Nature or Nurture? An Analysis of Rational Addiction to Mobile Social Applications

Through the lens of rational addiction theory (Becker and Murphy, 1988), this study investigates whether addiction to mobile social apps should be viewed as a rational behavior rather than an uncontrollable, irrational disorder. To derive the analytical model, this study extends the rational addiction framework to include a utility-level network effect as the key factor that regulates the inter-temporal consumption of mobile social apps. Further, to validate empirically the rational addiction model in this context, we gathered and analyzed longitudinal panel data on the weekly app usage of thousands of smartphone users. The findings suggest that consistent with the rational addiction theory, users of mobile social apps are rational and forward-looking. They determine their current consumption based on both past and future consumption and the utility derived from network effects. However, the extent of rational addiction to mobile social apps varies considerably across diverse demographic groups and app categories

Lightweight and Robust Representation of Economic Scales from Satellite Imagery

Satellite imagery has long been an attractive data source that provides a wealth of information on human-inhabited areas. While super resolution satellite images are rapidly becoming available, little study has focused on how to extract meaningful information about human habitation patterns and economic scales from such data. We present READ, a new approach for obtaining essential spatial representation for any given district from high-resolution satellite imagery based on deep neural networks. Our method combines transfer learning and embedded statistics to efficiently learn critical spatial characteristics of arbitrary size areas and represent them into a fixed-length vector with minimal information loss. Even with a small set of labels, READ can distinguish subtle differences between rural and urban areas and infer the degree of urbanization. An extensive evaluation demonstrates the model outperforms the state-of-the-art in predicting economic scales, such as population density for South Korea (R^2=0.9617), and shows a high potential use for developing countries where district-level economic scales are not known.Comment: Accepted for oral presentation at AAAI 202

Attenuating MKRN1 E3 ligase-mediated AMPKα suppression increases tolerance against metabolic stresses in mice

The 5′ adenosine monophosphate-activated protein kinase (AMPK) is an essential energy sensor in the cell, which, at low energy levels, instigates the cellular energy-generating systems along with suppression of the anabolic signaling pathways. The activation of AMPK through phosphorylation is a well-known process; however, activation alone is not sufficient, and knowledge about the other regulatory networks of post-translational modifications connecting the activities of AMPK to systemic metabolic syndromes is important, which is still lacking. The recent studies on Makorin Ring Finger Protein 1 (MKRN1) mediating the ubiquitination and proteasome-dependent degradation of AMPKa implicate that the post-translational modification of AMPK, regulating its protein homeostasis, could impose significant systemic metabolic effects (Lee et al. Nat Commun 9:3404). In this study, MKRN1 was identified as a novel E3 ligase for both AMPKα1 and α2. Mouse embryonic fibroblasts, genetically deleted for Mkrmn1, and Ampkα1 and α2, became stabilized with the suppression of lipogenesis pathways and an increase in nutrient consumption and mitochondria regeneration. Of note, the Mkrn1 knockout mice fed normal chow displayed no obvious phenotypic defects or abnormality, whereas the Mkrn1-null mice exhibited strong tolerance to metabolic stresses induced by high-fat diet (HFD). Thus, these mice, when compared with the HFD-induced wild type, were resistant to obesity, diabetes, and non-alcoholic fatty liver disease. Interestingly, in whole-body Mkrn1 knockout mouse, only the liver and white and brown adipose tissues displayed anincrease in the active phosphorylated AMPK levels, but no other organs, such as the hypothalamus, skeletal muscles, or pancreas, displayed such increases. Specific ablation of MKRN1 in the mouse liver using adenovirus prevented HFD-induced lipid accumulation in the liver and blood, implicating MKRN1 as a possible therapeutic target for metabolic syndromes, such as obesity, type II diabetes, and fat liver diseases. This study would provide a crucial perspective on the importance of post-translational regulation of AMPK in metabolic pathways and will help researchers develop novel therapeutic strategies that target not only AMPK but also its regulators

Switchable tribology of ferroelectrics

Switchable tribological properties of ferroelectrics offer an alternative route to visualize and control ferroelectric domains. Here, we observe the switchable friction and wear behavior of ferroelectrics using a nanoscale scanning probe—down domains have lower friction coefficients and show slower wear rates than up domains and can be used as smart masks. This asymmetry is enabled by flexoelectrically coupled polarization in the up and down domains under a sufficiently high contact force. Moreover, we determine that this polarization-sensitive tribological asymmetry is widely applicable across various ferroelectrics with different chemical compositions and crystalline symmetry. Finally, using this switchable tribology and multi-pass patterning with a domain-based dynamic smart mask, we demonstrate three-dimensional nanostructuring exploiting the asymmetric wear rates of up and down domains, which can, furthermore, be scaled up to technologically relevant (mm–cm) size. These findings demonstrate that ferroelectrics are electrically tunable tribological materials at the nanoscale for versatile applications.Peer ReviewedPostprint (published version

Modulatory role of phospholipase D in the activation of signal transducer and activator of transcription (STAT)-3 by thyroid oncogenic kinase RET/PTC

<p>Abstract</p> <p>Background</p> <p>RET/PTC (rearranged in transformation/papillary thyroid carcinomas) gene rearrangements are the most frequent genetic alterations identified in papillary thyroid carcinoma. Although it has been established that RET/PTC kinase plays a crucial role in intracellular signaling pathways that regulate cellular transformation, growth, and proliferation in thyroid epithelial cells, the upstream signaling that leads to the activation of RET/PTC is largely unknown. Based on the observation of high levels of PLD expression in human papillary thyroid cancer tissues, we investigated whether PLD plays a role in the regulating the RET/PTC-induced STAT3 activation.</p> <p>Methods</p> <p>Cancer tissue samples were obtained from papillary thyroid cancer patients (n = 6). The expression level of PLD was examined using immunohistochemistry and western blotting. Direct interaction between RET/PTC and PLD was analyzed by co-immunoprecipitation assay. PLD activity was assessed by measuring the formation of [³H]phosphatidylbutanol, the product of PLD-mediated transphosphatidylation, in the presence of <it>n</it>-butanol. The transcriptional activity of STAT3 was assessed by m67 luciferase reporter assay.</p> <p>Results</p> <p>In human papillary thyroid cancer, the expression levels of PLD2 protein were higher than those in the corresponding paired normal tissues. PLD and RET/PTC could be co-immunoprecipitated from cells where each protein was over-expressed. In addition, the activation of PLD by pervanadate triggered phosphorylation of tyrosine 705 residue on STAT-3, and its phosphorylation was dramatically higher in TPC-1 cells (from papillary carcinoma) that have an endogenous RET/PTC1 than in ARO cells (from anaplastic carcinoma) without alteration of total STAT-3 expression. Moreover, the RET/PTC-mediated transcriptional activation of STAT-3 was synergistically increased by over-expression of PLD, whereas the PLD activity as a lipid hydrolyzing enzyme was not affected by RET/PTC.</p> <p>Conclusion</p> <p>These findings led us to suggest that the PLD synergistically functions to activate the STAT3 signaling by interacting directly with the thyroid oncogenic kinase RET/PTC.</p

Attenuating MKRN1 E3 ligase-mediated AMPKα suppression increases tolerance against metabolic stresses in mice

The 5′ adenosine monophosphate-activated protein kinase (AMPK) is an essential energy sensor in the cell, which, at low energy levels, instigates the cellular energy-generating systems along with suppression of the anabolic signaling pathways. The activation of AMPK through phosphorylation is a well-known process; however, activation alone is not sufficient, and knowledge about the other regulatory networks of post-translational modifications connecting the activities of AMPK to systemic metabolic syndromes is important, which is still lacking. The recent studies on Makorin Ring Finger Protein 1 (MKRN1) mediating the ubiquitination and proteasome-dependent degradation of AMPKa implicate that the post-translational modification of AMPK, regulating its protein homeostasis, could impose significant systemic metabolic effects (Lee et al. Nat Commun 9:3404). In this study, MKRN1 was identified as a novel E3 ligase for both AMPKα1 and α2. Mouse embryonic fibroblasts, genetically deleted for Mkrmn1, and Ampkα1 and α2, became stabilized with the suppression of lipogenesis pathways and an increase in nutrient consumption and mitochondria regeneration. Of note, the Mkrn1 knockout mice fed normal chow displayed no obvious phenotypic defects or abnormality, whereas the Mkrn1-null mice exhibited strong tolerance to metabolic stresses induced by high-fat diet (HFD). Thus, these mice, when compared with the HFD-induced wild type, were resistant to obesity, diabetes, and non-alcoholic fatty liver disease. Interestingly, in whole-body Mkrn1 knockout mouse, only the liver and white and brown adipose tissues displayed anincrease in the active phosphorylated AMPK levels, but no other organs, such as the hypothalamus, skeletal muscles, or pancreas, displayed such increases. Specific ablation of MKRN1 in the mouse liver using adenovirus prevented HFD-induced lipid accumulation in the liver and blood, implicating MKRN1 as a possible therapeutic target for metabolic syndromes, such as obesity, type II diabetes, and fat liver diseases. This study would provide a crucial perspective on the importance of post-translational regulation of AMPK in metabolic pathways and will help researchers develop novel therapeutic strategies that target not only AMPK but also its regulators.© 2018 Han et al

Effect of Process Control Agent on the Microstructure of Ni-Based ODS Superalloy Produced by Mechanical Alloying and Sintering

The effects of different types of process control agents (PCA) on the microstructure evolution of Ni-based oxide dispersion-strengthened superalloy have been investigated. Alloy synthesis was performed on elemental powders having a nominal composition of Ni-15Cr-4.5Al-4W-2.5Ti-2Mo-2Ta-0.15Zr-1.1Y2O3 in wt % using high energy ball milling for 5 h. The prepared powders are consolidated by spark plasma sintering at 1000°C. Results indicated that the powder ball-milled with ethanol as PCA showed large particle size, low carbon content and homogeneous distribution of elemental powders compared with the powder by stearic acid. The sintered alloy prepared by ethanol as PCA exhibited a homogeneous microstructure with fine precipitates at the grain boundaries. The microstructural characteristics have been discussed on the basis of function of the PCA

Conflict between Two Selves: Mobile Temptation and Self-Control through Precommitment

This study investigates the effectiveness of diverse precommitment mechanisms as self-control measures against mobile temptation, which refers to an uncontrollable desire and craving to consume mobile applications. These precommitment systems are made available by app-blocking options that are downloadable on smartphones at user discretion to restrict access to apps. On the basis of Thaler and Shefrin’s (1981) self-control framework, we identify and evaluate rule-based (spatial and temporal) and incentive-driven (social- and reinforcement-based) precommitment schemes. Mixed results are found with respect to the effectiveness of rule-driven precommitment schemes: Rigid temporal precommitment effectively facilitates sustained self-control and motivates users to increase block time, but contrary to expectations, the less stringent flexible spatial precommitment outperforms rigid spatial precommitment. The findings also suggest that both social- and reinforcement-based methods successfully advance sustainable command over oneself and therefore aid users in increasing voluntarily implemented block time