House Prices and Consumption

I study the consumption responses of heterogeneous households following changes in both house prices and interest rates. I show the common assumption that household period utility is separable in housing and consumption can be consistent with the observed co-movement between these two series only in the absence of housing transaction costs. When these costs are introduced into dynamic stochastic general equilibrium (DSGE) models characterized by separable preferences, consumption no longer increases after a rise in house prices. As it is well known, transaction costs are an important ingredient in house sales. I address this issue by developing a model that allows for non-separable preferences in housing and consumption alongside housing transaction costs. The results of my model closely match the aggregate data. Furthermore, it predicts that credit-constrained households will be substantially more responsive to changes in both house prices and interest rates than unconstrained households. Following a rise in house prices, consumption among constrained households increases by far more than the consumption of unconstrained households. Following a rise in interest rates, constrained households' consumption falls by more than that of unconstrained households. I trace this differing responsiveness in consumption to the house loan-to-value ratio of credit-constrained households. Higher loan-to-value ratios imply larger differences in their elasticity of response relative to unconstrained households. I also find that these differences widen with the degree of complementarity between housing and consumption. These predictions of my model are confirmed by household data from the Consumer Expenditure Surveys.DSGE, House Prices, Heterogeneous Households, Elasticity of Intra-Temporal Substitution (EIS), Complementarity, Credit

Klinische und molekulargenetische Charakterisierung von Patienten mit Kongenitalen Myasthenen Syndromen

Die kongenitalen myasthenen Syndrome (CMS) bilden klinisch und pathogenetisch eine heterogene Gruppe von relativ seltenen hereditären Erkrankungen des Kindesalters. Sie werden durch unterschiedliche genetische Defekte im Bereich der neuromuskulären Endplatte verursacht und manifestieren sich mit variabler Symptomatik, bei der eine belastungs- und tageszeitabhängige Muskelschwäche das herausragende Kennzeichen ist. Man unterscheidet synaptische, prä- und postsynaptische CMS-Formen. Während der letzten Jahre hat sich gezeigt, dass die postsynaptischen Störungen bei weitem überwiegen, vor allem solche, bei denen die Mutationen in den Untereinheiten des Azetylcholinrezeptor (AChR) liegen. Dabei haben sich vor allem Mutationen im Gen, das für die Epsilon (e) -Untereinheit des AChR kodiert, als besonders häufig erwiesen. Der Hauptschwerpunkt dieser Arbeit lag deshalb auf der genauen Untersuchung des Gens kodierend für die e-Untereinheit bei unseren CMS-Patienten. Im Rahmen dieser Arbeit wurden 86 CMS-Patienten aus 71 nicht-verwandten Familien mit Hilfe eines Fragebogens rekrutiert und anschließend molekulargenetisch untersucht. Unter den 71 CMS-Familien waren 21 Familien, die aus Deutschland stammten, und 50 Familien nicht-deutscher Abstammung. Alle Patienten zeigten typische CMS-Symptome. Die zwölf Exons des Gens der e-Untereinheit des AChR einschließlich der Spleiß-Donor- und Spleiß-Akzeptor-Sequenzen sowie die Promotorregion wurden sequenziert. Bei 40 der 86 CMS-Patienten wurden unterschiedliche Frameshift-Mutationen entdeckt, die zu einer verminderten Expression des AChR führen. Die Frameshift-Mutation e1267delG wurde bei 33 Patienten aus 26 nicht-verwandten Familien entdeckt. Alle e1267delG-Patienten stammen aus der Volksgruppe der Roma oder kommen aus südosteuropäischen Ländern. Die Mutation e1267delG wurde bei 58% (26/45) der CMS-Familien, die nicht-deutscher Abstammung sind, gefunden im Vergleich zu 0% (0/26) der Familien mit deutscher Abstammung. Bei sechs CMS-Patienten zeigten sich Spleiß-Mutationen, deren Pathogenität aus Muskel-RNA bewiesen wurde. Bei zwei Patienten konnten Promotormutationen nachgewiesen werden, die ebenfalls zu einer beeinträchtigten AChR-Expression führen. Bei sechs Patienten fanden sich Missense-Mutationen, die nicht vorbeschrieben sind und deren pathophysiologische Konsequenzen noch geklärt werden müssen. Bei 36 CMS-Patienten aus unserer 86 CMS-Patienten umfassenden Population konnten keine Mutationen im Gen der e-Untereinheit des AChR gefunden werden. Mutationen anderer Gene könnten verantwortlich sein für CMS bei diesen Patienten. Die Mutations-suche in diesen Genen könnte, zumindest in geeigneten Familien mit mehreren betroffenen und nicht betroffenen Mitgliedern, mittels begrenzter Kopplungsanalyse durch Ausschluss oder nähere Eingrenzung einzelner Genloci vereinfacht werden. Wir finden bei Patienten mit Mutationen im e-Gen des AChR häufiger eine Ptose, eine Ophthalmoparese, ein als generalisiertes oder als bulbär und fazial beschriebenes Krankheitsbild, ein Dekrement, einen gutartigen Verlauf, sowie eine Krankheits-manifestion vor Vollendung des zweiten Lebensjahres. Krisenhafte Verschlechterungen findet man dagegen häufiger bei CMS-Patienten, die keine Mutationen im e-Gen haben. Mutationen im CHAT-Gen könnten dafür verantwortlich sein. Da CMS durch verschiedene strukturelle oder funktionelle Abnormalitäten an der Synapse bedingt sind, ist eine präzise elektrophysiologische und/oder genetische Klassifikation der CMS wichtig für Patienten. Genetische Beratung und pränatale Diagnostik können nur durchgeführt werden, wenn eine exakte Diagnostik auf molekularer Ebene verfügbar ist. Außerdem hat die exakte Klassifizierung kongenitaler myasthener Syndrome für die betroffenen Patienten große Bedeutung, da sich daraus unterschiedliche Konsequenzen hinsichtlich Prognose, Vererbbarkeit und Behandlungs-möglichkeiten ergeben. Die Analyse ursächlicher genetischer Defekte wird die Grundlage für eine sichere und verlässliche Einordnung von CMS bilden und möglicherweise die bisher erforderlichen invasiven Verfahren ablösen. Darüber hinaus sind durch die genaue Kenntnis des ursächlichen Defektes und der patho-physiologischen Zusammenhänge in Zukunft auch neue Therapiemöglichkeiten für CMS-Patienten zu erwarten

House Prices and Consumption

I study the consumption responses of heterogeneous households following changes in both house prices and interest rates. I show the common assumption that household period utility is separable in housing and consumption can be consistent with the observed co-movement between these two series only in the absence of housing transaction costs. When these costs are introduced into dynamic stochastic general equilibrium (DSGE) models characterized by separable preferences, consumption no longer increases after a rise in house prices. As it is well known, transaction costs are an important ingredient in house sales. I address this issue by developing a model that allows for non-separable preferences in housing and consumption alongside housing transaction costs. The results of my model closely match the aggregate data. Furthermore, it predicts that credit-constrained households will be substantially more responsive to changes in both house prices and interest rates than unconstrained households. Following a rise in house prices, consumption among constrained households increases by far more than the consumption of unconstrained households. Following a rise in interest rates, constrained households' consumption falls by more than that of unconstrained households. I trace this differing responsiveness in consumption to the house loan-to-value ratio of credit-constrained households. Higher loan-to-value ratios imply larger differences in their elasticity of response relative to unconstrained households. I also find that these differences widen with the degree of complementarity between housing and consumption. These predictions of my model are confirmed by household data from the Consumer Expenditure Surveys

South Koreans' attitudes toward foreigners, minorities and multiculturalism

노트 : Paper prepared for presentation at the annual meeting of the American Sociological Association, Boston, MA from August 1-4, 2008

Defect structure of BZCYYb17 and theoretical behavior and performance of SOFC’s with BZCYYb17 electrolyte

In this work, maximum power density of SOFC with BZCYYb17(BaZr0.1Ce0.7Y0.1Yb0.1O3-d) electrolyte as the function of thickness was calculated by integrating partial conductivities of charge carriers under various DC bias conditions at a fixed oxygen chemical potential gradient at both sides of the electrolyte. The partial conductivities were calculated by fitting various total conductivities in diverse thermodynamic conditions (temperature, partial pressure of oxygen and partial pressure of vapor) using equations from defect model. From the fitting, not only we can get the partial conductivities as a function of temperature, oxygen partial pressure and hydrogen partial pressure but also mobility of each carriers and reaction constant of oxidation and hydration. Spatial distribution of oxygen chemical potential and hydrogen chemical potential across the electrolyte were calculated based on Choudhury and Patterson’s model by considering zero electrode polarization. At positive voltage conditions corresponding to SOFC and SOEC, the high conductivity region near n-type to p-type transition was expanded, but ad negative cell voltage conditions, the low conductivity region near n-type to p-type transition was expanded. The current- voltage characteristics in different conditions with temperature and thickness dependence were calculated with vapor partial pressure of each electrode is 0.03, oxygen partial pressure of the cathode 0.21 and hydrogen partial pressure of the anode 0.97

Evaluation of the high temperature solid Oxide cells using La0.1Sr0.9Co0.8Fe0.2O3-δ

The performance of the SOCs using La0.1Sr0.9Co0.8Fe0.2O3-δ (LSCF1982) was characterized by I-V measurement and electrochemical impedance spectroscopy (EIS). The distribution function of relaxation times of EIS was used to analyze the polarization resistance of the cells. The fitting was performed using the appropriate equivalent circuit through DRT analysis. Furthermore, we co-electrolyzed CO2 and H2O to obtain H2 / CO syngas as well as water splitting. The composition of syngas was investigated by gas chromatography and controlled by varying in-let gas composition

Effects of non-genetically and genetically modified organism (maize-soybean) diet on growth performance, nutrient digestibility, carcass weight, and meat quality of broiler chicken

Objective This study was conducted to compare growth performance, nutrient digestibility and meat quality of broilers fed a genetically modified organism (GMO) diet or a non-GMO diet. Methods A total of 840 broilers with an initial body weight of 43.03 g per chick were randomly allocated into 1 of the following 2 dietary treatments lasted for 32 days (15 broilers per pen with 28 replicates per treatment): i) Trt 1, GMO maize-soybean meal based diet; ii) Trt 2, non-GMO maize soybean meal based diet. Both diets were maize-soybean meal diets. The GMO qualitative analysis, proximate analysis and amino acid analysis of the feed ingredient samples were carried out. Diets were formulated based on a nutrient matrix derived from analysis results. Growth performance was measured on day 0, 7, 17, and 32. And all other response criteria were measured on day 32. Results The analysis results showed that the total Lys, Met, Thr of non-GMO grains were lower than that of GMO grains, the protein content of GMO soybean meal was higher than that of non-GMO soybean meal. Feed intake and feed conversion rate (FCR) were greater (p0.05). Conclusion These results indicated that non-GMO diet showed a negative effect on growth performance but nutrient digestibility, blood profile, carcass weight and meat quality were not affected by non-GMO diets