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

Sent on Tuesday, 2010 Apr 20
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.	Nature. 2010 Mar 4;464(7285):104-7. Circulating mitochondrial DAMPs cause inflammatory responses to injury. Zhang Q, Raoof M, Chen Y, Sumi Y, Sursal T, Junger W, Brohi K, Itagaki K, Hauser CJ. Department of Surgery, Division of Trauma, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA. Comment in: Nature. 2010 Mar 4;464(7285):41-2. Abstract Injury causes a systemic inflammatory response syndrome (SIRS) that is clinically much like sepsis. Microbial pathogen-associated molecular patterns (PAMPs) activate innate immunocytes through pattern recognition receptors. Similarly, cellular injury can release endogenous 'damage'-associated molecular patterns (DAMPs) that activate innate immunity. Mitochondria are evolutionary endosymbionts that were derived from bacteria and so might bear bacterial molecular motifs. Here we show that injury releases mitochondrial DAMPs (MTDs) into the circulation with functionally important immune consequences. MTDs include formyl peptides and mitochondrial DNA. These activate human polymorphonuclear neutrophils (PMNs) through formyl peptide receptor-1 and Toll-like receptor (TLR) 9, respectively. MTDs promote PMN Ca(2+) flux and phosphorylation of mitogen-activated protein (MAP) kinases, thus leading to PMN migration and degranulation in vitro and in vivo. Circulating MTDs can elicit neutrophil-mediated organ injury. Cellular disruption by trauma releases mitochondrial DAMPs with evolutionarily conserved similarities to bacterial PAMPs into the circulation. These signal through innate immune pathways identical to those activated in sepsis to create a sepsis-like state. The release of such mitochondrial 'enemies within' by cellular injury is a key link between trauma, inflammation and SIRS. PMCID: PMC2843437 [Available on 2010/9/4]
	PMID: 20203610 [PubMed - indexed for MEDLINE]
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	Publication Types: Research Support, N.I.H., Extramural Research Support, U.S. Gov't, Non-P.H.S. MeSH Terms: Acute Lung Injury/immunology Acute Lung Injury/pathology Animals Calcium Signaling Cells, Cultured CpG Islands/immunology DNA, Mitochondrial/blood DNA, Mitochondrial/immunology Femur/injuries Fractures, Bone/immunology Fractures, Bone/pathology Humans Immunity, Innate/immunology Liver/immunology Liver/injuries Liver/pathology Male Mitochondria/immunology* Mitochondria/secretion* Mitogen-Activated Protein Kinases/metabolism Muscle, Skeletal/immunology Muscle, Skeletal/pathology N-Formylmethionine Leucyl-Phenylalanine/immunology N-Formylmethionine Leucyl-Phenylalanine/metabolism Neutrophils/enzymology Neutrophils/immunology Neutrophils/metabolism Phosphorylation Rats Rats, Sprague-Dawley Receptors, Formyl Peptide/metabolism Sepsis/immunology Sepsis/metabolism Sepsis/microbiology Systemic Inflammatory Response Syndrome/blood Systemic Inflammatory Response Syndrome/complications* Systemic Inflammatory Response Syndrome/immunology* Systemic Inflammatory Response Syndrome/pathology Toll-Like Receptor 9/metabolism Wounds and Injuries/blood Wounds and Injuries/complications* Wounds and Injuries/immunology* Wounds and Injuries/pathology Substances: DNA, Mitochondrial Receptors, Formyl Peptide TLR9 protein, human Toll-Like Receptor 9 N-Formylmethionine Leucyl-Phenylalanine Mitogen-Activated Protein Kinases

2.	Nature. 2010 Mar 4;464(7285):59-65. A human gut microbial gene catalogue established by metagenomic sequencing. Qin J, Li R, Raes J, Arumugam M, Burgdorf KS, Manichanh C, Nielsen T, Pons N, Levenez F, Yamada T, Mende DR, Li J, Xu J, Li S, Li D, Cao J, Wang B, Liang H, Zheng H, Xie Y, Tap J, Lepage P, Bertalan M, Batto JM, Hansen T, Le Paslier D, Linneberg A, Nielsen HB, Pelletier E, Renault P, Sicheritz-Ponten T, Turner K, Zhu H, Yu C, Li S, Jian M, Zhou Y, Li Y, Zhang X, Li S, Qin N, Yang H, Wang J, Brunak S, Doré J, Guarner F, Kristiansen K, Pedersen O, Parkhill J, Weissenbach J; MetaHIT Consortium, Bork P, Ehrlich SD, Wang J. Collaborators: Antolin M, Artiguenave F, Blottiere H, Borruel N, Bruls T, Casellas F, Chervaux C, Cultrone A, Delorme C, Denariaz G, Dervyn R, Forte M, Friss C, van de Guchte M, Guedon E, Haimet F, Jamet A, Juste C, Kaci G, Kleerebezem M, Knol J, Kristensen M, Layec S, Le Roux K, Leclerc M, Maguin E, Minardi RM, Oozeer R, Rescigno M, Sanchez N, Tims S, Torrejon T, Varela E, de Vos W, Winogradsky Y, Zoetendal E. BGI-Shenzhen, Shenzhen 518083, China. Abstract To understand the impact of gut microbes on human health and well-being it is crucial to assess their genetic potential. Here we describe the Illumina-based metagenomic sequencing, assembly and characterization of 3.3 million non-redundant microbial genes, derived from 576.7 gigabases of sequence, from faecal samples of 124 European individuals. The gene set, approximately 150 times larger than the human gene complement, contains an overwhelming majority of the prevalent (more frequent) microbial genes of the cohort and probably includes a large proportion of the prevalent human intestinal microbial genes. The genes are largely shared among individuals of the cohort. Over 99% of the genes are bacterial, indicating that the entire cohort harbours between 1,000 and 1,150 prevalent bacterial species and each individual at least 160 such species, which are also largely shared. We define and describe the minimal gut metagenome and the minimal gut bacterial genome in terms of functions present in all individuals and most bacteria, respectively.
	PMID: 20203603 [PubMed - indexed for MEDLINE]
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	Publication Types: Comparative Study Research Support, Non-U.S. Gov't MeSH Terms: Adult Bacteria/classification Bacteria/genetics Bacteria/isolation & purification Bacteria/metabolism Cohort Studies Contig Mapping Denmark Feces/microbiology Gastrointestinal Tract/microbiology* Genes, Bacterial/genetics Genes, Essential/genetics Genome, Bacterial/genetics Genomics* Health Humans Inflammatory Bowel Diseases/genetics Metagenome/genetics* Obesity/genetics Open Reading Frames/genetics Overweight/genetics Sequence Analysis, DNA Spain

3.	Nature. 2010 Mar 4;464(7285):44. Obituary: Marshall Nirenberg (1927-2010). Caskey CT.
	PMID: 20203601 [PubMed - indexed for MEDLINE]
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	Publication Types: Biography Historical Article News Portraits MeSH Terms: Animals Genetic Code/genetics* History, 20th Century Molecular Biology/history* National Institutes of Health (U.S.) Nobel Prize Protein Biosynthesis United States Personal Name as Subject: Nirenberg M

4.	Nature. 2010 Mar 4;464(7285):41-2. Clinical immunology: Culprits with evolutionary ties. Calfee CS, Matthay MA. Comment on: Nature. 2010 Mar 4;464(7285):104-7.
	PMID: 20203598 [PubMed - indexed for MEDLINE]
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	Publication Types: Comment News MeSH Terms: Acute Lung Injury/immunology Acute Lung Injury/pathology Animals DNA, Mitochondrial/blood DNA, Mitochondrial/immunology Humans Immunity, Innate/immunology* Mitochondria/immunology* Mitochondria/secretion* N-Formylmethionine Leucyl-Phenylalanine/immunology N-Formylmethionine Leucyl-Phenylalanine/metabolism Neutrophils/enzymology Neutrophils/immunology Sepsis/immunology Sepsis/metabolism Sepsis/microbiology Systemic Inflammatory Response Syndrome/blood Systemic Inflammatory Response Syndrome/complications* Systemic Inflammatory Response Syndrome/immunology* Systemic Inflammatory Response Syndrome/pathology Wounds and Injuries/blood Wounds and Injuries/complications* Wounds and Injuries/immunology* Wounds and Injuries/pathology Substances: DNA, Mitochondrial N-Formylmethionine Leucyl-Phenylalanine

5.	Nature. 2010 Mar 4;464(7285):22-4. Chinese bioscience: The sequence factory. Cyranoski D.
	PMID: 20203579 [PubMed - indexed for MEDLINE]
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	Publication Types: News MeSH Terms: Academies and Institutes/economics Academies and Institutes/trends* Animals Breeding/economics China Genomics/economics Genomics/instrumentation Genomics/trends* Human Genome Project Humans Outsourced Services/economics Sequence Analysis, DNA/economics Sequence Analysis, DNA/instrumentation Sequence Analysis, DNA/trends* Workload

6.	Nature. 2010 Mar 4;464(7285):7. Do scientists really need a PhD? [No authors listed]
	PMID: 20203559 [PubMed - indexed for MEDLINE]
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	Publication Types: Editorial MeSH Terms: Age Factors China Education, Graduate/trends* Genomics/education Genomics/manpower Research/education* Research/manpower Research Personnel/education* Research Personnel/trends

7.	Nature. 2010 Mar 4;464(7285):90-4. Epub 2010 Feb 21. Metabolic streamlining in an open-ocean nitrogen-fixing cyanobacterium. Tripp HJ, Bench SR, Turk KA, Foster RA, Desany BA, Niazi F, Affourtit JP, Zehr JP. Ocean Sciences Department, University of California, Santa Cruz, 1156 High Street, Santa Cruz, California 95064, USA. Abstract Nitrogen (N(2))-fixing marine cyanobacteria are an important source of fixed inorganic nitrogen that supports oceanic primary productivity and carbon dioxide removal from the atmosphere. A globally distributed, periodically abundant N(2)-fixing marine cyanobacterium, UCYN-A, was recently found to lack the oxygen-producing photosystem II complex of the photosynthetic apparatus, indicating a novel metabolism, but remains uncultivated. Here we show, from metabolic reconstructions inferred from the assembly of the complete UCYN-A genome using massively parallel pyrosequencing of paired-end reads, that UCYN-A has a photofermentative metabolism and is dependent on other organisms for essential compounds. We found that UCYN-A lacks a number of major metabolic pathways including the tricarboxylic acid cycle, but retains sufficient electron transport capacity to generate energy and reducing power from light. Unexpectedly, UCYN-A has a reduced genome (1.44 megabases) that is structurally similar to many chloroplasts and some bacteria, in that it contains inverted repeats of ribosomal RNA operons. The lack of biosynthetic pathways for several amino acids and purines suggests that this organism depends on other organisms, either in close association or in symbiosis, for critical nutrients. However, size fractionation experiments using natural populations have so far not provided evidence of a symbiotic association with another microorganism. The UCYN-A cyanobacterium is a paradox in evolution and adaptation to the marine environment, and is an example of the tight metabolic coupling between microorganisms in oligotrophic oceanic microbial communities.
	PMID: 20173737 [PubMed - indexed for MEDLINE]
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	Publication Types: Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. MeSH Terms: Carbon/metabolism Chromosomes, Bacterial/genetics Cyanobacteria/classification Cyanobacteria/cytology Cyanobacteria/genetics* Cyanobacteria/metabolism* Electron Transport Genome, Bacterial/genetics* Genomics Marine Biology Molecular Sequence Data Nitrogen/metabolism* Nitrogen Fixation/genetics Nitrogen Fixation/physiology* Oceans and Seas Oxidoreductases/genetics Seawater/microbiology* Substances: Carbon Nitrogen Oxidoreductases nitrogenase reductase Secondary Source ID: GENBANK/CP001842