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Träfflista för sökning "WFRF:(Guo Fei) srt2:(2010-2014)"

Sökning: WFRF:(Guo Fei) > (2010-2014)

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1.
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2.
  • Feng, Feng, et al. (författare)
  • Room-temperature large magnetic-dielectric coupling in new phase anatase VTiO4
  • 2013
  • Ingår i: Chemical Communications. - : Royal Society of Chemistry (RSC). - 1359-7345 .- 1364-548X. ; 49:89, s. 10462-10464
  • Tidskriftsartikel (refereegranskat)abstract
    • The synthetic new-phase VTiO4, as a new solid solution structure of anatase type, brings a large magnetodielectric ratio (Delta epsilon/epsilon(0)) of 7.2% at 300 K, representing a new simple-oxide structural catalogue exhibiting a room-temperature large magnetic-dielectric effect.
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3.
  • Wang, Guo-dong, et al. (författare)
  • The genomics of selection in dogs and the parallel evolution between dogs and humans
  • 2013
  • Ingår i: Nature Communications. - : Nature Publishing Group. - 2041-1723. ; 4, s. 1860-
  • Tidskriftsartikel (refereegranskat)abstract
    • The genetic bases of demographic changes and artificial selection underlying domestication are of great interest in evolutionary biology. Here we perform whole-genome sequencing of multiple grey wolves, Chinese indigenous dogs and dogs of diverse breeds. Demographic analysis show that the split between wolves and Chinese indigenous dogs occurred 32,000 years ago and that the subsequent bottlenecks were mild. Therefore, dogs may have been under human selection over a much longer time than previously concluded, based on molecular data, perhaps by initially scavenging with humans. Population genetic analysis identifies a list of genes under positive selection during domestication, which overlaps extensively with the corresponding list of positively selected genes in humans. Parallel evolution is most apparent in genes for digestion and metabolism, neurological process and cancer. Our study, for the first time, draws together humans and dogs in their recent genomic evolution.
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4.
  • Wei, Ting, et al. (författare)
  • Developed and developing world responsibilities for historical climate change and CO2 mitigation
  • 2012
  • Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 0027-8424 .- 1091-6490. ; 109:32, s. 12911-12915
  • Tidskriftsartikel (refereegranskat)abstract
    • At the United Nations Framework Convention on Climate Change Conference in Cancun, in November 2010, the Heads of State reached an agreement on the aim of limiting the global temperature rise to 2 degrees C relative to preindustrial levels. They recognized that long-term future warming is primarily constrained by cumulative anthropogenic greenhouse gas emissions, that deep cuts in global emissions are required, and that action based on equity must be taken to meet this objective. However, negotiations on emission reduction among countries are increasingly fraught with difficulty, partly because of arguments about the responsibility for the ongoing temperature rise. Simulations with two earth-system models (NCAR/CESM and BNU-ESM) demonstrate that developed countries had contributed about 60-80%, developing countries about 20-40%, to the global temperature rise, upper ocean warming, and sea-ice reduction by 2005. Enacting pledges made at Cancun with continuation to 2100 leads to a reduction in global temperature rise relative to business as usual with a 1/3-2/3 (CESM 33-67%, BNU-ESM 35-65%) contribution from developed and developing countries, respectively. To prevent a temperature rise by 2 degrees C or more in 2100, it is necessary to fill the gap with more ambitious mitigation efforts.
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5.
  • Wu, Wei, et al. (författare)
  • Roles of Mitogen-Activated Protein Kinases in the Modulation of Endothelial Cell Function Following Thermal Injury
  • 2011
  • Ingår i: Shock. - : Biomedical Press. - 1073-2322 .- 1540-0514. ; 35:6, s. 618-625
  • Tidskriftsartikel (refereegranskat)abstract
    • Several mitogen-activated protein kinases (MAPKs) are activated during thermal injury, and the p38 MAPK is specifically involved in endothelial cell (EC) actin and myosin rearrangement (stress-fiber formation) with ensuing cellular contraction and enhanced vessel permeability. Inhibition of p38 MAPK and extracellular signal-related kinase MAPK by their inhibitors SB203580 and PD98059, respectively, significantly reduces burn serum-induced EC stress-fiber formation, whereas SB203580 also inhibits burn serum-induced EC tight-junction damage and thereby general blood vessel hyperpermeability. The JNK MAPK inhibitor, SP600125, on the contrary, influences neither stress-fiber formation nor EC tight-junction damage. Extracellular signal-related kinase MAPK inhibition significantly decreases burn serum-induced Monocyte chemotactic protein-1 (MCP-1) release, whereas SB203580 and SP600125 have only limited such effects. Western blotting, real-time reverse transcriptase-polymerase chain reaction, and confocal laser scanning microscopy proved that SP600125 significantly inhibits burn serum-induced intercellular adhesion molecule 1 expression, whereas SB203580 depresses the expression of P selectin. In vivo studies, using the dominant negative adenoviral approach of MAPK kinase 3b and MAPK kinase 6b to block p38 MAPKs, and MKK4 and MKK7 to block JNK MAPKs, show that the latter MAPKs are involved in the regulation of P selectin and intercellular adhesion molecule 1 expression, respectively, following thermal injury. Taken together, the results suggest that several MAPKs play important, although different, roles in general EC alterations following burn injuries.
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