Does Age Matter in Mobile User Experience? Impact of Age on Relative Importance of Antecedents of Mobile User Experience

Interest in user experience (UX) has grown as both academics and practitioners perceive that focusing on functional usability provides only a limited understanding of human computer interaction. UX is a comprehensive concept that goes beyond usability and utilitarian aspects of technology use, to include the non-utilitarian, aesthetic, emotional and experiential aspects. A growing body of research based on Hassenzahl’s basic UX model has examined the impact of hedonic and pragmatic product attributes on user perceptions of beauty and goodness of the technology, and their subsequent impact on satisfaction. However, the influence of age on these relationships has largely been ignored. We conducted a survey of children, young adults and the elderly’s mobile phone UX, and conducted a multi-group analysis of the UX model. We found that age really matters in mobile phone user experience. While prior research has focused on young adults, the important determinants of UX for children and the elderly differed significantly. In accordance with the UX model, young adults’ UX evaluation was influenced by both pragmatic and hedonic qualities. Children and the elderly on the other hand focused on hedonic qualities. Our study has implications for the study and practice of UX design

Mal-Netminer: Malware Classification Approach based on Social Network Analysis of System Call Graph

As the security landscape evolves over time, where thousands of species of malicious codes are seen every day, antivirus vendors strive to detect and classify malware families for efficient and effective responses against malware campaigns. To enrich this effort, and by capitalizing on ideas from the social network analysis domain, we build a tool that can help classify malware families using features driven from the graph structure of their system calls. To achieve that, we first construct a system call graph that consists of system calls found in the execution of the individual malware families. To explore distinguishing features of various malware species, we study social network properties as applied to the call graph, including the degree distribution, degree centrality, average distance, clustering coefficient, network density, and component ratio. We utilize features driven from those properties to build a classifier for malware families. Our experimental results show that influence-based graph metrics such as the degree centrality are effective for classifying malware, whereas the general structural metrics of malware are less effective for classifying malware. Our experiments demonstrate that the proposed system performs well in detecting and classifying malware families within each malware class with accuracy greater than 96%.Comment: Mathematical Problems in Engineering, Vol 201

Phosphorylation of α-syntrophin is responsible for its subcellular localization and interaction with dystrophin in muscle cells

79-85Syntrophin is a well-known adaptor protein that links intracellular proteins with the dystrophin-glycoprotein complex (DGC) at the sarcolemma. However, little is known about the underlying mechanism that regulates the intracellular localization of α-syntrophin and its interaction with dystrophin. In this study, we demonstrate that α-syntrophin phosphorylation determines its intracellular localization and interaction with dystrophin in muscle cells. α-Syntrophin, a predominant isoform in skeletal muscles, directly interacts with ion channels, enzymes, receptors, and DGC proteins. Despite α-syntrophin being a potential signaling molecule, most studies focus on its function as a dystrophin-associated protein. However, we previously reported that α-syntrophin has a variety of DGC-independent functions to modulate cell migration, differentiation, survival, and protein stability. According to the results of the in vitro phosphorylation assays using subcellular fractions, the phosphorylated α-syntrophin accumulated only at the plasma membrane, and this event occurred regardless of dystrophin expression. However, the α-syntrophin interacting with dystrophin at the membrane was not in a phosphorylated state. We also identified that protein kinase C (PKC) was involved in the phosphorylation of α-syntrophin, which restricted α-syntrophin to interact with dystrophin. In conclusion, we demonstrate that the phosphorylation of α-syntrophin by PKC regulates its intracellular localization and interaction with dystrophin

Phosphorylation of α-syntrophin is responsible for its subcellular localization and interaction with dystrophin in muscle cells

Syntrophin is a well-known adaptor protein that links intracellular proteins with the dystrophin-glycoprotein complex (DGC) at the sarcolemma. However, little is known about the underlying mechanism that regulates the intracellular localization of α-syntrophin and its interaction with dystrophin. In this study, we demonstrate that α-syntrophin phosphorylation determines its intracellular localization and interaction with dystrophin in muscle cells. α-Syntrophin, a predominant isoform in skeletal muscles, directly interacts with ion channels, enzymes, receptors, and DGC proteins. Despite α-syntrophin being a potential signaling molecule, most studies focus on its function as a dystrophin-associated protein. However, we previously reported that α-syntrophin has a variety of DGC-independent functions to modulate cell migration, differentiation, survival, and protein stability. According to the results of the in vitro phosphorylation assays using subcellular fractions, the phosphorylated α-syntrophin accumulated only at the plasma membrane, and this event occurred regardless of dystrophin expression. However, the α-syntrophin interacting with dystrophin at the membrane was not in a phosphorylated state. We also identified that protein kinase C (PKC) was involved in the phosphorylation of α-syntrophin, which restricted α-syntrophin to interact with dystrophin. In conclusion, we demonstrate that the phosphorylation of α-syntrophin by PKC regulates its intracellular localization and interaction with dystrophin

Ductile Fracture Simulation of Full-scale Circumferential Cracked Pipes: (II) Stainless Steel

AbstractThis paper reports ductile fracture simulation of full-scale circumferentially cracked pipes using finite element (FE) damage analysis. In the structural integrity, without experimental investigations or with few ones, it is not an easy task to properly evaluate the crack initiation and crack propagation of large-scale components with a crack-like defect. Unfortunately, from an economic perspective, performing experiments of large-scale components would be consequently unfavorable. For these reasons, ductile fracture simulation using FE damage analysis to predict crack behavior is one efficient way to replace the test procedures. In order to simulate ductile tearing of large-scale cracked pipes, element-size-dependent critical damage model based on the stress-modified fracture strain model is proposed. To evaluate fracture behavior of full-scale cracked pipes, tensile and C(T) specimens are calibrated by FE analysis technique. Tensile properties and fracture toughness of stainless steel at 288oC are taken from Battelle Pipe Fracture Encyclopedia. After calibrations, simulated results of the full-scale pipes with a circumferential crack are compared with test data to validate the proposed method

Piper retrofractum

Photoaging occurs by UVB-irradiation and involves production of reactive oxygen species (ROS) and overexpression of matrix metalloproteinases (MMPs), leading to extracellular matrix damage. Piper retrofractum Vahl. is used as a traditional medicine for antiflatulence, expectorant, sedative, and anti-irritant; however, its antiphotoaging effect has not yet been studied. The current study investigated the antiphotoaging effect of standardized Piper retrofractum extract (PRE) on UVB-damaged human dermal fibroblasts and hairless mouse skin. PRE treatment activated the peroxisome proliferator-activated receptor delta (PPARδ) and the adenosine monophosphate-activated protein kinase (AMPK), consequently upregulating mitochondrial synthesis and reducing ROS production. Additionally, PRE inhibited MMPs expression via suppressing mitogen-activated protein kinase (MAPK) and activator protein-1 (AP-1). PRE downregulated UVB-induced inflammatory reactions by inhibiting the nuclear factor-kappa B (NF-κB) activity. PRE also enhanced transforming growth factor-beta (TGF-β) and the Smad signaling pathway, thereby promoting procollagen gene transcription. Furthermore, oral administration of PRE (300 mg/kg/day) similarly regulated the signaling pathways and increased antioxidant enzyme expression, thus attenuating physiological deformations, such as wrinkle formation and erythema response. Collectively, these results suggest that PRE acts as a potent antiphotoaging agent via PPARδ and AMPK activation

Global analyses of endonucleolytic cleavage in mammals reveal expanded repertoires of cleavage-inducing small RNAs and their targets.

In mammals, small RNAs are important players in post-transcriptional gene regulation. While their roles in mRNA destabilization and translational repression are well appreciated, their involvement in endonucleolytic cleavage of target RNAs is poorly understood. Very few microRNAs are known to guide RNA cleavage. Endogenous small interfering RNAs are expected to induce target cleavage, but their target genes remain largely unknown. We report a systematic study of small RNA-mediated endonucleolytic cleavage in mouse through integrative analysis of small RNA and degradome sequencing data without imposing any bias toward known small RNAs. Hundreds of small cleavage-inducing RNAs and their cognate target genes were identified, significantly expanding the repertoire of known small RNA-guided cleavage events. Strikingly, both small RNAs and their target sites demonstrated significant overlap with retrotransposons, providing evidence for the long-standing speculation that retrotransposable elements in mRNAs are leveraged as signals for gene targeting. Furthermore, our analysis showed that the RNA cleavage pathway is also present in human cells but affecting a different repertoire of retrotransposons. These results show that small RNA-guided cleavage is more widespread than previously appreciated. Their impact on retrotransposons in non-coding regions shed light on important aspects of mammalian gene regulation