The welfare effects of property tax classification in an urban area: A general equilibrium computational approach

Thesis advisor: Donald RichterTaxing different classes of property at different effective rates is a widespread occurrence in the United States, even though the practice violates many state constitutions. For purposes of tax discrimination, urban real property is commonly divided according to the use to which the property is applied. Typically, the major property categories considered are residential and business, or residential, commercial, and industrial. This thesis investigates the structural and welfare effects of a change from a tax structure in an urban area that classifies property by use for tax purposes to one that does not discriminate in its treatment of property. To accomplish this, long run equilibrium models of urban spatial location are developed. In all models wage rates, and for one model output price of a composite commodity produced in the urban area, can vary in response to the change in tax policy. Conditions guaranteeing the existence of equilibrium for some of the models are developed, and proofs of the existence of equilibrium for those models are provided. Due to the analytical intractability of the models, the tax policy changes are simulated numerically through the use of a fixed point algorithm. The models are stylized, to the extent possible, to the Boston metropolitan area. In particular, the classification tax structure and parameterization of the functions of the model are chosen so that a resultant equilibrium resembles the Boston metropolitan area in or around 1980. General equilibrium versions of compensating and equivalent variations in income are used as measures of welfare change. The qualitative welfare results obtained are quite robust. In all of the simulations conducted there is a welfare gain in moving from the particular classification tax structure used to one in which all property is taxed at the same effective rate.Thesis (PhD) — Boston College, 1984.Submitted to: Boston College. Graduate School of Arts and Sciences.Discipline: Economics

Investigating investment in biopharmaceutical R&D

Recent studies have highlighted a reduction in projected financial returns associated with biopharmaceutical R&D, owing to decreased productivity, increases in costs and flattening revenue per new drug, prompting calls for dramatic revisions to R&D models. On the basis of previous financial modelling, the simplest hypothesis would be that new investment in such R&D should be minimal and focused on biologics in preference to small molecules, as the internal rate of return on investment for biologics projects has been reported to be higher (Nat. Rev. Drug Discov. 8, 609–610; 2009). We sought to discern how investors have been acting in recent years, and so examined investment trends in nascent public biopharmaceutical companies located in the United States by constructing a database of such companies that had US initial public offerings (IPOs) between 2010 and 2014 (see Supplementary information S1 (box) for details). We then analysed the characteristics of the 113 companies that met our inclusion criteria, including their corporate strategy and therapeutic modality focus. Here, we present the key findings from this analysis and discuss its implications based on our own financial modelling.United States. National Institutes of Health (NIANIH/R01AG043560

Recognition of the Major Histocompatibility Complex (MHC) class Ib molecule H2-Q10 by the natural killer cell receptor Ly49C

Murine natural killer (NK) cells are regulated by the interaction of Ly49 receptors with major histocompatibility complex class I molecules (MHC-I). Although the ligands for inhibitory Ly49 were considered to be restricted to classical MHC (MHC-Ia), we have shown that the non-classical MHC molecule (MHC-Ib) H2-M3 was a ligand for the inhibitory Ly49A. Here we establish that another MHC-Ib, H2-Q10, is a bona fide ligand for the inhibitory Ly49C receptor. H2-Q10 bound to Ly49C with a marginally lower affinity (∼5 μm) than that observed between Ly49C and MHC-Ia (H-2Kb/H-2Dd, both ∼1 μm), and this recognition could be prevented by cis interactions with H-2K in situ. To understand the molecular details underpinning Ly49·MHC-Ib recognition, we determined the crystal structures of H2-Q10 and Ly49C bound H2-Q10. Unliganded H2-Q10 adopted a classical MHC-I fold and possessed a peptide-binding groove that exhibited features similar to those found in MHC-Ia, explaining the diverse peptide binding repertoire of H2-Q10. Ly49C bound to H2-Q10 underneath the peptide binding platform to a region that encompassed residues from the α1, α2, and α3 domains, as well as the associated β2-microglobulin subunit. This docking mode was conserved with that previously observed for Ly49C·H-2Kb. Indeed, structure-guided mutation of Ly49C indicated that Ly49C·H2-Q10 and Ly49C·H-2Kb possess similar energetic footprints focused around residues located within the Ly49C β4-stand and L5 loop, which contact the underside of the peptide-binding platform floor. Our data provide a structural basis for Ly49·MHC-Ib recognition and demonstrate that MHC-Ib represent an extended family of ligands for Ly49 molecules