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Sent on Thursday, 2011 Apr 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.	Science. 2011 Apr 15;332(6027):309-10. Genomics. Genomics, biobanks, and the trade-secret model. Mitchell R, Conley JM, Davis AM, Cadigan RJ, Dobson AW, Gladden RQ. Source Institute for Genome Sciences and Policy and English Department, Duke University, Durham, NC 27708, USA. rmitch@duke.edu
	PMID: 21493846 [PubMed - indexed for MEDLINE]
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2.	Science. 2011 Apr 15;332(6027):306; author reply 306. The risks and benefits of re-consent. Forsberg JS, Hansson MG, Eriksson S. Comment on Science. 2011 Jan 21;331(6015):287-8.
	PMID: 21493845 [PubMed - indexed for MEDLINE]
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3.	Science. 2011 Apr 15;332(6027):300-1. Retrotransposons. Do jumping genes spawn diversity? Vogel G.
	PMID: 21493838 [PubMed - indexed for MEDLINE]
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1.	N Engl J Med. 2011 Apr 14;364(15):1477-8; author reply 1478-9. Case 2-2011: a woman with shock after treatment of a furuncle. Pollock AA. Comment on N Engl J Med. 2011 Jan 20;364(3):266-75.
	PMID: 21488792 [PubMed - indexed for MEDLINE]
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2.	N Engl J Med. 2011 Apr 14;364(15):1478; author reply 1478-9. Case 2-2011: a woman with shock after treatment of a furuncle. Milazzo L, Antinori S. Comment on N Engl J Med. 2011 Jan 20;364(3):266-75.
	PMID: 21488791 [PubMed - indexed for MEDLINE]
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3.	N Engl J Med. 2011 Apr 14;364(15):1472; author reply 1474-5. Cholesterol efflux capacity and atherosclerosis. Gupta A. Comment on N Engl J Med. 2011 Jan 13;364(2):127-35.
	PMID: 21488784 [PubMed - indexed for MEDLINE]
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4.	N Engl J Med. 2011 Apr 14;364(15):1472-3; author reply 1474-5. Cholesterol efflux capacity and atherosclerosis. Aeddula NR, Trivedi N, Pathireddy S. Comment on N Engl J Med. 2011 Jan 13;364(2):127-35.
	PMID: 21488783 [PubMed - indexed for MEDLINE]
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5.	Lancet. 2011 Apr 9;377(9773):1256-63. Cytomegalovirus gly coprotein-B vaccine with MF59 adjuvant in transplant recipients: a phase 2 randomised placebo-controlled trial. Griffiths PD, Stanton A, McCarrell E, Smith C, Osman M, Harber M, Davenport A, Jones G, Wheeler DC, O'Beirne J, Thorburn D, Patch D, Atkinson CE, Pichon S, Sweny P, Lanzman M, Woodford E, Rothwell E, Old N, Kinyanjui R, Haque T, Atabani S, Luck S, Prideaux S, Milne RS, Emery VC, Burroughs AK. Source Centre for Virology, UCL Medical School, London, UK. p.griffiths@medsch.ucl.ac.uk Comment in Lancet. 2011 Apr 9;377(9773):1216-8. Abstract BACKGROUND: Cytomegalovirus end-organ disease can be prevented by giving ganciclovir when viraemia is detected in allograft recipients. Values of viral load correlate with development of end-organ disease and are moderated by pre-existing natural immunity. Our aim was to determine whether vaccine-induced immunity could do likewise. METHODS: We undertook a phase-2 randomised placebo controlled trial in adults awaiting kidney or liver transplantation at the Royal Free Hospital, London, UK. Exclusion criteria were pregnancy, receipt of blood products (except albumin) in the previous 3 months, and simultaneous multiorgan transplantation. 70 patients seronegative and 70 seropositive for cytomegalovirus were randomly assigned from a scratch-off randomisation code in a 1:1 ratio to receive either cytomegalovirus glycoprotein-B vaccine with MF59 adjuvant or placebo, each given at baseline, 1 month and 6 months later. If a patient was transplanted, no further vaccinations were given and serial blood samples were tested for cytomegalovirus DNA by real-time quantitative PCR (rtqPCR). Any patient with one blood sample containing more than 3000 cytomegalovirus genomes per mL received ganciclovir until two consecutive undetectable cytomegalovirus DNA measurements. Safety and immunogenicity were coprimary endpoints and were assessed by intention to treat in patients who received at least one dose of vaccine or placebo. This trial is registered with ClinicalTrials.gov, NCT00299260. FINDINGS: 67 patients received vaccine and 73 placebo, all of whom were evaluable. Glycoprotein-B antibody titres were significantly increased in both seronegative (geometric mean titre 12,537 (95% CI 6593-23,840) versus 86 (63-118) in recipients of placebo recipients; p<0.0001) and seropositive (118,395; 64,503-217,272) versus 24,682 (17,909-34,017); p<0.0001) recipients of vaccine. In those who developed viraemia after transplantation, glycoprotein-B antibody titres correlated inversely with duration of viraemia (p=0.0022). In the seronegative patients with seropositive donors, the duration of viraemia (p=0.0480) and number of days of ganciclovir treatment (p=0.0287) were reduced in vaccine recipients. INTERPRETATION: Although cytomegalovirus disease occurs in the context of suppressed cell-mediated immunity post-transplantation, humoral immunity has a role in reduction of cytomegalovirus viraemia. Vaccines containing cytomegalovirus glycoprotein B merit further assessment in transplant recipients. FUNDING: National Institute of Allergy and Infectious Diseases, Grant R01AI051355 and Wellcome Trust, Grant 078332. Sponsor: University College London (UCL). Copyright © 2011 Elsevier Ltd. All rights reserved.
	PMID: 21481708 [PubMed - indexed for MEDLINE]
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6.	Lancet. 2011 Apr 9;377(9773):1216-8. A cytomegalovirus vaccine tames the troll of transplantation. Schleiss MR. Source Center for Infectious Diseases and Microbiology Translational Research, Division of Pediatric Infectious Diseases, Department of Pediatrics, University of Minnesota Medical School, Minneapolis, MN 55455, USA. schleiss@umn.edu Comment on Lancet. 2011 Apr 9;377(9773):1256-63.
	PMID: 21481691 [PubMed - indexed for MEDLINE]
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7.	Science. 2011 Apr 8;332(6026):186-7. Immunology. Eosinophils forestall obesity. Maizels RM, Allen JE. Source Centre for Immunity, Infection and Evolution and the Institute for Immunology and Infection Research, University of Edinburgh, Edinburgh EH9 3JT, UK. r.maizels@ed.ac.uk Comment on Science. 2011 Apr 8;332(6026):243-7.
	PMID: 21474746 [PubMed - indexed for MEDLINE]
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8.	Lancet. 2011 Apr 9;377(9773):1276-87. Epub 2011 Mar 28. Osteoporosis: now and the future. Rachner TD, Khosla S, Hofbauer LC. Source Division of Endocrinology, Diabetes, and Bone Diseases, Dresden Technical University Medical Centre, Dresden, Germany. Abstract Osteoporosis is a common disease characterised by a systemic impairment of bone mass and microarchitecture that results in fragility fractures. With an ageing population, the medical and socioeconomic effect of osteoporosis, particularly postmenopausal osteoporosis, will increase further. A detailed knowledge of bone biology with molecular insights into the communication between bone-forming osteoblasts and bone-resorbing osteoclasts and the orchestrating signalling network has led to the identification of novel therapeutic targets. Novel treatment strategies have been developed that aim to inhibit excessive bone resorption and increase bone formation. The most promising novel treatments include: denosumab, a monoclonal antibody for receptor activator of NF-κB ligand, a key osteoclast cytokine; odanacatib, a specific inhibitor of the osteoclast protease cathepsin K; and antibodies against the proteins sclerostin and dickkopf-1, two endogenous inhibitors of bone formation. This overview discusses these novel therapies and explains their underlying physiology. Copyright © 2011 Elsevier Ltd. All rights reserved.
	PMID: 21450337 [PubMed - indexed for MEDLINE]
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9.	Science. 2011 Apr 8;332(6026):243-7. Epub 2011 Mar 24. Eosinophils sustain adipose alternatively activated macrophages associated with glucos e homeostasis. Wu D, Molofsky AB, Liang HE, Ricardo-Gonzalez RR, Jouihan HA, Bando JK, Chawla A, Locksley RM. Source Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94143-0795, USA. Comment in Science. 2011 Apr 8;332(6026):186-7. Abstract Eosinophils are associated with helminth immunity and allergy, often in conjunction with alternatively activated macrophages (AAMs). Adipose tissue AAMs are necessary to maintain glucose homeostasis and are induced by the cytokine interleukin-4 (IL-4). Here, we show that eosinophils are the major IL-4-expressing cells in white adipose tissues of mice, and, in their absence, AAMs are greatly attenuated. Eosinophils migrate into adipose tissue by an integrin-dependent process and reconstitute AAMs through an IL-4- or IL-13-dependent process. Mice fed a high-fat diet develop increased body fat, impaired glucose tolerance, and insulin resistance in the absence of eosinophils, and helminth-induced adipose tissue eosinophilia enhances glucose tolerance. Our results suggest that eosinophils play an unexpected role in metabolic homeostasis through maintenance of adipose AAMs.
	PMID: 21436399 [PubMed - indexed for MEDLINE]
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1.	Lancet. 2011 Mar 26;377(9771):1048. Key indicators of health in the USA. [No authors listed]
	PMID: 21440793 [PubMed - indexed for MEDLINE]
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2.	Nat Genet. 2011 Mar;43(3):178-9. A twist on admixture mapping. Chanock SJ. Comment on: Nat Genet. 2011 Mar;43(3):237-41. Abstract A new study uses genome-wide SNP genotypes to identify a subset of children undergoing therapy for acute lymphoblastic leukemia that are at increased risk for relapse. Borrowing from the classical approach of admixture mapping, the work shows how genome-wide assessment of genetic ancestry can be used as a biomarker for disease outcome.
	PMID: 21350496 [PubMed - indexed for MEDLINE]
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3.	Nat Genet. 2011 Mar;43(3):269-76. Epub 2011 Feb 13. Discovery and genotyping of genome structural polymorphism by sequencing on a population scale. Handsaker RE, Korn JM, Nemesh J, McCarroll SA. Department of Genetics, Harvard Medical School, Boston, Massachusetts, USA. Abstract Accurate and complete analysis of genome variation in large populations will be required to understand the role of genome variation in complex disease. We present an analytical framework for characterizing genome deletion polymorphism in populations using sequence data that are distributed across hundreds or thousands of genomes. Our approach uses population-level concepts to reinterpret the technical features of sequence data that often reflect structural variation. In the 1000 Genomes Project pilot, this approach identified deletion polymorphism across 168 genomes (sequenced at 4 × average coverage) with sensitivity and specificity unmatched by other algorithms. We also describe a way to determine the allelic state or genotype of each deletion polymorphism in each genome; the 1000 Genomes Project used this approach to type 13,826 deletion polymorphisms (48-995,664 bp) at high accuracy in populations. These methods offer a way to relate genome structural polymorphism to complex disease in populations.
	PMID: 21317889 [PubMed - indexed for MEDLINE]
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4.	Nat Genet. 2011 Mar;43(3):237-41. Epub 2011 Feb 6. Ancestry and pharmacogenomics of relapse in acute lymphoblastic leukemia. Yang JJ, Cheng C, Devidas M, Cao X, Fan Y, Campana D, Yang W, Neale G, Cox NJ, Scheet P, Borowitz MJ, Winick NJ, Martin PL, Willman CL, Bowman WP, Camitta BM, Carroll A, Reaman GH, Carroll WL, Loh M, Hunger SP, Pui CH, Evans WE, Relling MV. Department of Pharmaceutical Sciences, St. Jude Children's Research Hospital, Memphis, Tennessee, USA. Comment in: Nat Genet. 2011 Mar;43(3):178-9. Abstract Although five-year survival rates for childhood acute lymphoblastic leukemia (ALL) are now over 80% in most industrialized countries, not all children have benefited equally from this progress. Ethnic differences in survival after childhood ALL have been reported in many clinical studies, with poorer survival observed among African Americans or those with Hispanic ethnicity when compared with European Americans or Asians. The causes of ethnic differences remain uncertain, although both genetic and non-genetic factors are likely important. Interrogating genome-wide germline SNP genotypes in an unselected large cohort of children with ALL, we observed that the component of genomic variation that co-segregated with Native American ancestry was associated with risk of relapse (P = 0.0029) even after adjusting for known prognostic factors (P = 0.017). Ancestry-related differences in relapse risk were abrogated by the addition of a single extra phase of chemotherapy, indicating that modifications to therapy can mitigate the ancestry-related risk of relapse.
	PMID: 21297632 [PubMed - indexed for MEDLINE]
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1.	Lancet. 2011 Apr 2;377(9772):1153-4; author reply 1154. Artesunate for severe malaria in African children. Obaro SK. Comment on: Lancet. 2010 Nov 13;376(9753):1647-57.
	PMID: 21459208 [PubMed - indexed for MEDLINE]

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1.	Science. 2011 Mar 25;331(6024):1612-6. CD40 agonists alter tumor stroma and show efficacy against pancreatic carcinoma in mice and humans. Beatty GL, Chiorean EG, Fishman MP, Saboury B, Teitelbaum UR, Sun W, Huhn RD, Song W, Li D, Sharp LL, Torigian DA, O'Dwyer PJ, Vonderheide RH. Abramson Family Cancer Research Institute, University of Pennsylvania School of Medicine, 421 Curie Boulevard, Philadelphia, PA 19104, USA. Abstract Immunosuppressive tumor microenvironments can restrain antitumor immunity, particularly in pancreatic ductal adenocarcinoma (PDA). Because CD40 activation can reverse immune suppression and drive antitumor T cell responses, we tested the combination of an agonist CD40 antibody with gemcitabine chemotherapy in a small cohort of patients with surgically incurable PDA and observed tumor regressions in some patients. We reproduced this treatment effect in a genetically engineered mouse model of PDA and found unexpectedly that tumor regression required macrophages but not T cells or gemcitabine. CD40-activated macrophages rapidly infiltrated tumors, became tumoricidal, and facilitated the depletion of tumor stroma. Thus, cancer immune surveillance does not necessarily depend on therapy-induced T cells; rather, our findings demonstrate a CD40-dependent mechanism for targeting tumor stroma in the treatment of cancer.
	PMID: 21436454 [PubMed - indexed for MEDLINE]
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2.	Nature. 2011 Mar 17;471(7338):308-9. Vision: Dicer leaps into view. Meister G. Comment on: Nature. 2011 Mar 17;471(7338):325-30.
	PMID: 21412326 [PubMed - indexed for MEDLINE]
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3.	Nature. 2011 Mar 17;471(7338):325-30. Epub 2011 Feb 6. DICER1 deficit induces Alu RNA toxicity in age-related macular degeneration. Kaneko H, Dridi S, Tarallo V, Gelfand BD, Fowler BJ, Cho WG, Kleinman ME, Ponicsan SL, Hauswirth WW, Chiodo VA, Karikó K, Yoo JW, Lee DK, Hadziahmetovic M, Song Y, Misra S, Chaudhuri G, Buaas FW, Braun RE, Hinton DR, Zhang Q, Grossniklaus HE, Provis JM, Madigan MC, Milam AH, Justice NL, Albuquerque RJ, Blandford AD, Bogdanovich S, Hirano Y, Witta J, Fuchs E, Littman DR, Ambati BK, Rudin CM, Chong MM, Provost P, Kugel JF, Goodrich JA, Dunaief JL, Baffi JZ, Ambati J. Department of Ophthalmology & Visual Sciences, University of Kentucky, Lexington, Kentucky 40506, USA. Comment in: Nature. 2011 Mar 17;471(7338):308-9. Abstract Geographic atrophy (GA), an untreatable advanced form of age-related macular degeneration, results from retinal pigmented epithelium (RPE) cell degeneration. Here we show that the microRNA (miRNA)-processing enzyme DICER1 is reduced in the RPE of humans with GA, and that conditional ablation of Dicer1, but not seven other miRNA-processing enzymes, induces RPE degeneration in mice. DICER1 knockdown induces accumulation of Alu RNA in human RPE cells and Alu-like B1 and B2 RNAs in mouse RPE. Alu RNA is increased in the RPE of humans with GA, and this pathogenic RNA induces human RPE cytotoxicity and RPE degeneration in mice. Antisense oligonucleotides targeting Alu/B1/B2 RNAs prevent DICER1 depletion-induced RPE degeneration despite global miRNA downregulation. DICER1 degrades Alu RNA, and this digested Alu RNA cannot induce RPE degeneration in mice. These findings reveal a miRNA-independent cell survival function for DICER1 involving retrotransposon transcript degradation, show that Alu RNA can directly cause human pathology, and identify new targets for a major cause of blindness.
	PMID: 21297615 [PubMed - indexed for MEDLINE]
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1.	N Engl J Med. 2011 Mar 24;364(12):1144-53. Genomics and drug response. Wang L, McLeod HL, Weinshilboum RM. Division of Clinical Pharmacology, Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Medical School, Mayo Clinic, Rochester, MN 55905, USA. Free Article
	PMID: 21428770 [PubMed - indexed for MEDLINE]
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2.	N Engl J Med. 2011 Mar 24;364(12):1126-33. Carbamazepine-induced toxic effects and HLA-B*1502 screening in Taiwan. Chen P, Lin JJ, Lu CS, Ong CT, Hsieh PF, Yang CC, Tai CT, Wu SL, Lu CH, Hsu YC, Yu HY, Ro LS, Lu CT, Chu CC, Tsai JJ, Su YH, Lan SH, Sung SF, Lin SY, Chuang HP, Huang LC, Chen YJ, Tsai PJ, Liao HT, Lin YH, Chen CH, Chung WH, Hung SI, Wu JY, Chang CF, Chen L, Chen YT, Shen CY; Taiwan SJS Consortium. Collaborators: Su JJ, Lee MJ, Yen DJ, Liao KK, Hong CJ, Chen C, Su MS, Chuang CP, Chen CM, Lin KP, Lin JC, Chang CA, Yuan RY, Hu CJ, Yu CM, Shen JJ, Kuo YT, Sung JY, Lai TC, Wang KC, Wang CJ, Wang HC, Yeh JH, Hsu WC, Huang KL, Chiang TR, Chung WH, Chang YJ, Hsu WC, Lin KL, Wu YL, Huang CR, Chen YC, Chien HU, Wu TC, Sung CY, Lee YY, Hsieh MJ, Huang KL, His MS, Lee TH, Lyu RK, Yeh TH, Chuang WL, Chen CC, Huang CC, Chang HS, Wu YR, Lai SC, Chu NS, Kuo HC, Huang YZ, Weng YH, Ruy SJ, Fung HC, Chen RS, Chen ST, Chang TY, Hsieh HY, Tsai YT, Cheng MY, Yip BS, Chou PC, Kuo TM, Tsai PC, Tsai CH, Liu CH, Kuo HT, Chou IC, Yang YW, Hsu YT, Tsai TC, Lin KH, Lin JC, Liu CS, Chang MY, Wu CS, Wang HP, Hung PH, Kao YH, Lee CD, Hsiao MC, Wu CY, Wong TW, Yeh PS, Lin HJ, Ke DR, Cheng TJ, Lin KC, Chang CY, Chou CH, Tseng KY, Khor GT, Hsu CY, Liou CW, Chuang YC, Chang WN, Lai SL, Lin TK, Jen HM, Liu AB, Chen WH, Lin PY, Lee MT, Wei CY. Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan. Abstract BACKGROUND: Carbamazepine, an anticonvulsant and a mood-stabilizing drug, is the main cause of the Stevens-Johnson syndrome (SJS) and its related disease, toxic epidermal necrolysis (TEN), in Southeast Asian countries. Carbamazepine-induced SJS-TEN is strongly associated with the HLA-B*1502 allele. We sought to prevent carbamazepine-induced SJS-TEN by using HLA-B*1502 screening to prospectively identify subjects at genetic risk for the condition. METHODS: From 23 hospitals in Taiwan, we recruited 4877 candidate subjects who had not taken carbamazepine. We genotyped DNA purified from the subjects' peripheral blood to determine whether they carried the HLA-B*1502 allele. Those testing positive for HLA-B*1502 (7.7% of the total) were advised not to take carbamazepine and were given an alternative medication or advised to continue taking their prestudy medication; those testing negative (92.3%) were advised to take carbamazepine. We interviewed the subjects by telephone once a week for 2 months to monitor them for symptoms. We used the estimated historical incidence of SJS-TEN as a control. RESULTS: Mild, transient rash developed in 4.3% of subjects; more widespread rash developed in 0.1% of subjects, who were hospitalized. SJS-TEN did not develop in any of the HLA-B*1502-negative subjects receiving carbamazepine. In contrast, the estimated historical incidence of carbamazepine-induced SJS-TEN (0.23%) would translate into approximately 10 cases among study subjects (P<0.001). CONCLUSIONS: The identification of subjects carrying the HLA-B*1502 allele and the avoidance of carbamazepine therapy in these subjects was strongly associated with a decrease in the incidence of carbamazepine-induced SJS-TEN. (Funded by the National Science Council of Taiwan and the Taiwan Drug Relief Foundation.).
	PMID: 21428768 [PubMed - indexed for MEDLINE]
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1.	Science. 2011 Mar 18;331(6023):1387. Genomic medicine: the social science view. Kelly SE. Comment on: Science. 2011 Feb 4;331(6017):526-9.
	PMID: 21415338 [PubMed - indexed for MEDLINE]
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2.	Science. 2011 Mar 18;331(6023):1387. Genomic medicine: putting our tools to use. Schmidt M. Comment on: Science. 2011 Feb 4;331(6017):526-9.
	PMID: 21415335 [PubMed - indexed for MEDLINE]
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1.	Lancet. 2011 Mar 12;377(9769):900; author reply 901. Cholinesterase inhibitor treatment in patients with delirium. Berg RM, Möller K. Comment on: Lancet. 2010 Nov 27;376(9755):1829-37.
	PMID: 21397758 [PubMed - indexed for MEDLINE]
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2.	Nat Genet. 2011 Feb;43(2):88-9. The (new) new synthesis and epigenetic capacitors of morphological evolution. Ruden DM. Comment on: Nat Genet. 2011 Feb;43(2):153-8.
	PMID: 21270834 [PubMed - indexed for MEDLINE]
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3.	Nat Genet. 2011 Feb;43(2):87-8. A cornucopia of maize genes. Haley C. Comment on: Nat Genet. 2011 Feb;43(2):163-8. Nat Genet. 2011 Feb;43(2):159-62.
	PMID: 21270833 [PubMed - indexed for MEDLINE]
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