Towards an understanding of internet-based problem shopping behaviour: the concept of online shopping addiction and its proposed predictors

Abstract Background Compulsive and addictive forms of consumption and buying behaviour have been researched in both business and medical literature. Shopping enabled via the Internet now introduces new features to the shopping experience that translate to positive benefits for the shopper. Evidence now suggests that this new shopping experience may lead to problematic online shopping behaviour. This paper provides a theoretical review of the literature relevant to online shopping addiction (OSA). Based on this selective review, a conceptual model of OSA is presented. Method The selective review of the literature draws on searches within databases relevant to both clinical and consumer behaviour literature including EBSCO, ABI Pro-Quest, Web of Science — Social Citations Index, Medline, PsycINFO and Pubmed. The article reviews current thinking on problematic, and specifically addictive, behaviour in relation to online shopping. Results The review of the literature enables the extension of existing knowledge into the Internet-context. A conceptual model of OSA is developed with theoretical support provided for the inclusion of 7 predictor variables: low self-esteem, low self-regulation; negative emotional state; enjoyment; female gender; social anonymity and cognitive overload. The construct of OSA is defined and six component criteria of OSA are proposed based on established technological addiction criteria. Conclusions Current Internet-based shopping experiences may trigger problematic behaviours which can be classified on a spectrum which at the extreme end incorporates OSA. The development of a conceptual model provides a basis for the future measurement and testing of proposed predictor variables and the outcome variable OSA

Peptide utilization by nitrogen-starved Neurospora crassa.

Peptides ranging in size from a mean number of 30 residues down to dipeptides supported growth of a leucine auxotroph when used as both a nitrogen and leucine source. Under nitrogen-limiting conditions, the peptides induced extracellular peptidohydrolytic activity, hydrolyzing peptides to monomer amino acids. Growth of a leu-2 mutant of Neurospora crassa on those peptides transportable by the oligopeptide transport system did not result in induction of hydrolytic activity, whereas growth of a leu-2; gltR mutant on these same peptides resulted in induction of peptidohydrolytic activity. The induced extracellular proteolytic activity was shown to be analogous to that inducible by growth on proteins, e.g., bovine serum albumin

Subcellular localization of Aleutian mink disease parvovirus proteins and DNA during permissive infection of Crandell feline kidney cells.

Confocal microscopy allowed us to localize viral nonstructural (NS) and capsid (VP) proteins and DNA simultaneously in cells permissively infected with Aleutian mink disease parvovirus (ADV). Early after infection, NS proteins colocalized with viral DNA to form intranuclear inclusions, whereas VP proteins formed hollow intranuclear shells around the inclusions. Later, nuclei had irregular outlines and were virtually free of ADV products. In these cells, inclusions of viral DNA with or without associated NS protein were embedded in cytoplasmic VP protein. These findings implied that ADV replication within an infected cell is regulated spatially as well as temporally

Identification of genetic determinants of a tick-borne flavivirus associated with host-specific adaptation and pathogenicity

AbstractTick-borne flaviviruses are maintained in nature in an enzootic cycle involving a tick vector and a vertebrate host. Thus, the virus replicates in two disparate hosts, each providing selective pressures that can influence virus replication and pathogenicity. To identify viral determinants associated with replication in the individual hosts, plaque purified Langat virus (TP21pp) was adapted to growth in mouse or tick cell lines to generate two virus variants, MNBp20 and ISEp20, respectively. Virus adaptation to mouse cells resulted in four amino acid changes in MNBp20 relative to TP21pp, occurring in E, NS4A and NS4B. A comparison between TP21pp and ISEp20 revealed three amino acid modifications in M, NS3 and NS4A of ISEp20. ISEp20, but not MNBp20, was attenuated following intraperitoneal inoculation of mice. Following isolation from mice brains, additional mutations reproducibly emerged in E and NS3 of ISEp20 that were possibly compensatory for the initial adaptation to tick cells. Thus, our data implicate a role for E, M, NS3, NS4A and NS4B in host adaptation and pathogenicity of tick-borne flaviviruses