Essays on Stock Market Contagion: Evidence From the Americas

In this dissertation we examine the financial contagion from the U.S. to the Americas during the U.S. financial crisis. First, we examine the relationship between the U.S. perceived market volatility (VIX), perceived credit risk (TED spread), and the U.S. financial crisis, on the stock returns of these countries. Our findings suggest that VIX has negatively effects on the stock returns of all these countries and that this relationship increases significantly during the U.S. financial crisis. We also identify that increases in the TED spread, have negative effects on the stock market returns of Canada and Latin America, and this increases during the U.S. financial crisis. Our findings suggest that increases in market volatility and credit risk were contributing factors, of the financial contagion from the U.S. to the Americas, during the U.S. Financial Crisis. Second, we explore the role of perceived market volatility (VIX), individual investor sentiment, and institutional investor sentiment in the propagation of the U.S. financial crisis to the Americas. We confirm our findings from the previous essay in regards to VIX. We then find that individual and institutional investor sentiments positively affect the stock market returns of the countries in this study, and that the financial crisis has a positive effect on these relationships. We look in more detail and identify that institutional investor sentiment has a stronger effect than individual sentiment, highlighting the influence of institutional investors. Third, we study the effects of the 2008–2009 U.S. financial crisis, oil price returns, and U.S. market volatility, on the stock market returns of six oil producing countries in the Americas. We find evidence of contagion from the U.S. to the other oil producers during the U.S. financial crisis, finding positive effects on the conditional correlations between oil price returns and the oil producers’ stock market returns. We find evidence that due to the U.S. financial crisis, the conditional correlations between stock market returns and oil prices increase substantially, and that these correlations remain higher than the pre-crisis period

RNA microarray analysis in prenatal mouse cochlea reveals novel IGF-I target genes: implication of MEF2 and FOXM1 transcription factors

Background: Insulin-like growth factor-I (IGF-I) provides pivotal cell survival and differentiation signals during inner ear development throughout evolution. Homozygous mutations of human IGF1 cause syndromic sensorineural deafness, decreased intrauterine and postnatal growth rates, and mental retardation. In the mouse, deficits in IGF-I result in profound hearing loss associated with reduced survival, differentiation and maturation of auditory neurons. Nevertheless, little is known about the molecular basis of IGF-I activity in hearing and deafness. Methodology/Principal Findings: A combination of quantitative RT-PCR, subcellular fractionation and Western blotting, along with in situ hybridization studies show IGF-I and its high affinity receptor to be strongly expressed in the embryonic and postnatal mouse cochlea. The expression of both proteins decreases after birth and in the cochlea of E18.5 embryonic Igf1(-/-) null mice, the balance of the main IGF related signalling pathways is altered, with lower activation of Akt and ERK1/2 and stronger activation of p38 kinase. By comparing the Igf1(-/-) and Igf1(+/+) transcriptomes in E18.5 mouse cochleae using RNA microchips and validating their results, we demonstrate the up-regulation of the FoxM1 transcription factor and the misexpression of the neural progenitor transcription factors Six6 and Mash1 associated with the loss of IGF-I. Parallel, in silico promoter analysis of the genes modulated in conjunction with the loss of IGF-I revealed the possible involvement of MEF2 in cochlear development. E18.5 Igf1(+/+) mouse auditory ganglion neurons showed intense MEF2A and MEF2D nuclear staining and MEF2A was also evident in the organ of Corti. At P15, MEF2A and MEF2D expression were shown in neurons and sensory cells. In the absence of IGF-I, nuclear levels of MEF2 were diminished, indicating less transcriptional MEF2 activity. By contrast, there was an increase in the nuclear accumulation of FoxM1 and a corresponding decrease in the nuclear cyclin-dependent kinase inhibitor p27(Kip1). Conclusions/Significance: We have defined the spatiotemporal expression of elements involved in IGF signalling during inner ear development and reveal novel regulatory mechanisms that are modulated by IGF-I in promoting sensory cell and neural survival and differentiation. These data will help us to understand the molecular bases of human sensorineural deafness associated to deficits in IGF-I

Scala with Explicit Nulls

The Scala programming language unifies the object-oriented and functional styles of programming. One common source of errors in Scala programs is null references. In this dissertation, I present a modification to the Scala type system that makes nullability explicit in the types. This allows us to turn runtime errors into compile-time errors. I have implemented this design for explicit nulls as a fork of the Dotty (Scala 3) compiler. I evaluate the design by migrating a number of Scala libraries to use explicit nulls. In the second part of the dissertation, I give a theoretical foundation for explicit nulls. I do this in two, independent ways. First, I give a denotational semantics for type nullification, a key part of the explicit nulls design. Separately, I present a core calculus for null interoperability that models how languages with explicit nulls (like Scala) interact with languages where null remains implicit (like Java). Using the concept of blame from gradual typing, I show that if a well-typed program fails with certain kinds of nullability errors, an implicitly-nullable subterm can always be blamed for the failure

Enhancing On-line Blended Learning Systems Using a New Human-Computer Interaction Educational Methodology

Non

Collapse of optical binding under secondary irradiation

When an optically trapped and bound micrometer-sized chain of particles is subjected to a suitably oriented secondary laser beam above a threshold level of intensity, the structure will collapse. The effect arises from modifications to the interparticle energy landscapes owing to the superposition of optically induced potentials. From the theory it also emerges that, for particles separated by near-field distances, optically induced assemblies may be continuously transformed between linear, spherical, and lamellar forms. The results show scope for the optical fabrication of moldable nanoscale structures