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

Sent on Friday, 2010 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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PubMed Results

Items 1 - 7 of 7

1.	Science. 2010 May 14;328(5980):805. Scientific facilities. Sweden bets on new lab to spruce up its bioscience future. Travis J.
	PMID: 20466895 [PubMed - indexed for MEDLINE]
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	Publication Types: News MeSH Terms: Biological Science Disciplines* Facility Design and Construction Foundations Genome, Plant* Genomics* Humans Laboratories* Picea/genetics* Sequence Analysis, DNA Sweden

2.	Nat Genet. 2010 May;42(5):366-8. Chipping away at the genetics of smoking behavior. Amos CI, Spitz MR, Cinciripini P. Departments of Epidemiology and Behavioral Sciences, University of Texas MD Anderson Cancer Center, Houston, Texas, USA. camos@mdanderson.org Comment on: Nat Genet. 2010 May;42(5):441-7. Nat Genet. 2010 May;42(5):448-53. Nat Genet. 2010 May;42(5):436-40. Abstract Three large consortia present comprehensive analyses that identify genetic factors influencing smoking initiation, intensity and cessation. The genetic architecture of these three phases of smoking behavior appears to be largely distinct.
	PMID: 20428092 [PubMed - indexed for MEDLINE]
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	Publication Types: Comment MeSH Terms: Chromosome Mapping Family Health Health Behavior Humans Models, Genetic Nicotine/metabolism Pharmacogenetics/methods Receptors, Nicotinic/metabolism Sequence Analysis, DNA Smoking/genetics* Smoking Cessation/methods* Tobacco Use Disorder/genetics* Twin Studies as Topic Substances: Receptors, Nicotinic Nicotine

3.	Nat Genet. 2010 May;42(5):365-6. Copy number variation and human genome maps. McCarroll SA. Department of Genetics, Harvard Medical School, Boston, Massachusetts, USA. mccarroll@genetics.med.harvard.edu Comment on: Nat Genet. 2010 May;42(5):385-91. Nat Genet. 2010 May;42(5):400-5. Abstract Maps of human genome copy number variation (CNV) are maturing into useful resources for complex disease genetics. Four new studies increase the resolution of CNV maps and seek to locate human phenotypic variation on these maps.
	PMID: 20428091 [PubMed - indexed for MEDLINE]
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	Publication Types: Comment MeSH Terms: Base Sequence Chromosome Mapping Epigenesis, Genetic Gene Dosage* Genetic Variation Genome Genome, Human* Genomics Humans Linkage Disequilibrium Molecular Sequence Data Mutation Nucleic Acid Hybridization Phenotype Polymorphism, Single Nucleotide

4.	Nat Genet. 2010 May;42(5):363. Conventional wisdom. [No authors listed] Abstract Recent agreement on stable reference sequences for reporting human genetic variants now allows us to mandate the use of the allele naming conventions developed by the Human Genome Variation Society.
	PMID: 20428090 [PubMed - indexed for MEDLINE]
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	Publication Types: Editorial MeSH Terms: Alleles Databases, Genetic/standards* Europe Exons Genetic Variation Genetics/standards* Genome Genome, Human* Humans National Library of Medicine (U.S.) Open Reading Frames Programming Languages Software Terminology as Topic United States

5.	Nat Genet. 2010 May;42(5):441-7. Epub 2010 Apr 25. Genome-wide meta-analyses identify multiple loci associated with smoking behavior. Tobacco and Genetics Consortium. Collaborators: Furberg H, Kim Y, Dackor J, Boerwinkle E, Franceschini N, Ardissino D, Bernardinelli L, Mannucci PL, Mauri F, Merlini PA, Absher D, Assimes TL, Fortmann SP, Iribarren C, Knowles JW, Quertermous T, Ferrucci L, Tanaka T, Bis JC, Furberg CD, Haritunians T, McKnight B, Psaty BM, Taylor KD, Thacker EL, Almgren P, Groop L, Ladenvall C, Boehnke M, Jackson AU, Mohlke KL, Stringham HM, Tuomilehto J, Benjamin EJ, Hwang SJ, Levy D, Preis SR, Vasan RS, Duan J, Gejman PV, Levinson DF, Sanders AR, Shi J, Lips EH, McKay JD, Agudo A, Barzan L, Bencko V, Benhamou S, Castellsague X, Canova C, Conway DI, Fabianova E, Foretova L, Janout V, Healy CM, Holcátová I, Kjaerheim K, Lagiou P, Lissowska J, Lowry R, Macfarlane TV, Mates D, Richiardi L, Rudnai P, Szeszenia-Dabrowska N, Zaridze D, Znaor A, Lathrop M, Brennan P, Bandinelli S, Frayling TM, Guralnik JM, Milaneschi Y, Perry JR, Altshuler D, Elosua R, Kathiresan S, Lucas G, Melander O, O'Donnell CJ, Salomaa V, Schwartz SM, Voight BF, Penninx BW, Smit JH, Vogelzangs N, Boomsma DI, de Geus EJ, Vink JM, Willemsen G, Chanock SJ, Gu F, Hankinson SE, Hunter DJ, Hofman A, Tiemeier H, Uitterlinden AG, van Duijn CM, Walter S, Chasman DI, Everett BM, Paré G, Ridker PM, Li MD, Maes HH, Audrain-McGovern J, Posthuma D, Thornton LM, Lerman C, Kaprio J, Rose JE, Ioannidis JP, Kraft P, Lin DY, Sullivan PF. Department of Genetics, University of North Carolina, Chapel Hill, NC 27710, USA. Comment in: Nat Genet. 2010 May;42(5):366-8. Abstract Consistent but indirect evidence has implicated genetic factors in smoking behavior. We report meta-analyses of several smoking phenotypes within cohorts of the Tobacco and Genetics Consortium (n = 74,053). We also partnered with the European Network of Genetic and Genomic Epidemiology (ENGAGE) and Oxford-GlaxoSmithKline (Ox-GSK) consortia to follow up the 15 most significant regions (n > 140,000). We identified three loci associated with number of cigarettes smoked per day. The strongest association was a synonymous 15q25 SNP in the nicotinic receptor gene CHRNA3 (rs1051730[A], beta = 1.03, standard error (s.e.) = 0.053, P = 2.8 x 10(-73)). Two 10q25 SNPs (rs1329650[G], beta = 0.367, s.e. = 0.059, P = 5.7 x 10(-10); and rs1028936[A], beta = 0.446, s.e. = 0.074, P = 1.3 x 10(-9)) and one 9q13 SNP in EGLN2 (rs3733829[G], beta = 0.333, s.e. = 0.058, P = 1.0 x 10(-8)) also exceeded genome-wide significance for cigarettes per day. For smoking initiation, eight SNPs exceeded genome-wide significance, with the strongest association at a nonsynonymous SNP in BDNF on chromosome 11 (rs6265[C], odds ratio (OR) = 1.06, 95% confidence interval (Cl) 1.04-1.08, P = 1.8 x 10(-8)). One SNP located near DBH on chromosome 9 (rs3025343[G], OR = 1.12, 95% Cl 1.08-1.18, P = 3.6 x 10(-8)) was significantly associated with smoking cessation.
	PMID: 20418890 [PubMed - indexed for MEDLINE]
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	Publication Types: Meta-Analysis Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't MeSH Terms: Age Factors Alleles Chromosome Mapping Female Genome Genome-Wide Association Study* Genotype Humans Male Molecular Epidemiology/methods Odds Ratio Phenotype Polymorphism, Single Nucleotide* Receptors, Nicotinic/genetics Smoking/genetics* Substances: CHRNA3 protein, human Receptors, Nicotinic Grant Support: K07 CA118412/CA/NCI NIH HHS/United States

6.	Nat Genet. 2010 May;42(5):448-53. Epub 2010 Apr 25. Sequence variants at CHRNB3-CHRNA6 and CYP2A6 affect smoking behavior. Thorgeirsson TE, Gudbjartsson DF, Surakka I, Vink JM, Amin N, Geller F, Sulem P, Rafnar T, Esko T, Walter S, Gieger C, Rawal R, Mangino M, Prokopenko I, Mägi R, Keskitalo K, Gudjonsdottir IH, Gretarsdottir S, Stefansson H, Thompson JR, Aulchenko YS, Nelis M, Aben KK, den Heijer M, Dirksen A, Ashraf H, Soranzo N, Valdes AM, Steves C, Uitterlinden AG, Hofman A, Tönjes A, Kovacs P, Hottenga JJ, Willemsen G, Vogelzangs N, Döring A, Dahmen N, Nitz B, Pergadia ML, Saez B, De Diego V, Lezcano V, Garcia-Prats MD, Ripatti S, Perola M, Kettunen J, Hartikainen AL, Pouta A, Laitinen J, Isohanni M, Huei-Yi S, Allen M, Krestyaninova M, Hall AS, Jones GT, van Rij AM, Mueller T, Dieplinger B, Haltmayer M, Jonsson S, Matthiasson SE, Oskarsson H, Tyrfingsson T, Kiemeney LA, Mayordomo JI, Lindholt JS, Pedersen JH, Franklin WA, Wolf H, Montgomery GW, Heath AC, Martin NG, Madden PA, Giegling I, Rujescu D, Järvelin MR, Salomaa V, Stumvoll M, Spector TD, Wichmann HE, Metspalu A, Samani NJ, Penninx BW, Oostra BA, Boomsma DI, Tiemeier H, van Duijn CM, Kaprio J, Gulcher JR; ENGAGE Consortium, McCarthy MI, Peltonen L, Thorsteinsdottir U, Stefansson K. [1] deCODE Genetics, Reykjavik, Iceland. [2] Center for Biomolecular Science and Engineering, Jack Baskin School of Engineering, University of California, Santa Cruz, California, USA. Comment in: Nat Genet. 2010 May;42(5):366-8. Abstract Smoking is a common risk factor for many diseases. We conducted genome-wide association meta-analyses for the number of cigarettes smoked per day (CPD) in smokers (n = 31,266) and smoking initiation (n = 46,481) using samples from the ENGAGE Consortium. In a second stage, we tested selected SNPs with in silico replication in the Tobacco and Genetics (TAG) and Glaxo Smith Kline (Ox-GSK) consortia cohorts (n = 45,691 smokers) and assessed some of those in a third sample of European ancestry (n = 9,040). Variants in three genomic regions associated with CPD (P < 5 x 10(-8)), including previously identified SNPs at 15q25 represented by rs1051730[A] (effect size = 0.80 CPD, P = 2.4 x 10(-69)), and SNPs at 19q13 and 8p11, represented by rs4105144[C] (effect size = 0.39 CPD, P = 2.2 x 10(-12)) and rs6474412-T (effect size = 0.29 CPD, P = 1.4 x 10(-8)), respectively. Among the genes at the two newly associated loci are genes encoding nicotine-metabolizing enzymes (CYP2A6 and CYP2B6) and nicotinic acetylcholine receptor subunits (CHRNB3 and CHRNA6), all of which have been highlighted in previous studies of smoking and nicotine dependence. Nominal associations with lung cancer were observed at both 8p11 (rs6474412[T], odds ratio (OR) = 1.09, P = 0.04) and 19q13 (rs4105144[C], OR = 1.12, P = 0.0006).
	PMID: 20418888 [PubMed - indexed for MEDLINE]
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	Publication Types: Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't MeSH Terms: Alleles Aryl Hydrocarbon Hydroxylases/genetics* Cohort Studies Female Genetic Variation* Genome-Wide Association Study Genomics Humans Lung Neoplasms/genetics Male Odds Ratio Phenotype Receptors, Nicotinic/genetics* Smoking/genetics* Tobacco Use Disorder/genetics Substances: CHRNA6 protein, human CHRNB3 protein, human Receptors, Nicotinic Aryl Hydrocarbon Hydroxylases coumarin 7-hydroxylase Grant Support: R01 DA 017932/DA/NIDA NIH HHS/United States

7.	Nat Genet. 2010 May;42(5):392-9. Epub 2010 Mar 28. From transcriptome analysis to therapeutic anti-CD40L treatment in the SOD1 model of amyotrophic lateral sclerosis. Lincecum JM, Vieira FG, Wang MZ, Thompson K, De Zutter GS, Kidd J, Moreno A, Sanchez R, Carrion IJ, Levine BA, Al-Nakhala BM, Sullivan SM, Gill A, Perrin S. ALS Therapy Development Institute, Cambridge, Massachusetts, USA. Abstract Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by progressive loss of motor neurons. Using unbiased transcript profiling in an ALS mouse model, we identified a role for the co-stimulatory pathway, a key regulator of immune responses. Furthermore, we observed that this pathway is upregulated in the blood of 56% of human patients with ALS. A therapy using a monoclonal antibody to CD40L was developed that slows weight loss, delays paralysis and extends survival in an ALS mouse model. This work demonstrates that unbiased transcript profiling can identify cellular pathways responsive to therapeutic intervention in a preclinical model of human disease.
	PMID: 20348957 [PubMed - indexed for MEDLINE]
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	Publication Types: Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. MeSH Terms: Amyotrophic Lateral Sclerosis/genetics* Amyotrophic Lateral Sclerosis/metabolism Animals CD40 Ligand/antagonists & inhibitors* CD40 Ligand/immunology Disease Models, Animal Female Gene Expression Profiling Humans Immune System Inflammation Macrophages/metabolism Male Mice Mice, Transgenic Signal Transduction Superoxide Dismutase/genetics* Superoxide Dismutase/metabolism Substances: CD40 Ligand superoxide dismutase 1 Superoxide Dismutase