What's new for 'JKB_daily1' in PubMed
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Sender's message: Sepsis or genomics or altitude: JKB_daily1
Sent on Tuesday, 2012 December 11Search: (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 |
| 1. | Science. 2012 Nov 30;338(6111):1161-2. doi: 10.1126/science.1232327.Epidemiology. Outsmarting outbreaks.Walker MJ, Beatson SA.School of Chemistry and Molecular Biosciences and Australian Infectious Diseases Research Centre, University of Queensland, St. Lucia, QLD 4072, Australia. mark.walker@uq.edu.au |
| PMID: 23197523 [PubMed - indexed for MEDLINE] | |
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| 2. | Science. 2012 Nov 16;338(6109):917-21. doi: 10.1126/science.1222454.Unlike bone, cartilage regeneration remains elusive.Huey DJ, Hu JC, Athanasiou KA.Department of Biomedical Engineering, University of California, Davis, 1 Shields Avenue, Davis, CA 95616, USA. AbstractArticular cartilage was predicted to be one of the first tissues to successfully be regenerated, but this proved incorrect. In contrast, bone (but also vasculature and cardiac tissues) has seen numerous successful reparative approaches, despite consisting of multiple cell and tissue types and, thus, possessing more complex design requirements. Here, we use bone-regeneration successes to highlight cartilage-regeneration challenges: such as selecting appropriate cell sources and scaffolds, creating biomechanically suitable tissues, and integrating to native tissue. We also discuss technologies that can address the hurdles of engineering a tissue possessing mechanical properties that are unmatched in human-made materials and functioning in environments unfavorable to neotissue growth. |
| PMID: 23161992 [PubMed - indexed for MEDLINE] | |
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| 3. | Science. 2012 Nov 16;338(6109):883. doi: 10.1126/science.338.6109.883-a.Small science: high stakes.Gamazon ER.Comment on
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| PMID: 23161975 [PubMed - indexed for MEDLINE] | |
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| 4. | Science. 2012 Nov 16;338(6109):882-3. doi: 10.1126/science.338.6109.882-c.Small science: big science will prevail.Siminovitch L.Comment on
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| PMID: 23161974 [PubMed - indexed for MEDLINE] | |
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| 5. | Science. 2012 Nov 16;338(6109):882. doi: 10.1126/science.338.6109.882-b.Small science: view from developing nations.Slippers B.Comment on
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| PMID: 23161973 [PubMed - indexed for MEDLINE] | |
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| 6. | Science. 2012 Nov 16;338(6109):882. doi: 10.1126/science.338.6109.882-a.Small science: radical innovation.Berlekamp E.Comment on
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| PMID: 23161972 [PubMed - indexed for MEDLINE] | |
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| 7. | Science. 2012 Nov 9;338(6108):758-67.Presidential address. Transposable elements, epigenetics, and genome evolution.Fedoroff NV.King Abdullah University of Science and Technology, Saudi Arabia. nvf1@psu.edu |
| PMID: 23145453 [PubMed - indexed for MEDLINE] | |
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| 8. | Science. 2012 Nov 9;338(6108):768-72. doi: 10.1126/science.1224577.Hepcidin and the iron-infection axis.Drakesmith H, Prentice AM.Molecular Immunology Group and Medical Research Council (MRC) Human Immunology Unit, MRC Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Oxford, UK. alexander.drakesmith@ndm.ox.ac.uk AbstractIron lies at the center of a battle for nutritional resource between higher organisms and their microbial pathogens. The iron status of the human host affects the pathogenicity of numerous infections including malaria, HIV-1, and tuberculosis. Hepcidin, an antimicrobial-like peptide hormone, has emerged as the master regulator of iron metabolism. Hepcidin controls the absorption of dietary iron and the distribution of iron among cell types in the body, and its synthesis is regulated by both iron and innate immunity. We describe how hepcidin integrates signals from diverse physiological inputs, forming a key molecular bridge between iron trafficking and response to infection. |
| PMID: 23139325 [PubMed - indexed for MEDLINE] | |
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| 9. | Science. 2012 Nov 2;338(6107):581. doi: 10.1126/science.1231607.The scientist as world citizen.King MC. Free Article |
| PMID: 23118152 [PubMed - indexed for MEDLINE] | |
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| 10. | Science. 2012 Oct 26;338(6106):487-8. doi: 10.1126/science.1215229.IBI series winner. A mutant search--Caenorhabditis elegans and gene discovery.LaRue CC, Padilla PA.Department of Biological Sciences, University of North Texas, Denton TX 76203, USA. |
| PMID: 23112325 [PubMed - indexed for MEDLINE] | |
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| 11. | Nature. 2012 Nov 15;491(7424):454-7. doi: 10.1038/nature11508. Epub 2012 Oct 14.Long non-coding antisense RNA controls Uchl1 translation through an embedded SINEB2 repeat.Carrieri C, Cimatti L, Biagioli M, Beugnet A, Zucchelli S, Fedele S, Pesce E, Ferrer I, Collavin L, Santoro C, Forrest AR, Carninci P, Biffo S, Stupka E, Gustincich S.Area of Neuroscience, International School for Advanced Studies (SISSA), via Bonomea 265, 34136 Trieste, Italy. AbstractMost of the mammalian genome is transcribed. This generates a vast repertoire of transcripts that includes protein-coding messenger RNAs, long non-coding RNAs (lncRNAs) and repetitive sequences, such as SINEs (short interspersed nuclear elements). A large percentage of ncRNAs are nuclear-enriched with unknown function. Antisense lncRNAs may form sense-antisense pairs by pairing with a protein-coding gene on the opposite strand to regulate epigenetic silencing, transcription and mRNA stability. Here we identify a nuclear-enriched lncRNA antisense to mouse ubiquitin carboxy-terminal hydrolase L1 (Uchl1), a gene involved in brain function and neurodegenerative diseases. Antisense Uchl1 increases UCHL1 protein synthesis at a post-transcriptional level, hereby identifying a new functional class of lncRNAs. Antisense Uchl1 activity depends on the presence of a 5' overlapping sequence and an embedded inverted SINEB2 element. These features are shared by other natural antisense transcripts and can confer regulatory activity to an artificial antisense to green fluorescent protein. Antisense Uchl1 function is under the control of stress signalling pathways, as mTORC1 inhibition by rapamycin causes an increase in UCHL1 protein that is associated to the shuttling of antisense Uchl1 RNA from the nucleus to the cytoplasm. Antisense Uchl1 RNA is then required for the association of the overlapping sense protein-coding mRNA to active polysomes for translation. These data reveal another layer of gene expression control at the post-transcriptional level. |
| PMID: 23064229 [PubMed - indexed for MEDLINE] | |
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| 12. | Nature. 2012 Oct 4;490(7418):44-6. doi: 10.1038/490044a.Genomics: Resident risks.Oh J, Segre JA.Comment on |
| PMID: 23038462 [PubMed - indexed for MEDLINE] | |
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| 13. | Nature. 2012 Oct 4;490(7418):31-2. doi: 10.1038/490031a.Nobel success: What makes a great lab?Bynum W.University College London, UK. w.bynum@ucl.ac.uk |
| PMID: 23038449 [PubMed - indexed for MEDLINE] | |
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| 14. | Nature. 2012 Oct 4;490(7418):55-60. doi: 10.1038/nature11450. Epub 2012 Sep 26.A metagenome-wide association study of gut microbiota in type 2 diabetes.Qin J, Li Y, Cai Z, Li S, Zhu J, Zhang F, Liang S, Zhang W, Guan Y, Shen D, Peng Y, Zhang D, Jie Z, Wu W, Qin Y, Xue W, Li J, Han L, Lu D, Wu P, Dai Y, Sun X, Li Z, Tang A, Zhong S, Li X, Chen W, Xu R, Wang M, Feng Q, Gong M, Yu J, Zhang Y, Zhang M, Hansen T, Sanchez G, Raes J, Falony G, Okuda S, Almeida M, LeChatelier E, Renault P, Pons N, Batto JM, Zhang Z, Chen H, Yang R, Zheng W, Li S, Yang H, Wang J, Ehrlich SD, Nielsen R, Pedersen O, Kristiansen K, Wang J.BGI-Shenzhen, Shenzhen 518083, China. Comment in
AbstractAssessment and characterization of gut microbiota has become a major research area in human disease, including type 2 diabetes, the most prevalent endocrine disease worldwide. To carry out analysis on gut microbial content in patients with type 2 diabetes, we developed a protocol for a metagenome-wide association study (MGWAS) and undertook a two-stage MGWAS based on deep shotgun sequencing of the gut microbial DNA from 345 Chinese individuals. We identified and validated approximately 60,000 type-2-diabetes-associated markers and established the concept of a metagenomic linkage group, enabling taxonomic species-level analyses. MGWAS analysis showed that patients with type 2 diabetes were characterized by a moderate degree of gut microbial dysbiosis, a decrease in the abundance of some universal butyrate-producing bacteria and an increase in various opportunistic pathogens, as well as an enrichment of other microbial functions conferring sulphate reduction and oxidative stress resistance. An analysis of 23 additional individuals demonstrated that these gut microbial markers might be useful for classifying type 2 diabetes. |
| PMID: 23023125 [PubMed - indexed for MEDLINE] | |
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| 15. | Science. 2012 Nov 9;338(6108):795-8. doi: 10.1126/science.1226625. Epub 2012 Sep 27.Coagulation factor X activates innate immunity to human species C adenovirus.Doronin K, Flatt JW, Di Paolo NC, Khare R, Kalyuzhniy O, Acchione M, Sumida JP, Ohto U, Shimizu T, Akashi-Takamura S, Miyake K, MacDonald JW, Bammler TK, Beyer RP, Farin FM, Stewart PL, Shayakhmetov DM.Department of Medicine, University of Washington, Seattle, WA 98195, USA. Comment in
AbstractAlthough coagulation factors play a role in host defense for "living fossils" such as horseshoe crabs, the role of the coagulation system in immunity in higher organisms remains unclear. We modeled the interface of human species C adenovirus (HAdv) interaction with coagulation factor X (FX) and introduced a mutation that abrogated formation of the HAdv-FX complex. In vivo genome-wide transcriptional profiling revealed that FX-binding-ablated virus failed to activate a distinct network of nuclear factor κB-dependent early-response genes that are activated by HAdv-FX complex downstream of TLR4/MyD88/TRIF/TRAF6 signaling. Our study implicates host factor "decoration" of the virus as a mechanism to trigger an innate immune sensor that responds to a misplacement of coagulation FX from the blood into intracellular macrophage compartments upon virus entry into the cell. |
| PMID: 23019612 [PubMed - indexed for MEDLINE] | |
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| 17. | Nature. 2012 Oct 4;490(7418):49-54. doi: 10.1038/nature11413. Epub 2012 Sep 19.The oyster genome reveals stress adaptation and complexity of shell formation.Zhang G, Fang X, Guo X, Li L, Luo R, Xu F, Yang P, Zhang L, Wang X, Qi H, Xiong Z, Que H, Xie Y, Holland PW, Paps J, Zhu Y, Wu F, Chen Y, Wang J, Peng C, Meng J, Yang L, Liu J, Wen B, Zhang N, Huang Z, Zhu Q, Feng Y, Mount A, Hedgecock D, Xu Z, Liu Y, Domazet-Lošo T, Du Y, Sun X, Zhang S, Liu B, Cheng P, Jiang X, Li J, Fan D, Wang W, Fu W, Wang T, Wang B, Zhang J, Peng Z, Li Y, Li N, Wang J, Chen M, He Y, Tan F, Song X, Zheng Q, Huang R, Yang H, Du X, Chen L, Yang M, Gaffney PM, Wang S, Luo L, She Z, Ming Y, Huang W, Zhang S, Huang B, Zhang Y, Qu T, Ni P, Miao G, Wang J, Wang Q, Steinberg CE, Wang H, Li N, Qian L, Zhang G, Li Y, Yang H, Liu X, Wang J, Yin Y, Wang J.Institute of Oceanology, Chinese Academy of Sciences, Qingdao 266071, China. AbstractThe Pacific oyster Crassostrea gigas belongs to one of the most species-rich but genomically poorly explored phyla, the Mollusca. Here we report the sequencing and assembly of the oyster genome using short reads and a fosmid-pooling strategy, along with transcriptomes of development and stress response and the proteome of the shell. The oyster genome is highly polymorphic and rich in repetitive sequences, with some transposable elements still actively shaping variation. Transcriptome studies reveal an extensive set of genes responding to environmental stress. The expansion of genes coding for heat shock protein 70 and inhibitors of apoptosis is probably central to the oyster's adaptation to sessile life in the highly stressful intertidal zone. Our analyses also show that shell formation in molluscs is more complex than currently understood and involves extensive participation of cells and their exosomes. The oyster genome sequence fills a void in our understanding of the Lophotrochozoa. |
| PMID: 22992520 [PubMed - indexed for MEDLINE] | |
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| 18. | Nature. 2012 Oct 18;490(7420):421-5. doi: 10.1038/nature11428. Epub 2012 Sep 16.A FOXO3-IRF7 gene regulatory circuit limits inflammatory sequelae of antiviral responses.Litvak V, Ratushny AV, Lampano AE, Schmitz F, Huang AC, Raman A, Rust AG, Bergthaler A, Aitchison JD, Aderem A.Seattle Biomedical Research Institute, Seattle, Washington 98109, USA. AbstractAntiviral responses must be tightly regulated to defend rapidly against infection while minimizing inflammatory damage. Type 1 interferons (IFN-I) are crucial mediators of antiviral responses and their transcription is regulated by a variety of transcription factors; principal among these is the family of interferon regulatory factors (IRFs). The IRF gene regulatory networks are complex and contain multiple feedback loops. The tools of systems biology are well suited to elucidate the complex interactions that give rise to precise coordination of the interferon response. Here we have used an unbiased systems approach to predict that a member of the forkhead family of transcription factors, FOXO3, is a negative regulator of a subset of antiviral genes. This prediction was validated using macrophages isolated from Foxo3-null mice. Genome-wide location analysis combined with gene deletion studies identified the Irf7 gene as a critical target of FOXO3. FOXO3 was identified as a negative regulator of Irf7 transcription and we have further demonstrated that FOXO3, IRF7 and IFN-I form a coherent feed-forward regulatory circuit. Our data suggest that the FOXO3-IRF7 regulatory circuit represents a novel mechanism for establishing the requisite set points in the interferon pathway that balances the beneficial effects and deleterious sequelae of the antiviral response. |
| PMID: 22982991 [PubMed - indexed for MEDLINE] | |
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| 19. | Nat Genet. 2012 Sep;44(9):1066-71. doi: 10.1038/ng.2376. Epub 2012 Aug 19.A mixed-model approach for genome-wide association studies of correlated traits in structured populations.Korte A, Vilhjálmsson BJ, Segura V, Platt A, Long Q, Nordborg M.Gregor Mendel Institute, Austrian Academy of Sciences, Vienna, Austria. AbstractGenome-wide association studies (GWAS) are a standard approach for studying the genetics of natural variation. A major concern in GWAS is the need to account for the complicated dependence structure of the data, both between loci as well as between individuals. Mixed models have emerged as a general and flexible approach for correcting for population structure in GWAS. Here, we extend this linear mixed-model approach to carry out GWAS of correlated phenotypes, deriving a fully parameterized multi-trait mixed model (MTMM) that considers both the within-trait and between-trait variance components simultaneously for multiple traits. We apply this to data from a human cohort for correlated blood lipid traits from the Northern Finland Birth Cohort 1966 and show greatly increased power to detect pleiotropic loci that affect more than one blood lipid trait. We also apply this approach to an Arabidopsis thaliana data set for flowering measurements in two different locations, identifying loci whose effect depends on the environment. |
| PMID: 22902788 [PubMed - indexed for MEDLINE] | |
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| 20. | Nat Genet. 2012 Sep;44(9):1015-9. doi: 10.1038/ng.2368. Epub 2012 Aug 19.Evidence of widespread selection on standing variation in Europe at height-associated SNPs.Turchin MC, Chiang CW, Palmer CD, Sankararaman S, Reich D; Genetic Investigation of ANthropometric Traits (GIANT) Consortium, Hirschhorn JN.Division of Genetics, Children's Hospital Boston, Massachusetts, USA. AbstractStrong signatures of positive selection at newly arising genetic variants are well documented in humans(1-8), but this form of selection may not be widespread in recent human evolution(9). Because many human traits are highly polygenic and partly determined by common, ancient genetic variation, an alternative model for rapid genetic adaptation has been proposed: weak selection acting on many pre-existing (standing) genetic variants, or polygenic adaptation(10-12). By studying height, a classic polygenic trait, we demonstrate the first human signature of widespread selection on standing variation. We show that frequencies of alleles associated with increased height, both at known loci and genome wide, are systematically elevated in Northern Europeans compared with Southern Europeans (P < 4.3 × 10(-4)). This pattern mirrors intra-European height differences and is not confounded by ancestry or other ascertainment biases. The systematic frequency differences are consistent with the presence of widespread weak selection (selection coefficients ∼10(-3)-10(-5) per allele) rather than genetic drift alone (P < 10(-15)). |
| PMID: 22902787 [PubMed - indexed for MEDLINE] | |
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| 21. | Nature. 2012 Oct 4;490(7418):107-11. doi: 10.1038/nature11351. Epub 2012 Aug 19.Rapid induction of inflammatory lipid mediators by the inflammasome in vivo.von Moltke J, Trinidad NJ, Moayeri M, Kintzer AF, Wang SB, van Rooijen N, Brown CR, Krantz BA, Leppla SH, Gronert K, Vance RE.Department of Molecular and Cell Biology, Division of Immunology and Pathogenesis, University of California at Berkeley, Berkeley, California 94720, USA. AbstractDetection of microbial products by host inflammasomes is an important mechanism of innate immune surveillance. Inflammasomes activate the caspase-1 (CASP1) protease, which processes the cytokines interleukin (IL)-1β and IL-18, and initiates a lytic host cell death called pyroptosis. To identify novel CASP1 functions in vivo, we devised a strategy for cytosolic delivery of bacterial flagellin, a specific ligand for the NAIP5 (NLR family, apoptosis inhibitory protein 5)/NLRC4 (NLR family, CARD-domain-containing 4) inflammasome. Here we show that systemic inflammasome activation by flagellin leads to a loss of vascular fluid into the intestine and peritoneal cavity, resulting in rapid (less than 30 min) death in mice. This unexpected response depends on the inflammasome components NAIP5, NLRC4 and CASP1, but is independent of the production of IL-1β or IL-18. Instead, inflammasome activation results, within minutes, in an 'eicosanoid storm'--a pathological release of signalling lipids, including prostaglandins and leukotrienes, that rapidly initiate inflammation and vascular fluid loss. Mice deficient in cyclooxygenase-1, a critical enzyme in prostaglandin biosynthesis, are resistant to these rapid pathological effects of systemic inflammasome activation by either flagellin or anthrax lethal toxin. Inflammasome-dependent biosynthesis of eicosanoids is mediated by the activation of cytosolic phospholipase A(2) in resident peritoneal macrophages, which are specifically primed for the production of eicosanoids by high expression of eicosanoid biosynthetic enzymes. Our results therefore identify eicosanoids as a previously unrecognized cell-type-specific signalling output of the inflammasome with marked physiological consequences in vivo. |
| PMID: 22902502 [PubMed - indexed for MEDLINE] | |
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| 22. | Nature. 2012 Oct 4;490(7418):116-20. doi: 10.1038/nature11378. Epub 2012 Aug 12.Burkitt lymphoma pathogenesis and therapeutic targets from structural and functional genomics.Schmitz R, Young RM, Ceribelli M, Jhavar S, Xiao W, Zhang M, Wright G, Shaffer AL, Hodson DJ, Buras E, Liu X, Powell J, Yang Y, Xu W, Zhao H, Kohlhammer H, Rosenwald A, Kluin P, Müller-Hermelink HK, Ott G, Gascoyne RD, Connors JM, Rimsza LM, Campo E, Jaffe ES, Delabie J, Smeland EB, Ogwang MD, Reynolds SJ, Fisher RI, Braziel RM, Tubbs RR, Cook JR, Weisenburger DD, Chan WC, Pittaluga S, Wilson W, Waldmann TA, Rowe M, Mbulaiteye SM, Rickinson AB, Staudt LM.Metabolism Branch Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA. Comment in
AbstractBurkitt's lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. The normal germinal centre B cell is the presumed cell of origin for both BL and diffuse large B-cell lymphoma (DLBCL), yet gene expression analysis suggests that these malignancies may use different oncogenic pathways. BL is subdivided into a sporadic subtype that is diagnosed in developed countries, the Epstein-Barr-virus-associated endemic subtype, and an HIV-associated subtype, but it is unclear whether these subtypes use similar or divergent oncogenic mechanisms. Here we used high-throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways in BL that cooperate with MYC, the defining oncogene of this cancer. In 70% of sporadic BL cases, mutations affecting the transcription factor TCF3 (E2A) or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival phosphatidylinositol-3-OH kinase pathway in BL, in part by augmenting tonic B-cell receptor signalling. In 38% of sporadic BL cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. These findings suggest opportunities to improve therapy for patients with BL. |
| PMID: 22885699 [PubMed - indexed for MEDLINE] | |
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