What's new for 'JKB_daily1' in PubMed

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

Sent on Wednesday, 2014 June 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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PubMed Results

Items 1 - 7 of 7

1.	N Engl J Med. 2014 Jun 12;370(24):2342-5. doi: 10.1056/NEJMcibr1403629. Translating the genomic revolution - targeted genome editing in primates. Cathomen T, Ehl S.
	PMID: 24918378 [PubMed - indexed for MEDLINE]
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2.	Nature. 2014 May 8;509(7499):162-3. doi: 10.1038/509162a. Q&A: Canopy composer. Jones D, Hoffman J.
	PMID: 24805330 [PubMed - indexed for MEDLINE]
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3.	Nature. 2014 May 8;509(7499):148-9. doi: 10.1038/509148a. Imaging: Cancer caught in the act. Lok C. Author information: Nature in Cambridge, Massachusetts.
	PMID: 24805326 [PubMed - indexed for MEDLINE]
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4.	Nature. 2014 May 8;509(7499):171-2. doi: 10.1038/nature13332. Epub 2014 Apr 30. Biodiversity: Supply and demand. Mooers AO. Author information: Biology Department and the Human Evolutionary Studies Program, Simon Fraser University, Burnaby, British Columbia V5A1S6, Canada. Comment on Niche filling slows the diversification of Himalayan songbirds. [Nature. 2014] Niche filling slows the diversification of Himalayan songbirds.Price TD, Hooper DM, Buchanan CD, Johansson US, Tietze DT, Alström P, Olsson U, Ghosh-Harihar M, Ishtiaq F, Gupta SK, et al. Nature. 2014 May 8; 509(7499):222-5. Epub 2014 Apr 30.
	PMID: 24776802 [PubMed - indexed for MEDLINE]
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5.	Nature. 2014 May 8;509(7499):222-5. doi: 10.1038/nature13272. Epub 2014 Apr 30. Niche filling slows the diversification of Himalayan songbirds. Price TD1, Hooper DM1, Buchanan CD1, Johansson US2, Tietze DT3, Alström P4, Olsson U5, Ghosh-Harihar M6, Ishtiaq F6, Gupta SK6, Martens J7, Harr B8, Singh P6, Mohan D6. Author information: 1Department of Ecology and Evolution, University of Chicago, Chicago, Illinois 60637, USA. 21] Department of Ecology and Evolution, University of Chicago, Chicago, Illinois 60637, USA [2] Department of Zoology, Swedish Museum of Natural History, 10405 Stockholm, Sweden. 31] Department of Ecology and Evolution, University of Chicago, Chicago, Illinois 60637, USA [2] Institute of Pharmacy and Molecular Biotechnology, University of Heidelberg, Im Neuenheimer Feld 364, 69120 Heidelberg, Germany. 41] Key Laboratory of Zoological Systematics and Evolution, Institute of Zoology, Chinese Academy of Sciences, 1 Beichen West Road, Chaoyang District, Beijing 100101, China [2] Swedish Species Information Centre, Swedish University of Agricultural Sciences, Box 7007, 75007 Uppsala, Sweden. 5Systematics and Biodiversity, Department of Biology and Environmental Sciences, University of Gothenburg, 40530 Gothenburg, Sweden. 6Wildlife Institute of India, PO Box 18, Chandrabani, Dehradun 248001, India. 7Institute of Zoology, Johannes Gutenberg University, Mainz 55099, Germany. 8Max Planck Institute for Evolutionary Biology, August Thienemannstrasse 2, 24306 Plön, Germany. Comment in Biodiversity: Supply and demand. [Nature. 2014] Biodiversity: Supply and demand.Mooers AO. Nature. 2014 May 8; 509(7499):171-2. Epub 2014 Apr 30. Abstract Speciation generally involves a three-step process--range expansion, range fragmentation and the development of reproductive isolation between spatially separated populations. Speciation relies on cycling through these three steps and each may limit the rate at which new species form. We estimate phylogenetic relationships among all Himalayan songbirds to ask whether the development of reproductive isolation and ecological competition, both factors that limit range expansions, set an ultimate limit on speciation. Based on a phylogeny for all 358 species distributed along the eastern elevational gradient, here we show that body size and shape differences evolved early in the radiation, with the elevational band occupied by a species evolving later. These results are consistent with competition for niche space limiting species accumulation. Even the elevation dimension seems to be approaching ecological saturation, because the closest relatives both inside the assemblage and elsewhere in the Himalayas are on average separated by more than five million years, which is longer than it generally takes for reproductive isolation to be completed; also, elevational distributions are well explained by resource availability, notably the abundance of arthropods, and not by differences in diversification rates in different elevational zones. Our results imply that speciation rate is ultimately set by niche filling (that is, ecological competition for resources), rather than by the rate of acquisition of reproductive isolation.
	PMID: 24776798 [PubMed - indexed for MEDLINE]
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6.	Nature. 2014 May 8;509(7499):230-4. doi: 10.1038/nature13168. Epub 2014 Apr 13. Listeria monocytogenes exploits efferocytosis to promote cell-to-cell spread. Czuczman MA1, Fattouh R2, van Rijn JM3, Canadien V2, Osborne S2, Muise AM4, Kuchroo VK5, Higgins DE6, Brumell JH7. Author information: 11] Cell Biology Program, Hospital for Sick Children, Toronto, Ontario M5G0A4, Canada [2] Department of Molecular Genetics, University of Toronto, Toronto, Ontario M5S1A8, Canada. 2Cell Biology Program, Hospital for Sick Children, Toronto, Ontario M5G0A4, Canada. 3Department of Cell Biology and Institute of Biomembranes, University Medical Center Utrecht, 3584 CX Utrecht, the Netherlands. 41] Cell Biology Program, Hospital for Sick Children, Toronto, Ontario M5G0A4, Canada [2] Division of Gastroenterology, Hepatology, and Nutrition, Department of Paediatrics, Hospital for Sick Children, Toronto, Ontario M5G1X8, Canada [3] Institute of Medical Science, University of Toronto, Toronto, Ontario M5S1A8, Canada [4] Sickkids IBD Centre, Hospital for Sick Children, Toronto, Ontario M5G1X8, Canada. 5Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. 6Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts 02115, USA. 71] Cell Biology Program, Hospital for Sick Children, Toronto, Ontario M5G0A4, Canada [2] Department of Molecular Genetics, University of Toronto, Toronto, Ontario M5S1A8, Canada [3] Institute of Medical Science, University of Toronto, Toronto, Ontario M5S1A8, Canada [4] Sickkids IBD Centre, Hospital for Sick Children, Toronto, Ontario M5G1X8, Canada. Comment in Bacterial pathogenesis: Pirate bacteria hijack efferocytosis. [Nat Rev Microbiol. 2014] Bacterial pathogenesis: Pirate bacteria hijack efferocytosis.Kåhrström CT. Nat Rev Microbiol. 2014 Jun; 12(6):396-7. Epub 2014 Apr 28. Abstract Efferocytosis, the process by which dying or dead cells are removed by phagocytosis, has an important role in development, tissue homeostasis and innate immunity. Efferocytosis is mediated, in part, by receptors that bind to exofacial phosphatidylserine (PS) on cells or cellular debris after loss of plasma membrane asymmetry. Here we show that a bacterial pathogen, Listeria monocytogenes, can exploit efferocytosis to promote cell-to-cell spread during infection. These bacteria can escape the phagosome in host cells by using the pore-forming toxin listeriolysin O (LLO) and two phospholipase C enzymes. Expression of the cell surface protein ActA allows L. monocytogenes to activate host actin regulatory factors and undergo actin-based motility in the cytosol, eventually leading to formation of actin-rich protrusions at the cell surface. Here we show that protrusion formation is associated with plasma membrane damage due to LLO's pore-forming activity. LLO also promotes the release of bacteria-containing protrusions from the host cell, generating membrane-derived vesicles with exofacial PS. The PS-binding receptor TIM-4 (encoded by the Timd4 gene) contributes to efficient cell-to-cell spread by L. monocytogenes in macrophages in vitro and growth of these bacteria is impaired in Timd4(-/-) mice. Thus, L. monocytogenes promotes its dissemination in a host by exploiting efferocytosis. Our results indicate that PS-targeted therapeutics may be useful in the fight against infections by L. monocytogenes and other bacteria that use similar strategies of cell-to-cell spread during infection.
	PMID: 24739967 [PubMed - indexed for MEDLINE]
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7.	Nature. 2014 May 8;509(7499):235-9. doi: 10.1038/nature13152. Epub 2014 Apr 13. NRROS negatively regulates reactive oxygen species during host defence and autoimmunity. Noubade R1, Wong K2, Ota N2, Rutz S2, Eidenschenk C2, Valdez PA1, Ding J2, Peng I2, Sebrell A3, Caplazi P4, DeVoss J2, Soriano RH5, Sai T3, Lu R2, Modrusan Z5, Hackney J6, Ouyang W2. Author information: 11] Department of Immunology, Genentech Inc., 1 DNA Way, South San Francisco, California 94080, USA [2] Flexus Biosciences, 75 Shoreway Road, Suite D, San Carlos, California 94070, USA (R.N.); American Society for Biochemistry and Molecular Biology, 11200 Rockville Pike, Suite 302, Rockville, Maryland 20852, USA (P.A.V.). 2Department of Immunology, Genentech Inc., 1 DNA Way, South San Francisco, California 94080, USA. 3Department of Antibody Engineering, Genentech Inc., 1 DNA Way, South San Francisco, California 94080, USA. 4Department of Pathology, Genentech Inc., 1 DNA Way, South San Francisco, California 94080, USA. 5Department of Molecular Biology, Genentech Inc., 1 DNA Way, South San Francisco, California 94080, USA. 6Department of Bioinformatics, Genentech Inc., 1 DNA Way, South San Francisco, California 94080, USA. Abstract Reactive oxygen species (ROS) produced by phagocytes are essential for host defence against bacterial and fungal infections. Individuals with defective ROS production machinery develop chronic granulomatous disease. Conversely, excessive ROS can cause collateral tissue damage during inflammatory processes and therefore needs to be tightly regulated. Here we describe a protein, we termed negative regulator of ROS (NRROS), which limits ROS generation by phagocytes during inflammatory responses. NRROS expression in phagocytes can be repressed by inflammatory signals. NRROS-deficient phagocytes produce increased ROS upon inflammatory challenges, and mice lacking NRROS in their phagocytes show enhanced bactericidal activity against Escherichia coli and Listeria monocytogenes. Conversely, these mice develop severe experimental autoimmune encephalomyelitis owing to oxidative tissue damage in the central nervous system. Mechanistically, NRROS is localized to the endoplasmic reticulum, where it directly interacts with nascent NOX2 (also known as gp91(phox) and encoded by Cybb) monomer, one of the membrane-bound subunits of the NADPH oxidase complex, and facilitates the degradation of NOX2 through the endoplasmic-reticulum-associated degradation pathway. Thus, NRROS provides a hitherto undefined mechanism for regulating ROS production--one that enables phagocytes to produce higher amounts of ROS, if required to control invading pathogens, while minimizing unwanted collateral tissue damage.
	PMID: 24739962 [PubMed - indexed for MEDLINE]
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What's new for 'JKB_daily1' in PubMed

This message contains My NCBI what's new results from the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).
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Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Tuesday, 2014 June 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 - 5 of 5

1.	Nat Med. 2014 May;20(5):469-70. doi: 10.1038/nm.3558. Neonates, antibiotics and the microbiome. Thanabalasuriar A, Kubes P. Author information: Calvin, Phoebe & Joan Snyder Institute for Chronic Diseases and the Department of Physiology and Pharmacology, University of Calgary, Calgary, Alberta, Canada. Comment on The microbiota regulates neutrophil homeostasis and host resistance to Escherichia coli K1 sepsis in neonatal mice. [Nat Med. 2014] The microbiota regulates neutrophil homeostasis and host resistance to Escherichia coli K1 sepsis in neonatal mice.Deshmukh HS, Liu Y, Menkiti OR, Mei J, Dai N, O'Leary CE, Oliver PM, Kolls JK, Weiser JN, Worthen GS. Nat Med. 2014 May; 20(5):524-30. Epub 2014 Apr 20.
	PMID: 24804751 [PubMed - indexed for MEDLINE]
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2.	Science. 2014 May 2;344(6183):510-3. doi: 10.1126/science.1252076. Genomic signatures of specialized metabolism in plants. Chae L1, Kim T, Nilo-Poyanco R, Rhee SY. Author information: 1Department of Plant Biology, Carnegie Institution for Science, Stanford, CA 94305, USA. Abstract All plants synthesize basic metabolites needed for survival (primary metabolism), but different taxa produce distinct metabolites that are specialized for specific environmental interactions (specialized metabolism). Because evolutionary pressures on primary and specialized metabolism differ, we investigated differences in the emergence and maintenance of these processes across 16 species encompassing major plant lineages from algae to angiosperms. We found that, relative to their primary metabolic counterparts, genes coding for specialized metabolic functions have proliferated to a much greater degree and by different mechanisms and display lineage-specific patterns of physical clustering within the genome and coexpression. These properties illustrate the differential evolution of specialized metabolism in plants, and collectively they provide unique signatures for the potential discovery of novel specialized metabolic processes.
	PMID: 24786077 [PubMed - indexed for MEDLINE]
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3.	Nat Med. 2014 May;20(5):484-92. doi: 10.1038/nm.3527. Epub 2014 Apr 20. Pten deletion in RIP-Cre neurons protects against type 2 diabetes by activating the anti-inflammatory reflex. Wang L1, Opland D2, Tsai S3, Luk CT4, Schroer SA3, Allison MB2, Elia AJ5, Furlonger C6, Suzuki A7, Paige CJ8, Mak TW9, Winer DA10, Myers MG Jr2, Woo M11. Author information: 11] Toronto General Research Institute, University Health Network, Toronto, Ontario, Canada. [2] Department of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada. [3] Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada. 2Department of Molecular and Integrative Physiology, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA. 3Toronto General Research Institute, University Health Network, Toronto, Ontario, Canada. 41] Toronto General Research Institute, University Health Network, Toronto, Ontario, Canada. [2] Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada. [3] Institute of Medical Science, University of Toronto, Toronto, Ontario, Canada. 51] The Campbell Family Institute for Breast Cancer Research, Toronto, Ontario, Canada. [2] Ontario Cancer Institute, Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario, Canada. 6Ontario Cancer Institute, Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario, Canada. 7Division of Cancer Genetics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan. 81] Department of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada. [2] Ontario Cancer Institute, Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario, Canada. [3] Department of Immunology, University of Toronto, Toronto, Ontario, Canada. 91] Department of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada. [2] The Campbell Family Institute for Breast Cancer Research, Toronto, Ontario, Canada. [3] Ontario Cancer Institute, Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario, Canada. [4] Department of Immunology, University of Toronto, Toronto, Ontario, Canada. 101] Toronto General Research Institute, University Health Network, Toronto, Ontario, Canada. [2] Department of Immunology, University of Toronto, Toronto, Ontario, Canada. [3] Department of Pathology, University Health Network, University of Toronto, Toronto, Ontario, Canada. [4] Division of Endocrinology and Metabolism, Department of Medicine, University Health Network, University of Toronto, Toronto, Ontario, Canada. 111] Toronto General Research Institute, University Health Network, Toronto, Ontario, Canada. [2] Department of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada. [3] Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada. [4] Institute of Medical Science, University of Toronto, Toronto, Ontario, Canada. [5] Division of Endocrinology and Metabolism, Department of Medicine, University Health Network, University of Toronto, Toronto, Ontario, Canada. Comment in A new role for the brain in metabolic control. [Nat Med. 2014] A new role for the brain in metabolic control.Carvalheira JB, Odegaard JI, Chawla A. Nat Med. 2014 May; 20(5):472-3. Abstract Inflammation has a critical role in the development of insulin resistance. Recent evidence points to a contribution by the central nervous system in the modulation of peripheral inflammation through the anti-inflammatory reflex. However, the importance of this phenomenon remains elusive in type 2 diabetes pathogenesis. Here we show that rat insulin-2 promoter (Rip)-mediated deletion of Pten, a gene encoding a negative regulator of PI3K signaling, led to activation of the cholinergic anti-inflammatory pathway that is mediated by M2 activated macrophages in peripheral tissues. As such, Rip-cre(+) Pten(flox/flox) mice showed lower systemic inflammation and greater insulin sensitivity under basal conditions compared to littermate controls, which were abolished when the mice were treated with an acetylcholine receptor antagonist or when macrophages were depleted. After feeding with a high-fat diet, the Pten-deleted mice remained markedly insulin sensitive, which correlated with massive subcutaneous fat expansion. They also exhibited more adipogenesis with M2 macrophage infiltration, both of which were abolished after disruption of the anti-inflammatory efferent pathway by left vagotomy. In summary, we show that Pten expression in Rip(+) neurons has a critical role in diabetes pathogenesis through mediating the anti-inflammatory reflex.
	PMID: 24747746 [PubMed - indexed for MEDLINE]
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4.	Nat Med. 2014 May;20(5):524-30. doi: 10.1038/nm.3542. Epub 2014 Apr 20. The microbiota regulates neutrophil homeostasis and host resistance to Escherichia coli K1 sepsis in neonatal mice. Deshmukh HS1, Liu Y2, Menkiti OR1, Mei J2, Dai N2, O'Leary CE3, Oliver PM3, Kolls JK4, Weiser JN5, Worthen GS1. Author information: 11] Division of Neonatology, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA. [2] Department of Pediatrics, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA. 2Division of Neonatology, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA. 3Department of Pathology and Laboratory Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA. 4Department of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA. 51] Department of Pediatrics, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA. [2] Department of Microbiology, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA. Comment in Neonates, antibiotics and the microbiome. [Nat Med. 2014] Neonates, antibiotics and the microbiome.Thanabalasuriar A, Kubes P. Nat Med. 2014 May; 20(5):469-70. Abstract Neonatal colonization by microbes, which begins immediately after birth, is influenced by gestational age and the mother's microbiota and is modified by exposure to antibiotics. In neonates, prolonged duration of antibiotic therapy is associated with increased risk of late-onset sepsis (LOS), a disorder controlled by neutrophils. A role for the microbiota in regulating neutrophil development and susceptibility to sepsis in the neonate remains unclear. We exposed pregnant mouse dams to antibiotics in drinking water to limit transfer of maternal microbes to the neonates. Antibiotic exposure of dams decreased the total number and composition of microbes in the intestine of the neonates. This was associated with decreased numbers of circulating and bone marrow neutrophils and granulocyte/macrophage-restricted progenitor cells in the bone marrow of antibiotic-treated and germ-free neonates. Antibiotic exposure of dams reduced the number of interleukin-17 (IL-17)-producing cells in the intestine and production of granulocyte colony-stimulating factor (G-CSF). Granulocytopenia was associated with impaired host defense and increased susceptibility to Escherichia coli K1 and Klebsiella pneumoniae sepsis in antibiotic-treated neonates, which could be partially reversed by administration of G-CSF. Transfer of a normal microbiota into antibiotic-treated neonates induced IL-17 production by group 3 innate lymphoid cells (ILCs) in the intestine, increasing plasma G-CSF levels and neutrophil numbers in a Toll-like receptor 4 (TLR4)- and myeloid differentiation factor 88 (MyD88)-dependent manner and restored IL-17-dependent resistance to sepsis. Specific depletion of ILCs prevented IL-17- and G-CSF-dependent granulocytosis and resistance to sepsis. These data support a role for the intestinal microbiota in regulation of granulocytosis, neutrophil homeostasis and host resistance to sepsis in neonates. PMCID: PMC4016187 [Available on 2014/11/1]
	PMID: 24747744 [PubMed - indexed for MEDLINE]
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5.	Nat Med. 2014 May;20(5):518-23. doi: 10.1038/nm.3516. Epub 2014 Apr 13. Immunosuppression in acutely decompensated cirrhosis is mediated by prostaglandin E2. O'Brien AJ1, Fullerton JN1, Massey KA2, Auld G1, Sewell G3, James S1, Newson J1, Karra E1, Winstanley A4, Alazawi W5, Garcia-Martinez R6, Cordoba J7, Nicolaou A2, Gilroy DW1. Author information: 1Centre for Clinical Pharmacology and Therapeutics, Division of Medicine, University College London, London, UK. 2Manchester Pharmacy School, Faculty of Medical and Human Sciences, University of Manchester, Manchester, UK. 3Division of Medicine, University College London, London, UK. 4Department of Histopathology, University College London Hospitals, London, UK. 5Liver Unit, Centre for Digestive Diseases, Blizard Institute of Cell and Molecular Science, Queen Mary University of London, London, UK. 6Hospital Clínic de Barcelona, Servicio de Hepatología, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. 7Centro de Investigacion Biomédica en Red de Enfermedades Hepaticas y Digestivas, Instituto de Salud Carlos III, Madrid, Spain. Comment in Tying up PGE2 with albumin to relieve immunosuppression in cirrhosis. [Nat Med. 2014] Tying up PGE2 with albumin to relieve immunosuppression in cirrhosis.Arroyo V, Moreau R. Nat Med. 2014 May; 20(5):467-9. Abstract Liver disease is one of the leading causes of death worldwide. Patients with cirrhosis display an increased predisposition to and mortality from infection due to multimodal defects in the innate immune system; however, the causative mechanism has remained elusive. We present evidence that the cyclooxygenase (COX)-derived eicosanoid prostaglandin E2 (PGE2) drives cirrhosis-associated immunosuppression. We observed elevated circulating concentrations (more than seven times as high as in healthy volunteers) of PGE2 in patients with acute decompensation of cirrhosis. Plasma from these and patients with end-stage liver disease (ESLD) suppressed macrophage proinflammatory cytokine secretion and bacterial killing in vitro in a PGE2-dependent manner via the prostanoid type E receptor-2 (EP2), effects not seen with plasma from patients with stable cirrhosis (Child-Pugh score grade A). Albumin, which reduces PGE2 bioavailability, was decreased in the serum of patients with acute decompensation or ESLD (<30 mg/dl) and appears to have a role in modulating PGE2-mediated immune dysfunction. In vivo administration of human albumin solution to these patients significantly improved the plasma-induced impairment of macrophage proinflammatory cytokine production in vitro. Two mouse models of liver injury (bile duct ligation and carbon tetrachloride) also exhibited elevated PGE2, reduced circulating albumin concentrations and EP2-mediated immunosuppression. Treatment with COX inhibitors or albumin restored immune competence and survival following infection with group B Streptococcus. Taken together, human albumin solution infusions may be used to reduce circulating PGE2 levels, attenuating immune suppression and reducing the risk of infection in patients with acutely decompensated cirrhosis or ESLD.
	PMID: 24728410 [PubMed - indexed for MEDLINE]
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What's new for 'JKB_daily1' in PubMed

This message contains My NCBI what's new results from the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).
Do not reply directly to this message.

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

Sent on Tuesday, 2014 June 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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PubMed Results

Items 1 - 4 of 4

1.	Nature. 2014 May 1;509(7498):S14-5. doi: 10.1038/509S14a. Diagnostics: Detection drives defence. Kanthor R.
	PMID: 24784424 [PubMed - indexed for MEDLINE]
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2.	Nature. 2014 May 1;509(7498):105-9. doi: 10.1038/nature13148. Epub 2014 Mar 30. Quantitative proteomics identifies NCOA4 as the cargo receptor mediating ferritinophagy. Mancias JD1, Wang X2, Gygi SP3, Harper JW3, Kimmelman AC2. Author information: 11] Division of Genomic Stability and DNA Repair, Department of Radiation Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA [2] Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA [3] Harvard Radiation Oncology Program, Boston, Massachusetts 02115, USA [4] Department of Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA. 2Division of Genomic Stability and DNA Repair, Department of Radiation Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA. 3Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA. Abstract Autophagy, the process by which proteins and organelles are sequestered in double-membrane structures called autophagosomes and delivered to lysosomes for degradation, is critical in diseases such as cancer and neurodegeneration. Much of our understanding of this process has emerged from analysis of bulk cytoplasmic autophagy, but our understanding of how specific cargo, including organelles, proteins or intracellular pathogens, are targeted for selective autophagy is limited. Here we use quantitative proteomics to identify a cohort of novel and known autophagosome-enriched proteins in human cells, including cargo receptors. Like known cargo receptors, nuclear receptor coactivator 4 (NCOA4) was highly enriched in autophagosomes, and associated with ATG8 proteins that recruit cargo-receptor complexes into autophagosomes. Unbiased identification of NCOA4-associated proteins revealed ferritin heavy and light chains, components of an iron-filled cage structure that protects cells from reactive iron species but is degraded via autophagy to release iron through an unknown mechanism. We found that delivery of ferritin to lysosomes required NCOA4, and an inability of NCOA4-deficient cells to degrade ferritin led to decreased bioavailable intracellular iron. This work identifies NCOA4 as a selective cargo receptor for autophagic turnover of ferritin (ferritinophagy), which is critical for iron homeostasis, and provides a resource for further dissection of autophagosomal cargo-receptor connectivity.
	PMID: 24695223 [PubMed - indexed for MEDLINE]
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3.	Nat Genet. 2014 May;46(5):492-7. doi: 10.1038/ng.2939. Epub 2014 Mar 30. Low copy number of the salivary amylase gene predisposes to obesity. Falchi M1, El-Sayed Moustafa JS2, Takousis P3, Pesce F4, Bonnefond A5, Andersson-Assarsson JC6, Sudmant PH7, Dorajoo R8, Al-Shafai MN9, Bottolo L10, Ozdemir E3, So HC11, Davies RW12, Patrice A13, Dent R14, Mangino M15, Hysi PG15, Dechaume A16, Huyvaert M16, Skinner J17, Pigeyre M18, Caiazzo R18, Raverdy V13, Vaillant E16, Field S19, Balkau B20, Marre M21, Visvikis-Siest S22, Weill J23, Poulain-Godefroy O16, Jacobson P24, Sjostrom L24, Hammond CJ15, Deloukas P25, Sham PC11, McPherson R26, Lee J27, Tai ES28, Sladek R29, Carlsson LM24, Walley A30, Eichler EE31, Pattou F18, Spector TD32, Froguel P33. Author information: 11] Department of Genomics of Common Disease, Imperial College London, London, UK. [2] [3] [4]. 21] Department of Genomics of Common Disease, Imperial College London, London, UK. [2]. 3Department of Genomics of Common Disease, Imperial College London, London, UK. 41] Department of Genomics of Common Disease, Imperial College London, London, UK. [2] Renal, Dialysis and Transplant Unit, Department of Emergency and Organ Transplantation (D.E.T.O.), University of Bari "Aldo Moro", Bari, Italy. 51] CNRS UMR 8199, Lille Pasteur Institute, Lille, France. [2] Lille 2 University, Lille, France. [3] Qatar Biomedical Research Institute (QBRI), Qatar Foundation, Doha, Qatar. [4] European Genomic Institute for Diabetes (EGID), Lille, France. 61] Department of Genomics of Common Disease, Imperial College London, London, UK. [2] Department of Molecular and Clinical Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. [3] Center for Cardiovascular and Metabolic Research, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. 7Department of Genome Sciences, University of Washington, Seattle, Washington, USA. 81] Department of Genomics of Common Disease, Imperial College London, London, UK. [2] Genome Institute of Singapore, Agency for Science, Technology and Research, Singapore. 91] Department of Genomics of Common Disease, Imperial College London, London, UK. [2] Research Division, Qatar Foundation, Doha, Qatar. 10Department of Mathematics, Imperial College London, London, UK. 11Department of Psychiatry, University of Hong Kong, Hong Kong, China. 12Cardiovascular Research Methods Centre, University of Ottawa Heart Institute, Ottawa, Ontario, Canada. 131] European Genomic Institute for Diabetes (EGID), Lille, France. [2] INSERM UMR 859, Lille, France. [3] Centre Hospitalier Régional Universitaire (CHRU) Lille, Lille, France. 14Bariatric Program, Ottawa Hospital, Ottawa, Ontario, Canada. 15Department of Twin Research & Genetic Epidemiology, King's College London, St. Thomas' Hospital Campus, London, UK. 161] CNRS UMR 8199, Lille Pasteur Institute, Lille, France. [2] Lille 2 University, Lille, France. [3] European Genomic Institute for Diabetes (EGID), Lille, France. 17Norwich Medical School, University of East Anglia, Norwich, UK. 181] Lille 2 University, Lille, France. [2] European Genomic Institute for Diabetes (EGID), Lille, France. [3] INSERM UMR 859, Lille, France. [4] Centre Hospitalier Régional Universitaire (CHRU) Lille, Lille, France. 19Wellcome Trust Sanger Institute, Hinxton, UK. 201] Centre de Recherche en Epidémiologie et Santé des Populations, INSERM U1018, Epidemiology of Diabetes, Obesity and Chronic Kidney Disease over the Life Course, Villejuif, France. [2] Université Paris-Sud 11, UMRS 1018, Villejuif, France. 211] Department of Endocrinology, Diabetology and Nutrition, Bichat-Claude Bernard University Hospital, Assistance Publique-Hôpitaux de Paris (AP-HP), Paris, France. [2] INSERM U695, Paris 7 University, Paris, France. 22INSERM UMR 1122 Interactions Géne-Environnement en Physiopathologie Cardio-Vasculaire, Université de Lorraine, Nancy, France. 23Paediatric Endocrine Unit, Lille Teaching Hospital, Lille, France. 241] Department of Molecular and Clinical Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. [2] Center for Cardiovascular and Metabolic Research, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. 251] Wellcome Trust Sanger Institute, Hinxton, UK. [2] William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK. [3] Princess Al-Jawhara Al-Brahim Centre of Excellence in Research of Hereditary Disorders (PACER-HD), King Abdulaziz University, Jeddah, Saudi Arabia. 261] Atherogenomics Laboratory, University of Ottawa Heart Institute, Ottawa, Ontario, Canada. [2] Division of Cardiology, University of Ottawa Heart Institute, Ottawa, Ontario, Canada. 27Saw Swee Hock School of Public Health, National University of Singapore, National University Hospital System, Singapore. 281] Saw Swee Hock School of Public Health, National University of Singapore, National University Hospital System, Singapore. [2] Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, National University Hospital System, Singapore. [3] Duke-National University of Singapore Graduate Medical School, Singapore. 291] Department of Human Genetics, Faculty of Medicine, McGill University, Montreal, Quebec, Canada. [2] Department of Medicine, Faculty of Medicine, McGill University, Montreal, Quebec, Canada. [3] McGill University and Génome Québec Innovation Centre, Montreal, Quebec, Canada. 301] Department of Genomics of Common Disease, Imperial College London, London, UK. [2] Section of Genomic Medicine, National Heart and Lung Institute, Imperial College London, London, UK. 311] Department of Genome Sciences, University of Washington, Seattle, Washington, USA. [2] Howard Hughes Medical Institute, Seattle, Washington, USA. 321] Department of Twin Research & Genetic Epidemiology, King's College London, St. Thomas' Hospital Campus, London, UK. [2]. 331] Department of Genomics of Common Disease, Imperial College London, London, UK. [2] CNRS UMR 8199, Lille Pasteur Institute, Lille, France. [3] Lille 2 University, Lille, France. [4] Qatar Biomedical Research Institute (QBRI), Qatar Foundation, Doha, Qatar. [5] European Genomic Institute for Diabetes (EGID), Lille, France. [6] [7]. Abstract Common multi-allelic copy number variants (CNVs) appear enriched for phenotypic associations compared to their biallelic counterparts. Here we investigated the influence of gene dosage effects on adiposity through a CNV association study of gene expression levels in adipose tissue. We identified significant association of a multi-allelic CNV encompassing the salivary amylase gene (AMY1) with body mass index (BMI) and obesity, and we replicated this finding in 6,200 subjects. Increased AMY1 copy number was positively associated with both amylase gene expression (P = 2.31 × 10(-14)) and serum enzyme levels (P < 2.20 × 10(-16)), whereas reduced AMY1 copy number was associated with increased BMI (change in BMI per estimated copy = -0.15 (0.02) kg/m(2); P = 6.93 × 10(-10)) and obesity risk (odds ratio (OR) per estimated copy = 1.19, 95% confidence interval (CI) = 1.13-1.26; P = 1.46 × 10(-10)). The OR value of 1.19 per copy of AMY1 translates into about an eightfold difference in risk of obesity between subjects in the top (copy number > 9) and bottom (copy number < 4) 10% of the copy number distribution. Our study provides a first genetic link between carbohydrate metabolism and BMI and demonstrates the power of integrated genomic approaches beyond genome-wide association studies.
	PMID: 24686848 [PubMed - indexed for MEDLINE]
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4.	Nature. 2014 May 1;509(7498):91-5. doi: 10.1038/nature13176. Epub 2014 Mar 16. Identification of genomic alterations in oesophageal squamous cell cancer. Song Y1, Li L2, Ou Y3, Gao Z2, Li E4, Li X2, Zhang W5, Wang J6, Xu L7, Zhou Y6, Ma X5, Liu L5, Zhao Z5, Huang X6, Fan J5, Dong L5, Chen G6, Ma L5, Yang J6, Chen L6, He M6, Li M6, Zhuang X6, Huang K6, Qiu K6, Yin G6, Guo G6, Feng Q6, Chen P6, Wu Z8, Wu J9, Ma L5, Zhao J6, Luo L6, Fu M5, Xu B10, Chen B7, Li Y6, Tong T5, Wang M5, Liu Z5, Lin D5, Zhang X6, Yang H6, Wang J6, Zhan Q5. Author information: 11] State Key Laboratory of Molecular Oncology, Cancer Institute and Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China [2]. 21] BGI-Shenzhen, Shenzhen 518083, Guangdong 518083, China [2]. 31] State Key Laboratory of Molecular Oncology, Cancer Institute and Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China [2] Department of Neurosurgery, Chinese PLA General Hospital, Beijing 100853, China [3]. 41] Department of Biochemistry and Molecular Biology, The Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area, Shantou University Medical College, Shantou 515041, Guangdong, China [2]. 5State Key Laboratory of Molecular Oncology, Cancer Institute and Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China. 6BGI-Shenzhen, Shenzhen 518083, Guangdong 518083, China. 7Institute of Oncologic Pathology, Shantou University Medical College, Shantou 515041, Guangdong, China. 8Department of Tumor Surgery, Shantou Central Hospital, Affiliated Shantou Hospital of Sun Yat-sen University, Shantou 515041, Guangdong, China. 9Department of Biochemistry and Molecular Biology, The Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area, Shantou University Medical College, Shantou 515041, Guangdong, China. 10Department of Neurosurgery, Chinese PLA General Hospital, Beijing 100853, China. Abstract Oesophageal cancer is one of the most aggressive cancers and is the sixth leading cause of cancer death worldwide. Approximately 70% of global oesophageal cancer cases occur in China, with oesophageal squamous cell carcinoma (ESCC) being the histopathological form in the vast majority of cases (>90%). Currently, there are limited clinical approaches for the early diagnosis and treatment of ESCC, resulting in a 10% five-year survival rate for patients. However, the full repertoire of genomic events leading to the pathogenesis of ESCC remains unclear. Here we describe a comprehensive genomic analysis of 158 ESCC cases, as part of the International Cancer Genome Consortium research project. We conducted whole-genome sequencing in 17 ESCC cases and whole-exome sequencing in 71 cases, of which 53 cases, plus an additional 70 ESCC cases not used in the whole-genome and whole-exome sequencing, were subjected to array comparative genomic hybridization analysis. We identified eight significantly mutated genes, of which six are well known tumour-associated genes (TP53, RB1, CDKN2A, PIK3CA, NOTCH1, NFE2L2), and two have not previously been described in ESCC (ADAM29 and FAM135B). Notably, FAM135B is identified as a novel cancer-implicated gene as assayed for its ability to promote malignancy of ESCC cells. Additionally, MIR548K, a microRNA encoded in the amplified 11q13.3-13.4 region, is characterized as a novel oncogene, and functional assays demonstrate that MIR548K enhances malignant phenotypes of ESCC cells. Moreover, we have found that several important histone regulator genes (MLL2 (also called KMT2D), ASH1L, MLL3 (KMT2C), SETD1B, CREBBP and EP300) are frequently altered in ESCC. Pathway assessment reveals that somatic aberrations are mainly involved in the Wnt, cell cycle and Notch pathways. Genomic analyses suggest that ESCC and head and neck squamous cell carcinoma share some common pathogenic mechanisms, and ESCC development is associated with alcohol drinking. This study has explored novel biological markers and tumorigenic pathways that would greatly improve therapeutic strategies for ESCC.
	PMID: 24670651 [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 May 30;344(6187):970-2. doi: 10.1126/science.1255648. Translational genomics. Clues from the resilient. Friend SH1, Schadt EE2. Author information: 1Sage Bionetworks, Seattle, WA, 98109 USA Icahn School of Medicine at Mount Sinai, Department of Genetics and Genomic Sciences and the Icahn Institute for Genomics and Multiscale Biology, New York, NY 10029, USA. friend@sagebase.org eric.schadt@exchange.mssm.edu. 2Icahn School of Medicine at Mount Sinai, Department of Genetics and Genomic Sciences and the Icahn Institute for Genomics and Multiscale Biology, New York, NY 10029, USA. friend@sagebase.org eric.schadt@exchange.mssm.edu.
	PMID: 24876479 [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 May 23;344(6186):807-8. doi: 10.1126/science.1255074. Translational genomics. Targeting the host immune response to fight infection. Baillie JK. Author information: Roslin Institute, University of Edinburgh, Midlothian EH25 9RG, UK, and Intensive Care Unit, Royal Infirmary of Edinburgh, Edinburgh EH16 4SA, UK. j.k.baillie@ed.ac.uk.
	PMID: 24855243 [PubMed - indexed for MEDLINE]
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2.	Science. 2014 May 23;344(6186):801-2. doi: 10.1126/science.1255117. Cancer immunology. Identifying the infiltrators. Perdiguero EG1, Geissmann F2. Author information: 1Center for Molecular and Cellular Biology of Inflammation-CMCBI, Division of Immunology Infection & Inflammatory Diseases, King's College London, UK. 2Center for Molecular and Cellular Biology of Inflammation-CMCBI, Division of Immunology Infection & Inflammatory Diseases, King's College London, UK. frederic.geissmann@kcl.ac.uk. Comment on The cellular and molecular origin of tumor-associated macrophages. [Science. 2014] The cellular and molecular origin of tumor-associated macrophages.Franklin RA, Liao W, Sarkar A, Kim MV, Bivona MR, Liu K, Pamer EG, Li MO. Science. 2014 May 23; 344(6186):921-5. Epub 2014 May 8.
	PMID: 24855239 [PubMed - indexed for MEDLINE]
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3.	Science. 2014 May 23;344(6186):921-5. doi: 10.1126/science.1252510. Epub 2014 May 8. The cellular and molecular origin of tumor-associated macrophages. Franklin RA1, Liao W2, Sarkar A3, Kim MV1, Bivona MR3, Liu K4, Pamer EG3, Li MO5. Author information: 1Immunology Program, Memorial Sloan Kettering Cancer Center (MSKCC), New York, NY 10065, USA. Graduate Program in Immunology and Microbial Pathogenesis, Weill Cornell Graduate School of Medical Sciences, Cornell University, New York, NY 10065, USA. 2New York Genome Center, New York, NY 10022, USA. 3Immunology Program, Memorial Sloan Kettering Cancer Center (MSKCC), New York, NY 10065, USA. 4Department of Microbiology and Immunology, Columbia University, New York, NY 10032, USA. 5Immunology Program, Memorial Sloan Kettering Cancer Center (MSKCC), New York, NY 10065, USA. lim@mskcc.org. Comment in Cancer immunology. Identifying the infiltrators. [Science. 2014] Cancer immunology. Identifying the infiltrators.Perdiguero EG, Geissmann F. Science. 2014 May 23; 344(6186):801-2. Abstract Long recognized as an evolutionarily ancient cell type involved in tissue homeostasis and immune defense against pathogens, macrophages are being rediscovered as regulators of several diseases, including cancer. Here we show that in mice, mammary tumor growth induces the accumulation of tumor-associated macrophages (TAMs) that are phenotypically and functionally distinct from mammary tissue macrophages (MTMs). TAMs express the adhesion molecule Vcam1 and proliferate upon their differentiation from inflammatory monocytes, but do not exhibit an "alternatively activated" phenotype. TAM terminal differentiation depends on the transcriptional regulator of Notch signaling, RBPJ; and TAM, but not MTM, depletion restores tumor-infiltrating cytotoxic T cell responses and suppresses tumor growth. These findings reveal the ontogeny of TAMs and a discrete tumor-elicited inflammatory response, which may provide new opportunities for cancer immunotherapy. Copyright © 2014, American Association for the Advancement of Science.
	PMID: 24812208 [PubMed - indexed for MEDLINE]
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