria vectors means that only a small fraction of the genome, mainly on the X chromosome, has not crossed species boundaries. Our results suggest that traits enhancing vectorial capacity may be gained through interspecific gene flow, including between nonsister species. Copyright © 2015, American Association for the Advancement of Science.
	PMID: 25431491 [PubMed - indexed for MEDLINE]
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2.	Nat Genet. 2014 Nov;46(11):1220-6. doi: 10.1038/ng.3117. Epub 2014 Oct 12. Genomic analyses provide insights into the history of tomato breeding. Lin T1, Zhu G2, Zhang J3, Xu X4, Yu Q5, Zheng Z2, Zhang Z2, Lun Y2, Li S2, Wang X2, Huang Z2, Li J2, Zhang C2, Wang T3, Zhang Y3, Wang A4, Zhang Y6, Lin K6, Li C7, Xiong G8, Xue Y9, Mazzucato A10, Causse M11, Fei Z12, Giovannoni JJ12, Chetelat RT13, Zamir D14, Städler T15, Li J4, Ye Z3, Du Y2, Huang S1. Abstract The histories of crop domestication and breeding are recorded in genomes. Although tomato is a model species for plant biology and breeding, the nature of human selection that altered its genome remains largely unknown. Here we report a comprehensive analysis of tomato evolution based on the genome sequences of 360 accessions. We provide evidence that domestication and improvement focused on two independent sets of quantitative trait loci (QTLs), resulting in modern tomato fruit ∼100 times larger than its ancestor. Furthermore, we discovered a major genomic signature for modern processing tomatoes, identified the causative variants that confer pink fruit color and precisely visualized the linkage drag associated with wild introgressions. This study outlines the accomplishments as well as the costs of historical selection and provides molecular insights toward further improvement.
	PMID: 25305757 [PubMed - indexed for MEDLINE]
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3.	Nat Genet. 2014 Nov;46(11):1173-86. doi: 10.1038/ng.3097. Epub 2014 Oct 5. Defining the role of common variation in the genomic and biological architecture of adult human height. Wood AR1, Esko T2, Yang J3, Vedantam S4, Pers TH5, Gustafsson S6, Chu AY7, Estrada K8, Luan J9, Kutalik Z10, Amin N11, Buchkovich ML12, Croteau-Chonka DC13, Day FR9, Duan Y14, Fall T15, Fehrmann R16, Ferreira T17, Jackson AU18, Karjalainen J16, Lo KS19, Locke AE18, Mägi R20, Mihailov E21, Porcu E22, Randall JC23, Scherag A24, Vinkhuyzen AA25, Westra HJ16, Winkler TW26, Workalemahu T27, Zhao JH9, Absher D28, Albrecht E29, Anderson D30, Baron J31, Beekman M32, Demirkan A33, Ehret GB34, Feenstra B35, Feitosa MF36, Fischer K37, Fraser RM38, Goel A39, Gong J40, Justice AE41, Kanoni S42, Kleber ME43, Kristiansson K44, Lim U45, Lotay V46, Lui JC31, Mangino M47, Mateo Leach I48, Medina-Gomez C49, Nalls MA50, Nyholt DR51, Palmer CD4, Pasko D1, Pechlivanis S52, Prokopenko I53, Ried JS29, Ripke S54, Shungin D55, Stancáková A56, Strawbridge RJ57, Sung YJ58, Tanaka T59, Teumer A60, Trompet S61, van der Laan SW62, van Setten J63, Van Vliet-Ostaptchouk JV64, Wang Z65, Yengo L66, Zhang W 67, Afzal U67, Arnlöv J68, Arscott GM69, Bandinelli S70, Barrett A71, Bellis C72, Bennett AJ71, Berne C73, Blüher M74, Bolton JL38, Böttcher Y75, Boyd HA35, Bruinenberg M76, Buckley BM77, Buyske S78, Caspersen IH79, Chines PS80, Clarke R81, Claudi-Boehm S82, Cooper M30, Daw EW36, De Jong PA83, Deelen J32, Delgado G84, Denny JC85, Dhonukshe-Rutten R86, Dimitriou M87, Doney AS88, Dörr M89, Eklund N90, Eury E66, Folkersen L57, Garcia ME91, Geller F35, Giedraitis V92, Go AS93, Grallert H94, Grammer TB84, Gräßler J95, Grönberg H96, de Groot LC86, Groves CJ71, Haessler J40, Hall P96, Haller T37, Hallmans G97, Hannemann A98, Hartman CA99, Hassinen M100, Hayward C101, Heard-Costa NL102, Helmer Q103, Hemani G3, Henders AK51, Hillege HL104, Hlatky MA105, Hoffmann W106, Hoffmann P107, Holmen O108, Houwing-Duistermaat JJ 109, Illig T110, Isaacs A111, James AL112, Jeff J46, Johansen B79, Johansson Å113, Jolley J114, Juliusdottir T17, Junttila J115, Kho AN116, Kinnunen L44, Klopp N110, Kocher T117, Kratzer W118, Lichtner P119, Lind L120, Lindström J44, Lobbens S66, Lorentzon M121, Lu Y122, Lyssenko V123, Magnusson PK96, Mahajan A17, Maillard M124, McArdle WL125, McKenzie CA126, McLachlan S38, McLaren PJ127, Menni C47, Merger S82, Milani L37, Moayyeri A47, Monda KL128, Morken MA80, Müller G129, Müller-Nurasyid M130, Musk AW131, Narisu N80, Nauck M132, Nolte IM133, Nöthen MM134, Oozageer L135, Pilz S136, Rayner NW137, Renstrom F138, Robertson NR139, Rose LM7, Roussel R140, Sanna S22, Scharnagl H141, Scholtens S133, Schumacher FR142, Schunkert H143, Scott RA9, Sehmi J67, Seufferlein T118, Shi J144, Silventoinen K145, Smit JH146, Smith AV147, Smolonska J148, Stanton AV149, Stirrups K150, Stott DJ151, Stringham HM18, Sundström J120, Swertz MA16, Syvänen AC152, Tayo BO153, Thorleifsson G154, Tyrer JP155, van Dijk S156, van Schoor NM157, van der Velde N158, van Heemst D159, van Oort FV160, Vermeulen SH161, Verweij N48, Vonk JM133, Waite LL28, Waldenberger M162, Wennauer R163, Wilkens LR45, Willenborg C 164, Wilsgaard T165, Wojczynski MK36, Wong A166, Wright AF101, Zhang Q36, Arveiler D167, Bakker SJ168, Beilby J169, Bergman RN170, Bergmann S171, Biffar R172, Blangero J72, Boomsma DI173, Bornstein SR95, Bovet P174, Brambilla P175, Brown MJ176, Campbell H38, Caulfield MJ177, Chakravarti A178, Collins R81, Collins FS80, Crawford DC179, Cupples LA180, Danesh J181, de Faire U182, den Ruijter HM183, Erbel R184, Erdmann J164, Eriksson JG185, Farrall M39, Ferrannini E186, Ferrières J187, Ford I188, Forouhi NG9, Forrester T126, Gansevoort RT168, Gejman PV189, Gieger C29, Golay A190, Gottesman O46, Gudnason V147, Gyllensten U113, Haas DW191, Hall AS192, Harris TB91, Hattersley AT193, Heath AC194, Hengstenberg C143, Hicks AA195, Hindorff LA196, Hingorani AD197, Hofman A198, Hovingh GK199, Humphries SE200, Hunt SC201, Hypponen E202, Jacobs KB203, Jarvelin MR204, Jousilahti P44, Jula AM44, Kaprio J205, Kastelein JJ199, Kayser M206, Kee F207, Keinanen-Kiukaanniemi SM208, Kiemeney LA209, Kooner JS210, Kooperberg C40, Koskinen S44, Kovacs P74, Kraja AT36, Kumari M211, Kuusisto J212, Lakka TA213, Langenberg C214, Le Marchand L45, Lehtimäki T215, Lupoli S216, Madden PA194, Männistö S44, Manunta P217, Marette A218, Matise TC219, McKnight B220, Meitinger T221, Moll FL222, Montgomery GW51, Morris AD88, Morris AP223, Murray JC224, Nelis M37, Ohlsson C121, Oldehinkel AJ99, Ong KK225, Ouwehand WH114, Pasterkamp G62, Peters A226, Pramstaller PP227, Price JF38, Qi L228, Raitakari OT229, Rankinen T230, Rao DC231, Rice TK232, Ritchie M233, Rudan I234, Salomaa V44, Samani NJ235, Saramies J236, Sarzynski MA230, Schwarz PE237, Sebert S238, Sever P239, Shuldiner AR240, Sinisalo J241, Steinthorsdottir V154, Stolk RP133, Tardif JC242, Tönjes A74 , Tremblay A243, Tremoli E244, Virtamo J44, Vohl MC245; Electronic Medical Records and Genomics (eMEMERGEGE) Consortium; MIGen Consortium; PAGEGE Consortium; LifeLines Cohort Study, Amouyel P246, Asselbergs FW247, Assimes TL105, Bochud M174, Boehm BO248, Boerwinkle E249, Bottinger EP46, Bouchard C230, Cauchi S66, Chambers JC250, Chanock SJ251, Cooper RS153, de Bakker PI252, Dedoussis G87, Ferrucci L59, Franks PW253, Froguel P254, Groop LC255, Haiman CA142, Hamsten A57, Hayes MG116, Hui J256, Hunter DJ257, Hveem K108, Jukema JW258, Kaplan RC259, Kivimaki M211, Kuh D166, Laakso M212, Liu Y260, Martin NG51, März W261, Melbye M262, Moebus S52, Munroe PB177, Njølstad I165, Oostra BA263, Palmer CN88, Pedersen NL96, Perola M264, Pérusse L265, Peters U40, Powell JE3, Power C266, Quertermous T105, Rauramaa R267, Reinmaa E37, Ridker PM268, Rivadeneira F49, Rotter JI269, Saaristo TE270, Saleheen D271, Schlessinger D272, Slagboom PE32, Snieder H133, Spector TD47, Strauch K273, Stumvoll M74, Tuomilehto J274, Uusitupa M275, van der Harst P276, Völzke H106, Walker M277, Wareham NJ9, Watkins H39, Wichmann HE278, Wilson JF38, Zanen P279, Deloukas P280, Heid IM281, Lindgren CM282, Mohlke KL12, Speliotes EK283, Thorsteinsdottir U284, Barroso I285, Fox CS286, North KE287, Strachan DP288, Beckmann JS289, Berndt SI251, Boehnke M18, Borecki IB36, McCarthy MI290, Metspalu A21, Stefansson K284, Uitterlinden AG49, van Duijn CM291, Franke L16 , Willer CJ292, Price AL293, Lettre G242, Loos RJ294, Weedon MN1, Ingelsson E295, O'Connell JR296, Abecasis GR18, Chasman DI268, Goddard ME297, Visscher PM3, Hirschhorn JN298, Frayling TM1. Collaborators: McCarty CA, Starren J, Peissig P, Berg R, Rasmussen L, Linneman J, Miller A, Choudary V, Chen L, Waudby C, Kitchner T, Reeser J, Fost N, Ritchie M, Wilke RA, Chisholm RL, Avila PC, Greenland P, Hayes M, Kho A, Kibbe WA, Lemke AA, Lowe WL, Smith ME, Wolf WA, Pacheco JA, Thompson WK, Humowiecki J, Law M, Chute C, Kullo I, Koenig B, de Andrade M, Bielinski S, Pathak J, Savova G, Wu J, Henriksen J, Ding K, Hart L, Palbicki J, Larson EB, Newton K, Ludman E, Spangler L, Hart G, Carrell D, Jarvik G, Crane P, Burke W, Fullerton SM, Trinidad SB, Carlson C, Hutchinson F, McDavid A, Roden DM, Clayton E, Haines JL, Masys DR, Churchill LR, Cornfield D, Crawford D, Darbar D, Denny JC, Malin BA, Ritchie MD, Schildcrout JS, Xu H, Ramirez AH, Basford M, Pulley J, Alizadeh B, de Boer RA, Boezen HM, Bruinenberg M, Franke L, van der Harst P, Hillege HL, van der Klauw MM, Navis G, Ormel J, Postma DS, Rosmalen JG, Slaets JP, Snieder H, Stolk RP, Wolffenbuttel BH, Wijmenga C, Kathiresan S, Voight BF, Purcell S, Musunuru K, Ardissino D, Mannucci PM, Anand S, Engert JC, Samani NJ, Schunkert H, Erdmann J, Reilly MP, Rader DJ, Morgan T, Spertus JA, Stoll M, Girelli D, McKeown PP, Patterson CC, Siscovick DS, O'Donnell CJ, Elosua R, Peltonen L, Salomaa V, Schwartz SM, Melander O, Altshuler D, Ardissino D, Merlini PA, Berzuini C, Bernardinelli L, Peyvandi F, Tubaro M, Celli P, Ferrario M, Fetiveau R, Marziliano N, Casari G, Galli M, Ribichini F, Rossi M, Bernardi F, Zonzin P, Piazza A, Mannucci PM, Schwartz SM, Siscovick DS, Yee J, Friedlander Y, Elosua R, Marrugat J, Lucas G, Subirana I, Sala J, Ramos R, Kathiresan S, Meigs JB, Williams G, Nathan DM, MacRae CA, O'Donnell CJ, Salomaa V, Havulinna AS, Peltonen L, Melander O, Berglund G, Voight B, Kathiresan S, Hirschhorn JN, Asselta R, Duga S, Spreafico M, Musunuru K, Daly MJ, Purcell S, Voight BF, Purcell S, Nemesh J, Korn JM, McCarroll SA, Schwartz SM, Yee J, Kathiresan S, Lucas G, Subirana I, Elosua R, Surti A, Guiducci C, Gianniny L, Mirel D, Parkin M, Burtt N, Gabriel SB, Samani NJ, Thompson JR, Braund PS, Wright BJ, Balmforth AJ, Ball SG, Hall AS, Schunkert I, Erdmann J, Linsel-Nitschke P, Lieb W, Ziegler A, König IR, Hengstenberg C, Fischer M, Stark K, Grosshennig A, Preuss M, Wichmann HE, Schreiber S, Schunkert H, Samani NJ, Erdmann J, Ouwehand W, Hengstenberg C, Deloukas P, Scholz M, Cambien F, Goodall A, Reilly MP, Li M, Chen Z, Wilensky R, Matthai W, Qasim A, Hakonarson HH, Devaney J, Burnett MS, Pichard AD, Kent KM, Satler L, Lindsay JM, Waksman R, Knouff CW, Waterworth DM, Walker MC, Mooser V, Epstein SE, Rader DJ, Scheffold T, Berger K, Stoll M, Huge A, Girelli D, Martinelli N, Olivieri O, Corrocher R, Morgan T, Spertus JA, McKeown PP, Patterson CC, Schunkert H, Erdmann J, Linsel-Nitschke P, Lieb W, Ziegler A, König I, Hengstenberg C, Fischer M, Stark K, Grosshennig A, Preuss M, Wichmann HE, Schreiber S, Hólm H, Thorleifsson G, Thorsteinsdottir U, Stefansson K, Engert JC, Do R, Xie C, Anand S, Kathiresan S, Ardissino D, Mannucci PM, Siscovick D, O'Donnell CJ, Samani NJ, Melander O, Elosua R, Peltonen L, Salomaa V, Schwartz SM, Altshuler D, Matise T, Buyske S, Higashio J, Williams R, Nato A, Ambite JL, Deelman E, Manolio T, Hindorff L, North KE, Heiss G, Taylor K, Franceschini N, Avery C, Graff M, Lin D, Quibrera M, Cochran B, Kao L, Umans J, Cole S, MacCluer J, Person S, Pankow J, Gross M, Boerwinkle E, Fornage M, Durda P, Jenny N, Patsy B, Arnold A, Buzkova P, Crawford D, Haines J, Murdock D, Glenn K, Brown-Gentry K, Thornton-Wells T, Dumitrescu L, Jeff J, Bush WS, Mitchell SL, Goodloe R, Wilson S, Boston J, Malinowski J, Restrepo N, Oetjens M, Fowke J, Zheng W, Spencer K, Ritchie M, Pendergrass S, Le Marchand L, Wilkens L, Park L, Tiirikainen M, Kolonel L, Lim U, Cheng I, Wang H, Shohet R, Haiman C, Stram D, Henderson B, Monroe K, Schumacher F, Kooperberg C, Peters U, Anderson G, Carlson C, Prentice R, LaCroix A, Wu C, Carty C, Gong J, Rosse S, Young A, Haessler J, Kocarnik J, Lin Y, Jackson R, Duggan D, Kuller L. Abstract Using genome-wide data from 253,288 individuals, we identified 697 variants at genome-wide significance that together explained one-fifth of the heritability for adult height. By testing different numbers of variants in independent studies, we show that the most strongly associated ∼2,000, ∼3,700 and ∼9,500 SNPs explained ∼21%, ∼24% and ∼29% of phenotypic variance. Furthermore, all common variants together captured 60% of heritability. The 697 variants clustered in 423 loci were enriched for genes, pathways and tissue types known to be involved in growth and together implicated genes and pathways not highlighted in earlier efforts, such as signaling by fibroblast growth factors, WNT/β-catenin and chondroitin sulfate-related genes. We identified several genes and pathways not previously connected with human skeletal growth, including mTOR, osteoglycin and binding of hyaluronic acid. Our results indicate a genetic architecture for human height that is characterized by a very large but finite number (thousands) of causal variants. PMCID: PMC4250049 [Available on 2015/5/1]
	PMID: 25282103 [PubMed - indexed for MEDLINE]
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4.	Nat Genet. 2014 Nov;46(11):1205-11. doi: 10.1038/ng.3114. Epub 2014 Oct 5. Recombination drives genome evolution in outbreak-related Legionella pneumophila isolates. Sánchez-Busó L1, Comas I1, Jorques G2, González-Candelas F1. Abstract Legionella pneumophila is a strictly environmental pathogen and the etiological agent of legionellosis. It is known that non-vertical processes have a major role in the short-term evolution of pathogens, but little is known about the relevance of these and other processes in environmental bacteria. We report the whole-genome sequencing of 69 L. pneumophila strains linked to recurrent outbreaks in a single location (Alcoy, Spain) over 11 years. We found some examples where the genome sequences of isolates of the same sequence type and outbreak did not cluster together and were more closely related to sequences from different outbreaks. Our analyses identify 16 recombination events responsible for almost 98% of the SNPs detected in the core genome and an apparent acceleration in the evolutionary rate. These results have profound implications for the understanding of microbial populations and for public health interventions in Legionella outbreak investigations.
	PMID: 25282102 [PubMed - indexed for MEDLINE]
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5.	Nat Genet. 2014 Nov;46(11):1160-5. doi: 10.1038/ng.3101. Epub 2014 Sep 28. Genome-wide analysis of noncoding regulatory mutations in cancer. Weinhold N1, Jacobsen A2, Schultz N1, Sander C1, Lee W3. Comment in Second call for pan-cancer analysis. [Nat Genet. 2014] Second call for pan-cancer analysis.[No authors listed]Nat Genet. 2014 Dec; 46(12):1251. Abstract Cancer primarily develops because of somatic alterations in the genome. Advances in sequencing have enabled large-scale sequencing studies across many tumor types, emphasizing the discovery of alterations in protein-coding genes. However, the protein-coding exome comprises less than 2% of the human genome. Here we analyze the complete genome sequences of 863 human tumors from The Cancer Genome Atlas and other sources to systematically identify noncoding regions that are recurrently mutated in cancer. We use new frequency- and sequence-based approaches to comprehensively scan the genome for noncoding mutations with potential regulatory impact. These methods identify recurrent mutations in regulatory elements upstream of PLEKHS1, WDR74 and SDHD, as well as previously identified mutations in the TERT promoter. SDHD promoter mutations are frequent in melanoma and are associated with reduced gene expression and poor prognosis. The non-protein-coding cancer genome remains widely unexplored, and our findings represent a step toward targeting the entire genome for clinical purposes. PMCID: PMC4217527 [Available on 2015/5/1]
	PMID: 25261935 [PubMed - indexed for MEDLINE]
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6.	Nat Genet. 2014 Nov;46(11):1227-32. doi: 10.1038/ng.3095. Epub 2014 Sep 21. PRC2 is recurrently inactivated through EED or SUZ12 loss in malignant peripheral nerve sheath tumors. Lee W1, Teckie S2, Wiesner T3, Ran L3, Prieto Granada CN4, Lin M5, Zhu S3, Cao Z3, Liang Y3, Sboner A6, Tap WD7, Fletcher JA8, Huberman KH9, Qin LX10, Viale A9, Singer S11, Zheng D12, Berger MF13, Chen Y14, Antonescu CR4, Chi P14. Abstract Malignant peripheral nerve sheath tumors (MPNSTs) represent a group of highly aggressive soft-tissue sarcomas that may occur sporadically, in association with neurofibromatosis type I (NF1 associated) or after radiotherapy. Using comprehensive genomic approaches, we identified loss-of-function somatic alterations of the Polycomb repressive complex 2 (PRC2) components (EED or SUZ12) in 92% of sporadic, 70% of NF1-associated and 90% of radiotherapy-associated MPNSTs. MPNSTs with PRC2 loss showed complete loss of trimethylation at lysine 27 of histone H3 (H3K27me3) and aberrant transcriptional activation of multiple PRC2-repressed homeobox master regulators and their regulated developmental pathways. Introduction of the lost PRC2 component in a PRC2-deficient MPNST cell line restored H3K27me3 levels and decreased cell growth. Additionally, we identified frequent somatic alterations of CDKN2A (81% of all MPNSTs) and NF1 (72% of non-NF1-associated MPNSTs), both of which significantly co-occur with PRC2 alterations. The highly recurrent and specific inactivation of PRC2 components, NF1 and CDKN2A highlights their critical and potentially cooperative roles in MPNST pathogenesis. PMCID: PMC4249650 [Available on 2015/5/1]
	PMID: 25240281 [PubMed - indexed for MEDLINE]
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