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

Sent on Wednesday, 2014 December 24
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. 2014 Dec 12;346(6215):1254390. doi: 10.1126/science.1254390. Epub 2014 Dec 11. Evidence for a single loss of mineralized teeth in the common avian ancestor. Meredith RW1, Zhang G2, Gilbert MT3, Jarvis ED4, Springer MS5. Abstract Edentulism, the absence of teeth, has evolved convergently among vertebrates, including birds, turtles, and several lineages of mammals. Instead of teeth, modern birds (Neornithes) use a horny beak (rhamphotheca) and a muscular gizzard to acquire and process food. We performed comparative genomic analyses representing lineages of nearly all extant bird orders and recovered shared, inactivating mutations within genes expressed in both the enamel and dentin of teeth of other vertebrate species, indicating that the common ancestor of modern birds lacked mineralized teeth. We estimate that tooth loss, or at least the loss of enamel caps that provide the outer layer of mineralized teeth, occurred about 116 million years ago. Copyright © 2014, American Association for the Advancement of Science.
	PMID: 25504730 [PubMed - indexed for MEDLINE]

2.	Science. 2014 Dec 12;346(6215):1311-20. doi: 10.1126/science.1251385. Epub 2014 Dec 11. Comparative genomics reveals insights into avian genome evolution and adaptation. Zhang G1, Li C2, Li Q2, Li B3, Larkin DM4, Lee C5, Storz JF6, Antunes A7, Greenwold MJ8, Meredith RW9, Ödeen A10, Cui J11, Zhou Q12, Xu L13, Pan H3, Wang Z14, Jin L3, Zhang P3, Hu H3, Yang W3, Hu J3, Xiao J3, Yang Z3, Liu Y3, Xie Q3, Yu H3, Lian J3, Wen P3, Zhang F3, Li H3, Zeng Y3, Xiong Z3, Liu S14, Zhou L3, Huang Z3, An N3, Wang J15, Zheng Q3, Xiong Y3, Wang G3, Wang B3, Wang J3, Fan Y16, da Fonseca RR17, Alfaro-Núñez A17, Schubert M17, Orlando L17, Mourier T17, Howard JT18, Ganapathy G18, Pfenning A18, Whitney O18, Rivas MV18, Hara E18, Smith J18, Farré M4, Narayan J19, Slavov G19, Romanov MN20, Borges R7, Machado JP21, Khan I7, Springer MS22, Gatesy J22, Hoffmann FG23, Opazo JC24, Håstad O25, Sawyer RH8, Kim H26, Kim KW27, Kim HJ28, Cho S28, Li N29, Huang Y30, Bruford MW31, Zhan X32, Dixon A33, Bertelsen MF34, Derryberry E35, Warren W36, Wilson RK36, Li S37, Ray DA38, Green RE39, O'Brien SJ40, Griffin D20, Johnson WE41, Haussler D39, Ryder OA42, Willerslev E17, Graves GR43, Alström P44, Fjeldså J45, Mindell DP46, Edwards SV47, Braun EL48, Rahbek C49, Burt DW50, Houde P51, Zhang Y3, Yang H52, Wang J3; Avian Genome Consortium, Jarvis ED53, Gilbert MT54, Wang J55. Collaborators: Ye C, Liang S, Yan Z, Zepeda ML, Campos PF, Vargas Velazquez AM, Samaniego JA, Avila-Arcos M, Martin MD, Barnett R, Ribeiro AM, Mello CV, Lovell PV, Almeida D, Maldonado E, Pereira J, Sunagar K, Philip S, Dominguez-Bello MG, Bunce M, Lambert D, Brumfield RT, Sheldon FH, Holmes EC, Gardner PP, Steeves TE, Stadler PF, Burge SW, Lyons E, Smith J, McCarthy F, Pitel F, Rhoads D, Froman DP. Abstract Birds are the most species-rich class of tetrapod vertebrates and have wide relevance across many research fields. We explored bird macroevolution using full genomes from 48 avian species representing all major extant clades. The avian genome is principally characterized by its constrained size, which predominantly arose because of lineage-specific erosion of repetitive elements, large segmental deletions, and gene loss. Avian genomes furthermore show a remarkably high degree of evolutionary stasis at the levels of nucleotide sequence, gene synteny, and chromosomal structure. Despite this pattern of conservation, we detected many non-neutral evolutionary changes in protein-coding genes and noncoding regions. These analyses reveal that pan-avian genomic diversity covaries with adaptations to different lifestyles and convergent evolution of traits. Copyright © 2014, American Association for the Advancement of Science.
	PMID: 25504712 [PubMed - indexed for MEDLINE]

3.	Science. 2014 Dec 12;346(6215):1308-9. doi: 10.1126/science.346.6215.1308. Avian genomes. A flock of genomes. Introduction. Zhang G, Jarvis ED, Gilbert MT.
	PMID: 25504710 [PubMed - indexed for MEDLINE]

4.	Science. 2014 Dec 12;346(6215):1275-6. doi: 10.1126/science.346.6215.1275. Genomics. Bird genomes give new perches to old friends. Pennisi E.
	PMID: 25504693 [PubMed - indexed for MEDLINE]

5.	Science. 2014 Dec 5;346(6214):1187-8. doi: 10.1126/science.aaa3177. Human Genomics. Sleeping dogs of the genome. Gorbunova V1, Boeke JD2, Helfand SL3, Sedivy JM4.
	PMID: 25477445 [PubMed - indexed for MEDLINE]
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6.	Science. 2014 Dec 5;346(6214):1167-70. doi: 10.1126/science.346.6214.1167. Unknown significance. Couzin-Frankel J.
	PMID: 25477439 [PubMed - indexed for MEDLINE]
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What's new for 'JKB_daily1' in PubMed

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

Sent on Friday, 2014 December 19
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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1.	Science. 2014 Nov 21;346(6212):1000-3. doi: 10.1126/science.1261754. Nucleoside reverse transcriptase inhibitors possess intrinsic anti-inflammatory activity. Fowler BJ1, Gelfand BD2, Kim Y3, Kerur N3, Tarallo V 4, Hirano Y3, Amarnath S5, Fowler DH5, Radwan M6, Young MT6, Pittman K7, Kubes P7, Agarwal HK8, Parang K8, Hinton DR9, Bastos-Carvalho A3, Li S3, Yasuma T3, Mizutani T3, Yasuma R3, Wright C3, Ambati J10. Abstract Nucleoside reverse transcriptase inhibitors (NRTIs) are mainstay therapeutics for HIV that block retrovirus replication. Alu (an endogenous retroelement that also requires reverse transcriptase for its life cycle)-derived RNAs activate P2X7 and the NLRP3 inflammasome to cause cell death of the retinal pigment epithelium in geographic atrophy, a type of age-related macular degeneration. We found that NRTIs inhibit P2X7-mediated NLRP3 inflammasome activation independent of reverse transcriptase inhibition. Multiple approved and clinically relevant NRTIs prevented caspase-1 activation, the effector of the NLRP3 inflammasome, induced by Alu RNA. NRTIs were efficacious in mouse models of geographic atrophy, choroidal neovascularization, graft-versus-host disease, and sterile liver inflammation. Our findings suggest that NRTIs are ripe for drug repurposing in P2X7-driven diseases. Copyright © 2014, American Association for the Advancement of Science.
	PMID: 25414314 [PubMed - indexed for MEDLINE]

What's new for 'JKB_daily1' in PubMed

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

Sent on Thursday, 2014 December 18
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 - 4 of 4

1.	Nat Med. 2014 Oct;20(10):1124-5. doi: 10.1038/nm.3696. Lasker Award winner Mary-Claire King. King MC.
	PMID: 25295950 [PubMed - indexed for MEDLINE]
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2.	Nat Med. 2014 Oct;20(10):1103-4. doi: 10.1038/nm.3722. Genome editing: a tool for research and therapy: towards a functional understanding of variants for molecular diagnostics using genome editing. Tsai SQ1, Iafrate AJ1, Joung JK1.
	PMID: 25295940 [PubMed - indexed for MEDLINE]
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3.	Nat Med. 2014 Oct;20(10):1082-3. doi: 10.1038/nm1014-1082. New platform for cataloging hundreds of proteins gets test drive. Powell K.
	PMID: 25295926 [PubMed - indexed for MEDLINE]
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4.	Nat Med. 2014 Oct;20(10):1211-6. doi: 10.1038/nm.3640. Epub 2014 Sep 14. An extracorporeal blood-cleansing device for sepsis therapy. Kang JH1, Super M2, Yung CW3, Cooper RM4, Domansky K5, Graveline AR5, Mammoto T6, Berthet JB5, Tobin H6, Cartwright MJ5, Watters AL5, Rottman M2, Waterhouse A5, Mammoto A6, Gamini N5, Rodas MJ5, Kole A5, Jiang A6, Valentin TM5, Diaz A5, Takahashi K7, Ingber DE8. Abstract Here we describe a blood-cleansing device for sepsis therapy inspired by the spleen, which can continuously remove pathogens and toxins from blood without first identifying the infectious agent. Blood flowing from an infected individual is mixed with magnetic nanobeads coated with an engineered human opsonin--mannose-binding lectin (MBL)--that captures a broad range of pathogens and toxins without activating complement factors or coagulation. Magnets pull the opsonin-bound pathogens and toxins from the blood; the cleansed blood is then returned back to the individual. The biospleen efficiently removes multiple Gram-negative and Gram-positive bacteria, fungi and endotoxins from whole human blood flowing through a single biospleen unit at up to 1.25 liters per h in vitro. In rats infected with Staphylococcus aureus or Escherichia coli, the biospleen cleared >90% of bacteria from blood, reduced pathogen and immune cell infiltration in multiple organs and decreased inflammatory cytokine levels. In a model of endotoxemic shock, the biospleen increased survival rates after a 5-h treatment.
	PMID: 25216635 [PubMed - indexed for MEDLINE]
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What's new for 'JKB_daily1' in PubMed

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

Sent on Wednesday, 2014 December 17
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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PubMed Results

Items 1 - 10 of 10

1.	N Engl J Med. 2014 Nov 27;371(22):e34. doi: 10.1056/NEJMicm1314314. Images in clinical medicine. Emphysematous pyelonephritis. Chen CY1, Chen CJ. Free Article
	PMID: 25427126 [PubMed - indexed for MEDLINE]
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2.	Nature. 2014 Nov 13;515(7526):189-91. doi: 10.1038/515189a. Mental health: depression needs large human-genetics studies. Hyman S1.
	PMID: 25391945 [PubMed - indexed for MEDLINE]
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3.	Nature. 2014 Nov 13;515(7526):S6-7. doi: 10.1038/515S6a. Q&A: healthy progress. Serjeant G, Mallapaty S.
	PMID: 25390144 [PubMed - indexed for MEDLINE]
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4.	Science. 2014 Nov 28;346(6213):1113-8. doi: 10.1126/science.aaa0114. Epub 2014 Nov 6. Paleogenomics. Genomic structure in Europeans dating back at least 36,200 years. Seguin-Orlando A1, Korneliussen TS1, Sikora M1, Malaspinas AS1, Manica A2, Moltke I3, Albrechtsen A4, Ko A5, Margaryan A1, Moiseyev V6, Goebel T7, Westaway M5, Lambert D5, Khartanovich V6, Wall JD8, Nigst PR9, Foley RA10, Lahr MM11, Nielsen R12, Orlando L1, Willerslev E13. Abstract The origin of contemporary Europeans remains contentious. We obtained a genome sequence from Kostenki 14 in European Russia dating from 38,700 to 36,200 years ago, one of the oldest fossils of anatomically modern humans from Europe. We find that Kostenki 14 shares a close ancestry with the 24,000-year-old Mal'ta boy from central Siberia, European Mesolithic hunter-gatherers, some contemporary western Siberians, and many Europeans, but not eastern Asians. Additionally, the Kostenki 14 genome shows evidence of shared ancestry with a population basal to all Eurasians that also relates to later European Neolithic farmers. We find that Kostenki 14 contains more Neandertal DNA that is contained in longer tracts than present Europeans. Our findings reveal the timing of divergence of western Eurasians and East Asians to be more than 36,200 years ago and that European genomic structure today dates back to the Upper Paleolithic and derives from a metapopulation that at times stretched from Europe to central Asia. Copyright © 2014, American Association for the Advancement of Science.
	PMID: 25378462 [PubMed - indexed for MEDLINE]
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5.	Nat Genet. 2014 Oct;46(10):1044. doi: 10.1038/ng.3099. David H. Dressler 1941-2014. Potter H1.
	PMID: 25257081 [PubMed - indexed for MEDLINE]
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6.	Nat Genet. 2014 Oct;46(10):1043. doi: 10.1038/ng.3115. Growing quality. [No authors listed]
	PMID: 25257080 [PubMed - indexed for MEDLINE]
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7.	Nat Genet. 2014 Oct;46(10):1140-6. doi: 10.1038/ng.3089. Epub 2014 Sep 14. An activating NLRC4 inflammasome mutation causes autoinflammation with recurrent macrophage activation syndrome. Canna SW1, de Jesus AA2, Gouni S1, Brooks SR3, Marrero B2, Liu Y2, DiMattia MA4, Zaal KJ5, Sanchez GA6, Kim H2, Chapelle D6, Plass N6, Huang Y2, Villarino AV1, Biancotto A7, Fleisher TA8, Duncan JA9, O'Shea JJ1, Benseler S10, Grom A11, Deng Z3, Laxer RM12, Goldbach-Mansky R2. Comment in NLRC4 gets out of control. [Nat Genet. 2014] NLRC4 gets out of control.Khameneh HJ, Mortellaro A. Nat Genet. 2014 Oct; 46(10):1048-9. Autoinflammation: NLRC4 mutation causes rare autoinflammatory disease. [Nat Rev Rheumatol. 2014] Autoinflammation: NLRC4 mutation causes rare autoinflammatory disease.Bernard NJ. Nat Rev Rheumatol. 2014 Nov; 10(11):635. Epub 2014 Sep 30. Abstract Inflammasomes are innate immune sensors that respond to pathogen- and damage-associated signals with caspase-1 activation, interleukin (IL)-1β and IL-18 secretion, and macrophage pyroptosis. The discovery that dominant gain-of-function mutations in NLRP3 cause the cryopyrin-associated periodic syndromes (CAPS) and trigger spontaneous inflammasome activation and IL-1β oversecretion led to successful treatment with IL-1-blocking agents. Herein we report a de novo missense mutation (c.1009A > T, encoding p.Thr337Ser) affecting the nucleotide-binding domain of the inflammasome component NLRC4 that causes early-onset recurrent fever flares and macrophage activation syndrome (MAS). Functional analyses demonstrated spontaneous inflammasome formation and production of the inflammasome-dependent cytokines IL-1β and IL-18, with the latter exceeding the levels seen in CAPS. The NLRC4 mutation caused constitutive caspase-1 cleavage in cells transduced with mutant NLRC4 and increased production of IL-18 in both patient-derived and mutant NLRC4-transduced macrophages. Thus, we describe a new monoallelic inflammasome defect that expands the monogenic autoinflammatory disease spectrum to include MAS and suggests new targets for therapy. PMCID: PMC4177369 [Available on 2015/4/1]
	PMID: 25217959 [PubMed - indexed for MEDLINE]
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8.	Nat Genet. 2014 Oct;46(10):1089-96. doi: 10.1038/ng.3075. Epub 2014 Aug 24. Population genomics of Populus trichocarpa identifies signatures of selection and adaptive trait associations. Evans LM1, Slavov GT2, Rodgers-Melnick E1, Martin J3, Ranjan P4, Muchero W4, Brunner AM5, Schackwitz W3, Gunter L4, Chen JG4, Tuskan GA6, DiFazio SP1. Abstract Forest trees are dominant components of terrestrial ecosystems that have global ecological and economic importance. Despite distributions that span wide environmental gradients, many tree populations are locally adapted, and mechanisms underlying this adaptation are poorly understood. Here we use a combination of whole-genome selection scans and association analyses of 544 Populus trichocarpa trees to reveal genomic bases of adaptive variation across a wide latitudinal range. Three hundred ninety-seven genomic regions showed evidence of recent positive and/or divergent selection and enrichment for associations with adaptive traits that also displayed patterns consistent with natural selection. These regions also provide unexpected insights into the evolutionary dynamics of duplicated genes and their roles in adaptive trait variation.
	PMID: 25151358 [PubMed - indexed for MEDLINE]
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9.	Nat Genet. 2014 Oct;46(10):1051-9. doi: 10.1038/ng.3073. Epub 2014 Aug 24. An integrated genomics approach identifies drivers of proliferation in luminal-subtype human breast cancer. Gatza ML1, Silva GO2, Parker JS1, Fan C3, Perou CM4. Abstract Elucidating the molecular drivers of human breast cancers requires a strategy that is capable of integrating multiple forms of data and an ability to interpret the functional consequences of a given genetic aberration. Here we present an integrated genomic strategy based on the use of gene expression signatures of oncogenic pathway activity (n = 52) as a framework to analyze DNA copy number alterations in combination with data from a genome-wide RNA-mediated interference screen. We identify specific DNA amplifications and essential genes within these amplicons representing key genetic drivers, including known and new regulators of oncogenesis. The genes identified include eight that are essential for cell proliferation (FGD5, METTL6, CPT1A, DTX3, MRPS23, EIF2S2, EIF6 and SLC2A10) and are uniquely amplified in patients with highly proliferative luminal breast tumors, a clinical subset of patients for which few therapeutic options are effective. This general strategy has the potential to identify therapeutic targets within amplicons through an integrated use of genomic data sets.
	PMID: 25151356 [PubMed - indexed for MEDLINE]
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10.	Nature. 2014 Nov 13;515(7526):261-3. doi: 10.1038/nature13685. Epub 2014 Aug 20. Comparative population genomics in animals uncovers the determinants of genetic diversity. Romiguier J1, Gayral P2, Ballenghien M3, Bernard A3, Cahais V3, Chenuil A4, Chiari Y5, Dernat R3, Duret L6, Faivre N3, Loire E3, Lourenco JM3, Nabholz B3, Roux C1, Tsagkogeorga G7, Weber AA4, Weinert LA8, Belkhir K3, Bierne N3, Glémin S3, Galtier N3. Abstract Genetic diversity is the amount of variation observed between DNA sequences from distinct individuals of a given species. This pivotal concept of population genetics has implications for species health, domestication, management and conservation. Levels of genetic diversity seem to vary greatly in natural populations and species, but the determinants of this variation, and particularly the relative influences of species biology and ecology versus population history, are still largely mysterious. Here we show that the diversity of a species is predictable, and is determined in the first place by its ecological strategy. We investigated the genome-wide diversity of 76 non-model animal species by sequencing the transcriptome of two to ten individuals in each species. The distribution of genetic diversity between species revealed no detectable influence of geographic range or invasive status but was accurately predicted by key species traits related to parental investment: long-lived or low-fecundity species with brooding ability were genetically less diverse than short-lived or highly fecund ones. Our analysis demonstrates the influence of long-term life-history strategies on species response to short-term environmental perturbations, a result with immediate implications for conservation policies.
	PMID: 25141177 [PubMed - indexed for MEDLINE]
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What's new for 'JKB_daily1' in PubMed

This message contains My NCBI what's new results from the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).
Do not reply directly to this message.

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

Sent on Tuesday, 2014 December 16
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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PubMed Results

Items 1 - 10 of 10

1.	Science. 2014 Nov 14;346(6211):1256272. doi: 10.1126/science.1256272. Synthetic biology. Genomically encoded analog memory with precise in vivo DNA writing in living cell populations. Farzadfard F1, Lu TK2. Comment in Synthetic biology. Dynamic genome engineering in living cells. [Science. 2014] Synthetic biology. Dynamic genome engineering in living cells.Ausländer S, Fussenegger M. Science. 2014 Nov 14; 346(6211):813-4. Abstract Cellular memory is crucial to many natural biological processes and sophisticated synthetic biology applications. Existing cellular memories rely on epigenetic switches or recombinases, which are limited in scalability and recording capacity. In this work, we use the DNA of living cell populations as genomic "tape recorders" for the analog and distributed recording of long-term event histories. We describe a platform for generating single-stranded DNA (ssDNA) in vivo in response to arbitrary transcriptional signals. When coexpressed with a recombinase, these intracellularly expressed ssDNAs target specific genomic DNA addresses, resulting in precise mutations that accumulate in cell populations as a function of the magnitude and duration of the inputs. This platform could enable long-term cellular recorders for environmental and biomedical applications, biological state machines, and enhanced genome engineering strategies. Copyright © 2014, American Association for the Advancement of Science.
	PMID: 25395541 [PubMed - indexed for MEDLINE]
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2.	Science. 2014 Nov 7;346(6210):763-7. doi: 10.1126/science.1257570. Epub 2014 Nov 6. Phylogenomics resolves the timing and pattern of insect evolution. Misof B1, Liu S2, Meusemann K3, Peters RS4, Donath A5, Mayer C5, Frandsen PB6, Ware J7, Flouri T8, Beutel RG9, Niehuis O5, Petersen M5, Izquierdo-Carrasco F8, Wappler T10, Rust J10, Aberer AJ8, Aspöck U11, Aspöck H12, Bartel D13, Blanke A14, Berger S8, Böhm A13, Buckley TR15, Calcott B16, Chen J17, Friedrich F18, Fukui M19, Fujita M20, Greve C5, Grobe P5, Gu S17, Huang Y2, Jermiin LS21, Kawahara AY22, Krogmann L23, Kubiak M18, Lanfear R24, Letsch H25, Li Y2, Li Z17, Li J17, Lu H17, Machida R20, Mashimo Y20, Kapli P26, McKenna DD27, Meng G2, Nakagaki Y20, Navarrete-Heredia JL28, Ott M29, Ou Y17, Pass G13, Podsiadlowski L30, Pohl H9, von Reumont BM31, Schütte K32, Sekiya K20, Shimizu S20, Slipinski A33, Stamatakis A34, Song W2, Su X2, Szucsich NU13, Tan M2, Tan X17, Tang M2, Tang J17, Timelthaler G13, Tomizuka S20, Trautwein M35, Tong X36, Uchifune T37, Walzl MG13, Wiegmann BM38, Wilbrandt J5, Wipfler B9, Wong TK21, Wu Q2, Wu G17, Xie Y17, Yang S2, Yang Q2, Yeates DK33, Yoshizawa K39, Zhang Q2, Zhang R2, Zhang W17, Zhang Y17, Zhao J2, Zhou C2, Zhou L2, Ziesmann T5, Zou S17, Li Y17, Xu X17, Zhang Y2, Yang H17, Wang J17, Wang J40, Kjer KM41, Zhou X42. Abstract Insects are the most speciose group of animals, but the phylogenetic relationships of many major lineages remain unresolved. We inferred the phylogeny of insects from 1478 protein-coding genes. Phylogenomic analyses of nucleotide and amino acid sequences, with site-specific nucleotide or domain-specific amino acid substitution models, produced statistically robust and congruent results resolving previously controversial phylogenetic relations hips. We dated the origin of insects to the Early Ordovician [~479 million years ago (Ma)], of insect flight to the Early Devonian (~406 Ma), of major extant lineages to the Mississippian (~345 Ma), and the major diversification of holometabolous insects to the Early Cretaceous. Our phylogenomic study provides a comprehensive reliable scaffold for future comparative analyses of evolutionary innovations among insects. Copyright © 2014, American Association for the Advancement of Science.
	PMID: 25378627 [PubMed - indexed for MEDLINE]
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3.	Science. 2014 Nov 7;346(6210):698-9. doi: 10.1126/science.1258871. Evolution. Searching for new branches on the tree of life. Woyke T1, Rubin EM2.
	PMID: 25378606 [PubMed - indexed for MEDLINE]
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4.	Science. 2014 Nov 7;346(6210):684-5. doi: 10.1126/science.346.6210.684. Infectious Diseases. Delays hinder Ebola genomics. Vogel G.
	PMID: 25378599 [PubMed - indexed for MEDLINE]
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5.	Nature. 2014 Oct 30;514(7524):548. doi: 10.1038/514548a. Geneticists tap human knockouts. Callaway E.
	PMID: 25355341 [PubMed - indexed for MEDLINE]
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6.	Nature. 2014 Oct 23;514(7523):438-40. doi: 10.1038/nature13758. Epub 2014 Oct 1. Lung disease: Treatment by cell transplant. Thomassen MJ1, Kavuru MS2. Comment on Pulmonary macrophage transplantation therapy. [Nature. 2014] Pulmonary macrophage transplantation therapy.Suzuki T, Arumugam P, Sakagami T, Lachmann N, Chalk C, Sallese A, Abe S, Trapnell C, Carey B, Moritz T, et al. Nature. 2014 Oct 23; 514(7523):450-4. Epub 2014 Oct 1.
	PMID: 25274303 [PubMed - indexed for MEDLINE]
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7.	Nature. 2014 Oct 23;514(7523):450-4. doi: 10.1038/nature13807. Epub 2014 Oct 1. Pulmonary macrophage transplantation therapy. Suzuki T1, Arumugam P2, Sakagami T1, Lachmann N3, Chalk C1, Sallese A1, Abe S1, Trapnell C4, Carey B1, Moritz T3, Malik P2, Lutzko C2, Wood RE5, Trapnell BC6. Comment in Lung disease: Treatment by cell transplant. [Nature. 2014] Lung disease: Treatment by cell transplant.Thomassen MJ, Kavuru MS. Nature. 2014 Oct 23; 514(7523):438-40. Epub 2014 Oct 1. Abstract Bone-marrow transplantation is an effective cell therapy but requires myeloablation, which increases infection risk and mortality. Recent lineage-tracing studies documenting that resident macrophage populations self-maintain independently of haematological progenitors prompted us to consider organ-targeted, cell-specific therapy. Here, using granulocyte-macrophage colony-stimulating factor (GM-CSF) receptor-β-deficient (Csf2rb(-/-)) mice that develop a myeloid cell disorder identical to hereditary pulmonary alveolar proteinosis (hPAP) in children with CSF2RA or CSF2RB mutations, we show that pulmonary macrophage transplantation (PMT) of either wild-type or Csf2rb-gene-corrected macrophages without myeloablation was safe and well-tolerated and that one administration corrected the lung disease, secondary systemic manifestations and normalized disease-related biomarkers, and prevented disease-specific mortality. PMT-derived alveolar macrophages persisted for at least one year as did therapeutic effects. Our findings identify mechanisms regulating alveolar macrophage population size in health and disease, indicate that GM-CSF is required for phenotypic determination of alveolar macrophages, and support translation of PMT as the first specific therapy for children with hPAP. PMCID: PMC4236859 [Available on 2015/4/23]
	PMID: 25274301 [PubMed - indexed for MEDLINE]
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8.	Science. 2014 Nov 7;346(6210):751-5. doi: 10.1126/science.1255638. Epub 2014 Sep 18. Quality control of inner nuclear membrane proteins by the Asi complex. Foresti O1, Rodriguez-Vaello V1, Funaya C2, Carvalho P3. Comment in Cell Biology. Local synthesis and disposal. [Science. 2014] Cell Biology. Local synthesis and disposal.Shao S, Hegde RS. Science. 2014 Nov 7; 346(6210):701-2. Protein quality control: Nuclear membrane proteins in check. [Nat Rev Mol Cell Biol. 2014] Protein quality control: Nuclear membrane proteins in check.Baumann K. Nat Rev Mol Cell Biol. 2014 Nov; 15(11):700-1. Epub 2014 Oct 15. Abstract Misfolded proteins in the endoplasmic reticulum (ER) are eliminated by a quality control system called ER-associated protein degradation (ERAD). However, it is unknown how misfolded proteins in the inner nuclear membrane (INM), a specialized ER subdomain, are degraded. We used a quantitative proteomics approach to reveal an ERAD branch required for INM protein quality control in yeast. This branch involved the integral membrane proteins Asi1, Asi2, and Asi3, which assembled into an Asi complex. Besides INM misfolded proteins, the Asi complex promoted the degradation of functional regulators of sterol biosynthesis. Asi-mediated ERAD was required for ER homeostasis, which suggests that spatial segregation of protein quality control systems contributes to ER function. Copyright © 2014, American Association for the Advancement of Science.
	PMID: 25236469 [PubMed - indexed for MEDLINE]
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9.	Nature. 2014 Oct 23;514(7523):494-7. doi: 10.1038/nature13591. Epub 2014 Aug 20. Pre-Columbian mycobacterial genomes reveal seals as a source of New World human tuberculosis. Bos KI1, Harkins KM2, Herbig A3, Coscolla M4, Weber N5, Comas I6, Forrest SA7, Bryant JM8, Harris SR8, Schuenemann VJ7, Campbell TJ9, Majander K7, Wilbur AK10, Guichon RA11, Wolfe Steadman DL12, Cook DC13, Niemann S14, Behr MA15, Zumarraga M16, Bastida R17, Huson D5, Nieselt K5, Young D18, Parkhill J8, Buikstra JE10, Gagneux S19, Stone AC10, Krause J20. Abstract Modern strains of Mycobacterium tuberculosis from the Americas are closely related to those from Europe, supporting the assumption that human tuberculosis was introduced post-contact. This notion, however, is incompatible with archaeological evidence of pre-contact tuberculosis in the New World. Comparative genomics of modern isolates suggests that M. tuberculosis attained its worldwide distribution following human dispersals out of Africa during the Pleistocene epoch, although this has yet to be confirmed with ancient calibration points. Here we present three 1,000-year-old mycobacterial genomes from Peruvian human skeletons, revealing that a member of the M. tuberculosis complex caused human disease before contact. The ancient strains are distinct from known human-adapted forms and are most closely related to those adapted to seals and sea lions. Two independent dating approaches suggest a most recent common ancestor for the M. tuberculosis complex less than 6,000 years ago, which supports a Holocene dispersal of the disease. Our results implicate sea mammals as having played a role in transmitting the disease to humans across the ocean.
	PMID: 25141181 [PubMed - indexed for MEDLINE]
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10.	PLoS One. 2014 Jan 22;9(1):e81229. doi: 10.1371/journal.pone.0081229. eCollection 2014. Network analysis reveals distinct clinical syndromes underlying acute mountain sickness. Hall DP1, MacCormick IJ2, Phythian-Adams AT2, Rzechorzek NM3, Hope-Jones D2, Cosens S2, Jackson S2, Bates MG4, Collier DJ5, Hume DA6, Freeman T6, Thompson AA7, Baillie JK8. Abstract Acute mountain sickness (AMS) is a common problem among visitors at high altitude, and may progress to life-threatening pulmonary and cerebral oedema in a minority of cases. International consensus defines AMS as a constellation of subjective, non-specific symptoms. Specifically, headache, sleep disturbance, fatigue and dizziness are given equal diagnostic weighting. Different pathophysiological mechanisms are now thought to underlie headache and sleep disturbance during acute exposure to high altitude. Hence, these symptoms may not belong together as a single syndrome. Using a novel visual analogue scale (VAS), we sought to undertake a systematic exploration of the symptomatology of AMS using an unbiased, data-driven approach originally designed for analysis of gene expression. Symptom scores were collected from 292 subjects during 1110 subject-days at altitudes between 3650 m and 5200 m on Apex expeditions to Bolivia and Kilimanjaro. Three distinct patterns of symptoms were consistently identified. Although fatigue is a ubiquitous finding, sleep disturbance and headache are each commonly reported without the other. The commonest pattern of symptoms was sleep disturbance and fatigue, with little or no headache. In subjects reporting severe headache, 40% did not report sleep disturbance. Sleep disturbance correlates poorly with other symptoms of AMS (Mean Spearman correlation 0.25). These results challenge the accepted paradigm that AMS is a single disease process and describe at least two distinct syndromes following acute ascent to high altitude. This approach to analysing symptom patterns has potential utility in other clinical syndromes. PMCID: PMC3898916 Free PMC Article
	PMID: 24465370 [PubMed - indexed for MEDLINE]
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