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Sender's message: Sepsis or genomics or altitude: JKB_daily1
Sent on Tuesday, 2015 January 27
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(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]))View complete results in PubMed (results may change over time).
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| 1. | Science. 2015 Jan 16;347(6219):250-4. doi: 10.1126/science.1258732.Bishop CM1, Spivey RJ1, Hawkes LA2, Batbayar N3, Chua B4, Frappell PB5, Milsom WK4, Natsagdorj T6, Newman SH7, Scott GR8, Takekawa JY9, Wikelski M10, Butler PJ11.AbstractThe physiological and biomechanical requirements of flight at high altitude have been the subject of much interest. Here, we uncover a steep relation between heart rate and wingbeat frequency (raised to the exponent 3.5) and estimated metabolic power and wingbeat frequency (exponent 7) of migratory bar-headed geese. Flight costs increase more rapidly than anticipated as air density declines, which overturns prevailing expectations that this species should maintain high-altitude flight when traversing the Himalayas. Instead, a "roller coaster" strategy, of tracking the underlying terrain and discarding large altitude gains only to recoup them later in the flight with occasional benefits from orographic lift, is shown to be energetically advantageous for flights over the Himalayas. Copyright © 2015, American Association for the Advancement of Science. |
| PMID: 25593180 [PubMed - indexed for MEDLINE] |
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| 2. | Science. 2015 Jan 16;347(6219):248-50. doi: 10.1126/science.1259172. Epub 2014 Nov 20.Chen FH1, Dong GH1, Zhang DJ2, Liu XY3, Jia X2, An CB2, Ma MM2, Xie YW2, Barton L4, Ren XY5, Zhao ZJ6, Wu XH7, Jones MK8.AbstractOur understanding of when and how humans adapted to living on the Tibetan Plateau at altitudes above 2000 to 3000 meters has been constrained by a paucity of archaeological data. Here we report data sets from the northeastern Tibetan Plateau indicating that the first villages were established only by 5200 calendar years before the present (cal yr B.P.). Using these data, we tested the hypothesis that a novel agropastoral economy facilitated year-round living at higher altitudes since 3600 cal yr B.P. This successful subsistence strategy facilitated the adaptation of farmers-herders to the challenges of global temperature decline during the late Holocene. Copyright © 2015, American Association for the Advancement of Science. |
| PMID: 25593179 [PubMed - indexed for MEDLINE] |
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| 3. | Nature. 2014 Dec 11;516(7530):198-206. doi: 10.1038/nature14046.Hussein SM1, Puri MC2, Tonge PD1, Benevento M3, Corso AJ4, Clancy JL5, Mosbergen R6, Li M1, Lee DS7, Cloonan N8, Wood DL8, Munoz J3, Middleton R9, Korn O6, Patel HR10, White CA11, Shin JY12, Gauthier ME8, Lê Cao KA8, Kim JI7, Mar JC13, Shakiba N14, Ritchie W9, Rasko JE15, Grimmond SM8, Zandstra PW11, Wells CA16, Preiss T17, Seo JS18, Heck AJ3, Rogers IM19, Nagy A20.AbstractSomatic cell reprogramming to a pluripotent state continues to challenge many of our assumptions about cellular specification, and despite major efforts, we lack a complete molecular characterization of the reprograming process. To address this gap in knowledge, we generated extensive transcriptomic, epigenomic and proteomic data sets describing the reprogramming routes leading from mouse embryonic fibroblasts to induced pluripotency. Through integrative analysis, we reveal that cells transition through distinct gene expression and epigenetic signatures and bifurcate towards reprogramming transgene-dependent and -independent stable pluripotent states. Early transcriptional events, driven by high levels of reprogramming transcription factor expression, are associated with widespread loss of histone H3 lysine 27 (H3K27me3) trimethylation, representing a general opening of the chromatin state. Maintenance of high transgene levels leads to re-acquisition of H3K27me3 and a stable pluripotent state that is alternative to the embryonic stem cell (ESC)-like fate. Lowering transgene levels at an intermediate phase, however, guides the process to the acquisition of ESC-like chromatin and DNA methylation signature. Our data provide a comprehensive molecular description of the reprogramming routes and is accessible through the Project Grandiose portal at http://www.stemformatics.org. |
| PMID: 25503233 [PubMed - indexed for MEDLINE] |
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| 4. | Nature. 2014 Dec 11;516(7530):242-5. doi: 10.1038/nature13760. Epub 2014 Sep 28.Jacobs FM1, Greenberg D2, Nguyen N3, Haeussler M4, Ewing AD5, Katzman S4, Paten B4, Salama SR6, Haussler D6.AbstractThroughout evolution primate genomes have been modified by waves of retrotransposon insertions. For each wave, the host eventually finds a way to repress retrotransposon transcription and prevent further insertions. In mouse embryonic stem cells, transcriptional silencing of retrotransposons requires KAP1 (also known as TRIM28) and its repressive complex, which can be recruited to target sites by KRAB zinc-finger (KZNF) proteins such as murine-specific ZFP809 which binds to integrated murine leukaemia virus DNA elements and recruits KAP1 to repress them. KZNF genes are one of the fastest growing gene families in primates and this expansion is hypothesized to enable primates to respond to newly emerged retrotransposons. However, the identity of KZNF genes battling retrotransposons currently active in the human genome, such as SINE-VNTR-Alu (SVA) and long interspersed nuclear element 1 (L1), is unknown. Here we show that two primate-specific KZNF genes rapidly evolved to repress these two distinct retrotransposon families shortly after they began to spread in our ancestral genome. ZNF91 underwent a series of structural changes 8-12 million years ago that enabled it to repress SVA elements. ZNF93 evolved earlier to repress the primate L1 lineage until ∼12.5 million years ago when the L1PA3-subfamily of retrotransposons escaped ZNF93's restriction through the removal of the ZNF93-binding site. Our data support a model where KZNF gene expansion limits the activity of newly emerged retrotransposon classes, and this is followed by mutations in these retrotransposons to evade repression, a cycle of events that could explain the rapid expansion of lineage-specific KZNF genes. |
| PMID: 25274305 [PubMed - indexed for MEDLINE] |
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