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Träfflista för sökning "WFRF:(Blake R. S.) srt2:(2005-2009)"

Sökning: WFRF:(Blake R. S.) > (2005-2009)

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2.
  • Monks, P. S., et al. (författare)
  • Atmospheric composition change : global and regional air quality
  • 2009
  • Ingår i: Atmospheric Environment. - : Elsevier BV. - 1352-2310 .- 1873-2844. ; 43:33, s. 5268-5350
  • Forskningsöversikt (refereegranskat)abstract
    • Air quality transcends all scales with in the atmosphere from the local to the global with handovers and feedbacks at each scale interaction. Air quality has manifold effects on health, ecosystems heritage and, climate. In this review the state of scientific understanding in relation to global and regional air quality is outlined. The review discusses air quality, in terms of emissions, processing and transport of trace gases and aerosols. New insights into the characterization of both natural and anthropogenic emissions are reviewed looking at both natural (e.g. dust and lightning) as well as plant emissions. Trends in anthropogenic emissions both by region and globally are discussed as well as biomass burning emissions. In terms of chemical processing the major air quality elements of ozone, non-methane hydrocarbons, nitrogen oxides and aerosols are covered. A number of topics are presented as a way of integrating the process view into the atmospheric context; these include the atmospheric oxidation efficiency, halogen and HOx chemistry, nighttime chemistry, tropical chemistry, heat waves, megacities, biomass burning and the regional hot spot of the Mediterranean. New findings with respect to the transport of pollutants across the scales are discussed, in particular the move to quantify the impact of long-range transport on regional air quality. Gaps and research questions that remain intractable are identified. The review concludes with a focus of research and policy questions for the coming decade. In particular, the policy challenges for concerted air quality and climate change policy (co-benefit) are discussed.
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3.
  • Haas, Brian J., et al. (författare)
  • Genome sequence and analysis of the Irish potato famine pathogen Phytophthora infestans
  • 2009
  • Ingår i: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 461:7262, s. 393-398
  • Tidskriftsartikel (refereegranskat)abstract
    • Phytophthora infestans is the most destructive pathogen of potato and a model organism for the oomycetes, a distinct lineage of fungus-like eukaryotes that are related to organisms such as brown algae and diatoms. As the agent of the Irish potato famine in the mid-nineteenth century, P. infestans has had a tremendous effect on human history, resulting in famine and population displacement(1). To this day, it affects world agriculture by causing the most destructive disease of potato, the fourth largest food crop and a critical alternative to the major cereal crops for feeding the world's population(1). Current annual worldwide potato crop losses due to late blight are conservatively estimated at $6.7 billion(2). Management of this devastating pathogen is challenged by its remarkable speed of adaptation to control strategies such as genetically resistant cultivars(3,4). Here we report the sequence of the P. infestans genome, which at similar to 240 megabases (Mb) is by far the largest and most complex genome sequenced so far in the chromalveolates. Its expansion results from a proliferation of repetitive DNA accounting for similar to 74% of the genome. Comparison with two other Phytophthora genomes showed rapid turnover and extensive expansion of specific families of secreted disease effector proteins, including many genes that are induced during infection or are predicted to have activities that alter host physiology. These fast-evolving effector genes are localized to highly dynamic and expanded regions of the P. infestans genome. This probably plays a crucial part in the rapid adaptability of the pathogen to host plants and underpins its evolutionary potential.
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4.
  • Lee, J. H., et al. (författare)
  • Resistin is elevated following traumatic joint injury and causes matrix degradation and release of inflammatory cytokines from articular cartilage in vitro
  • 2009
  • Ingår i: Osteoarthritis and Cartilage. - 1063-4584. ; 17:5, s. 613-620
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: Resistin is a secreted factor that is elevated in rheumatoid arthritis (RA) and believed to drive joint inflammation in vivo. This study was undertaken to determine if resistin is present in the joint following joint injury and to elucidate the role of resistin in cartilage degradation. Methods: The level of resistin was measured in paired synovial fluid (SF) and serum samples from patients following joint injury (anterior cruciate ligament, ACL or meniscus tear). Localization of resistin was visualized by immunohistochemistry of synovial tissue and cartilage from healthy and CA donors. Mouse and human cartilage cultures were used to assess the effect of resistin on cartilage metabolism. Results: In trauma patients, resistin levels declined with increasing time post injury. The resistin levels were highest in samples collected up to 1 week following traumatic injury (SF: 2980 pg/ml, serum: 7901 pg/ml) and lowest in samples collected 6-26 years post injury (SF: 686 pg/ml, serum: 5682 pg/ml). Resistin was shown to be expressed in macrophage-like cells in both healthy and OA synovial tissue. Treatment of mouse cartilage cultures with recombinant resistin led to a dose dependent loss of proteoglycan and induction of inflammatory cytokine and PGE(2) production. Recombinant resistin inhibited proteoglycan synthesis in human cartilage explants. Conclusion: Resistin is elevated both systemically and locally in the weeks immediately following joint injury and has a direct effect on cartilage matrix turnover and cytokine production. Resistin may play a role in the early stages of trauma-induced CA and may represent a new therapeutic target to slow joint destruction in CA. (C) 2008 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.
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