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

Sent on Saturday, 2014 February 01
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 - 3 of 3

1.	Nature. 2014 Jan 9;505(7482):174-9. doi: 10.1038/nature12826. Elephant shark genome provides unique insights into gnathostome evolution. Venkatesh B1, Lee AP2, Ravi V2, Maurya AK3, Lian MM2, Swann JB4, Ohta Y5, Flajnik MF5, Sutoh Y6, Kasahara M6, Hoon S7, Gangu V7, Roy SW8, Irimia M9, Korzh V10, Kondrychyn I10, Lim ZW2, Tay BH2, Tohari S2, Kong KW7, Ho S7, Lorente-Galdos B11, Quilez J11, Marques-Bonet T11, Raney BJ12, Ingham PW3, Tay A2, Hillier LW13, Minx P13, Boehm T4, Wilson RK13, Brenner S2, Warren WC13. Author information: 11] Comparative Genomics Laboratory, Institute of Molecular and Cell Biology, A*STAR, Biopolis, Singapore 138673 [2] Department of Paediatrics, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 119228. 2Comparative Genomics Laboratory, Institute of Molecular and Cell Biology, A*STAR, Biopolis, Singapore 138673. 3Developmental and Biomedical Genetics Laboratory, Institute of Molecular and Cell Biology, A*STAR, Biopolis, Singapore 138673. 4Department of Developmental Immunology, Max-Planck-Institute of Immunobiology and Epigenetics, Stuebeweg 51, 79108 Freiburg, Germany. 5Department of Microbiology and Immunology, University of Maryland, Baltimore, Maryland 21201, USA. 6Department of Pathology, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan. 7Molecular Engineering Laboratory, Biomedical Sciences Institutes, A*STAR, Biopolis, Singapore 138673. 8Department of Biology, San Francisco State University, San Francisco, California 94132, USA. 9Banting and Best Department of Medical Research and Donnelly Centre, University of Toronto, Toronto, Ontario M5S 3E1, Canada. 10Fish Developmental Biology Laboratory, Institute of Molecular and Cell Biology, A*STAR, Biopolis, Singapore 138673. 111] Institut de Biologia Evolutiva (UPF-CSIC), PRBB, 08003 Barcelona, Spain [2] Institució Catalana de Recerca i Estudis Avançats (ICREA), 08010 Barcelona, Catalonia, Spain. 12Center for Biomolecular Science and Engineering, School of Engineering, University of California Santa Cruz, Santa Cruz, California 95064, USA. 13The Genome Institute at Washington University, St Louis, Missouri 63108, USA. Abstract The emergence of jawed vertebrates (gnathostomes) from jawless vertebrates was accompanied by major morphological and physiological innovations, such as hinged jaws, paired fins and immunoglobulin-based adaptive immunity. Gnathostomes subsequently diverged into two groups, the cartilaginous fishes and the bony vertebrates. Here we report the whole-genome analysis of a cartilaginous fish, the elephant shark (Callorhinchus milii). We find that the C. milii genome is the slowest evolving of all known vertebrates, including the 'living fossil' coelacanth, and features extensive synteny conservation with tetrapod genomes, making it a good model for comparative analyses of gnathostome genomes. Our functional studies suggest that the lack of genes encoding secreted calcium-binding phosphoproteins in cartilaginous fishes explains the absence of bone in their endoskeleton. Furthermore, the adaptive immune system of cartilaginous fishes is unusual: it lacks the canonical CD4 co-receptor and most transcription factors, cytokines and cytokine receptors related to the CD4 lineage, despite the presence of polymorphic major histocompatibility complex class II molecules. It thus presents a new model for understanding the origin of adaptive immunity.
	PMID: 24402279 [PubMed - indexed for MEDLINE]
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2.	Nature. 2014 Jan 9;505(7482):160. doi: 10.1038/505160c. Environment: Himalayas already have hazard network. Uprety Y1, Chaudhary RP1, Chettri N2. Author information: 1Research Centre for Applied Science and Technology, Tribhuvan University, Kathmandu, Nepal. 2ICIMOD, Kathmandu, Nepal. Comment on The Himalayas must be protected. [Nature. 2013] The Himalayas must be protected.Pandit MK. Nature. 2013 Sep 19; 501(7467):283.
	PMID: 24402272 [PubMed - indexed for MEDLINE]
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3.	Nature. 2014 Jan 9;505(7482):218-22. doi: 10.1038/nature12799. Epub 2013 Dec 15. Mycobacteria manipulate macrophage recruitment through coordinated use of membrane lipids. Cambier CJ1, Takaki KK2, Larson RP3, Hernandez RE4, Tobin DM2, Urdahl KB5, Cosma CL2, Ramakrishnan L6. Author information: 1Department of Immunology, University of Washington, Seattle, Washington 98195, USA. 2Department of Microbiology, University of Washington, Seattle, Washington 98195, USA. 31] Department of Immunology, University of Washington, Seattle, Washington 98195, USA [2] Seattle Biomedical Research Institute, Seattle, Washington 98109, USA. 4Department of Pediatrics, University of Washington, Seattle, Washington 98195, USA. 51] Department of Immunology, University of Washington, Seattle, Washington 98195, USA [2] Seattle Biomedical Research Institute, Seattle, Washington 98109, USA [3] Department of Pediatrics, University of Washington, Seattle, Washington 98195, USA. 61] Department of Immunology, University of Washington, Seattle, Washington 98195, USA [2] Department of Microbiology, University of Washington, Seattle, Washington 98195, USA [3] Department of Medicine, University of Washington, Seattle, Washington 98195, USA. Abstract The evolutionary survival of Mycobacterium tuberculosis, the cause of human tuberculosis, depends on its ability to invade the host, replicate, and transmit infection. At its initial peripheral infection site in the distal lung airways, M. tuberculosis infects macrophages, which transport it to deeper tissues. How mycobacteria survive in these broadly microbicidal cells is an important question. Here we show in mice and zebrafish that M. tuberculosis, and its close pathogenic relative Mycobacterium marinum, preferentially recruit and infect permissive macrophages while evading microbicidal ones. This immune evasion is accomplished by using cell-surface-associated phthiocerol dimycoceroserate (PDIM) lipids to mask underlying pathogen-associated molecular patterns (PAMPs). In the absence of PDIM, these PAMPs signal a Toll-like receptor (TLR)-dependent recruitment of macrophages that produce microbicidal reactive nitrogen species. Concordantly, the related phenolic glycolipids (PGLs) promote the recruitment of permissive macrophages through a host chemokine receptor 2 (CCR2)-mediated pathway. Thus, we have identified coordinated roles for PDIM, known to be essential for mycobacterial virulence, and PGL, which (along with CCR2) is known to be associated with human tuberculosis. Our findings also suggest an explanation for the longstanding observation that M. tuberculosis initiates infection in the relatively sterile environment of the lower respiratory tract, rather than in the upper respiratory tract, where resident microflora and inhaled environmental microbes may continually recruit microbicidal macrophages through TLR-dependent signalling.
	PMID: 24336213 [PubMed - indexed for MEDLINE]
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