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

Sent on Thursday, 2012 May 31
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.	Nat Genet. 2012 Mar 28;44(4):357. doi: 10.1038/ng.2244. Your data are not a product. [No authors listed]
	PMID: 22456731 [PubMed - indexed for MEDLINE]

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Sent on Wednesday, 2012 May 30
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. 2012 May 18;336(6083):934-7. Epub 2012 Apr 26. Quantitative sequencing of 5-methylcytosine and 5-hydroxymethylcytosine at single-base resolution. Booth MJ, Branco MR, Ficz G, Oxley D, Krueger F, Reik W, Balasubramanian S. Source Department of Chemistry, University of Cambridge, Cambridge CB2 1EW, UK. Abstract 5-Methylcytosine can be converted to 5-hydroxymethylcytosine (5hmC) in mammalian DNA by the ten-eleven translocation (TET) enzymes. We introduce oxidative bisulfite sequencing (oxBS-Seq), the first method for quantitative mapping of 5hmC in genomic DNA at single-nucleotide resolution. Selective chemical oxidation of 5hmC to 5-formylcytosine (5fC) enables bisulfite conversion of 5fC to uracil. We demonstrate the utility of oxBS-Seq to map and quantify 5hmC at CpG islands (CGIs) in mouse embryonic stem (ES) cells and identify 800 5hmC-containing CGIs that have on average 3.3% hydroxymethylation. High levels of 5hmC were found in CGIs associated with transcriptional regulators and in long interspersed nuclear elements, suggesting that these regions might undergo epigenetic reprogramming in ES cells. Our results open new questions on 5hmC dynamics and sequence-specific targeting by TETs.
	PMID: 22539555 [PubMed - indexed for MEDLINE]

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Sent on Saturday, 2012 May 26
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. 2012 May 11;336(6082):740-3. Recent explosive human population growth has resulted in an excess of rare genetic variants. Keinan A, Clark AG. Source Department of Biological Statistics and Computational Biology, Cornell University, Ithaca, NY 14853, USA. ak735@cornell.edu Abstract Human populations have experienced recent explosive growth, expanding by at least three orders of magnitude over the past 400 generations. This departure from equilibrium skews patterns of genetic variation and distorts basic principles of population genetics. We characterized the empirical signatures of explosive growth on the site frequency spectrum and found that the discrepancy in rare variant abundance across demographic modeling studies is mostly due to differences in sample size. Rapid recent growth increases the load of rare variants and is likely to play a role in the individual genetic burden of complex disease risk. Hence, the extreme recent human population growth needs to be taken into consideration in studying the genetics of complex diseases and traits.
	PMID: 22582263 [PubMed - indexed for MEDLINE]
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2.	Science. 2012 May 11;336(6082):673-4. Research priorities. ELSI 2.0 for genomics and society. Kaye J, Meslin EM, Knoppers BM, Juengst ET, Deschênes M, Cambon-Thomsen A, Chalmers D, De Vries J, Edwards K, Hoppe N, Kent A, Adebamowo C, Marshall P, Kato K. Source HeLEX, Department of Public Health, University of Oxford, OX3 7LF, Oxford, UK. jane.kaye@law.ox.ac.uk
	PMID: 22582247 [PubMed - indexed for MEDLINE]
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3.	Nature. 2012 Apr 18;484(7394):320-1. doi: 10.1038/484320a. Sensory biology: Search for the compass needles. Mouritsen H. Comment on Nature. 2012 Apr 19;484(7394):367-70.
	PMID: 22517155 [PubMed - indexed for MEDLINE]
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4.	Nature. 2012 Apr 17;484(7394):302-3. doi: 10.1038/484302a. Gene hunt is on for mental disability. Callaway E.
	PMID: 22517145 [PubMed - indexed for MEDLINE]
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5.	Nature. 2012 Apr 11;484(7394):367-70. doi: 10.1038/nature11046. Clusters of iron-rich cells in the upper beak of pigeons are macrophages not magnetosensitive neurons. Treiber CD, Salzer MC, Riegler J, Edelman N, Sugar C, Breuss M, Pichler P, Cadiou H, Saunders M, Lythgoe M, Shaw J, Keays DA. Source Institute of Molecular Pathology, Dr Bohr-Gasse, 1030 Vienna, Austria. Comment in Nature. 2012 Apr 19;484(7394):320-1. Abstract Understanding the molecular and cellular mechanisms that mediate magnetosensation in vertebrates is a formidable scientific problem. One hypothesis is that magnetic information is transduced into neuronal impulses by using a magnetite-based magnetoreceptor. Previous studies claim to have identified a magnetic sense system in the pigeon, common to avian species, which consists of magnetite-containing trigeminal afferents located at six specific loci in the rostral subepidermis of the beak. These studies have been widely accepted in the field and heavily relied upon by both behavioural biologists and physicists. Here we show that clusters of iron-rich cells in the rostro-medial upper beak of the pigeon Columbia livia are macrophages, not magnetosensitive neurons. Our systematic characterization of the pigeon upper beak identified iron-rich cells in the stratum laxum of the subepidermis, the basal region of the respiratory epithelium and the apex of feather follicles. Using a three-dimensional blueprint of the pigeon beak created by magnetic resonance imaging and computed tomography, we mapped the location of iron-rich cells, revealing unexpected variation in their distribution and number--an observation that is inconsistent with a role in magnetic sensation. Ultrastructure analysis of these cells, which are not unique to the beak, showed that their subcellular architecture includes ferritin-like granules, siderosomes, haemosiderin and filopodia, characteristics of iron-rich macrophages. Our conclusion that these cells are macrophages and not magnetosensitive neurons is supported by immunohistological studies showing co-localization with the antigen-presenting molecule major histocompatibility complex class II. Our work necessitates a renewed search for the true magnetite-dependent magnetoreceptor in birds.
	PMID: 22495303 [PubMed - indexed for MEDLINE]
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6.	Nature. 2012 Mar 28;484(7394):339-44. doi: 10.1038/nature10960. A unique regulatory phase of DNA methylation in the early mammalian embryo. Smith ZD, Chan MM, Mikkelsen TS, Gu H, Gnirke A, Regev A, Meissner A. Source Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA. Abstract DNA methylation is highly dynamic during mammalian embryogenesis. It is broadly accepted that the paternal genome is actively depleted of 5-methylcytosine at fertilization, followed by passive loss that reaches a minimum at the blastocyst stage. However, this model is based on limited data, and so far no base-resolution maps exist to support and refine it. Here we generate genome-scale DNA methylation maps in mouse gametes and from the zygote through post-implantation. We find that the oocyte already exhibits global hypomethylation, particularly at specific families of long interspersed element 1 and long terminal repeat retroelements, which are disparately methylated between gametes and have lower methylation values in the zygote than in sperm. Surprisingly, the oocyte contributes a unique set of differentially methylated regions (DMRs)--including many CpG island promoters--that are maintained in the early embryo but are lost upon specification and absent from somatic cells. In contrast, sperm-contributed DMRs are largely intergenic and become hypermethylated after the blastocyst stage. Our data provide a genome-scale, base-resolution timeline of DNA methylation in the pre-specified embryo, when this epigenetic modification is most dynamic, before returning to the canonical somatic pattern. PMCID: PMC3331945 [Available on 2012/10/19]
	PMID: 22456710 [PubMed - indexed for MEDLINE]
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Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Wednesday, 2012 May 23
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.	Lancet. 2012 May 5;379(9827):1705-11. Epub 2012 Mar 29. Point-of-care genetic testing for personalisation of antiplatelet treatment (RAPID GENE): a prospective, randomised, proof-of-concept trial. Roberts JD, Wells GA, Le May MR, Labinaz M, Glover C, Froeschl M, Dick A, Marquis JF, O'Brien E, Goncalves S, Druce I, Stewart A, Gollob MH, So DY. Source Division of Cardiology, University of Ottawa Heart Institute, Ottawa, ON, Canada. Comment in Lancet. 2012 May 5;379(9827):1680-2. Abstract BACKGROUND: Prospective assessment of pharmacogenetic strategies has been limited by an inability to undertake bedside genetic testing. The CYP2C19*2 allele is a common genetic variant associated with increased rates of major adverse events in individuals given clopidogrel after percutaneous coronary intervention (PCI). We used a novel point-of-care genetic test to identify carriers of the CYP2C19*2 allele and aimed to assess a pharmacogenetic approach to dual antiplatelet treatment after PCI. METHODS: Between Aug 26, 2010, and July 7, 2011, 200 patients were enrolled into our prospective, randomised, proof-of-concept study. Patients undergoing PCI for acute coronary syndrome or stable angina were randomly assigned to rapid point-of-care genotyping or to standard treatment. Individuals in the rapid genotyping group were screened for the CYP2C19*2 allele. Carriers were given 10 mg prasugrel daily, and non-carriers and patients in the standard treatment group were given 75 mg clopidogrel daily. The primary endpoint was the proportion of CYP2C19*2 carriers with high on-treatment platelet reactivity (P2Y12 reactivity unit [PRU] value of more than 234) after 1 week of dual antiplatelet treatment, which is a marker associated with increased adverse cardiovascular events. Interventional cardiologists and data analysts were masked to genetic status and treatment. Patients were not masked to treatment allocation. All analyses were by intention to treat. This study is registered with ClinicalTrials.gov, NCT01184300. FINDINGS: After randomisation, 187 patients completed follow-up (91 rapid genotyping group, 96 standard treatment). 23 individuals in each group carried at least one CYP2C19*2 allele. None of the 23 carriers in the rapid genotyping group had a PRU value of more than 234 at day 7, compared with seven (30%) given standard treatment (p=0·0092). The point-of-care genetic test had a sensitivity of 100% (95% CI 92·3-100) and a specificity of 99·3% (96·3-100). INTERPRETATION: Point-of-care genetic testing after PCI can be done effectively at the bedside and treatment of identified CYP2C19*2 carriers with prasugrel can reduce high on-treatment platelet reactivity. FUNDING: Spartan Biosciences. Copyright © 2012 Elsevier Ltd. All rights reserved.
	PMID: 22464343 [PubMed - indexed for MEDLINE]
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2.	Blood. 2012 Feb 23;119(8):1810-20. Epub 2011 Dec 20. Therapeutic applications of macrophage colony-stimulating factor-1 (CSF-1) and antagonists of CSF-1 receptor (CSF-1R) signaling. Hume DA, MacDonald KP. Source Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Edinburgh, United Kingdom. david.hume@roslin.ed.ac.uk Abstract Macrophage-colony stimulating factor (CSF-1) signaling through its receptor (CSF-1R) promotes the differentiation of myeloid progenitors into heterogeneous populations of monocytes, macrophages, dendritic cells, and bone-resorbing osteoclasts. In the periphery, CSF-1 regulates the migration, proliferation, function, and survival of macrophages, which function at multiple levels within the innate and adaptive immune systems. Macrophage populations elicited by CSF-1 are associated with, and exacerbate, a broad spectrum of pathologies, including cancer, inflammation, and bone disease. Conversely, macrophages can also contribute to immunosuppression, disease resolution, and tissue repair. Recombinant CSF-1, antibodies against the ligand and the receptor, and specific inhibitors of CSF-1R kinase activity have been each been tested in a range of animal models and in some cases, in patients. This review examines the potential clinical uses of modulators of the CSF-1/CSF-1R system. We conclude that CSF-1 promotes a resident-type macrophage phenotype. As a treatment, CSF-1 has therapeutic potential in tissue repair. Conversely, inhibition of CSF-1R is unlikely to be effective in inflammatory disease but may have utility in cancer.
	PMID: 22186992 [PubMed - indexed for MEDLINE]
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Sent on Saturday, 2012 May 19
Search: (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))

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1.	Nature. 2012 Apr 5;484(7392):133. Turning point: Jessica Ware. Interviewed by Virginia Gewin. Ware J.
	PMID: 22486001 [PubMed - indexed for MEDLINE]
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2.	Nature. 2012 Apr 4;484(7392):55-61. doi: 10.1038/nature10944. The genomic basis of adaptive evolution in threespine sticklebacks. Jones FC, Grabherr MG, Chan YF, Russell P, Mauceli E, Johnson J, Swofford R, Pirun M, Zody MC, White S, Birney E, Searle S , Schmutz J, Grimwood J, Dickson MC, Myers RM, Miller CT, Summers BR, Knecht AK, Brady SD, Zhang H, Pollen AA, Howes T, Amemiya C; Broad Institute Genome Sequencing Platform & Whole Genome Assembly Team, Baldwin J, Bloom T, Jaffe DB, Nicol R, Wilkinson J, Lander ES, Di Palma F, Lindblad-Toh K, Kingsley DM. Source Department of Developmental Biology, Beckman Center B300, Stanford University School of Medicine, Stanford California 94305, USA. Comment in Nature. 2012 Apr 5;484(7392):46-7. Abstract Marine stickleback fish have colonized and adapted to thousands of streams and lakes formed since the last ice age, providing an exceptional opportunity to characterize genomic mechanisms underlying repeated ecological adaptation in nature. Here we develop a high-quality reference genome assembly for threespine sticklebacks. By sequencing the genomes of twenty additional individuals from a global set of marine and freshwater populations, we identify a genome-wide set of loci that are consistently associated with marine-freshwater divergence. Our results indicate that reuse of globally shared standing genetic variation, including chromosomal inversions, has an important role in repeated evolution of distinct marine and freshwater sticklebacks, and in the maintenance of divergent ecotypes during early stages of reproductive isolation. Both coding and regulatory changes occur in the set of loci underlying marine-freshwater evolution, but regulatory changes appear to predominate in this well known example of repeated adaptive evolution in nature. PMCID: PMC3322419 [Available on 2012/10/5]
	PMID: 22481358 [PubMed - indexed for MEDLINE]
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3.	Nature. 2012 Apr 4;484(7392):21-3. doi: 10.1038/484021a. Infectious disease: Blowing in the wind. Frazer J.
	PMID: 22481336 [PubMed - indexed for MEDLINE]
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4.	Nature. 2012 Apr 2;484(7392):19. doi: 10.1038/484019a. Glaciologists to target third pole. Qiu J.
	PMID: 22481333 [PubMed - indexed for MEDLINE]
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5.	Nature. 2012 Mar 18;484(7392):101-4. doi: 10.1038/nature10905. Endospore abundance, microbial growth and necromass turnover in deep sub-seafloor sediment. Lomstein BA, Langerhuus AT, D'Hondt S, Jørgensen BB, Spivack AJ. Source Department of Bioscience, Section for Microbiology, Aarhus University, Building 1540, Ny Munkegade 114, DK-8000 Aarhus C, Denmark. bente.lomstein@biology.au.dk Abstract Two decades of scientific ocean drilling have demonstrated widespread microbial life in deep sub-seafloor sediment, and surprisingly high microbial-cell numbers. Despite the ubiquity of life in the deep biosphere, the large community sizes and the low energy fluxes in this vast buried ecosystem are not yet understood. It is not known whether organisms of the deep biosphere are specifically adapted to extremely low energy fluxes or whether most of the observed cells are in a dormant, spore-like state. Here we apply a new approach--the D:L-amino-acid model--to quantify the distributions and turnover times of living microbial biomass, endospores and microbial necromass, as well as to determine their role in the sub-seafloor carbon budget. The approach combines sensitive analyses of unique bacterial markers (muramic acid and D-amino acids) and the bacterial endospore marker, dipicolinic acid, with racemization dynamics of stereo-isomeric amino acids. Endospores are as abundant as vegetative cells and microbial activity is extremely low, leading to microbial biomass turnover times of hundreds to thousands of years. We infer from model calculations that biomass production is sustained by organic carbon deposited from the surface photosynthetic world millions of years ago and that microbial necromass is recycled over timescales of hundreds of thousands of years.
	PMID: 22425999 [PubMed - indexed for MEDLINE]
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1.	N Engl J Med. 2012 May 3;366(18):1734-6. The monocyte in atherosclerosis--should I stay or should I go now? Gerszten RE, Tager AM. Source Massachusetts General Hospital and Harvard Medical School, Boston, USA.
	PMID: 22551134 [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. 2012 Apr 27;336(6080):433. Science policy. The payoff of federal R&D: iPod, Google, and Human Genome Project. Lane E, Ham B.
	PMID: 22548216 [PubMed - indexed for MEDLINE]
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2.	Science. 2012 Apr 27;336(6080):425-6. Cell Biology. Using cell-to-cell variability--a new era in molecular biology. Pelkmans L. Source Institute of Molecular Life Sciences, University of Zurich, Zürich, Switzerland. lucas.pelkmans@imls.uzh.ch
	PMID: 22539709 [PubMed - indexed for MEDLINE]
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3.	Science. 2012 Apr 27;336(6080):420-1. Immunology. Select inflammasome assembly. Caffrey DR, Fitzgerald KA. Source Division of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA. Comment on Science. 2012 Apr 27;336(6080):481-5.
	PMID: 22539706 [PubMed - indexed for MEDLINE]
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4.	Science. 2012 Apr 27;336(6080):481-5. Epub 2012 Mar 29. GBP5 promotes NLRP3 inflammasome assembly and immunity in mammals. Shenoy AR, Wellington DA, Kumar P, Kassa H, Booth CJ, Cresswell P, MacMicking JD. Source Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, CT 06510, USA. Comment in Science. 2012 Apr 27;336(6080):420-1. Abstract Inflammasomes are sensory complexes that alert the immune system to the presence of infection or tissue damage. These complexes assemble NLR (nucleotide binding and oligomerization, leucine-rich repeat) or ALR (absent in melanoma 2-like receptor) proteins to activate caspase-1 cleavage and interleukin (IL)-1β/IL-18 secretion. Here, we identified a non-NLR/ALR human protein that stimulates inflammasome assembly: guanylate binding protein 5 (GBP5). GBP5 promoted selective NLRP3 inflammasome responses to pathogenic bacteria and soluble but not crystalline inflammasome priming agents. Generation of Gbp5(-/-) mice revealed pronounced caspase-1 and IL-1β/IL-18 cleavage defects in vitro and impaired host defense and Nlrp3-dependent inflammatory responses in vivo. Thus, GBP5 serves as a unique rheostat for NLRP3 inflammasome activation and extends our understanding of the inflammasome complex beyond its core machinery.
	PMID: 22461501 [PubMed - indexed for MEDLINE]
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Sent on Wednesday, 2012 May 09
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1.	Lancet. 2012 Apr 21;379(9825):1484; author reply 1484-5. Paediatric hospital-acquired bacteraemia in developing countries. Wolkewitz M, Di Termini S, Cooper B, Meerpohl J, Schumacher M. Comment on Lancet. 2011 Dec 10;378(9808):2021-7.
	PMID: 22521064 [PubMed - indexed for MEDLINE]
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2.	Lancet. 2012 Apr 21;379(9825):1483-4; author reply 1484-5. Paediatric hospital-acquired bacteraemia in developing countries. Das RR. Comment on Lancet. 2011 Dec 10;378(9808):2021-7.
	PMID: 22521062 [PubMed - indexed for MEDLINE]
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3.	Lancet. 2012 Apr 21;379(9825):1462. New hope for sepsis. [No authors listed]
	PMID: 22521056 [PubMed - indexed for MEDLINE]
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4.	Science. 2012 Apr 20;336(6079):353-5. Recent plant diversity changes on Europe's mountain summits. Pauli H, Gottfried M, Dullinger S, Abdaladze O, Akhalkatsi M, Benito Alonso JL, Coldea G, Dick J, Erschbamer B, Fernández Calzado R, Ghosn D, Holten JI, Kanka R, Kazakis G, Kollár J, Larsson P, Moiseev P, Moiseev D, Molau U, Molero Mesa J, Nagy L, Pelino G, Puşcaş M, Rossi G, Stanisci A, Syverhuset AO, Theurillat JP, Tomaselli M, Unterluggauer P, Villar L, Vittoz P, Grabherr G. Source Institute of Mountain Research, Austrian Academy of Sciences, c/o University of Vienna, 1030 Wien, Austria. Abstract In mountainous regions, climate warming is expected to shift species' ranges to higher altitudes. Evidence for such shifts is still mostly from revisitations of historical sites. We present recent (2001 to 2008) changes in vascular plant species richness observed in a standardized monitoring network across Europe's major mountain ranges. Species have moved upslope on average. However, these shifts had opposite effects on the summit floras' species richness in boreal-temperate mountain regions (+3.9 species on average) and Mediterranean mountain regions (-1.4 species), probably because recent climatic trends have decreased the availability of water in the European south. Because Mediterranean mountains are particularly rich in endemic species, a continuation of these trends might shrink the European mountain flora, despite an average increase in summit species richness across the region.
	PMID: 22517860 [PubMed - indexed for MEDLINE]
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5.	Nature. 2012 Mar 29;483(7391):637-9. Epigenetics: Marked for success. Ledford H.
	PMID: 22468273 [PubMed - indexed for MEDLINE]
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6.	Nature. 2012 Mar 28;483(7391):603-7. doi: 10.1038/nature11003. The Cancer Cell Line Encyclopedia enables predictive modelling of anticancer drug sensitivity. Barretina J, Caponigro G, Stransky N, Venkatesan K, Margolin AA, Kim S, Wilson CJ, Lehár J, Kryukov GV, Sonkin D, Reddy A, Liu M, Murray L, Berger MF, Monahan JE, Morais P, Meltzer J, Korejwa A, Jané-Valbuena J, Mapa FA, Thibault J, Bric-Furlong E, Raman P, Shipway A, Engels IH, Cheng J, Yu GK, Yu J, Aspesi P Jr, de Silva M, Jagtap K, Jones MD, Wang L, Hatton C, Palescandolo E, Gupta S, Mahan S, Sougnez C, Onofrio RC, Liefeld T, MacConaill L, Winckler W, Reich M, Li N, Mesirov JP, Gabriel SB, Getz G, Ardlie K, Chan V, Myer VE, Weber BL, Porter J, Warmuth M, Finan P, Harris JL, Meyerson M, Golub TR, Morrissey MP, Sellers WR, Schlegel R, Garraway LA. Source The Broad Institute of Harvard and MIT, Cambridge, Massachusetts 02142, USA. Comment in Nature. 2012 Mar 29;483(7391):544-5. Abstract The systematic translation of cancer genomic data into knowledge of tumour biology and therapeutic possibilities remains challenging. Such efforts should be greatly aided by robust preclinical model systems that reflect the genomic diversity of human cancers and for which detailed genetic and pharmacological annotation is available. Here we describe the Cancer Cell Line Encyclopedia (CCLE): a compilation of gene expression, chromosomal copy number and massively parallel sequencing data from 947 human cancer cell lines. When coupled with pharmacological profiles for 24 anticancer drugs across 479 of the cell lines, this collection allowed identification of genetic, lineage, and gene-expression-based predictors of drug sensitivity. In addition to known predictors, we found that plasma cell lineage correlated with sensitivity to IGF1 receptor inhibitors; AHR expression was associated with MEK inhibitor efficacy in NRAS-mutant lines; and SLFN11 expression predicted sensitivity to topoisomerase inhibitors. Together, our results indicate that large, annotated cell-line collections may help to enable preclinical stratification schemata for anticancer agents. The generation of genetic predictions of drug response in the preclinical setting and their incorporation into cancer clinical trial design could speed the emergence of 'personalized' therapeutic regimens. PMCID: PMC3320027 [Available on 2012/9/29]
	PMID: 22460905 [PubMed - indexed for MEDLINE]
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7.	Nature. 2012 Mar 28;483(7391):570-5. doi: 10.1038/nature11005. Systematic identification of genomic markers of drug sensitivity in cancer cells. Garnett MJ, Edelman EJ, Heidorn SJ, Greenman CD, Dastur A, Lau KW, Greninger P, Thompson IR, Luo X, Soares J, Liu Q, Iorio F, Surdez D, Chen L, Milano RJ, Bignell GR, Tam AT, Davies H, Stevenson JA, Barthorpe S, Lutz SR, Kogera F, Lawrence K, McLaren-Douglas A, Mitropoulos X, Mironenko T, Thi H, Richardson L, Zhou W, Jewitt F, Zhang T, O'Brien P, Boisvert JL, Price S, Hur W, Yang W, Deng X, Butler A, Choi HG, Chang JW, Baselga J, Stamenkovic I, Engelman JA, Sharma SV, Delattre O, Saez-Rodriguez J, Gray NS, Settleman J, Futreal PA, Haber DA, Stratton MR, Ramaswamy S, McDermott U, Benes CH. Source Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton CB10 1SA, UK. Comment in Nature. 2012 Mar 29;483(7391):544-5. Abstract Clinical responses to anticancer therapies are often restricted to a subset of patients. In some cases, mutated cancer genes are potent biomarkers for responses to targeted agents. Here, to uncover new biomarkers of sensitivity and resistance to cancer therapeutics, we screened a panel of several hundred cancer cell lines--which represent much of the tissue-type and genetic diversity of human cancers--with 130 drugs under clinical and preclinical investigation. In aggregate, we found that mutated cancer genes were associated with cellular response to most currently available cancer drugs. Classic oncogene addiction paradigms were modified by additional tissue-specific or expression biomarkers, and some frequently mutated genes were associated with sensitivity to a broad range of therapeutic agents. Unexpected relationships were revealed, including the marked sensitivity of Ewing's sarcoma cells harbouring the EWS (also known as EWSR1)-FLI1 gene translocation to poly(ADP-ribose) polymerase (PARP) inhibitors. By linking drug activity to the functional complexity of cancer genomes, systematic pharmacogenomic profiling in cancer cell lines provides a powerful biomarker discovery platform to guide rational cancer therapeutic strategies.
	PMID: 22460902 [PubMed - indexed for MEDLINE]
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8.	Nature. 2012 Mar 28;483(7391):546-8. doi: 10.1038/483546a. Cancer: Clinical trials unite mice and humans. Johnson L. Comment on Nature. 2012 Mar 29;483(7391):613-7.
	PMID: 22460895 [PubMed - indexed for MEDLINE]
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9.	Nature. 2012 Mar 28;483(7391):520-2. doi: 10.1038/483520a. Flu surveillance lacking. Butler D.
	PMID: 22460875 [PubMed - indexed for MEDLINE]
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10.	Nature. 2012 Mar 18;483(7391):613-7. doi: 10.1038/nature10937. A murine lung cancer co-clinical trial identifies genetic modifiers of therapeutic response. Chen Z, Cheng K, Walton Z, Wang Y, Ebi H, Shimamura T, Liu Y, Tupper T, Ouyang J, Li J, Gao P, Woo MS, Xu C, Yanagita M, Altabef A, Wang S, Lee C, Nakada Y, Peña CG, Sun Y, Franchetti Y, Yao C, Saur A, Cameron MD, Nishino M, Hayes DN, Wilkerson MD, Roberts PJ, Lee CB, Bardeesy N, Butaney M, Chirieac LR, Costa DB, Jackman D, Sharpless NE, Castrillon DH, Demetri GD, Jänne PA, Pandolfi PP, Cantley LC, Kung AL, Engelman JA, Wong KK. Source Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA. Comment in Nature. 2012 Mar 29;483(7391):546-8. Abstract Targeted therapies have demonstrated efficacy against specific subsets of molecularly defined cancers. Although most patients with lung cancer are stratified according to a single oncogenic driver, cancers harbouring identical activating genetic mutations show large variations in their responses to the same targeted therapy. The biology underlying this heterogeneity is not well understood, and the impact of co-existing genetic mutations, especially the loss of tumour suppressors, has not been fully explored. Here we use genetically engineered mouse models to conduct a 'co-clinical' trial that mirrors an ongoing human clinical trial in patients with KRAS-mutant lung cancers. This trial aims to determine if the MEK inhibitor selumetinib (AZD6244) increases the efficacy of docetaxel, a standard of care chemotherapy. Our studies demonstrate that concomitant loss of either p53 (also known as Tp53) or Lkb1 (also known as Stk11), two clinically relevant tumour suppressors, markedly impaired the response of Kras-mutant cancers to docetaxel monotherapy. We observed that the addition of selumetinib provided substantial benefit for mice with lung cancer caused by Kras and Kras and p53 mutations, but mice with Kras and Lkb1 mutations had primary resistance to this combination therapy. Pharmacodynamic studies, including positron-emission tomography (PET) and computed tomography (CT), identified biological markers in mice and patients that provide a rationale for the differential efficacy of these therapies in the different genotypes. These co-clinical results identify predictive genetic biomarkers that should be validated by interrogating samples from patients enrolled on the concurrent clinical trial. These studies also highlight the rationale for synchronous co-clinical trials, not only to anticipate the results of ongoing human clinical trials, but also to generate clinically relevant hypotheses that can inform the analysis and design of human studies.
	PMID: 22425996 [PubMed - indexed for MEDLINE]
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