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Sent on Friday, 2011 Oct 28
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 - 5 of 5

1.	Nature. 2011 Oct 19;478(7369):334-5. doi: 10.1038/478334b. Chemical biology: Many faces of a cancer-supporting protein. Darby JF, Workman P.
	PMID: 22012391 [PubMed - indexed for MEDLINE]
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2.	Nature. 2011 Oct 19;478(7369):287. doi: 10.1038/478287a. Genomic medicine has failed the poor. Bak er S. Source Oxford University Clinical Research Unit. sbaker@oucru.org
	PMID: 22012349 [PubMed - indexed for MEDLINE]
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3.	Science. 2011 Oct 14;334(6053):177; author reply 177. Comment on "Changes in climatic water balance drive downhill shifts in plant species' optimum elevations". Stephenson NL, Das AJ. Source US Geological Survey, Western Ecological Research Center, Three Rivers, CA 93271, USA. nstephenson@usgs.gov Comment on Science. 2011 Jan 21;331(6015):324-7. Abstract Crimmins et al. (Reports, 21 January 2011, p. 324) attributed an apparent downward elevational shift of California plant species to a precipitation-induced decline in climatic water deficit. We show that the authors miscalculated deficit, that the apparent decline in species' elevations is likely a consequence of geographic biases, and that unlike temperature changes, precipitation changes should not be expected to cause coordinated directional shifts in species' elevations. Free Article
	PMID: 21998371 [PubMed - indexed for MEDLINE]
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4.	Science. 2011 Oct 14;334(6053):177; author reply 177. Comment on "Changes in climatic water balance dri ve downhill shifts in plant species' optimum elevations". Hijmans RJ. Source Department of Environmental Science and Policy, University of California, Davis, Davis, CA 95616, USA. rhijmans@ucdavis.edu Comment on Science. 2011 Jan 21;331(6015):324-7. Abstract Crimmins et al. (Reports, 21 January 2011, p. 324) reported that plant species moved downhill between 1935 and 2005. They compared plot data for two time periods, ignoring that the modern plots were farther north than the historical plots. I contend that there is no support for a general downhill shift after correcting for this geographic bias. Free Article
	PMID: 21998370 [PubMed - indexed for MEDLINE]
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5.	Science. 2011 Oct 14;334(6053):177; author reply 177. Comment on "Changes in climatic water balance dri ve downhill shifts in plant species' optimum elevations". Wolf A, Anderegg WR. Source Department of Ecology and Evolutionary Biology, Princeton University, Princeton, NJ 08544, USA. adamwolf@princeton.edu Comment on Science. 2011 Jan 21;331(6015):324-7. Abstract Crimmins et al. (Reports, 21 January 2011, p. 324) presented a study that purports to show that plants in California are shifting downslope to maintain a constant water deficit. We argue that the results are limited in scope to just a handful of woody species in one part of the state and are confounded by methodological errors. Free Article
	PMID: 21998369 [PubMed - indexed for MEDLINE]
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Sent on Thursday, 2011 Oct 20
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. 2011 Oct 7;334(6052):15. Genomics is not enough. Chakravarti A. Free Article
	PMID: 21980079 [PubMed - indexed for MEDLINE]
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2.	N Engl J Med. 2011 Sep 29;365(13):1201-11. Treatment of neonatal sepsis with intravenous immune g lobulin. INIS Collaborative Group, Brocklehurst P, Farrell B, King A, Juszczak E, Darlow B, Haque K, Salt A, Stenson B, Tarnow-Mordi W. Collaborators: García RT, Raineri A, Falcó O, Redondo F, Farri M, Funes SM, Burgaretta C, Ramirez L, Fernandez F, Levinson L, Agudo E, Bisbal M, Guerrero M, Szyld E, Brazda G, Deguer CA, Ceriani Cernadas JM, Cravedi V, Leyton A, Prado A, Herrera NR, Murad M, Aguirre JD, Arosio S, Picón C, Posse N, Rolón SV, Vacou P, Buking C, Soto Conti CP, Deckert M, Kronemberger M, Navarro I, Collino E, Peyrano AJ, Bouceau N, Bruni MT, Parga L, Varela DM, Levinson L, Sachetti P, Alem MI, Camusso HC, Oviedo A, Ponce de León PA, Díaz R, Morante J, Puig G, del Barco M, Filtrín MR, Oliveira F, Halac E, Alberto G, Meskell S, Reynolds G, Craven P, Hobson L, Meredith K, Chambers C, Phelps J, Morris S, Buchan J, Glover R, Sarunac J, Guaran R, Pazanin N, Stack J, Casalaz D, Saker S, Wilson D, Hayes M, Kopp H, Lewis T, Coughtrey H, Davies K, Simeon L, Cartwright D, Hermann G, Pritchard M, Mills J, Perkins L, Plover C, Butterley K, Dargaville P, Ryan G, Graudins I, Lui K, Michalowski J, Gibson M, Jeffrey M, Klucklow M, Evans N, Hay J, Reid S, Callanan K, Doyle L, Wong S, Fa P, Luig M, Tarnow-Mordi W, Twible B, Bhatia V, Goodchild L, Western K, Cossey V, Dahl M, Reinholdt J, Hoest B, Vad Pedersen L, Dellagrammaticas H, Iacovidou N, Bradfield L, Murphy BP, Ryan CA, Gojic M, Vasiljevic B, Darlow B, McNeill N, Pugh-Williams D, Broadbent R, McCaffrey F, Johnson O, Bushell T, L'Anson J, Wong M, Battin M, Anderson-Hawke K, Kennedy A, Brown J, Kumar P, Butler S, Hale A, Harris D, Elder D, Gibson M, Bali S, Cubitt A, Jones L, Rackham O, Macrae E, Staines J, Konig S, Wong E, Marshall F, Saeed MA, Maybor C, Rose SJ, Chatfield SL, Szpara S, Elliot L, Soe T, Nycyk J, Perry M, Freeman D, Rogahn D, Kirby H, Madar J, Adiotomre P, Watkinson J, Al Hilaly NH, Wijetunge V, Simpson J, Wakefield R, Ainsworth S, McCormack K, Peters M, Tighe H, Cruwys M, Hoong MC, Crosbie E, Knapton A, Lal MK, Whalley B, Pentelow H, Rao P, Doyle H, Chang J, Lam S, Jani BR, West G, Kirby D, Kumararatne B, Gopinathan V, Irving D, Hendry S, Ibrahim M, McGahon A, Nicholl R, Campbell C, Dorling J, Cousins R, Kisat H, Rao R, Sheehy D, Brazier J, Thambapillai RE, Powls A, Provan S, Fox P, Rubin S, Barry WC, Handley L, Henwood J, Murdoch E, Bhadoria R, Shoilan C, Lama M, Shahili S, Afshar K, Yadav M, Munyard P, Nichols P, Collinson A, Mill H, Al-Muzaffar I, Fernandez M, McCormick J, Stenson B, McCullagh K, Sweet D, Deshpande S, Taplin M, Barrow L, Lawn C, Cousins J, Pike A, Shephard R, Speirs C, Emmerson A, Mercy J, Groves CR, Jain A, Waite C, Otunla T, Woodford M, Arya R, Qasim M, Sivashankar S, Armstrong S, Coombs RC, Garvie D, Holmes S, Gupta A, Bradshaw JM, Satodia P, Glennard A, Webb RD, Frost J, Wilson N, Long D, O'Brien S, Ibhanesebhor S, McManus A, Garg A, Triance G, Blades J, Russell-Taylor M, Bowden L, O'Brien R. Source National Perinatal Epidemiology Unit, University of Oxford, Old Road Campus, Headington, Oxford OX3 7LF, United Kingdom. Abstract BACKGROUND: Neonatal sepsis is a major cause of death and complications despite antibiotic treatment. Effective adjunctive treatments are needed. Newborn infants are relatively deficient in endogenous immunoglobulin. Meta-analyses of trials of intravenous immune globulin for suspected or proven neonatal sepsis suggest a reduced rate of death from any cause, but the trials have been small and have varied in quality. METHODS: At 113 hospitals in nine countries, we enrolled 3493 infants receiving antibiotics for suspected or proven serious infection and randomly assigned them to receive two infusions of either polyvalent IgG immune globulin (at a dose of 500 mg per kilogram of body weight) or matching placebo 48 hours apart. The primary outcome was death or major disability at the age of 2 years. RESULTS: There was no significant between-group difference in the rates of the primary outcome, which occurred in 686 of 1759 infants (39.0%) who received intravenous immune globulin and in 677 of 1734 infants (39.0%) who received placebo (relative risk, 1.00; 95% confidence interval, 0.92 to 1.08). Similarly, there were no significant differences in the rates of secondary outcomes, including the incidence of subsequent sepsis episodes. In follow-up of 2-year-old infants, there were no significant differences in the rates of major or nonmajor disability or of adverse events. CONCLUSIONS: Therapy with intravenous immune globulin had no effect on the outcomes of suspected or proven neonatal sepsis.
	PMID: 21962214 [PubMed - indexed for MEDLINE]
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3.	Science. 2011 Oct 7;334(6052):94-8. Epub 2011 Sep 22. An Ab original Australian genome reveals separate human dispersals into Asia. Rasmussen M, Guo X, Wang Y, Lohmueller KE, Rasmussen S, Albrechtsen A, Skotte L, Lindgreen S, Metspalu M, Jombart T, Kivisild T, Zhai W, Eriksson A, Manica A, Orlando L, De La Vega FM, Tridico S, Metspalu E, Nielsen K, Ávila-Arcos MC, Moreno-Mayar JV, Muller C, Dortch J, Gilbert MT, Lund O, Wesolowska A, Karmin M, Weinert LA, Wang B, Li J, Tai S, Xiao F, Hanihara T, van Driem G, Jha AR, Ricaut FX, de Knijff P, Migliano AB, Gallego Romero I, Kristiansen K, Lambert DM, Brunak S, Forster P, Brinkmann B, Nehlich O, Bunce M, Richards M, Gupta R, Bustamante CD, Krogh A, Foley RA, Lahr MM, Balloux F, Sicheritz-Pontén T, Villems R, Nielsen R, Wang J, Willerslev E. Source Centre for GeoGenetics, Natural History Museum of Denmark, Øster Voldgade 5-7, 1350 Copenhagen, Denmark. Abstract We present an Aboriginal Australian genomic sequence obtained from a 100-year-old lock of hair donated by an Aboriginal man from southern Western Australia in the early 20th century. We detect no evidence of European admixture and estimate contamination levels to be below 0.5%. We show that Aboriginal Australians are descendants of an early human dispersal into eastern Asia, possibly 62,000 to 75,000 years ago. This dispersal is separate from the one that gave rise to modern Asians 25,000 to 38,000 years ago. We also find evidence of gene flow between populations of the two dispersal waves prior to the divergence of Native Americans from modern Asian ancestors. Our findings support the hypothesis that present-day Aboriginal Australians descend from the earliest humans to occupy Australia, likely representing one of the oldest continuous populations outside Africa.
	PMID: 21940856 [PubMed - indexed for MEDLINE]
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4.	Nature. 2011 Sep 15;477(7364):359-61. Biomedical illustration: From monsters to molecules. Lok C.
	PMID: 21928542 [PubMed - indexed for MEDLINE]
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5.	Nature. 2011 Sep 14;477(7364):326-9. doi: 10.1038/nature10432. Sequence-based characterization of structural variation in the mouse genome. Yalcin B, Wong K, Agam A, Goodson M, Keane TM, Gan X, Nellåker C, Goodstadt L, Nicod J, Bhomra A, Hernandez-Pliego P, Whitley H, Cleak J, Dutton R, Janowitz D, Mott R, Adams DJ, Flint J. Source The Wellcome Trust Centre for Human Genetics, Roosevelt Drive, Oxford OX3 7BN, UK. Abstract Structural variation is widespread in mammalian genomes and is an important cause of disease, but just how abundant and important structural variants (SVs) are in shaping phenotypic variation remains unclear. Without knowing how many SVs there are, and how they arise, it is difficult to discover what they do. Combining experimental with automated analyses, we identified 711,920 SVs at 281,243 sites in the genomes of thirteen classical and four wild-derived inbred mouse strains. The majority of SVs are less than 1 kilobase in size and 98% are deletions or insertions. The breakpoints of 160,000 SVs were mapped to base pair resolution, allowing us to infer that insertion of retrotransposons causes more than half of SVs. Yet, despite their prevalence, SVs are less likely than other sequence variants to cause gene expression or quantitative phenotypic variation. We identified 24 SVs that disrupt coding exons, acting as rare variants of large effect on gene function. One-third of the genes so affected have immunological functions.
	PMID: 21921916 [PubMed - indexed for MEDLINE]
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6.	Nature. 2011 Sep 14;477(7364):289-94. doi: 10.1038/nature10413. Mouse genomic variation and its effect on phenotypes and gene regulation. Keane TM, Goodstadt L, Danecek P, White MA, Wong K, Yalcin B, Heger A, Agam A, Slater G, Goodson M, Furlotte NA, Eskin E, Nellåker C, Whitley H, Cleak J, Janowitz D, Hernandez-Pliego P, Edwards A, Belgard TG, Oliver PL, McIntyre RE, Bhomra A, Nicod J, Gan X, Yuan W, van der Weyden L, Steward CA, Bala S, Stalker J, Mott R, Durbin R, Jackson IJ, Czechanski A, Guerra-Assunção JA, Donahue LR, Reinholdt LG, Payseur BA, Ponting CP, Birney E, Flint J, Adams DJ. Source The Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1HH, UK. Abstract We report genome sequences of 17 inbred strains of laboratory mice and identify almost ten times more variants than previously known. We use these genomes to explore the phylogenetic history of the laboratory mouse and to examine the functional consequences of allele-specific variation on transcript abundance, revealing that at least 12% of transcripts show a significant tissue-specific expression bias. By identifying candidate functional variants at 718 quantitative trait loci we show that the molecular nature of functional variants and their position relative to genes vary according to the effect size of the locus. These sequences provide a starting point for a new era in the functional analysis of a key model organism.
	PMID: 21921910 [PubMed - indexed for MEDLINE]
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Sent on Wednesday, 2011 Oct 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. 2011 Sep 30;333(6051):1825; author reply 1825. Comment on "The response of vegetation on the Andean flank in western Amazonia to Pleistocene climate change". Punyasena SW, Dalling JW, Jaramillo C, Turner BL. Source Department of Plant Biology, University of Illinois, 505 South Goodwin Avenue, Urbana, IL 61801-3750, USA. punyasena@life.illinois.edu Comment on Science. 2011 Feb 25;331(6020):1055-8. Abstract Cárdenas et al. (Reports, 25 February 2011, p. 1055) used the presence of Podocarpus pollen and wood to infer ≥5°C cooling of Andean forests during Quaternary glacial periods. We show that (i) Podocarpus has a wide elevation range in the Neotropics, and (ii) edaphic factors cannot be discounted as a factor governing its distribution. Paleoecologists should therefore reevaluate Podocarpus as a cool-temperature proxy. Free Article
	PMID: 21960612 [PubMed - indexed for MEDLINE]
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2.	Science. 2011 Sep 30;333(6051):1818-9. Epidemiology. Outbreak detectives embrace the genome era.Kupferschmidt K.
	PMID: 21960605 [PubMed - indexed for MEDLINE]
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1.	Nat Genet. 2011 Aug 14;43(9):908-12. doi: 10.1038/ng.874. A20 (TNFAIP3) deficiency in myeloid cells triggers erosive polyarthritis resembling rheumatoid arthritis. Matmati M, Jacques P, Maelfait J, Verheugen E, Kool M, Sze M, Geboes L, Louagie E, Guire CM, Vereecke L, Chu Y, Boon L, Staelens S, Matthys P, Lambrecht BN, Schmidt-Supprian M, Pasparakis M, Elewaut D, Beyaert R, van Loo G. Source Department for Molecular Biomedical Research, Unit of Molecular Signal Transduction in Inflammation, Vlaams Instituut voor Biotechnologie, Ghent, Belgium. Comment in Nat Genet. 2011 Sep;43(9):822-3. Abstract A20 (TNFAIP3) is a protein that is involved in the negative feedback regulation of NF-κB signaling in response to specific proinflammatory stimuli in different cell types and has been suggested as a susceptibility gene for rheumatoid arthritis. To define the contribution of A20 to rheumatoid arthritis pathology, we generated myeloid-specific A20-deficient mice and show that specific ablation of Tnfaip3 in myeloid cells results in spontaneous development of a severe destructive polyarthritis with many features of rheumatoid arthritis. Myeloid-A20-deficient mice have high levels of inflammatory cytokines in their serum, consistent with a sustained NF-κB activation and higher TNF production by macrophages. Destructive polyarthritis in myeloid A20 knockout mice was TLR4-MyD88 and IL-6 dependent but was TNF independent. Myeloid A20 deficiency also promoted osteoclastogenesis in mice. Together, these observations indicate a critical and cell-specific function for A20 in the etiology of rheumatoid arthritis, supporting the idea of developing A20 modulatory drugs as cell-targeted therapies.
	PMID: 21841782 [PubMed - indexed for MEDLINE]

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1.	Nature. 2011 Sep 6;477(7363):146. doi: 10.1038/477146a. A radical approach to mental illness. Interview by Alison Abbott. Weinberger D.
	PMID: 21900988 [PubMed - indexed for MEDLINE]
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2.	Nature. 2011 Aug 10;477(7363):207-10. doi: 10.1038/nature10342. The genome sequence of Atlantic cod reveals a unique immune system. Star B, Nederbragt AJ, Jentoft S, Grimholt U, Malmstrøm M, Gregers TF, Rounge TB, Paulsen J, Solbakken MH, Sharma A, Wetten OF, Lanzén A, Winer R, Knight J, Vogel JH, Aken B, Andersen O, Lagesen K, Tooming-Klunderud A, Edvardsen RB, Tina KG, Espelund M, Nepal C, Previti C, Karlsen BO, Moum T, Skage M, Berg PR, Gjøen T, Kuhl H, Thorsen J, Malde K, Reinhardt R, Du L, Johansen SD, Searle S, Lien S, Nilsen F, Jonassen I, Omholt SW, Stenseth NC, Jakobsen KS. Source Centre for Ecological and Evolutionary Synthesis, Department of Biology, University of Oslo, PO Box 1066, Blindern, N-0316 Oslo, Norway. Comment in Nat Rev Immunol. 2011 Sep;11(9):570. Abstract Atlantic cod (Gadus morhua) is a large, cold-adapted teleost that sustains long-standing commercial fisheries and incipient aquaculture. Here we present the genome sequence of Atlantic cod, showing evidence for complex thermal adaptations in its haemoglobin gene cluster and an unusual immune architecture compared to other sequenced vertebrates. The genome assembly was obtained exclusively by 454 sequencing of shotgun and paired-end libraries, and automated annotation identified 22,154 genes. The major histocompatibility complex (MHC) II is a conserved feature of the adaptive immune system of jawed vertebrates, but we show that Atlantic cod has lost the genes for MHC II, CD4 and invariant chain (Ii) that are essential for the function of this pathway. Nevertheless, Atlantic cod is not exceptionally susceptible to disease under natural conditions. We find a highly expanded number of MHC I genes and a unique composition of its Toll-like receptor (TLR) families. This indicates how the Atlantic cod immune system has evolved compensatory mechanisms in both adaptive and innate immunity in the absence of MHC II. These observations affect fundamental assumptions about the evolution of the adaptive immune system and its components in vertebrates.
	PMID: 21832995 [PubMed - indexed for MEDLINE]
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3.	J Bone Miner Res. 2011 Jul;26(7):1517-32. doi: 10.1002/jbmr.354. Osteal macrophages promote in vivo intramembranous bone healing in a mouse tibial injury model. Alexander KA, Chang MK, Maylin ER, Kohler T, Müller R, Wu AC, Van Rooijen N, Sweet MJ, Hume DA, Raggatt LJ, Pettit AR. Source The University of Queensland, UQ Centre for Clinical Research, Herston, Australia. Abstract Bone-lining tissues contain a population of resident macrophages termed osteomacs that interact with osteoblasts in vivo and control mineralization in vitro. The role of osteomacs in bone repair was investigated using a mouse tibial bone injury model that heals primarily through intramembranous ossification and progresses through all major phases of stabilized fracture repair. Immunohistochemical studies revealed that at least two macrophage populations, F4/80(+) Mac-2(-/low) TRACP(-) osteomacs and F4/80(+) Mac-2(hi) TRACP(-) inflammatory macrophages, were present within the bone injury site and persisted throughout the healing time course. In vivo depletion of osteomacs/macrophages (either using the Mafia transgenic mouse model or clodronate liposome delivery) or osteoclasts (recombinant osteoprotegerin treatment) established that osteomacs were required for deposition of collagen type 1(+) (CT1(+)) matrix and bone mineralization in the tibial injury model, as assessed by quantitative immunohistology and micro-computed tomography. Conversely, administration of the macrophage growth factor colony-stimulating factor 1 (CSF-1) increased the number of osteomacs/macrophages at the injury site significantly with a concurrent increase in new CT1(+) matrix deposition and enhanced mineralization. This study establishes osteomacs as participants in intramembranous bone healing and as targets for primary anabolic bone therapies. Copyright © 2011 American Society for Bone and Mineral Research.
	PMID: 21305607 [PubMed - indexed for MEDLINE]
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Sent on Wednesday, 2011 Oct 05
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. 2011 Sep 23;333(6050):1755-8. Disentangling the drivers of β diversity along latitudinal and elevational gradients. Kraft NJ, Comita LS, Chase JM, Sanders NJ, Swenson NG, Crist TO, Stegen JC, Vellend M, Boyle B, Anderson MJ, Cornell HV, Davies KF, Freestone AL, Inouye BD, Harrison SP, Myers JA. Source Biodiversity Research Centre, University of British Columbia, Vancouver, British Columbia V6T 1Z4, Canada. nkraft@biodiversity.ubc.ca Abstract Understanding spatial variation in biodiversity along environmental gradients is a central theme in ecology. Differences in species compositional turnover among sites (β diversity) occurring along gradients are often used to infer variation in the processes structuring communities. Here, we show that sampling alone predicts changes in β diversity caused simply by changes in the sizes of species pools. For example, forest inventories sampled along latitudinal and elevational gradients show the well-documented pattern that β diversity is higher in the tropics and at low elevations. However, after correcting for variation in pooled species richness (γ diversity), these differences in β diversity disappear. Therefore, there is no need to invoke differences in the mechanisms of community assembly in temperate versus tropical systems to explain these global-scale patterns of β diversity.
	PMID: 21940897 [PubMed - indexed for MEDLINE]

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1.	Nat Genet. 2011 Jul 27;43(8):724-6. doi: 10.1038/ng.897. Epigenetic variation and cellular Darwinism. Issa JP. Comment on Nat Genet. 2011 Aug;43(8):768-75.
	PMID: 21792236 [PubMed - indexed for MEDLINE]
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2.	Nat Genet. 2011 Jul 24;43(8):741-3. doi: 10.1038/ng.877. Analyses of X-linked and autosomal genetic variation in population-scale whole genome sequencing. Gottipati S, Arbiza L, Siepel A, Clark AG, Keinan A. Source Department of Biological Statistics and Computational Biology, Cornell University, Ithaca, New York, USA. Abstract The ratio of genetic diversity on chromosome X to that on the autosomes is sensitive to both natural selection and demography. On the basis of whole-genome sequences of 69 females, we report that whereas this ratio increases with genetic distance from genes across populations, it is lower in Europeans than in West Africans independent of proximity to genes. This relative reduction is most parsimoniously explained by differences in demographic history without the need to invoke natural selection. PMCID: PMC3145052 [Available on 2012/1/24]
	PMID: 21775991 [PubMed - indexed for MEDLINE]
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3.	Nat Genet. 2011 Jul 17;43(8):732-4. doi: 10.1038/ng.883. NBEAL2 is mutated in gray platelet syndrome and is required for biogenesis of platelet α-granules. Gunay-Aygun M, Falik-Zaccai TC, Vilboux T, Zivony-Elboum Y, Gumruk F, Cetin M, Khayat M, Boerkoel CF, Kfir N, Huang Y, Maynard D, Dorward H, Berger K, Kleta R, Anikster Y, Arat M, Freiberg AS, Kehrel BE, Jurk K, Cruz P, Mullikin JC, White JG, Huizing M, Gahl WA. Source Section on Human Biochemical Genetics, Medical Genetics Branch, National Human Genome Research Institute, US National Institutes of Health, Bethesda, Maryland, USA. mgaygun@mail.nih.gov Abstract Gray platelet syndrome (GPS) is an autosomal recessive bleeding disorder that is characterized by large platelets that lack α-granules. Here we show that mutations in NBEAL2 (neurobeachin-like 2), which encodes a BEACH/ARM/WD40 domain protein, cause GPS and that megakaryocytes and platelets from individuals with GPS express a unique combination of NBEAL2 transcripts. Proteomic analysis of sucrose-gradient subcellular fractions of platelets indicated that NBEAL2 localizes to the dense tubular system (endoplasmic reticulum) in platelets. PMCID: PMC3154019 [Available on 2012/1/17]
	PMID: 21765412 [PubMed - indexed for MEDLINE]
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4.	Nat Genet. 2011 Jun 26;43(8):768-75. doi: 10.1038/ng.865. Increased methylation variation in epigenetic domains across cancer types. Hansen KD, Timp W, Bravo HC, Sabunciyan S, Langmead B, McDonald OG, Wen B, Wu H, Liu Y, Diep D, Briem E, Zhang K, Irizarry RA, Feinberg AP. Source Department of Biostatistics, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, USA. Comment in Nat Genet. 2011 Aug;43(8):724-6. Abstract Tumor heterogeneity is a major barrier to effective cancer diagnosis and treatment. We recently identified cancer-specific differentially DNA-methylated regions (cDMRs) in colon cancer, which also distinguish normal tissue types from each other, suggesting that these cDMRs might be generalized across cancer types. Here we show stochastic methylation variation of the same cDMRs, distinguishing cancer from normal tissue, in colon, lung, breast, thyroid and Wilms' tumors, with intermediate variation in adenomas. Whole-genome bisulfite sequencing shows these variable cDMRs are related to loss of sharply delimited methylation boundaries at CpG islands. Furthermore, we find hypomethylation of discrete blocks encompassing half the genome, with extreme gene expression variability. Genes associated with the cDMRs and large blocks are involved in mitosis and matrix remodeling, respectively. We suggest a model for cancer involving loss of epigenetic stability of well-defined genomic domains that underlies increased methylation variability in cancer that may contribute to tumor heterogeneity. PMCID: PMC3145050 [Available on 2011/12/26]
	PMID: 21706001 [PubMed - indexed for MEDLINE]
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