Recent Developments in Quantitative Finance: An Overview

Quantitative finance combines mathematical finance, financial statistics, financial econometrics and empirical finance to provide a solid quantitative foundation for the analysis of financial issues. The purpose of this special issue on “Recent developments in quantitative finance” is to highlight some areas of research in which novel methods in quantitative finance have contributed significantly to the analysis of financial issues, specifically fast methods for large-scale non-elliptical portfolio optimization, the impact of acquisitions on new technology stocks: the Google-Motorola case, the effects of firm characteristics and recognition policy on employee stock options prices after controlling for self-selection, searching for landmines in equity markets, whether CEO incentive pay improves bank performance, using a quantile regression analysis of U.S. commercial banks, testing price pressure, information, feedback trading, and smoothing effects for energy exchange traded funds, actuarial implications of structural changes in El Niño-Southern Oscillation Index dynamics, credit spreads and bankruptcy information from options data, QMLE of a standard exponential ACD model: asymptotic distribution and residual correlation, and using two-part quantile regression to analyze how earnings shocks affect stock repurchases

Recent Developments in Quantitative Finance: An Overview

Quantitative finance combines mathematical finance, financial statistics, financial econometrics and empirical finance to provide a solid quantitative foundation for the analysis of financial issues. The purpose of this special issue on “Recent developments in quantitative finance” is to highlight some areas of research in which novel methods in quantitative finance have contributed significantly to the analysis of financial issues, specifically fast methods for large-scale non-elliptical portfolio optimization, the impact of acquisitions on new technology stocks: the Google-Motorola case, the effects of firm characteristics and recognition policy on employee stock options prices after controlling for self-selection, searching for landmines in equity markets, whether CEO incentive pay improves bank performance, using a quantile regression analysis of U.S. commercial banks, testing price pressure, information, feedback trading, and smoothing effects for energy exchange traded funds, actuarial implications of structural changes in El Niño-Southern Oscillation Index dynamics, credit spreads and bankruptcy information from options data, QMLE of a standard exponential ACD model: asymptotic distribution and residual correlation, and using two-part quantile regression to analyze how earnings shocks affect stock repurchases

The Enamel Phenotype in Homozygous Fam83h Truncation Mice

BackgroundTruncation FAM83H mutations cause human autosomal dominant hypocalcified amelogenesis imperfecta (ADHCAI), an inherited disorder characterized by severe hardness defects in dental enamel. No enamel defects were observed in Fam83h null mice suggesting that Fam83h truncation mice would better replicate human mutations.MethodsWe generated and characterized a mouse model (Fam83hTr/Tr) expressing a truncated FAM83H protein (amino acids 1â 296), which recapitulated the ADHCAIâ causing human FAM83H p.Tyr297* mutation.ResultsDay 14 and 7â week Fam83hTr/Tr molars exhibited rough enamel surfaces and slender cusps resulting from hypoplastic enamel defects. The lateral third of the Fam83hTr/Tr incisor enamel layer was thinner, with surface roughness and altered enamel rod orientation, suggesting disturbed enamel matrix secretion. Regular electron density in mandibular incisor enamel indicated normal enamel maturation. Only mildly increased posteruption attrition of Fam83hTr/Tr molar enamel was observed at 7â weeks. Histologically, the Fam83hTr/Tr enamel organ, including ameloblasts, and enamel matrices at sequential stages of amelogenesis exhibited comparable morphology without overt abnormalities, except irregular and less evident ameloblast Tomes’ processes in specific areas.ConclusionsConsidering Fam83hâ /â mice showed no enamel phenotype, while Fam83hTr/Tr (p.Tyr297*) mice displayed obvious enamel malformations, we conclude that FAM83H truncation mutations causing ADHCAI in humans disturb amelogenesis through a neomorphic mechanism, rather than haploinsufficiency.FAM83H truncation mutations cause inherited enamel malformations in humans. Previously we showed that no enamel malformations are observed in Fam83h null mice. Here we demonstrate that truncation of FAM83H in mice causes enamel malformations. This figure shows how the lateral incisor enamel (on the left) is thinner in the Fam83h truncation mouse than it is in wild-type.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/149571/1/mgg3724-sup-0004-DataS4.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/149571/2/mgg3724-sup-0003-DataS3.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/149571/3/mgg3724-sup-0001-DataS1.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/149571/4/mgg3724-sup-0002-DataS2.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/149571/5/mgg3724_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/149571/6/mgg3724.pd

Regioselectivity in the Ring Opening of Epoxides for the Synthesis of Aminocyclitols from D-(-)-Quinic Acid

[[abstract]]Efficient syntheses of four aminocyclitols are reported. Each synthesis is accomplished in eight steps starting from D-(-)-quinic acid. The key step involves a highly regioselective ring opening of epoxides by sodium azide.[[journaltype]]國外[[incitationindex]]SCI[[booktype]]電子版[[countrycodes]]CH

Critical roles for WDR72 in calcium transport and matrix protein removal during enamel maturation

Defects in WDR72 (WD repeat‐containing protein 72) cause autosomal recessive hypomaturation amelogenesis imperfecta. We generated and characterized Wdr72‐knockout/lacZ‐knockin mice to investigate the role of WDR72 in enamel formation. In all analyses, enamel formed by Wdr72 heterozygous mice was indistinguishable from wild‐type enamel. Without WDR72, enamel mineral density increased early during the maturation stage but soon arrested. The null enamel layer was only a tenth as hard as wild‐type enamel and underwent rapid attrition following eruption. Despite the failure to further mineralize enamel deposited during the secretory stage, ectopic mineral formed on the enamel surface and penetrated into the overlying soft tissue. While the proteins in the enamel matrix were successfully degraded, the digestion products remained inside the enamel. Interactome analysis of WDR72 protein revealed potential interactions with clathrin‐associated proteins and involvement in ameloblastic endocytosis. The maturation stage mandibular incisor enamel did not stain with methyl red, indicating that the enamel did not acidify beneath ruffle‐ended ameloblasts. Attachment of maturation ameloblasts to the enamel layer was weakened, and SLC24A4, a critical ameloblast calcium transporter, did not localize appropriately along the ameloblast distal membrane. Fewer blood vessels were observed in the papillary layer supporting ameloblasts. Specific WDR72 expression by maturation stage ameloblasts explained the observation that enamel thickness and rod decussation (established during the secretory stage) are normal in the Wdr72 null mice. We conclude that WDR72 serves critical functions specifically during the maturation stage of amelogenesis and is required for both protein removal and enamel mineralization.We generated knockout mice lacking the ability to make WDR72. Deletion of WDR72 caused retention of degraded enamel proteins within the mineral layer and significantly reduced mineralization. The null enamel layer was only a tenth as hard as wild‐type enamel and underwent rapid attrition following eruption. Attachment of maturation ameloblasts to the enamel layer was weakened, and SLC24A4, a critical ameloblast calcium transporter, did not localize appropriately along the ameloblast distal membrane. Interactome analysis of WDR72 protein revealed potential involvement in ameloblastic endocytosis.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/112233/1/mgg3143.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/112233/2/mgg3143-sup-0001-SuppInfo.pd