Spatial Econometric Approaches to Estimating Hedonic Property Value Models

The inclusion of spatial correlation of house price in hedonic pricing model may produce better marginal implicit price estimate(s) of the environmental variable(s) of interest. Most applications where a spatial econometric model is applied to the estimation of a hedonic property value model have used either a spatial lag model or a spatial autoregressive (SAR) error model. Incorrect spatial specification may produce even worse estimate outcome than OLS. Three issues regarding the specification of a spatial hedonic pricing model are considered. First, we question the "convention" of row-standardizing the spatial weights matrix. Second, we argue that the spatial error component (SEC) model is more theoretically intuitive and appealing for modeling house price. Third, we explore whether the choice of spatial model is important, empirically, using a large house sale dataset that includes measures of proximity to landfills. With one exception, estimated marginal implicit prices are fairly robust across all models.row-standardization, spatial econometrics, SEC model, SAR error model, spatial lag model, hedonic pricing, landfill, house price, Public Economics,

Joint vector magnetograph observations at BBSO, Huairou Station and Mees Solar Observatory

Joint vector magnetograph observations were carried out at Big Bear Solar Observatory (BBSO), Huairou Solar Observing Station (Huairou), and Mees Solar Observatory (MSO) in late September 1989. Comparisons of vector magnetograms obtained at the three stations show a high degree of consistency in the morphology of both longitudinal and transverse fields. Quantitative comparisons show the presence of noise, cross-talk between longitudinal field and transverse field, Faraday rotation and signal saturation effects in the magnetograms. We have tried to establish how the scatter in measurements from different instruments is apportioned between these sources of error

Analyzing the Binding of Co(II)-specific Inhibitors to the Methionyl Aminopeptidases from \u3cem\u3eEscherichia coli\u3c/em\u3e and \u3cem\u3ePyrococcus furiosus\u3c/em\u3e

Methionine aminopeptidases (MetAPs) represent a unique class of protease that is capable of the hydrolytic removal of an N-terminal methionine residue from nascent polypeptide chains. MetAPs are physiologically important enzymes; hence, there is considerable interest in developing inhibitors that can be used as antiangiogenic and antimicrobial agents. A detailed kinetic and spectroscopic study has been performed to probe the binding of a triazole-based inhibitor and a bestatin-based inhibitor to both Mn(II)- and Co(II)-loaded type-I (Escherichia coli) and type-II (Pyrococcus furiosus) MetAPs. Both inhibitors were found to be moderate competitive inhibitors. The triazole-type inhibitor was found to interact with both active-site metal ions, while the bestatin-type inhibitor was capable of switching its mode of binding depending on the metal in the active site and the type of MetAP enzyme

Investigation of the transient fuel preburner manifold and combustor

A computational fluid dynamics (CFD) model with finite rate reactions, FDNS, was developed to study the start transient of the Space Shuttle Main Engine (SSME) fuel preburner (FPB). FDNS is a time accurate, pressure based CFD code. An upwind scheme was employed for spatial discretization. The upwind scheme was based on second and fourth order central differencing with adaptive artificial dissipation. A state of the art two-equation k-epsilon (T) turbulence model was employed for the turbulence calculation. A Pade' Rational Solution (PARASOL) chemistry algorithm was coupled with the point implicit procedure. FDNS was benchmarked with three well documented experiments: a confined swirling coaxial jet, a non-reactive ramjet dump combustor, and a reactive ramjet dump combustor. Excellent comparisons were obtained for the benchmark cases. The code was then used to study the start transient of an axisymmetric SSME fuel preburner. Predicted transient operation of the preburner agrees well with experiment. Furthermore, it was also found that an appreciable amount of unburned oxygen entered the turbine stages

Chromosomal Distribution of Genes Conferring Tolerance to Abiotic Stresses Versus That of Genes Controlling Resistance to Biotic Stresses in Plants

Tolerance to abiotic stresses caused by environmental conditions can prevent yield loss in crops for sustaining agricultural productivity [1]. Resistance to biotic stresses caused by diseases and insects can prevent or reduce yield loss in crops [2]. For each crop or plant species, there are many abiotic threats, such as changes in temperature, soil salinity/alkalinity, water shortage, and soil contaminants, as well as biotic challenges from pathogens (bacteria, viruses, and fungi), insects, and nematodes. Plants need to possess genes conferring tolerance to these abiotic stresses to adapt to the changing environment, due to global climate changes, in which they are growing. Due to the coevolution of plants and stress-causing organisms [3], plants need to possess multiple resistance genes to deal with the rise of new virulence in stress-causing organisms. Plant breeders are constantly looking for new resistance genes to combat evolving organisms that pose a threat to susceptible crops. As a result, plant geneticists have identified many resistance genes in various crops, and molecular geneticists have developed molecular markers for most of those genes. Similarly, researchers are investigating plant mechanisms and underlying genetic systems involved in plant tolerance to abiotic stresses, hoping to breed crops resilient to adverse environmental conditions. With the advent of whole-genome sequencing in many important crops, it is time to map the detailed chromosomal locations of known genes that are involved in tolerance to various abiotic stresses as well as in the resistance to biotic stresses in important plant species. In the Special Issue, Mapping Abiotic Stress-Tolerance Genes in Plants of International Journal of Molecular Sciences, 21 papers, including two reviews and 19 research articles, were published [4–24]. Eleven research articles [3,25–34] were published in the Special Issue “Mapping Plant Genes that Confer Resistance to Biotic Stress.” In this editorial, I firstly express my appreciation to all authors for their contribution to the two Special Issues. Secondly, I will compare the chromosomal distribution patterns of genes for the two types of stresses that plants faced (Tables 1 and 2). The evidence obtained supports my long-held hypothesis that genes conferring resistance to biotic stresses are more likely to be located in the distal portion of chromosomes than the proximal portion in order to adapt to the host-pest coevolution. On the other hand, abiotic-stress tolerance genes should have a lower ratio of distal to proximal distribution than that for biotic stresses to maintain the stability of genes regulating plant growth and development. Knowing the relationship between gene functions and their chromosomal distribution patterns, plant breeders can select the most appropriate and efficient method to improve crops for withstanding stresses and ensuring productivity and food security

G protein-coupled receptor kinase-2 (GRK-2) regulates serotonin metabolism through the monoamine oxidase AMX-2 in Caenorhabditis elegans.

G protein-coupled receptors (GPCRs) regulate many animal behaviors. GPCR signaling is mediated by agonist-promoted interactions of GPCRs with heterotrimeric G proteins, GPCR kinases (GRKs), and arrestins. To further elucidate the role of GRKs in regulating GPCR-mediated behaviors, we utilized the genetic model system Caenorhabditis elegans Our studies demonstrate that grk-2 loss-of-function strains are egg laying-defective and contain low levels of serotonin (5-HT) and high levels of the 5-HT metabolite 5-hydroxyindole acetic acid (5-HIAA). The egg laying defect could be rescued by the expression of wild type but not by catalytically inactive grk-2 or by the selective expression of grk-2 in hermaphrodite-specific neurons. The addition of 5-HT or inhibition of 5-HT metabolism also rescued the egg laying defect. Furthermore, we demonstrate that AMX-2 is the primary monoamine oxidase that metabolizes 5-HT in C. elegans, and we also found that grk-2 loss-of-function strains have abnormally high levels of AMX-2 compared with wild-type nematodes. Interestingly, GRK-2 was also found to interact with and promote the phosphorylation of AMX-2. Additional studies reveal that 5-HIAA functions to inhibit egg laying in a manner dependent on the 5-HT receptor SER-1 and the G protein GOA-1. These results demonstrate that GRK-2 modulates 5-HT metabolism by regulating AMX-2 function and that 5-HIAA may function in the SER-1 signaling pathway

Spin-Fluctuation-Induced Non-Fermi-Liquid Behavior with suppressed superconductivity in LiFe1−x_{1-x}Cox_{x}As

A series of LiFe$_{1-x}$Co$_{x}$As compounds with different Co concentrations have been studied by transport, optical spectroscopy, angle-resolved photoemission spectroscopy and nuclear magnetic resonance. We observed a Fermi liquid to non-Fermi liquid to Fermi liquid (FL-NFL-FL) crossover alongside a monotonic suppression of the superconductivity with increasing Co content. In parallel to the FL-NFL-FL crossover, we found that both the low-energy spin fluctuations and Fermi surface nesting are enhanced and then diminished, strongly suggesting that the NFL behavior in LiFe$_{1-x}$Co$_{x}$As is induced by low-energy spin fluctuations which are very likely tuned by Fermi surface nesting. Our study reveals a unique phase diagram of LiFe$_{1-x}$Co$_{x}$As where the region of NFL is moved to the boundary of the superconducting phase, implying that they are probably governed by different mechanisms.Comment: 10 pages, 11 figure

Alternate cyclin D1 mRNA splicing modulates P27\u3csup\u3eKlP1\u3c/sup\u3e binding and cell migration

Cyclin D1 is an important cell cycle regulator but in cancer its overexpression also increases cellular migration mediated by p27KlP1 stabilization and RhoA inhibition. Recently, a common polymorphism at the exon 4-intron 4 boundary of the human cyclin D1 gene within a splice donor region was associated with an altered risk of developing cancer. Altered RNA splicing caused by this polymorphism gives rise to a variant cyclin D1 isoform termed cyclin D1b, which has the same N-terminus as the canonical cyclin D1a isoform but a distinct C-terminus. In this study we show that these different isoforms have unique properties with regard to the cellular migration function of cyclin D1. Whereas they displayed little difference in transcriptional co-repression assays on idealized reporter genes, microarray cDNA expression analysis revealed differential regulation of genes including those that influence cellular migration. Additionally, while cyclin D1a stabilized p27KIP1 and inhibited RhoA-induced ROCK kinase activity, promoting cellular migration, cyclin D1b failed to stabilize p27KIP1 or inhibit ROCK kinase activity and had no effect on migration. Our findings argue that alternate splicing is an important determinant of the function of cyclin D1 in cellular migration