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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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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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