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

Sent on Friday, 2014 October 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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PubMed Results

Items 1 - 9 of 9

1.	Nature. 2014 Oct 2;514(7520):E2. doi: 10.1038/nature13689. Kruidenier et al. reply. Kruidenier L1, Chung CW2, Cheng Z3, Liddle J1, Che K4, Joberty G5, Bantscheff M5, Bountra C6, Bridges A2, Diallo H1, Eberhard D5, Hutchinson S2, Jones E2, Katso R2, Leveridge M2, Mander PK1, Mosley J2, Ramirez-Molina C1, Rowland P2, Schofield CJ6, Sheppard RJ1, Smith JE1, Swales C7, Tanner R2, Thomas P2, Tumber A6, Drewes G5, Oppermann U4, Patel DJ3, Lee K8, Wilson DM1. Author information: 1Epinova DPU, Immuno-Inflammation Therapy Area, GlaxoSmithKline R&D, Medicines Research Centre, Gunnels Wood Road, Stevenage SG1 2NY, UK. 2Platform Technology and Science, GlaxoSmithKline R&D, Medicines Research Centre, Gunnels Wood Road, Stevenage SG1 2NY, UK. 3Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, New York 10065, USA. 41] Structural Genomics Consortium, University of Oxford, Old Road Campus, Roosevelt Drive, Headington OX3 7DQ, UK [2] Botnar Research Centre, NIHR Biomedical Research Unit, University of Oxford OX3 7LD, UK. 5Cellzome AG, Meyerhofstrasse 1, 69117 Heidelberg, Germany. 6Structural Genomics Consortium, University of Oxford, Old Road Campus, Roosevelt Drive, Headington OX3 7DQ, UK. 7Botnar Research Centre, NIHR Biomedical Research Unit, University of Oxford OX3 7LD, UK. 81] Epinova DPU, Immuno-Inflammation Therapy Area, GlaxoSmithKline R&D, Medicines Research Centre, Gunnels Wood Road, Stevenage SG1 2NY, UK [2] Pfizer, Biotherapeutics R&D, 200 Cambridgepark Drive, Cambridge, Massachusetts 02140, USA. Comment on A selective jumonji H3K27 demethylase inhibitor modulates the proinflammatory macrophage response. [Nature. 2012] A selective jumonji H3K27 demethylase inhibitor modulates the proinflammatory macrophage response.Kruidenier L, Chung CW, Cheng Z, Liddle J, Che K, Joberty G, Bantscheff M, Bountra C, Bridges A, Diallo H, et al. Nature. 2012 Aug 16; 488(7411):404-8. Inhibition of demethylases by GSK-J1/J4. [Nature. 2014] Inhibition of demethylases by GSK-J1/J4.Heinemann B, Nielsen JM, Hudlebusch HR, Lees MJ, Larsen DV, Boesen T, Labelle M, Gerlach LO, Birk P, Helin K. Nature. 2014 Oct 2; 514(7520):E1-2.
	PMID: 25279927 [PubMed - indexed for MEDLINE]
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2.	Nature. 2014 Oct 2;514(7520):E1-2. doi: 10.1038/nature13688. Inhibition of demethylases by GSK-J1/J4. Heinemann B1, Nielsen JM1, Hudlebusch HR1, Lees MJ2, Larsen DV1, Boesen T1, Labelle M1, Gerlach LO1, Birk P1, Helin K3. Author information: 1EpiTherapeutics Aps, Ole Maaløes Vej 3, 2200 Copenhagen, Denmark. 2Biotech Research and Innovation Centre (BRIC), University of Copenhagen, Ole Maaløes Vej 5, 2200 Copenhagen, Denmark. 31] Biotech Research and Innovation Centre (BRIC), University of Copenhagen, Ole Maaløes Vej 5, 2200 Copenhagen, Denmark [2] Centre for Epigenetics, University of Copenhagen, Ole Maaløes Vej 5, 2200 Copenhagen, Denmark [3] The Danish Stem Cell Center (DanStem), University of Copenhagen, Blegdamsvej 3, 2200 Copenhagen, Denmark. Comment in Kruidenier et al. reply. [Nature. 2014] Kruidenier et al. reply.Kruidenier L, Chung CW, Cheng Z, Liddle J, Che K, Joberty G, Bantscheff M, Bountra C, Bridges A, Diallo H, et al. Nature. 2014 Oct 2; 514(7520):E2. Comment on A selective jumonji H3K27 demethylase inhibitor modulates the proinflammatory macrophage response. [Nature. 2012] A selective jumonji H3K27 demethylase inhibitor modulates the proinflammatory macrophage response.Kruidenier L, Chung CW, Cheng Z, Liddle J, Che K, Joberty G, Bantscheff M, Bountra C, Bridges A, Diallo H, et al. Nature. 2012 Aug 16; 488(7411):404-8.
	PMID: 25279926 [PubMed - indexed for MEDLINE]
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3.	Nature. 2014 Oct 2;514(7520):59-64. doi: 10.1038/nature13786. Biogeography and individuality shape function in the human skin metagenome. Oh J1, Byrd AL1, Deming C1, Conlan S1; NISC Comparative Sequencing Program, Kong HH2, Segre JA3. Collaborators: Barnabas B, Blakesley R, Bouffard G, Brooks S, Coleman H, Dekhtyar M, Gregory M, Guan X, Gupta J, Han J, Ho SL, Legaspi R, Maduro Q, Masiello C, Maskeri B, McDowell J, Montemayor C, Mullikin J, Park M, Riebow N, Schandler K, Schmidt B, Sison C, Stantripop M, Thomas J, Thomas P, Vemulapalli M, Young A. Author information: 1Translational and Functional Genomics Branch, National Human Genome Research Institute, NIH, Bethesda, Maryland 20892, USA. 21] Dermatology Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA [2]. 31] Translational and Functional Genomics Branch, National Human Genome Research Institute, NIH, Bethesda, Maryland 20892, USA [2]. Comment in Microbiology: An integrated view of the skin microbiome. [Nature. 2014] Microbiology: An integrated view of the skin microbiome.Schloss PD. Nature. 2014 Oct 2; 514(7520):44-5. Abstract The varied topography of human skin offers a unique opportunity to study how the body's microenvironments influence the functional and taxonomic composition of microbial communities. Phylogenetic marker gene-based studies have identified many bacteria and fungi that colonize distinct skin niches. Here metagenomic analyses of diverse body sites in healthy humans demonstrate that local biogeography and strong individuality define the skin microbiome. We developed a relational analysis of bacterial, fungal and viral communities, which showed not only site specificity but also individual signatures. We further identified strain-level variation of dominant species as heterogeneous and multiphyletic. Reference-free analyses captured the uncharacterized metagenome through the development of a multi-kingdom gene catalogue, which was used to uncover genetic signatures of species lacking reference genomes. This work is foundational for human disease studies investigating inter-kingdom interactions, metabolic changes and strain tracking, and defines the dual influence of biogeography and individuality on microbial composition and function. PMCID: PMC4185404 [Available on 2015/4/1]
	PMID: 25279917 [PubMed - indexed for MEDLINE]
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4.	Nature. 2014 Oct 2;514(7520):24-6. doi: 10.1038/514024a. The first South Americans: Extreme living. Fraser B.
	PMID: 25279901 [PubMed - indexed for MEDLINE]
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5.	Nature. 2014 Oct 2;514(7520):16-7. doi: 10.1038/514016a. Tibetan plateau gets wired up for monsoon prediction. Qiu J.
	PMID: 25279896 [PubMed - indexed for MEDLINE]
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6.	Nature. 2014 Oct 2;514(7520):13-4. doi: 10.1038/514013a. Fast genetic sequencing saves newborn lives. Reardon S.
	PMID: 25279893 [PubMed - indexed for MEDLINE]
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7.	Science. 2014 Sep 26;345(6204):1251086. doi: 10.1126/science.1251086. Epigenetic programming of monocyte-to-macrophage differentiation and trained innate immunity. Saeed S1, Quintin J2, Kerstens HH1, Rao NA1, Aghajanirefah A1, Matarese F1, Cheng SC2, Ratter J2, Berentsen K1, van der Ent MA1, Sharifi N1, Janssen-Megens EM1, Ter Huurne M1, Mandoli A1, van Schaik T1, Ng A3, Burden F4, Downes K4, Frontini M4, Kumar V5, Giamarellos-Bourboulis EJ6, Ouwehand WH4, van der Meer JW2, Joosten LA2, Wijmenga C5, Martens JH1, Xavier RJ3, Logie C7, Netea MG8, Stunnenberg HG7. Author information: 1Department of Molecular Biology, Faculties of Science and Medicine, Radboud Institute for Molecular Life Sciences, Radboud University, 6500 HB Nijmegen, Netherlands. 2Department of Internal Medicine, Radboud University Medical Center, 6525 GA Nijmegen, Netherlands. 3Center for Computational and Integrative Biology and Gastrointestinal Unit, Massachusetts General Hospital, Harvard School of Medicine, Boston, MA 02114, USA. Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, MA 02142, USA. 4Department of Haematology, University of Cambridge, Cambridge, UK. National Health Service, Blood and Transplant Cambridge Centre, Cambridge Biomedical Campus, Cambridge CB0 2PT, UK. 5University of Groningen, University Medical Center Groningen, Department of Genetics, Groningen, Netherlands. 6Fourth Department of Internal Medicine, University of Athens, Medical School, 1 Rimini Street, 12462 Athens, Greece. 7Department of Molecular Biology, Faculties of Science and Medicine, Radboud Institute for Molecular Life Sciences, Radboud University, 6500 HB Nijmegen, Netherlands. h.stunnenberg@ncmls.ru.nl mihai.netea@radboudumc.nl c.logie@ncmls.ru.nl. 8Department of Internal Medicine, Radboud University Medical Center, 6525 GA Nijmegen, Netherlands. h.stunnenberg@ncmls.ru.nl mihai.netea@radboudumc.nl c.logie@ncmls.ru.nl. Abstract Monocyte differentiation into macrophages represents a cornerstone process for host defense. Concomitantly, immunological imprinting of either tolerance or trained immunity determines the functional fate of macrophages and susceptibility to secondary infections. We characterized the transcriptomes and epigenomes in four primary cell types: monocytes and in vitro-differentiated naïve, tolerized, and trained macrophages. Inflammatory and metabolic pathways were modulated in macrophages, including decreased inflammasome activation, and we identified pathways functionally implicated in trained immunity. β-glucan training elicits an exclusive epigenetic signature, revealing a complex network of enhancers and promoters. Analysis of transcription factor motifs in deoxyribonuclease I hypersensitive sites at cell-type-specific epigenetic loci unveiled differentiation and treatment-specific repertoires. Altogether, we provide a resource to understand the epigenetic changes that underlie innate immunity in humans. Copyright © 2014, American Association for the Advancement of Science.
	PMID: 25258085 [PubMed - indexed for MEDLINE]
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8.	Science. 2014 Sep 26;345(6204):1250684. doi: 10.1126/science.1250684. mTOR- and HIF-1α-mediated aerobic glycolysis as metabolic basis for trained immunity. Cheng SC1, Quintin J1, Cramer RA2, Shepardson KM2, Saeed S3, Kumar V4, Giamarellos-Bourboulis EJ5, Martens JH3, Rao NA3, Aghajanirefah A3, Manjeri GR6, Li Y4, Ifrim DC1, Arts RJ1, van der Meer BM4, Deen PM7, Logie C3, O'Neill LA8, Willems P6, van de Veerdonk FL1, van der Meer JW1, Ng A9, Joosten LA1, Wijmenga C4, Stunnenberg HG4, Xavier RJ9, Netea MG10. Author information: 1Department of Internal Medicine, Radboud University Medical Center, 6525 GA Nijmegen, Netherlands. 2Department of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Hanover, NH 03755, USA. 3Department of Molecular Biology, Faculties of Science and Medicine, Nijmegen Centre for Molecular Life Sciences, Radboud University, 6500 HB Nijmegen, Netherlands. 4Department of Genetics, University of Groningen, University Medical Center Groningen, Groningen, Netherlands. 54th Department of Internal Medicine, University of Athens Medical School, 12462 Athens, Greece. 6Department of Biochemistry, Faculties of Science and Medicine, Nijmegen Centre for Molecular Life Sciences, Radboud University, 6500 HB Nijmegen, Netherlands. 7Department of Physiology, Radboud University Medical Center, 6525 GA Nijmegen, Netherlands. 8School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin 2, Ireland. 9Center for Computational and Integrative Biology and Gastrointestinal Unit, Massachusetts General Hospital, Harvard School of Medicine, Boston, MA 02114, USA. Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. 10Department of Internal Medicine, Radboud University Medical Center, 6525 GA Nijmegen, Netherlands. mihai.netea@radboudumc.nl. Abstract Epigenetic reprogramming of myeloid cells, also known as trained immunity, confers nonspecific protection from secondary infections. Using histone modification profiles of human monocytes trained with the Candida albicans cell wall constituent β-glucan, together with a genome-wide transcriptome, we identified the induced expression of genes involved in glucose metabolism. Trained monocytes display high glucose consumption, high lactate production, and a high ratio of nicotinamide adenine dinucleotide (NAD(+)) to its reduced form (NADH), reflecting a shift in metabolism with an increase in glycolysis dependent on the activation of mammalian target of rapamycin (mTOR) through a dectin-1-Akt-HIF-1α (hypoxia-inducible factor-1α) pathway. Inhibition of Akt, mTOR, or HIF-1α blocked monocyte induction of trained immunity, whereas the adenosine monophosphate-activated protein kinase activator metformin inhibited the innate immune response to fungal infection. Mice with a myeloid cell-specific defect in HIF-1α were unable to mount trained immunity against bacterial sepsis. Our results indicate that induction of aerobic glycolysis through an Akt-mTOR-HIF-1α pathway represents the metabolic basis of trained immunity. Copyright © 2014, American Association for the Advancement of Science.
	PMID: 25258083 [PubMed - indexed for MEDLINE]
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9.	Nature. 2014 Oct 2;514(7520):47-53. doi: 10.1038/nature13777. Epub 2014 Aug 29. Reversion of advanced Ebola virus disease in nonhuman primates with ZMapp. Qiu X1, Wong G2, Audet J2, Bello A2, Fernando L1, Alimonti JB1, Fausther-Bovendo H2, Wei H3, Aviles J1, Hiatt E4, Johnson A4, Morton J4, Swope K4, Bohorov O5, Bohorova N5, Goodman C5, Kim D5, Pauly MH5, Velasco J5, Pettitt J6, Olinger GG6, Whaley K5, Xu B7, Strong JE8, Zeitlin L5, Kobinger GP9. Author information: 1National Laboratory for Zoonotic Diseases and Special Pathogens, Public Health Agency of Canada, Winnipeg, Manitoba R3E 3R2, Canada. 21] National Laboratory for Zoonotic Diseases and Special Pathogens, Public Health Agency of Canada, Winnipeg, Manitoba R3E 3R2, Canada [2] Department of Medical Microbiology, University of Manitoba, Winnipeg, Manitoba R3E 0J9, Canada. 31] National Laboratory for Zoonotic Diseases and Special Pathogens, Public Health Agency of Canada, Winnipeg, Manitoba R3E 3R2, Canada [2] Institute of Infectious Disease, Henan Centre for Disease Control and Prevention, Zhengzhou, 450012 Henan, China. 4Kentucky BioProcessing, Owensboro, Kentucky 42301, USA. 5Mapp Biopharmaceutical Inc., San Diego, California 92121, USA. 61] United States Army Medical Research Institute of Infectious Diseases (USAMRIID), Frederick, Maryland 21702, USA [2] Integrated Research Facility, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Frederick, Maryland 21702, USA. 7Institute of Infectious Disease, Henan Centre for Disease Control and Prevention, Zhengzhou, 450012 Henan, China. 81] National Laboratory for Zoonotic Diseases and Special Pathogens, Public Health Agency of Canada, Winnipeg, Manitoba R3E 3R2, Canada [2] Department of Medical Microbiology, University of Manitoba, Winnipeg, Manitoba R3E 0J9, Canada [3] Department of Pediatrics and Child Health, University of Manitoba, Winnipeg, Manitoba R3A 1S1, Canada. 91] National Laboratory for Zoonotic Diseases and Special Pathogens, Public Health Agency of Canada, Winnipeg, Manitoba R3E 3R2, Canada [2] Department of Medical Microbiology, University of Manitoba, Winnipeg, Manitoba R3E 0J9, Canada [3] Department of Immunology, University of Manitoba, Winnipeg, Manitoba R3E 0T5, Canada [4] Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA. Comment in Medical research: Ebola therapy protects severely ill monkeys. [Nature. 2014] Medical research: Ebola therapy protects severely ill monkeys.Geisbert TW. Nature. 2014 Oct 2; 514(7520):41-3. Epub 2014 Aug 29. Abstract Without an approved vaccine or treatments, Ebola outbreak management has been limited to palliative care and barrier methods to prevent transmission. These approaches, however, have yet to end the 2014 outbreak of Ebola after its prolonged presence in West Africa. Here we show that a combination of monoclonal antibodies (ZMapp), optimized from two previous antibody cocktails, is able to rescue 100% of rhesus macaques when treatment is initiated up to 5 days post-challenge. High fever, viraemia and abnormalities in blood count and blood chemistry were evident in many animals before ZMapp intervention. Advanced disease, as indicated by elevated liver enzymes, mucosal haemorrhages and generalized petechia could be reversed, leading to full recovery. ELISA and neutralizing antibody assays indicate that ZMapp is cross-reactive with the Guinean variant of Ebola. ZMapp exceeds the efficacy of any other therapeutics described so far, and results warrant further development of this cocktail for clinical use.
	PMID: 25171469 [PubMed - indexed for MEDLINE]
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