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Sent on Saturday, 2014 November 15
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. 2014 Nov 6;371(19):1833-7. doi: 10.1056/NEJMcps1313772. Clinical problem-solving. A chilly fever. Price C, Ashbaugh C, Miller AL, Loscalzo J.
	PMID: 25372092 [PubMed - indexed for MEDLINE]
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2.	Science. 2014 Oct 31;346(6209):641-6. doi: 10.1126/science.1258705. Innate immunity. A Spaetzle-like role for nerve growth factor β in vertebrate immunity to Staphylococcus aureus. Hepburn L1, Prajsnar TK2, Klapholz C1, Moreno P3, Loynes CA4, Ogryzko NV5, Brown K6, Schiebler M1, Hegyi K1, Antrobus R3, Hammond KL4, Connolly J7, Ochoa B8, Bryant C9, Otto M10, Surewaard B11, Seneviratne SL12, Grogono DM13, Cachat J14, Ny T15, Kaser A16, Török ME16, Peacock SJ17, Holden M18, Blundell T8, Wang L19, Ligoxygakis P19, Minichiello L20, Woods CG21, Foster SJ7, Renshaw SA22, Floto RA23. Author information: 1Cambridge Institute for Medical Research, University of Cambridge, UK. Department of Medicine, University of Cambridge, UK. 2Krebs Institute, University of Sheffield, Western Bank, Sheffield, S10 2TN, UK. Department of Molecular Biology and Biotechnology, University of Sheffield, Western Bank, Sheffield, S10 2TN, UK. Bateson Centre, University of Sheffield, Western Bank, Sheffield, S10 2TN, UK. 3Cambridge Institute for Medical Research, University of Cambridge, UK. 4Bateson Centre, University of Sheffield, Western Bank, Sheffield, S10 2TN, UK. Department of Infection and Immunity, University of Sheffield, Western Bank, Sheffield, S10 2TN, UK. 5Bateson Centre, University of Sheffield, Western Bank, Sheffield, S10 2TN, UK. 6Cambridge Institute for Medical Research, University of Cambridge, UK. Department of Medicine, University of Cambridge, UK. Cambridge Centre for Lung Infection, Papworth Hospital, Cambridge, UK. 7Krebs Institute, University of Sheffield, Western Bank, Sheffield, S10 2TN, UK. Department of Molecular Biology and Biotechnology, University of Sheffield, Western Bank, Sheffield, S10 2TN, UK. 8Department of Biochemistry, University of Cambridge, UK. 9Department of Veterinary Medicine, University of Cambridge, UK. 10Laboratory of Human Bacterial Pathogenesis, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, USA. 11Department of Medical Microbiology, University Medical Centre, Utrecht, Netherlands. 12Department of Clinical Immunology, Royal Free Hospital London, UK. 13Department of Medicine, University of Cambridge, UK. Cambridge Centre for Lung Infection, Papworth Hospital, Cambridge, UK. 14Department of Pathology and Immunology, Geneva University, Switzerland. 15Department of Medical Biochemistry and Biophysics, Umea University, Sweden. 16Department of Medicine, University of Cambridge, UK. 17Department of Medicine, University of Cambridge, UK. Wellcome Trust Sanger Institute, Hinxton, UK. 18Wellcome Trust Sanger Institute, Hinxton, UK. School of Medicine, University of St. Andrews, UK. 19Biochemistry Department, Oxford University, UK. 20Pharmacology Department, Oxford University, UK. 21Cambridge Institute for Medical Research, University of Cambridge, UK. Department of Medical Genetics, University of Cambridge, UK. 22Krebs Institute, University of Sheffield, Western Bank, Sheffield, S10 2TN, UK. Bateson Centre, University of Sheffield, Western Bank, Sheffield, S10 2TN, UK. Department of Infection and Immunity, University of Sheffield, Western Bank, Sheffield, S10 2TN, UK. arf27@cam.ac.uk s.a.renshaw@sheffield.ac.uk. 23Cambridge Institute for Medical Research, University of Cambridge, UK. Department of Medicine, University of Cambridge, UK. Cambridge Centre for Lung Infection, Papworth Hospital, Cambridge, UK. arf27@cam.ac.uk s.a.renshaw@sheffield.ac.uk. Abstract Many key components of innate immunity to infection are shared between Drosophila and humans. However, the fly Toll ligand Spaetzle is not thought to have a vertebrate equivalent. We have found that the structurally related cystine-knot protein, nerve growth factor β (NGFβ), plays an unexpected Spaetzle-like role in immunity to Staphylococcus aureus infection in chordates. Deleterious mutations of either human NGFβ or its high-affinity receptor tropomyosin-related kinase receptor A (TRKA) were associated with severe S. aureus infections. NGFβ was released by macrophages in response to S. aureus exoproteins through activation of the NOD-like receptors NLRP3 and NLRP4 and enhanced phagocytosis and superoxide-dependent killing, stimulated proinflammatory cytokine production, and promoted calcium-dependent neutrophil recruitment. TrkA knockdown in zebrafish increased susceptibility to S. aureus infection, confirming an evolutionarily conserved role for NGFβ-TRKA signaling in pathogen-specific host immunity. Copyright © 2014, American Association for the Advancement of Science.
	PMID: 25359976 [PubMed - indexed for MEDLINE]
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Sent on Friday, 2014 November 14
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. 2014 Oct 16;514(7522):395-6. Molecular biology: Genetic touch-ups. Perkel JM.
	PMID: 25325097 [PubMed - indexed for MEDLINE]
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2.	Nature. 2014 Oct 16;514(7522):282. doi: 10.1038/514282a. Giant gene banks take on disease. Check Hayden E.
	PMID: 25318499 [PubMed - indexed for MEDLINE]
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Sent on Wednesday, 2014 November 12
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 Oct 24;346(6208):510. doi: 10.1126/science.346.6208.510. A double dose of advice. Wang H. Author information: Huan (Sharon) Wang is now a postdoc working in the lab of Peter Sorger at Harvard Medical School. For more on life, science, and careers, visit www.sciencecareers.org.
	PMID: 25342808 [PubMed - indexed for MEDLINE]
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2.	Science. 2014 Oct 24;346(6208):466-9. doi: 10.1126/science.1258260. Paleoindian settlement of the high-altitude Peruvian Andes. Rademaker K1, Hodgins G2, Moore K3, Zarrillo S4, Miller C5, Bromley GR6, Leach P7, Reid DA8, Álvarez WY9, Sandweiss DH10. Author information: 1Department of Anthropology, South Stevens Hall, University of Maine, Orono, ME 04469-5773, USA. Department of Early Prehistory and Quaternary Ecology, Schloß Hohentübingen, Burgsteige 11, 72070 Tübingen, Germany. Climate Change Institute, Bryand Global Sciences Center, University of Maine, Orono, ME 04469, USA. kurt.rademaker@umit.maine.edu. 2Accelerator Mass Spectrometry Laboratory, Department of Physics and School of Anthropology, University of Arizona, Tucson, AZ 85721, USA. 3University of Pennsylvania Museum, 3260 South Street, Philadelphia, PA 19104, USA. 4Department of Anthropology and Archaeology, Earth Sciences Building, Room 806, 844 Campus Place Northwest, Calgary, British Columbia, Canada. 5Institute for Archaeological Sciences, University of Tübingen, Rümelinstrasse 23, 72070 Tübingen, Germany. Senckenberg Centre for Human Evolution and Paleoenvironment, University of Tübingen, Rümelinstrasse 23, 72070 Tübingen, Germany. 6Climate Change Institute, Bryand Global Sciences Center, University of Maine, Orono, ME 04469, USA. 7Department of Anthropology, 354 Mansfield Road, University of Connecticut, Storrs, CT 06269-1176, USA. 8Department of Anthropology, University of Illinois at Chicago, Behavioral Sciences Building, 1007 West Harrison Street, Chicago, IL 60607-7139, USA. 9Arequipa, Peru. 10Department of Anthropology, South Stevens Hall, University of Maine, Orono, ME 04469-5773, USA. Climate Change Institute, Bryand Global Sciences Center, University of Maine, Orono, ME 04469, USA. Abstract Study of human adaptation to extreme environments is important for understanding our cultural and genetic capacity for survival. The Pucuncho Basin in the southern Peruvian Andes contains the highest-altitude Pleistocene archaeological sites yet identified in the world, about 900 meters above confidently dated contemporary sites. The Pucuncho workshop site [4355 meters above sea level (masl)] includes two fishtail projectile points, which date to about 12.8 to 11.5 thousand years ago (ka). Cuncaicha rock shelter (4480 masl) has a robust, well-preserved, and well-dated occupation sequence spanning the past 12.4 thousand years (ky), with 21 dates older than 11.5 ka. Our results demonstrate that despite cold temperatures and low-oxygen conditions, hunter-gatherers colonized extreme high-altitude Andean environments in the Terminal Pleistocene, within about 2 ky of the initial entry of humans to South America. Copyright © 2014, American Association for the Advancement of Science.
	PMID: 25342802 [PubMed - indexed for MEDLINE]
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3.	Science. 2014 Oct 24;346(6208):433. doi: 10.1126/science.346.6208.433-a. Ebola: mobility data. Halloran ME1, Vespignani A2, Bharti N3, Feldstein LR4, Alexander KA5, Ferrari M3, Shaman J6, Drake JM7, Porco T8, Eisenberg JN9, Del Valle SY10, Lofgren E11, Scarpino SV12, Eisenberg MC9, Gao D8, Hyman JM13, Eubank S14, Longini IM Jr15. Author information: 1Fred Hutchinson Cancer Research Center, University of Washington, Seattle, WA 98109, USA. Department of Biostatistics, University of Washington, Seattle, WA 98195, USA. betz@u.washington.edu. 2Department of Physics, Northeastern University, Boston, MA 02115, USA. 3Department of Biology, Pennsylvania State University, University Park, PA 16802, USA. 4Fred Hutchinson Cancer Research Center, University of Washington, Seattle, WA 98109, USA. Department of Epidemiology, University of Washington, Seattle, WA 98195, USA. 5Department of Fish and Wildlife Conservation, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061, USA. 6Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University, New York, NY 10032, USA. 7Odum School of Ecology, University of Georgia, Athens, GA 30602, USA. 8Francis I. Proctor Foundation, University of California, San Francisco, CA 94143, USA. 9Department of Epidemiology, University of Michigan, Ann Arbor, MI 48109, USA. 10Los Alamos National Laboratory, Los Alamos, NM 87545, USA. 11Virginia Bioinformatics Institute, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061, USA. 12Santa Fe Institute, Santa Fe, NM 87501, USA. 13Department of Mathematics, Tulane University, New Orleans, LA 70118, USA. 14Virginia Bioinformatics Institute, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061, USA. Department of Population Health Sciences, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061, USA. 15Department of Biostatistics, University of Florida, Gainesville, FL 32611, USA.
	PMID: 25342792 [PubMed - indexed for MEDLINE]
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Sent on Tuesday, 2014 November 11
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.	BMC Genomics. 2013 Sep 20;14:632. doi: 10.1186/1471-2164-14-632. An expression atlas of human primary cells: inference of gene function from coexpression networks. Mabbott NA1, Baillie JK, Brown H, Freeman TC, Hume DA. Author information: 1The Roslin Institute and Royal (Dick) School of Veterinary Studies, The University of Edinburgh, Easter Bush, Midlothian, Edinburgh EH25 9RG, UK. neil.mabbott@roslin.ed.ac.uk. Abstract BACKGROUND: The specialisation of mammalian cells in time and space requires genes associated with specific pathways and functions to be co-ordinately expressed. Here we have combined a large number of publically available microarray datasets derived from human primary cells and analysed large correlation graphs of these data. RESULTS: Using the network analysis tool BioLayout Express3D we identify robust co-associations of genes expressed in a wide variety of cell lineages. We discuss the biological significance of a number of these associations, in particular the coexpression of key transcription factors with the genes that they are likely to control. CONCLUSIONS: We consider the regulation of genes in human primary cells and specifically in the human mononuclear phagocyte system. Of particular note is the fact that these data do not support the identity of putative markers of antigen-presenting dendritic cells, nor classification of M1 and M2 activation states, a current subject of debate within immunological field. We have provided this data resource on the BioGPS web site (http://biogps.org/dataset/2429/primary-cell-atlas/) and on macrophages.com (http://www.macrophages.com/hu-cell-atlas). PMCID: PMC3849585 Free PMC Article
	PMID: 24053356 [PubMed - indexed for MEDLINE]

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Sent on Saturday, 2014 November 08
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. 2014 Sep 25;513(7519):501-6. doi: 10.1038/nature13704. Epub 2014 Sep 14. Asian monsoons in a late Eocene greenhouse world. Licht A1, van Cappelle M2, Abels HA3, Ladant JB4, Trabucho-Alexandre J5, France-Lanord C6, Donnadieu Y4, Vandenberghe J7, Rigaudier T6, Lécuyer C 8, Terry D Jr9, Adriaens R10, Boura A11, Guo Z12, Soe AN13, Quade J14, Dupont-Nivet G15, Jaeger JJ16. Author information: 11] Institut de Paléoprimatologie, Paléontologie Humaine: Evolution et Paléoenvironnements, UMR CNRS 7262, Université de Poitiers, 86000 Poitiers, France [2] Centre de Recherches Pétrographiques et Géochimiques, UMR CNRS 7358, Université de Lorraine 54501 Vandoeuvre les Nancy, France [3] Department of Geosciences, University of Arizona, Tucson, Arizona 85721, USA. 21] Department of Earth Sciences, Universiteit Utrecht, 3584CD, Utrecht, The Netherlands [2] Department of Earth Science and Engineering, Imperial College London, London SW7 2AZ, UK. 31] Department of Earth Sciences, Universiteit Utrecht, 3584CD, Utrecht, The Netherlands [2] Department of Earth and Environmental Sciences, Katholieke Universiteit Leuven, 3001 Leuven, Belgium. 4Laboratoire des Sciences du Climat et de l'Environnement, UMR CNRS 8212, 91198 Gif-sur-Yvette, France. 5Department of Earth Sciences, Durham University, Durham DH1 3LE, UK. 6Centre de Recherches Pétrographiques et Géochimiques, UMR CNRS 7358, Université de Lorraine 54501 Vandoeuvre les Nancy, France. 7Department of Earth Sciences, Vrije Universiteit, 1081HV Amsterdam, The Netherlands. 8Laboratoire de Géologie de Lyon, Terre, Planètes, Environnement, UMR CNRS 5276, Université de Lyon, Institut Universitaire de France, 69622 Lyon, France. 9Department of Earth and Environmental Science, Temple University, Philadelphia, Pennsylvania 19122, USA. 10Department of Earth and Environmental Sciences, Katholieke Universiteit Leuven, 3001 Leuven, Belgium. 11Centre de Recherche sur la Paléodiversité et les Paléoenvironnements - UPMC, MNHN, CNRS, 75005 Paris, France. 12Key Laboratory of Orogenic Belts and Crustal Evolution, Peking University, 100871 Beijing, China. 13Department of Geology, Defence Services Academy, Pyin Oo Lwin, Myanmar. 14Department of Geosciences, University of Arizona, Tucson, Arizona 85721, USA. 151] Department of Earth Sciences, Universiteit Utrecht, 3584CD, Utrecht, The Netherlands [2] Key Laboratory of Orogenic Belts and Crustal Evolution, Peking University, 100871 Beijing, China [3] Géosciences Rennes, UMR CNRS 6118, Université de Rennes, 35042 Rennes Cedex, France [4] Universität Potsdam, Institute of Earth and Environmental Science, 14476 Potsdam, Germany. 16Institut de Paléoprimatologie, Paléontologie Humaine: Evolution et Paléoenvironnements, UMR CNRS 7262, Université de Poitiers, 86000 Poitiers, France. Abstract The strong present-day Asian monsoons are thought to have originated between 25 and 22 million years (Myr) ago, driven by Tibetan-Himalayan uplift. However, the existence of older Asian monsoons and their response to enhanced greenhouse conditions such as those in the Eocene period (55-34 Myr ago) are unknown because of the paucity of well-dated records. Here we show late Eocene climate records revealing marked monsoon-like patterns in rainfall and wind south and north of the Tibetan-Himalayan orogen. This is indicated by low oxygen isotope values with strong seasonality in gastropod shells and mammal teeth from Myanmar, and by aeolian dust deposition in northwest China. Our climate simulations support modern-like Eocene monsoonal rainfall and show that a reinforced hydrological cycle responding to enhanced greenhouse conditions counterbalanced the negative effect of lower Tibetan relief on precipitation. These strong monsoons later weakened with the global shift to icehouse conditions 34 Myr ago.
	PMID: 25219854 [PubMed - indexed for MEDLINE]
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2.	Nature. 2014 Sep 25;513(7519):559-63. doi: 10.1038/nature13490. Epub 2014 Jul 13. Functional polarization of tumour-associated macrophages by tumour-derived lactic acid. Colegio OR1, Chu NQ2, Szabo AL2, Chu T2, Rhebergen AM2, Jairam V2, Cyrus N2, Brokowski CE2, Eisenbarth SC3, Phillips GM4, Cline GW5, Phillips AJ4, Medzhitov R6. Author information: 11] Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06519-1612, USA [2] Department of Dermatology, Yale University School of Medicine, New Haven, Connecticut 06520-8059, USA [3] Yale-New Haven Transplantation Center, Yale University School of Medicine, New Haven, Connecticut 06519-1369, USA [4] Yale Cancer Center, Yale University School of Medicine, New Haven, Connecticut 06520-8028, USA. 2Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06519-1612, USA. 31] Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06519-1612, USA [2] Department of Laboratory Medicine, Yale University School of Medicine, New Haven, Connecticut 06520-8035, USA. 4Department of Chemistry, Yale University School of Medicine, New Haven, Connecticut 06520-8107, USA. 5Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06520-8020, USA. 61] Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06519-1612, USA [2] Yale Cancer Center, Yale University School of Medicine, New Haven, Connecticut 06520-8028, USA [3] Howard Hughes Medical Institute, Chevy Chase, Maryland 20815-6789, USA. Comment in Tumor cells hijack macrophages via lactic acid. [Immunol Cell Biol. 2014] Tumor cells hijack macrophages via lactic acid.Bronte V. Immunol Cell Biol. 2014 Sep; 92(8):647-9. Epub 2014 Aug 5. Abstract Macrophages have an important role in the maintenance of tissue homeostasis. To perform this function, macrophages must have the capacity to monitor the functional states of their 'client cells': namely, the parenchymal cells in the various tissues in which macrophages reside. Tumours exhibit many features of abnormally developed organs, including tissue architecture and cellular composition. Similarly to macrophages in normal tissues and organs, macrophages in tumours (tumour-associated macrophages) perform some key homeostatic functions that allow tumour maintenance and growth. However, the signals involved in communication between tumours and macrophages are poorly defined. Here we show that lactic acid produced by tumour cells, as a by-product of aerobic or anaerobic glycolysis, has a critical function in signalling, through inducing the expression of vascular endothelial growth factor and the M2-like polarization of tumour-associated macrophages. Furthermore, we demonstrate that this effect of lactic acid is mediated by hypoxia-inducible factor 1α (HIF1α). Finally, we show that the lactate-induced expression of arginase 1 by macrophages has an important role in tumour growth. Collectively, these findings identify a mechanism of communication between macrophages and their client cells, including tumour cells. This communication most probably evolved to promote homeostasis in normal tissues but can also be engaged in tumours to promote their growth.
	PMID: 25043024 [PubMed - indexed for MEDLINE]
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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 Oct 17;346(6207):296-8. doi: 10.1126/science.1256396. Epub 2014 Oct 16. Science and Regulation. Changes on the horizon for consumer genomics in the EU. Kalokairinou L1, Howard HC2, Borry P3. Author information: 1Department of Public Health and Primary Care, University of Leuven, B-3000 Leuven, Belgium. 2Center for Research Ethics and Bioethics, Uppsala University, SE-751 22 Uppsala, Sweden. 3Department of Public Health and Primary Care, University of Leuven, B-3000 Leuven, Belgium. pascal.borry@med.kuleuven.be.
	PMID: 25324369 [PubMed - indexed for MEDLINE]
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2.	Nat Med. 2014 Sep;20(9):1062-8. doi: 10.1038/nm.3623. Epub 2014 Aug 17. In vivo proteomic imaging analysis of caveolae reveals pumping system to penetrate solid tumors. Oh P1, Testa JE1, Borgstrom P2, Witkiewicz H1, Li Y1, Schnitzer JE1. Author information: 11] Proteogenomics Research Institute for Systems Medicine, San Diego, California, USA. [2] Sidney Kimmel Cancer Center, San Diego, California, USA. 21] Sidney Kimmel Cancer Center, San Diego, California, USA. [2]. Abstract Technologies are needed to map and image biological barriers in vivo that limit solid tumor delivery and, ultimately, the effectiveness of imaging and therapeutic agents. Here we integrate proteomic and imaging analyses of caveolae at the blood-tumor interface to discover an active transendothelial portal to infiltrate tumors. A post-translationally modified form of annexin A1 (AnnA1) is selectively concentrated in human and rodent tumor caveolae. To follow trafficking, we generated a specific AnnA1 antibody that targets caveolae in the tumor endothelium. Intravital microscopy of caveolae-immunotargeted fluorophores even at low intravenous doses showed rapid and robust pumping across the endothelium to enter mammary, prostate and lung tumors. Within 1 h, the fluorescence signal concentrated throughout tumors to exceed the peak levels in blood. This transvascular pumping required the expression of caveolin 1 and annexin A1. Tumor uptake with other antibodies were >100-fold less. This proteomic imaging strategy reveals a unique target, antibody and caveolae pumping system for solid tumor penetration.
	PMID: 25129480 [PubMed - indexed for MEDLINE]
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3.	Nature. 2014 Oct 9;514(7521):187-92. doi: 10.1038/nature13683. Epub 2014 Aug 6. Inflammatory caspases are innate immune receptors for intracellular LPS. Shi J1, Zhao Y2, Wang Y3, Gao W3, Ding J4, Li P3, Hu L3, Shao F5. Author information: 11] Peking University-Tsinghua University-National Institute of Biological Sciences Joint Graduate Program, National Institute of Biological Sciences, Beijing 102206, China [2] National Institute of Biological Sciences, Beijing 102206, China [3]. 21] National Institute of Biological Sciences, Beijing 102206, China [2]. 3National Institute of Biological Sciences, Beijing 102206, China. 41] National Institute of Biological Sciences, Beijing 102206, China [2] National Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China. 51] Peking University-Tsinghua University-National Institute of Biological Sciences Joint Graduate Program, National Institute of Biological Sciences, Beijing 102206, China [2] National Institute of Biological Sciences, Beijing 102206, China [3] National Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China [4] National Institute of Biological Sciences, Beijing, Collaborative Innovation Center for Cancer Medicine, Beijing 102206, China. Comment in Host response: new LPS receptors discovered. [Nat Rev Microbiol. 2014] Host response: new LPS receptors discovered.Nunes-Alves C. Nat Rev Microbiol. 2014 Oct; 12(10):658. Epub 2014 Aug 19. Abstract The murine caspase-11 non-canonical inflammasome responds to various bacterial infections. Caspase-11 activation-induced pyroptosis, in response to cytoplasmic lipopolysaccharide (LPS), is critical for endotoxic shock in mice. The mechanism underlying cytosolic LPS sensing and the responsible pattern recognition receptor are unknown. Here we show that human monocytes, epithelial cells and keratinocytes undergo necrosis upon cytoplasmic delivery of LPS. LPS-induced cytotoxicity was mediated by human caspase-4 that could functionally complement murine caspase-11. Human caspase-4 and the mouse homologue caspase-11 (hereafter referred to as caspase-4/11) and also human caspase-5, directly bound to LPS and lipid A with high specificity and affinity. LPS associated with endogenous caspase-11 in pyroptotic cells. Insect-cell purified caspase-4/11 underwent oligomerization upon LPS binding, resulting in activation of the caspases. Underacylated lipid IVa and lipopolysaccharide from Rhodobacter sphaeroides (LPS-RS) could bind to caspase-4/11 but failed to induce their oligomerization and activation. LPS binding was mediated by the CARD domain of the caspase. Binding-deficient CARD-domain point mutants did not respond to LPS with oligomerization or activation and failed to induce pyroptosis upon LPS electroporation or bacterial infections. The function of caspase-4/5/11 represents a new mode of pattern recognition in immunity and also an unprecedented means of caspase activation.
	PMID: 25119034 [PubMed - indexed for MEDLINE]
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