High-Mobility Workers’ Expectations of Mobile Business Applications

The popularity of smartphones has provided new opportunities for mobile (m)-businesses in recent years. This study implements a qualitative research design using the Delphi method and attempts to gain an insight into the expected value of m-business apps from the high-mobility workers’ perspective. Three major value propositions are gathered during the study, including ubiquity, time efficiency, and collaboration. We also conclude that task-technology fit is a key factor when pursuing user satisfaction due to the limited screen size of smartphones. In the context of m-business, users expect simple interfaces instead of sophisticated functions or training sessions. The work-life conflict was investigated as a potential reason for resistance to m-business; however, none of the interviewees in this study identified such conflicts

Radiative and flavor-violating transitions of leptons from interactions with color-octet particles

It has been recently proposed that neutrino mass could originate from Yukawa interactions of leptons with new colored particles. This raises the interesting possibility of testing mass generation through copious production of those particles at hadron colliders. A realistic assessment of it however should take into account how large those interactions could be from available precision results. In this work we make a systematic analysis to the flavor structure in Yukawa couplings, provide a convenient parametrization to it, and investigate the rare radiative and pure leptonic decays of the muon and tau leptons. For general values of parameters the muon decays set stringent constraints on the couplings, and all rare tau decays are far below the current experimental sensitivity. However, there is room in parameter space in which the muon decays could be significantly suppressed by destructive interference between colored particles without generically reducing the couplings themselves. This is also the region of parameters that is relevant to collider physics. We show that for this part of parameter space some tau decays can reach or are close to the current level of precision.Comment: 20 pages, 7 figure

Commentary on the Regulation of Viral Proteins in Autophagy Process

The ability to subvert intracellular antiviral defenses is necessary for virus to survive as its replication occurs only in the host cells. Viruses have to modulate cellular processes and antiviral mechanisms to their own advantage during the entire virus life cycle. Autophagy plays important roles in cell regulation. Its function is not only to catabolize aggregate proteins and damaged organelles for recycling but also to serve as innate immunity to remove intracellular pathogenic elements such as viruses. Nevertheless, some viruses have evolved to negatively regulate autophagy by inhibiting its formation. Even more, some viruses have employed autophagy to benefit their replication. To date, there are more and more growing evidences uncovering the functions of many viral proteins to regulate autophagy through different cellular pathways. In this review, we will discuss the relationship between viruses and autophagy and summarize the current knowledge on the functions of viral proteins contributing to affect autophagy process

Mutations in the PKM2 exon-10 region are associated with reduced allostery and increased nuclear translocation.

PKM2 is a key metabolic enzyme central to glucose metabolism and energy expenditure. Multiple stimuli regulate PKM2's activity through allosteric modulation and post-translational modifications. Furthermore, PKM2 can partner with KDM8, an oncogenic demethylase and enter the nucleus to serve as a HIF1α co-activator. Yet, the mechanistic basis of the exon-10 region in allosteric regulation and nuclear translocation remains unclear. Here, we determined the crystal structures and kinetic coupling constants of exon-10 tumor-related mutants (H391Y and R399E), showing altered structural plasticity and reduced allostery. Immunoprecipitation analysis revealed increased interaction with KDM8 for H391Y, R399E, and G415R. We also found a higher degree of HIF1α-mediated transactivation activity, particularly in the presence of KDM8. Furthermore, overexpression of PKM2 mutants significantly elevated cell growth and migration. Together, PKM2 exon-10 mutations lead to structure-allostery alterations and increased nuclear functions mediated by KDM8 in breast cancer cells. Targeting the PKM2-KDM8 complex may provide a potential therapeutic intervention

The Interplay of Reovirus with Autophagy

Autophagy participates in multiple fundamental physiological processes, including survival, differentiation, development, and cellular homeostasis. It eliminates cytoplasmic protein aggregates and damaged organelles by triggering a series of events: sequestering the protein substrates into double-membrane vesicles, fusing the vesicles with lysosomes, and then degrading the autophagic contents. This degradation pathway is also involved in various disorders, for instance, cancers and infectious diseases. This paper provides an overview of modulation of autophagy in the course of reovirus infection and also the interplay of autophagy and reovirus

Lepton Flavor Violating Muon Decays in a Model of Electroweak-Scale Right-Handed Neutrinos

The small neutrino mass observed in neutrino oscillations is nicely explained by the seesaw mechanism. Rich phenomenology is generally expected if the heavy neutrinos are not much heavier than the electroweak scale. A model with this feature built in has been suggested recently by Hung. The model keeps the standard gauge group but introduces chirality-flipped partners for the fermions. In particular, a right-handed neutrino forms a weak doublet with a charged heavy lepton, and is thus active. We analyze the lepton flavor structure in gauge interactions. The mixing matrices in charged currents (CC) are generally non-unitary, and their deviation from unitarity induces flavor changing neutral currents (FCNC). We calculate the branching ratios for the rare decays \mu\to e\gamma and \mu\to ee\bar e due to the gauge interactions. Although the former is generally smaller than the latter by three orders of magnitude, parameter regions exist in which \mu\to e\gamma is reachable in the next generation of experiments even if the current stringent bound on \mu\to ee\bar e is taken into account. If light neutrinos dominate for \mu\to e\gamma, the latter cannot set a meaningful bound on unitarity violation in the mixing matrix of light leptons due to significant cancelation between CC and FCNC contributions. Instead, the role is taken over by the decay \mu\to ee\bar e.Comment: 11 pages, 2 figures. v2: added 2 refs and improved a comment on previous work; no other changes. v3: proofread version for PLB; added a few clarifying sentences in paragraph before eq (17) plus minor editting change

FASTSNP: an always up-to-date and extendable service for SNP function analysis and prioritization

Single nucleotide polymorphism (SNP) prioritization based on the phenotypic risk is essential for association studies. Assessment of the risk requires access to a variety of heterogeneous biological databases and analytical tools. FASTSNP (function analysis and selection tool for single nucleotide polymorphisms) is a web server that allows users to efficiently identify and prioritize high-risk SNPs according to their phenotypic risks and putative functional effects. A unique feature of FASTSNP is that the functional effect information used for SNP prioritization is always up-to-date, because FASTSNP extracts the information from 11 external web servers at query time using a team of web wrapper agents. Moreover, FASTSNP is extendable by simply deploying more Web wrapper agents. To validate the results of our prioritization, we analyzed 1569 SNPs from the SNP500Cancer database. The results show that SNPs with a high predicted risk exhibit low allele frequencies for the minor alleles, consistent with a well-known finding that a strong selective pressure exists for functional polymorphisms. We have been using FASTSNP for 2 years and FASTSNP enables us to discover a novel promoter polymorphism. FASTSNP is available at