An Affective Model for Unauthorized Sharing of Software

Software piracy has been studied by academics, software firms, law enforcement agents and policy makers for many years. Previous research in software piracy either did not differentiate between unauthorized copying and unauthorized sharing, or focused only on unauthorized copying. We believe the motivating factors behind the two behaviors are quite different because beneficiaries of the behaviors are different. In this paper, we consider unauthorized sharing as a kind of helping behavior and draw on relevant literature to see if the motivations behind unauthorized sharing can be better appreciated from an affective perspective. We tested the affective model of unauthorized sharing based on empirical data obtained from a large-scale survey. We found from the survey that both perceived affordability and perceived convenience could arouse sympathy or annoyance with the unauthorized copier, and their effects were mediated by perceived controllability of the need of unauthorized copying. Our results support the strong effects of affective factors on the moral obligation of unauthorized sharing

Risk of Using Pirated Software and its Impact on Software Protection Strategies

The software protection strategy of software developer and the inherent risk to end user in using pirated software are two major factors that affect a user’s decision on whether to purchase or pirate a software product. This paper analyzes the optimal protection strategy for software developer in horizontally and vertically differentiated markets. We find that the implementation cost of software protection constitutes the primary factor for software developers to determine their software protection strategies. However, in a vertically differentiated market, the lower quality product should always adopt a non-protection strategy, regardless of the protection implementation cost. In other cases, protection would only be optimal if the protection implementation cost to the software developer is relatively small. These findings are consistent with anecdotal evidence

The Role of Morality in Digital Piracy: Understanding the Deterrent and Motivational Effects of Moral Reasoning in Different Piracy Contexts

Digital piracy has been a chronic issue in intellectual property protection. With the prevalence of online technologies, digital piracy has become even more rampant, as digital resources can now be accessed and disseminated easily through the Internet. While the antecedents of piracy behaviors have been studied for years, previous studies often focus on a specific type of behavior or pirated content and the findings are far from conclusive. They do not paint a coherent picture of the impacts of antecedents. In this study, we focus on the role of morality by revealing the different levels of moral reasoning that can both deter and motivate users’ piracy intentions. Furthermore, we differentiate between two types of piracy behaviors (unauthorized copying/downloading vs. unauthorized sharing) and two categories of digital products (application software vs. music/movies), so that the differential impacts of the various antecedents can be assessed and articulated more clearly. We empirically evaluated the models in the four piracy contexts using a sample of 3,426 survey participants from a sizable IT-literate society. Our findings indicate the conflicting roles of morality in piracy intention and demonstrate its differential impacts across the two types of piracy behaviors, which can be generalized across the two categories of digital products. Our study sheds new light on end users’ considerations in accessing and disseminating unauthorized digital content. It also informs the design of copyright protection policies and sanction measures with different levels of specificity

Trauma and depressive symptomatology in middle-aged persons at high risk of dementia: the PREVENT Dementia Study

Objective: Depression and trauma are associated with changes in brain regions implicated in Alzheimer’s disease. The present study examined associations between childhood trauma, depression, adult cognitive functioning and risk of dementia. Methods: Data from 378 participants in the PREVENT Dementia Study aged 40–59 years. Linear and logistic models were used to assess associations between childhood trauma, depression, dementia risk, cognitive test scores and hippocampal volume. Results: Childhood trauma was associated with depression and reduced hippocampal volume but not current cognitive function or dementia risk. Poorer performance on a delayed face/name recall task was associated with depression. Childhood trauma was associated with lower hippocampal volume however poorer cognitive performance was mediated by depression rather than structural brain differences. Conclusion: Depressive symptomatology may be associated with dementia risk via multiple pathways, and future studies should consider subtypes of depressive symptomatology when examining its relationship to dementia

Bcar1/p130Cas is essential for ventricular development and neural crest cell remodelling of the cardiac outflow tract.

AIM: The adapter protein p130Cas, encoded by the Bcar1 gene, is a key regulator of cell movement, adhesion, and cell cycle control in diverse cell types. Bcar1 constitutive knockout mice are embryonic lethal by embryonic days (E) 11.5-12.5, but the role of Bcar1 in embryonic development remains unclear. Here, we investigated the role of Bcar1 specifically in cardiovascular development and defined the cellular and molecular mechanisms disrupted following targeted Bcar1 deletions. METHODS AND RESULTS: We crossed Bcar1 floxed mice with Cre transgenic lines allowing for cell-specific knockout either in smooth muscle and early cardiac tissues (SM22-Cre), mature smooth muscle cells (smMHC-Cre), endothelial cells (Tie2-Cre), second heart field cells (Mef2c-Cre), or neural crest cells (NCC) (Pax3-Cre) and characterised these conditional knock outs using a combination of histological and molecular biology techniques.Conditional knockout of Bcar1 in SM22-expressing smooth muscle cells and cardiac tissues (Bcar1SM22KO) was embryonically lethal from E14.5-15.5 due to severe cardiovascular defects, including abnormal ventricular development and failure of outflow tract (OFT) septation leading to a single outflow vessel reminiscent of persistent truncus arteriosus. SM22-restricted loss of Bcar1 was associated with failure of OFT cushion cells to undergo differentiation to septal mesenchymal cells positive for SMC-specific α-actin, and disrupted expression of proteins and transcription factors involved in epithelial-to-mesenchymal transformation (EMT). Furthermore, knockout of Bcar1 specifically in NCC (Bcar1PAX3KO) recapitulated part of the OFT septation and aortic sac defects seen in the Bcar1SM22KO mutants, indicating a cell-specific requirement for Bcar1 in NCC essential for OFT septation. In contrast, conditional knockouts of Bcar1 in differentiated smooth muscle, endothelial cells, and second heart field cells survived to term and were phenotypically normal at birth and post-natally. CONCLUSIONS: Our work reveals a cell-specific requirement for Bcar1 in NCC, early myogenic and cardiac cells, essential for OFT septation, myocardialisation and EMT/cell cycle regulation and differentiation to myogenic lineages. TRANSLATIONAL PERSPECTIVE: The molecular pathways coordinating cardiogenesis and the remodelling of the OFT are complex, and dysregulation of these pathways causes human heart defects. Our findings highlight a specific requirement for Bcar1 essential for cardiogenesis. Furthermore, the failure of OFT septation in Bcar1SM22KO mice resembles persistent truncus arteriosus (PTA), a feature of several human congenital heart diseases, including DiGeorge Syndrome. Our findings have implications for the mechanisms underlying the pathogenesis of congenital heart disease, and suggest that mice with conditional Bcar1 deletions may be useful models for dissecting mechanisms involved in the pathogenesis of human heart defects

Elucidating the aetiology of human Campylobacter coli infections

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