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

Sent on Saturday, 2011 May 28
Search (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))
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1.	N Engl J Med. 2011 May 19;364(20):1932-42. Genomics and the eye. Sheffield VC, Stone EM. Source Department of Pediatrics, Howard Hughes Medical Institute, University of Iowa Carver College of Medicine, Iowa City, IA, USA. Free Article
	PMID: 21591945 [PubMed - indexed for MEDLINE]

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Sent on Thursday, 2011 May 26
Search (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))
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1.	Science. 2011 May 13;332(6031):848-52. Role for piRNAs and noncoding RNA in de novo DNA methylation of the imprinted mouse Rasgrf1 locus. Watanabe T, Tomizawa S, Mitsuya K, Totoki Y, Yamamoto Y, Kuramochi-Miyagawa S, Iida N, Hoki Y, Murphy PJ, Toyoda A, Gotoh K, Hiura H, Arima T, Fujiyama A, Sado T, Shibata T, Nakano T, Lin H, Ichiyanagi K, Soloway PD, Sasaki H. Source Division of Human Genetics and Department of Integrated Genetics, National Institute of Genetics, Research Organization of Information and Systems, Mishima, Shizuoka, 411-8540, Japan. toshwatatoshiakiwatanabe@gmail.com Abstract Genomic imprinting causes parental origin-specific monoallelic gene expression through differential DNA methylation established in the parental germ line. However, the mechanisms underlying how specific sequences are selectively methylated are not fully understood. We have found that the components of the PIWI-interacting RNA (piRNA) pathway are required for de novo methylation of the differentially methylated region (DMR) of the imprinted mouse Rasgrf1 locus, but not other paternally imprinted loci. A retrotransposon sequence within a noncoding RNA spanning the DMR was targeted by piRNAs generated from a different locus. A direct repeat in the DMR, which is required for the methylation and imprinting of Rasgrf1, served as a promoter for this RNA. We propose a model in which piRNAs and a target RNA direct the sequence-specific methylation of Rasgrf1.
	PMID: 21566194 [PubMed - indexed for MEDLINE]
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2.	Science. 2011 May 13;332(6031):767. The birth of the operon. Jacob F. Free Article
	PMID: 21566161 [PubMed - indexed for MEDLINE]
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3.	Nature. 2011 Mar 31;471(7340):637-41. SHARPIN forms a linear ubiquitin ligase complex regulating NF-κB activity and apoptosis. Ikeda F, Deribe YL, Skånland SS, Stieglitz B, Grabbe C, Franz-Wachtel M, van Wijk SJ, Goswami P, Nagy V, Terzic J, Tokunaga F, Androulidaki A, Nakagawa T, Pasparakis M, Iwai K, Sundberg JP, Schaefer L, Rittinger K, Macek B, Dikic I. Source Frankfurt Institute for Molecular Life Sciences and Institute of Biochemistry II, Goethe University School of Medicine, Theodor-Stern-Kai 7, D-60590 Frankfurt, Main, Germany. Abstract SHARPIN is a ubiquitin-binding and ubiquitin-like-domain-containing protein which, when mutated in mice, results in immune system disorders and multi-organ inflammation. Here we report that SHARPIN functions as a novel component of the linear ubiquitin chain assembly complex (LUBAC) and that the absence of SHARPIN causes dysregulation of NF-κB and apoptotic signalling pathways, explaining the severe phenotypes displayed by chronic proliferative dermatitis (cpdm) in SHARPIN-deficient mice. Upon binding to the LUBAC subunit HOIP (also known as RNF31), SHARPIN stimulates the formation of linear ubiquitin chains in vitro and in vivo. Coexpression of SHARPIN and HOIP promotes linear ubiquitination of NEMO (also known as IKBKG), an adaptor of the IκB kinases (IKKs) and subsequent activation of NF-κB signalling, whereas SHARPIN deficiency in mice causes an impaired activation of the IKK complex and NF-κB in B cells, macrophages and mouse embryonic fibroblasts (MEFs). This effect is further enhanced upon concurrent downregulation of HOIL-1L (also known as RBCK1), another HOIP-binding component of LUBAC. In addition, SHARPIN deficiency leads to rapid cell death upon tumour-necrosis factor α (TNF-α) stimulation via FADD- and caspase-8-dependent pathways. SHARPIN thus activates NF-κB and inhibits apoptosis via distinct pathways in vivo. PMCID: PMC3085511 [Available on 2012/3/31]
	PMID: 21455181 [PubMed - indexed for MEDLINE]
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4.	Nature. 2011 Mar 31;471(7340):578. Microbial sequences benefit health now. Cartwright EJ , Köser CU, Peacock SJ. Comment on Nature. 2011 Feb 10;470(7333):140.
	PMID: 21455159 [PubMed - indexed for MEDLINE]
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Sent on Saturday, 2011 May 21
Search (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))
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1.	Science. 2011 May 6;332(6030):726-9. Relationship between clinical signs and transmission of an infectious disease and the implications for control. Charleston B, Bankowski BM, Gubbins S, Chase-Topping ME, Schley D, Howey R, Barnett PV, Gibson D, Juleff ND, Woolhouse ME. Source Institute for Animal Health, Pirbright Laboratory, Ash Road, Woking, Surrey GU24 0NF, UK. bryan.charleston@bbsrc.ac.uk Abstract Control of many infectious diseases relies on the detection of clinical cases and the isolation, removal, or treatment of cases and their contacts. The success of such "reactive" strategies is influenced by the fraction of transmission occurring before signs appear. We performed experimental studies of foot-and-mouth disease transmission in cattle and estimated this fraction at less than half the value expected from detecting virus in body fluids, the standard proxy measure of infectiousness. This is because the infectious period is shorter (mean 1.7 days) than currently realized, and animals are not infectious until, on average, 0.5 days after clinical signs appear. These results imply that controversial preemptive control measures may be unnecessary; instead, efforts should be directed at early detection of infection and rapid intervention.
	PMID: 21551063 [PubMed - indexed for MEDLINE]
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2.	Science. 2011 May 6;332(6030):717-21. A family of IFN-gamma-inducible 65-kD GTPases protects against bacterial in fection. Kim BH, Shenoy AR, Kumar P, Das R, Tiwari S, MacMicking JD. Source Section of Microbial Pathogenesis, Boyer Centre for Molecular Medicine, Yale University School of Medicine, New Haven, CT 06510, USA. Abstract Immune interferon gamma (IFN-γ) is essential for mammalian host defense against intracellular pathogens. IFN-γ induces nearly 2000 host genes, yet few have any assigned function. Here, we examined a complete mouse 65-kilodalton (kD) guanylate-binding protein (Gbp) gene family as part of a 43-member IFN-γ-inducible guanosine triphosphatase (GTPase) superfamily in mouse and human genomes. Family-wide loss-of-function analysis found that at least four Gbps--Gbp1, Gbp6, Gbp7, and Gbp10--conferred cell-autonomous immunity to listerial or mycobacterial infection within macrophages and gene-deficient animals. These Gbps solicited host defense proteins, including the phagocyte oxidase, antimicrobial peptides, and autophagy effectors, to kill intracellular bacteria. Thus, specific 65-kD Gbps coordinate a potent oxidative and vesicular trafficking program to protect the host from infection.
	PMID: 21551061 [PubMed - indexed for MEDLINE]
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3.	Science. 2011 May 6;332(6030):639. Indigenous genomics. Hayes V. Free Article
	PMID: 21551033 [PubMed - indexed for MEDLINE]
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Sent on Thursday, 2011 May 19
Search (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))
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1.	Nature. 2011 May 12;473(7346):208-11. Novel pathway for assimilation of dimethylsulphoniopropionate widespread in marine bacteria. Reisch CR, Stoudemayer MJ, Varaljay VA, Amster IJ, Moran MA, Whitman WB. Source Department of Microbiology, University of Georgia, Athens, Georgia 30602, USA. Abstract Dimethylsulphoniopropionate (DMSP) accounts for up to 10% of carbon fixed by marine phytoplankton in ocean surface waters, producing an estimated 11.7-103 Tmol S per year, most of which is processed by marine bacteria through the demethylation/demethiolation pathway. This pathway releases methanethiol (MeSH) instead of the climatically active gas dimethylsulphide (DMS) and enables marine microorganisms to assimilate the reduced sulphur. Despite recognition of this critical microbial transformation for over two decades, the biochemical pathway and enzymes responsible have remained unidentified. Here we show that three new enzymes related to fatty acid β-oxidation constitute the pathway that assimilates methylmercaptopropionate (MMPA), the first product of DMSP demethylation/demethiolation, and that two previously unknown coenzyme A (CoA) derivatives, 3-methylmercaptopropionyl-CoA (MMPA-CoA) and methylthioacryloyl-CoA (MTA-CoA), are formed as novel intermediates. A member of the marine roseobacters, Ruegeria pomeroyi DSS-3, requires the MMPA-CoA pathway for MMPA assimilation and MeSH production. This pathway and the ability to produce MeSH from MMPA are present in diverse bacteria, and the ubiquitous SAR11 clade bacterium Pelagibacter ubique possesses enzymes for at least the first two steps. Analysis of marine metagenomic data indicates that the pathway is widespread among bacterioplankton in the ocean surface waters, making it one of the most important known routes for acquisition of reduced carbon and sulphur by surface ocean heterotrophs.
	PMID: 21562561 [PubMed - indexed for MEDLINE]
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2.	Nature. 2011 May 12;473(7346):155. Baruch Blumberg (1925-2011). Alter H. < h3 class="label">Source Department of Transfusion Medicine, Clinical Center, NIH, Bethesda, Maryland, USA. halter@dtm.cc.nih.gov
	PMID: 21562549 [PubMed - indexed for MEDLINE]
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3.	Nature. 2011 May 12;473(7346):174-80. Epub 2011 Apr 20. Enterotypes of the human gut microbiome. Arumugam M, Raes J, Pelletier E, Le Paslier D, Yamada T, Mende DR, Fernandes GR, Tap J, Bruls T, Batto JM, Bertalan M, Borruel N, Casellas F, Fernandez L, Gautier L, Hansen T, Hattori M, Hayashi T, Kleerebezem M, Kurokawa K, Leclerc M, Levenez F, Manichanh C, Nielsen HB, Nielsen T, Pons N, Poulain J, Qin J, Sicheritz-Ponten T, Tims S, Torrents D, Ugarte E, Zoetendal EG, Wang J, Guarner F, Pedersen O, de Vos WM, Brunak S, Doré J; MetaHIT Consortium, Antolín M, Artiguenave F, Blottiere HM, Almeida M, Brechot C, Cara C, Chervaux C, Cultrone A, Delorme C, Denariaz G, Dervyn R, Foerstner KU, Friss C, van de Guchte M, Guedon E, Haimet F, Huber W, van Hylckama-Vlieg J, Jamet A, Juste C, Kaci G, Knol J, Lakhdari O, Layec S, Le Roux K, Maguin E, Mérieux A, Melo Minardi R, M'rini C, Muller J, Oozeer R, Parkhill J, Renault P, Rescigno M, Sanchez N, Sunagawa S, Torrejon A, Turner K, Vandemeulebrouck G, Varela E, Winogradsky Y, Zeller G, Weissenbach J, Ehrlich SD, Bork P. Source European Molecular Biology Laboratory, Meyerhofstrasse 1, 69117 Heidelberg, Germany. Abstract Our knowledge of species and functional composition of the human gut microbiome is rapidly increasing, but it is still based on very few cohorts and little is known about variation across the world. By combining 22 newly sequenced faecal metagenomes of individuals from four countries with previously published data sets, here we identify three robust clusters (referred to as enterotypes hereafter) that are not nation or continent specific. We also confirmed the enterotypes in two published, larger cohorts, indicating that intestinal microbiota variation is generally stratified, not continuous. This indicates further the existence of a limited number of well-balanced host-microbial symbiotic states that might respond differently to diet and drug intake. The enterotypes are mostly driven by species composition, but abundant molecular functions are not necessarily provided by abundant species, highlighting the importance of a functional analysis to understand microbial communities. Although individual host properties such as body mass index, age, or gender cannot explain the observed enterotypes, data-driven marker genes or functional modules can be identified for each of these host properties. For example, twelve genes significantly correlate with age and three functional modules with the body mass index, hinting at a diagnostic potential of microbial markers.
	PMID: 21508958 [PubMed - indexed for MEDLINE]
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Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Tuesday, 2011 May 17
Search (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))
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1.	Nat Med. 2011 Mar;17(3):304-12. Taming the dragon: genomic biomarkers to individualize the treatment of cancer. Majewski IJ, Bernards R. Source Division of Molecular Carcinogenesis, Centre for Biomedical Genetics, The Netherlands Cancer Institute, Amsterdam, The Netherlands. Abstract The gradual shift from cytotoxic drugs to highly selective, targeted therapeutic agents for cancer requires a parallel effort to characterize cancers at the molecular level to guide the choice of therapy for the individual patient. Here we review the genomic technologies that can be used to develop these drug response indicators, or biomarkers. We also discuss hurdles in their development and the implementation of biomarkers in clinical practice.
	PMID: 21386834 [PubMed - indexed for MEDLINE]
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2.	Nat Med. 2011 Mar;17(3):297-303. Cancer genomics: from discovery science to personalized medicine. Chin L, Andersen JN, Futreal PA. Source Belfer Institute for Applied Cancer Science, Dana-Farber Cancer Institute, Boston, Massachusetts, USA. lynda_chin@dfci.harvard.edu Abstract Recent advances in genome technologies and the ensuing outpouring of genomic information related to cancer have accelerated the convergence of discovery science and clinical medicine. Successful examples of translating cancer genomics into therapeutics and diagnostics reinforce its potential to make possible personalized cancer medicine. However, the bottlenecks along the path of converting a genome discovery into a tangible clinical endpoint are numerous and formidable. In this Perspective, we emphasize the importance of establishing the biological relevance of a cancer genomic discovery in realizing its clinical potential and discuss some of the major obstacles to moving from the bench to the bedside.
	PMID: 21383744 [PubMed - indexed for MEDLINE]
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3.	Nat Med. 2011 Mar;17(3):285-6. B cells and macrophages in cancer: yin and yang. Mantovani A.
	PMID: 21383737 [PubMed - indexed for MEDLINE]
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4.	Nat Med. 2011 Mar;17(3):270. When it takes two to tango, FDA suggests a new regulatory dance. Dolgin E.
	PMID: 21383727 [PubMed - indexed for MEDLINE]
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5.	Nat Med. 2011 Mar;17(3):262-5. A close look at cancer. Farrell A.
	PMID: 21383721 [PubMed - indexed for MEDLINE]
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Sent on Wednesday, 2011 May 11
Search (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))
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1.	N Engl J Med. 2011 May 5;364(18):1779; author reply 1779-80. Dialysis catheters and recombinant tissue plasminogen activator. Allon M. Comment on N Engl J Med. 2011 Jan 27;364(4):303-12.
	PMID: 21542758 [PubMed - indexed for MEDLINE]
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2.	N Engl J Med. 2011 May 5;364(18):1773-4. Leishmania--a pa rasitized parasite. Scott P. Source School of Veterinary Medicine, University of Pennsylvania, Philadelphia, USA.
	PMID: 21542750 [PubMed - indexed for MEDLINE]
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3.	Nature. 2011 May 5;473(7345):97-100. Epub 2011 Apr 10. An cestral polyploidy in seed plants and angiosperms. Jiao Y, Wickett NJ, Ayyampalayam S, Chanderbali AS, Landherr L, Ralph PE, Tomsho LP, Hu Y, Liang H, Soltis PS, Soltis DE, Clifton SW, Schlarbaum SE, Schuster SC, Ma H, Leebens-Mack J, dePamphilis CW. Source Intercollege Graduate Degree Program in Plant Biology, The Pennsylvania State University, University Park, Pennsylvania 16802, USA. Abstract Whole-genome duplication (WGD), or polyploidy, followed by gene loss and diploidization has long been recognized as an important evolutionary force in animals, fungi and other organisms, especially plants. The success of angiosperms has been attributed, in part, to innovations associated with gene or whole-genome duplications, but evidence for proposed ancient genome duplications pre-dating the divergence of monocots and eudicots remains equivocal in analyses of conserved gene order. Here we use comprehensive phylogenomic analyses of sequenced plant genomes and more than 12.6 million new expressed-sequence-tag sequences from phylogenetically pivotal lineages to elucidate two groups of ancient gene duplications-one in the common ancestor of extant seed plants and the other in the common ancestor of extant angiosperms. Gene duplication events were intensely concentrated around 319 and 192 million years ago, implicating two WGDs in ancestral lineages shortly before the diversification of extant seed plants and extant angiosperms, respectively. Significantly, these ancestral WGDs resulted in the diversification of regulatory genes important to seed and flower development, suggesting that they were involved in major innovations that ultimately contributed to the rise and eventual dominance of seed plants and angiosperms. ©2011 Macmillan Publishers Limited. All rights reserved
	PMID: 21478875 [PubMed - indexed for MEDLINE]
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Sent on Tuesday, 2011 May 10
Search (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))
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1.	Nat Genet. 2011 Mar 29;43(4):279. Crowdsourcing human mutations. [No authors listed] Comment on Nat Genet. 2007 Apr;39(4):423. Nat Genet. 2011;43(4):281-3. Nat Genet. 2011;43(4):295-301. Abstract The first Human Variome microattribution review shows that data citation and publication credit can work as incentives for systematic curation of gene variant and phenotype data. Analysis of the formal assertions in both databases and journal articles argues for better separation of data structures from narrative so that they can better support one another to communicate meaning.
	PMID: 21445067 [PubMed - indexed for MEDLINE]
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2.	Nat Genet. 2011 Mar 20;43(4):295-301. Systematic documentation and analysis of human genetic variation in hemoglobinopathies using the microattribution approach. Giardine B, Borg J, Higgs DR, Peterson KR, Philipsen S, Maglott D, Singleton BK, Anstee DJ, Basak AN, Clark B, Costa FC, Faustino P, Fedosyuk H, Felice AE, Francina A, Galanello R, Gallivan MV, Georgitsi M, Gibbons RJ, Giordano PC, Harteveld CL, Hoyer JD, Jarvis M, Joly P, Kanavakis E, Kollia P, Menzel S, Miller W, Moradkhani K, Old J, Papachatzopoulou A, Papadakis MN, Papadopoulos P, Pavlovic S, Perseu L, Radmilovic M, Riemer C, Satta S, Schrijver I, Stojiljkovic M, Thein SL, Traeger-Synodinos J, Tully R, Wada T, Waye JS, Wiemann C, Zukic B, Chui DH, Wajcman H, Hardison RC, Patrinos GP. Source Pennsylvania State University, Center for Comparative Genomics and Bioinformatics, University Park, Philadelphia, Pennsylvania, USA. Comment in Nat Genet. 2011;43(4):279. Abstract We developed a series of interrelated locus-specific databases to store all published and unpublished genetic variation related to hemoglobinopathies and thalassemia and implemented microattribution to encourage submission of unpublished observations of genetic variation to these public repositories. A total of 1,941 unique genetic variants in 37 genes, encoding globins and other erythroid proteins, are currently documented in these databases, with reciprocal attribution of microcitations to data contributors. Our project provides the first example of implementing microattribution to incentivise submission of all known genetic variation in a defined system. It has demonstrably increased the reporting of human variants, leading to a comprehensive online resource for systematically describing human genetic variation in the globin genes and other genes contributing to hemoglobinopathies and thalassemias. The principles established here will serve as a model for other systems and for the analysis of other common and/or complex human genetic diseases.
	PMID: 21423179 [PubMed - indexed for MEDLINE]
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1.	Lancet. 2011 Apr 23;377(9775):1397. The legacies of Francis Galton. Rose H, Rose S. Source h.s.rose@lse.ac.uk
	PMID: 21539010 [PubMed - indexed for MEDLINE]

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1.	Nature. 2011 Mar 24;471(7339):467-72. Initial genome sequencing and analysis of multiple myeloma. Chapman MA, Lawrence MS, Keats JJ, Cibulskis K, Sougnez C, Schinzel AC, Harview CL, Brunet JP, Ahmann GJ, Adli M, Anderson KC, Ardlie KG, Auclair D, Baker A, Bergsagel PL, Bernstein BE, Drier Y, Fonseca R, Gabriel SB, Hofmeister CC, Jagannath S, Jakubowiak AJ, Krishnan A, Levy J, Liefeld T, Lonial S, Mahan S, Mfuko B, Monti S, Perkins LM, Onofrio R, Pugh TJ, Rajkumar SV, Ramos AH, Siegel DS, Sivachenko A, Stewart AK, Trudel S, Vij R, Voet D, Winckler W, Zimmerman T, Carpten J, Trent J, Hahn WC, Garraway LA, Meyerson M, Lander ES, Getz G, Golub TR. Source The Eli and Edythe L. Broad Institute, 7 Cambridge Center, Cambridge, Massachusetts 02412, USA. Abstract Multiple myeloma is an incurable malignancy of plasma cells, and its pathogenesis is poorly understood. Here we report the massively parallel sequencing of 38 tumour genomes and their comparison to matched normal DNAs. Several new and unexpected oncogenic mechanisms were suggested by the pattern of somatic mutation across the data set. These include the mutation of genes involved in protein translation (seen in nearly half of the patients), genes involved in histone methylation, and genes involved in blood coagulation. In addition, a broader than anticipated role of NF-κB signalling was indicated by mutations in 11 members of the NF-κB pathway. Of potential immediate clinical relevance, activating mutations of the kinase BRAF were observed in 4% of patients, suggesting the evaluation of BRAF inhibitors in multiple myeloma clinical trials. These results indicate that cancer genome sequencing of large collections of samples will yield new insights into cancer not anticipated by existing knowledge.
	PMID: 21430775 [PubMed - indexed for MEDLINE]
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2.	Nature. 2011 Mar 24;471(7339):425. Genome builders face the competition. Hayden EC.
	PMID: 21430748 [PubMed - indexed for MEDLINE]
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3.	Nature. 2011 Mar 24;471(7339):E8-9; author reply E9-10. In defence of inclusive fitness theory. H erre EA, Wcislo WT. Comment on Nature. 2010 Aug 26;466(7310):1057-62. Abstract Arising from M. A. Nowak, C. E. Tarnita & E. O. Wilson 466, 1057-1062 (2010); Nowak et al. reply. Arguably the defining characteristic of the scientific process is its capacity for self-criticism and correction. Nowak et al. challenge proposed connections between relatedness and the evolution of eusociality, suggest instead that defensible nests and "spring-loaded" traits are key, and present alternative modelling approaches. They then dismiss the utility of Hamilton's insight that relatedness has a profound evolutionary effect, formalized in his widely accepted inclusive fitness theory as Hamilton's rule ("Rise and fall of inclusive fitness theory"). However, we believe that Nowak et al. fail to make their case for logical, theoretical and empirical reasons.
	PMID: 21430725 [PubMed - indexed for MEDLINE]
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4.	Nature. 2011 Mar 24;471(7339):E6-8; author reply E9-10. Inclusive fitness in evolution. Fer riere R, Michod RE. Comment on Nature. 2010 Aug 26;466(7310):1057-62. Abstract Arising from M. A. Nowak, C. E. Tarnita & E. O. Wilson 466, 1057-1062 (2010); Nowak et al. reply. For over fifty years, the evolution of social behaviour has been guided by the concept of inclusive fitness as a measure of evolutionary success. Nowak et al. argue that inclusive fitness should be abandoned. In so doing, however, they misrepresent the role that inclusive fitness has played in the theory of social evolution by which understanding social behaviour in a variety of disciplines has developed and flourished. By discarding inclusive fitness on the basis of its limitations, they create a conceptual tension which, we argue, is unnecessary, and potentially dangerous for evolutionary biology.
	PMID: 21430724 [PubMed - indexed for MEDLINE]
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5.	Nature. 2011 Mar 24;471(7339):E5-6; author reply E9-10. Kin selection and eusociality. S trassmann JE, Page RE Jr, Robinson GE, Seeley TD. Comment on Nature. 2010 Aug 26;466(7310):1057-62. Abstract Arising from M. A. Nowak, C. E. Tarnita & E. O. Wilson 466, 1057-1062 (2010); Nowak et al. reply. Hamilton described a selective process in which individuals affect kin (kin selection), developed a novel modelling strategy for it (inclusive fitness), and derived a rule to describe it (Hamilton's rule). Nowak et al. assert that inclusive fitness is not the best modelling strategy, and also that its production has been "meagre". The former may be debated by theoreticians, but the latter is simply incorrect. There is abundant evidence to demonstrate that inclusive fitness, kin selection and Hamilton's rule have been extraordinarily productive for understanding the evolution of sociality.
	PMID: 21430723 [PubMed - indexed for MEDLINE]
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6.	Nature. 2011 Mar 24;471(7339):E4-5; author reply E9-10. Only full-sibling families evolved eusociality. Boomsma JJ, Beekman M, Cornwallis CK, Griffin AS, Holman L, Hughes WO, Keller L, Oldroyd BP, Ratnieks FL. Comment on Nature. 2010 Aug 26;466(7310):1057-62. Abstract Arising from M. A. Nowak, C. E. Tarnita & E. O. Wilson 466, 1057-1062 (2010); Nowak et al. reply. The paper by Nowak et al. has the evolution of eusociality as its title, but it is mostly about something else. It argues against inclusive fitness theory and offers an alternative modelling approach that is claimed to be more fundamental and general, but which, we believe, has no practical biological meaning for the evolution of eusociality. Nowak et al. overlook the robust empirical observation that eusociality has only arisen in clades where mothers are associated with their full-sibling offspring; that is, in families where the average relatedness of offspring to siblings is as high as to their own offspring, independent of population structure or ploidy. We believe that this omission makes the paper largely irrelevant for understanding the evolution of eusociality.
	PMID: 21430722 [PubMed - indexed for MEDLINE]
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7.	Nature. 2011 Mar 24;471(7339):E1-4; author reply E9-10. Inclusive fitness theory and eusociality. Abbot P, Abe J, Alcock J, Alizon S, Alpedrinha JA, Andersson M, Andre JB, van Baalen M, Balloux F, Balshine S, Barton N, Beukeboom LW, Biernaskie JM, Bilde T, Borgia G, Breed M, Brown S, Bshary R, Buckling A, Burley NT, Burton-Chellew MN, Cant MA, Chapuisat M, Charnov EL, Clutton-Brock T, Cockburn A, Cole BJ, Colegrave N, Cosmides L, Couzin ID, Coyne JA, Creel S, Crespi B, Curry RL, Dall SR, Day T, Dickinson JL, Dugatkin LA, El Mouden C, Emlen ST, Evans J, Ferriere R, Field J, Foitzik S, Foster K, Foster WA, Fox CW, Gadau J, Gandon S, Gardner A, Gardner MG, Getty T, Goodisman MA, Grafen A, Grosberg R, Grozinger CM, Gouyon PH, Gwynne D, Harvey PH, Hatchwell BJ, Heinze J, Helantera H, Helms KR, Hill K, Jiricny N, Johnstone RA, Kacelnik A, Kiers ET, Kokko H, Komdeur J, Korb J, Kronauer D, Kümmerli R, Lehmann L, Linksvayer TA, Lion S, Lyon B, Marshall JA, McElreath R, Michalakis Y, Michod RE, Mock D, Monnin T, Montgomerie R, Moore AJ, Mueller UG, Noë R, Okasha S, Pamilo P, Parker GA, Pedersen JS, Pen I, Pfennig D, Queller DC, Rankin DJ, Reece SE, Reeve HK, Reuter M, Roberts G, Robson SK, Roze D, Rousset F, Rueppell O, Sachs JL, Santorelli L, Schmid-Hempel P, Schwarz MP, Scott-Phillips T, Shellmann-Sherman J, Sherman PW, Shuker DM, Smith J, Spagna JC, Strassmann B, Suarez AV, Sundström L, Taborsky M, Taylor P, Thompson G, Tooby J, Tsutsui ND, Tsuji K, Turillazzi S, Ubeda F, Vargo EL, Voelkl B, Wenseleers T, West SA, West-Eberhard MJ, Westneat DF, Wiernasz DC, Wild G, Wrangham R, Young AJ, Zeh DW, Zeh JA, Zink A. Comment on Nature. 2010 Aug 26;466(7310):1057-62. Abstract Arising from M. A. Nowak, C. E. Tarnita & E. O. Wilson 466, 1057-1062 (2010); Nowak et al. reply. Nowak et al. argue that inclusive fitness theory has been of little value in explaining the natural world, and that it has led to negligible progress in explaining the evolution of eusociality. However, we believe that their arguments are based upon a misunderstanding of evolutionary theory and a misrepresentation of the empirical literature. We will focus our comments on three general issues.
	PMID: 21430721 [PubMed - indexed for MEDLINE]
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8.	Nature. 2011 Mar 24;471(7339):S12-3. Epigenetics: Unravelling the cancer code. Brower V.< /td>
	PMID: 21430711 [PubMed - indexed for MEDLINE]
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