What's new for 'JKB_daily1' in PubMed

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

Sent on Saturday, 2011 Mar 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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PubMed Results

Items 1 - 3 of 3

1.	Nature. 2011 Mar 10;471(7337):173-4. Host-pathogen interaction: Culprit within a culprit. Olivier M.
	PMID: 21390122 [PubMed - indexed for MEDLINE]
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2.	Nature. 2011 Mar 10;471(7337):166. Infrastructure vital to genome success. Yuille M. Commen t on: Nature. 2011 Feb 10;470(7333):187-97.
	PMID: 21390116 [PubMed - indexed for MEDLINE]
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3.	Nature. 2011 Mar 10;471(7337):159-60. Biobanks need publicity. Gaskell G, Gottweis H. London School of Economics and Political Science, London WC2A 2AE, UK. g.gaskell@lse.ac.uk
	PMID: 21390108 [PubMed - indexed for MEDLINE]
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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, 2011 Mar 22
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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PubMed Results

Items 1 - 5 of 5

1.	Nature. 2011 Mar 3;471(7336):125-6. Canada: Quebec's research ambitions. Hoag H.
	PMID: 21416812 [PubMed - indexed for MEDLINE]
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2.	Nature. 2011 Mar 3;471(7336):110-4. Sensitivity to antitubulin chemotherapeutics is regulated by MCL1 and FBW7. Wertz IE, Kusam S, Lam C, Okamoto T, Sandoval W, Anderson DJ, Helgason E, Ernst JA, Eby M, Liu J, Belmont LD, Kaminker JS, O'Rourke KM, Pujara K, Kohli PB, Johnson AR, Chiu ML, Lill JR, Jackson PK, Fairbrother WJ, Seshagiri S, Ludlam MJ, Leong KG, Dueber EC, Maecker H, Huang DC, Dixit VM. Department of Early Discovery Biochemistry, Genentech, South San Francisco, California 94080, USA. ingrid@gene.com Abstract Microtubules have pivotal roles in fundamental cellular processes and are targets of antitubulin chemotherapeutics. Microtubule-targeted agents such as Taxol and vincristine are prescribed widely for various malignancies, including ovarian and breast adenocarcinomas, non-small-cell lung cancer, leukaemias and lymphomas. These agents arrest cells in mitosis and subsequently induce cell death through poorly defined mechanisms. The strategies that resistant tumour cells use to evade death induced by antitubulin agents are also unclear. Here we show that the pro-survival protein MCL1 (ref. 3) is a crucial regulator of apoptosis triggered by antitubulin chemotherapeutics. During mitotic arrest, MCL1 protein levels decline markedly, through a post-translational mechanism, potentiating cell death. Phosphorylation of MCL1 directs its interaction with the tumour-suppressor protein FBW7, which is the substrate-binding component of a ubiquitin ligase complex. The polyubiquitylation of MCL1 then targets it for proteasomal degradation. The degradation of MCL1 was blocked in patient-derived tumour cells that lacked FBW7 or had loss-of-function mutations in FBW7, conferring resistance to antitubulin agents and promoting chemotherapeutic-induced polyploidy. Additionally, primary tumour samples were enriched for FBW7 inactivation and elevated MCL1 levels, underscoring the prominent roles of these proteins in oncogenesis. Our findings suggest that profiling the FBW7 and MCL1 status of tumours, in terms of protein levels, messenger RNA levels and genetic status, could be useful to predict the response of patients to antitubulin chemotherapeutics.
	PMID: 21368834 [PubMed - indexed for MEDLINE]
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3.	Nature. 2011 Mar 3;471(7336):95-8. Phylogenomic analyses unravel annelid evolution. Struck T H, Paul C, Hill N, Hartmann S, Hösel C, Kube M, Lieb B, Meyer A, Tiedemann R, Purschke G, Bleidorn C. University of Osnabrück, FB05 Biology/Chemistry, AG Zoology, Barbarastrasse 11, 49069 Osnabrück, Germany. struck@biologie.uni-osnabrueck.de Comment in: Nature. 2011 Mar 3;471(7336):44-5. Abstract Annelida, the ringed worms, is a highly diverse animal phylum that includes more than 15,000 described species and constitutes the dominant benthic macrofauna from the intertidal zone down to the deep sea. A robust annelid phylogeny would shape our understanding of animal body-plan evolution and shed light on the bilaterian ground pattern. Traditionally, Annelida has been split into two major groups: Clitellata (earthworms and leeches) and polychaetes (bristle worms), but recent evidence suggests that other taxa that were once considered to be separate phyla (Sipuncula, Echiura and Siboglinidae (also known as Pogonophora)) should be included in Annelida. However, the deep-level evolutionary relationships of Annelida are still poorly understood, and a robust reconstruction of annelid evolutionary history is needed. Here we show that phylogenomic analyses of 34 annelid taxa, using 47,953 amino acid positions, recovered a well-supported phylogeny with strong support for major splits. Our results recover chaetopterids, myzostomids and sipunculids in the basal part of the tree, although the position of Myzostomida remains uncertain owing to its long branch. The remaining taxa are split into two clades: Errantia (which includes the model annelid Platynereis), and Sedentaria (which includes Clitellata). Ancestral character trait reconstructions indicate that these clades show adaptation to either an errant or a sedentary lifestyle, with alteration of accompanying morphological traits such as peristaltic movement, parapodia and sensory perception. Finally, life history characters in Annelida seem to be phylogenetically informative.
	PMID: 21368831 [PubMed - indexed for MEDLINE]
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4.	Nature. 2011 Mar 3;471(7336):20-4. Epidemiology: Study of a lifetime. Pearson H.
	PMID: 21368799 [PubMed - indexed for MEDLINE]
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5.	Nature. 2011 Mar 3;471(7336):68-73. Epub 2011 Feb 2. Hotspots of aberrant epigenomic reprogramming in human induced pluripotent stem cells. Lister R, Pelizzola M, Kida YS, Hawkins RD, Nery JR, Hon G, Antosiewicz-Bourget J, O'Malley R, Castanon R, Klugman S, Downes M, Yu R, Stewart R, Ren B, Thomson JA, Evans RM, Ecker JR. Genomic Analysis Laboratory, The Salk Institute for Biological Studies, La Jolla, California 92037, USA. Comment in: Nature. 2011 Mar 3;471(7336):46-7. Abstract Induced pluripotent stem cells (iPSCs) offer immense potential for regenerative medicine and studies of disease and development. Somatic cell reprogramming involves epigenomic reconfiguration, conferring iPSCs with characteristics similar to embryonic stem (ES) cells. However, it remains unknown how complete the reestablishment of ES-cell-like DNA methylation patterns is throughout the genome. Here we report the first whole-genome profiles of DNA methylation at single-base resolution in five human iPSC lines, along with methylomes of ES cells, somatic cells, and differentiated iPSCs and ES cells. iPSCs show significant reprogramming variability, including somatic memory and aberrant reprogramming of DNA methylation. iPSCs share megabase-scale differentially methylated regions proximal to centromeres and telomeres that display incomplete reprogramming of non-CG methylation, and differences in CG methylation and histone modifications. Lastly, differentiation of iPSCs into trophoblast cells revealed that errors in reprogramming CG methylation are transmitted at a high frequency, providing an iPSC reprogramming signature that is maintained after differentiation.
	PMID: 21289626 [PubMed - indexed for MEDLINE]
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What's new for 'JKB_daily1' in PubMed

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

Sent on Saturday, 2011 Mar 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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PubMed Results

Item 1 of 1

1.	Nat Med. 2011 Feb;17(2):179-88. Epub 2011 Jan 9. The NLRP3 inflammasome instigates obesity-induced inflammation and insulin resistance. Vandanmagsar B, Youm YH, Ravussin A, Galgani JE, Stadler K, Mynatt RL, Ravussin E, Stephens JM, Dixit VD. Laboratory of Neuroendocrine-Immunology, Louisiana State University, Baton Rouge, Louisiana, USA. Comment in: Nat Med. 2011 Feb;17(2):164-5. Abstract The emergence of chronic inflammation during obesity in the absence of overt infection or well-defined autoimmune processes is a puzzling phenomenon. The Nod-like receptor (NLR) family of innate immune cell sensors, such as the nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (Nlrp3, but also known as Nalp3 or cryopyrin) inflammasome are implicated in recognizing certain nonmicrobial originated 'danger signals' leading to caspase-1 activation and subsequent interleukin-1β (IL-1β) and IL-18 secretion. We show that calorie restriction and exercise-mediated weight loss in obese individuals with type 2 diabetes is associated with a reduction in adipose tissue expression of Nlrp3 as well as with decreased inflammation and improved insulin sensitivity. We further found that the Nlrp3 inflammasome senses lipotoxicity-associated increases in intracellular ceramide to induce caspase-1 cleavage in macrophages and adipose tissue. Ablation of Nlrp3 in mice prevents obesity-induced inflammasome activation in fat depots and liver as well as enhances insulin signaling. Furthermore, elimination of Nlrp3 in obese mice reduces IL-18 and adipose tissue interferon-γ (IFN-γ) expression, increases naive T cell numbers and reduces effector T cell numbers in adipose tissue. Collectively, these data establish that the Nlrp3 inflammasome senses obesity-associated danger signals and contributes to obesity-induced inflammation and insulin resistance.
	PMID: 21217695 [PubMed - indexed for MEDLINE]

What's new for 'JKB_daily1' in PubMed

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

Sent on Friday, 2011 Mar 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]))
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PubMed Results

Items 1 - 2 of 2

1.	Lancet. 2011 Feb 5;377(9764):526. Mind the gap! An unusual metabolic acidosis. Myall K, Sidney J, Marsh A. Department of Anaesthesia, Frenchay Hospital, Bristol, UK. katemyall@gmail.com
	PMID: 21296238 [PubMed - indexed for MEDLINE]
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2.	Lancet. 2011 Feb 5;377(9764):464-5; author reply 465. Anticoagulation: improve care quality or use new alternatives? You JH. Comment on: Lancet. 2010 Sep 18;376(9745):975-83.
	PMID: 21296230 [PubMed - indexed for MEDLINE]
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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, 2011 Mar 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]))
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PubMed Results

Items 1 - 16 of 16

1.	Science. 2011 Feb 25;331(6020):1055-8. The response of vegetation on the Andean flank in western Amazonia to Pleistocene climate change. Cárdenas ML, Gosling WD, Sherlock SC, Poole I, Pennington RT, Mothes P. Department of Earth and Environmental Sciences, CEPSAR, The Open University, Walton Hall, Milton Keynes MK7 6AA, UK. m.l.cardenas@open.ac.uk Abstract A reconstruction of past environmental change from Ecuador reveals the response of lower montane forest on the Andean flank in western Amazonia to glacial-interglacial global climate change. Radiometric dating of volcanic ash indicates that deposition occurred ~324,000 to 193,000 years ago during parts of Marine Isotope Stages 9, 7, and 6. Fossil pollen and wood preserved within organic sediments suggest that the composition of the forest altered radically in response to glacial-interglacial climate change. The presence of Podocarpus macrofossils ~1000 meters below the lower limit of their modern distribution indicates a relative cooling of at least 5°C during glacials and persistence of wet conditions. Interglacial deposits contain thermophilic palms suggesting warm and wet climates. Hence, global temperature change can radically alter vegetation communities and biodiversity in this region.
	PMID: 21350174 [PubMed - indexed for MEDLINE]
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2.	Science. 2011 Feb 25;331(6020):1027. Genome-sequencing anniversary. The genome dances. Lerman L. Liz Lerman Dance Exchange, Takoma Park, MD, USA.
	PMID: 21350168 [PubMed - indexed for MEDLINE]
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3.	Science. 2011 Feb 25;331(6020):1026. Genome-sequencing anniversary. The meaning of the Human Genome Project for n europsychiatric disorders. Hyman SE. Harvard University, MA, USA.
	PMID: 21350167 [PubMed - indexed for MEDLINE]
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4.	Science. 2011 Feb 25;331(6020):1026. Genome-sequencing anniversary. A healthy son. King MC. University of Washington, Seattle, WA, USA.
	PMID: 21350166 [PubMed - indexed for MEDLINE]
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5.	Science. 2011 Feb 25;331(6020):1026-7. Genome-sequencing anniversary. Socializing genetic diseases. Rabeharisoa V. Centre de sociologie de l'innovation, MINES ParisTech, Paris, France.
	PMID: 21350165 [PubMed - indexed for MEDLINE]
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6.	Science. 2011 Feb 25;331(6020):1025. Genome-sequencing anniversary. Fruits of genome sequences for biology.Botstein D. Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, NJ, USA.
	PMID: 21350164 [PubMed - indexed for MEDLINE]
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7.	Science. 2011 Feb 25;331(6020):1025-6. Genome-sequencing anniversary. Presenting the human genome: now in 3D! Ruan Y. Genome Institute of Singapore, Singapore, Republic of Singapore.
	PMID: 21350163 [PubMed - indexed for MEDLINE]
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8.	Science. 2011 Feb 25;331(6020):1024. Genome-sequencing anniversary. The accelerator. Lander ES. Broad Institute of Harvard and MIT, Cambridge, MA, USA.
	PMID: 21350161 [PubMed - indexed for MEDLINE]
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9.	Science. 2011 Feb 25;331(6020):1024-5. Genome-sequencing anniversary. Making sense of the data. Donnelly P. Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK.
	PMID: 21350160 [PubMed - indexed for MEDLINE]
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10.	Science. 2011 Feb 25;331(6020):1015-6. Genetics. Systems genetics. Nadeau JH, Dudley AM. Institute for Systems Biology, 1441 North 34th Street, Seattle, WA 98103, USA. jnadeau@systemsbiology.org
	PMID: 21350153 [PubMed - indexed for MEDLINE]
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11.	Science. 2011 Feb 25;331(6020):1009. Human genome 10th anniversary. Probing pronghorn mating preferences.Pennisi E.
	PMID: 21350146 [PubMed - indexed for MEDLINE]
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12.	Science. 2011 Feb 25;331(6020):1008-9. Human genome 10th anniversary. Digging deep into the microbiome. Pennisi E.
	PMID: 21350145 [PubMed - indexed for MEDLINE]
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13.	Science. 2011 Feb 25;331(6020):1007-8. Human genome 10th anniversary. Tackling the mystery of the disappearing f rogs. Pennisi E.
	PMID: 21350144 [PubMed - indexed for MEDLINE]
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14.	Science. 2011 Feb 25;331(6020):1006-7. Human genome 10th anniversary. Using DNA to reveal a mosquito's history.< /a> Pennisi E.
	PMID: 21350143 [PubMed - indexed for MEDLINE]
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15.	Science. 2011 Feb 25;331(6020):1005. Human genome 10th anniversary. Beyond human: new faces, fields exploit genomics. Pennisi E.
	PMID: 21350142 [PubMed - indexed for MEDLINE]
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16.	Science. 2011 Feb 25;331(6020):1005-6. Human genome 10th anniversary. Tracing the tree of life. Pennisi E.
	PMID: 21350141 [PubMed - indexed for MEDLINE]
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What's new for 'JKB_daily1' in PubMed

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

Sent on Wednesday, 2011 Mar 09
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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PubMed Results

Items 1 - 6 of 6

1.	Science. 2011 Feb 18;331(6019):874. Genome-sequencing anniversary. The genomic foundation is shifting. Mattick JS. Institute for Molecular Bioscience, University of Queensland, St. Lucia, Queensland, Australia.
	PMID: 21330534 [PubMed - indexed for MEDLINE]
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2.	Science. 2011 Feb 18;331(6019):874. Genome-sequencing anniversary. Famine in the presence of the genomic data fea st. Hoal E. Department of Biomedical Sciences, Faculty of Health Sciences, Stellenbosch University, Tygerberg, South Africa.
	PMID: 21330533 [PubMed - indexed for MEDLINE]
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3.	Science. 2011 Feb 18;331(6019):873. Genome-sequencing anniversary. Of mice and humans. Yamanaka S. Center for iPS Cell Research and Application, Kyoto University, Kyoto, Japan.
	PMID: 21330532 [PubMed - indexed for MEDLINE]
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4.	Science. 2011 Feb 18;331(6019):873. Genome-sequencing anniversary. Human genome sequencing: celebrating 10 years. Al-Gazali L. Department of Pediatrics, United Arab Emirates University, Al-Ain, United Arab Emirates.
	PMID: 21330531 [PubMed - indexed for MEDLINE]
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5.	Science. 2011 Feb 18;331(6019):872. Genome-sequencing anniversary. A living constitution. Jasanoff S. John F. Kennedy School of Government, Harvard University, Cambridge, MA, USA.
	PMID: 21330528 [PubMed - indexed for MEDLINE]
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6.	Science. 2011 Feb 18;331(6019):861-2. Genomics. Deflating the genomic bubble. Evans JP, Meslin EM, Marteau TM, Caulfield T. Department of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. jpevans@med.unc.edu
	PMID: 21330519 [PubMed - indexed for MEDLINE]
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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, 2011 Mar 03
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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PubMed Results

Items 1 - 15 of 15

1.	Nature. 2011 Feb 17;470(7334):338-9. Genomics: Drugs, diabetes and cancer. Birnbaum MJ, Shaw RJ.
	PMID: 21331030 [PubMed - indexed for MEDLINE]
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2.	Nature. 2011 Feb 17;470(7334):327-9. Health-care hit or miss? Hersh W, Jacko JA, Greenes R, Tan J, Janies D, Embi PJ, Payne PR.
	PMID: 21331020 [PubMed - indexed for MEDLINE]
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3.	Nature. 2011 Feb 17;470(7334):305-6. Devil in the details. [No authors listed]
	PMID: 21 330998 [PubMed - indexed for MEDLINE]
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4.	Science. 2011 Feb 11;331(6018):775-8. Leishmania RNA virus controls the severity of mucocutaneous leishmaniasis. Ives A, Ronet C, Prevel F, Ruzzante G, Fuertes-Marraco S, Schutz F, Zangger H, Revaz-Breton M, Lye LF, Hickerson SM, Beverley SM, Acha-Orbea H, Launois P, Fasel N, Masina S. Department of Biochemistry, University of Lausanne, 1066 Epalinges, Switzerland. Abstract Mucocutaneous leishmaniasis is caused by infections with intracellular parasites of the Leishmania Viannia subgenus, including Leishmania guyanensis. The pathology develops after parasite dissemination to nasopharyngeal tissues, where destructive metastatic lesions form with chronic inflammation. Currently, the mechanisms involved in lesion development are poorly understood. Here we show that metastasizing parasites have a high Leishmania RNA virus-1 (LRV1) burden that is recognized by the host Toll-like receptor 3 (TLR3) to induce proinflammatory cytokines and chemokines. Paradoxically, these TLR3-mediated immune responses rendered mice more susceptible to infection, and the animals developed an increased footpad swelling and parasitemia. Thus, LRV1 in the metastasizing parasites subverted the host immune response to Leishmania and promoted parasite persistence.
	PMID: 21311023 [PubMed - indexed for MEDLINE]
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5.	Science. 2011 Feb 11;331(6018):728-9. On the future of genomic data. Kahn SD. Illumina, 9885 Towne Centre Drive, San Diego, CA 92121, USA. Abstract Many of the challenges in genomics derive from the informatics needed to store and analyze the raw sequencing data that is available from highly multiplexed sequencing technologies. Because single week-long sequencing runs today can produce as much data as did entire genome centers a few years ago, the need to process terabytes of information has become de rigueur for many labs engaged in genomic research. The availability of deep (and large) genomic data sets raises concerns over information access, data security, and subject/patient privacy that must be addressed for the field to continue its rapid advances.
	PMID: 21311016 [PubMed - indexed for MEDLINE]
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6.	Science. 2011 Feb 11;331(6018):691. Genome-sequencing anniversary. What will drive genomics over the next 10 year s? Caplan A. Center for Bioethics, University of Pennsylvania, Philadelphia, PA, USA.
	PMID: 21311001 [PubMed - indexed for MEDLINE]
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7.	Science. 2011 Feb 11;331(6018):691. Genome-sequencing anniversary. An anniversary party. Stefánsson K. deCode Genetics, Reykjavik, Iceland.
	PMID: 21311000 [PubMed - indexed for MEDLINE]
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8.	Science. 2011 Feb 11;331(6018):691. Genome-sequencing anniversary. First steps on a long road. Schadt E. Pacific Biosciences of California, Menlo Park, CA, USA.
	PMID: 21310999 [PubMed - indexed for MEDLINE]
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9.	Science. 2011 Feb 11;331(6018):690. Genome-sequencing anniversary. Personal genomes: for one and for all. Wang J. Beijing Genome Institute.
	PMID: 21310998 [PubMed - indexed for MEDLINE]
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10.	Science. 2011 Feb 11;331(6018):690-1. Genome-sequencing anniversary. My genome, my identity, my health. Royal CD. Institute for Genome Sciences & Policy and Department of African and African American Studies, Duke University, Durham, NC, USA.
	PMID: 21310996 [PubMed - indexed for MEDLINE]
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11.	Science. 2011 Feb 11;331(6018):689. Genome-sequencing anniversary. My genome. Tutu D.
	PMID: 21310994 [PubMed - indexed for MEDLINE]
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12.	Science. 2011 Feb 11;331(6018):689-90. Genome-sequencing anniversary. Genome literacy. Dermitzakis ET. Department of Genetic Medicine and Development, University of Geneva Medical School, Geneva, Switzerland.
	PMID: 21310993 [PubMed - indexed for MEDLINE]
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13.	Science. 2011 Feb 11;331(6018):666-8. Human genome 10th anniversary. Will computers crash genomics? Pennisi E.
	PMID: 21310981 [PubMed - indexed for MEDLINE]
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14.	Science. 2011 Feb 11;331(6018):662-5. Human genome 10th anniversary. What would you do? Couzin-Frankel J.
	PMID: 21310980 [PubMed - indexed for MEDLINE]
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15.	Science. 2011 Feb 11;331(6018):660. Biomedical research. The genome project: what will it do as a teenager? Inte rview by Jocelyn Kaiser. Green E.
	PMID: 21310978 [PubMed - indexed for MEDLINE]
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Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Tuesday, 2011 Mar 01
Search (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))
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Items 1 - 9 of 9

1.	Nature. 2011 Feb 10;470(7333):289-94. Genomics: Genomes in three dimensions. Baker M. Nature and Nature Methods.
	PMID: 21307943 [PubMed - indexed for MEDLINE]
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2.	Nature. 2011 Feb 10;470(7333):284-8. lncRNAs transactivate STAU1-mediated mRNA decay by duplexing with 3' UTRs via Alu elements. Gong C, Maquat LE. Department of Biochemistry and Biophysics, School of Medicine and Dentistry, University of Rochester, Rochester, New York 14642, USA. Abstract Staufen 1 (STAU1)-mediated messenger RNA decay (SMD) involves the degradation of translationally active mRNAs whose 3'-untranslated regions (3' UTRs) bind to STAU1, a protein that binds to double-stranded RNA. Earlier studies defined the STAU1-binding site within ADP-ribosylation factor 1 (ARF1) mRNA as a 19-base-pair stem with a 100-nucleotide apex. However, we were unable to identify comparable structures in the 3' UTRs of other targets of SMD. Here we show that STAU1-binding sites can be formed by imperfect base-pairing between an Alu element in the 3' UTR of an SMD target and another Alu element in a cytoplasmic, polyadenylated long non-coding RNA (lncRNA). An individual lncRNA can downregulate a subset of SMD targets, and distinct lncRNAs can downregulate the same SMD target. These are previously unappreciated functions of non-coding RNAs and Alu elements. Not all mRNAs that contain an Alu element in the 3' UTR are targeted for SMD even in the presence of a complementary lncRNA that targets other mRNAs for SMD. Most known trans-acting RNA effectors consist of fewer than 200 nucleotides, and these include small nucleolar RNAs and microRNAs. Our finding that the binding of STAU1 to mRNAs can be transactivated by lncRNAs uncovers an unexpected strategy that cells use to recruit proteins to mRNAs and mediate the decay of these mRNAs. We name these lncRNAs half-STAU1-binding site RNAs (1/2-sbsRNAs).
	PMID: 21307942 [PubMed - indexed for MEDLINE]
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3.	Nature. 2011 Feb 10;470(7333):204-13. Charting a course for genomic medicine from base pairs to bedside. Green ED, Guyer MS; National Human Genome Research Institute. Collaborators: Green ED, Guyer MS, Manolio TA, Peterson JL. National Human Genome Research Institute, National Institutes of Health, 31 Center Dr., Bethesda, Maryland 20892-2152, USA. egreen@nhgri.nih.gov Abstract There has been much progress in genomics in the ten years since a draft sequence of the human genome was published. Opportunities for understanding health and disease are now unprecedented, as advances in genomics are harnessed to obtain robust foundational knowledge about the structure and function of the human genome and about the genetic contributions to human health and disease. Here we articulate a 2011 vision for the future of genomics research and describe the path towards an era of genomic medicine.
	PMID: 21307933 [PubMed - indexed for MEDLINE]
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4.	Nature. 2011 Feb 10;470(7333):198-203. A decade's perspective on DNA sequencing technology. Mardis ER. The Genome Center at Washington University School of Medicine, Department of Genetics, Washington University School of Medicine, St Louis, Missouri 63108, USA. emardis@wustl.edu Abstract The decade since the Human Genome Project ended has witnessed a remarkable sequencing technology explosion that has permitted a multitude of questions about the genome to be asked and answered, at unprecedented speed and resolution. Here I present examples of how the resulting information has both enhanced our knowledge and expanded the impact of the genome on biomedical research. New sequencing technologies have also introduced exciting new areas of biological endeavour. The continuing upward trajectory of sequencing technology development is enabling clinical applications that are aimed at improving medical diagnosis and treatment.
	PMID: 21307932 [PubMed - indexed for MEDLINE]
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5.	Nature. 2011 Feb 10;470(7333):187-97. Initial impact of the sequencing of the human genome. Lander ES. Broad Institute of MIT and Harvard, 7 Cambridge Center, Cambridge, Massachusetts 02142, USA. lander@broadinstitute.org Abstract The sequence of the human genome has dramatically accelerated biomedical research. Here I explore its impact, in the decade since its publication, on our understanding of the biological functions encoded in the genome, on the biological basis of inherited diseases and cancer, and on the evolution and history of the human species. I also discuss the road ahead in fulfilling the promise of genomics for medicine.
	PMID: 21307931 [PubMed - indexed for MEDLINE]
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6.	Nature. 2011 Feb 10;470(7333):163-5. Too many roads not taken. Edwards AM, Isserlin R, Bader GD, Frye SV, Willson TM, Yu FH. University of Toronto, Toronto, Ontario M5G 1L7, Canada. aled.edwards@utoronto.ca
	PMID: 21307913 [PubMed - indexed for MEDLINE]
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7.	Nature. 2011 Feb 10;470(7333):161-2. Evolution: a can of worms. Maxmen A.
	PMID: 21307912 [PubMed - indexed for MEDLINE]
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8.	Nature. 2011 Feb 10;470(7333):155. Gene reading steps up a gear. Ledford H.
	PMID: 21307910 [PubMed - indexed for MEDLINE]
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9.	Nature. 2011 Feb 10;470(7333):140. Best is yet to come. [No authors listed]
	PMID: 21307 892 [PubMed - indexed for MEDLINE]
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