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

Sent on Wednesday, 2011 Aug 31
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.	Science. 2011 Aug 19;333(6045):1024-6. Rapid range shifts of species associated with high levels of climate warming. Chen IC, Hill JK, Ohlemüller R, Roy DB, Thomas CD. Source Department of Biology, University of York, Wentworth Way, York YO10 5DD, UK. Abstract The distributions of many terrestrial organisms are currently shifting in latitude or elevation in response to changing climate. Using a meta-analysis, we estimated that the distributions of species have recently shifted to higher elevations at a median rate of 11.0 meters per decade, and to higher latitudes at a median rate of 16.9 kilometers per decade. These rates are approximately two and three times faster than previously reported. The distances moved by species are greatest in studies showing the highest levels of warming, with average latitudinal shifts being generally sufficient to track temperature changes. However, individual species vary greatly in their rates of change, suggesting that the range shift of each species depends on multiple internal species traits and external drivers of change. Rapid average shifts derive from a wide diversity of responses by individual species.
	PMID: 21852500 [PubMed - indexed for MEDLINE]
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2.	Science. 2011 Aug 19;333(6045):984-8. Partitioning regulatory mechanisms of within-host malaria dynamics using th e effective propagation number. Metcalf CJ, Graham AL, Huijben S, Barclay VC, Long GH, Grenfell BT, Read AF, Bjørnstad ON. Source Department of Zoology, Oxford University, Oxford OX1 3PS, UK. charlotte.metcalf@zoo.ox.ac.uk Comment in Science. 2011 Aug 19;333(6045):943-4. Abstract Immune clearance and resource limitation (via red blood cell depletion) shape the peaks and troughs of malaria parasitemia, which in turn affect disease severity and transmission. Quantitatively partitioning the relative roles of these effects through time is challenging. Using data from rodent malaria, we estimated the effective propagation number, which reflects the relative importance of contrasting within-host control mechanisms through time and is sensitive to the inoculating parasite dose. Our analysis showed that the capacity of innate responses to restrict initial parasite growth saturates with parasite dose and that experimentally enhanced innate immunity can affect parasite density indirectly via resource depletion. Such a statistical approach offers a tool to improve targeting of drugs or vaccines for human therapy by revealing the dynamics and interactions of within-host regulatory mechanisms.
	PMID: 21852493 [PubMed - indexed for MEDLINE]
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3.	Science. 2011 Aug 19;333(6045):943-4. Microbiology. Quantifying malaria dynamics within the host. Day KP, Fowkes FJ. Source Division of Parasitology, Department of Microbiology, New York University School of Medicine, New York, NY 10016, USA. karen.day@nyumc.org Comment on Science. 2011 Aug 19;333(6045):984-8.
	PMID: 21852478 [PubMed - indexed for MEDLINE]
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4.	Nature. 2011 Jul 20;475(7356):348-52. doi: 10.1038/nature10242. An integrated semiconductor device enabling non-o ptical genome sequencing. Rothberg JM, Hinz W, Rearick TM, Schultz J, Mileski W, Davey M, Leamon JH, Johnson K, Milgrew MJ, Edwards M, Hoon J, Simons JF, Marran D, Myers JW, Davidson JF, Branting A, Nobile JR, Puc BP, Light D, Clark TA, Huber M, Branciforte JT, Stoner IB, Cawley SE, Lyons M, Fu Y, Homer N, Sedova M, Miao X, Reed B, Sabina J, Feierstein E, Schorn M, Alanjary M, Dimalanta E, Dressman D, Kasinskas R, Sokolsky T, Fidanza JA, Namsaraev E, McKernan KJ, Williams A, Roth GT, Bustillo J. Source Ion Torrent by Life Technologies, Suite 100, 246 Goose Lane, Guilford, Connecticut 06437, USA. Jonathan.Rothberg@Lifetech.com Abstract The seminal importance of DNA sequencing to the life sciences, biotechnology and medicine has driven the search for more scalable and lower-cost solutions. Here we describe a DNA sequencing technology in which scalable, low-cost semiconductor manufacturing techniques are used to make an integrated circuit able to directly perform non-optical DNA sequencing of genomes. Sequence data are obtained by directly sensing the ions produced by template-directed DNA polymerase synthesis using all-natural nucleotides on this massively parallel semiconductor-sensing device or ion chip. The ion chip contains ion-sensitive, field-effect transistor-based sensors in perfect register with 1.2 million wells, which provide confinement and allow parallel, simultaneous detection of independent sequencing reactions. Use of the most widely used technology for constructing integrated circuits, the complementary metal-oxide semiconductor (CMOS) process, allows for low-cost, large-scale production and scaling of the device to higher densities and larger array sizes. We show the performance of the system by sequencing three bacterial genomes, its robustness and scalability by producing ion chips with up to 10 times as many sensors and sequencing a human genome.
	PMID: 21776081 [PubMed - indexed for MEDLINE]
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5.	Nature. 2011 Jul 20;475(7356):278. doi: 10.1038/475278a. Chip chips away at the cost of a genome. Zakaib GD.
	PMID: 21776054 [PubMed - indexed for MEDLINE]
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Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Tuesday, 2011 Aug 30
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.	Hepatology. 2011 Jun;53(6):2003-15. doi: 10.1002/hep.24315. Macrophage therapy for murine liver fibrosis recruits host effector cells improving fibrosis, regeneration, and function. Thomas JA, Pope C, Wojtacha D, Robson AJ, Gordon-Walker TT, Hartland S, Ramachandran P, Van Deemter M, Hume DA, Iredale JP, Forbes SJ. Source MRC Centre for Inflammation Research, University of Edinburgh, Edinburgh, UK. Abstract Clinical studies of bone marrow (BM) cell therapy for liver cirrhosis are under way but the mechanisms of benefit remain undefined. Cells of the monocyte-macrophage lineage have key roles in the development and resolution of liver fibrosis. Therefore, we tested the therapeutic effects of these cells on murine liver fibrosis. Advanced liver fibrosis was induced in female mice by chronic administration of carbon tetrachloride. Unmanipulated, syngeneic macrophages, their specific BM precursors, or unfractionated BM cells were delivered during liver injury. Mediators of inflammation, fibrosis, and regeneration were measured. Donor cells were tracked by sex-mismatch and green fluorescent protein expression. BM-derived macrophage (BMM) delivery resulted in early chemokine up-regulation with hepatic recruitment of endogenous macrophages and neutrophils. These cells delivered matrix metalloproteinases-13 and -9, respectively, into the hepatic scar. The effector cell infiltrate was accompanied by increased levels of the antiinflammatory cytokine interleukin 10. A reduction in hepatic myofibroblasts was followed by reduced fibrosis detected 4 weeks after macrophage infusion. Serum albumin levels were elevated at this time. Up- regulation of the liver progenitor cell mitogen tumor necrosis factor-like weak inducer of apoptosis (TWEAK) preceded expansion of the progenitor cell compartment. Increased expression of colony stimulating factor-1, insulin-like growth factor-1, and vascular endothelial growth factor also followed BMM delivery. In contrast to the effects of differentiated macrophages, liver fibrosis was not significantly altered by the application of macrophage precursors and was exacerbated by whole BM. CONCLUSION: Macrophage cell therapy improves clinically relevant parameters in experimental chronic liver injury. Paracrine signaling to endogenous cells amplifies the effect. The benefits from this single, defined cell type suggest clinical potential. Copyright © 2011 American Association for the Study of Liver Diseases.
	PMID: 21433043 [PubMed - indexed for MEDLINE]

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

Sent on Thursday, 2011 Aug 25
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 - 3 of 3

1.	Nature. 2011 Jul 13;475(7355):163-5. doi: 10.1038/475163a. Genomics for the world. Bustamante CD, Burchard EG, De la Vega FM. Source Department of Genetics, Stanford University School of Medicine, Stanford, California 94305, USA. cdbustam@stanford.edu
	PMID: 21753830 [PubMed - indexed for MEDLINE]
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2.	Nature. 2011 Jul 10;475(7355):189-95. doi: 10.1038/nature10158. Genome sequence and analysis of the tuber crop potato. Potato Genome Sequencing Consortium, Xu X, Pan S, Cheng S, Zhang B, Mu D, Ni P, Zhang G, Yang S, Li R, Wang J, Orjeda G, Guzman F, Torres M, Lozano R, Ponce O, Martinez D, De la Cruz G, Chakrabarti SK, Patil VU, Skryabin KG, Kuznetsov BB, Ravin NV, Kolganova TV, Beletsky AV, Mardanov AV, Di Genova A, Bolser DM, Martin DM, Li G, Yang Y, Kuang H, Hu Q, Xiong X, Bishop GJ, Sagredo B, Mejía N, Zagorski W, Gromadka R, Gawor J, Szczesny P, Huang S, Zhang Z, Liang C, He J, Li Y, He Y, Xu J, Zhang Y, Xie B, Du Y, Qu D, Bonierbale M, Ghislain M, Herrera Mdel R, Giuliano G, Pietrella M, Perrotta G, Facella P, O'Brien K, Feingold SE, Barreiro LE, Massa GA, Diambra L, Whitty BR, Vaillancourt B, Lin H, Massa AN, Geoffroy M, Lundback S, DellaPenna D, Buell CR, Sharma SK, Marshall DF, Waugh R, Bryan GJ, Destefanis M, Nagy I, Milbourne D, Thomson SJ, Fiers M, Jacobs JM, Nielsen KL, Sønderkær M, Iovene M, Torres GA, Jiang J, Veilleux RE, Bachem CW, de Boer J, Borm T, Kloosterman B, van Eck H, Datema E, Hekkert BL, Goverse A, van Ham RC, Visser RG. Source BGI-Shenzhen, Chinese Ministry of Agricultural, Key Lab of Genomics, Beishan Industrial Zone, Yantian District, Shenzhen 518083, China. Abstract Potato (Solanum tuberosum L.) is the world's most important non-grain food crop and is central to global food security. It is clonally propagated, highly heterozygous, autotetraploid, and suffers acute inbreeding depression. Here we use a homozygous doubled-monoploid potato clone to sequence and assemble 86% of the 844-megabase genome. We predict 39,031 protein-coding genes and present evidence for at least two genome duplication events indicative of a palaeopolyploid origin. As the first genome sequence of an asterid, the potato genome reveals 2,642 genes specific to this large angiosperm clade. We also sequenced a heterozygous diploid clone and show that gene presence/absence variants and other potentially deleterious mutations occur frequently and are a likely cause of inbreeding depression. Gene family expansion, tissue-specific expression and recruitment of genes to new pathways contributed to the evolution of tuber development. The potato genome sequence provides a platform for genetic improvement of this vital crop. ©2011 Macmillan Publishers Limited. All rights reserved
	PMID: 21743474 [PubMed - indexed for MEDLINE]
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3.	Nature. 2011 Jun 8;475(7355):222-5. doi: 10.1038/nature10138. CCL2 recruits inflammatory monocytes to facilitate breast-tumour metastasis. Qian BZ, Li J, Zhang H, Kitamura T, Zhang J, Campion LR, Kaiser EA, Snyder LA, Pollard JW. Source Department of Developmental and Molecular Biology, Center for the Study of Reproductive Biology and Women's Health, Albert Einstein College of Medicine, New York, New York 10461, USA. Abstract Macrophages, which are abundant in the tumour microenvironment, enhance malignancy. At metastatic sites, a distinct population of metastasis-associated macrophages promotes the extravasation, seeding and persistent growth of tumour cells. Here we define the origin of these macrophages by showing that Gr1-positive inflammatory monocytes are preferentially recruited to pulmonary metastases but not to primary mammary tumours in mice. This process also occurs for human inflammatory monocytes in pulmonary metastases of human breast cancer cells. The recruitment of these inflammatory monocytes, which express CCR2 (the receptor for chemokine CCL2), as well as the subsequent recruitment of metastasis-associated macrophages and their interaction with metastasizing tumour cells, is dependent on CCL2 synthesized by both the tumour and the stroma. Inhibition of CCL2-CCR2 signalling blocks the recruitment of inflammatory monocytes, inhibits metastasis in vivo and prolongs the survival of tumour-bearing mice. Depletion of tumour-cell-derived CCL2 also inhibits metastatic seeding. Inflammatory monocytes promote the extravasation of tumour cells in a process that requires monocyte-derived vascular endothelial growth factor. CCL2 expression and macrophage infiltration are correlated with poor prognosis and metastatic disease in human breast cancer. Our data provide the mechanistic link between these two clinical associations and indicate new therapeutic targets for treating metastatic breast cancer. ©2011 Macmillan Publishers Limited. All rights reserved
	PMID: 21654748 [PubMed - indexed for MEDLINE]
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Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Saturday, 2011 Aug 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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1.	Nature. 2011 Jun 19;475(7354):110-3. doi: 10.1038/nature10134. Intravenous gammaglobulin suppresses inflammation through a novel T(H)2 pathway. Anthony RM, Kobayashi T, Wermeling F, Ravetch JV. Source Laboratory of Molecular Genetics and Immunology, The Rockefeller University, 1230 York Avenue, New York, New York 10065, USA. Abstract High-dose intravenous immunoglobulin is a widely used therapeutic preparation of highly purified immunoglobulin G (IgG) antibodies. It is administered at high doses (1-2 grams per kilogram) for the suppression of autoantibody-triggered inflammation in a variety of clinical settings. This anti-inflammatory activity of intravenous immunoglobulin is triggered by a minor population of IgG crystallizable fragments (Fcs), with glycans terminating in α2,6 sialic acids (sFc) that target myeloid regulatory cells expressing the lectin dendritic-cell-specific ICAM-3 grabbing non-integrin (DC-SIGN; also known as CD209). Here, to characterize this response in detail, we generated humanized DC-SIGN mice (hDC-SIGN), and demonstrate that the anti-inflammatory activity of intravenous immunoglobulin can be recapitulated by the transfer of bone-marrow-derived sFc-treated hDC-SIGN(+) macrophages or dendritic cells into naive recipients. Furthermore, sFc administration results in the production of IL-33, which, in turn, induces expansion of IL-4-producing basophils that promote increased expression of the inhibitory Fc receptor FcγRIIB on effector macrophages. Systemic administration of the T(H)2 cytokines IL-33 or IL-4 upregulates FcγRIIB on macrophages, and suppresses serum-induced arthritis. Consistent with these results, transfer of IL-33-treated basophils suppressed induced arthritic inflammation. This novel DC-SIGN-T(H)2 pathway initiated by an endogenous ligand, sFc, provides an intrinsic mechanism for maintaining immune homeostasis that could be manipulated to provide therapeutic benefit in autoimmune diseases. ©2011 Macmillan Publishers Limited. All rights reserved
	PMID: 21685887 [PubMed - indexed for MEDLINE]

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Sent on Friday, 2011 Aug 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.	N Engl J Med. 2011 Aug 11;365(6):486-8. Incomplete care--on the trail of flaws in the system. Gandhi TK, Zuccotti G, Lee TH. Source Partners HealthCare System and Harvard Medical School, Boston, USA. Free Article
	PMID: 21830964 [PubMed - indexed for MEDLINE]
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2.	Science. 2011 Aug 5;333(6043):711. Retrospective. Lennart Philipson (1929-2011). Simons K, Mattaj IW. Source Max Planck Institute of Molecular Cell Biology and Genetics, Pfotenhauerstrasse 108, Dresden 01307, Germany. simons@mpi-cbg.de
	PMID: 21817041 [PubMed - indexed for MEDLINE]
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3.	Science. 2011 Aug 5;333(6043):762-5. Epub 2011 Jul 14. The plant cell wall-decomposing machinery underlies the f unctional diversity of forest fungi. Eastwood DC, Floudas D, Binder M, Majcherczyk A, Schneider P, Aerts A, Asiegbu FO, Baker SE, Barry K, Bendiksby M, Blumentritt M, Coutinho PM, Cullen D, de Vries RP, Gathman A, Goodell B, Henrissat B, Ihrmark K, Kauserud H, Kohler A, LaButti K, Lapidus A, Lavin JL, Lee YH, Lindquist E, Lilly W, Lucas S, Morin E, Murat C, Oguiza JA, Park J, Pisabarro AG, Riley R, Rosling A, Salamov A, Schmidt O, Schmutz J, Skrede I, Stenlid J, Wiebenga A, Xie X, Kües U, Hibbett DS, Hoffmeister D, Högberg N, Martin F, Grigoriev IV, Watkinson SC. Source College of Science, University of Swansea, Singleton Park, Swansea SA2 8PP, UK. d.c.eastwood@swansea.ac.uk Abstract Brown rot decay removes cellulose and hemicellulose from wood--residual lignin contributing up to 30% of forest soil carbon--and is derived from an ancestral white rot saprotrophy in which both lignin and cellulose are decomposed. Comparative and functional genomics of the "dry rot" fungus Serpula lacrymans, derived from forest ancestors, demonstrated that the evolution of both ectomycorrhizal biotrophy and brown rot saprotrophy were accompanied by reductions and losses in specific protein families, suggesting adaptation to an intercellular interaction with plant tissue. Transcriptome and proteome analysis also identified differences in wood decomposition in S. lacrymans relative to the brown rot Postia placenta. Furthermore, fungal nutritional mode diversification suggests that the boreal forest biome originated via genetic coevolution of above- and below-ground biota.
	PMID: 21764756 [PubMed - indexed for MEDLINE]
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4.	Nat Med. 2011 Jun;17(6):738-43. Epub 2011 May 22. A clinical microchip for evaluation of single immune cells rev eals high functional heterogeneity in phenotypically similar T cells. Ma C, Fan R, Ahmad H, Shi Q, Comin-Anduix B, Chodon T, Koya RC, Liu CC, Kwong GA, Radu CG, Ribas A, Heath JR. Source NanoSystems Biology Cancer Center, California Institute of Technology, Pasadena, California, USA. Abstract Cellular immunity has an inherent high level of functional heterogeneity. Capturing the full spectrum of these functions requires analysis of large numbers of effector molecules from single cells. We report a microfluidic platform designed for highly multiplexed (more than ten proteins), reliable, sample-efficient (∼1 × 10(4) cells) and quantitative measurements of secreted proteins from single cells. We validated the platform by assessment of multiple inflammatory cytokines from lipopolysaccharide (LPS)-stimulated human macrophages and comparison to standard immunotechnologies. We applied the platform toward the ex vivo quantification of T cell polyfunctional diversity via the simultaneous measurement of a dozen effector molecules secreted from tumor antigen-specific cytotoxic T lymphocytes (CTLs) that were actively responding to tumor and compared against a cohort of healthy donor controls. We observed profound, yet focused, functional heterogeneity in active tumor antigen-specific CTLs, with the major functional phenotypes quantitatively identified. The platform represents a new and informative tool for immune monitoring and clinical assessment.
	PMID: 21602800 [PubMed - indexed for MEDLINE]
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Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Wednesday, 2011 Aug 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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1.	FEBS Lett. 2011 Jun 6;585(11):1589-94. Epub 2011 Apr 6. Retrotransposons: mobile and mutagenic from conception to death. Faulkner GJ. Source Division of Genetics and Genomics, The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush, UK. geoff.faulkner@roslin.ed.ac.uk Abstract Mobile genetic elements feature prominently in mammalian genome evolution. Several transposition-competent retrotransposon families (L1, Alu, SVA) remain active in the human germ line, leading to pathogenesis as well as genome structural variation across the global population. High-throughput screening approaches have recently been developed to detect retrotransposon insertion polymorphisms. Evidence produced by these and other genome-scale technologies indicates an expanded role for retrotransposition in human biology, including somatic mobilisation in the developing embryo and in neural cells. Copyright © 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
	PMID: 21477589 [PubMed - indexed for MEDLINE]

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Sent on Saturday, 2011 Aug 06
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.	N Engl J Med. 2011 Jul 28;365(4):347-57. Microbial genomics and infectious diseases. Relman DA. Source Department of Medicine, Stanford University, Stanford, California, USA. relman@stanford.edu Free Article
	PMID: 21793746 [PubMed - indexed for MEDLINE]

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1.	Science. 2011 Jul 22;333(6041):411-2. Evolution. Seeing the trees in your terrace. Kubatko LS, Pearl DK. Source Department of Statistics, The Ohio State University, Columbus, OH 43210, USA. lkubatko@stat.osu.edu Comment on Science. 2011 Jul 22;333(6041):448-50.
	PMID: 21778387 [PubMed - indexed for MEDLINE]
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2.	Science. 2011 Jul 22;333(6041):405; author reply 405. Comment on "Activation of β-catenin in dendritic cells r egulates immunity versus tolerance in the intestine". Murphy KM. Source Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. kmurphy@wustl.edu Comment on Science. 2010 Aug 13;329(5993):849-53. Abstract Manicassamy et al. (Reports, 13 August 2010, p. 849) deleted β-catenin in intestinal immune cells using a CD11c-driven Cre recombinase, which decreased anti-inflammatory mediators and increased inflammatory bowel disease. However, the deletion of β-catenin in macrophages remains a caveat to their interpretation that Wnt signaling programs dendritic cells into a tolerogenic state. Development of strains expressing Cre in a more finely lineage-restricted pattern may help resolve this issue. Free Article
	PMID: 21778384 [PubMed - indexed for MEDLINE]
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3.	Nature. 2011 Jul 17;475(7357):514-8. doi: 10.1038/nature10228. Control of TH17 cells occurs in the smal l intestine. Esplugues E, Huber S, Gagliani N, Hauser AE, Town T, Wan YY, O'Connor W Jr, Rongvaux A, Van Rooijen N, Haberman AM, Iwakura Y, Kuchroo VK, Kolls JK, Bluestone JA, Herold KC, Flavell RA. Source Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA. enric.esplugues@yale.edu Abstract Interleukin (IL)-17-producing T helper cells (T(H)17) are a recently identified CD4(+) T cell subset distinct from T helper type 1 (T(H)1) and T helper type 2 (T(H)2) cells. T(H)17 cells can drive antigen-specific autoimmune diseases and are considered the main population of pathogenic T cells driving experimental autoimmune encephalomyelitis (EAE), the mouse model for multiple sclerosis. The factors that are needed for the generation of T(H)17 cells have been well characterized. However, where and how the immune system controls T(H)17 cells in vivo remains unclear. Here, by using a model of tolerance induced by CD3-specific antibody, a model of sepsis and influenza A viral infection (H1N1), we show that pro-inflammatory T(H)17 cells can be redirected to and controlled in the small intestine. T(H)17-specific IL-17A secretion induced expression of the chemokine CCL20 in the small intestine, facilitating the migration of these cells specifically to the small intestine via the CCR6/CCL20 axis. Moreover, we found that T(H)17 cells are controlled by two different mechanisms in the small intestine: first, they are eliminated via the intestinal lumen; second, pro-inflammatory T(H)17 cells simultaneously acquire a regulatory phenotype with in vitro and in vivo immune-suppressive properties (rT(H)17). These results identify mechanisms limiting T(H)17 cell pathogenicity and implicate the gastrointestinal tract as a site for control of T(H)17 cells. PMCID: PMC3148838 [Available on 2012/1/28]
	PMID: 21765430 [PubMed - indexed for MEDLINE]
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4.	Nature. 2011 Jul 13;475(7357):493-6. doi: 10.1038/nature10231. Inference of human population history from individual whole-genome sequences. Li H, Durbin R. Source The Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK. Abstract The history of human population size is important for understanding human evolution. Various studies have found evidence for a founder event (bottleneck) in East Asian and European populations, associated with the human dispersal out-of-Africa event around 60 thousand years (kyr) ago. However, these studies have had to assume simplified demographic models with few parameters, and they do not provide a precise date for the start and stop times of the bottleneck. Here, with fewer assumptions on population size changes, we present a more detailed history of human population sizes between approximately ten thousand and a million years ago, using the pairwise sequentially Markovian coalescent model applied to the complete diploid genome sequences of a Chinese male (YH), a Korean male (SJK), three European individuals (J. C. Venter, NA12891 and NA12878 (ref. 9)) and two Yoruba males (NA18507 (ref. 10) and NA19239). We infer that European and Chinese populations had very similar population-size histories before 10-20 kyr ago. Both populations experienced a severe bottleneck 10-60 kyr ago, whereas African populations experienced a milder bottleneck from which they recovered earlier. All three populations have an elevated effective population size between 60 and 250 kyr ago, possibly due to population substructure. We also infer that the differentiation of genetically modern humans may have started as early as 100-120 kyr ago, but considerable genetic exchanges may still have occurred until 20-40 kyr ago.
	PMID: 21753753 [PubMed - indexed for MEDLINE]
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5.	Nature. 2011 Jul 6;475(7357):506-9. doi: 10.1038/nature10307. Legionella pneumophila SidD is a deAMPylase that modifies Rab1. Tan Y, Luo ZQ. Source Department of Biological Sciences, Purdue University, 915 West State Street, West Lafayette, Indiana 47907, USA. Abstract Legionella pneumophila actively modulates host vesicle trafficking pathways to facilitate its intracellular replication with effectors translocated by the Dot/Icm type IV secretion system (T4SS). The SidM/DrrA protein functions by locking the small GTPase Rab1 into an active form by its guanine nucleotide exchange factor (GEF) and AMPylation activity. Here we demonstrate that the L. pneumophila protein SidD preferably deAMPylates Rab1. We found that the deAMPylation activity of SidD could suppress the toxicity of SidM to yeast and is required to release Rab1 from bacterial phagosomes efficiently. A molecular mechanism for the temporal control of Rab1 activity in different phases of L. pneumophila infection is thus established. These observations indicate that AMPylation-mediated signal transduction is a reversible process regulated by specific enzymes. PMCID: PMC3146296 [Available on 2012/1/28]
	PMID: 21734656 [PubMed - indexed for MEDLINE]
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6.	Science. 2011 Jul 22;333(6041):453-6. Epub 2011 Jun 16. De-AMPylation of the small GTPase Rab1 by the pathogen Legionella pneumophila. Neunuebel MR, Chen Y, Gaspar AH, Backlund PS Jr, Yergey A, Machner MP. Source Cell Biology and Metabolism Program, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA. Abstract The bacterial pathogen Legionella pneumophila exploits host cell vesicle transport by transiently manipulating the activity of the small guanosine triphosphatase (GTPase) Rab1. The effector protein SidM recruits Rab1 to the Legionella-containing vacuole (LCV), where it activates Rab1 and then AMPylates it by covalently adding adenosine monophosphate (AMP). L. pneumophila GTPase-activating protein LepB inactivates Rab1 before its removal from LCVs. Because LepB cannot bind AMPylated Rab1, the molecular events leading to Rab1 inactivation are unknown. We found that the effector protein SidD from L. pneumophila catalyzed AMP release from Rab1, generating de-AMPylated Rab1 accessible for inactivation by LepB. L. pneumophila mutants lacking SidD were defective for Rab1 removal from LCVs, identifying SidD as the missing link connecting the processes of early Rab1 accumulation and subsequent Rab1 removal during infection.
	PMID: 21680813 [PubMed - indexed for MEDLINE]
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7.	Science. 2011 Jul 22;333(6041):448-50. Epub 2011 Jun 16. Terraces in phylogenetic tree space. Sanderson MJ, McMahon MM, Steel M. Source Department of Ecology and Evolutionary Biology, University of Arizona, Tucson, AZ 85721, USA. sanderm@email.arizona.edu Comment in Science. 2011 Jul 22;333(6041):411-2. Abstract A key step in assembling the tree of life is the construction of species-rich phylogenies from multilocus--but often incomplete--sequence data sets. We describe previously unknown structure in the landscape of solutions to the tree reconstruction problem, comprising sometimes vast "terraces" of trees with identical quality, arranged on islands of phylogenetically similar trees. Phylogenetic ambiguity within a terrace can be characterized efficiently and then ameliorated by new algorithms for obtaining a terrace's maximum-agreement subtree or by identifying the smallest set of new targets for additional sequencing. Algorithms to find optimal trees or estimate Bayesian posterior tree distributions may need to navigate strategically in the neighborhood of large terraces in tree space.
	PMID: 21680810 [PubMed - indexed for MEDLINE]
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8.	PLoS One. 2011 Jan 7;6(1):e15723. Macrophage activation and differentiation signals regulate schlafen-4 gene expr ession: evidence for Schlafen-4 as a modulator of myelopoiesis. van Zuylen WJ, Garceau V, Idris A, Schroder K, Irvine KM, Lattin JE, Ovchinnikov DA, Perkins AC, Cook AD, Hamilton JA, Hertzog PJ, Stacey KJ, Kellie S, Hume DA, Sweet MJ. Source The University of Queensland, Institute for Molecular Bioscience, Queensland, Australia. Abstract BACKGROUND: The ten mouse and six human members of the Schlafen (Slfn) gene family all contain an AAA domain. Little is known of their function, but previous studies suggest roles in immune cell development. In this report, we assessed Slfn regulation and function in macrophages, which are key cellular regulators of innate immunity. METHODOLOGY/PRINCIPAL FINDINGS: Multiple members of the Slfn family were up-regulated in mouse bone marrow-derived macrophages (BMM) by the Toll-like Receptor (TLR)4 agonist lipopolysaccharide (LPS), the TLR3 agonist Poly(I∶C), and in disease-affected joints in the collagen-induced model of rheumatoid arthritis. Of these, the most inducible was Slfn4. TLR agonists that signal exclusively through the MyD88 adaptor protein had more modest effects on Slfn4 mRNA levels, thus implicating MyD88-independent signalling and autocrine interferon (IFN)-β in inducible expression. This was supported by the substantial reduction in basal and LPS-induced Slfn4 mRNA expression in IFNAR-1⁻/⁻ BMM. LPS causes growth arrest in macrophages, and other Slfn family genes have been implicated in growth control. Slfn4 mRNA levels were repressed during macrophage colony-stimulating factor (CSF-1)-mediated differentiation of bone marrow progenitors into BMM. To determine the role of Slfn4 in vivo, we over-expressed the gene specifically in macrophages in mice using a csf1r promoter-driven binary expression system. Transgenic over-expression of Slfn4 in myeloid cells did not alter macrophage colony formation or proliferation in vitro. Monocyte numbers, as well as inflammatory macrophages recruited to the peritoneal cavity, were reduced in transgenic mice that specifically over-expressed Slfn4, while macrophage numbers and hematopoietic activity were increased in the livers and spleens. CONCLUSIONS: Slfn4 mRNA levels were up-regulated during macrophage activation but down-regulated during differentiation. Constitutive Slfn4 expression in the myeloid lineage in vivo perturbs myelopoiesis. We hypothesise that the down-regulation of Slfn4 gene expression during macrophage differentiation is a necessary step in development of this lineage. PMCID: PMC3017543 Free PMC Article
	PMID: 21249125 [PubMed - indexed for MEDLINE]
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