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- All Subjects: Biology
- Creators: Arizona State University
Description
In two independent and thematically relevant chapters, I empirically investigate consumers’ mobile channel usage behaviors. In the first chapter, I examine the impact of mobile use in online higher education. With the prevalence of affordable mobile devices, higher education institutions anticipate that learning facilitated through mobile access can make education more accessible and effective, while some critics of mobile learning worry about the efficacy of small screens and possible distraction factors. I analyze individual-level data from Massive Open Online Courses. To resolve self-selection issues in mobile use, I exploit changes in the number of mobile-friendly, short video lectures in one course (“non-focal course”) as an instrumental variable for a learner’s mobile intensity in the other course (“focal course”), and vice versa, among learners who have taken both courses during the same semester. Results indicate that high mobile intensity impedes, or at most does not improve course engagement due mainly to mobile distractions from doing activities unrelated to learning. Finally, I discuss practical implications for researchers and higher education institutions to improve the effectiveness of mobile learning. In the second chapter, I investigate the impact of mobile users’ popular app adoption on their app usage behaviors. The adoption of popular apps can serve as a barrier to the use of other apps given popular apps’ addictive nature and users’ limited time resources, while it can stimulate the exploration of other apps by inspiring interest in experimentation with similar technologies. I use individual-level app usage data and develop a joint model of the number of apps used and app usage duration. Results indicate that popular app adoption stimulates users to explore new apps at app stores and allocate more time to them such that it increases both the number of apps used and app usage duration for apps excluding the popular app. Such positive spillover effects are heterogeneous across app categories and user characteristics. I draw insights for app developers, app platforms, and media planners by determining which new apps to release in line with the launch of popular apps, when to release such apps, and to whom distribution should be targeted.
ContributorsLee, Mi Hyun (Author) / Park, Sungho (Thesis advisor) / Han, Sang Pil (Committee member) / Kim, Sunghoon (Committee member) / Arizona State University (Publisher)
Created2018
Description
Obesity impairs skeletal muscle maintenance and regeneration, a condition that can progressively lead to muscle loss, but the mechanisms behind it are unknown. Muscle is primarily composed of multinucleated cells called myotubes which are derived by the fusion of mononucleated myocytes. A key mediator in this process is the cellular fusion protein syncytin-1. This led to the hypothesis that syncytin-1 could be decreased in the muscle of obese/insulin resistant individuals. In contrast, it was found that obese/insulin resistant subjects had higher syncytin-1 expression in the muscle compared to that of the lean subjects. Across the subjects, syncytin-1 correlated significantly with body mass index, percent body fat, blood glucose and HbA1c levels, insulin sensitivity and muscle protein fractional synthesis rate. The concentrations of specific plasma fatty acids, such as the saturated fatty acid (palmitate) and monounsaturated fatty acid (oleate) are known to be altered in obese/insulin resistant humans, and also to influence the protein synthesis in muscle. Therefore, it was evaluated that the effects of palmitate and oleate on syncytin-1 expression, as well as 4E-BP1 phosphorylation, a key mechanism regulating muscle protein synthesis in insulin stimulated C2C12 myotubes. The results showed that treatment with 20 nM insulin, 300 µM oleate, 300 µM oleate +20 nM insulin and 300 µM palmitate + 300 µM oleate elevated 4E-BP1 phosphorylation. At the same time, 20 nM insulin, 300 µM palmitate, 300 µM oleate + 20 nM insulin and 300 µM palmitate + 300 µM oleate elevated syncytin-1 expression. Insulin stimulated muscle syncytin-1 expression and 4E-BP1 phosphorylation, and this effect was comparable to that observed in the presence of oleate alone. However, the presence of palmitate + oleate diminished the stimulatory effect of insulin on muscle syncytin-1 expression and 4E-BP1 phosphorylation. These findings indicate oleate but not palmitate increased total 4E-BP1 phosphorylation regardless of insulin and the presence of palmitate in insulin mediated C2C12 cells. The presence of palmitate inhibited the upregulation of total 4EB-P1 phosphorylation. Palmitate but not oleate increased syncytin-1 expression in insulin mediated C2C12 myotubes. It is possible that chronic hyperinsulinemia in obesity and/or elevated levels of fatty acids such as palmitate in plasma could have contributed to syncytin-1 overexpression and decreased muscle protein fractional synthesis rate in obese/insulin resistant human muscle.
ContributorsRavichandran, Jayachandran (Author) / Katsanos, Christos (Thesis advisor) / Coletta, Dawn (Committee member) / Dickinson, Jared (Committee member) / Arizona State University (Publisher)
Created2017
Description
In a 2004 paper, John Nagy raised the possibility of the existence of a hypertumor \emph{i.e.}, a focus of aggressively reproducing parenchyma cells that invade part or all of a tumor. His model used a system of nonlinear ordinary differential equations to find a suitable set of conditions for which these hypertumors exist. Here that model is expanded by transforming it into a system of nonlinear partial differential equations with diffusion, advection, and a free boundary condition to represent a radially symmetric tumor growth. Two strains of parenchymal cells are incorporated; one forming almost the entirety of the tumor while the much more aggressive strain
appears in a smaller region inside of the tumor. Simulations show that if the aggressive strain focuses its efforts on proliferating and does not contribute to angiogenesis signaling when in a hypoxic state, a hypertumor will form. More importantly, this resultant aggressive tumor is paradoxically prone to extinction and hypothesize is the cause of necrosis in many vascularized tumors.
appears in a smaller region inside of the tumor. Simulations show that if the aggressive strain focuses its efforts on proliferating and does not contribute to angiogenesis signaling when in a hypoxic state, a hypertumor will form. More importantly, this resultant aggressive tumor is paradoxically prone to extinction and hypothesize is the cause of necrosis in many vascularized tumors.
ContributorsAlvarez, Roberto L (Author) / Milner, Fabio A (Thesis advisor) / Nagy, John D. (Committee member) / Kuang, Yang (Committee member) / Thieme, Horst (Committee member) / Mahalov, Alex (Committee member) / Smith, Hal (Committee member) / Arizona State University (Publisher)
Created2014