24 research outputs found

    Mobile wallet inhibitors: Developing a comprehensive theory using an integrated model

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    © 2018 Elsevier Ltd The concept of the mobile wallet is increasingly adopted in developed and developing countries for improving the scale, productivity, and excellence of banking services. Oman is one of the most growing countries of the Middle Eastern economies. Acceptance of mobile wallets in Oman is being hindered by various inhibitors. There is no study in the Middle Eastern countries that addressed the concerns of probable inhibitors influencing mobile wallet acceptance from expert's perspective. In this study, eleven key inhibitors to mobile wallet adoption are identified from the literature and expert's feedback. This study employed Interpretive Structural Modelling (ISM) in conjunction with fuzzy MICMAC to reveal the intricate relationship among inhibitors to mobile wallet acceptance. To the end, an integrated hierarchical model is developed to understand the influence of a particular inhibitor on others. ‘Anxiety towards new technology’ ‘Lack of new technology skills’ ‘Lack of awareness of mobile wallet benefits’ and ‘Complexity of new technology’ have been reported as key inhibitors to promote mobile wallets in Oman. This study also suggests several recommendations for banking organizations and policymakers in developing the effective model to popularize mobile wallets in Oman

    Bone marrow mesenchymal/fibroblastic stromal cells induce a distinctive EMT-like phenotype in AML cells

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    The development of epithelial-to-mesenchymal transition (EMT) like features is emerging as a critical factor involved in the pathogenesis of acute myeloid leukaemia (AML). However, the extracellular signals and the signalling pathways in AML that may regulate EMT remain largely unstudied. We found that the bone marrow (BM) mesenchymal/fibroblastic cell line HS5 induces an EMT-like migratory phenotype in AML cells. AML cells underwent a strong increase of vimentin (VIM) levels that was not mirrored to the same extent by changes of expression of the other EMT core proteins SNAI1 and SNAI2. We validated these particular pattern of co-expression of core-EMT markers in AML cells by performing an in silico analysis using datasets of human tumours. Our data showed that in AML the expression levels of VIM does not completely correlate with the co-expression of core EMT markers observed in epithelial tumours. We also found that vs epithelial tumours, AML cells display a distinct patterns of co-expression of VIM and the actin binding and adhesion regulatory proteins that regulate F-actin dynamics and integrin-mediated adhesions involved in the invasive migration in cells undergoing EMT. We conclude that the BM stroma induces an EMT related pattern of migration in AML cells in a process involving a distinctive regulation of EMT markers and of regulators of cell adhesion and actin dynamics that should be further investigated. Understanding the tumour specific signalling pathways associated with the EMT process may contribute to the development of new tailored therapies for AML as well as in different types of cancers
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