Fintech in the time of COVID-19: Technological adoption during crises

We document the effects of the COVID-19 pandemic on digital finance and fintech adoption. Drawing on mobile application data from a globally representative sample, we find that the spread of COVID- 19 and related government lockdowns led to a sizeable increase in the rate of finance app downloads. We then analyze factors that may have driven this effect on the demand-side and better understand the “winners” from this digital acceleration on the supply-side. Our overall results suggest that traditional incumbents saw the largest growth in their digital offerings during the initial period, but that "BigTech" companies and newer fintech providers ultimately outperformed them over time. Finally, we drill-down further on the adoption of fintech apps pertaining to both the asset and liability side of the traditional bank balance sheet, to explore the implications that the accelerated trends in digitization may have for the future landscape of financial intermediation

Don’t Stay Put: Ride the (Credit) Wave

Information asymmetries and enforcement problems often limit commercial lenders’ entry into low-income markets. Using detailed credit registry data with more than 32 million bank-borrower loan observations, we study the “failed” entry of commercial lenders into Bolivia’s microfinance market in the mid-1990s, which led to an over-indebtedness crisis. Tracing borrowers’ credit outcomes for nearly 10 years, we find that despite the commercial lenders’ poorly adapted lending technologies, stronger adverse selection, and moral hazard problems, the increase in competition carried significant short-term and long-term credit benefits to borrowers by forcing microfinance institutions to improve their loan terms and reduce rents

Interacting quantum walk on a two-leg flux ladder: Emergence of re-entrant dynamics

We study the quench dynamics of interacting bosons on a two-leg flux ladder by implementing the continuous-time quantum walk and explore the combined effect of the magnetic field and onsite interaction in the presence of uniform flux. We show that in the regime of weak interaction, the magnetic field substantially slows down the spreading of the particles' wavefunction during the dynamics. However, in the presence of strong interaction, we obtain an interesting re-entrant behaviour in the dynamics where the radial velocity associated to the spreading first increases, then decreases, and increases again as a function of the flux strength. We also find a re-entrant dynamics in the chiral motion of the particles as a function of interaction for fixed flux strengths.Comment: 6 pages, 7Fig

Quasi-Degenerate Neutrinos in Type II Seesaw Models

We present an analysis of normal and inverted hierarchical neutrino mass models within the framework of tri-bi-maximal (TBM) mixing. Considering the neutrinos to be quasi-degenerate (QDN), we study two different neutrino mass models with mass eigenvalues $(m_1, -m_2, m_3)$ and $(m_1, m_2, m_3)$ for both normal hierarchical (NH) and inverted hierarchical (IH) cases. Parameterizing the neutrino mass matrix using best fit oscillation and cosmology data for a QDN scenario, we find the right-handed Majorana mass matrix using type I seesaw formula for two types of Dirac neutrino mass matrices: charged lepton (CL) type and up quark (UQ) type. Incorporating the presence of type II seesaw term which arises naturally in generic left-right symmetric models (LRSM) along with type I term, we compare the predictions for neutrino mass parameters with the experimental values. Within such a framework and incorporating both oscillation as well as cosmology data, we show that QDN scenario of neutrino masses can still survive in nature with some minor exceptions. A viable extension of the standard model with an abelian gauged flavor symmetry is briefly discussed which can give rise to the desired structure of the Dirac and Majorana mass matrices.Comment: Version 2: Typos corrected, texts+tables rearranged, conclusion unchanged. Accepted for publication in Physical Review

Novel mutation predicted to disrupt SGOL1 protein function

Cell cycle alterations are the major cause of cancers in human. The proper segregation of sister chromatids during the cell division process defines the fate of daughter cells which is efficiently maintained by various proteomic complexes and signaling cascades. Shugosin (SGOL1) is one among those proteins which are required for phosphatise 2A protein (PP2A) localization to centromeres during division. This localization actively manages the adherence of sister chromatids at the centromeric region until the checkpoint signals are received. Wide evidences of SGOL1 genomic variants have been studied for their correlation with chromosomal instability and chromatid segregation errors. Here we used computational methods to prioritize the Single Nucleotide Polymorphism’s (SNP’s) capable of disrupting the normal functionality of SGOL1 protein. L54Q, a mutation predicted as deleterious in this study was found to be located in N-terminal coiled coil domain which is effectively involved in the proper localization of PP2A to centromere. We further examined the effect of this mutation over the translational efficiency of the SGOL1 coding gene. Our analysis revealed major structural consequences of mutation over folding conformation of the 3rd exon. Further we carried molecular dynamic simulations to unravel the structural variations induced by this mutation in SGOL1 N-terminal coiled coil domain. Root mean square deviation (RMSD), root mean square fluctuation (RMSF), H-Bond scores further supported our result. The result obtained in our study will provide a landmark to future research in understanding genotype-phenotype association of damaging non-synonymous SNPs (nsSNPs) in several other centromere proteins as done in SGOL1 and will be helpful to forecast their role in chromosomal instabilities and solid tumor formation.Keywords: SGOL1; Molecular Dynamics Simulation; Gromacs; PhD-SNP; SIFT; Polyphen; MutPredThe Egyptian Journal of Medical Human Genetics (2013) 14, 149–15