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

Sent on Wednesday, 2014 January 29
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 - 3 of 3

1.	Nature. 2014 Jan 2;505(7481):27. doi: 10.1038/505027a. Frederick Sanger (1918-2013). Walker J. Author information: Medical Research Council Laboratory of Molecular Biology.
	PMID: 24380948 [PubMed - indexed for MEDLINE]
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2.	Nature. 2014 Jan 2;505(7481):14-7. doi: 10.1038/505014a. Behaviour and biology: The accidental epigeneticist. Hall SS. Author information: New York University.
	PMID: 24380939 [PubMed - indexed for MEDLINE]
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3.	Nature. 2014 Jan 2;505(7481):87-91. doi: 10.1038/nature12736. Epub 2013 Nov 20. Upper Palaeolithic Siberian genome reveals dual ancestry of Native Americans. Raghavan M1, Skoglund P2, Graf KE3, Metspalu M4, Albrechtsen A5, Moltke I6, Rasmussen S7, Stafford TW Jr8, Orlando L9, Metspalu E10, Karmin M11, Tambets K12, Rootsi S12, Mägi R13, Campos PF9, Balanovska E14, Balanovsky O15, Khusnutdinova E16, Litvinov S17, Osipova LP18, Fedorova SA19, Voevoda MI20, DeGiorgio M21, Sicheritz-Ponten T22, Brunak S22, Demeshchenko S23, Kivisild T24, Villems R25, Nielsen R21, Jakobsson M26, Willerslev E9. Author information: 11] Centre for GeoGenetics, Natural History Museum of Denmark, University of Copenhagen, Øster Voldgade 5-7, 1350 Copenhagen, Denmark [2]. 21] Department of Evolutionary Biology, Uppsala University, Norbyvägen 18D, Uppsala 752 36, Sweden [2]. 3Center for the Study of the First Americans, Texas A&M University, TAMU-4352, College Station, Texas 77845-4352, USA. 41] Estonian Biocentre, Evolutionary Biology group, Tartu 51010, Estonia [2] Department of Integrative Biology, University of California, Berkeley, California 94720, USA [3] Department of Evolutionary Biology, University of Tartu, Tartu 51010, Estonia. 5The Bioinformatics Centre, Department of Biology, University of Copenhagen, Ole Maaløes Vej 5, Copenhagen 2200, Denmark. 61] The Bioinformatics Centre, Department of Biology, University of Copenhagen, Ole Maaløes Vej 5, Copenhagen 2200, Denmark [2] Department of Human Genetics, The University of Chicago, Chicago, Illinois 60637, USA. 7Center for Biological Sequence Analysis, Technical University of Denmark, Kongens Lyngby 2800, Denmark. 81] Centre for GeoGenetics, Natural History Museum of Denmark, University of Copenhagen, Øster Voldgade 5-7, 1350 Copenhagen, Denmark [2] AMS 14C Dating Centre, Department of Physics and Astronomy, University of Aarhus, Ny Munkegade 120, Aarhus DK-8000, Denmark. 9Centre for GeoGenetics, Natural History Museum of Denmark, University of Copenhagen, Øster Voldgade 5-7, 1350 Copenhagen, Denmark. 10Department of Evolutionary Biology, University of Tartu, Tartu 51010, Estonia. 111] Estonian Biocentre, Evolutionary Biology group, Tartu 51010, Estonia [2] Department of Evolutionary Biology, University of Tartu, Tartu 51010, Estonia. 12Estonian Biocentre, Evolutionary Biology group, Tartu 51010, Estonia. 13Estonian Genome Center, University of Tartu, Tartu 51010, Estonia. 14Research Centre for Medical Genetics, Russian Academy of Medical Sciences, Moskvorechie Street 1, Moscow 115479, Russia. 151] Research Centre for Medical Genetics, Russian Academy of Medical Sciences, Moskvorechie Street 1, Moscow 115479, Russia [2] Vavilov Institute of General Genetics, Russian Academy of Sciences, Gubkina Street 3, Moscow 119991, Russia. 161] Institute of Biochemistry and Genetics, Ufa Scientific Centre, Russian Academy of Sciences, Ufa, Bashkorostan 450054, Russia [2] Biology Department, Bashkir State University, Ufa, Bashkorostan 450074, Russia. 171] Estonian Biocentre, Evolutionary Biology group, Tartu 51010, Estonia [2] Institute of Biochemistry and Genetics, Ufa Scientific Centre, Russian Academy of Sciences, Ufa, Bashkorostan 450054, Russia. 18The Institute of Cytology and Genetics, Center for Brain Neurobiology and Neurogenetics, Siberian Branch of the Russian Academy of Sciences, Lavrentyeva Avenue, Novosibirsk 630090, Russia. 19Department of Molecular Genetics, Yakut Research Center of Complex Medical Problems, Russian Academy of Medical Sciences and North-Eastern Federal University, Yakutsk, Sakha (Yakutia) 677010, Russia. 201] The Institute of Cytology and Genetics, Center for Brain Neurobiology and Neurogenetics, Siberian Branch of the Russian Academy of Sciences, Lavrentyeva Avenue, Novosibirsk 630090, Russia [2] Institute of Internal Medicine, Siberian Branch of the Russian Academy of Medical Sciences, Borisa Bogatkova 175/1, Novosibirsk 630089, Russia. 21Department of Integrative Biology, University of California, Berkeley, California 94720, USA. 221] Center for Biological Sequence Analysis, Technical University of Denmark, Kongens Lyngby 2800, Denmark [2] Novo Nordisk Foundation Center for Biosustainability, Technical University of Denmark, Kongens Lyngby 2800, Denmark. 23The State Hermitage Museum, 2, Dvortsovaya Ploshchad, St. Petersberg 190000, Russia. 241] Estonian Biocentre, Evolutionary Biology group, Tartu 51010, Estonia [2] Department of Biological Anthropology, University of Cambridge, Cambridge CB2 1QH, UK. 251] Estonian Biocentre, Evolutionary Biology group, Tartu 51010, Estonia [2] Department of Evolutionary Biology, University of Tartu, Tartu 51010, Estonia [3] Estonian Academy of Sciences, Tallinn 10130, Estonia. 261] Department of Evolutionary Biology, Uppsala University, Norbyvägen 18D, Uppsala 752 36, Sweden [2] Science for Life Laboratory, Uppsala University, Norbyvägen 18D, 752 36 Uppsala, Sweden. Abstract The origins of the First Americans remain contentious. Although Native Americans seem to be genetically most closely related to east Asians, there is no consensus with regard to which specific Old World populations they are closest to. Here we sequence the draft genome of an approximately 24,000-year-old individual (MA-1), from Mal'ta in south-central Siberia, to an average depth of 1×. To our knowledge this is the oldest anatomically modern human genome reported to date. The MA-1 mitochondrial genome belongs to haplogroup U, which has also been found at high frequency among Upper Palaeolithic and Mesolithic European hunter-gatherers, and the Y chromosome of MA-1 is basal to modern-day western Eurasians and near the root of most Native American lineages. Similarly, we find autosomal evidence that MA-1 is basal to modern-day western Eurasians and genetically closely related to modern-day Native Americans, with no close affinity to east Asians. This suggests that populations related to contemporary western Eurasians had a more north-easterly distribution 24,000 years ago than commonly thought. Furthermore, we estimate that 14 to 38% of Native American ancestry may originate through gene flow from this ancient population. This is likely to have occurred after the divergence of Native American ancestors from east Asian ancestors, but before the diversification of Native American populations in the New World. Gene flow from the MA-1 lineage into Native American ancestors could explain why several crania from the First Americans have been reported as bearing morphological characteristics that do not resemble those of east Asians. Sequencing of another south-central Siberian, Afontova Gora-2 dating to approximately 17,000 years ago, revealed similar autosomal genetic signatures as MA-1, suggesting that the region was continuously occupied by humans throughout the Last Glacial Maximum. Our findings reveal that western Eurasian genetic signatures in modern-day Native Americans derive not only from post-Columbian admixture, as commonly thought, but also from a mixed ancestry of the First Americans.
	PMID: 24256729 [PubMed - indexed for MEDLINE]
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Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Friday, 2014 January 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 - 8 of 8

1.	Science. 2014 Jan 10;343(6167):204-8. doi: 10.1126/science.1244705. Internalization of Salmonella by macrophages induces formation of nonreplicating persisters. Helaine S, Cheverton AM, Watson KG, Faure LM, Matthews SA, Holden DW. Author information: Section of Microbiology, Medical Research Council Centre for Molecular Bacteriology and Infection, Imperial College London, Armstrong Road, London SW7 2AZ, UK. Abstract Many bacterial pathogens cause persistent infections despite repeated antibiotic exposure. Bacterial persisters are antibiotic-tolerant cells, but little is known about their growth status and the signals and pathways leading to their formation in infected tissues. We used fluorescent single-cell analysis to identify Salmonella persisters during infection. These were part of a nonreplicating population formed immediately after uptake by macrophages and were induced by vacuolar acidification and nutritional deprivation, conditions that also induce Salmonella virulence gene expression. The majority of 14 toxin-antitoxin modules contributed to intracellular persister formation. Some persisters resumed intracellular growth after phagocytosis by naïve macrophages. Thus, the vacuolar environment induces phenotypic heterogeneity, leading to either bacterial replication or the formation of nonreplicating persisters that could provide a reservoir for relapsing infection.
	PMID: 24408438 [PubMed - indexed for MEDLINE]
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2.	Science. 2014 Jan 10;343(6167):117. doi: 10.1126/science.1247701. EMBO at 50. Nurse P. Author information: Paul Nurse is Secretary General of EMBO.
	PMID: 24408402 [PubMed - indexed for MEDLINE]
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3.	N Engl J Med. 2014 Jan 9;370(2):158. doi: 10.1056/NEJMicm1306161. Images in clinical medicine. Emphysematous aortitis after endovascular graft. Huang YL, Wu MT. Author information: Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan. Free Article
	PMID: 24401053 [PubMed - indexed for MEDLINE]
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4.	Nat Med. 2013 Nov;19(11):1423-37. doi: 10.1038/nm.3394. Microenvironmental regulation of tumor progression and metastasis. Quail DF, Joyce JA. Author information: Cancer Biology and Genetics Program, Memorial Sloan-Kettering Cancer Center, New York, New York, USA. Abstract Cancers develop in complex tissue environments, which they depend on for sustained growth, invasion and metastasis. Unlike tumor cells, stromal cell types within the tumor microenvironment (TME) are genetically stable and thus represent an attractive therapeutic target with reduced risk of resistance and tumor recurrence. However, specifically disrupting the pro-tumorigenic TME is a challenging undertaking, as the TME has diverse capacities to induce both beneficial and adverse consequences for tumorigenesis. Furthermore, many studies have shown that the microenvironment is capable of normalizing tumor cells, suggesting that re-education of stromal cells, rather than targeted ablation per se, may be an effective strategy for treating cancer. Here we discuss the paradoxical roles of the TME during specific stages of cancer progression and metastasis, as well as recent therapeutic attempts to re-educate stromal cells within the TME to have anti-tumorigenic effects.
	PMID: 24202395 [PubMed - indexed for MEDLINE]
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5.	Nat Med. 2013 Nov;19(11):1368-9. doi: 10.1038/nm.3387. An endogenous factor mediates shock-induced injury. Ward PA. Author information: Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan, USA. Comment on Cold-inducible RNA-binding protein (CIRP) triggers inflammatory responses in hemorrhagic shock and sepsis. [Nat Med. 2013] Cold-inducible RNA-binding protein (CIRP) triggers inflammatory responses in hemorrhagic shock and sepsis.Qiang X, Yang WL, Wu R, Zhou M, Jacob A, Dong W, Kuncewitch M, Ji Y, Yang H, Wang H, et al. Nat Med. 2013 Nov; 19(11):1489-95. Epub 2013 Oct 6.
	PMID: 24202382 [PubMed - indexed for MEDLINE]
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6.	Nat Med. 2013 Nov;19(11):1354-5. doi: 10.1038/nm1113-1354. Pharmacogenetic tests yield bonus benefit: better drug adherence. Dolgin E.
	PMID: 24202373 [PubMed - indexed for MEDLINE]
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7.	Nat Med. 2013 Nov;19(11):1529-33. doi: 10.1038/nm.3351. Epub 2013 Oct 27. Loss of immune escape mutations during persistent HCV infection in pregnancy enhances replication of vertically transmitted viruses. Honegger JR, Kim S, Price AA, Kohout JA, McKnight KL, Prasad MR, Lemon SM, Grakoui A, Walker CM. Author information: 1] The Center for Vaccines and Immunity, Nationwide Children's Hospital, Columbus, Ohio, USA. [2] Department of Pediatrics, The Ohio State University School of Medicine, Columbus, Ohio, USA. Abstract Globally, about 1% of pregnant women are persistently infected with the hepatitis C virus (HCV). Mother-to-child transmission of HCV occurs in 3-5% of pregnancies and accounts for most new childhood infections. HCV-specific CD8(+) cytotoxic T lymphocytes (CTLs) are vital in the clearance of acute HCV infections, but in the 60-80% of infections that persist, these cells become functionally exhausted or select for mutant viruses that escape T cell recognition. Increased HCV replication during pregnancy suggests that maternofetal immune tolerance mechanisms may further impair HCV-specific CTLs, limiting their selective pressure on persistent viruses. To assess this possibility, we characterized circulating viral quasispecies during and after consecutive pregnancies in two women. This revealed a loss of some escape mutations in HLA class I epitopes during pregnancy that was associated with emergence of more fit viruses. CTL selective pressure was reimposed after childbirth, at which point escape mutations in these epitopes again predominated in the quasispecies and viral load dropped sharply. Importantly, the viruses transmitted perinatally were those with enhanced fitness due to reversion of escape mutations. Our findings indicate that the immunoregulatory changes of pregnancy reduce CTL selective pressure on HCV class I epitopes, thereby facilitating vertical transmission of viruses with optimized replicative fitness. PMCID: PMC3823809 [Available on 2014/5/1]
	PMID: 24162814 [PubMed - indexed for MEDLINE]
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8.	Nat Med. 2013 Nov;19(11):1489-95. doi: 10.1038/nm.3368. Epub 2013 Oct 6. Cold-inducible RNA-binding protein (CIRP) triggers inflammatory responses in hemorrhagic shock and sepsis. Qiang X, Yang WL, Wu R, Zhou M, Jacob A, Dong W, Kuncewitch M, Ji Y, Yang H, Wang H, Fujita J, Nicastro J, Coppa GF, Tracey KJ, Wang P. Author information: 1] Center for Translational Research, The Feinstein Institute for Medical Research, Manhasset, New York, USA. [2]. Comment in An endogenous factor mediates shock-induced injury. [Nat Med. 2013] An endogenous factor mediates shock-induced injury.Ward PA. Nat Med. 2013 Nov; 19(11):1368-9. Abstract A systemic inflammatory response is observed in patients undergoing hemorrhagic shock and sepsis. Here we report increased levels of cold-inducible RNA-binding protein (CIRP) in the blood of individuals admitted to the surgical intensive care unit with hemorrhagic shock. In animal models of hemorrhage and sepsis, CIRP is upregulated in the heart and liver and released into the circulation. In macrophages under hypoxic stress, CIRP translocates from the nucleus to the cytosol and is released. Recombinant CIRP stimulates the release of tumor necrosis factor-α (TNF-α) and HMGB1 from macrophages and induces inflammatory responses and causes tissue injury when injected in vivo. Hemorrhage-induced TNF-α and HMGB1 release and lethality were reduced in CIRP-deficient mice. Blockade of CIRP using antisera to CIRP attenuated inflammatory cytokine release and mortality after hemorrhage and sepsis. The activity of extracellular CIRP is mediated through the Toll-like receptor 4 (TLR4)-myeloid differentiation factor 2 (MD2) complex. Surface plasmon resonance analysis indicated that CIRP binds to the TLR4-MD2 complex, as well as to TLR4 and MD2 individually. In particular, human CIRP amino acid residues 106-125 bind to MD2 with high affinity. Thus, CIRP is a damage-associated molecular pattern molecule that promotes inflammatory responses in shock and sepsis. PMCID: PMC3826915 [Available on 2014/5/1]
	PMID: 24097189 [PubMed - indexed for MEDLINE]
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1.	Nature. 2013 Dec 19;504(7480):377. doi: 10.1038/504377a. Adrienne Asch (1946-2013). Roberts D. Author information: University of Pennsylvania, Philadelphia, Pennsylvania.
	PMID: 24352283 [PubMed - indexed for MEDLINE]
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2.	Nature. 2013 Dec 19;504(7480):389-93. doi: 10.1038/nature12831. Epub 2013 Nov 27. Inconsistency in large pharmacogenomic studies. Haibe-Kains B1, El-Hachem N2, Birkbak NJ3, Jin AC4, Beck AH5, Aerts HJ6, Quackenbush J7. Author information: 11] Institut de Recherches Cliniques de Montréal, University of Montreal, Montreal, Quebec, Canada [2] Ontario Cancer Institute, Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario M5G 2M9, Canada. 2Institut de Recherches Cliniques de Montréal, University of Montreal, Montreal, Quebec, Canada. 3Center for Biological Sequence Analysis, Department of Systems Biology, Technical University of Denmark, 2800 Kgs, Lyngby, Denmark. 4Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA. 51] Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA [2]. 61] Department of Biostatistics and Computational Biology and Center for Cancer Computational Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA [2] Department of Radiation Oncology & Radiology, Dana-Farber Cancer Institute, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02215, USA [3] Department of Radiation Oncology, Maastricht University, Maastricht 6200 MD, The Netherlands [4]. 71] Department of Biostatistics and Computational Biology and Center for Cancer Computational Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA [2] Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA [3]. Comment in Cancer: Discrepancies in drug sensitivity. [Nature. 2013] Cancer: Discrepancies in drug sensitivity.Weinstein JN, Lorenzi PL. Nature. 2013 Dec 19; 504(7480):381-3. Epub 2013 Nov 27. Abstract Two large-scale pharmacogenomic studies were published recently in this journal. Genomic data are well correlated between studies; however, the measured drug response data are highly discordant. Although the source of inconsistencies remains uncertain, it has potential implications for using these outcome measures to assess gene-drug associations or select potential anticancer drugs on the basis of their reported results.
	PMID: 24284626 [PubMed - indexed for MEDLINE]
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3.	Nature. 2013 Dec 19;504(7480):381-3. doi: 10.1038/nature12839. Epub 2013 Nov 27. Cancer: Discrepancies in drug sensitivity. Weinstein JN, Lorenzi PL. Author information: Department of Bioinformatics and Computational Biology and the Department of Systems Biology, University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA. Comment on Inconsistency in large pharmacogenomic studies. [Nature. 2013] Inconsistency in large pharmacogenomic studies.Haibe-Kains B, El-Hachem N, Birkbak NJ, Jin AC, Beck AH, Aerts HJ, Quackenbush J. Nature. 2013 Dec 19; 504(7480):389-93. Epub 2013 Nov 27.
	PMID: 24284624 [PubMed - indexed for MEDLINE]
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1.	Science. 2013 Dec 20;342(6165):1241089. doi: 10.1126/science.1241089. The Amborella genome and the evolution of flowering plants. Amborella Genome Project. Collaborators: Albert VA, Barbazuk WB, dePamphilis CW, Der JP, Leebens-Mack J, Ma H, Palmer JD, Rounsley S, Sankoff D, Schuster SC, Soltis DE, Soltis PS, Wessler SR, Wing RA, Albert VA, Ammiraju JS, Barbazuk WB, Chamala S, Chanderbali AS, dePamphilis CW, Der JP, Determann R, Leebens-Mack J, Ma H, Ralph P, Rounsley S, Schuster SC, Soltis DE, Soltis PS, Talag J, Tomsho L, Walts B, Wanke S, Wing RA, Albert VA, Barbazuk WB, Chamala S, Chanderbali AS, Chang TH, Determann R, Lan T, Soltis DE, Soltis PS, Arikit S, Axtell MJ, Ayyampalayam S, Barbazuk WB, Burnette JM 3rd, Chamala S, De Paoli E, dePamphilis CW, Der JP, Estill JC, Farrell NP, Harkess A, Jiao Y, Leebens-Mack J, Liu K, Mei W, Meyers BC, Shahid S, Wafula E, Walts B, Wessler SR, Zhai J, Zhang X, Albert VA, Carretero-Paulet L, dePamphilis CW, Der JP, Jiao Y, Leebens-Mack J, Lyons E, Sankoff D, Tang H, Wafula E, Zheng C, Albert VA, Altman NS, Barbazuk WB, Carretero-Paulet L, dePamphilis CW, Der JP, Estill JC, Jiao Y, Leebens-Mack J, Liu K, Mei W, Wafula E, Altman NS, Arikit S, Axtell MJ, Chamala S, Chanderbali AS, Chen F, Chen JQ, Chiang V, De Paoli E, dePamphilis CW, Der JP, Determann R, Fogliani B, Guo C, Harholt J, Harkess A, Job C, Job D, Kim S, Kong H, Leebens-Mack J, Li G, Li L, Liu J, Ma H, Meyers BC, Park J, Qi X, Rajjou L, Burtet-Sarramegna V, Sederoff R, Shahid S, Soltis DE, Soltis PS, Sun YH, Ulvskov P, Villegente M, Xue JY, Yeh TF, Yu X, Zhai J, Acosta JJ, Albert VA, Barbazuk WB, Bruenn RA, Chamala S, de Kochko A, dePamphilis CW, Der JP, Herrera-Estrella LR, Ibarra-Laclette E, Kirst M, Leebens-Mack J , Pissis SP, Poncet V, Schuster SC, Soltis DE, Soltis PS, Tomsho L. Comment in Genomics. Genomic clues to the ancestral flowering plant. [Science. 2013] Genomics. Genomic clues to the ancestral flowering plant.Adams K. Science. 2013 Dec 20; 342(6165):1456-7. Abstract Amborella trichopoda is strongly supported as the single living species of the sister lineage to all other extant flowering plants, providing a unique reference for inferring the genome content and structure of the most recent common ancestor (MRCA) of living angiosperms. Sequencing the Amborella genome, we identified an ancient genome duplication predating angiosperm diversification, without evidence of subsequent, lineage-specific genome duplications. Comparisons between Amborella and other angiosperms facilitated reconstruction of the ancestral angiosperm gene content and gene order in the MRCA of core eudicots. We identify new gene families, gene duplications, and floral protein-protein interactions that first appeared in the ancestral angiosperm. Transposable elements in Amborella are ancient and highly divergent, with no recent transposon radiations. Population genomic analysis across Amborella's native range in New Caledonia reveals a recent genetic bottleneck and geographic structure with conservation implications.
	PMID: 24357323 [PubMed - indexed for MEDLINE]
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2.	Nat Genet. 2013 Nov;45(11):1263. doi: 10.1038/ng.2825. Taking pan-cancer analysis global. [No authors listed] Abstract Although federated cooperation is politically desirable, uniform data quality and standards are essential and should not be reinvented from scratch. The International Cancer Genome Consortium (ICGC) will do well to start with the data standards of The Cancer Genome Atlas (TCGA) and the Pediatric Cancer Genome Consortium if it is to succeed in genomic analysis across cancer types.
	PMID: 24165723 [PubMed - indexed for MEDLINE]
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1.	Nature. 2013 Dec 12;504(7479):200. doi: 10.1038/504200a. India faces uphill battle on biodiversity. Padma TV.
	PMID: 24336266 [PubMed - indexed for MEDLINE]

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1.	Nature. 2013 Nov 21;503(7476):342. doi: 10.1038/503342c. Heritability: Smarten up on intelligence genetics. Velden M. Author information: Department of Psychology, University of Mainz, Germany. Comment on Ethics: Taboo genetics. [Nature. 2013] Ethics: Taboo genetics.Hayden EC. Nature. 2013 Oct 3; 502(7469):26-8.
	PMID: 24256795 [PubMed - indexed for MEDLINE]
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2.	Nature. 2013 Nov 21;503(7476):365-70. doi: 10.1038/nature12790. Epub 2013 Nov 13. Activated ClpP kills persisters and eradicates a chronic biofilm infection. Conlon BP, Nakayasu ES, Fleck LE, LaFleur MD, Isabella VM, Coleman K, Leonard SN, Smith RD, Adkins JN, Lewis K. Author information: Antimicrobial Discovery Center, Department of Biology, Northeastern University, Boston, Massachusetts 02115, USA. Comment in Antibiotics: Killing the survivors. [Nature. 2013] Antibiotics: Killing the survivors.Gerdes K, Ingmer H. Nature. 2013 Nov 21; 503(7476):347-9. Epub 2013 Nov 13. Abstract Chronic infections are difficult to treat with antibiotics but are caused primarily by drug-sensitive pathogens. Dormant persister cells that are tolerant to killing by antibiotics are responsible for this apparent paradox. Persisters are phenotypic variants of normal cells and pathways leading to dormancy are redundant, making it challenging to develop anti-persister compounds. Biofilms shield persisters from the immune system, suggesting that an antibiotic for treating a chronic infection should be able to eradicate the infection on its own. We reasoned that a compound capable of corrupting a target in dormant cells will kill persisters. The acyldepsipeptide antibiotic (ADEP4) has been shown to activate the ClpP protease, resulting in death of growing cells. Here we show that ADEP4-activated ClpP becomes a fairly nonspecific protease and kills persisters by degrading over 400 proteins, forcing cells to self-digest. Null mutants of clpP arise with high probability, but combining ADEP4 with rifampicin produced complete eradication of Staphylococcus aureus biofilms in vitro and in a mouse model of a chronic infection. Our findings indicate a general principle for killing dormant cells-activation and corruption of a target, rather than conventional inhibition. Eradication of a biofilm in an animal model by activating a protease suggests a realistic path towards developing therapies to treat chronic infections.
	PMID: 24226776 [PubMed - indexed for MEDLINE]
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3.	Nature. 2013 Nov 21;503(7476):352-3. doi: 10.1038/nature12707. Epub 2013 Nov 6. HIV: Slipping under the radar. Goff SP. Author information: Departments of Microbiology & Immunology and Biochemistry & Molecular Biophysics, Columbia University, New York, New York 10032, USA. Comment on HIV-1 evades innate immune recognition through specific cofactor recruitment. [Nature. 2013] HIV-1 evades innate immune recognition through specific cofactor recruitment.Rasaiyaah J, Tan CP, Fletcher AJ, Price AJ, Blondeau C, Hilditch L, Jacques DA, Selwood DL, James LC, Noursadeghi M, et al. Nature. 2013 Nov 21; 503(7476):402-5. Epub 2013 Nov 6.
	PMID: 24196714 [PubMed - indexed for MEDLINE]
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4.	Nature. 2013 Nov 21;503(7476):402-5. doi: 10.1038/nature12769. Epub 2013 Nov 6. HIV-1 evades innate immune recognition through specific cofactor recruitment. Rasaiyaah J, Tan CP, Fletcher AJ, Price AJ, Blondeau C, Hilditch L, Jacques DA, Selwood DL, James LC, Noursadeghi M, Towers GJ. Author information: University College London, Medical Research Council Centre for Medical Molecular Virology, Division of Infection and Immunity, University College London, 90 Gower Street, London WC1E 6BT, UK. Comment in HIV: Slipping under the radar. [Nature. 2013] HIV: Slipping under the radar.Goff SP. Nature. 2013 Nov 21; 503(7476):352-3. Epub 2013 Nov 6. Abstract Human immunodeficiency virus (HIV)-1 is able to replicate in primary human macrophages without stimulating innate immunity despite reverse transcription of genomic RNA into double-stranded DNA, an activity that might be expected to trigger innate pattern recognition receptors. We reasoned that if correctly orchestrated HIV-1 uncoating and nuclear entry is important for evasion of innate sensors then manipulation of specific interactions between HIV-1 capsid and host factors that putatively regulate these processes should trigger pattern recognition receptors and stimulate type 1 interferon (IFN) secretion. Here we show that HIV-1 capsid mutants N74D and P90A, which are impaired for interaction with cofactors cleavage and polyadenylation specificity factor subunit 6 (CPSF6) and cyclophilins (Nup358 and CypA), respectively, cannot replicate in primary human monocyte-derived macrophages because they trigger innate sensors leading to nuclear translocation of NF-κB and IRF3, the production of soluble type 1 IFN and induction of an antiviral state. Depletion of CPSF6 with short hairpin RNA expression allows wild-type virus to trigger innate sensors and IFN production. In each case, suppressed replication is rescued by IFN-receptor blockade, demonstrating a role for IFN in restriction. IFN production is dependent on viral reverse transcription but not integration, indicating that a viral reverse transcription product comprises the HIV-1 pathogen-associated molecular pattern. Finally, we show that we can pharmacologically induce wild-type HIV-1 infection to stimulate IFN secretion and an antiviral state using a non-immunosuppressive cyclosporine analogue. We conclude that HIV-1 has evolved to use CPSF6 and cyclophilins to cloak its replication, allowing evasion of innate immune sensors and induction of a cell-autonomous innate immune response in primary human macrophages.
	PMID: 24196705 [PubMed - indexed for MEDLINE]
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