Explaining Adoption of Pervasive Retail Systems with a Model based on UTAUT2 and the Extended Privacy Calculus

The advent of e-commerce puts traditional retail companies under a lot of pressure. A way retailers try to attract more customers to their physical stores is by offering online services on the retail sales floor. Such services are enabled through pervasive retail systems. These systems, however, do not only offer new opportunities but also bear risks for retailers because they heavily depend on privacy-related data, which customers could perceive as a potential privacy threat. In the present paper, we thus investigate the antecedents of customers’ usage intention towards such systems and the trade-off between the perceived benefits and the perceived privacy costs that are associated with their use. To this end, we propose a model based on the most recent version of the Unified Theory of Acceptance and Use of Technology (UTAUT2) and the Extended Privacy Calculus Theory. We validate our model considering a smart fitting room application and show that the model is able to explain 67.1% of the variance in the behavioral intention to use the system and 43.1% of the variance in a person’s willingness to disclose private information. Our results can be leveraged to design pervasive systems that are perceived as valuable instead of privacy threatening

Extracellular glutamate accumulates only in final, ischemic stage of progressive epidural mass lesion in cats

Epidural mass lesions may cause ischemia due to progressive intracranial hypertension. In order to 1) investigate the impact of intracranial pressure (ICP) on accumulation of neuroactive substances, and 2) test the significance of neurochemical monitoring for early prediction of fatal outcome, we gradually raised ICP in cats by inflation of an epidural balloon: We assessed extracellular substrate alterations in the contralateral cortex in relation to changes of ICP, cerebral perfusion pressure (CPP) and mean arterial blood pressure (MABP). In a complementary experiment, regional cerebral blood flow was assessed by sequential positron emission tomography (PET).peer-reviewe

Formulating efficient software solution for digital image processing system

© 2015 John Wiley & Sons, Ltd. Digital image processing systems are complex, being usually composed of different computer vision libraries. Algorithm implementations cannot be directly used in conjunction with algorithms developed using other computer vision libraries. This paper formulates a software solution by proposing a processor with the capability of handling different types of image processing algorithms, which allow the end users to install new image processing algorithms from any library. This approach has other functionalities like capability to process one or more images, manage multiple processing jobs simultaneously and maintain the manner in which an image was processed for later use. It is a computational efficient and promising technique to handle variety of image processing algorithms. To promote the reusability and adaptation of the package for new types of analysis, a feature of sustainability is established. The framework is integrated and tested on a medical imaging application, and the software is made freely available for the reader. Future work involves introducing the capability to connect to another instance of processing service with better performance

Analysis of microglial BDNF function and expression in the motor cortex

Brain-derived neurotrophic factor (BDNF) is a neurotrophin that regulates several aspects of brain function. Although numerous studies have demonstrated the expression and function of BDNF in neurons, its expression in microglia remains controversial. Using a combination of genetic tools and fluorescence imaging, we analyzed BDNF expression patterns and investigated the effect of microglial Bdnf deletion on neuronal activity, early-stage spine formation, and microglia-neuron attraction in the motor cortex. We did not detect BDNF expression in microglia at the transcriptional or translational level, in physiological or pathological conditions, and none of the assessed neuronal functions were found to be affected in conditional Bdnf knockout mice. Our results suggest that microglia do not express BDNF in sufficient amounts to modulate neuronal function

Analysis of microglial BDNF function and expression in the motor cortex

Brain-derived neurotrophic factor (BDNF) is a neurotrophin that regulates several aspects of brain function. Although numerous studies have demonstrated the expression and function of BDNF in neurons, its expression in microglia remains controversial. Using a combination of genetic tools and fluorescence imaging, we analyzed BDNF expression patterns and investigated the effect of microglial Bdnf deletion on neuronal activity, early-stage spine formation, and microglia-neuron attraction in the motor cortex. We did not detect BDNF expression in microglia at the transcriptional or translational level, in physiological or pathological conditions, and none of the assessed neuronal functions were found to be affected in conditional Bdnf knockout mice. Our results suggest that microglia do not express BDNF in sufficient amounts to modulate neuronal function

Microglia shape presynaptic properties at developing glutamatergic synapses

Deficient neuron-microglia signaling during brain development is associated with abnormal synaptic maturation. However, the precise impact of deficient microglia function on synaptic maturation and the mechanisms involved remain poorly defined. Here we report that mice defective in neuron-to-microglia signaling via the fractalkine receptor (Cx3cr1 KO) show reduced microglial branching and altered motility and develop widespread deficits in glutamatergic neurotransmission. We characterized the functional properties of CA3-CA1 synapses in hippocampal slices from these mice and found that they display altered glutamatergic release probability, maintaining immature properties also at late developmental stages. In particular, CA1 synapses of Cx3cr1 KO show (i) immature AMPA/NMDA ratio across developmental time, displaying a normal NMDA component and a defective AMPA component of EPSC; (ii) defective functional connectivity, as demonstrated by reduced current amplitudes in the input/output curve; and (iii) greater facilitation in the paired pulse ratio (PPR), suggesting decreased release probability. In addition, minimal stimulation experiments revealed that excitatory synapses have normal potency, but an increased number of failures, confirming a deficit in presynaptic release. Consistently, KO mice were characterized by higher number of silent synapses in comparison to WT. The presynaptic deficits were corrected by performing experiments in conditions of high release probability (Ca2+ /Mg2+ ratio 8), where excitatory synapses showed normal synaptic multiplicity, AMPA/NMDA ratio, and proportion of silent synapses. These results establish that neuron-microglia interactions profoundly influence the functional maturation of excitatory presynaptic function

Microglia complement signaling promotes neuronal elimination and normal brain functional connectivity

Complement signaling is thought to serve as an opsonization signal to promote the phagocytosis of synapses by microglia. However, while its role in synaptic remodeling has been demonstrated in the retino-thalamic system, it remains unclear whether complement signaling mediates synaptic pruning in the brain more generally. Here we found that mice lacking the Complement receptor 3, the major microglia complement receptor, failed to show a deficit in either synaptic pruning or axon elimination in the developing mouse cortex. Instead, mice lacking Complement receptor 3 exhibited a deficit in the perinatal elimination of neurons in the cortex, a deficit that is associated with increased cortical thickness and enhanced functional connectivity in these regions in adulthood. These data demonstrate a role for complement in promoting neuronal elimination in the developing cortex