855 resultados para multimodal terminals
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Federal Highway Administration, Safety Design Division, McLean, Va.
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Federal Highway Administration, Office of Research, Development, and Technology, Washington, D.C.
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Transportation Department, Office of University Research, Washington, D.C.
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Mode of access: Internet.
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Originally presented as the author's thesis (M.A.), University of Illinois at Urbana-Champaign.
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Thesis (M.S.)--University of Illinois.
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"31 July 1973."
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Includes index.
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Includes index.
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Mode of access: Internet.
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Mode of access: Internet.
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I denna uppsats undersöker jag vilka modelläsare som skapas i två olika sorters mejl från Greenpeace i Sverige till personer som engagerar sig i organisationens arbete. Jag gör en multimodal textanalys med utgångspunkt i dialogism och sociosemiotisk teori, och jag använder analysmetoder från den systemisk-funktionella grammatiken. Resultatet visar att de två mejltyperna i det stora hela är mycket lika varandra, men att det finns vissa skillnader och att de olika mejltyperna därigenom konstruerar delvis olika modelläsare som verkliga läsare måste förhålla sig till. Modelläsarna skapas genom realiseringar av olika språkliga och visuella betydelseskapande resurser som t.ex. presuppositioner, processer, distans och språk- och bildhandlingar. Det gemensamma för modelläsarna är att de sympatiserar med Greenpeace, har en aktiv aktörsroll och har en nära och jämlik relation till organisationen.
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Thesis (Master's)--University of Washington, 2016-06
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beta2-Laminin is important for the formation of neuromuscular junctions in vertebrates. Previously, we have inactivated the gene that encodes for beta2-laminin in mice and observed predominantly prejunctional structural defects. In this study, we have used both intra- and extracellular recording methods to investigate evoked neurotransmission in beta2-laminin-deficient mice, from postnatal day 8 (P8) through to day 18(P18). Our results confirmed that there was a decrease in the frequency of spontaneous release, but no change in the postjunctional response to such release. Analysis of evoked neurotransmission showed an increase in the frequency of stimuli that failed to elicit an evoked postjunctional response in the mutants compared to litter mate controls, resulting in a 50% reduction in mean quantal content at mutant terminals. Compared to littermate controls, beta2-laminin-deficient terminals showed greater synaptic depression when subjected to high frequency stimulation. Furthermore, the paired pulse ratio of the first two stimuli was significantly lower in beta2-laminin mutant terminals. Statistical analysis of the binomial parameters of release showed that the decrease in quantal content was due to a decrease in the number of release sites without any significant change in the average probability of release. This suggestion was supported by the observation of fewer synaptic vesicle protein 2 (SV2)-positive varicosities in beta2-laminin-deficient terminals and by ultrastructural observations showing smaller terminal profiles and increased Schwann cell invasion in beta2-laminin mutants; the differences between beta2-laminin mutants and wild-type mice were the same at both P8 and P18. From these results we conclude that beta2-laminin plays a role in the early structural development of the neuromuscular junction. We also suggest that transmitter release activity may act as a deterrent to Schwarm cell invasion in the absence of beta2-laminin.