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 September 21Search: (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. | Science. 2013 Sep 13;341(6151):1250-3. doi: 10.1126/science.1240988.Cytoplasmic LPS activates caspase-11: implications in TLR4-independent endotoxic shock.Hagar JA, Powell DA, Aachoui Y, Ernst RK, Miao EA.Department of Microbiology and Immunology and Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. Comment in
AbstractInflammatory caspases, such as caspase-1 and -11, mediate innate immune detection of pathogens. Caspase-11 induces pyroptosis, a form of programmed cell death, and specifically defends against bacterial pathogens that invade the cytosol. During endotoxemia, however, excessive caspase-11 activation causes shock. We report that contamination of the cytoplasm by lipopolysaccharide (LPS) is the signal that triggers caspase-11 activation in mice. Specifically, caspase-11 responds to penta- and hexa-acylated lipid A, whereas tetra-acylated lipid A is not detected, providing a mechanism of evasion for cytosol-invasive Francisella. Priming the caspase-11 pathway in vivo resulted in extreme sensitivity to subsequent LPS challenge in both wild-type and Tlr4-deficient mice, whereas Casp11-deficient mice were relatively resistant. Together, our data reveal a new pathway for detecting cytoplasmic LPS. |
| PMID: 24031018 [PubMed - indexed for MEDLINE] | |
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| 2. | Science. 2013 Sep 13;341(6151):1239-42. doi: 10.1126/science.1239352.Marine taxa track local climate velocities.Pinsky ML, Worm B, Fogarty MJ, Sarmiento JL, Levin SA.Department of Ecology and Evolutionary Biology, Princeton University, Princeton, NJ 08544, USA. malin.pinsky@rutgers.edu AbstractOrganisms are expected to adapt or move in response to climate change, but observed distribution shifts span a wide range of directions and rates. Explanations often emphasize biological distinctions among species, but general mechanisms have been elusive. We tested an alternative hypothesis: that differences in climate velocity-the rate and direction that climate shifts across the landscape-can explain observed species shifts. We compiled a database of coastal surveys around North America from 1968 to 2011, sampling 128 million individuals across 360 marine taxa. Climate velocity explained the magnitude and direction of shifts in latitude and depth much more effectively than did species characteristics. Our results demonstrate that marine species shift at different rates and directions because they closely track the complex mosaic of local climate velocities. |
| PMID: 24031017 [PubMed - indexed for MEDLINE] | |
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| 3. | Science. 2013 Sep 13;341(6151):1184-5. doi: 10.1126/science.1243939.Immunology. Sensing endotoxins from within.Kagan JC.Harvard Medical School and Division of Gastroenterology, Boston Children's Hospital, Boston, MA 02115, USA. jonathan.kagan@childrens.harvard.edu Comment on |
| PMID: 24031006 [PubMed - indexed for MEDLINE] | |
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| 4. | Science. 2013 Sep 13;341(6151):1163. doi: 10.1126/science.341.6151.1163.Genomics. Researchers to explore promise, risks of sequencing newborns' DNA.Kaiser J. |
| PMID: 24030994 [PubMed - indexed for MEDLINE] | |
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| 5. | Science. 2013 Sep 13;341(6151):1182-4. doi: 10.1126/science.1240880. Epub 2013 Aug 29.Evolution. What, where, and when?Knapp S.Natural History Museum, London, UK. s.knapp@nhm.ac.uk |
| PMID: 23989953 [PubMed - indexed for MEDLINE] | |
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| 6. | Science. 2013 Sep 13;341(6151):1246-9. doi: 10.1126/science.1240248. Epub 2013 Jul 25.Noncanonical inflammasome activation by intracellular LPS independent of TLR4.Kayagaki N, Wong MT, Stowe IB, Ramani SR, Gonzalez LC, Akashi-Takamura S, Miyake K, Zhang J, Lee WP, Muszyński A, Forsberg LS, Carlson RW, Dixit VM.Department of Physiological Chemistry, Genentech, South San Francisco, CA 94080, USA. kayagaki@gene.com Comment in
AbstractGram-negative bacteria including Escherichia coli, Citrobacter rodentium, Salmonella typhimurium, and Shigella flexneri are sensed in an ill-defined manner by an intracellular inflammasome complex that activates caspase-11. We show that macrophages loaded with synthetic lipid A, E. coli lipopolysaccharide (LPS), or S. typhimurium LPS activate caspase-11 independently of the LPS receptor Toll-like receptor 4 (TLR4). Consistent with lipid A triggering the noncanonical inflammasome, LPS containing a divergent lipid A structure antagonized caspase-11 activation in response to E. coli LPS or Gram-negative bacteria. Moreover, LPS-mutant E. coli failed to activate caspase-11. Tlr4(-/-) mice primed with TLR3 agonist polyinosinic:polycytidylic acid [poly(I:C)] to induce pro-caspase-11 expression were as susceptible as wild-type mice were to sepsis induced by E. coli LPS. These data unveil a TLR4-independent mechanism for innate immune recognition of LPS. |
| PMID: 23887873 [PubMed - indexed for MEDLINE] | |
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posted by JKB @ 03:30
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