Mössbauer Effect studies of ferroelectric phase transitions in the PbZrO₃ - PbTiO₃ - BiFeO₃ ternary system

The Mössbauer Effect was used to measure the phase transitions in the following ferroelectric compounds: 95% PbZ4₀.₈Ti₀.₂ - 5% BiFeO₃ [and] 95% PbZ4₀.₇Ti₀.₃ - 5% BiFeO₃ and in the antiferroelectric compound: 95% PbZrO₃ - 5% BiFeO₃. The parameters obtained were the area under the resonance peak, the isomer shift, and the electric quadrupole splitting, all as a function of temperature. The ionicity, electric field gradient, and Debye temperature were determined for room temperature. The data are discussed in terms of the lattice vibration model of ferroelectrics and antiferroelectrics, and the structural phase transitions as recently defined for these compounds. The ionicity is determined and discussed in relation to crystal distortion and Curie temperature. The electric field gradient is related to the relative polarizations of the different samples. A discussion of the mixture of charge states on the A and B ion sites of the perovskite structure, and the oxygen defect problem in these compounds, completes the discussion --Abstract, page i

The 2007 HMDA data

Mortgage loans ; Bank loans

The 2006 HMDA data

Analyzes the 2006 data collected under the Home Mortgage Disclosure Act (HMDA). The review focuses primarily on the pricing information in the data. Includes an assessment of factors that account for the variation in rates of serious delinquency on mortgage loans across U.S. metropolitan area counties observed as of March 31, 2007, with information drawn from the HMDA data on the incidence of higher-priced lending and from credit scores by geographic area.Mortgage loans ; Bank loans

The 2009 HMDA data: the mortgage market in a time of low interest rates and economic distress

Mortgages ; Home Mortgage Disclosure Act

The 2008 HMDA data: the mortgage market during a turbulent year

The data that mortgage lending institutions reported for 2008 under the Home Mortgage Disclosure Act of 1975 (HMDA) reflect the ongoing difficulties in the housing and mortgage markets. This article presents a number of key findings from a review of the 2008 HMDA data. In particular, it documents a reduction in lending activity that was experienced by all groups of borrowers, highlights the Federal Housing Administration's greatly expanded role in the mortgage market, and examines how atypical changes in the interest rate environment affected the incidence of reported higher-priced lending in 2008 relative to earlier years.Mortgages ; Home Mortgage Disclosure Act

Ex-Th17 Foxp3+ T cells - a novel subset of Foxp3+ T cells induced in cancer

Th17 and regulatory T (Treg) cells are integral in maintaining immune homeostasis and Th17-Treg misbalance associates with inflammation.\ud \ud We demonstrate that in addition to natural (n)Treg and induced (i)Treg cells developed from naïve precursors, Th17 cells are a novel source of Foxp3+ cells by converting into ex-Th17 Foxp3+ cells, and this helps to reconcile the contradictory information about the relevance in particularly of Th17 subset in immune surveillance.\ud \ud We identified IL-17A+Foxp3+ double-positive and ex-IL-17-producing IL-17A-Foxp3+ T cells to be the underlying mechanism of immune regulation in mesenchymal stem cell-mediated prolonged allograft survival. Further, we identified accumulation of IL17A+Foxp3+ and ex-Th17 Foxp3+ cells in tumor bearing mice, indicating progressive direct Th17-into-Treg cell conversion as a novel phenomenon in cancer.\ud \ud Moreover, we determined the importance of the Th17 cell plasticity for tumor induction and/or progression in ROR-g-/- mice. Our data indicate that RORgt is required not only for Th17 development, but also for effective Treg cell induction. TGF-b1 induced Foxp3 expression was reduced in ROR-g -/- cells. Further, tumor bearing ROR-g-/- mice showed significantly less Foxp3+ Treg cells, but higher IFNg+ Tcells compared to wild type animals.\ud \ud Increased infiltration of IL17+ and FoxP3+ CD4+ T cells in the human ovarian cancer ascites, with the presence of a distinct IL17+FoxP3+ subset, and a significant correlation between tumor-associated Th17 and Treg cells demonstrates the existence of Th17-Foxp3+ T cell inter-relationship in cancer patients.\ud \ud Yin-yang of IL17+ and Foxp3+ is important principle for improved clinical approaches targeting responses against self, allo and/or neo-self

Synergistic Effects of Traffic-Related Air Pollution and Exposure to Violence on Urban Asthma Etiology

Background: Disproportionate life stress and consequent physiologic alteration (i.e., immune dysregulation) has been proposed as a major pathway linking socioeconomic position, environmental exposures, and health disparities. Asthma, for example, disproportionately affects lower-income urban communities, where air pollution and social stressors may be elevated. Objectives: We aimed to examine the role of exposure to violence (ETV), as a chronic stressor, in altering susceptibility to traffic-related air pollution in asthma etiology. Methods: We developed geographic information systems (GIS)–based models to retrospectively estimate residential exposures to traffic-related pollution for 413 children in a community-based pregnancy cohort, recruited in East Boston, Massachusetts, between 1987 and 1993, using monthly nitrogen dioxide measurements for 13 sites over 18 years. We merged pollution estimates with questionnaire data on lifetime ETV and examined the effects of both on childhood asthma etiology. Results: Correcting for potential confounders, we found an elevated risk of asthma with a 1-SD (4.3 ppb) increase in NO2 exposure solely among children with above-median ETV [odds ratio (OR) = 1.63; 95% confidence interval (CI), 1.14–2.33)]. Among children always living in the same community, with lesser exposure measurement error, this association was magnified (OR = 2.40; 95% CI, 1.48–3.88). Of multiple exposure periods, year-of-diagnosis NO$_2$ was most predictive of asthma outcomes. Conclusions: We found an association between traffic-related air pollution and asthma solely among urban children exposed to violence. Future studies should consider socially patterned susceptibility, common spatial distributions of social and physical environmental factors, and potential synergies among these. Prospective assessment of physical and social exposures may help determine causal pathways and critical exposure periods

Feedback modeling of non-esterified fatty acids in rats after nicotinic acid infusions

A feedback model was developed to describe the tolerance and oscillatory rebound seen in non-esterified fatty acid (NEFA) plasma concentrations following intravenous infusions of nicotinic acid (NiAc) to male Sprague-Dawley rats. NiAc was administered as an intravenous infusion over 30 min (0, 1, 5 or 20 μmol kg−1 of body weight) or over 300 min (0, 5, 10 or 51 μmol kg−1 of body weight), to healthy rats (n = 63), and serial arterial blood samples were taken for measurement of NiAc and NEFA plasma concentrations. Data were analyzed using nonlinear mixed effects modeling (NONMEM). The disposition of NiAc was described by a two-compartment model with endogenous turnover rate and two parallel capacity-limited elimination processes. The plasma concentration of NiAc was driving NEFA (R) turnover via an inhibitory drug-mechanism function acting on the formation of NEFA. The NEFA turnover was described by a feedback model with a moderator distributed over a series of transit compartments, where the first compartment (M1) inhibited the formation of R and the last compartment (MN) stimulated the loss of R. All processes regulating plasma NEFA concentrations were assumed to be captured by the moderator function. The potency, IC50, of NiAc was 45 nmol L−1, the fractional turnover rate kout was 0.41 L mmol−1 min−1 and the turnover rate of moderator ktol was 0.027 min−1. A lower physiological limit of NEFA was modeled as a NiAc-independent release (kcap) of NEFA into plasma and was estimated to 0.032 mmol L−1 min−1. This model can be used to provide information about factors that determine the time-course of NEFA response following different modes, rates and routes of administration of NiAc. The proposed model may also serve as a preclinical tool for analyzing and simulating drug-induced changes in plasma NEFA concentrations after treatment with NiAc or NiAc analogues