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Träfflista för sökning "WFRF:(Cleveland D) srt2:(2002-2004)"

Sökning: WFRF:(Cleveland D) > (2002-2004)

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  • Garrison, D.R, et al. (författare)
  • Critical factors in student satisfaction and success : Facilitating student role adjustment in online communities of inquiry
  • 2004
  • Ingår i: Elements of quality online education. - : Sloan Consortium. - 9780967774169 ; , s. 29-38
  • Bokkapitel (refereegranskat)abstract
    • The purpose of this study is to validate an instrument to study role adjustment of students new to anonline community of inquiry. The community of inquiry conceptual model for online learning was usedto shape this research and identify the core elements and conditions associated with role adjustment toonline learning (Garrison, Anderson and Archer, 2000). Through a factor analytic process it is shown thatthe instrument did reflect the theoretical model. It was also useful in refining the items for thequestionnaire. The instrument is for use in future research designed to measure and understand studentrole adjustment in online learning.
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3.
  • Liu, Jian, et al. (författare)
  • Toxicity of familial ALS-linked SOD1 mutants from selective recruitment to spinal mitochondria
  • 2004
  • Ingår i: Neuron. - : Cell Press. - 0896-6273 .- 1097-4199. ; 43:1, s. 5-17
  • Tidskriftsartikel (refereegranskat)abstract
    • One cause of amyotrophic lateral sclerosis (ALS) is mutation in ubiquitously expressed copper/zinc superoxide dismutase (SOD1), but the mechanism of toxicity to motor neurons is unknown. Multiple disease-causing mutants, but not wild-type SOD1, are now demonstrated to be recruited to mitochondria, but only in affected tissues. This is independent of the copper chaperone for SOD1 and dismutase activity. Highly preferential association with spinal cord mitochondria is seen in human ALS for a mutant SOD1 that accumulates only to trace cytoplasmic levels. Despite variable proportions that are successfully imported, nearly constant amounts of SOD1 mutants and covalently damaged adducts of them accumulate as apparent import intermediates and/or are tightly aggregated or crosslinked onto integral membrane components on the cytoplasmic face of those mitochondria. These findings implicate damage from action of spinal cord-specific factors that recruit mutant SOD1 to spinal mitochondria as the basis for their selective toxicity in ALS.
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