From Albéniz to Arbós: the Orchestration of Iberia

Enrique Arbós's five orchestrations of pieces from Iberia, the masterly piano work by his close friend, Isaac Albéniz, are among the most frequently programmed works in the Spanish orchestral repertoire today. Increased academic interest in Albéniz's orchestral output has revealed that Arbós's orchestration of Albéniz's piano solo, "El Puerto," from Iberia, bears striking similarities with Albéniz's unpublished orchestration of the same piece. Although Albéniz asked Arbós to take over the task of orchestrating "El Puerto," little is known about the details of this arrangement. To shed light on this issue, I have carefully reviewed the overlapping biographies of these two composers, as well as thoroughly analyzed the two scores for the first time. I conclude that Arbós's orchestration of "El Puerto" is indeed a revision of Albéniz's orchestration, and that this revision was a natural result of their close relationship.

Characterization of Borrelia burgdorferi Gene Product BBD18 for Its Role(s) in Pathogen Biology and Infectivity

bbd18 is a differentially expressed Borrelia burgdorferi gene that is transcribed at almost undetectable levels in spirochetes grown in vitro but dramatically upregulated during tick infection. The gene also displays low yet detectable expression at various times in tissues of murine hosts. As the gene product bears no homology to known proteins, its biological significance remains enigmatic. To understand the gene function, we created isogenic bbd18-deletion mutants as well as genetically-complemented isolates from an infectious wild-type B. burgdorferi strain. Compared to parental isolates, bbd18 mutants - but not complemented spirochetes - displayed slower in vitro growth. The bbd18 mutants also reflect significantly reduced ability to persist or remain undetectable both in immunocompetent and SCID mice, yet were able to survive in ticks. This suggests BBD18 function is essential in mammalian hosts but redundant in the arthropod vector. Notably, although bbd18 expression and in vitro growth defects are restored in the complemented isolates, their phenotype is similar to the mutants - being unable to persist in mice but able to survive in ticks. Despite low expression in cultured wild-type B. burgdorferi, bbd18 deletion downregulated several genes. Interestingly, expression of some, including ospD and bbi39, could be complemented, while that of others could not be restored via bbd18 re-expression. Correspondingly, bbd18 mutants displayed altered production of several proteins, and similar to RNA levels, some were restored in the bbd18 complement and others not. To understand how bbd18 deletion results in apparently permanent and noncomplementable phenotypic defects, we sought to genetically disturb the DNA topology surrounding the bbd18 locus without deleting the gene. Spirochetes with an antibiotic cassette inserted downstream of the gene, between bbd17 and bbd18, were significantly attenuated in mice, while a similar upstream insertion, between bbd18 and bbd19, did not affect infectivity, suggesting that an unidentified cis element downstream of bbd18 may encode a virulence-associated factor critical for infection.

My Four Thousand Bibles

This collection exhibits the relationships between generations of mothers and daughters that are often frayed by misgivings about each others’ perspectives and situations. My Four Thousand Bibles is an emotive critique of ideologies that yield these generational problems, while it embraces the fluidity of spirit, being both intimate and echoing. The collection traces an arch of disquietude from a pressurized girlhood, which for the speaker bears the inevitable condition of guilt, unknowingness, and loving faith. Complemented by the records of her grandmother from poor Appalachia and by the challenges of love and partnership, the speaker’s understanding of herself and her position in time develops patience as an observer and participator in the world’s larger turning.

Essays on Financial Constraints, R&D Investments, and Competition

This dissertation consists of two chapters of theoretical studies that investigate the effect of financial constraints and market competition on research and development (R&D) investments. In the first chapter, I explore the impact of financial constraints on two different types of R&D investments. In the second chapter, I examine the impact of market competition on the relationship between financial constraints and R&D investments. In the first chapter, I develop a dynamic monopoly model to study a firm’s R&D strategy. Contrary to intuition, I show that a financially constrained firm may invest more aggressively in R&D projects than an unconstrained firm. Financial constraints introduce a risk that a firm may run out of money before its project bears fruit, which leads to involuntary termination on an otherwise positive-NPV project. For a company that relies on cash flow from assets in place to keep its R&D project alive, early success can be relatively important. I find that when the discovery process can be expedited by heavier investment (“accelerable” projects), a financially constrained company may find it optimal to “over”-invest in order to raise the probability of project survival. The over-investment will not happen if the project is only “scalable” (investment scales up payoffs). The model generates several testable implications regarding over-investment and project values. In the second chapter, I study the effects of competition on R&D investments in a duopoly framework. Using a homogeneous duopoly model where two unconstrained firms compete head to head in an R&D race, I find that competition has no effect on R&D investment if the project is not accelerable, and the competing firms are not constrained. In a heterogeneous duopoly model where a financially constrained firm competes against an unconstrained firm, I discover interesting strategic interactions that lead to preemption by the constrained firm in equilibrium. The unconstrained competitor responds to its constrained rival’s investment in an inverted-U shape fashion. When the constrained competitor has high cash flow risk, it accelerates the innovation in equilibrium, while the unconstrained firm invests less aggressively and waits for its rival to quit the race due to shortage of funds.