Testing the Distance-Duality Relation with a Combination of Cosmological Distance Observations

In this paper, we propose an accurate test of the distance-duality (DD) relation, $\eta=D_{L}(z)(1+z)^{-2}/D_{A}(z)=1$ (where $D_{L}$ and $D_{A}$ are the luminosity distances and angular diameter distances, respectively), with a combination of cosmological observational data of Type Ia Supernave (SNe Ia) from Union2 set and the galaxy cluster sample under an assumption of spherical model. In order to avoid bias brought by redshift incoincidence between observational data and to consider redshift error bars of both clusters and SNe Ia in analysis, we carefully choose the SNe Ia points which have the minimum acceptable redshift difference of the galaxy cluster sample ($|\Delta z|_{\rm min} =\sigma_{z, \rm SN}+\sigma_{z, \rm cluster}$). By assuming $\eta$ a constant and functions of the redshift parameterized by six different expressions, we find that there exists no conceivable evidence for variations in the DD relation concerning with observational data, since it is well satisfied within $1\sigma$ confidence level for most cases. Further considering different values of $\Delta z$ in constraining, we also find that the choosing of $\Delta z$ may play an important role in this model-independent test of the distance-duality relation for the spherical sample of galaxy clusters.Comment: 9 pages, 4 figures, 1 table. accepted for publication in Res. Astron. Astrophy

An approximation scheme for semilinear parabolic PDEs with convex and coercive Hamiltonians

We propose an approximation scheme for a class of semilinear parabolic equations that are convex and coercive in their gradients. Such equations arise often in pricing and portfolio management in incomplete markets and, more broadly, are directly connected to the representation of solutions to backward stochastic differential equations. The proposed scheme is based on splitting the equation in two parts, the first corresponding to a linear parabolic equation and the second to a Hamilton-Jacobi equation. The solutions of these two equations are approximated using, respectively, the Feynman-Kac and the Hopf-Lax formulae. We establish the convergence of the scheme and determine the convergence rate, combining Krylov's shaking coefficients technique and Barles-Jakobsen's optimal switching approximation.Comment: 24 page

Towards transcriptome-wide studies of mRNA translation in tissues from cancer patients

Gene expression consists of multiple strictly regulated steps, including transcription, RNA modification, splicing, messenger RNA (mRNA) transport, mRNA degradation, mRNA translation and protein degradation. mRNA translation, the most energy consuming step, plays a critical role in gene expression via global and selective control of protein synthesis. Translation is a complex process that is commonly divided into initiation, elongation and termination. Among these, translation initiation is widely acknowledged as the rate-limiting step for mRNA translation. The mammalian/mechanistic target of rapamycin (mTOR) pathway, as one important regulator of translation initiation, delivers vital signaling by phosphorylating eIF4E binding proteins (4E-BPs) thereby facilitating eIF4F complex formation which participates in eukaryotic cap dependent translation. Increased mTOR activity and dysregulation of translation have been observed in many diseases, such as cancer as well as immune and metabolic disorders. Sequence and structure features of the mRNA, the translational apparatus and trans-acting proteins facilitate or restrict translation regulation of an mRNA. Moreover, these factors can potentially alter the translational efficiency of an mRNA thereby impacting protein levels without changes in mRNA levels. Accordingly, a well-established technique to study translatomes, polysome profiling, separates efficiently translated mRNA from total mRNA into multiple fractions based on the number of ribosomes bound on the mRNA. Extraction of these fractions is a time consuming and laborious process, which makes polysome profiling inconvenient for large experiments or samples with low RNA amounts. Until now, these shortcomings have prevented assessments of translatomes in patient tissue samples. This thesis introduces an optimized non-linear sucrose gradient which consistently enriches the efficiently translated mRNA in merely one or two fractions, thus reducing sample handling 5-10 fold and saving time in the lab 10-20 fold. When combined with smart-seq2 RNA sequencing, translatomes can be obtained from samples with low amount of RNA and small bio-banked tissues. mRNA yields and translatomes acquired from the optimized gradients resemble those obtained from the standard linear gradients. Thus, this optimized polysome-profiling technique expands the usage of the methodology to small tissue samples and primary cells in large study designs. Insulin sensitive mRNA translation has been observed in cancer cells derived from insulin insensitive organs, for instance breast. It is largely unknown that if this insulin sensitivity resembles that of cells from insulin sensitive organs or if cancer cells tailor a novel program. To this end, this thesis explored insulin’s effect on metabolomes and translatomes in human primary myotubes, human mammary epithelial cells immortalized with human telomerase (HMEC/hTERT) and the MCF7 breast cancer cells. The data indicates that MCF7 cells have developed pathological responses to insulin induction that differ from those observed in cells from insulin sensitive or insensitive organs. The exploration of mechanisms concealed behind this discrepancy would disclose a potential strategy for cancer treatment through annulment of cancer specific effects of insulin. The role of mRNA translation during treatments with experimental anti-cancer drugs or those used in the clinic is largely unknown. We examined the effect on translation of one such experimental drug called “Reactivation of p53 and induction of tumor cell apoptosis” (RITA). The α subunit of eukaryotic initiation factor 2 (eIF2α) is a key regulator of translation initiation. We found eIF2α to be phosphorylated during RITA treatment and to be involved in RITA induced apoptosis and repression of mRNA translation. This activity of RITA is independent of TP53 and mTOR pathway. The inhibition of eIF2α phosphorylation counteracts the impact of RITA on apoptosis and clonogenicity. Another aspect of this thesis explored regulation of translation in immune cells. Short post- infusion persistence restricts treatment of hematological malignancies via adoptive infusion of stimulated natural killer (NK) cells. Interleukin-15 (IL-15) was demonstrated to hold stronger ability than IL-2 to maintain antitumor functions of NK cells after cytokine deprivation. To explore the mechanism underlying these differences, a transcriptome wide study through polysome-profiling technique was applied. Further, the role of mTOR pathway in this superiority of IL-15 was also investigated. Coupled with clinical outcome of patients with B-cell lymphoma, IL-15 but not IL-2 is argued to be implemented in adoptive NK cell cancer therapy. In conclusion, in order to facilitate studies of the translatome for samples with low amount of RNA and small bio-banked tissues, the optimized non-linear gradient was designed. Its performance in aforementioned samples for large experiment set and general applicability was verified to be satisfying. The study on cancer specific effects of insulin unraveled the prospect to selectively target insulin/IGF1 dependent effects on metabolomes and/or translatomes for cancer therapy. As two important pathways regulating translation initiation, the effect of mTOR in immune cell functions and eIF2α in RITA induced apoptosis were unveiled and explored

In-class Multitasking among College Students

The use of mobile devices in class has become a common scene on the college campus. The negative effects of in-class multitasking behaviors have been identified in many educational settings, including colleges. This study investigates the factors that drive college students to multitask and seeks to understand the relationship between learning engagement and multitasking behaviors in the classroom. This study also explores whether polychronic traits relate to multitasking behavior. A total of 282 survey samples were collected from college students in Taiwan. The results confirmed our hypotheses: (1) Students’ multitasking motivation, including social and emotional needs, positively relates to their in-class multitasking. (2) Polychronic traits positively relate to in-class multitasking. (3) Learning engagement negatively relates to in-class multitasking behavior. (4) Polychronic traits negatively relate to learning engagement. (5) Low course difficulty level relates to more frequent in-class multitasking behaviors. The implications of the study are also discussed

Essays on bank diversification

This thesis, which consists of four studies, investigates bank diversification in the context of bank stability, banks’ market power, and bank competition, by constructing new diversification indicators to capture the degree of diversification at the market and country levels. The first essay empirically tests a theory regarding the influence of diversification on bank systemic risk and investigates whether this effect is different for bank standalone risk. I construct a new country-level diversification measure to reflect the risk distribution among banks, which makes my study more suitable to evaluate the mechanical reasons behind the theory tested than traditionally used bank-level diversification indicators. My results confirm the Wagner’s theory according to which diversification leads to more systemic risk but less bank standalone risk. The second essay investigates the role of the regulatory environment, bank size, and capital in the diversification-bank stability nexus, which extends my findings in the first essay. I find that the negative relationship between diversification and bank systemic stability becomes weaker in countries with greater supervisory power of regulatory agencies, higher stringency of capital regulations, more restrictions on the scope of banks’ activities, and more private monitoring. Moreover, I show that bank size and capital alleviate the negative diversification-systemic stability relationship, which implies that larger and well-capitalized banks are less subject to systemic risk when the degree of diversification in a country is high. To the best of my knowledge, my study is the first to confirm the moderating role of cross-country regulatory environments and banks’ essential characteristics in the relationship between diversification and bank stability. The third essay investigates how diversification influences banks’ market power, which fills the gap in the literature regarding the lack of analyses showing whether diversification can be a determinant or source of banks’ market power. Diversification may enable banks to gain market power from obtaining new sources of revenues but could also weaken market power by inducing new costs. I find an inverse U-shaped relationship between revenue diversification and banks’ market power in both lending and funding markets. This implies that diversification is an important determinant or source of banks’ market power and potentially affects market power by changing banks’ output prices and marginal costs of production, or a combination of both. In addition, this inverse U-shaped relationship is much more manifest in large banks than in small banks, which indicates that it is dominated by large banks. The last essay investigates the role of market diversification in the relationship between competition and bank stability in the dimensions of individual bank stability and systemic stability, by constructing novel market-level diversification measures. My study is important to reconcile the mixed conclusions regarding the competition-stability nexus in the literature by considering the potential changing associations between competition and bank stability conditional on different degrees of diversification in the market. I find that the negative relationship between competition and systemic stability is exacerbated when the market diversification is high while this negative competition-systemic stability relationship turns to be positive when the market diversification is low. However, I do not find a significant interacting effect of market diversification on the competition-individual bank stability relationship. Lastly, I show a positive association between competition and diversification, which suggests that restrictions in banks’ diversification activities in a competitive environment may help in maintaining systemic stability. My research provides useful implications for bank managers and policymakers. First, it offers bank managers knowledge of how diversified activities are related to banks’ standalone and systemic risks and suggests the feasibility of managing banks’ market power by formulating an appropriate diversification strategy. Second, from the policymaking perspective, my study proposes that promoting diversification would be beneficial to bank standalone stability if banks’ diversification strategy is well formulated and executed but could bring additional costs to banks and exacerbate systemic stability