Curtin University

About: Curtin University is a education organization based out in Perth, Western Australia, Australia. It is known for research contribution in the topics: Population & Zircon. The organization has 14257 authors who have published 48997 publications receiving 1336531 citations. The organization is also known as: WAIT & Western Australian Institute of Technology.

Consuming luxury brands: The relevance of the ‘Rarity Principle’

Abstract: This paper extends work on the influence of awareness, purchase and dream values of luxury brands on two counts. First, it introduces a measure on consumers' ‘dislike’ for certain luxury brands of high awareness. The justification is consumers may be aware of a well-known brand but need not necessarily like it. Second, the Rarity Principle suggests that in order to maintain prestige, luxury brands must sustain high levels of awareness and tightly controlled brand diffusion to enhance exclusivity. This study in Singapore supports the notion that Asian consumers hold different perceptions in the ownership of luxury brands compared to the West. The findings show that the popularity of a brand may propel the dream value of the brand. Increasing awareness yields higher levels of brand preference, which generates stronger purchase intentions. This clearly rejects the Rarity Principle, which exists in the USA findings. Therefore, in order for luxury brands to be successful, they have to be promoted through active-marketing communication. The focus must be on strengthening the brand image and delivering benefits that the brands could provide.

Species coextinctions and the biodiversity crisis.

Abstract: To assess the coextinction of species (the loss of a species upon the loss of another), we present a probabilistic model, scaled with empirical data. The model examines the relationship between coextinction levels (proportion of species extinct) of affiliates and their hosts across a wide range of coevolved interspecific systems: pollinating Ficus wasps and Ficus, parasites and their hosts, butterflies and their larval host plants, and ant butterflies and their host ants. Applying a nomographic method based on mean host specificity (number of host species per affiliate species), we estimate that 6300 affiliate species are “coendangered” with host species currently listed as endangered. Current extinction estimates need to be recalibrated by taking species coextinctions into account.

The genetic basis for the association of the 8.1 ancestral haplotype (A1, B8, DR3) with multiple immunopathological diseases

Abstract: An individual's major histocompatibility complex (MHC) ancestral haplotype (AH) is the clearest single determinant of susceptibility to MHC associated immunopathological disease, as it defines the alleles carried at all loci in the MHC. However, the direct effects of any of the 150-200 genes that constitute the MHC are difficult to determine since recombination only occurs at defined hotspots. This review concerns the 8.1 AH (HLA-A1, C7, B8, C4AQ0, C4B1, DR3, DQ2), which is carried by most Caucasians with HLA-B8. It is associated with accelerated human immunodeficiency virus (HIV) disease, and susceptibility to insulin-dependent diabetes mellitus (IDDM), systemic lupus erythematosus, dermatitis herpetiformis, common variable immunodeficiency and IgA deficiency, myasthenia gravis and several other conditions. We have mapped susceptibility genes for HIV, IDDM and myasthenia gravis to the central MHC between HLA-B and the tumour necrosis factor or complement genes. Here we consider which of the remaining 8.1-associated diseases are more closely associated with HLA-DR3 and/or DQ2. Several candidate genes in the central MHC have the potential to modulate immune or inflammatory responses in an antigen-independent manner, as is seen in studies of cultured cells from healthy carriers of the 8.1 AH. Hence these genes may act as a common co-factor in the diverse immunopathological conditions associated with the 8.1 AH.

Predictors of breastfeeding duration: evidence from a cohort study.

Abstract: OBJECTIVE. To report the duration of breastfeeding among a population of Australian women and to identify factors that are associated with the duration of full breastfeeding to 6 months and any breastfeeding to 12 months. METHODS. Participants were 587 women who were recruited from 2 maternity hospitals in Perth and completed a baseline questionnaire just before or shortly after discharge from the hospital. Women were followed up by telephone interview at 4, 10, 16, 22, 32, 40, and 52 weeks postpartum. Data collected included sociodemographic, biomedical, hospital-related, and psychosocial factors associated with the initiation and the duration of breastfeeding. Cox9s proportional hazards model was used to identify factors that were associated with the risk for discontinuing full breastfeeding before 6 months and any breastfeeding before 12 months. RESULTS. At 6 months of age, fewer than one half of infants were receiving any breast milk (45.9%), and only 12% were being fully breastfed. By 12 months, only 19.2% of infants were still receiving any breast milk. Breastfeeding duration was independently, positively associated with maternal infant feeding attitudes and negatively associated with breastfeeding difficulties in the first 4 weeks, maternal smoking, introduction of a pacifier, and early return to work. CONCLUSIONS. Relatively few women achieved the international recommendations for duration of full and overall breastfeeding. Women should receive anticipatory guidance while still in the hospital on how to prevent or manage common breastfeeding difficulties and should be discouraged from introducing a pacifier before 10 weeks, if at all. Improved maternity leave provisions and more flexible working conditions may help women to remain at home with their infants longer and/or to combine successfully breastfeeding with employment outside the home.

Alzheimer's beta-amyloid peptides compete for insulin binding to the insulin receptor

Abstract: The amyloid- (A) peptide is neurotoxic and associated with the pathology of Alzheimer’s disease (AD). We investigated the effect of A peptides on insulin binding to the insulin receptor because it is known that (1) A and insulin are both amyloidogenic peptides sharing a common sequence recognition motif, (2) A and insulin are substrates for the same insulin degrading enzyme, and (3) impaired glucose metabolism is a characteristic event in the pathology of AD. We discovered that A1–40 and A1–42, the main physiological forms, reduced insulin binding and receptor autophosphorylation. The reduction in binding was caused by a decrease in the affinity of insulin binding to the insulin receptor. This reduction was independent of the receptor concentration. The reverse, control peptide A40–1 did not reduce insulin binding or insulin receptor autophosphorylation. These results demonstrate that A is a direct competitive inhibitor of insulin binding and action. We speculate that the increased levels of A in Alzheimer’s disease may be linked to the associated insulin resistance that has been observed previously in this disease.