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 Tuesday, 2014 September 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]))

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 - 5 of 5

1.	Nature. 2014 Aug 7;512(7512):35-6. doi: 10.1038/nature13647. Epub 2014 Jul 20. HIV: Early treatment may not be early enough. Deng K1, Siliciano RF2. Author information: 1Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. 21] Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. [2] Howard Hughes Medical Institute, Baltimore. Comment on Rapid seeding of the viral reservoir prior to SIV viraemia in rhesus monkeys. [Nature. 2014] Rapid seeding of the viral reservoir prior to SIV viraemia in rhesus monkeys.Whitney JB, Hill AL, Sanisetty S, Penaloza-MacMaster P, Liu J, Shetty M, Parenteau L, Cabral C, Shields J, Blackmore S, et al. Nature. 2014 Aug 7; 512(7512):74-7. Epub 2014 Jul 20.
	PMID: 25043038 [PubMed - indexed for MEDLINE]
	Related citations

2.	Nature. 2014 Aug 7;512(7512):69-73. doi: 10.1038/nature13322. Epub 2014 Jun 29. Negative regulation of the NLRP3 inflammasome by A20 protects against arthritis. Vande Walle L1, Van Opdenbosch N1, Jacques P2, Fossoul A1, Verheugen E2, Vogel P3, Beyaert R4, Elewaut D2, Kanneganti TD3, van Loo G5, Lamkanfi M6. Author information: 11] Department of Medical Protein Research, VIB, Ghent B-9000, Belgium [2] Department of Biochemistry, Ghent University, Ghent B-9000, Belgium. 2Department of Rheumatology, Ghent University, Ghent B-9000, Belgium. 3Department of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA. 41] Inflammation Research Center, VIB, Ghent B-9052, Belgium [2] Department of Biomedical Molecular Biology, Ghent University, Ghent B-9052, Belgium. 51] Inflammation Research Center, VIB, Ghent B-9052, Belgium [2] Department of Biomedical Molecular Biology, Ghent University, Ghent B-9052, Belgium [3]. 61] Department of Medical Protein Research, VIB, Ghent B-9000, Belgium [2] Department of Biochemistry, Ghent University, Ghent B-9000, Belgium [3]. Comment in Experimental arthritis: Inflammasome-driven arthritis: a new model of RA? [Nat Rev Rheumatol. 2014] Experimental arthritis: Inflammasome-driven arthritis: a new model of RA?Onuora S. Nat Rev Rheumatol. 2014 Aug; 10(8):445. Epub 2014 Jul 15. Abstract Rheumatoid arthritis is a chronic autoinflammatory disease that affects 1-2% of the world's population and is characterized by widespread joint inflammation. Interleukin-1 is an important mediator of cartilage destruction in rheumatic diseases, but our understanding of the upstream mechanisms leading to production of interleukin-1β in rheumatoid arthritis is limited by the absence of suitable mouse models of the disease in which inflammasomes contribute to pathology. Myeloid-cell-specific deletion of the rheumatoid arthritis susceptibility gene A20/Tnfaip3 in mice (A20(myel-KO) mice) triggers a spontaneous erosive polyarthritis that resembles rheumatoid arthritis in patients. Rheumatoid arthritis in A20(myel-KO) mice is not rescued by deletion of tumour necrosis factor receptor 1 (ref. 2). Here we show, however, that it crucially relies on the Nlrp3 inflammasome and interleukin-1 receptor signalling. Macrophages lacking A20 have increased basal and lipopolysaccharide-induced expression levels of the inflammasome adaptor Nlrp3 and proIL-1β. As a result, A20-deficiency in macrophages significantly enhances Nlrp3 inflammasome-mediated caspase-1 activation, pyroptosis and interleukin-1β secretion by soluble and crystalline Nlrp3 stimuli. In contrast, activation of the Nlrc4 and AIM2 inflammasomes is not altered. Importantly, increased Nlrp3 inflammasome activation contributes to the pathology of rheumatoid arthritis in vivo, because deletion of Nlrp3, caspase-1 and the interleukin-1 receptor markedly protects against rheumatoid-arthritis-associated inflammation and cartilage destruction in A20(myel-KO) mice. These results reveal A20 as a novel negative regulator of Nlrp3 inflammasome activation, and describe A20(myel-KO) mice as the first experimental model to study the role of inflammasomes in the pathology of rheumatoid arthritis. PMCID: PMC4126806 [Available on 2015/2/7]
	PMID: 25043000 [PubMed - indexed for MEDLINE]
	Related citations

3.	Nature. 2014 Aug 7;512(7512):74-7. doi: 10.1038/nature13594. Epub 2014 Jul 20. Rapid seeding of the viral reservoir prior to SIV viraemia in rhesus monkeys. Whitney JB1, Hill AL2, Sanisetty S3, Penaloza-MacMaster P3, Liu J3, Shetty M3, Parenteau L3, Cabral C3, Shields J3, Blackmore S3, Smith JY3, Brinkman AL3, Peter LE3, Mathew SI3, Smith KM3, Borducchi EN3, Rosenbloom DI2, Lewis MG4, Hattersley J5, Li B5, Hesselgesser J5, Geleziunas R5, Robb ML6, Kim JH6, Michael NL6, Barouch DH1. Author information: 11] Center for Virology and Vaccine Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA [2] Ragon Institute of MGH, MIT and Harvard, Cambridge, Massachusetts 02139, USA. 2Program for Evolutionary Dynamics, Harvard University, Cambridge, Massachusetts 02138 USA. 3Center for Virology and Vaccine Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA. 4Bioqual, Rockville, Maryland 20852, USA. 5Gilead Sciences, Foster City, California 94404, USA. 6US Military HIV Research Program, Walter Reed Army Institute of Research, Silver Spring, Maryland 20910, USA. Comment in HIV: Early treatment may not be early enough. [Nature. 2014] HIV: Early treatment may not be early enough.Deng K, Siliciano RF. Nature. 2014 Aug 7; 512(7512):35-6. Epub 2014 Jul 20. Abstract The viral reservoir represents a critical challenge for human immunodeficiency virus type 1 (HIV-1) eradication strategies. However, it remains unclear when and where the viral reservoir is seeded during acute infection and the extent to which it is susceptible to early antiretroviral therapy (ART). Here we show that the viral reservoir is seeded rapidly after mucosal simian immunodeficiency virus (SIV) infection of rhesus monkeys and before systemic viraemia. We initiated suppressive ART in groups of monkeys on days 3, 7, 10 and 14 after intrarectal SIVMAC251 infection. Treatment with ART on day 3 blocked the emergence of viral RNA and proviral DNA in peripheral blood and also substantially reduced levels of proviral DNA in lymph nodes and gastrointestinal mucosa as compared with treatment at later time points. In addition, treatment on day 3 abrogated the induction of SIV-specific humoral and cellular immune responses. Nevertheless, after discontinuation of ART following 24 weeks of fully suppressive therapy, virus rebounded in all animals, although the monkeys that were treated on day 3 exhibited a delayed viral rebound as compared with those treated on days 7, 10 and 14. The time to viral rebound correlated with total viraemia during acute infection and with proviral DNA at the time of ART discontinuation. These data demonstrate that the viral reservoir is seeded rapidly after intrarectal SIV infection of rhesus monkeys, during the 'eclipse' phase, and before detectable viraemia. This strikingly early seeding of the refractory viral reservoir raises important new challenges for HIV-1 eradication strategies. PMCID: PMC4126858 [Available on 2015/2/7]
	PMID: 25042999 [PubMed - indexed for MEDLINE]
	Related citations

4.	J Leukoc Biol. 2014 Aug;96(2):167-83. doi: 10.1189/jlb.6HI0313-169R. Epub 2014 Apr 10. Analysis of the transcriptional networks underpinning the activation of murine macrophages by inflammatory mediators. Raza S1, Barnett MW1, Barnett-Itzhaki Z2, Amit I2, Hume DA1, Freeman TC3. Author information: 1The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Scotland, United Kingdom; and. 2Department of Immunology, Weizmann Institute of Science, Rehovot, Israel. 3The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Scotland, United Kingdom; and tom.freeman@roslin.ed.ac.uk. Comment in Editorial: you give me fever: transcriptional responses to LPS. [J Leukoc Biol. 2014] Editorial: you give me fever: transcriptional responses to LPS.Bowdish DM. J Leukoc Biol. 2014 Aug; 96(2):161-3. Abstract Macrophages respond to the TLR4 agonist LPS with a sequential transcriptional cascade controlled by a complex regulatory network of signaling pathways and transcription factors. At least two distinct pathways are currently known to be engaged by TLR4 and are distinguished by their dependence on the adaptor molecule MyD88. We have used gene expression microarrays to define the effects of each of three variables--LPS dose, LPS versus IFN-β and -γ, and genetic background--on the transcriptional response of mouse BMDMs. Analysis of correlation networks generated from the data has identified subnetworks or modules within the macrophage transcriptional network that are activated selectively by these variables. We have identified mouse strain-specific signatures, including a module enriched for SLE susceptibility candidates. In the modules of genes unique to different treatments, we found a module of genes induced by type-I IFN but not by LPS treatment, suggesting another layer of complexity in the LPS-TLR4 signaling feedback control. We also observe that the activation of the complement system, in common with the known activation of MHC class 2 genes, is reliant on IFN-γ signaling. Taken together, these data further highlight the exquisite nature of the regulatory systems that control macrophage activation, their likely relevance to disease resistance/susceptibility, and the appropriate response of these cells to proinflammatory stimuli. © 2014 Society for Leukocyte Biology.
	PMID: 24721704 [PubMed - indexed for MEDLINE]
	Related citations

5.	J Leukoc Biol. 2014 Aug;96(2):265-74. doi: 10.1189/jlb.2A0114-006R. Epub 2014 Mar 20. Pleiotropic effects of extended blockade of CSF1R signaling in adult mice. Sauter KA1, Pridans C1, Sehgal A1, Tsai YT2, Bradford BM1, Raza S1, Moffat L1, Gow DJ1, Beard PM1, Mabbott NA1, Smith LB2, Hume DA3. Author information: 1The Roslin Institute and Royal (Dick) School of Veterinary Studies and. 2Medical Research Council Centre for Reproductive Health, The Queen's Medical Research Institute, University of Edinburgh, Scotland, United Kingdom. 3The Roslin Institute and Royal (Dick) School of Veterinary Studies and david.hume@roslin.ed.ac.uk. Abstract We investigated the role of CSF1R signaling in adult mice using prolonged treatment with anti-CSF1R antibody. Mutation of the CSF1 gene in the op/op mouse produces numerous developmental abnormalities. Mutation of the CSF1R has an even more penetrant phenotype, including perinatal lethality, because of the existence of a second ligand, IL-34. These effects on development provide limited insight into functions of CSF1R signaling in adult homeostasis. The carcass weight and weight of several organs (spleen, kidney, and liver) were reduced in the treated mice, but overall body weight gain was increased. Despite the complete loss of Kupffer cells, there was no effect on liver gene expression. The treatment ablated OCL, increased bone density and trabecular volume, and prevented the decline in bone mass seen in female mice with age. The op/op mouse has a deficiency in pancreatic β cells and in Paneth cells in the gut wall. Only the latter was reproduced by the antibody treatment and was associated with increased goblet cell number but no change in villus architecture. Male op/op mice are infertile as a result of testosterone insufficiency. Anti-CSF1R treatment ablated interstitial macrophages in the testis, but there was no sustained effect on testosterone or LH. The results indicate an ongoing requirement for CSF1R signaling in macrophage and OCL homeostasis but indicate that most effects of CSF1 and CSF1R mutations are due to effects on development. © 2014 Society for Leukocyte Biology.
	PMID: 24652541 [PubMed - indexed for MEDLINE]
	Related citations

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 Saturday, 2014 September 27
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 - 4 of 4

1.	Nature. 2014 Sep 11;513(7517):195-201. doi: 10.1038/nature13679. Gibbon genome and the fast karyotype evolution of small apes. Carbone L1, Harris RA2, Gnerre S3, Veeramah KR4, Lorente-Galdos B5, Huddleston J6, Meyer TJ7, Herrero J8, Roos C9, Aken B10, Anaclerio F11, Archidiacono N11, Baker C12, Barrell D10, Batzer MA13, Beal K14, Blancher A15, Bohrson CL16, Brameier M9, Campbell MS17, Capozzi O11, Casola C18, Chiatante G11, Cree A19, Damert A20, de Jong PJ21, Dumas L22, Fernandez-Callejo M5, Flicek P14, Fuchs NV23, Gut I24, Gut M24, Hahn MW25, Hernandez-Rodriguez J5, Hillier LW26, Hubley R27, Ianc B20, Izsvák Z23, Jablonski NG28, Johnstone LM29, Karimpour-Fard A22, Konkel MK13, Kostka D30, Lazar NH31, Lee SL19, Lewis LR19, Liu Y19, Locke DP32, Mallick S33, Mendez FL34, Muffato M14, Nazareth LV19, Nevonen KA35, O'Bleness M22, Ochis C20, Odom DT36, Pollard KS37, Quilez J5, Reich D33, Rocchi M11, Schumann GG38, Searle S39, Sikela JM22, Skollar G40, Smit A26, Sonmez K41, ten Hallers B42, Terhune E35, Thomas GW25, Ullmer B43, Ventura M11, Walker JA13, Wall JD44, Walter L9, Ward MC45, Wheelan SJ16, Whelan CW46, White S39, Wilhelm LJ35, Woerner AE29, Yandell M17, Zhu B42, Hammer MF29, Marques-Bonet T47, Eichler EE6, Fulton L26, Fronick C26, Muzny DM19, Warren WC26, Worley KC19, Rogers J19, Wilson RK26, Gibbs RA19. Author information: 11] Oregon Health &Science University, Department of Behavioral Neuroscience, 3181 SW Sam Jackson Park Road Portland, Oregon 97239, USA. [2] Oregon National Primate Research Center, Division of Neuroscience, 505 NW 185th Avenue, Beaverton, Oregon 97006, USA. [3] Oregon Health &Science University, Department of Molecular &Medical Genetics, 3181 SW Sam Jackson Park Road, Portland, Oregon 97239, USA. [4] Oregon Health &Science University, Bioinformatics and Computational Biology Division, Department of Medical Informatics &Clinical Epidemiology, 3181 SW Sam Jackson Park Road, Portland, Oregon 97239, USA. 2Baylor College of Medicine, Department of Molecular and Human Genetics, One Baylor Plaza, Houston, Texas 77030, USA. 3Nabsys, 60 Clifford Street, Providence, Rhode Island 02903, USA. 41] University of Arizona, ARL Division of Biotechnology, Tucson, Arizona 85721, USA. [2] Stony Brook University, Department of Ecology and Evolution, Stony Brook, New York 11790, USA. 5IBE, Institut de Biologia Evolutiva (UPF-CSIC), Universitat Pompeu Fabra, PRBB, Doctor Aiguader, 88, 08003 Barcelona, Spain. 61] Department of Genome Sciences, University of Washington School of Medicine, Seattle, Washington 98195, USA. [2] Howard Hughes Medical Institute, 1705 NE Pacific Street, Seattle, Washington 98195, USA. 7Oregon Health &Science University, Department of Behavioral Neuroscience, 3181 SW Sam Jackson Park Road Portland, Oregon 97239, USA. 81] European Molecular Biology Laboratory, European Bioinformatics Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SD, UK. [2] The Genome Analysis Centre, Norwich Research Park, Norwich NR4 7UH, UK. [3] Bill Lyons Informatics Center, UCL Cancer Institute, University College London, London WC1E 6DD, UK (J.He); Seven Bridges Genomics, Cambridge, Massachusetts 02138, USA (D.P.L.); Department of Genetics, Stanford University School of Medicine, Stanford, California 94305, USA (F.L.M.); BioNano Genomics, San Diego, California 92121, USA (B.t.H.); University of Chicago, Department of Human Genetics, Chicago, Illinois 60637, USA (M.C.W.); Stanley Center for Psychiatric Research, Broad Institute, Cambridge, Massachusetts 02138, USA (C.W.W.); The CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China (B.Z.). 9Leibniz Institute for Primate Research, Gene Bank of Primates, German Primate Center, Göttingen 37077, Germany. 101] European Molecular Biology Laboratory, European Bioinformatics Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SD, UK. [2] European Bioinformatics Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SD, UK. 11University of Bari, Department of Biology, Via Orabona 4, 70125, Bari, Italy. 12Department of Genome Sciences, University of Washington School of Medicine, Seattle, Washington 98195, USA. 13Louisiana State University, Department of Biological Sciences, Baton Rouge, Louisiana 70803, USA. 14European Molecular Biology Laboratory, European Bioinformatics Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SD, UK. 15University of Paul Sabatier, Toulouse 31062, France. 16The Johns Hopkins University School of Medicine, Department of Oncology, Division of Biostatistics and Bioinformatics, Baltimore, Maryland 21205, USA. 17University of Utah, Salt Lake City, Utah 84112, USA. 18Texas A&M University, Department of Ecosystem Science and Management, College Station, Texas 77843, USA. 19Human Genome Sequencing Center, Department of Molecular and Human Genetics, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA. 20Babes-Bolyai-University, Institute for Interdisciplinary Research in Bio-Nano-Sciences, Molecular Biology Center, Cluj-Napoca 400084, Romania. 21Children's Hospital Oakland Research Institute, BACPAC Resources, Oakland, California 94609, USA. 22University of Colorado School of Medicine, Department of Biochemistry and Molecular Genetics, Aurora, Colorado 80045, USA. 23Max Delbrück Center for Molecular Medicine, Berlin 13125, Germany. 24Centro Nacional de Análisis Genómico (CNAG), Parc Científic de Barcelona, Barcelona 08028, Spain. 25Indiana University, School of Informatics and Computing, Bloomington, Indiana 47408, USA. 26The Genome Center at Washington University, Washington University School of Medicine, 4444 Forest Park Avenue, Saint Louis, Missouri 63108, USA. 27Institute for Systems Biology, Seattle, Washington 98109-5234, USA. 28The Pennsylvania State University, Department of Anthropology, University Park, Pennsylvania 16802, USA. 29University of Arizona, ARL Division of Biotechnology, Tucson, Arizona 85721, USA. 30University of Pittsburgh School of Medicine, Department of Developmental Biology, Department of Computational and Systems Biology, Pittsburg, Pennsylvania 15261, USA. 31Oregon Health &Science University, Bioinformatics and Computational Biology Division, Department of Medical Informatics &Clinical Epidemiology, 3181 SW Sam Jackson Park Road, Portland, Oregon 97239, USA. 321] The Genome Center at Washington University, Washington University School of Medicine, 4444 Forest Park Avenue, Saint Louis, Missouri 63108, USA. [2] Bill Lyons Informatics Center, UCL Cancer Institute, University College London, London WC1E 6DD, UK (J.He); Seven Bridges Genomics, Cambridge, Massachusetts 02138, USA (D.P.L.); Department of Genetics, Stanford University School of Medicine, Stanford, California 94305, USA (F.L.M.); BioNano Genomics, San Diego, California 92121, USA (B.t.H.); University of Chicago, Department of Human Genetics, Chicago, Illinois 60637, USA (M.C.W.); Stanley Center for Psychiatric Research, Broad Institute, Cambridge, Massachusetts 02138, USA (C.W.W.); The CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China (B.Z.). 33Harvard Medical School, Department of Genetics, Boston, Massachusetts 02115, USA. 341] University of Arizona, ARL Division of Biotechnology, Tucson, Arizona 85721, USA. [2] Bill Lyons Informatics Center, UCL Cancer Institute, University College London, London WC1E 6DD, UK (J.He); Seven Bridges Genomics, Cambridge, Massachusetts 02138, USA (D.P.L.); Department of Genetics, Stanford University School of Medicine, Stanford, California 94305, USA (F.L.M.); BioNano Genomics, San Diego, California 92121, USA (B.t.H.); University of Chicago, Department of Human Genetics, Chicago, Illinois 60637, USA (M.C.W.); Stanley Center for Psychiatric Research, Broad Institute, Cambridge, Massachusetts 02138, USA (C.W.W.); The CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China (B.Z.). 35Oregon National Primate Research Center, Division of Neuroscience, 505 NW 185th Avenue, Beaverton, Oregon 97006, USA. 361] European Bioinformatics Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SD, UK. [2] University of Cambridge, Cancer Research UK-Cambridge Institute, Cambridge CB2 0RE, UK. 371] University of California, Gladstone Institutes, San Francisco, California 94158-226, USA. [2] Institute for Human Genetics, University of California, San Francisco, California 94143-0794, USA. [3] Division of Biostatistics, University of California, San Francisco, California 94143-0794, USA. 38Paul Ehrlich Institute, Division of Medical Biotechnology, 63225 Langen, Germany. 39European Bioinformatics Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SD, UK. 40Gibbon Conservation Center, 19100 Esguerra Rd, Santa Clarita, California 91350, USA. 411] Oregon Health &Science University, Bioinformatics and Computational Biology Division, Department of Medical Informatics &Clinical Epidemiology, 3181 SW Sam Jackson Park Road, Portland, Oregon 97239, USA. [2] Oregon Health &Science University, Center for Spoken Language Understanding, Institute on Development and Disability, Portland, Oregon 97239, USA. 421] Children's Hospital Oakland Research Institute, BACPAC Resources, Oakland, California 94609, USA. [2] Bill Lyons Informatics Center, UCL Cancer Institute, University College London, London WC1E 6DD, UK (J.He); Seven Bridges Genomics, Cambridge, Massachusetts 02138, USA (D.P.L.); Department of Genetics, Stanford University School of Medicine, Stanford, California 94305, USA (F.L.M.); BioNano Genomics, San Diego, California 92121, USA (B.t.H.); University of Chicago, Department of Human Genetics, Chicago, Illinois 60637, USA (M.C.W.); Stanley Center for Psychiatric Research, Broad Institute, Cambridge, Massachusetts 02138, USA (C.W.W.); The CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China (B.Z.). 43Louisiana State University, School of Electrical Engineering and Computer Science, Baton Rouge, Louisiana 70803, USA. 441] Institute for Human Genetics, University of California, San Francisco, California 94143-0794, USA. [2] Division of Biostatistics, University of California, San Francisco, California 94143-0794, USA. 451] University of Cambridge, Cancer Research UK-Cambridge Institute, Cambridge CB2 0RE, UK. [2] Bill Lyons Informatics Center, UCL Cancer Institute, University College London, London WC1E 6DD, UK (J.He); Seven Bridges Genomics, Cambridge, Massachusetts 02138, USA (D.P.L.); Department of Genetics, Stanford University School of Medicine, Stanford, California 94305, USA (F.L.M.); BioNano Genomics, San Diego, California 92121, USA (B.t.H.); University of Chicago, Department of Human Genetics, Chicago, Illinois 60637, USA (M.C.W.); Stanley Center for Psychiatric Research, Broad Institute, Cambridge, Massachusetts 02138, USA (C.W.W.); The CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China (B.Z.). 461] Oregon Health &Science University, Center for Spoken Language Understanding, Institute on Development and Disability, Portland, Oregon 97239, USA. [2] Bill Lyons Informatics Center, UCL Cancer Institute, University College London, London WC1E 6DD, UK (J.He); Seven Bridges Genomics, Cambridge, Massachusetts 02138, USA (D.P.L.); Department of Genetics, Stanford University School of Medicine, Stanford, California 94305, USA (F.L.M.); BioNano Genomics, San Diego, California 92121, USA (B.t.H.); University of Chicago, Department of Human Genetics, Chicago, Illinois 60637, USA (M.C.W.); Stanley Center for Psychiatric Research, Broad Institute, Cambridge, Massachusetts 02138, USA (C.W.W.); The CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China (B.Z.). 471] IBE, Institut de Biologia Evolutiva (UPF-CSIC), Universitat Pompeu Fabra, PRBB, Doctor Aiguader, 88, 08003 Barcelona, Spain. [2] Centro Nacional de Análisis Genómico (CNAG), Parc Científic de Barcelona, Barcelona 08028, Spain. Comment in Genomics: Something to swing about. [Nature. 2014] Genomics: Something to swing about.O'Neill MJ, O'Neill RJ. Nature. 2014 Sep 11; 513(7517):174-5. Abstract Gibbons are small arboreal apes that display an accelerated rate of evolutionary chromosomal rearrangement and occupy a key node in the primate phylogeny between Old World monkeys and great apes. Here we present the assembly and analysis of a northern white-cheeked gibbon (Nomascus leucogenys) genome. We describe the propensity for a gibbon-specific retrotransposon (LAVA) to insert into chromosome segregation genes and alter transcription by providing a premature termination site, suggesting a possible molecular mechanism for the genome plasticity of the gibbon lineage. We further show that the gibbon genera (Nomascus, Hylobates, Hoolock and Symphalangus) experienced a near-instantaneous radiation ∼5 million years ago, coincident with major geographical changes in southeast Asia that caused cycles of habitat compression and expansion. Finally, we identify signatures of positive selection in genes important for forelimb development (TBX5) and connective tissues (COL1A1) that may have been involved in the adaptation of gibbons to their arboreal habitat.
	PMID: 25209798 [PubMed - indexed for MEDLINE]
	Related citations

2.	Nature. 2014 Sep 11;513(7517):S8-9. doi: 10.1038/513S8a. Personalized medicine: Special treatment. Eisenstein M.
	PMID: 25208073 [PubMed - indexed for MEDLINE]
	Related citations

3.	Science. 2014 Aug 29;345(6200):1005-6. doi: 10.1126/science.1259452. AIDS/HIV. Rekindled HIV infection. Siliciano JD1, Siliciano RF2. Author information: 1Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA. 2Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Howard Hughes Medical Institute, Baltimore, MD, USA. rsiliciano@jhmi.edu.
	PMID: 25170139 [PubMed - indexed for MEDLINE]
	Related citations

4.	Nature. 2014 Sep 11;513(7517):237-41. doi: 10.1038/nature13449. Epub 2014 Jun 11. Innate immune sensing of bacterial modifications of Rho GTPases by the Pyrin inflammasome. Xu H1, Yang J2, Gao W3, Li L3, Li P3, Zhang L3, Gong YN3, Peng X3, Xi JJ4, Chen S3, Wang F3, Shao F5. Author information: 11] National Institute of Biological Sciences, Beijing 102206, China [2]. 21] National Institute of Biological Sciences, Beijing 102206, China [2] National Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China [3]. 3National Institute of Biological Sciences, Beijing 102206, China. 4Department of Biomedical Engineering, College of Engineering, Peking University, Beijing 100871, China. 51] National Institute of Biological Sciences, Beijing 102206, China [2] National Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China [3] National Institute of Biological Sciences, Beijing, Collaborative Innovation Center for Cancer Medicine, Beijing 102206, China. Abstract Cytosolic inflammasome complexes mediated by a pattern recognition receptor (PRR) defend against pathogen infection by activating caspase 1. Pyrin, a candidate PRR, can bind to the inflammasome adaptor ASC to form a caspase 1-activating complex. Mutations in the Pyrin-encoding gene, MEFV, cause a human autoinflammatory disease known as familial Mediterranean fever. Despite important roles in immunity and disease, the physiological function of Pyrin remains unknown. Here we show that Pyrin mediates caspase 1 inflammasome activation in response to Rho-glucosylation activity of cytotoxin TcdB, a major virulence factor of Clostridium difficile, which causes most cases of nosocomial diarrhoea. The glucosyltransferase-inactive TcdB mutant loses the inflammasome-stimulating activity. Other Rho-inactivating toxins, including FIC-domain adenylyltransferases (Vibrio parahaemolyticus VopS and Histophilus somni IbpA) and Clostridium botulinum ADP-ribosylating C3 toxin, can also biochemically activate the Pyrin inflammasome in their enzymatic activity-dependent manner. These toxins all target the Rho subfamily and modify a switch-I residue. We further demonstrate that Burkholderia cenocepacia inactivates RHOA by deamidating Asn 41, also in the switch-I region, and thereby triggers Pyrin inflammasome activation, both of which require the bacterial type VI secretion system (T6SS). Loss of the Pyrin inflammasome causes elevated intra-macrophage growth of B. cenocepacia and diminished lung inflammation in mice. Thus, Pyrin functions to sense pathogen modification and inactivation of Rho GTPases, representing a new paradigm in mammalian innate immunity.
	PMID: 24919149 [PubMed - indexed for MEDLINE]
	Related citations

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 Thursday, 2014 September 25
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 - 3 of 3

1.	Nature. 2014 Sep 4;513(7516):40-1. doi: 10.1038/nature13659. Epub 2014 Aug 20. Biological techniques: Edit the genome to understand it. Urnov FD. Comment on Saturation editing of genomic regions by multiplex homology-directed repair. [Nature. 2014] Saturation editing of genomic regions by multiplex homology-directed repair.Findlay GM, Boyle EA, Hause RJ, Klein JC, Shendure J. Nature. 2014 Sep 4; 513(7516):120-3.
	PMID: 25141180 [PubMed - indexed for MEDLINE]
	Related citations

2.	Nature. 2014 Sep 4;513(7516):120-3. doi: 10.1038/nature13695. Saturation editing of genomic regions by multiplex homology-directed repair. Findlay GM1, Boyle EA1, Hause RJ2, Klein JC2, Shendure J2. Author information: 11] Department of Genome Sciences, University of Washington, Seattle, Washington 98195, USA [2]. 2Department of Genome Sciences, University of Washington, Seattle, Washington 98195, USA. Comment in Biological techniques: Edit the genome to understand it. [Nature. 2014] Biological techniques: Edit the genome to understand it.Urnov FD. Nature. 2014 Sep 4; 513(7516):40-1. Epub 2014 Aug 20. Abstract Saturation mutagenesis--coupled to an appropriate biological assay--represents a fundamental means of achieving a high-resolution understanding of regulatory and protein-coding nucleic acid sequences of interest. However, mutagenized sequences introduced in trans on episomes or via random or "safe-harbour" integration fail to capture the native context of the endogenous chromosomal locus. This shortcoming markedly limits the interpretability of the resulting measurements of mutational impact. Here, we couple CRISPR/Cas9 RNA-guided cleavage with multiplex homology-directed repair using a complex library of donor templates to demonstrate saturation editing of genomic regions. In exon 18 of BRCA1, we replace a six-base-pair (bp) genomic region with all possible hexamers, or the full exon with all possible single nucleotide variants (SNVs), and measure strong effects on transcript abundance attributable to nonsense-mediated decay and exonic splicing elements. We similarly perform saturation genome editing of a well-conserved coding region of an essential gene, DBR1, and measure relative effects on growth that correlate with functional impact. Measurement of the functional consequences of large numbers of mutations with saturation genome editing will potentially facilitate high-resolution functional dissection of both cis-regulatory elements and trans-acting factors, as well as the interpretation of variants of uncertain significance observed in clinical sequencing. PMCID: PMC4156553 [Available on 2015/3/4]
	PMID: 25141179 [PubMed - indexed for MEDLINE]
	Related citations

3.	Nature. 2014 Sep 4;513(7516):59-64. doi: 10.1038/nature13568. Epub 2014 Jul 23. Alterations of the human gut microbiome in liver cirrhosis. Qin N1, Yang F2, Li A2, Prifti E3, Chen Y2, Shao L1, Guo J4, Le Chatelier E5, Yao J6, Wu L4, Zhou J4, Ni S4, Liu L4, Pons N5, Batto JM5, Kennedy SP5, Leonard P5, Yuan C4, Ding W4, Chen Y4, Hu X4, Zheng B6, Qian G4, Xu W4, Ehrlich SD7, Zheng S8, Li L6. Author information: 11] State Key Laboratory for Diagnosis and Treatment of Infectious Disease, The First Affiliated Hospital, College of Medicine, Zhejiang University, 310003 Hangzhou, China [2] Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Zhejiang University, 310003 Hangzhou, China [3]. 21] State Key Laboratory for Diagnosis and Treatment of Infectious Disease, The First Affiliated Hospital, College of Medicine, Zhejiang University, 310003 Hangzhou, China [2]. 31] Metagenopolis, Institut National de la Recherche Agronomique, 78350 Jouy en Josas, France [2]. 4State Key Laboratory for Diagnosis and Treatment of Infectious Disease, The First Affiliated Hospital, College of Medicine, Zhejiang University, 310003 Hangzhou, China. 5Metagenopolis, Institut National de la Recherche Agronomique, 78350 Jouy en Josas, France. 61] State Key Laboratory for Diagnosis and Treatment of Infectious Disease, The First Affiliated Hospital, College of Medicine, Zhejiang University, 310003 Hangzhou, China [2] Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Zhejiang University, 310003 Hangzhou, China. 71] Metagenopolis, Institut National de la Recherche Agronomique, 78350 Jouy en Josas, France [2] King's College London, Centre for Host-Microbiome Interactions, Dental Institute Central Office, Guy's Hospital, London Bridge, London SE1 9RT, UK. 81] Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Zhejiang University, 310003 Hangzhou, China [2] Key Laboratory of Combined Multi-organ Transplantation, Ministry of Public Health, the First Affiliated Hospital, Zhejiang University, 310003 Hangzhou, China. Abstract Liver cirrhosis occurs as a consequence of many chronic liver diseases that are prevalent worldwide. Here we characterize the gut microbiome in liver cirrhosis by comparing 98 patients and 83 healthy control individuals. We build a reference gene set for the cohort containing 2.69 million genes, 36.1% of which are novel. Quantitative metagenomics reveals 75,245 genes that differ in abundance between the patients and healthy individuals (false discovery rate < 0.0001) and can be grouped into 66 clusters representing cognate bacterial species; 28 are enriched in patients and 38 in control individuals. Most (54%) of the patient-enriched, taxonomically assigned species are of buccal origin, suggesting an invasion of the gut from the mouth in liver cirrhosis. Biomarkers specific to liver cirrhosis at gene and function levels are revealed by a comparison with those for type 2 diabetes and inflammatory bowel disease. On the basis of only 15 biomarkers, a highly accurate patient discrimination index is created and validated on an independent cohort. Thus microbiota-targeted biomarkers may be a powerful tool for diagnosis of different diseases.
	PMID: 25079328 [PubMed - indexed for MEDLINE]
	Related citations

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 Tuesday, 2014 September 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]))

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

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

PubMed Results

Item 1 of 1

1.	Science. 2014 Sep 5;345(6201):1173-7. doi: 10.1126/science.1256450. Multiple nutrient stresses at intersecting Pacific Ocean biomes detected by protein biomarkers. Saito MA1, McIlvin MR2, Moran DM2, Goepfert TJ2, DiTullio GR3, Post AF4, Lamborg CH2. Author information: 1Marine Chemistry and Geochemistry Department, Woods Hole Oceanographic Institution, Woods Hole, MA 02543, USA. msaito@whoi.edu. 2Marine Chemistry and Geochemistry Department, Woods Hole Oceanographic Institution, Woods Hole, MA 02543, USA. 3College of Charleston, Charleston, SC, USA. 4Marine Biological Laboratory, Woods Hole, MA 02543, USA. Comment in Ocean Science. Microbial proteins and oceanic nutrient cycles. [Science. 2014] Ocean Science. Microbial proteins and oceanic nutrient cycles.Moore CM. Science. 2014 Sep 5; 345(6201):1120-1. Abstract Marine primary productivity is strongly influenced by the scarcity of required nutrients, yet our understanding of these nutrient limitations is informed by experimental observations with sparse geographical coverage and methodological limitations. We developed a quantitative proteomic method to directly assess nutrient stress in high-light ecotypes of the abundant cyanobacterium Prochlorococcus across a meridional transect in the central Pacific Ocean. Multiple peptide biomarkers detected widespread and overlapping regions of nutritional stress for nitrogen and phosphorus in the North Pacific Subtropical Gyre and iron in the equatorial Pacific. Quantitative protein analyses demonstrated simultaneous stress for these nutrients at biome interfaces. This application of proteomic biomarkers to diagnose ocean metabolism demonstrated Prochlorococcus actively and simultaneously deploying multiple biochemical strategies for low-nutrient conditions in the oceans. Copyright © 2014, American Association for the Advancement of Science.
	PMID: 25190794 [PubMed - indexed for MEDLINE]

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 Thursday, 2014 September 18
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 - 2 of 2

1.	Nature. 2014 Jul 10;511(7508):167-76. doi: 10.1038/nature13312. Metabolism of stromal and immune cells in health and disease. Ghesquière B, Wong BW, Kuchnio A, Carmeliet P. Author information: 1] Laboratory of Angiogenesis and Neurovascular Link, Vesalius Research Center, Department of Oncology, University of Leuven, Leuven B-3000, Belgium [2] Laboratory of Angiogenesis and Neurovascular Link, Vesalius Research Center, VIB, Leuven B-3000, Belgium. Abstract Cancer cells have been at the centre of cell metabolism research, but the metabolism of stromal and immune cells has received less attention. Nonetheless, these cells influence the progression of malignant, inflammatory and metabolic disorders. Here we discuss the metabolic adaptations of stromal and immune cells in health and disease, and highlight how metabolism determines their differentiation and function.
	PMID: 25008522 [PubMed - indexed for MEDLINE]
	Related citations

2.	Nature. 2014 Jul 10;511(7508):184-90. doi: 10.1038/nature13323. Aryl hydrocarbon receptor control of a disease tolerance defence pathway. Bessede A1, Gargaro M2, Pallotta MT3, Matino D3, Servillo G3, Brunacci C3, Bicciato S4, Mazza EM4, Macchiarulo A5, Vacca C3, Iannitti R3, Tissi L3, Volpi C3, Belladonna ML3, Orabona C3, Bianchi R3, Lanz TV6, Platten M6, Della Fazia MA3, Piobbico D3, Zelante T3, Funakoshi H7, Nakamura T8, Gilot D9, Denison MS10, Guillemin GJ11, DuHadaway JB12, Prendergast GC12, Metz R13, Geffard M14, Boon L15, Pirro M16, Iorio A17, Veyret B14, Romani L3, Grohmann U3, Fallarino F3, Puccetti P3. Author information: 11] Department of Experimental Medicine, University of Perugia, 06132 Perugia, Italy [2] IMS Laboratory, University of Bordeaux, 33607 Pessac, France [3]. 21] Department of Experimental Medicine, University of Perugia, 06132 Perugia, Italy [2]. 3 Department of Experimental Medicine, University of Perugia, 06132 Perugia, Italy. 4Center for Genome Research, University of Modena and Reggio Emilia, 41125 Modena, Italy. 5Department of Chemistry and Technology of Drugs, University of Perugia, 06123 Perugia, Italy. 61] Experimental Neuroimmunology Unit, German Cancer Research Center, 69120 Heidelberg, Germany [2] Department of Neurooncology, University Hospital, 69120 Heidelberg, Germany. 7Center for Advanced Research and Education, Asahikawa Medical University, 078-8510 Asahikawa, Japan. 8Kringle Pharma Joint Research Division for Regenerative Drug Discovery, Center for Advanced Science and Innovation, Osaka University, 565-0871 Osaka, Japan. 9CNRS UMR6290, Institut de Génétique et Développement de Rennes, Université de Rennes 1, 35043 Rennes, France. 10Department of Environmental Toxicology, University of California, Davis, 95616 California, USA. 11Australian School of Advanced Medicine (ASAM), Macquarie University, 2109 New South Wales, Australia. 12Lankenau Institute for Medical Research, Wynnewood, 19096 Pennsylvania, USA. 13New Link Genetics Corporation, Ames, 50010 Iowa, USA. 14IMS Laboratory, University of Bordeaux, 33607 Pessac, France. 15Bioceros, 3584 Utrecht, The Netherlands. 16Department of Medicine, University of Perugia, 06132 Perugia, Italy. 17Department of Clinical Epidemiology & Biostatistics, McMaster University, Ontario L8S 4K1, Canada. Abstract Disease tolerance is the ability of the host to reduce the effect of infection on host fitness. Analysis of disease tolerance pathways could provide new approaches for treating infections and other inflammatory diseases. Typically, an initial exposure to bacterial lipopolysaccharide (LPS) induces a state of refractoriness to further LPS challenge (endotoxin tolerance). We found that a first exposure of mice to LPS activated the ligand-operated transcription factor aryl hydrocarbon receptor (AhR) and the hepatic enzyme tryptophan 2,3-dioxygenase, which provided an activating ligand to the former, to downregulate early inflammatory gene expression. However, on LPS rechallenge, AhR engaged in long-term regulation of systemic inflammation only in the presence of indoleamine 2,3-dioxygenase 1 (IDO1). AhR-complex-associated Src kinase activity promoted IDO1 phosphorylation and signalling ability. The resulting endotoxin-tolerant state was found to protect mice against immunopathology in Gram-negative and Gram-positive infections, pointing to a role for AhR in contributing to host fitness. PMCID: PMC4098076 [Available on 2015/2/10]
	PMID: 24930766 [PubMed - indexed for MEDLINE]
	Related citations