What's new for 'JKB_daily1' in PubMed

This message contains My NCBI what's new results from the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).
Do not reply directly to this message.

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

Sent on Friday, 2014 August 15
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]))

View complete results in PubMed (results may change over time).

Edit saved search settings, or unsubscribe from these e-mail updates.

PubMed Results

Items 1 - 7 of 7

1.	Science. 2014 Aug 1;345(6196):1251343. doi: 10.1126/science.1251343. Mobile DNA in cancer. Extensive transduction of nonrepetitive DNA mediated by L1 retrotransposition in cancer genomes. Tubio JM1, Li Y1, Ju YS1, Martincorena I1, Cooke SL1, Tojo M2, Gundem G1, Pipinikas CP3, Zamora J1, Raine K1, Menzies A1, Roman-Garcia P1, Fullam A1, Gerstung M1, Shlien A1, Tarpey PS1, Papaemmanuil E1, Knappskog S4, Van Loo P5, Ramakrishna M1, Davies HR1, Marshall J1, Wedge DC1, Teague JW1, Butler AP1, Nik-Zainal S6, Alexandrov L1, Behjati S1, Yates LR1, Bolli N7, Mudie L1, Hardy C1, Martin S1, McLaren S1, O'Meara S1, Anderson E1, Maddison M1, Gamble S1; ICGC Breast Cancer Group; ICGC Bone Cancer Group; ICGC Prostate Cancer Group, Foster C8, Warren AY9, Whitaker H10, Brewer D11, Eeles R12, Cooper C11, Neal D10, Lynch AG10, Visakorpi T13, Isaacs WB14, van't Veer L15, Caldas C10, Desmedt C16, Sotiriou C16, Aparicio S17, Foekens JA18, Eyfjörd JE19, Lakhani SR20, Thomas G21, Myklebost O22, Span PN23, Børresen-Dale AL22, Richardson AL24, Van de Vijver M25, Vincent-Salomon A26, Van den Eynden GG27, Flanagan AM28, Futreal PA29, Janes SM3, Bova GS13, Stratton MR1, McDermott U1, Campbell PJ30. Collaborators: Provenzano E, van de Vijver M, Richardson AL, Purdie C, Pinder S, MacGrogan G, Vincent-Salomon A, Larsimont D, Grabau D, Sauer T, Garred Ø, Ehinger A, Van den Eynden GG, van Deurzen CH, Salgado R, Brock JE, Lakhani SR, Giri DD, Arnould L, Jacquemier J, Treilleux I, Caldas C, Chin SF, Fatima A, Thompson AM, Stenhouse A, Foekens J, Martens J, Sieuwerts A, Brinkman A, Stunnenberg H, Span PN, Sweep F, Desmedt C, Sotiriou C, Thomas G, Broeks A, Langerod A, Aparicio S, Simpson P, van 't Veer L, Eyfjörd JE, Hilmarsdottir H, Jonasson JG, Børresen-Dale AL, Lee MT, Wong BH, Tan BK, Hooijer GK, Cooper C, Eeles R, Wedge D, Van Loo P, Gundem G, Alexandrov L, Kremeyer B, Butler A, Lynch A, Edwards S, Camacho N, Massie C, Kote-Jarai Z, Dennis N, Merson S, Zamora J, Kay J, Corbishley C, Thomas S, Nik-Zainai S, O'Meara S, Matthews L, Clark J, Hurst R, Mithen R, Cooke S, Raine K, Jones D, Menzies A, Stebbings L, Hinton J, Teague J, McLaren S , Mudie L, Hardy C, Anderson E, Joseph O, Goody V, Robinson B, Maddison M, Gamble S, Greenman C, Berney D, Hazell S, Livni N, Fisher C, Ogden C, Kumar P, Thompson A, Woodhouse C, Nicol D, Mayer E, Dudderidge T, Shah N, Gnanapragasam V, Campbell P, Futreal A, Easton D, Warren AY, Foster C, Stratton M, Whitaker H, McDermott U, Brewer D, Neal D. Author information: 1Wellcome Trust Sanger Institute, Hinxton, Cambridgeshire, UK. 2Department of Physiology, School of Medicine-Center for Resesarch in Molecular Medicine and Chronic Diseases, Instituto de Investigaciones Sanitarias, University of Santiago de Compostela, Spain. 3Lungs for Living Research Centre, Rayne Institute, University College London (UCL), London, UK. 4Wellcome Trust Sanger Institute, Hinxton, Cambridgeshire, UK. Department of Clinical Science, University of Bergen, Bergen, Norway. Department of Oncology, Haukeland University Hospital, Bergen, Norway. 5Wellcome Trust Sanger Institute, Hinxton, Cambridgeshire, UK. Human Genome Laboratory, Department of Human Genetics, VIB and KU Leuven, Leuven, Belgium. 6Wellcome Trust Sanger Institute, Hinxton, Cambridgeshire, UK. Cambridge University Hospitals National Health Service (NHS) Foundation Trust, Cambridge, UK. 7Wellcome Trust Sanger Institute, Hinxton, Cambridgeshire, UK. Department of Haematology, University of Cambridge, Cambridge, UK. 8University of Liverpool and HCA Pathology Laboratories, London, UK. 9Cambridge University Hospitals National Health Service (NHS) Foundation Trust, Cambridge, UK. 10Cancer Research UK (CRUK) Cambridge Institute, University of Cambridge, Cambridge, UK. 11Institute of Cancer Research, Sutton, London, UK. University of East Anglia, Norwich, UK. 12Institute of Cancer Research, Sutton, London, UK. 13Institute of Biosciences and Medical Technology-BioMediTech, University of Tampere and Tampere University Hospital, Tampere, Finland. 14Johns Hopkins University, Baltimore, MD, USA. 15Netherlands Cancer Institute, Amsterdam, Netherlands. 16Breast Cancer Translational Research Laboratory, Institut Jules Bordet, Université Libre de Bruxelles, Brussels, Belgium. 17British Columbia Cancer Agency, Vancouver, Canada. 18Department of Medical Oncology, Erasmus Medical Center Cancer Institute, Erasmus University Medical Center, Rotterdam, Netherlands. 19Cancer Research Laboratory, University of Iceland, Reykjavik, Iceland. 20School of Medicine, University of Queensland, Brisbane, Australia. Pathology Queensland, Royal Brisbane and Women's Hospital, Brisbane, Australia. UQ Centre for Clinical Research, University of Queensland, Brisbane, Australia. 21Université Lyon 1, Institut National du Cancer (INCa)-Synergie, Lyon, France. 22Institute for Cancer Research, Oslo University Hospital, Oslo, Norway. 23Department of Radiation Oncology and Department of Laboratory Medicine, Radboud University Medical Center, Nijmegen, Netherlands. 24Dana-Farber Cancer Institute, Boston, MA, USA. 25Department of Pathology, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, Netherlands. 26Institut Bergonié, 229 cours de l'Argone, 33076 Bordeaux, France. Institut Curie, Department of Tumor Biology, 26 rue d'Ulm, 75248 Paris cédex 05, France. 27Translational Cancer Research Unit and Department of Pathology, GZA Hospitals, Antwerp, Belgium. 28Royal National Orthopaedic Hospital, Middlesex, UK. UCL Cancer Institute, University College London, London, UK. 29Wellcome Trust Sanger Institute, Hinxton, Cambridgeshire, UK. MD Anderson Cancer Center, Houston, TX, USA. 30Wellcome Trust Sanger Institute, Hinxton, Cambridgeshire, UK. Cambridge University Hospitals National Health Service (NHS) Foundation Trust, Cambridge, UK. Department of Haematology, University of Cambridge, Cambridge, UK. pc8@sanger.ac.uk. Abstract Long interspersed nuclear element-1 (L1) retrotransposons are mobile repetitive elements that are abundant in the human genome. L1 elements propagate through RNA intermediates. In the germ line, neighboring, nonrepetitive sequences are occasionally mobilized by the L1 machinery, a process called 3' transduction. Because 3' transductions are potentially mutagenic, we explored the extent to which they occur somatically during tumorigenesis. Studying cancer genomes from 244 patients, we found that tumors from 53% of the patients had somatic retrotranspositions, of which 24% were 3' transductions. Fingerprinting of donor L1s revealed that a handful of source L1 elements in a tumor can spawn from tens to hundreds of 3' transductions, which can themselves seed further retrotranspositions. The activity of individual L1 elements fluctuated during tumor evolution and correlated with L1 promoter hypomethylation. The 3' transductions disseminated genes, exons, and regulatory elements to new locations, most often to heterochromatic regions of the genome. Copyright © 2014, American Association for the Advancement of Science.
	PMID: 25082706 [PubMed - indexed for MEDLINE]
	Related citations

2.	Science. 2014 Aug 1;345(6196):578-82. doi: 10.1126/science.1256942. Epub 2014 Jul 17. Coinfection. Virus-helminth coinfection reveals a microbiota-independent mechanism of immunomodulation. Osborne LC1, Monticelli LA1, Nice TJ2, Sutherland TE3, Siracusa MC1, Hepworth MR4, Tomov VT5, Kobuley D1, Tran SV1, Bittinger K6, Bailey AG6, Laughlin AL6, Boucher JL7, Wherry EJ8, Bushman FD6, Allen JE3, Virgin HW2, Artis D9. Author information: 1Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. 2Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. 3Institute of Immunology and Infection Research, Centre for Immunity, Infection and Evolution, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3JT, UK. 4Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Department of Medicine, Division of Gastroenterology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. 5Department of Medicine, Division of Gastroenterology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. 6Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. 7Laboratoire de Chimie et Biochimie Pharmacologiques et Toxicologiques, Université Paris Descartes, Paris, France. 8Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. 9Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. dartis@mail.med.upenn.edu. Comment in Immunology. How helminths go viral. [Science. 2014] Immunology. How helminths go viral.Maizels RM, Gause WC. Science. 2014 Aug 1; 345(6196):517-8. Epub 2014 Jul 31. Abstract The mammalian intestine is colonized by beneficial commensal bacteria and is a site of infection by pathogens, including helminth parasites. Helminths induce potent immunomodulatory effects, but whether these effects are mediated by direct regulation of host immunity or indirectly through eliciting changes in the microbiota is unknown. We tested this in the context of virus-helminth coinfection. Helminth coinfection resulted in impaired antiviral immunity and was associated with changes in the microbiota and STAT6-dependent helminth-induced alternative activation of macrophages. Notably, helminth-induced impairment of antiviral immunity was evident in germ-free mice, but neutralization of Ym1, a chitinase-like molecule that is associated with alternatively activated macrophages, could partially restore antiviral immunity. These data indicate that helminth-induced immunomodulation occurs independently of changes in the microbiota but is dependent on Ym1. Copyright © 2014, American Association for the Advancement of Science.
	PMID: 25082704 [PubMed - indexed for MEDLINE]
	Related citations

3.	Science. 2014 Aug 1;345(6196):573-7. doi: 10.1126/science.1254517. Epub 2014 Jun 26. Coinfection. Helminth infection reactivates latent γ-herpesvirus via cytokine competition at a viral promoter. Reese TA1, Wakeman BS2, Choi HS3, Hufford MM4, Huang SC1, Zhang X1, Buck MD1, Jezewski A1, Kambal A1, Liu CY1, Goel G5, Murray PJ6, Xavier RJ5, Kaplan MH4, Renne R3, Speck SH2, Artyomov MN1, Pearce EJ1, Virgin HW7. Author information: 1Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. 2Emory University Vaccine Center, Atlanta, GA 30322, USA. 3Department of Molecular Genetics and Microbiology, University of Florida, Gainesville, FL 32610, USA. 4Departments of Pediatrics and Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN 46202, USA. 5Center for Computational and Integrative Biology and Gastrointestinal Unit, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA. 6Departments of Infectious Diseases and Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA. 7Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. virgin@wustl.edu. Comment in Immunology. How helminths go viral. [Science. 2014] Immunology. How helminths go viral.Maizels RM, Gause WC. Science. 2014 Aug 1; 345(6196):517-8. Epub 2014 Jul 31. Abstract Mammals are coinfected by multiple pathogens that interact through unknown mechanisms. We found that helminth infection, characterized by the induction of the cytokine interleukin-4 (IL-4) and the activation of the transcription factor Stat6, reactivated murine γ-herpesvirus infection in vivo. IL-4 promoted viral replication and blocked the antiviral effects of interferon-γ (IFNγ) by inducing Stat6 binding to the promoter for an important viral transcriptional transactivator. IL-4 also reactivated human Kaposi's sarcoma-associated herpesvirus from latency in cultured cells. Exogenous IL-4 plus blockade of IFNγ reactivated latent murine γ-herpesvirus infection in vivo, suggesting a "two-signal" model for viral reactivation. Thus, chronic herpesvirus infection, a component of the mammalian virome, is regulated by the counterpoised actions of multiple cytokines on viral promoters that have evolved to sense host immune status. Copyright © 2014, American Association for the Advancement of Science.
	PMID: 24968940 [PubMed - indexed for MEDLINE]
	Related citations

4.	Nature. 2014 Jun 26;510(7506):473. doi: 10.1038/510473d. Embryo screening: update German view of genetic testing. Propping P, Schott H. Author information: University of Bonn, Germany.
	PMID: 24965640 [PubMed - indexed for MEDLINE]
	Related citations

5.	Nature. 2014 Jun 26;510(7506):473. doi: 10.1038/510473b. Ancient cultures: maize is not a clue to Puerto Rican origins. Pagán-Jiménez JR1, Rodríguez-Ramos R2, Oliver JR3. Author information: 1Leiden University, the Netherlands. 2University of Puerto Rico, Utuado, Puerto Rico. 3University College London, UK.
	PMID: 24965639 [PubMed - indexed for MEDLINE]
	Related citations

6.	Nature. 2014 Apr 24;508(7497):451-3. Medical genomics: Gather and use genetic data in health care. Ginsburg G.
	PMID: 24765668 [PubMed - indexed for MEDLINE]
	Related citations

7.	Nature. 2014 Apr 24;508(7497):488-93. doi: 10.1038/nature13151. Origins and functional evolution of Y chromosomes across mammals. Cortez D1, Marin R1, Toledo-Flores D2, Froidevaux L3, Liechti A3, Waters PD4, Grützner F2, Kaessmann H1. Author information: 11] Center for Integrative Genomics, University of Lausanne, 1015 Lausanne, Switzerland [2] Swiss Institute of Bioinformatics, 1015 Lausanne, Switzerland. 2The Robinson Research Institute, School of Molecular and Biomedical Science, University of Adelaide, Adelaide, South Australia 5005, Australia. 3Center for Integrative Genomics, University of Lausanne, 1015 Lausanne, Switzerland. 4School of Biotechnology and Biomolecular Sciences, UNSW Australia, Sydney, New South Wales 2052, Australia. Comment in Genetics: The vital Y chromosome. [Nature. 2014] Genetics: The vital Y chromosome.Clark AG. Nature. 2014 Apr 24; 508(7497):463-5. Abstract Y chromosomes underlie sex determination in mammals, but their repeat-rich nature has hampered sequencing and associated evolutionary studies. Here we trace Y evolution across 15 representative mammals on the basis of high-throughput genome and transcriptome sequencing. We uncover three independent sex chromosome originations in mammals and birds (the outgroup). The original placental and marsupial (therian) Y, containing the sex-determining gene SRY, emerged in the therian ancestor approximately 180 million years ago, in parallel with the first of five monotreme Y chromosomes, carrying the probable sex-determining gene AMH. The avian W chromosome arose approximately 140 million years ago in the bird ancestor. The small Y/W gene repertoires, enriched in regulatory functions, were rapidly defined following stratification (recombination arrest) and erosion events and have remained considerably stable. Despite expression decreases in therians, Y/W genes show notable conservation of proto-sex chromosome expression patterns, although various Y genes evolved testis-specificities through differential regulatory decay. Thus, although some genes evolved novel functions through spatial/temporal expression shifts, most Y genes probably endured, at least initially, because of dosage constraints.
	PMID: 24759410 [PubMed - indexed for MEDLINE]
	Related citations