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, 2013 June 01Search: (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 |
| 1. | Nature. 2013 May 9;497(7448):235-8. doi: 10.1038/nature12068.Future sea-level rise from Greenland's main outlet glaciers in a warming climate.Nick FM, Vieli A, Andersen ML, Joughin I, Payne A, Edwards TL, Pattyn F, van de Wal RS.Laboratoire de Glaciologie, Université Libre de Bruxelles, B-1050 Brussels, Belgium. faezeh.nick@unis.no AbstractOver the past decade, ice loss from the Greenland Ice Sheet increased as a result of both increased surface melting and ice discharge to the ocean. The latter is controlled by the acceleration of ice flow and subsequent thinning of fast-flowing marine-terminating outlet glaciers. Quantifying the future dynamic contribution of such glaciers to sea-level rise (SLR) remains a major challenge because outlet glacier dynamics are poorly understood. Here we present a glacier flow model that includes a fully dynamic treatment of marine termini. We use this model to simulate behaviour of four major marine-terminating outlet glaciers, which collectively drain about 22 per cent of the Greenland Ice Sheet. Using atmospheric and oceanic forcing from a mid-range future warming scenario that predicts warming by 2.8 degrees Celsius by 2100, we project a contribution of 19 to 30 millimetres to SLR from these glaciers by 2200. This contribution is largely (80 per cent) dynamic in origin and is caused by several episodic retreats past overdeepenings in outlet glacier troughs. After initial increases, however, dynamic losses from these four outlets remain relatively constant and contribute to SLR individually at rates of about 0.01 to 0.06 millimetres per year. These rates correspond to ice fluxes that are less than twice those of the late 1990s, well below previous upper bounds. For a more extreme future warming scenario (warming by 4.5 degrees Celsius by 2100), the projected losses increase by more than 50 per cent, producing a cumulative SLR of 29 to 49 millimetres by 2200. |
| PMID: 23657350 [PubMed - indexed for MEDLINE] | |
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| 2. | Nature. 2013 May 9;497(7448):188. doi: 10.1038/497188d.History: Non-coding RNA foreseen 48 years ago.Harris H.Comment on
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| PMID: 23657339 [PubMed - indexed for MEDLINE] | |
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| 3. | Nat Genet. 2013 Mar;45(3):325-9. doi: 10.1038/ng.2553. Epub 2013 Feb 10.Endogenous retroviruses function as species-specific enhancer elements in the placenta.Chuong EB, Rumi MA, Soares MJ, Baker JC.Department of Genetics, Stanford University School of Medicine, Stanford, California, USA. echuong@stanford.edu AbstractThe mammalian placenta is remarkably distinct between species, suggesting a history of rapid evolutionary diversification. To gain insight into the molecular drivers of placental evolution, we compared biochemically predicted enhancers in mouse and rat trophoblast stem cells (TSCs) and found that species-specific enhancers are highly enriched for endogenous retroviruses (ERVs) on a genome-wide level. One of these ERV families, RLTR13D5, contributes hundreds of mouse-specific histone H3 lysine 4 monomethylation (H3K4me1)- and histone H3 lysine 27 acetylation (H3K27ac)-defined enhancers that functionally bind Cdx2, Eomes and Elf5-core factors that define the TSC regulatory network. Furthermore, we show that RLTR13D5 is capable of driving gene expression in rat placental cells. Analysis in other tissues shows that species-specific ERV enhancer activity is generally restricted to hypomethylated tissues, suggesting that tissues permissive for ERV activity gain access to an otherwise silenced source of regulatory variation. Overall, our results implicate ERV enhancer co-option as a mechanism underlying the extensive evolutionary diversification of placental development. |
| PMID: 23396136 [PubMed - indexed for MEDLINE] | |
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| 4. | Nat Genet. 2013 Mar;45(3):285-9. doi: 10.1038/ng.2526. Epub 2013 Jan 20.Genomic sequencing of meningiomas identifies oncogenic SMO and AKT1 mutations.Brastianos PK, Horowitz PM, Santagata S, Jones RT, McKenna A, Getz G, Ligon KL, Palescandolo E, Van Hummelen P, Ducar MD, Raza A, Sunkavalli A, Macconaill LE, Stemmer-Rachamimov AO, Louis DN, Hahn WC, Dunn IF, Beroukhim R.Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA. Comment in
AbstractMeningiomas are the most common primary nervous system tumor. The tumor suppressor NF2 is disrupted in approximately half of all meningiomas, but the complete spectrum of genetic changes remains undefined. We performed whole-genome or whole-exome sequencing on 17 meningiomas and focused sequencing on an additional 48 tumors to identify and validate somatic genetic alterations. Most meningiomas had simple genomes, with fewer mutations, rearrangements and copy-number alterations than reported in other tumors in adults. However, several meningiomas harbored more complex patterns of copy-number changes and rearrangements, including one tumor with chromothripsis. We confirmed focal NF2 inactivation in 43% of tumors and found alterations in epigenetic modifiers in an additional 8% of tumors. A subset of meningiomas lacking NF2 alterations harbored recurrent oncogenic mutations in AKT1 (p.Glu17Lys) and SMO (p.Trp535Leu) and exhibited immunohistochemical evidence of activation of these pathways. These mutations were present in therapeutically challenging tumors of the skull base and higher grade. These results begin to define the spectrum of genetic alterations in meningiomas and identify potential therapeutic targets. |
| PMID: 23334667 [PubMed - indexed for MEDLINE] | |
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| 5. | High Alt Med Biol. 2012 Dec;13(4):263-8. doi: 10.1089/ham.2011.1097.Retinal vessel tortuosity in response to hypobaric hypoxia.MacCormick IJ, Somner J, Morris DS, MacGillivray TJ, Bourne RR, Huang SS, MacCormick A, Aspinall PA, Baillie JK, Thompson AA, Dhillon B.Malawi-Liverpool-Wellcome Trust Clinical Research Programme, College of Medicine, Blantyre, Malawi. Ian.maccormick@gmail.com AbstractPURPOSE:Retinal vascular tortuosity is associated with retinopathy of differing etiologies, including hypertension, diabetes, and hypoxia. However, detailed understanding of the underlying pathophysiology is lacking. The aim of this study was to map changes in tortuosity associated with hypoxia at high altitude, and to determine the influence of sildenafil and an antioxidant preparation on altitude-induced tortuosity. METHODS:We measured the tortuosity of retinal vessels using a semi-automated method in 35 young, healthy subjects exposed to hypobaric hypoxia for 7 days at 5200 m, and compared the measurements to those from the same vessels at sea level. These subjects simultaneously took part in a randomized double-blind placebo-controlled trial of sildenafil and antioxidant. Comparison of tortuosity between these subgroups was performed. RESULTS:High altitude was associated with the development of retinal tortuosity in individual vessels. A nonsignificant trend suggests this is limited by prophylaxis with sildenafil or antioxidant. CONCLUSIONS:Retinal vessel tortuosity increases rapidly at high altitude. We suggest that retinal vessel tortuosity at altitude may result from increased sheer stress causing elongation of vessel segments and that this might be limited by agents that act to preserve nitric oxide dependent vasodilation. Trial Registration Numbers: NCT00664001, NCT00627965. |
| PMID: 23270443 [PubMed - indexed for MEDLINE] | |
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