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

Sent on Wednesday, 2012 August 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

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1.	Nature. 2012 May 2;486(7403):420-8. doi: 10.1038/nature10831. Experimental adaptation of an influenza H5 HA confers respiratory droplet transmission to a reassortant H5 HA/H1N1 virus in ferrets. Imai M, Watanabe T, Hatta M, Das SC, Ozawa M, Shinya K, Zhong G, Hanson A, Katsura H, Watanabe S, Li C, Kawakami E, Yamada S, Kiso M, Suzuki Y, Maher EA, Neumann G, Kawaoka Y. Source Department of Pathobiological Sciences, University of Wisconsin-Madison, Madison, Wisconsin 53711, USA. Comment in Virology: bird flu in mammals. [Nature. 2012] Virology: bird flu in mammals.Yen HL, Peiris JS. Nature. 2012 May 2; 486(7403):332-3. Epub 2012 May 2. Abstract Highly pathogenic avian H5N1 influenza A viruses occasionally infect humans, but currently do not transmit efficiently among humans. The viral haemagglutinin (HA) protein is a known host-range determinant as it mediates virus binding to host-specific cellular receptors. Here we assess the molecular changes in HA that would allow a virus possessing subtype H5 HA to be transmissible among mammals. We identified a reassortant H5 HA/H1N1 virus-comprising H5 HA (from an H5N1 virus) with four mutations and the remaining seven gene segments from a 2009 pandemic H1N1 virus-that was capable of droplet transmission in a ferret model. The transmissible H5 reassortant virus preferentially recognized human-type receptors, replicated efficiently in ferrets, caused lung lesions and weight loss, but was not highly pathogenic and did not cause mortality. These results indicate that H5 HA can convert to an HA that supports efficient viral transmission in mammals; however, we do not know whether the four mutations in the H5 HA identified here would render a wholly avian H5N1 virus transmissible. The genetic origin of the remaining seven viral gene segments may also critically contribute to transmissibility in mammals. Nevertheless, as H5N1 viruses continue to evolve and infect humans, receptor-binding variants of H5N1 viruses with pandemic potential, including avian-human reassortant viruses as tested here, may emerge. Our findings emphasize the need to prepare for potential pandemics caused by influenza viruses possessing H5 HA, and will help individuals conducting surveillance in regions with circulating H5N1 viruses to recognize key residues that predict the pandemic potential of isolates, which will inform the development, production and distribution of effective countermeasures. PMCID: PMC3388103 [Available on 2012/12/21]
	PMID: 22722205 [PubMed - indexed for MEDLINE]
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2.	Nature. 2012 Apr 18;486(7403):346-52. The genomic and transcriptomic architecture of 2,000 breast tumours reveals novel subgroups. Curtis C, Shah SP, Chin SF, Turashvili G, Rueda OM, Dunning MJ, Speed D, Lynch AG, Samarajiwa S, Yuan Y, Gräf S, Ha G , Haffari G, Bashashati A, Russell R, McKinney S; METABRIC Group, Langerød A, Green A, Provenzano E, Wishart G, Pinder S, Watson P, Markowetz F, Murphy L, Ellis I, Purushotham A, Børresen-Dale AL, Brenton JD, Tavaré S, Caldas C, Aparicio S. Collaborators: Caldas C, Aparicio S, Curtis C, Shah SP, Caldas C, Aparicio S, Brenton JD, Ellis I, Huntsman D, Pinder S, Purushotham A, Murphy L, Caldas C, Aparicio S, Caldas C, Bardwell H, Chin SF, Curtis C, Ding Z, Gräf S, Jones L, Liu B, Lynch AG, Papatheodorou I, Sammut SJ, Wishart G, Aparicio S, Chia S, Gelmon K, Huntsman D, McKinney S, Speers C, Turashvili G, Watson P, Ellis I, Blamey R, Green A, Macmillan D, Rakha E, Purushotham A, Gillett C, Grigoriadis A, Pinder S, de Rinaldis E, Tutt A, Murphy L, Parisien M, Troup S, Caldas C, Chin SF, Chan D, Fielding C, Maia AT, McGuire S, Osborne M, Sayalero SM, Spiteri I, Hadfield J, Aparicio S, Turashvili G, Bell L, Chow K, Gale N, Huntsman D, Kovalik M, Ng Y, Prentice L, Caldas C, Tavaré S, Curtis C, Dunning MJ, Gräf S, Lynch AG, Rueda OM, Russell R, Samarajiwa S, Speed D, Markowetz F, Yuan Y, Brenton JD, Aparicio S, Shah SP, Bashashati A, Ha G, Haffari G, McKinney S. Source Department of Oncology, University of Cambridge, Hills Road, Cambridge CB2 2XZ, UK. Comment in Copy number aberrations define breast cancer subgroups. [Cancer Discov. 2012] Copy number aberrations define breast cancer subgroups.[No authors listed]Cancer Discov. 2012 Jun; 2(6):OF6. Epub 2012 Apr 26. Genomics: the breast cancer landscape. [Nature. 2012] Genomics: the breast cancer landscape.Gray J, Druker B. Nature. 2012 Jun 20; 486(7403):328-9. Epub 2012 Jun 20. Abstract The elucidation of breast cancer subgroups and their molecular drivers requires integrated views of the genome and transcriptome from representative numbers of patients. We present an integrated analysis of copy number and gene expression in a discovery and validation set of 997 and 995 primary breast tumours, respectively, with long-term clinical follow-up. Inherited variants (copy number variants and single nucleotide polymorphisms) and acquired somatic copy number aberrations (CNAs) were associated with expression in ~40% of genes, with the landscape dominated by cis- and trans-acting CNAs. By delineating expression outlier genes driven in cis by CNAs, we identified putative cancer genes, including deletions in PPP2R2A, MTAP and MAP2K4. Unsupervised analysis of paired DNA–RNA profiles revealed novel subgroups with distinct clinical outcomes, which reproduced in the validation cohort. These include a high-risk, oestrogen-receptor-positive 11q13/14 cis-acting subgroup and a favourable prognosis subgroup devoid of CNAs. Trans-acting aberration hotspots were found to modulate subgroup-specific gene networks, including a TCR deletion-mediated adaptive immune response in the 'CNA-devoid' subgroup and a basal-specific chromosome 5 deletion-associated mitotic network. Our results provide a novel molecular stratification of the breast cancer population, derived from the impact of somatic CNAs on the transcriptome.
	PMID: 22522925 [PubMed - indexed for MEDLINE]
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