1,217 research outputs found

    Adapting tam and ECT: continuance intention of e-shopping in Saudi Arabia

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    The objective of this study is to clarify the theoretical problem and identify factors that could explain the level of continuance intention of e-shopping in context of Saudi Arabia. The study proposes a revised technology acceptance model that integrates expectation confirmation theory to measure age differences with regard to continuance online shopping intentions. Structural equation model confirms model fit. The research findings confirm that Perceived usefulness, enjoyment, and subjective norms are determinants of online shopping continuance. The structural weights are mostly equivalent between the young and old groups, but the regression path from subjective norms to perceived usefulness is not invariant, with that relationship being stronger for the younger respondents. This research moves beyond online shopping intentions and includes factors affecting online shopping continuance. The model explains 65% of the intention to continue shopping online. The research findings suggest that online strategies cannot ignore either the direct and indirect effects on continuance intentions

    Characterisation of a novel interaction partner for Atg16L1 and its role in regulating autophagy

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    Macroautophagy (hereafter referred to as autophagy) is a highly conserved eukaryotic cellular response to starvation, resulting in the formation of double-membrane vesicles known as autophagosomes. These sequester cytoplasmic contents to the lysosome, where they are degraded to generate amino acids which can be used for protein synthesis during periods of nutrient deprivation. Membrane targeting of LC3, the major structural protein of the autophagosome, is essential for autophagy. LC3 is processed from its cytosolic form (LC3-I) to its lipidated form (LC3-II) in a series of ubiquitin-like conjugation events. Of particular importance is Atg16-like-1 (Atg16L1), which through its interactions with Atg5-Atg12, specifies the site of LC3 incorporation into the expanding autophagosomal membrane. In this study tools have been generated for the study and characterisation of Atg16L1 domains in cell culture. Atg16L1 -/- MEFs have also been generated and used for reconstitution experiments, which confirm that the coiled-coil domain of Atg16L1 is sufficient to restore autophagy in response to starvation and to a surrogate pathogen. A novel interaction between Atg16L1 and the serine/threonine kinase MEKK4 has been characterised in this study. Existing research has established an interaction between the pathogen recognition receptors NOD1/2 and Atg16L1. The NOD receptors are activated by bacterial peptidoglycan (PG), which has been shown to drive autophagy. Interestingly, MEKK4 inhibits NOD2 signalling by binding the downstream adaptor protein RIP2, leading to the hypothesis that MEKK4 may play a role in autophagy. The interaction was verified by co-immunoprecipitation, with domain analysis indicating that MEKK4 binds to the linker region of Atg16L1. The kinase activity of MEKK4 was also required for the interaction. The complex between Atg16L1 and MEKK4 persisted during starvation induced autophagy. Lipidation of LC3 in response to starvation required expression of MEKK4, with a redistribution of LC3 to large perinuclear aggregrates that co-localised with p62 and ubiquitin in siRNA silenced cells and CRISPR/Cas MEKK4 knockout cells. The aggregates were also able to recruit LC3 I, indicating a role of aggresome-like induced structures (ALIS). This thesis documents an interaction between Atg16L1 and MEKK4 that is vital for LC3 processing. The potential role for MEKK4 in regulating autophagy through Atg16L1 is discussed and experiments proposed to further explore this interaction in the context of autophagy

    Linearity in the non-deterministic call-by-value setting

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    We consider the non-deterministic extension of the call-by-value lambda calculus, which corresponds to the additive fragment of the linear-algebraic lambda-calculus. We define a fine-grained type system, capturing the right linearity present in such formalisms. After proving the subject reduction and the strong normalisation properties, we propose a translation of this calculus into the System F with pairs, which corresponds to a non linear fragment of linear logic. The translation provides a deeper understanding of the linearity in our setting.Comment: 15 pages. To appear in WoLLIC 201

    Confluence via strong normalisation in an algebraic \lambda-calculus with rewriting

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    The linear-algebraic lambda-calculus and the algebraic lambda-calculus are untyped lambda-calculi extended with arbitrary linear combinations of terms. The former presents the axioms of linear algebra in the form of a rewrite system, while the latter uses equalities. When given by rewrites, algebraic lambda-calculi are not confluent unless further restrictions are added. We provide a type system for the linear-algebraic lambda-calculus enforcing strong normalisation, which gives back confluence. The type system allows an abstract interpretation in System F.Comment: In Proceedings LSFA 2011, arXiv:1203.542

    Aedes nigrinus (Eckstein, 1918) (Diptera, Culicidae), a new country record for England, contrasted with Aedes sticticus (Meigen, 1838)

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    We report the discovery of Aedes nigrinus (Eckstein, 1918) in the New Forest of southern England, bringing to 36 the number of mosquito species recorded in Britain. Because it seems that this species has been misidentified previously in Britain as the morphologically similar Aedes sticticus (Meigen, 1838), the two species are contrasted and distinguished based on distinctive differences exhibited in the adult and larval stages. The pupa of Ae. nigrinus is unknown, but the pupa of Ae. sticticus is distinguished from the pupae of other species of Aedes by modification of the most recent key to British mosquitoes. The history of the mosquito fauna recorded in the UK is summarized and bionomical information is provided for the two species.Peer reviewe

    A novel Apaf-1–independent putative caspase-2 activation complex

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    CVaspase activation is a key event in apoptosis execution. In stress-induced apoptosis, the mitochondrial pathway of caspase activation is believed to be of central importance. In this pathway, cytochrome c released from mitochondria facilitates the formation of an Apaf-1 apoptosome that recruits and activates caspase-9. Recent data indicate that in some cells caspase-9 may not be the initiator caspase in stress-mediated apoptosis because caspase-2 is required upstream of mitochondria for the release of cytochrome c and other apoptogenic factors. To determine how caspase-2 is activated, we have studied the formation of a complex that mediates caspase-2 activation. Using gel filtration analysis of cell lysates, we show that caspase-2 is spontaneously recruited to a large protein complex independent of cytochrome c and Apaf-1 and that recruitment of caspase-2 to this complex is sufficient to mediate its activation. Using substrate-binding assays, we also provide the first evidence that caspase-2 activation may occur without processing of the precursor molecule. Our data are consistent with a model where caspase-2 activation occurs by oligomerization, independent of the Apaf-1 apoptosome
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